Puswhisperer Year Deux:

Another Year of Pus

Mark Crislip MD

edgydoc.com

Dedication

For Stephen R Jones MD

Chief of Medicine, Legacy Health.

My boss of 22 years whose enthusiasm and knowledge of medicine has always been an inspiration.

These are the collected essays from the second year (September 2009-2010) of my blog over at Medscape, Rubor, Dolor, Calor, Tumor.

I spent most of my professional life seeing acute infections in the hospital. These are some of the cases, details modified so that the patient cannot be identified, but the clinical particulars are exact.

Each entry as a goal: one case, one pearl (in medicine, a pearl is an important fact) and maybe one attempt at humor, your mileage will vary.

All the old typos, misspellings, and grammatical errors are fixed and entirely new ones inserted. An editor I am not.

Enjoy the whispers to the pus.

Thanks to Susan Yox over at Medscape who pretty much lets me run free with my prose.

Any Bug, Any time.

Sep 8, 2009

Any bug can cause any disease in any patient at any time. It is part of the allure of infectious diseases, and it is part of the aggravation. You never know what you are going to grow.

Common things are common, but this blog is more about uncommon things being uncommon.

Patient presents with a progressive sore throat. No risks, no trauma, just a 53 yo male a drinker and a smoker, who was out exercising when his throat becomes sore, then he had a fever, and then he was in the ER. Exam showed a red, swollen retropharynx, and the CT showed inflammation of the back of the throat, but no abscess or phlegmon (sounds so Jamaican. Where is the phelg, mon?) so much so he need intubation to protect his airway.

His WBC is also elevated, so he as a retropharyngeal cellulitis. Not yet abscess. Retropharyngeal cellulitis is usually a disease of children and usually due to a Streptococcus.

Imagine my surprise when the blood and aspiration of the back of the throat grew methicillin susceptible Staphylococcus aureus. S. aureus certainly causes abscesses in the neck, but Pubmed reveals a whopping 2 cases of S. aureus cellulitis of the retropharynx.

He isn't talking, due to the ET tube, but I assume he had some trauma. A bone perhaps, or a toothpick. I am most impressed with the damage a tortilla chip can do; they are edible ninja stars that can cut through an esophagus, especially if your mental status is altered and you are not chewing so well. I had one young guy, drunk on beer in a Mexican Restaurant, who had sudden chest pain eating his chips and he had lacerated his esophagus, leading to a whopping mediastinitis. Almost killed him. Those chips can be sharp.

Chew. Slowly. Carefully. Until you have a mouth full of mush. Only then is it safe to swallow.

POLL RESULTS

A Phelg is:

1. a farm animal. 3%

2. a fish. 11%

3. Miss Cleos star sign. 8%

4. one of Bob Marley’s children. 16%

5. a strain of ganja. 32%

6. Other Answers:

7. An outdoor public lavatory

8. a dyslexic phleg

9. phleg

Underdiagnosed?

Sep 12, 2009

There are clinical syndromes that I suspect are more common that we suspect, and I hope you do not find find this entry suspect.

Patient had a valve replacement complicated by a wound infection. Post op after the wound debridement there was a sudden change to a WBC of 35K climbing to 50k, renal failure, and hypotension requiring 4 pressors. That’s how old I am, I didn’t even know we HAD 4 pressors to use.

Exam has abdominal tenderness but no rebound, the rest of routine evaluation for infection is negative except her lactate also jumped.

50K for WBC is a leukemoid reaction and has a fairly narrow differential: miliary Tb, an abscess the size of my ego (my ego rivals Zaphod Beeblebrox in its breadth and depth) and something dead.

In this case, the something is probably bowel. Eventually a CT revealed thicken ilium and cecum and rectum, so the diagnosis is a confirmed as I can get since the patient is not going to the OR.

Why? I do not know. On possibility is late cholesterol emboli from the AVR. The other, and more likely, is the CT also demonstrated her vascular tree is filled with calcium. The relative hypotension of the anesthesia and sepsis led to a low flow state and ischemic/dead bowel.

I bet this occurs more often than we suspect in patients with hypotension. I not infrequently see patients who, after a prolonged episode of hypotension, have a leukocytosis and fever with no obvious source once the blood pressure normalizes. I have occasionally browbeat a GI doc into doing a quick colonic look see and there is often ischemic changes in the bowel. I wonder how often the post-op ileus we see is due to transient bowel ischemia. If you have bad enough coronary arteries to get a bypass, your mesenteric arteries are probably not in the best of health. Certainly, it is found in the open heart/pump patients if you go looking, but most of the time patients get better and who really wants a colonoscopy after a bypass? I don't even want one before.

Rationalization

Am J Med. 2006 Jun;119(6):527.e1-9.Characterization of ischemic colitis associated with myocardial infarction: an analysis of 23 patients. Cappell MS, Mahajan D, Kurupath V.

Poll Results

'Other' is included in poll questions to drive a funny response. I don't respond to 'other' as:

Humor does not belong in medicine. 0%

I am not funny. 12%

I have no sense of humor. 5%

You are funny enough for everyone. 39%

You are not half as funny as you think you are. 7%

Other Answers 37%

1. I'm just being annoyingly ironic.

2. You asked for it.

3. This is the Mark Crislip ™ Show. It's always best to ignore hecklers.

4. I was hoping for free beer

5. Heh.

6. I love funny!! I wear a funmeter it is always on high!!

7. a way to politely say "No comment" or I have no real opinion of my own.

In which I am tired and beat a metaphor to death, only to have it rise again.

Sep 14, 2009

Today I am beat. All day with H1N1 preparation meetings squeezed into patient care. This pandemic is already a major pain, and it hasn't even started yet.

Well, maybe. The CDC shows that since school started there is a big spike in flu-like illnesses. Crowd a bunch of vectors in classrooms all across the nation and, viola, flu. I was hoping that the flu would be kind enough to wait until the vaccine came out, but no such luck.

If we do not act soon, and we won’t and, due to a lack of vaccine, can't, it will spread fast in a susceptible population. Like zombies.

If there were a zombie outbreak, we will all be toast in no time.

"If the timescale of the outbreak increases, then the result is the doomsday scenario: an outbreak of zombies will result in the collapse of civilization, with every human infected, or dead," they wrote. "This is because human births and deaths will provide the undead with a limitless supply of new bodies to infect, resurrect and convert."

"How fast do we need to deal with the outbreak? Here's the equation they used, where S = susceptible, Z = zombies and R = removed. If an infection breaks out in a city of 500,000 people, the zombies will outnumber the susceptible in about three days."

Will quarantine work? Nope.

"In this case, the effect of quarantine is to slightly delay the time to eradication of humans."

Treatment? Under the assumption

"We are able to quickly produce a cure for ‘zombie-ism’. Our treatment would be able to allow the zombie individual to return to their human form again. Once human, however, the new human would again be susceptible to becoming a zombie; thus, our cure does not provide immunity. Those zombies who resurrected from the dead and who were given the cure were also able to return to life and live again as they did before entering the R class."

Under that assumption, "humans are not eradicated, but only exist in low numbers."

But that is our advantage over flu. We can induce immunity, which, due to antibody, is the equivalent to

"control (of) the zombie population by strategically destroying them at such times that our resources permit. It was assumed that it would be difficult to have the resources and coordination, so we would need to attack more than once, and with each attack, try and destroy more zombies."

Sounds like a flu vaccination program, and with good results: all zombies are gone.

"An outbreak of zombies infecting humans is likely to be disastrous unless extremely aggressive tactics are employed against the undead. While aggressive quarantine may eradicate the infection, this is unlikely to happen in practice. A cure would only result in some humans surviving the outbreak, although they will still coexist with zombies. Only sufficiently frequent attacks, with increasing force, will result in eradication, assuming the available resources can be mustered in time.”

Zombie? HIV? Influenza? Any real difference? Disease spread is disease spread, be it from being bitten by the undead, sex, coughing, sex or, worst case, all three.

At least I read World War Z and the Zombie Survival Guide. I will survive. Will you?

Rationalization

http://www.mathstat.uottawa.ca/~rsmith/Zombies.pdf

http://www.wired.com/wiredscience/2009/08/zombies/

Poll Results

I worry most about

Kuru from a zombie. 12%

Hepatitis C from a vampire. 21%

Chillblaines from a ghost. 3%

Rabies from a werewolf. 0%

Tomato stains from the Flying Spagetti Monster. 52%

Other Answers. 12%

1. Black lung from Santa Claus

2. Being eaten last by Cthulhu

3. consults from a homeopath.

Nothing to see Here, Keep Moving

Sep 16, 2009

Work is slow. Between the economy and the end of summer, people are not coming into the hospital. Thanks to the aggressive use of hand hygiene and best practice bundles, hospital-acquired infections are at an all-time low. And flu season has yet to start.

Problem is that my practice depends to the random bad luck of others and that bad luck can be decreased by simple things like hand-washing.

There was one clinical pearl today that I have never seen published.

The majority of cellulitis is due to streptococci. Patients get a red, hot tender leg with fevers and chills. Everyone knows what cellulitis looks like. In a subset of patients that have cellulitis, the first symptom is groin pain on the affected side. It can occur a few hours before on the onset of the rubor, dolor, calor, tumor and I think is due to inguinal lymphadenitis.

I did a Pubmed the other day and I cannot find a report that this is a manifestation of Group A strep cellulitis. So I want it to be called Crislip's sign.

I assume that someone will correct me and point me to a reference. And if there is a bored resident out there, it might be a good topic for a review. Just give me first author. I ask for so little.

Hopefully, someone will have real bad luck and I will have something to write about. But at least I have lots of time for H1N1 planning.

Poll Results

Crislip's sign is

Inguinal lymphadenitis with group A strep. 40%

Broken glove on exam. 8%

Hyper self esteem 23%

Constipation of the brain and diarrhea of the mouth. 13%

Has no vaccine to prevent it. Bummer. 15%

Other Answers 2%

1. Reflexive gripping of a conference room chair with hands and gluteal muscles in response to an urge to leap up and strangle another committee member.

A Rash of Vampires

Sep 18, 2009

I give a lot of doxycycline. Most of the MRSA is susceptible in my neck of the woods and it is better tolerated than tmp-sulfa.

And the nice thing about my wattle of the woods is that I do not have to worry much about some of the side effects of the medications, or so I thought.

One side effect is photosensitivity. The sun acts with the doxy to produce a real bad sunburn, and I have yet to see a case, for the obvious reason I live in Oregon. If there were rain sensitivity, now that would be a problem. I always warn patients to use the sun block if they are out in the direct sun.

I have a patient on long doxycycline for chronic osteo who had a big dose of sun and developed a severe sunburn when he forgot to use his sunblock. However, he continues to get blisters that are both itchy and painful in sun-exposed areas, and are flaking like psoriasis.

It doesn’t look like a drug rash.

I think its porphyria cutanea tarda (PCT), and it may have been set off by the doxycycline. There is a case where it is thought that doxycycline was a trigger for developing PCT.

Last century I had an AIDS patient with the disease who developed PCT late in the disease, perhaps because

"HIV infection may impair the hepatic cytochrome oxidase system, which could lead to an aberration in porphyrin metabolism and subsequently cause porphyria."

I remember the dermatologist telling me the diagnosis with a glee filled, isn’t it obvious tone of voice, so I am keen to not miss another case. I strive to avoid the scorn of my colleagues.

Keeping with our theme of the undead, it has been suggested that PCT is the origin of the vampire myth. This is mostly based on the sun sensitivity of both PCT sufferers and vampires. To quote the Wikipedia,

"Porphyria has been suggested as an explanation for the origin of vampire and werewolf legends, based upon certain perceived similarities between the condition and the folklore.

In January 1964, L. Illis' 1963 paper, "On Porphyria and the Aetiology of Werwolves," was published in Proceedings of the Royal Society of Medicine. Later, Nancy Garden argued for a connection between porphyria and the vampire belief in her 1973 book, Vampires. In 1985, biochemist David Dolphin's paper for the American Association for the Advancement of Science, "Porphyria, Vampires, and Werewolves: The Aetiology of European Metamorphosis Legends," gained widespread media coverage, thus popularizing the connection.

The theory has since faced heavy criticism, especially for the stigma it has placed on its sufferers. Norine Dresser's American Vampires: Fans, Victims, Practitioners (1989) treats the matter with more depth.

The theory also operates on a highly flawed premise, mainly in regard to a perceived harmful effect sunlight had on vampires."

I do not buy it as after repeated viewings of Buffy the Vampire Slayer (aka best show of all time), I never saw a vamp with a skin condition on the hands. Just the forehead.

Rationalization

http://www.medicinenet.com/script/main/art.asp?articlekey=51292

Hong Kong Med J. 2001 Jun;7(2):197-200. Porphyria cutanea tarda and melioidosis. Fung WK, Tam SC, Ho KM, Lam P, Lo KK.

Clin Infect Dis. 1995 Feb;20(2):348-51. Human immunodeficiency virus infection and porphyria cutanea tarda: coexistence of risk factors or causative association? McAlister F, McClean K, Hamilton PG, Houston S.

A Classic Association

Sep 22, 2009

Lady in her 60s with chronic arm lymphedema after a radical lymph node dissection for cancer.

She has the sudden onset of rubor, dolor, calor, tumor (there are those words yet again) and is admitted to the hospital for cellulitis.

While most signs and symptoms improve, the arm is slow to resolve the rubor and tumor.

I suggest ...

Patience.

In the old days every female with breast cancer (and, I suppose, the occasional male) had a radical mastectomy and lymph node dissection. They all had refractory lymphedema and recurrent infections, always with Group A strep.

It is unusual with the decline in lymph node dissections and the residents and medical students seem to be unaware of the association.

And it is slow to get better, especially if the arm in not kept raised like you are riding a subway. I presume that the arm is filled with the corpses of all the group A strep, and the poor outflow of the lymph prevents the dead bugs from being removed, perpetuating the erythema longer than normal. Or I could be writing out my ass, but I do not think so.

Like so much of medicine, practice has changed. Fewer patients get node dissections, and so fewer go on to get edema with recurrent infections.

So many of the changes in medicine that are for the better seem to result in fewer infections. Not a good thing, from my narrow, selfish, perspective. I wonder if this is a conspiracy of the left? Fox news needs to look into it.

Rationalization

Dermatol Online J. 2005 Dec 1;11(3):12. Erysipelas after breast cancer treatment (26 cases). Masmoudi A, Maaloul I, Turki H, Elloumi Y, Marrekchi S, Bouassida S, Ben Jemaa M, Zahaf A.

The M-I-C is K-E-Y

Sep 24, 2009

How am I going to work in the mouse? I saw Modest Mouse earlier in the week, but it does not fit into the theme. So let’s move on while I mull it over.

Almost a quarter of a century into ID and I am still flabbergasted as to the rapidity with which S. aureus can cause extensive disease. My specialty really should be called "let’s see if you can kill Staphylococcus."

The answer is increasingly no.

The patient is a homeless IVDA with 48 hours of an abscess in her axilla. She denies injecting in the armpit, is seen in the ER and put on TMP/Sulfa, but gets much worse as an outpatient, so is admitted with increasing chest wall pain and erythema.

She is thin, malnourished by both exam and labs. The axillary abscess is I&D'd and she is started on vancomycin. Over the next 48 hours, the infection progresses to cover her entire flank. CT shows a one huge abscess from the clavicle to the pelvis and into the buttock. Her chest wall is one big abscess. The cultures grow MRSA, resistant to TMP/Sulfa and the MIC to vancomycin is 1.5.

That's elevated. It's the M.I.C that is K.E.Y. to treating the M.R.U.S.A. But the U doesn't work. Most MRSA are the USA 300 strain, but most would not know that. Too obscure. So close yet so far. Back to MRSA.

As the MIC to vancomycin increases, the success rate for the treatment declines, maybe even for an MIC of >= 1.5, but especially if the MIC is >=2. That, combined with the horrible pharmacokinetics of vancomycin and a nutritionally bankrupt patient, ensures that failure is expected with the treatment with vancomycin.

I bet that this beast makes the Panton-Valentine leukocidin, a protein that dissolves human tissue like water on Elphaba. Unfortunately, the organism is resistant to clindamycin as well so no inhibiting protein synthesis for this organism.

What do give? Surgery. Nothing heals like cold steel. My current bias is daptomycin, but that is a bias. As best I can tell from the literature, all the agents for the treatment of MRSA are equally lousy. I await the new anti MRSA cephalosporins with impatience; I so want to kill S. aureus again.

Rationalization

Antimicrob Agents Chemother. 2008 Sep;52(9):3315-20. Epub 2008 Jun 30 Relationship between vancomycin MIC and failure among patients with methicillin-resistant Staphylococcus aureus bacteremia treated with vancomycin. Lodise TP, Graves J, Evans A, Graffunder E, Helmecke M, Lomaestro BM, Stellrecht K

Oh No

Sep 26, 2009

I am all about the cure. That’s what is nice about ID. Most of the time antibiotics will cure the infection and where antibiotics fail you often have surgery as a backup. One way or the other or perhaps both, I will get rid of the infection.

My old partner (Hey, Ray) used to say that people who got S. aureus infections for no reason did particularly worse with the organism. Needle users and chronically ill patients, he hypothesized, have, due to constant exposure, antibodies that help control the infection. Staph, while serious, is somewhat less aggressive as a result. If you do not have protective antibodies, when you get Staph, it rips right through you. I wonder if that is true.

Twice I have had patients with unknown bicuspid valves who have seeded the valve from a festering splinter. Neither had prior exposure to staph and the infection chewed the valve up in record time.

I recently had a patient with MSSA of a bicuspid valve who developed an aneurysm, but had the valve replaced and did well. At first.

It is traditional to continue antibiotics for 4 to 6 weeks after valve replacement to prevent the new valve from being infected. What and how long? Not known. Does it work? Not known. It seems to. In my experience I have had maybe 2 or three reinfections I can remember, but the three most dangerous words in medicine are "In my experience."

As we neared the end of the therapy, the WBC did not go down and the heart became more hyperdynamic. Repeat TEE showed a ring abscess and another aneurysm.

Crap. What causes the sinking feeling when you realize that something, despite doing everything right, may have gone horribly wrong?

"THE SINKING FEELING, OR THE "HOLLOW IN THE PIT OF THE stomach," is a widely prevalent phenomenon. Feldman (1969) regarded it as universal. It emerges in association with remembering and reality testing and has therapeutic significance. There are no specific references to it in the psychoanalytic literature.

In this paper, I offer a description of the sinking feeling, report clinical observations, suggest some of its determinants, and outline its potential usefulness in psychoanalytic therapy.

The sinking feeling is typically located low or deep in the abdomen, although some persons, both men and women, sense it in the chest or mediastinum. The location is not variable in the same person. The duration of the experience is brief, at most 10 seconds. The feeling is regarded as unpleasant, but is differentiated from pain, anxiety, or fear. An acute transitory depression best describes the feeling. "Oh no" seems to be a frequent verbal association, without specific referent."

Gee, thanks. But why? I can't find the physiology of the response that transient sense of dread and horror I associate with unexpected complications or, back in the day, asking a girl out for the first time.

Fortunately, I work with great surgeons. He went to the OR and had another reconstruction and was doing well when I left work. And he will get another long course of antibiotics.

Rationalization

http://www.pep-web.org/document.php?id=PSC.039.0321A

J Thorac Cardiovasc Surg. 2009 Feb;137(2):326-33. Epub 2008 Oct 23. Predictors of recurrence and reoperation for prosthetic valve endocarditis after valve replacement surgery for native valve endocarditis. Fedoruk LM, Jamieson WR, Ling H, Macnab JS, Germann E, Karim SS, Lichtenstein SV.

Ann Thorac Surg. 2000 May;69(5):1448-54. Surgery for active culture-positive endocarditis: determinants of early and late outcome. Alexiou C, Langley SM, Stafford H, Lowes JA, Livesey SA, Monro JL.

POLL RESULTS

I respond to unexpected complications at work with

that sinking feeling. 58%

crying. 0%

vomiting. 3%

passing out. 0%

What are you talking about? I don’t have complications. It is the fault of someone else. 35%

Other Answers 3%

1. Engaging my colleagues in a discussion of the issue usually creates confusion and side-discussions, which ease my dread of being the only clueless one.

More than Zits

Sep 28, 2009

Not the comic strip, although with a 16 yo at home, I find that particular comic strip especially funny of late.

55 yo male with back surgery and has a month of slowly increasing pain, but no fever, chills, sweats or other inflammatory sighs or symptoms. MRI shows discitis and a fluid collection.

CBC is normal, CRAP (C ReActive Protein) is elevated. Rain is wet. Fire is hot.

Post op wound infection. Thanks to the SCIP protocols, I do not get to see many of these. So off to the ER. Thin pus is found, gram stain negative and at three days’ cultures are negative.

What's it gonna be?

Heavy growth of an anaerobic gram-positive rod that is usually resistant to metronidazole grows at day five. Yes, you guessed it. P. acnes.

Despite its Stridex inducing name, P. acnes is not just for acne anymore. It grows in the base of hair follicles, especially greasy hair follicles, so it is more common in men and more common in craniotomy infections. I am becoming increasingly resistant to cranial infections.

Thing about P. acnes is that if you hold the cultures longer (up to two weeks) you will find it in prosthetic joint infections and catheter infections. Most of the time we don't look. And this organism really seems to not incite much of an immune response and can fester for years. My record is a craniotomy infection that manifested 8 years after the tumor was removed, and that duration is not unusual.

Look for P. acnes, it is probably there more than you suspect, especially if the cultures are negative in the first two days.

Treatment? I tend to use clindamycin over penicillin, as in my experience it is better, so you know I am talking out my butt, although there are no head to head trials.` Squeezing in front of a mirror doesn't work as well.

Rationalization

J Infect. 2008 Apr;56(4):257-60. Epub 2008 Mar 12. Propionibacterium acnes is a common colonizer of intravascular catheters.

Clin Infect Dis. 2008 Jun 15;46(12):1884-6. Propionibacterium acnes postoperative shoulder arthritis: an emerging clinical entity.

Cold Flusion

Sep 29, 2009

This is a quick entry to allow me to have a little spleen venting. And I am cross-posting this over at SBM.

Background for you youngsters. In 1989 two electrochemists Martin Fleischmann and Stanley Pons, announced they had successfully developed cold fusion: nuclear fusion at room temperature. Pons was chairman of the chemistry department at the University of Utah at the time and lent a fair amount of respectability to the announcement.

A great deal of brouhaha followed, but in the end "is heard no more: it is a tale Told by an idiot, full of sound and fury, Signifying nothing." Cold fusion was and is a bust, although millions were spent in pursuit of that pot of gold.

Fast forward to this week. Here is the data upon which important public health decisions are being made, in its entirety:

"new Canadian study — which has not yet been peer reviewed or published —that found those who receive the seasonal flu vaccine become two times more likely to get H1N1."

That is all I can find as of 8:15 on 9/29/9. Interesting but we do not have the data, the methodology, confirmatory data from similar or other populations.

There is some biologic plausibility for this effect. The flu vaccine or infection can increase the uptake of unrelated influenza strains into cells that have an Fc receptor.

So maybe it’s true. I don't know. No one knows. Yet. It is almost, but not quite, an unsubstantiated rumor, and it is not known if it is clinically relevant.

Evidently, the Canadians have decided to stop vaccination with seasonal flu as a result of that information. That’s it. And that makes little sense.

First, you have already have a population of people who already have had either the vaccine or influenza year after year after year after year. So everyone should already be at risk from this phenomenon, if real, from either having had influenza or the vaccine. They should already have the evil antibody, either from disease or vaccine. Please note. No one had had THIS year’s seasonal flu vaccine before the H1N1 hit. Its PRIOR years vaccines that may have led to this phenomenon. Stopping this year’s vaccination should be too little too late.

All that should happen by discontinuing the vaccination this year is denying protection from the seasonal flu but not preventing slight increased risk for H1N1. Instead they should go on to get seasonal flu, have an increased risk of dying as a result, and in the end have 'natural' antibody from disease that should increase the risk for H1N1 anyway.

Unless I am missing something (and I often am), it would appear stopping seasonal flu vaccination is a decision that should have no upside in preventing H1N1 but should increase morbidity and mortality from seasonal flu.

It just does not seem rational to stop the vaccination program on so little information and with the knowledge that if the effect is real, it is from prior years vaccinations. The horse is out of the barn. All that should happen is increasing the risk of seasonal flu and death without decreasing the risk of H1N1.

And in the end what I bet will happen is rather than getting two vaccines late, people will get no vaccines at all and flu will cut loose in Canada.

And that is assuming that this study is the real deal and will be reproduced and is clinically relevant. Or it all may be cold flusion.

Addendum.

I have been perseverating on this since I posted it last night. It occurs to me that the phenomena, if real and due to antibody, should not be one way. If prior exposure to the seasonal flu or the vaccine increases risk for H1N1, then H1N1 vaccine or disease should increase risk for seasonal flu. That leads to the following possibilities:

1) You have had flu or the vaccine in the past. You have the increased risk already. There is no data that the current vaccine will increase the preexisting risk and all you will do is be at risk for seasonal flu when it hits. Might as well get the vaccine for seasonal then get H1N1 vaccine when available.

2) You have never had the vaccine or the disease.

You avoid all vaccines. But you do not avoid the flu.

a) You get seasonal flu, then increase your risk for H1N1, and then you develop H1N1. So you get flu twice in a year.

b) You get H1N1, then increase your risk for seasonal flu, and then you develop seasonal flu. So you get flu twice in a year.

By avoiding the vaccine, you increase the risk of getting the disease twice.

So if you get the seasonal vaccine, you decrease the risk of seasonal influenza, but either way you slightly increase your risk for H1N1.

3) You avoid the vaccines and get lucky and avoid seasonal flu and H1N1. For this season. One day you will get flu unless you are a full-time lighthouse keeper. Then you are there with the rest of us.

Some clever person can run the numbers and calculate the relative risk of seasonal and H1N1 flu with each behavior. As best I can tell, the best bet is to get vaccinated, it is the best way to decrease your risk for getting ill.

Rationalization

J Infect Dis. 1994 Jan;169(1):200-3. Primary influenza A virus infection induces cross-reactive antibodies that enhance uptake of virus into Fc receptor-bearing cells. Gotoff R, Tamura M, Janus J, Thompson J, Wright P, Ennis FA.

Holding a Grudge

Oct 1, 2009

I can hold a grudge for a long time. Usually against those that produce standardized tests for the purpose of demonstrating competence in medicine. They always have a few questions I can't answer and I realize the answer after I have turned in the test.

Example to follow.

I saw a patient today with whopping cellulitis. What, exactly, is a cellulitis? Hepatitis is inflammation of the hepatic, pneumonitis is inflammation of pneumo (lung). But where is my celluli?

Anyway, she had erythema from foot to mid thigh that was exquisitely painful and she had a WBC of 34K. She was slow to get better on vancomycin and had an abscess that was I&D'd and grew Streptococcus agalactiae. So I changed her to ampicillin and I expect she will now get better.

The other name of this organism is Group B streptococcus. Now I knew all about group B streptococcus as an intern, but when I took the boards at the end of my internship they had a bunch of questions about S. agalactiae, which I had never, ever heard of. Could they be bothered to put Group B strep in parentheses after the entry? NOOOOooooooo. Expletives deleted. So I missed the question. 30 years and I am still bitter.

Group B strep is usually seen in two groups: invasive disease in recently pregnant females and their new offspring. Mom and/or baby get bacteremic at the time of delivery.

But it also occurs in older diabetics (and others with bad underlying medical problems), such as this patient. A Pubmed search reveals a smattering of reports in the adult of group B in the adult human, and there is a case in a brown cow (how? now?) and a bottle-nosed dolphin.

"Skin and soft tissues are the most common sites of focal group B streptococcal infections in adults, accounting for more than one third of infections in some reports. Cellulitis, foot ulcers, abscess, and infection of decubitus ulcers are common manifestations...Less common manifestations of skin and soft tissue infections are pyomyositis, blistering dactylitis, and necrotizing fasciitis, on occasion associated with toxic shock-like syndrome....Abscess formation was observed in 46% of these infections. Group B streptococcus was the only organism isolated from 71% of patients with an abscess. Appropriate drainage and parenteral antimicrobial therapy effected complete recovery in 89% of these patients."

I have to wonder what happened to the 11% that did not respond to therapy.

Nice thing about Strep is I can still kill it with some ampicillin. So kill it I will. I am still concerned about the extreme pain, but so far no sign of a nec fasc and it was not seen at the I&D. Hopefully tincture of time will take care of it. Does time come in a tincture? Or is it come as a suspension or a solution? A tincture is an alcoholic extract, so I suppose so. Alcohol has extracted some of my time, that’s for sure.

Rationalization

J S Afr Vet Assoc. 2009 Mar;80(1):17-22. Trends in udder health and emerging mastitogenic pathogens in South African dairy herds. Petzer IM, Karzis J, Watermeyer JC, van der Schans TJ, van Reenen R.

Loose (Stool) Associations

Oct 3, 2009

Recently the spouse of a colleague said that ID docs were all about lists. We carry in our minds lists of diseases and organisms and, in a Pavlovian response, generate a list of possibilities for any given sign or symptom.

Kind of true. I am all about associations. We ID docs do not have to reason from physiology, like a pulmonologist. Or a cardiologist. We ID docs have to have knowledge, often picayune knowledge, that also allows us to dominate in the game of Trivial Pursuit.

Say cat bite and I say Pasturella. Say salt water, I say Vibrio. Say toe-may-toe, I most certainly do not say toe-mah-toe, nor have I ever said po-tah-toe.

I get a call from one of the hospitalists after I had left the hospital last Friday.

So I have this patient with bad diarrhea (as, I suppose, to be contrasted with the good diarrhea) and the cultures of the stool are negative. But he has a gram negative in his blood and they are calling it Salmonella.

It happens.

And he has an aneurysm in his femoral artery. Any association?

Que the dramatic prairie dog.

Of course there is an association.

Salmonella loves to infect the clot of aneurysms. It is more common in abdominal aneurysms, but there are reports of involvement of the femoral artery as well. I have seen a few cases in my years in practice, so it does really happen.

The treatment, besides antibiotics, is resection of the mycotic aneurysm. Medical therapy? Not so much. When I got back after the weekend both the patient and the hospitalist were gone and I never found out what happened. Maybe it was just a dream...

Rationalization

Angiologia. 1993 Nov-Dec;45(6):210-3. [A ruptured mycotic aneurysm of the femoral artery due to Salmonella typhimurium] Calvo Cascallo J, Mundi Salvadó N, Cardona Fontanet M.

J Vasc Surg. 2009 Jan;49(1):66-70. Epub 2008 Oct 11. Selective medical treatment of infected aneurysms of the aorta in high-risk patients.,Hsu RB, Chang CI, Wu IH, Lin FY.

Fleas and Lice

Oct 5, 2009

I am on Occam kind of guy. One of my go to rules is Occam s razor: entia non sunt multiplicanda praeter necessitatem (Latin, translated as "entities must not be multiplied beyond necessity" But then, you knew that.)

Clinically it is usually used to suggest that all the patients admitting complaints should be understood by one underlying diagnosis. Of course, it’s nice in theory, but all too often the patients prefer to follow "Hickam's dictum, the counterargument to the use of Occam's razor in the medical profession." It states that the patient can have as many diagnoses as she damn well pleases. Like this patient.

Diabetic female presents with multiple red hot, swollen, painful joints. It is not unusual for a diabetic to have a septic knee, shoulder, ankle and wrist, and the tap of the joints grew MSSA. No surprise there. Polyarticular septic arthritis, while uncommon is not uncommon, if you know what I mean. I expected a group B streptococcus, but S. aureus was a distant second on the list. Blood cultures grew the same bug, so, despite a negative ECHO, she is going to be treated for endocarditis.

But.

All the joints have gout crystals in them. Lots of gout crystals. She had never had gout before. So which came first, the gout or the arthritis? Certainly, gouty joints are a fertile soil in which to grow bacteria. Until this case most of the infected gouty joints I have seen occurred after the joint was injected. Shhh. Don't tell anyone that.

The literature suggests it is the gout that comes first and that all gouty joints should be sent for culture. I have the opposite problem in that all septic appearing joints are not sent for crystals.

But sometimes it is Hickam who rules.

Tomorrow I get to spend the day do my certification exam, so tomorrow night I will give you all the answers.

Rationalization

Rheumatology (Oxford). 2003 Sep;42(9):1062-6. Epub 2003 Apr 16.Concomitant septic and gouty arthritis--an analysis of 30 cases. Yu KH, Luo SF, Liou LB, Wu YJ, Tsai WP, Chen JY, Ho HH.

Recertification

Oct 6, 2009

No cool cases or interesting references. I had to spend the day taking my ID recertification exam. I always do it with bitterness, as in 1989 I skipped taking the boards to write what would be an unfunded NIH grant, but if I had taken it I would have been grandfathered in. Assuming I passed. Crap.

The test was all on the computer; the age of the number 2 pencil and filling in the ovals is a thing of the past. Now, along with typewriters, dial phones, and no cable TV, I have more topics with which to bore the kids. I remember back in the day we had four function calculators and were happy to get them. My youngest, BTW, has TI 89 graphic calculator for school and he spends his time learning how to turn the numbers into upside down words. 7734 lives. The more things change.

Lots of security as well: multiple proofs of ID, fingerprinting, photographs. Unfortunately, the nano chips in my head could not be removed. I expect next time there will be polygraphs and body cavity searches. I can't wait.

What is interesting with the boards is the disconnect from the practice of ID and the testing of ID. I know tons of stuff about ID. There is also tons of stuff I do not bother to put in my brain as I can find it when I want it. The right answer for a lot of the questions should have been Google it or Pubmed it. So much knowledge these days is online and doesn’t need to be carried around in the brain. What you need to know is when to look it up.

So here are the answers from the ID recert: a bunch of a's, a smattering of b's, one c, a whole lot of d's and e's and, oddly, one m.

Glad that is over for 10 years. Just one more before I retire. Or die.

Poll Results

My favorite answer is:

a) 12% (5)

b) 15% (6)

c) 15% (6)

d) 17% (7)

e) 12% (5)

Other Answers 29% (12)

1. b or c

2. all of the above

3. all of the above

4. Go ask your mom. Or All of the above.

5. none of the above

6. Other

Top Ramosus

Oct 7, 2009

Work is so much nicer than taking a multiple-choice computer test.

A consult today was a neutropenic who had been admitted with fever. Common problem with a fairly standardized approach.

The blood cultures grew a gram-positive rod in the anaerobe bottle.

Hmmm. Anaerobes in the blood are not that common in the neutropenic, for reasons that I have never understood, especially given the predominance of anaerobes in the GI tract. Probably the oxygen in the blood. Keeps the anaerobes from growing well.

Turns out to be Clostridium ramosum.

Do you need to worry? I don't know. Maybe. Clostridium in the blood are almost binary in the their disease. Either it is nothing or the patient is in multiple organ system failure and rapidly dying. Very little in between.

C. ramosum can behave like C. perfringins or C. septicum. These cause overwhelming sepsis, often with severe hemolysis, in neutropenics, esp. in patients with either bowel cancer or lymphoma. The hypothesis is that the dead cancer from chemotherapy gives the organism a toe hold, and from there it spreads to cause almost certain death. I often say that these diseases are like falling out of an airplane without a parachute. Survival is rare. I did see one patient who had C. septium sepsis after chemo for lymphoma, refused antibiotics and survived.

I saw one C. ramosum years ago in the blood of a post-partum female and she was doing fine; it is part of normal vaginal flora and was a transient bacteremia in due to the trauma of delivery.

There are just a smattering of C. ramosum reports in the literature. A abscess here, a gas gangrene there. There is one interesting report to show this organism was found in high numbers in the gut of a strict vegetarian. I knew meat was good for me.

The patient today is, all things considered, doing fine. No focal complaints, nothing of note on exam. The chemo probably damaged the gut so the bug could slip in with the neutropenia, and due to underlying lung disease, the patient runs a lower than normal pO2. Everything conspired to let an anaerobe cause a bacteremia. So while the C. ramosum is a real bacteremia, it appears to be an unimportant bacteremia. In this patient. This time.

Rationalization

Med Oncol. 2002;19(4):267-72. A study of bacteremia in febrile neutropenic patients at a tertiary-care hospital with special reference to anaerobes. Mathur P, Chaudhry R, Kumar L, Kapil A, Dhawan B.

Microbiol Immunol. 2002;46(12):819-31. Fecal microbial diversity in a strict vegetarian as determined by molecular analysis and cultivation. Hayashi H, Sakamoto M, Benno Y.

Who is that masked man?

Oct 9, 2009

Not every (any?) title can be a gem.

First, some self-aggrandizement. There is a post of mine over at sciencebasedmedicine.org on influenza vaccine efficacy. It is excellent, but I expect nothing less from me.

Consults have been slow for the month of September and the hospitals have taken leave of their census, down for the last 8 weeks. ID, being the canary in the coal mine of hospitalizations, gets real slow, real fast. But I have influenza to keep me occupied.

Wednesday I spent the morning taking the cart around one of my hospitals giving influenza vaccines, both seasonal and H1N1, to all who wanted to decrease their chance of getting the flu. I did this last year as well, and I highly recommend it, especially for ID docs. It really brings home the message that you think the vaccine is important. You get to do a lot of teaching and answer questions. For those who are on the fence, I am careful not to say that they have to get the shot, and that they can think about the information and get back to us when they want to get the vaccine.

The person I feel sorry for is the nurse who helped me and who had to listen to the same lame jokes told over and over for three hours. She defines long suffering.

If you keep an eye on Google flu trends or the ER, you know that influenza is kicking into full gear and it is all H1N1. And we are running low on masks already. Do masks make a difference in influenza protection?

Maybe. In a JAMA study this week, surgical masks were just as good as N95 masks for preventing influenza. 23% (ow, that’s a lot) in each group done went and got the flu. This is contrasted to a report at ICCAC out of China where 25% of N95 users developed flu, but 46% of the surgical mask users developed flu. I will take a published study over a meeting poster any day. The 23% failure rate really suggests that the vaccine is going to be needed sooner rather than later if you want to avoid flu.

Since you may not be able to find a mask in the near future, perhaps you can stock up on Hanes 100% cotton T-shirts. There are instructions over at EID on how to make your own. And they probably will help, especially when combined with basic handwashing, etc. Me? I'm going to hold my breath. The blue color of my skin will match my eyes.

Rationalization

JAMA. 2009 Nov 4;302(17):1865-71. Epub 2009 Oct 1. Surgical mask vs N95 respirator for preventing influenza among health care workers: a randomized trial Loeb M, Dafoe N, Mahony J, John M, Sarabia A, Glavin V, Webby R, Smieja M, Earn DJ, Chong S, Webb A, Walter SD.

Simple Respiratory Mask Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 12, No. 6, June 2006 1033

PLoS One. 2008 Jul 9;3(7):e2618.Professional and home-made face masks reduce exposure to respiratory infections among the general population. van der Sande M, Teunis P, Sabel R.

POLL RESULTS

My primary defense against acquiring influenza will be

Washing my hands like Lady MacBeth. 51% (18)

Not inhaling like President Clinton. 14% (5)

Isolating myself like Howard Hughs. 11% (4)

Lie about my age to get the H1N1 flumist (http://en.wikipedia.org/wiki/Age_fabrication). 11% (4)

Use the bra/gas mask hybrid (see last reference). 9% (3)

Other Answers 3% (1)

1. Get vaccinated w/H1N1 injectable vaccine

What's in a name? A rose by any other name would smell as sweet.

Oct 11, 2009

Elderly patient comes in with urosepsis and on CT is found of have a pyelonephritis and obstruction of the ureter from a kidney stone.

Common clinical problem, the treatment is antibiotics and remove the obstruction. Usually it is E. coli or Proteus and the attending doesn't bother to call me. Occasionally more problematic organisms will rear their ugly head.

Candida parapsilosis as one example from earlier in the year. That was a tough one. Fluconazole doesn't get into the urine, C. parapsilosis is (relatively) resistant to fluconazole. Ampho is notoriously problematic when the creatinine is increasing from sepsis. We got away with a short course of ampho followed by high dose fluconazole.

This week the blood and the urine are growing an alpha hemolytic streptococcus.

In the old days, I would get the occasional call that the patient has S. viridans, not otherwise speciated, growing in significant amounts in the urine of the elderly. What do you make of it?

I always said that any bug can cause an infection in the urine, why not an alpha strep? The lab would not, as a rule, identify these organisms further. There was no need to. Now, thanks to the miracle of modern microbiologic advances, they can and do.

This patient had Aerococcus urinae in the blood and urine. Sometimes you know the origin of an organism from its name. In this case, it is found in the air, hence the name Aerococcus. Really.

"Aerococci are widely distributed and occur naturally in air, dust and vegetation; they also form part of the flora of meat-curing brines."

Other Aerococci are pathogenic in lobsters, where it causes gaffkemia, or red tail disease, with considerable mortality in captive populations. Now do you ever learn anything like that in the other blogs? No. They only bother with PRACTICAL information.

Oh, it’s also found in the urine, hence that last name. Here I thought I was named after a guy named urinae. They are different than most strep in that they form tetrads. There are about 40 references on Pubmed, with a smattering of cases of endocarditis and metastatic infections.

It is easily enough to kill with a penicillin, so I did. Take home? If the lab says there is a viridans strep in the urine, ask if it’s an Aerococcus. And avoid the lobsters with the red tails. Hey. Don't they all have red tails?

Rationalization

J Gen Microbiol. 1992 Feb;138(2):401-5. Phylogenetic analysis of some Aerococcus-like organisms from urinary tract infections: description of Aerococcus urinae sp. nov. Aguirre M, Collins MD.

Diagn Microbiol Infect Dis. 2005 Dec;53(4):289-92. Epub 2005 Nov 2. Clinical significance of Aerococcus urinae: a retrospective review. Sierra-Hoffman M, Watkins K, Jinadatha C, Fader R, Carpenter JL.

The oldest 730.27. Ever.

Oct 13, 2009

Last night I was watching the Discovery Channel special on Ardipithecus ramidus, the 4.4-million-year-old hominid fossil found in Ethiopia.

Ardi, as they call her, had many interesting features: small brains, grasping feet, bipedal, lived in a forest, and had small canine teeth. The skeleton suggests the chimp is not a direct ancestor of humans, but the divergence of the two species occurred earlier than supposed. The skeleton rewrote the understanding of early human evolution, although they never say with what font.

The most interesting feature was mentioned in passing. The creature had "infection of the left proximal ray 5 pedal phalanx."

4.4-million-year-old osteomyelitis of the foot. Presumably from a penetrating injury as this species predated footwear by a few million years.

I wonder if it was a S. aureus, or its evolutionary precursor, or some environmental organism picked up from grasping a pointy stick with the foot. I doubt it was a diabetic foot infection. Humans have had infections for as long as we have been a species.

Mummies have had evidence of both tubercular and bacterial osteomyelitis, but that is a mere several thousand-year-old. There is one skull, 500,000 years old that may have had tuberculosis meningitis. There has been leprosy found in a 4,000-year-old skeleton.

They have found fossilized human poo containing Enterobius vermicularis that is 7837 years old. No T.P. survived.

There may be a 1.2 million year old case of Brucella of the spine, although I cannot tell from the report why they think it is Brucella. It was spine osteo, and while a common manifestation of Brucella, it is also a common manifestation of Staphylococcus. And I suppose it was a proto-Brucella.

We sort of know when humans started wearing clothes thanks to lice. This bit of information is based on the fact that the human body louse appears to have diverged into two species about 100,000 years ago, one of which needs clothes to perpetuate. So it would appear that humans have been wearing clothes, which were infested with lice, for about 100,000 years.

Footwear came later, based on anatomical changes, perhaps in the middle to upper paleolithic, about 10 to 40,000 thousand years ago, presumptively with a decrease in osteomyelitis of the foot.

When the earliest ID doctor was, I cannot find. But it is oddly reassuring to think the focus of my professional life is as old as humanity.

Rationalization

Science 2 October 2009: Vol. 326 no. 5949 pp. 64, 75-86 Ardipithecus ramidus and the Paleobiology of Early Hominids Tim D. White1,*, Berhane Asfaw2, Yonas Beyene3, Yohannes Haile-Selassie4, C. Owen Lovejoy5, Gen Suwa6, Giday WoldeGabriel7

POLL RESULTS

The first human infection probably was

Postpartum tetanus. 16% (10)

influenza. 5% (3)

dental abscess. 42% (26)

Gonorrhea. 16% (10)

Salmonella gastroenteritis. 11% (7)

Other Answers 10% (6)

1. impossible to tell.

2. foot osteomyelitis

3. osteomyelitis

4. Another Viral entity

Ignorance with grace and style

Oct 15, 2009

Often I get asked to do a consult with a question that has no answer, at least not an answer that I can get without doing the patient some serious harm. Part of my job is to provide an answer based on my best bet, with not a lot of good data to back me up. To be a consultant is to learn how to be ignorant with grace and style (yes, yes, yes, I know. I am ignorant, but lack grace and style. I got that from the Dumb Ass post. Let’s move on, shall we?).

The patient is elderly, with liver failure. And COPD. And diabetes. And on steroids. And on a ventilator for the last two weeks recovering from a gram-negative pneumonia. And I had a fever. Just one. As they often do in the ICU for no apparent reason. With a normal white count.

A fever work up is done and the sputum, on day 2, has light growth Aspergillus.

Is it real? Should we treat it? Inquiring referral docs want to know.

Last century I would have said ignore it. It’s a contaminant. But now, I am not so certain.

Aspergillus is occasionally a pathogen in the ICU. Risk factors include liver failure and steroid use. Patients who are septic will follow their inflammatory response with a subsequent anti-inflammatory state that increases the risk for infection, and sepsis can cause the CD4 counts to plummet, increasing risk for infections like invasive Aspergillus.

So treat the Aspergillus? SHAZAM! No wisdom on Solomon. Darn. So I have to make the decisions with the wisdom of Mark, nothing if not potentially flawed. Is it better, initially to treat a disease that may not be there or not treat a disease that may be there?

Initially I treated with po voriconazole, and ordered a CT of the chest and a galactomannan assay.

CT shows patchy infiltrates but no consolidation/necrotic pneumonia and the galactomannan assay is pending. Clinically the patient is improving sooner than I would expect due to the voriconazole. The patient probably does not have invasive Aspergillus, so I am close to stopping the voriconazole after a short course.

My very first consult 20 years ago was an alcoholic with end-stage liver disease and refractory pneumonia who died the day after of my consult (remember association is not causation). Autopsy showed Aspergillus in the lung and in the heart. Not that anything I could have done would have altered the course, but one likes to make these diagnoses premortum.

Is the Aspergillus real? Short of an autopsy I can't say definitively. Does he need therapy? And if so, how long? Are lots of risks for diseases reason enough to continue therapy? I don't know. There are times when my pronouncements are a definitive as the 10 commandments, and sometimes it’s just my opinion. This falls into the latter.

I have to have an answer, and so I will provide one with grace and style.

Rationalization

Intensive Care Med. 2007 Oct;33(10):1694-703. Epub 2007 Jul 24. Management of invasive pulmonary aspergillosis in non-neutropenic critically ill patients. Trof RJ, Beishuizen A, Debets-Ossenkopp YJ, Girbes AR, Groeneveld AB.

J Crit Care. 2006 Dec;21(4):322-7.Click here to read Links Isolation of Aspergillus in critically ill patients: a potential marker of poor outcome. Khasawneh F, Mohamad T, Moughrabieh MK, Lai Z, Ager J, Soubani AO.

The Eyes Have It and It Gives Me the Creeps

Oct 17, 2009

The patient was minding their own business, going on with their ADL's, when, bam, it felt like they were punched in the eye. Over the next 24 yours the pain in the eye became unbearable and vision went to zero.

No past medical history, no trauma, no festering infections or dental work. No prior symptoms of any kind in the weeks leading up to the eye pain.

Ophthalmology found an endophthalmitis, which was tapped and grew Streptococcus mitis.

S. mitis? That’s a viridans strep. Hematogenous endophthalmitis (the ophthalmologists call it endogenous endophthalmitis; exogenous is from penetrating trauma) with S. mitis suggests endocarditis, but all blood cultures before antibiotics are negative.

What I am left with is a spontaneous eyeball infection from S. mitis. Three cases in the literature, two with a reason (endocarditis and line infection).

Pubmed also fails to reveal much in the way of spontaneous endophthalmitis, people have reasons to get their eye ball infected, and even then it is rare.

I can remember two other cases of eye ball infections in 25 years. One was S. pneumoniae from pneumonia, the eye spontaneously perforated. I cringe all these years later. There is something about the eye ball and infections that gives me the willies. The other was last year with both eyes being seeded from S. aureus endocarditis. Candida likes to cause fungus balls in the back of the eye, but rarely causes a vitreous infection and loss of vision.

Of course, every time you floss, every time you brush, there is a wee bit o' bacteremia, so this is probably due to dental hygiene and really really really bad luck. You are probably more likely to win the lottery than to have this occur.

Hmmmm. And endophthalmitis from mitis. They are spelled the same. That’s why it happened. Sympathetic magic. Works for the homeopaths.

Rationalization

Am J Ophthalmol. 1997 Feb;123(2):260-1. Endogenous endophthalmitis caused by Streptococcus mitis. Harrison SA, Bateman JB.

Eye. 2009 Apr;23(4):945-56. Epub 2008 Jul 4.Microbiological profile of culture-proven cases of exogenous and endogenous endophthalmitis: a 10-year retrospective study. Ramakrishnan R, Bharathi MJ, Shivkumar C, Mittal S, Meenakshi R, Khadeer MA, Avasthi A.

J Clin Periodontol. 2009 Apr;36(4):323-32. Epub 2009 Mar 11. Bacteraemia due to dental flossing. Crasta K, Daly CG, Mitchell D, Curtis B, Stewart D, Heitz-Mayfield LJ.

Unhealthy lifestyle

Oct 19, 2009

I lack a lifestyle. I have a life and I live it. Others, it appears, do have a lifestyle, and it involves intravenous drugs. And, to be daring and edgy, I am going to suggest that a lifestyle that involves intravenous drugs is not one that provides optimal health. There. I said it. Let the opprobrium begin.

The problem is that drugs have to be mixed into some sort of fluid before injection, and sterile water is not high on the list.

Tap water is the most frequently used, and tap water, while certainly clean, is not sterile. I have had patients use toilet water, water from the Culligan man, Willamette river water, puddle water and their own spit to dissolve their drugs. Ick.

The patient this week is a long-standing IVDA I have seen on and off for years with injection-related infections. She is slowing being consumed by her drugs and the subsequent malnutrition and other abuses that are hand maidens to addiction. It is sad to watch someone waste their life to heroin.

This time she is in with fevers and chills and grows two different gram-negative rods: Chryseobacterium and Delftia acidovorans. The first I have the heard of, it grows in water and decomposing organic material. The second? Not so much. It used to be called Comamonas. Does that help you? Not me.

It’s a gram-negative rod found in water, and there is a distinct paucity of clinical cases associated with this organism. Like two, one of which was an IVDA who got it from shooting up with tap water. Sound familiar?

I find it interesting the other things bacteria can do beside kill people. Delftia is also used to take excess nitrogen out of waste water. And it is found in the drinking water of the Space Station. And they are found in bee larvae.

Bee season is over (where do they go in the winter?) and she has not been in the space station or working in a sewage treatment plant, so I suppose it was from the tap water.

A little po ciprofloxicin and she is all better. But you can bet I am not going to let a bee crap on my food.

Rationalization

American Journal of Infectious Diseases / April, 2005 Delftia acidovorans bacteremia in an intravenous drug abuser

J Environ Sci (China). 2006;18(3):525-9. High nitrogen removal from wastewater with several new aerobic bacteria isolated from diverse ecosystems. Ping L, De-Li L, Nahimana L, Chen SL, Yang X, Zhao L.

Environ Microbiol. 2006 Feb;8(2):258-72. Diversity and phylotype consistency of bacteria in the guts of three bee species (Apoidea) at an oilseed rape field. Mohr KI, Tebbe CC.

Habitation (Elmsford). 2004;10(1):39-48. Evidence of pathogenic microbes in the International Space Station drinking water: reason for concern? La Duc MT, Sumner R, Pierson D, Venkat P, Venkateswaran K. Collaborators (1)

What does the Inky Dinky Do?

Oct 21, 2009

More of the same

When I was an intern, tattoos were not a fashion statement, but a sure sign of sociopathy. Not so much anymore, where everyone but me has a tat.

But sometimes, well, tats may be a sign that the individual with them is not necessarily going to be a model patient. Love and hate on opposite hands are a good tip off as are tats on the face, like a tear in the corner of the eye. Do NOT date anyone with a tattoo of a tear.

Patient today, with a prior aortic valve replacement for endocarditis from IVDA, is back with IVDA and MRSA in all the blood cultures.

TEE is negative for ring abscess, the tattoos are interesting, and the MRSA is only susceptible to vancomycin and the patient has a well-documented adverse reaction to vancomycin.

What to do?

I don't know. I think it’s time to fall back on the old ID stand by: wishful magical thinking. There is a grand total of one case of prosthetic valve IE treated with daptomycin and they were, surprisingly, successful.

Should I go with a higher dose of the daptomyin? No clinical trials with endocarditis, much less prosthetic valve endocarditis, just animal models and a few ventricular assist device infections. High dose daptomycin seems to be the trick of the day, and it appears to be as safe as 6 mg/kg/d. They always test these drugs on infections like cellulitis, where anything will probably work. When it comes to the real infections, where you really need a good study to guide therapy, I get nothing.

I think I will go with wishful magical thinking and give higher dose daptomycin, 8 mg/kg/d, although as he gets better he is getting ready to leave AMA and refusing antibiotics. It’s the power of the tattoos. They are destiny.

Rationalization

Heart Lung. 2005 Jan-Feb;34(1):69-71. Methicillin-resistant Staphylococcus aureus prosthetic aortic valve endocarditis with paravalvular abscess treated with daptomycin. Mohan SS, McDermott BP, Cunha BA.

Antimicrob Agents Chemother. 2009 Oct;53(10):4252-7. Epub 2009 Jul 27. Efficacy of high doses of daptomycin versus alternative therapies against experimental foreign-body infection by methicillin-resistant Staphylococcus aureus. Murillo O, Garrigós C, Pachón ME, Euba G, Verdaguer R, Cabellos C, Cabo J, Gudiol F, Ariza J.

Clin Infect Dis. 2009 Jul 15;49(2):177-80. Safety of high-dose intravenous daptomycin treatment: three-year cumulative experience in a clinical program. Figueroa DA, Mangini E, Amodio-Groton M, Vardianos B, Melchert A, Fana C, Wehbeh W, Urban CM, Segal-Maurer S.

POLL RESULTS

That tattoo that gives me pause is

1. anything in the small of the back. 7% (8)

2. faux Chinese symbols. 5% (6)

3. homemade of any kind. 20% (24)

4. the fake tear in the corner of the eye. 25% (30)

5. a bar code on the forehead. 40% (48)

6. Other Answers 3% (3)

7. Home-made tats on the face, or anything on the genitalia.

8. all tattoos

9. all of the above

A Perfect Storm

Oct 24, 2009

H1N1 is taking off big time and to judge from the CDC site and Google flu trends, the great Pacific Northwest is the epicenter of H1N1 activity. Whether due to increased testing or increased cases, we have more H1N1 than anyone.

Lucky us.

Oddly, the pandemic has not affected my clinical work all that much. Most cases are mild, outpatient diseases and do not reach the level of an ID evaluation. The hospital is manned and womanned by extremely good hospitalists and intensivists who don't break a sweat at a mere H1N1. So the only thing I seem to be needed for is meetings.

Lucky me.

Not entirely true. I do get to see the odd cases.

Staff, er I mean staph, pneumonia comes in three flavors. Figuratively speaking. I have never tasted a pneumonia.

One is hematogenous/septic embolic from right-sided endocarditis. Blood cultures are positive and the CXR shows multiple round peripheral infiltrates that cavitate.

The second is lobar pneumonia, usually seen in ventilated patients, and has, well, a lobar consolidation.

These are hard enough to treat, but the third type is the worst: post-influenza pneumonia with MRSA. This is the anti-Hannah Montana pneumonia, with the worst of both worlds. These patients get multiple lobar cavitating/necrotizing consolidations.

I have a case this week of post-influenza MRSA pneumonia. First a viral syndrome, then the MRSA marches down the airway into all the lobes, eating lung as it goes. Many of the MRSA make the Panton Valentine leukocidin, a protein that is to human tissues that water is to Elphaba. "I'm melting! Melting! Oh what a world, what a world! Who would have thought a good little girl like you could destroy my beautiful wickedness!?"

And, of course, as I have mentioned many times, all our antibiotics for MRSA stink on ice.

We may have a perfect storm, a once in a century confluence of a widespread virulent MRSA and a huge population of humans (at least 60 % in the US) susceptible to a rapidly spreading influenza. Put them together, shake, and you have an almost untreatable pneumonia. The few I have seen before this pandemic have been fatal.

In children the deaths are often due to, or perhaps contributed to, by bacterial superinfection.

"Among the 53 deaths in children, 32 children had specimens collected for bacterial culture from normally sterile sites and seven (21.9%) of the 32 were positive; Staphylococcus aureus was identified in five (71.4%) of the seven children. One S. aureus isolate was sensitive to methicillin, three were methicillin resistant, and one did not have sensitivity testing performed."

And we are just at the beginning of the pandemic. I expect more infections like this. It is the kind of work I really do not want.

Rationalization

J Thorac Imaging. 2008 Feb;23(1):13-9. Community-acquired methicillin-resistant Staphylococcus aureus pneumonia: radiographic and computed tomography findings. Nguyen ET, Kanne JP, Hoang LM, Reynolds S, Dhingra V, Bryce E, Müller NL.

POLL RESULTS

I imagine pneumonia tastes like

1. Unicorn tears. 5% (2)

2. Iron tinged rotten hamburger. 39% (15)

3. Brussel sprouts. 11% (4)

4. Vomit. The thought makes me vomit. Man, can't you come up with a better question. Jeeze 18% (7)

5. Teen spirit. 21% (8)

6. Other answers 5% (2)

7. Victory.

Read the Book

Oct 25, 2009

First patient is a new kidney transplant with slowly progressive hypoxia over two weeks despite azithromycin, on no PJP prophylaxis, a CXR that shows a slight patchy lower lobe infiltrate but the CT shows diffuse, patchy, multi-lobar involvement with tree in bud pattern. Cough is nonproductive and the patient is totally nontoxic on exam. Labs are normal except for an LDH of 300.

The second patient has 6 months of chronic cough, bilateral infiltrates, but no hypoxia. LDH is 225. She has been on no immunosuppressants for the last 6 months, although she had been on prednisone for an acute case of gout about six months ago around the onset of her cough.

First patient I thought for sure had PJP. He didn't. His bronch grew out heavy growth of a very resistant S. pneumoniae and once a quinolone was started he rapidly improved.

The second I thought for sure had aspiration or perhaps MAI. The bronch had lots of PJP.

I really wish patients would read the text book before coming to the hospital. The first patient was clinically NOT a bacterial pneumonia and that’s what he had.

The second had no reason for PJP and that’s what she had. She subsequently had a full work up looking for a reason for PJP and nothing was found. Just prednisone 6 months ago.

The first had a subacute, perhaps partially treated, bacterial pneumonia and the second had an opportunistic infection with no opportunity. Sigh. That’s not what the textbooks say these diseases behave like.

What is "tree in bud" you ask. Is it celebrating arbor day with a beer? Nope. It is

"...peripheral (within approximately 3–5 mm of the pleural surface), small (2–4 mm in diameter), centrilobular, and well-defined nodules of soft-tissue attenuation are connected to linear, branching opacities that have more than one contiguous branching site, thus resembling a tree in bud"

"The tree-in-bud pattern represents bronchiolar luminal impaction with mucus, pus, or fluid, which demarcates the normally invisible branching course of the peripheral airways. In addition, dilated and thickened walls of the peripheral airways and peribronchiolar inflammation can contribute to the visibility of affected bronchioles. In histopathologic studies, the tree-in-bud appearance correlates well with the presence of plugging of the small airways with mucus, pus, or fluid; dilated bronchioles; bronchiolar wall thickening; and peribronchiolar inflammation."

"Similarly, bronchogenic dissemination of atypical mycobacterial organisms or pyogenic bacteria can result in tree-in-bud opacities. Less frequently, the tree-in-bud sign is seen with viral and fungal infections and" can be a sign of PJP.

Except when it isn't.

Rationalization

Radiology. 2002 Mar;222(3):771-2. The tree-in-bud sign. Eisenhuber E.

I ain't never heard of that bug before, no how.

Oct 28, 2009

I have a patient with a long-term port for fluids and electrolytes. She has fevers and a deep, bone cold. Her white cells are low (not an uncommon early reaction to acute sepsis) and she is admitted for antibiotics and evaluation.

Usually line infections are due to various staphylococci, but a 1.5 days her blood is growing gram-negative rods.

OK. Happens. In my neck of the woods that is usually and Enterobacter or a Pseudomonas, so she is placed on a big gun, powerful, strong, super-duper, antibiotic of steel pending cultures.

And she grows Ralstonia paucula.

WTH! (See, I know the interweb/text shortcuts. JHDHYR?)

I have never heard of this particular bug. Have you? Liar.

Like Prince, it had another symbol in the past: CDC Group IV c-2. But unlike his purple Highness, it is a gram-negative rod.

There are a smattering of other cases in the literature. One case was due to contaminated blood and it is also presumed, in other cases, to be due to contamination. There are other Ralstonia spp.that cause disease.

We only have the one case, so it is hard to say it is due to contamination at the pharmacy level or inadvertent infection by the patient.

The line was pulled and grew the same bug and she did well of a course of po ciprofloxacin.

I do not know if there will be any other entries this week. I am off to IDSA in Philadelphia, to sit in a large, dark, cold room and desperately try to stave off sleep. I hope that this year they to not have the usual contingent of Dementors giving talks, sucking all the joy and happiness out of Infections Diseases.

But at least I will get to try a real Philly cheese steak. My life is almost complete.

Rationalization

J Clin Microbiol. 2001 January; 39(1): 381–384 Ralstonia paucula (Formerly CDC Group IV c-2): Unsuccessful Strain Differentiation with PCR-Based Methods, Study of the 16S-23S Spacer of the rRNA Operon, and Comparison with Other Ralstonia Species (R. eutropha, R. pickettii, R. gilardii, and R. solanacearum)

A case of Ralstonia paucula septicaemia in an intensive care patient following blood transfusion via a level-1 fast flow fluid warmer, successfully treated with meropenem. Abstract number: 1733_1202

Int J Syst Bacteriol. 1999 Apr;49 Pt 2:663-9. Assignment of Centers for Disease Control group IVc-2 to the genus Ralstonia as Ralstonia paucula sp. nov.

POLL RESULTS

The food I most want to eat before I die

1. Kobe beef in Japan 31% (27)

2. Philly cheese steak in Philly 13% (11)

3. Anything in Paris 36% (31)

4. Fish and Chips in London 8% (7)

5. A Big Mac, as I regret being a vegan 1% (1)

6. Other Answers 10% (9)

7. 25 years ago, I'd have said Breakfast in bed with Raquel Welch. But I'm too old and too married for that now.

8. Big Fat Sushi

9. Roasted pig at a lua in Hawaii

10. Lasagna

11. surprise me - something absolutely delightful that I've never heard of before and doesn't conflict with my moral values.

Major Strasser has been shot.

Nov 3, 2009

Back from IDSA. Four days trying to avoid a pressure sore. It is almost impossible to sit 12 hours a day, I think next year I am going to bring an inflatable donut to sit on. It will make the meeting, I hope, a little more bearable. I was rooting against Philly in the World Series. On Wed they won and there were drunks shouting and honking horns until 3 a.m. When they lost the next game, all was quiet and I got a good nights sleep. It is all about me.

The speakers were, by and large, not as Dementoroid as I had feared, although a few could be bottled and sold as a sleeping aid. Rather than a butterfly fluttering across the screen, you could have an academic reading you PowerPoint slides in a monotone. I learned stuff. I always do. What I don't know always seems to grow faster than what I can learn. The former is exponential, the latter linear. But it is good to be back home and back to work. It is so much more fun to see patients.

The consult today was an elderly female who had a large stroke intraop and now has a persisting WBC of 18K with no fever, no other abnormal labs, and a negative CXR. The CT of the head shows about 1/4 of the brain infarcted. It’s awful.

I call these the Captain Renault consult; it is my job to round up all the usual suspects. I went through the usual causes of an increased WBC with the resident but there was nothing pointing to an infection of labs, CXR or exam.

Then we talked about non-infectious causes of increased white counts (the uninteresting causes), then moved on to leukemoid reactions, which this patient does not have, but was a teaching point. Then I wondered, could a big CNS infarction lead to an increased WBC? I had never recognized it as a cause of an increased white count before, although I have credited both liver and myocardial infarctions with a leukocytosis. So why not?

So off to Pubmed and what do you know, the bigger the stroke, the higher the white count. I do so love the Pubmed.

I still have some usual suspects at large, but they should all be behind bars by tomorrow and I will blame the stroke for the increased WBC.

Rationalization

Stroke. 2008 Feb;39(2):355-60. Epub 2007 Dec 27. Early neutrophilia is associated with volume of ischemic tissue in acute stroke. Buck BH, Liebeskind DS, Saver JL, Bang OY, Yun SW, Starkman S, Ali LK, Kim D, Villablanca JP, Salamon N, Razinia T, Ovbiagele B.

Coke Does Not Always Add Life

Nov 5, 2009

Young male comes in with pneumonia. He has been ill at home for a week, but gets acutely more short of breath and cannot get out of bed.

The girlfriend calls an ambulance and he is admitted to the hospital heading into septic shock. He tries to die, but thanks to modern ICU support, he survives.

His nasal swab has H1N1, his sputum grows MRSA, and his blood has S. pneumoniae. He denied drug use before he was intubated, but the urine tox screen has cocaine and other mind-altering substances.

He has a negative HIV, but his CD4 counts are 200 and I am asked to weigh in on his antibiotics and immune function.

Sepsis, as well as a variety of other acute infections, can cause the CD4 to plummet, and it is why the CD4 counts in the ICU are a poor surrogate for HIV testing. Patients with a sepsis-induced decline in their CD4 count have a higher mortality than them what maintain their CD4's, but it may be a marker of severity of disease rather than cause and effect.

But, as always, there is more.

I have noticed that the drug using lifestyle is not necessarily a healthy lifestyle, and cocaine in particular is not good for you.

Coke users have more rapid progression of their HIV and this is in part due to the direct toxic effect of coke on T cells.

Cocaine kills T cells. And occasionally other cells as well.

That plus nutrition and non -adherence with their compliance (or is it non-compliance with their adherence?) with their HAART.

Whether the same effect occurs with Root Beer or Diet Rite I cannot say with certainty.

Rationalization

The Journal of Immunology, 2001, 166: 6952-6963. Sepsis-Induced Apoptosis Causes Progressive Profound Depletion of B and CD4+ T Lymphocytes in Humans

J Natl Med Assoc. 1993 April; 85(4): 293–296. Short-term declines in CD4 levels associated with cocaine use in HIV-1 seropositive, minority injecting drug users. N. S. Siddiqui, L. S. Brown, Jr.

http://tiny.cc/s9oZq

Int J Immunopharmacol. 1998 Dec;20(12):737-49. Interactive effects of cocaine and gender on thymocytes: a study of in vivo repeated cocaine exposure. Xu W, Flick T, Mitchell J, Knowles C, Ault K.

POLL RESULTS

I prefer to drink the immune boosting

1. Coke 13% (23)

2. Diet Coke 32% (59)

3. Coke One 3% (5)

4. Lime Coke 5% (9)

5. Hefeweizen 27% (49)

6. Other Answers 20% (37)

7. Mountain Dew

8. Bourbon.

9. Water

10. black coffee

11. Beer & wine

12. Coke Zero

13. vernor's diet ginger ale

14. green tea

15. water

16. single malt scotch

17. wine

18. Life water

19. caffeine-free diet Pepsi

20. corona light

21. guiness

22. cofe

23. Pepsi

24. water

25. blueberry/pineapple smoothie

26. water

27. yogurt smoothies

28. water

29. coffee

30. WATER

Hiccups

Nov 6, 2009

I had a busy day today. There are them what say the swine flu pandemic is a myth generated by big pharma to sell tamiflu and vaccines. I see no reason why this is not true. If it is on the interwebs, it can’t be a lie, can it? So I went around the hospital today sending all the people with 'flu' home, even if it met taking them off the ventilator. Posers. But when I was done had I freed up a lot of beds.

It was like the old bad days this week. One of the consults was a young gay male with months of decline, thrush, and admitted with altered mental status. His CD4 was < 30 and the CT of the head showed 8 ring enhancing masses in the brain. His toxoplasmosis serology was off the wall. It is probably CNS toxoplasmosis.

I have not seen a case of toxo this century and he has been placed on appropriate therapy (I try to avoid inappropriate therapy).

As much as I would like to blame the feline vermin, er, I mean cats, they are not the most common reason why people get toxo, although that is the common belief. It’s diet.

"In multivariate analysis, an elevated risk of recent T. gondii infection was associated with the following factors: eating raw ground beef; eating rare lamb; eating locally produced cured, dried, or smoked meat; working with meat; drinking unpasteurized goat’s milk (ick); and having 3 or more kittens."

Hmmm. In the context of the last sentence, the kittens do appear to be a food source. But, really, who could eat three or more kittens? I get full from just one. I presume they mean owning, not eating or birthing, the kittens. So while we tell pregnant women not to change the litter box, it is the streak tartar they should avoid.

This patient also has intractable hiccups as well. Why?

Perhaps the toxo is in the hiccup center; there is one case report of toxo in AIDS causing hiccups. There is, probably (any neurologist want to weigh in?), a brain stem focus for hiccups and he has a lesion in the brain stem. A brain lesion as a cause of intractable hiccups is unusual and perhaps he will respond to seizure medications. In the meantime, I do not expect is CNS lesions to get better for at least two weeks.

Rationalization

Clin Infect Dis. 1994 May;18(5):835. Hiccups, toxoplasmosis, and AIDS.

Clinical Infectious Diseases 2009;49:878-884 Risk Factors for Toxoplasma gondii Infection in the United States

POLL RESULTS

The other white meat is

1. chicken. 22% (14)

2. pork. 20% (13)

3. cat. 8% (5)

4. guinea pig. 27% (17)

5. tofu. 16% (10)

6. Other Answers 8% (5)

7. rattlesnake

8. Phlegm. Oh, wait - I meant Tofu! Darn!

9. Yak

10. I've had guinea pig and it is NOT the other white meat!!

Babe Ruth

Nov 8, 2009

No, not the candy bar. Mr. Ruth was famous for the number of home runs he hit, but most people do not remember that he also led the league in strikeouts.

I saw a patient with two weeks of fevers and a non-productive cough. He had a renal transplant about 6 months ago and has been doing fine on medications, back to work and normal activity.

He otherwise is healthy and he failed a course of azithromycin.

On exam he is non-toxic and some crackles in the upper lobe.

His labs are equally unimpressive with a normal WBC and creatinine.

CXR has an upper lobe patchy infiltrate with hilar adenopathy.

Bronch has WBC but no organisms seen. Key in my mind. What bugs do not show up in a gram stain? So what does he have?

I talk to the patient and he has cattle that he feeds hay and alfalfa he takes out of a barn with a small fork lift. No other exposure.

It’s not a bacterial pneumonia and he hasn't been anywhere of interest, so that narrows the options. You can, as a consultant, make a list of the possibilities in no particular order.

I like to rank order them, especially if I am looking for a zebra. Most of the time I am wrong, but occasionally I point to the right-field bleachers, take a swing, and hit it out of the park.

In my note I said, it is Nocardia >> Rhodococcus > Aspergillus >> Cryptococcus.

I called the lab and told them to look for those organisms, and three days later they called me to say it’s growing a Nocardia. Yippee and Skippy.

Why rank Nocardia first? First, he had a nontoxic pneumonia in a transplant patient.

Second, his only exposure was the cows and the barn. Nocardia grows in rotting organic material like mulch piles and hay. So I played the odds.

No one remembers when you are wrong with an odd diagnosis, but when you are right, your reputation is made. ID docs often blather on about the possible infecting organism but do not commit to what they think the patient really has.

Always commit to a diagnosis and see if events prove you right (sometimes) or wrong (usually). You will find, however, it makes you a sharper thinker if you commit. Plus, you get to brag. That's always fun.

Rationalization

Clin Infect Dis. 2002 Aug 15;35(4):390-4. Epub 2002 Jul 23.Nocardia infection in chronic granulomatous disease. Dorman SE, Guide SV, Conville PS, DeCarlo ES, Malech HL, Gallin JI, Witebsky FG, Holland SM.

Internist (Berl). 2005 Oct;46(10):1152-7. [Unusual infection with pulmonary round foci obtained through "hay packs"]. Pfosser A, Raake P, Reithmann C, Behr J, Steinbeck G.

Next time use a toothpick

Nov 11, 2009

In medical school you are taught (at least I was, I don't know what they treat those young whipper snappers today) to ask open-ended questions and let the patient tell their story in their own words.

I tend to do that, but often the patient doesn't tell me what I want to know and it is only with direct and specific questions can I get the clues I need to find an answer to the what and why of their infection.

One study showed that the average doc interrupts the patient after 18 seconds, and I am sympathetic to this as often the history that the patient tells me has little to do with determining what they have. Still, I let them talk at first and most do not talk than a minute or two before running out of stream.

Today I had a lady with two months of pain and redness in her low back. Studies eventually showed an abscess, it was drained and grew P. aeruginosa.

The heck. Not what I would have predicted. So why does she have this organism?

The usual history of the present illness gives no hint as to why there is a large abscess with an unusual organism in an unexpected place. From the patient’s point of view she had spontaneous, progressive low back pain with redness and swelling. No reason from the patient’s viewpoint for the infection. It’s all a mystery. So I start to fish.

Any trauma, I ask?

No.

Lifting injury?

No.

Surgery?

50 years ago, and chronic back pain without change ever since.

Hot tubs, swimming pools, saunas, any water exposure?

Just the home shower.

Any back injections? Steroids? For the pain?

No.

So no injury, trauma, lifting, overwork, anything?

No. Nothing.

Any acupuncture?

Oh yes. I get acupuncture for the pain in the back. But that could not be the reason. She uses plastic needles.

Bingo was his name-o.

There are 5 references of Pseudomonas infections following acupuncture and there are 344 references using acupuncture and infection as search terms. I have seen several post acupuncture infections in my career and what is striking about all of them it that it was not until I specifically asked about acupuncture did the patients fess up. All were of the opinion that the acupuncture could have nothing to do with their infection.

I like to tell the true story of the patient who had fevers, hepatitis and diffuse lymphadenopathy whose biopsy showed stellate granuloma. A dozen people asked him if he had pets. He said no. My boss, on Chief of Service Rounds, asked if he was around any cats. Why, yes, he replied, my roommate has a dozen cats. The patient had cat scratch disease, hence the stellate granuloma. It's all in how you ask the question, or whether you ask it at all.

Shame, really, because fake acupuncture with toothpicks is just as good (i.e., a placebo effect) as 'real' acupuncture but has none of the complications and costs less.

But then, as I have mentioned before, if you think disease can be cured by moving around chi, why worry about little things like bacteria?

Rationalization

Outbreak of invasive methicillin-resistant Staphylococcus aureus infection associated with acupuncture and joint injection. Murray RJ, Pearson JC, Coombs GW, Flexman JP, Golledge CL, Speers DJ, Dyer JR, McLellan DG, Reilly M, Bell JM, Bowen SF, Christiansen KJ. Infect Control Hosp Epidemiol. 2008 Sep;29(9):859-65.

Arch Intern Med. 2009 May 11;169(9):858-66. A randomized trial comparing acupuncture, simulated acupuncture, and usual care for chronic low back pain.Cherkin DC, Sherman KJ, Avins AL, Erro JH, Ichikawa L, Barlow WE, Delaney K, Hawkes R, Hamilton L, Pressman A, Khalsa PS, Deyo RA.

Expect What?

Nov 12, 2009

The ID literature is filled with odd case reports. Organisms that show up in places or patients where they do not belong. It is, at least for me, part of the allure of ID. One never knows what one is going to grow.

The authors of these one-off oddities always conclude something to the effect that although no one has ever seen such a case before, never, never, ever, now everyone needs to consider the authors unique etiology in their differential. Expect the unexpected. As if. I wish editors would ban that conclusion. Common things are common and that should usually guide our diagnostics, not some once in a million-year case report.

Young female, 19, zero medical problems, presents with fever, chills, RUQ pain. Common things? PID? Pyelo? Even gallbladder disease?

Nope.

CT shows a liver abscess.

OK. Wrong patient, no risk factors, no reason for a liver abscess.

Should be S. anginosus, maybe anaerobes, maybe even staph.

Nope.

The abscess grew H. influenza. Repeat of the history reveals no reason for this and evaluation of her immune system, such as one can do, finds zip.

A spontaneous H. influenza liver abscess in an adult.

In the literature there are 3 cases of H. influenza liver abscess, one of which was in a adult. So now with two reported, I can say in case after case H. influenza is a cause of liver abscess.

And now when you see a patient with a liver abscess, you too will have to consider H. influenza as a cause, even though you will never, ever, never see a case. Expect the unexpected.

Right.

Rationalization

Eur J Clin Microbiol. 1987 Feb;6(1):76-7. Liver abscess due to Haemophilus influenzae type b. Bradley J, Francis J, Wheatley T.

I Came As A Rat

Nov 14, 2009

Modest Mouse is one of my favorite artists at the moment and if Mr. Mouse comes to your town, I recommend you see him live. He puts on a great show and he is one weird, intense dude up on stage.

This week I covered my partner who is off on vacation and one his hospitals is a level one trauma center and that means ECMO. All the severe respiratory failure is in the trauma ICU on various fancy schmanzy forms of ventilator support and ECMO.

Both across the US and in Oregon, it looks like H1N1 cases are plummeting but we are still getting the occasional admit who go on to intubation.

I get called to opine on the need for antibiotics. Most patients get started on community-acquired pneumonia therapy and the standard in my neck of the woods is ceftriaxone and azithromycin. All the cultures are negative and there is nothing to suggest a bacterial process, so do I continue the admission antibiotics?

That was the question asked on both consults today, and the answer to both was no. Except.

Macrolides are interesting antibiotics. There are a growing number of studies to suggest that macrolides have modest immunomodulatory effects, and can decrease mortality with bacterial pneumonias.

But hows about influenza?

Well, in mice (see, the opening paragraph was leading towards something infectious disease related), macrolides decrease the inflammation associated with influenza.

In a Japanese study, macrolides led to a more rapid resolution of symptoms compared to cephalosporins for influenza and for influenza-like illnesses.

The presumption is that macrolides alter the evil humors, er, I mean cytokines to mitigate their adverse effects.

I am not the first to notice this, of course, and I found a nice review writing this post.

There are no randomized clinical trials and extrapolating from mice to humans is not a reliable practice. We are not mice. We are Devo.

Anyway, I have a certain affinity for the macrolide-immunomodulatory hypothesis, so I have been inclined to continue the macrolide because of the modest mouse effect. It took a while, but I got there. It took a Willful Suspension of Belief, but as a result I can Float On rather than Dig Your Grave. If it works, the World at Large may thank you. But enough Mr. Mouse song titles.

In the meantime, I think I am going to continue with the macrolide.

Rationalization

Am J Respir Crit Care Med. 1998 Mar;157(3 Pt 1):853-7. Therapeutic effect of erythromycin on influenza virus-induced lung injury in mice.

J Nippon Med Sch. 2002 Feb;69(1):53-7. Effect of macrolides on duration and resolution of symptoms and complication of pneumonia in children with influenza. Ninomiya K, Fukui T, Imai T, Matsui M, Matsuoka K.

POLL RESULTS

The animal humans most resemble is the

mouse. 10% (3)

sheep. 23% (7)

ape. 13% (4)

Hey, I use macrolides as well, don't you want to know that instead? 10% (3)

Hey, I do not use macrolides for influenza and I think I most resemble my dog. 35% (11)

Other Answers 10% (3)

Lemming.

Easter Island statues

Metastatic Zits

Nov 17, 2009

No. Not the cartoon strip, although I am suspicious the author is stalking my eldest son for ideas.

I had a patient who 6 months ago had an aortic valve replacement and pacemaker.

He had mild failure to thrive and very slowly progressive SOB that did not respond to lasix (isn't lasix like jello at this point, a brand name that has become generic? Or am I in denial?). A chest X-ray showed persisting pleural effusions which lead to a CT scan.

There is a large, non-dependent, loculated pleural fluid with a thick rind. Looks like empyema, but no fevers chills, night sweats or weight loss.

So off to VATs he goes.

The pleural fluid is not that impressive (20-30 monocytes) but the surgeon described an extensive, thick, inflammatory pleural peel.

The pleural fluid gram stain is negative but the tissue gram stain has gram-positive rods.

And it grows, not unexpectedly, Propionibacterium acnes.

P. acnes is an odd bug, extremely indolent and it does not cause much of an inflammatory response, but when you look for it in artificial joints or central lines (usually holding the cultures for at least 2 weeks) you will find it.

The more I look for P. acnes, the more I find it. And I am long out of puberty.

Empyema is distinctly unusual; there are two cases in the literature.

The long duration from surgical trauma to clinical manifestation is also not uncommon for P. acnes. I had a subdural empyema (well, the patient did, not me) that was 7 years in the making before presenting with a seizure. The surgeon told me the pus was odd, like old scrambled eggs. In texture, not taste.

The usual treatment is penicillin or clindamycin and squeezing in front of a mirror leads nowhere. While I always say the three most dangerous words in medicine are "in my experience", in my experience clindamycin is better than penicillin. Some data suggests that vancomycin and a third-generation cephalosporin are the best bet for CNS infections. It is one of the few anaerobes that are resistant to metronidazole.

If you have post-op infections with negative cultures, ask the lab to hold the cultures for 2 weeks. You may find P. acnes unless there is prior Clearasil use.

Rationalization

J Antimicrob Chemother. 2005 Feb;55(2):265-8. Epub 2004 Dec 8. In vitro activities of cefotaxime, vancomycin, quinupristin/dalfopristin, linezolid and other antibiotics alone and in combination against Propionibacterium acnes isolates from central nervous system infections. Mory F, Fougnot S, Rabaud C, Schuhmacher H, Lozniewski A.

POLL RESULTS

I think the following brand names are now generic:

1. lasix. 12% (9)

2. flagyl. 7% (5)

3. kleenex. 59% (45)

4. milk. 9% (7)

5. butter. 8% (6)

Other Answers 5% (4)

1. google (as in the verb)

That can't be normal

Nov 20, 2009

Young healthy males do not present with a large, necrotic lung abscess. That’s it. No history of note.

I mean people have to have reasons for large, necrotic lung abscesses: bad teeth, loss of consciousness, exposure to Tb. Something. My all-time oddest etiology was a 18-year-old female who had a lung abscess that I think was due to aspiration of spit from her saxophone. Saxophonists keep their airway open and if you lift the saxophone in the air, they run the risk of aspiration. I think it was a case of pneumonia from oral sax. And curiously, saxophone players have a shorter life expectancy and they tend to die not of a heroin overdose, but of lung disease. Google it. You will see I write the truth.

But this patient has a life duller than mine. Absolutely no reason for the lung abscess. He has been nowhere, done nothing.

He coughs up a sputum (not in my presence as it makes me barf big time) and cultures are negative.

CT shows, well, as you may have guessed, a large, necrotic lung abscess.

So he has a bronch. Initial cultures and gram stain are negative for bacteria but, annoyingly, the cultures grow moderate Aspergillus.

The real deal? Got me.

This was a big abscess, so off to the OR and it is removed and the pathology shows invasive Aspergillus.

History again suggests no reason whatsoever. Despite being a young Oregonian, he doesn't even smoke marijuana, a risk, perhaps, for pulmonary Aspergillus.

While he is probably a cure with the resection, I have put him on an ill-defined course of voriconazole and have sent his white cells off for testing for chronic granulomatous disease, although his history suggests, with no prior infections, that this will be fruitless, even though Aspergillus can grow on fruit.

Does Aspergillus cause invasive disease in normal people?

Yes and no. There are a smattering of cases of invasive Aspergillus in normal people, but the presence of Aspergillus is probably evidence that the patient has some probably undiagnosable defect in his white cell function. I should say that you now have to suspect Aspergillus in a patient with a necrotic lung abscess who is otherwise healthy, but I have ranted before on what a stupid conclusion that is for unusual cases. Why would I do that?

Rationalization

Chest. 1998 Aug;114(2):629-34. Acute community-acquired pneumonia due to Aspergillus in presumably immunocompetent hosts: clues for recognition of a rare but fatal disease.

Drug Intell Clin Pharm. 1986 Apr;20(4):289-91. Possible risk of invasive pulmonary aspergillosis with marijuana use during chemotherapy for small cell lung cancer. Sutton S, Lum BL, Torti FM.

Bacterial Mummies

Nov 21, 2009

After he died and was buried, there was concern the Beethoven may have been poisoned, so they decided to disinter him and perform another autopsy. When they opened the grave, instead of a coffin, they found steps leading into the earth, followed by a long hall that ended in a candle-lit room.

There, at a bench, sat Beethoven, furiously erasing music.

"Herr Beethoven, what are you doing?" cried someone.

"Decomposing." he replied.

Thank you, thank you, I will be here all week. Please don't forget to try the prime rib.

A year ago I treated bicuspid valve endocarditis with viridans streptococcus.

Patient received standard therapy and was clinically cured. No constitutional symptoms, blood cultures are negative, but the symptoms of aortic insufficiency were rate limiting her activity.

So off to the OR for a new valve, and, as long as he is in there, the surgeon sends off a gram stain and culture of the old vegetation.

It shows 1 to 2 WBCs and 1 plus gram-positive cocci. Now what do you do?

The gram stain of a vegetation can be positive long after the infection is cured, but how long? Up to six months and longer

"...it may take months for dead bacteria in a vegetation to be removed by phagocytosis and/or bacterial cell lysis."

I cannot find the world record for post cure positive gram stain.

When we die we partly decompose from enzymes in our cells, but mostly we decompose from bacteria and mold eating us. So what is going to decompose the decomposer? There are no bacteria in the vegetation to eat the bacteria. The vegetation is often a white cell-free environment so there are no WBCs in the vegetation to dispose of the bacteria either. So, while worrisome, it is to be expected that the preserved corpses of bacteria will exist in the vegetation, probably empty husks, mummy like, for prolonged periods.

So what to do? If the cultures are negative, then nothing. If the cultures are positive then another course of antibiotics. It is not out of consideration that it is a new, incubating, rather than relapsed, case of endocarditis.

Rationalization

Clin Infect Dis. 2003 Mar 15;36(6):697-704. Epub 2003 Mar 4. Gram stain, culture, and histopathological examination findings for heart valves removed because of infective endocarditis. Morris AJ, Drinkovic D, Pottumarthy S, Strickett MG, MacCulloch D, Lambie N, Kerr AR.

The Eyes Have It

Nov 23, 2009

Four days of progressively severe unilateral eye pain, and fevers and loss of vision is not a good thing.

Something about eye infection that makes me wince, one of two body parts that make me cringe when they are infected. And then the ophthalmologist comes along and sticks needles in the eye. EEEEuuuuueeeeee.

Hematogenous eye infections are uncommon, despite what seems to be a run of them this year; this the third time I have seen endophthalmitis of late. Not pun intended for once.

The first was Candida, not an unusual manifestation of line-related candida infection.

The second was due to S. aureus in a particularly nasty mitral valve endocarditis that seeded both eyes.

And now this case.

The classic cause with heroin use for eye ball infections is either B. cerus or C. albicans, but I was expecting a Strep or Staph as the patient is 6 months or so out of a treated case of endocarditis.

Both the eye and the blood cultures had streptococci by gram stain, and imagine my surprise when it grew S. pneumoniae. This organism does have a predilection for seeding the eye, but usually there is a reason. The last S. pneumoniae I saw, many years ago, actually ruptured on the way to the OR.

Part of the annoyance is that I cannot find a reason for the bacteremia. No pneumonia, no immunodeficiency, it is not an organism found in heroin. And there is no preceding eyeball trauma, usually present with this disease. She still has a mitral valve vegetation from the recent IE; I feel obligated to treat her for post-endocarditis endocarditis, but there are no other manifestations of endocarditis.

Distinctly unsatisfying to know the what but no clue as to the why, except bad luck. Unfortunately vision will probably be ruined in that eye.

Rationalization

Am J Ophthalmol. 2004 Aug;138(2):231-6. Endophthalmitis caused by Streptococcus pneumoniae. Miller JJ, Scott IU, Flynn HW Jr, Smiddy WE, Corey RP, Miller D.

More Mold

Nov 26, 2009

Steroids and diabetes are a bad combination. Opportunistic infections can occur, although usually the steroids are given by the medical-industrial complex.

Sometimes the steroids are endogenous. Cushing's syndrome can pump the steroids into the body with resultant diabetes and immunosuppression. Given the rarity of Cushing's, and I have now seen one in my career, it is unusual to see infectious complications of this disease.

Cough and fever in a Cushing patient leads to a CXR with multiple nodules that leads to a CT that confirms the nodules that leads to a biopsy that shows hyphae in the middle of the nodules, but cultures are negative. So they send the patient to me. They are still are trying to discover the source of the endogenous cortisol.

She is not all that ill from infection, although she does have the dramatic changes of Cushings. When you wonder about Cushing's or acromegaly, it is good to look at the patient’s driver’s license for comparison as a 'before' picture. The changes of these diseases can be slow and unnoticed. Given most people’s drivers license picture, acromegaly can be an improvement.

The CT pattern, with scattered small nodules, suggests an inhalation injury and the patient is a gardener, so perhaps it was airborne. The patient was never ill enough to think it was hematogenous, but I can't be sure. I suppose this is Aspergillus, but the fly in the ointment is frequent trips to SE Asia, and Penicillium can look the same on biopsy.

The lesions are getting better on voriconazole, so I can’t argue with success.

There are other cases (8 total on Pubmed, although one was in a horse. Poor Mr. Ed. Wilber always made fun of the stria) of invasive Aspergillus occurring in patients with Cushing's and no cases of Penicillium, so I suppose it’s Aspergillus. Still, I wish the organism had grown.

Rationalization

Ann Intern Med. 1984 Sep;101(3):334-8. Opportunistic infections in endogenous Cushing's syndrome. Graham BS, Tucker WS Jr.

Sore Throat

Dec 1, 2009

Sore throats are common. Most people tough them out and they go away.

Rarely, they get worser and worser with progressive fevers, chills, myalgias and prostration. That’s a sore throat worth a visit to the ER and subsequent admission.

No past medical history of note, she has a painful, swollen knot at the angle of the jaw and a CT shows inflammation of the salivary gland.

I haven't seen one of these in ages. There was a time, at the dawn of the ICU era, when parotitis was not an uncommon cause of ICU infections, but good fluid management and oral care have made nosocomial parotitis disappear.

All her blood cultures are growing S. aureus, so I think this is a bacteremia from the salivary gland. Oddly, on the CT there is no stone, the usual cause of bacterial parotitis.

The last one of these I took care of died of the disease. The patient seeded her prosthetic valve and she died of progressive endocarditis. Not this time. TIme and antibiotics and she got all better.

Part of therapy is to use antibiotics, the other is to get the saliva a flowin' with salivary-activating foods such as lemon, lemon drops, pickles and sauerkraut. Blech.

Is there data to support the use of salivary activating foods? Not that I can find. It is tradition. It does have a history going back to at least 1922, where, if you think you have it tough.

"Fenwick, in an article entitled "The Prevention of Parotitis During Rectal Feeding" states that he had patients suck an India rubber teat about two inches long, which had the desired effect. Collins state that is a good way to excite the secretion if the mouth and keep the current of saliva is to allow the patient to suck on a stick of lemon candy after the operation."

That was back in the days before antibiotics and parotitis had a 30% mortality rate, some dying from the embarrassment of rectal feeding. It was how Garfield was fed after he was shot; no wonder he died. The president, not the cat. Unfortunately.

Rationalization

Cal State J Med. 1922 September; 20(9): 301–303.CHRONIC SUPPURATIVE PAROTITIS WITH ACUTE EXACERBATIONS* Henry J. Profant

Oral Maxillofac Surg Clin North Am. 2009 Aug;21(3):269-74. The bacteriology of salivary gland infections. Brook I.

Follow-Ups

Dec 3, 2009

It has been a week of S. aureus. That is the organism that pays my mortgage. But there are no curious or unusual manifestations of S. aureus, just the ongoing issue of what to do with this or that bacteremia. So I thought I would give a pair of follow-ups as I thought perhaps you want to know what happened with some of the prior cases.

One case was the pulmonary Nocardia in the transplant patient. He kept being readmitted to the hospital with an increase in his creatinine, which eventually was attributed to his trimethoprim. His renal dysfunction resolved when he was changed to sulfamethoxazole alone.

"Trimethoprim can also reversibly increase serum creatinine concentration and reduce creatinine clearance without decreasing glomerular filtration rate both in people with normal renal function and in those with renal allografts. Trimethoprim alone can cause an important but reversible increase in serum creatinine concentration in acute uncomplicated cystitis and in chronic renal failure. The mechanism is probably competitive inhibition of tubular secretion of creatinine and does not signify a deterioration in renal function."

I felt comfortable with sulfa alone once the Nocardia was identified a N. nova, and it was susceptible to sulfa. It was hard finding oral sulfa. Seems no one uses it much any more.

N. nova also turns out to be a pathogen in cattle and dogs, and, as you may remember, he was a cattle rancher. I had credited his Nocardia to the hay in the barn he used to feed his cattle, but perhaps it was his cattle or even his dawg. I will never know with complete certainty.

He continues to improve on therapy and will likely be declared a cure sometime next year.

The other case is not so good. It was the AIDS patient with hiccups from CNS toxoplasmosis. The only thing that has improved is the hiccups. He remained slow to improve and MRI showed non-enhancing CNS lesions, as well as blood and a few of the lesions crossed the midline. His toxo serology was off the wall, but AIDS patients are more prone to follow Hickam's dictum than Occam's razor and most patients improve radiographically and clinically after 10-14 days.

Neuro was adamant that only cancer will cross the midline, and toxo usually enhances on MRI.

If you search for non-enhancing lesions in AIDS, its mostly PML and CNS lymphoma. There are only a few case reports of non-enhancing toxo. So eventually a brain biopsy was performed.

Pathology showed changes most consistent with toxoplasmosis although the parasite itself was not seen. The lesions are a little less bad on MRI after three weeks of therapy. But I remain worried that there is more going on in his brain than we know.

Rationalization

Hyperkalaemia and non-oliguric renal failure associated with trimethoprim. BMJ 1994; 308 doi: 10.1136/bmj.308.6926.454b (Published 12 February 1994)

Rev Inst Med Trop Sao Paulo. 2008 May-Jun;50(3):177-85. Epub 2008 May 14. Nocardiosis: an overview and additional report of 28 cases in cattle and dogs.

What is THAT doing THERE?

Dec 3, 2009

I received a request from an intern to see a consult today. Whenever I can get away with it, I have the referring doctor give me just a 5-word question. 5 words. That’s all. It saves me having to listen to the history that I am going to take anyway, and I prefer to get the information without the filter of the calling physician.

Few can do it. 'Why fever?' is the shortest I get. I would love a one-word question, but no one has provided me with one as of yet. The intern today said '56 year old male' and I said, 'That’s five.'

I know. What an a-hole.

She laughed and said he has a septic shoulder, what should we do about it.

I thanked her and said I would be all over it like a large, furry dog.

Septic shoulder? Probably going to be Staphylococcus, probably post-operative or IVDA. That’s the typical shoulder infection.

Wrong on all counts. Both the blood and the joint are growing E. coli. No IVDA, no recent surgery.

So what is THAT doing there?

The last E. coli septic joint I saw was a complication of urosepsis in a patient with advanced rheumatoid arthritis and that was last century.

E. coli, despite the fact that it is often found in the blood, rarely goes to joints. There are a whopping six cases in Pubmed with diabetes, gout and cirrhosis being underlying causes. This patient has none of the above, but does have underlying liver disease and tics, so we went looking in the abdomen for a source. Nothing.

I&D and a long course of IV antibiotics are to come as well.

5 words: What is THAT doing THERE?

Two word answer: No clue.

Sums it up.

POLL RESULTS

Short consult questions?

1. Infected? 18% (7)

2. Fever? 13% (5)

3. Therapy? 8% (3)

4. Insured? 20% (8)

5. Butthead? 38% (15)

6. Other Answers 5%

7. Dying?

8. Fix him please?

With three letters I predict the future.

Dec 5, 2009

Chemo for cancer has its side effects, but the side effects are usually better than death. Usually. The patient has cancer and HIV, with CD4 counts hovering just above the magic mark of 200, the point where you have to worry about opportunistic infections. Or do I? That is part of the problem. Is a CD4 count of 200 reliable when there is ongoing cancer chemo? Not if it is chemotherapy for lymphoma, but how about adenocarcinoma as in this case? I don't know.

So the patient has horrible diarrhea, constant, watery, almost levitating in severity, after getting chemo that includes 5-FU and comes in febrile, neutropenic, and dehydrated, or, as my renal attending always said, volume short. Instant coffee is dehydrated, not humans.

He has the full workup for fever and diarrhea and we don't find a reason, but the diarrhea persists, so a CT is done.

Colon and small bowel are markedly thickened. To have involvement of small and large bowel is odd with most infectious diseases, who have a predilection for either one or the other.

So I suspect CMV, although the CD4s are higher than one would expect for CMV.

So I suggest we walk down the CMV pathway with a colonoscopy, but, wait, says onc. This is probably DPD deficiency.

Huh? CDC deficiency? No DPD. Dihydropyrimidine dehydrogenase deficiency.

Huh?

I'll quote the Wikipedia

"Dihydropyrimidine dehydrogenase deficiency (DPD deficiency) is an autosomal recessive metabolic disorder in which there is absent or significantly decreased activity of dihydropyrimidine dehydrogenase, an enzyme involved in the metabolism of uracil and thymine.

Individuals with this condition may develop life-threatening toxicity following exposure to 5-fluorouracil (5-FU), a chemotherapy drug that is used in the treatment of cancer. . Beside 5-FU, widely prescribed oral fluoropyrimidine capecitabine (Xeloda) could put DPD-deficient patients at risk of experiencing severe or lethal toxicities as well.

Current research suggests that nearly 8% of the population has at least partial DPD deficiency. A diagnostics determination test for DPD deficiency is available and it is expected that with a potential 500,000 people in North America using 5-FU this form of testing will increase. The whole genetic events affecting the DPYD gene and possibly impacting on its function are far from being elucidated, and epigenetic regulations could probably play a major role in DPD deficiency. Dihydropyrimidine dehydrogenase deficiency has an autosomal recessive pattern of inheritance.

It is more common among African-Americans than it is among Caucasians."

That’s cool. But why do people have this mutation? Anything that occurs in 8% of the population must have been there for an evolutionary reason. Pubmed is quiet on the topic as is the Googles so I am going to speculate.

I bet that it is an infectious disease that has driven this mutation and I bet the infection will be malaria. There is probably no organism that has left more footprints on our genome than malaria: sickle cell, thalassemias and G6PD deficiency being prime examples.

I bet, and who wants to bet against me, that people with this mutation will have less severe malaria. Or maybe less severe TB. Or another chronic infections that have plagued mankind forever. But DPD will be protective against an infection.

Everything always gets down to an infection. Except, maybe, OB.

POLL RESULTS

The disease I expect to be found to due to an infectious disease will be

1. CFS 2% (1)

2. IBD 25% (12)

3. CAD 15% (7)

4. Pregnancy 8% (4)

5. Stupidity 46% (22)

6. Other Answers 4% (2)

7. Autism

It Wasn't the Cigarettes

Dec 7, 2009

Busy today in a slow way. The blog is about the weird and wonderful cases I see, but today was cases with vague problems and uncertain answers.

I think it would make the blog entry too 'Jack Torrance' to write "I don't know' over and over. The one symptom all my patients have is fever. I have an ongoing interest in fever and temperature regulation.

Fever, of course, is protective and all wings of the immune system work better at higher temperatures. One thing I had never considered is that being a mammal, with our temperature above ambient, is also protective against infections.

Insects can be infected with 50,000 different fungi and plants are susceptible to 270,000 fungi. Humans? Many fewer, maybe a couple of dozen pathogenic fungi at best and few that infect normal people. And it may be due to the fact that we are warmer than ambient temperature.

In a recent JID article they tested the growth characteristics of 4800 fungi at a variety of temperatures from 4 to 45 degrees C, and as the temperature went up, the number of fungi that could grow declined. They found for each increase in temperature of 1 degree C, they "excluded an additional 6% of fungal isolates, implying that fever could significantly increase the thermal exclusion zone."

Perhaps not being consumed by fungi helped drive the evolution of increased body temperature.

"Endothermy is associated with certain metabolic benefits and thermodynamic efficiency, but these benefits come at a high cost since endothermic vertebrates require <10 data-preserve-html-node="true" times more oxygen to support metabolism than do ectothermic vertebrates [8] . Our analysis suggests that part of the cost is mitigated by the creation of a thermal exclusionary zone that can protect against environmental microbes. Given the high metabolic cost of endothermy, the core temperatures of individual mammal and bird species are likely to be a compromise between its benefits and costs. If endothermy was selected for protection against infectious disease, then a case could be made that endothermy preceded homeothermy. Similarly, if one considers fever as a mechanism to extend the thermal exclusionary zone against environmental microbes such as fungi, increases in temperature of only 1-3 degree C can significantly reduce the proportion of such microbes that can inhabit the host."

Even cooler is they have found a burst in fungal fossils at the Cretaceous-Tertiary boundary when the dinosaurs died off.

A meteor hits earth, increasing the amount of organic material for fungi to feed on, the fungi proliferate to kill off the surviving dinosaurs, and we mammals remain, resistant to the fungi. It pays to be warm.

It wasn't the cigarettes after all.

Rationalization

Vertebrate Endothermy Restricts Most Fungi as Potential Pathogens. The Journal of Infectious Diseases 2009;200:16236

Fungal Genet Biol. 2005 Feb;42(2):98-106. Epub 2005 Jan 5. Fungal virulence, vertebrate endothermy, and dinosaur extinction: is there a connection?

Physiol Biochem Zool. 2004 Nov-Dec;77(6):1019-42. The evolution of endothermy in terrestrial vertebrates: Who? When? Why?

http://humormedication.wordpress.com/2010/02/24/gary-larson-dinosaurs/

POLL RESULTS

What killed the dinosaurs?

1. Meteor. 15% (6)

2. Global Warming. 2% (1)

3. Health Care Reform. 29% (12)

4. The Internet. 7% (3)

5. Boredom 34% (14)

6. Other Answers 12% (5)

7. String theory

8. Noah's ark floats by. “Was that TODAY” said Rex?

9. other dinosaurs

10. laziness

Cold and Cold

Dec 10, 2009

It is cold out. Twelve degrees this morning in what should be the mild Pacific Northwest. Where is global warming when you need it? I did my residency in Minneapolis, and that was cold. There was one month where the temperature did not get above zero. 12 degrees would have been short pants and sandals weather back in the day, but now? It is too cold for me.

I have an interest in the effect of weather on infections. Legionella goes up with warm, humid weather. The RSV season has shortened as mean temperature has increased. Most of the recent literature has focused on the effects of warming as a risk for a wide variety of infections.

But can you catch a cold because of cold weather? And if you can, why don't you catch a hot in the summer?

The incubation of the rhinovirus can be remarkably short: 8 to 10 hours, although the average is 16 hours. So based on incubation period it is reasonable that exposure to cold virus because of cold weather could lead to a cold symptoms that day.

But does it?

Cold weather also tends to be dry and tends to drive people together ("sharing office space increases the risk of the common cold") so teasing out temperature is not as simple as you would think. And then there is the whole issue of lack of sun and the resultant vitamin D decline, a probably minor reason why URI's increase in the winter.

The first epidemiologic study on weather and the cold, to validate long held beliefs, goes back to 1925 and there have been many studies since all trying to tease out the relationship between cold and the cold.

There was a study this year that suggested it is both cold and decreased humidity that spreads the cold:

"The average outdoor temperature decreased during the preceding three days of the onset of any RTIs, URTI, LRTI or common cold. The temperature for the preceding 14 days also showed a linear decrease for any RTI, URTI or common cold. Absolute humidity decreased linearly during the preceding three days before the onset of common cold, and during the preceding 14 days for all RTIs, common cold and LRTI."

However, most colds are transmitted indoors from contact with other people and their secretions, and not spread in the light of the moon on a cold winter night.

So my evening walk to the top of Mt. Scott may, in the cold weather, be putting me at risk for a cold. But only if those around me have a cold as well.

Rationalization

The Jeremiah Metzger lecture. Climatology and the common cold.

Respir Med. 2009 Mar;103(3):456-62. Epub 2008 Nov 1. Cold temperature and low humidity are associated with increased occurrence of respiratory tract infections.

Eur J Epidemiol. 1995 Apr;11(2):213-6. Shared office space and the risk of the common cold.

Sore Throat

Dec 13, 2009

It Sunday morning, I am on call and waiting for the ice to melt so I can get in to round. It is one of the reasons I live on a hill, it provides me with the occasional legitimate reason to take my time getting into work.

One of the cases I have to see is a severe sore throat with lymphadenopathy and early abscess formation on CT. Patient is barely out of his teens and no risk factors for anything odd like tularemia.

He has a classic 'hot potato/potatoe' voice. I quail at the thought of trying to spell some tubers correctly.

Hot potato voice is distinctive and occurs with peritonsillar abscess and sounds like someone talking with a mouth full of hot potatoes. Or does it?

Has the hot potato voice ever been subjected to scientific scrutiny? Mai oui.

"The "hot potato voice" is widely recognized as a symptom of peritonsillar cellulitis or abscess; yet there have been no studies assessing the resonance characteristics of the vocal tract in peritonsillitis. Analysis was undertaken of formant frequencies in the articulation of the vowels /i:/. /a:/ and /u:/ in six subjects with peritonsillitis and compared with articulation once the peritonsillitis had settled. Significant variation was found in F1 when articulating /i:/ and in F2 when articulating /a:/, which are explainable by dyskinesis of the peritonsillar musculature. These findings were compared with six subjects articulating the same vowels with and without a hot potato in their mouth. Variation was found in both F1 and F2 when articulating /i:/, which can be related to interference of the potato with movement of the anterior tongue. The changes in the vocal tract differ in these two cases and the title "hot potato voice" in peritonsillitis is a misnomer."

Damn. If it is a misnomer, then what should we call it?

The other interesting thing is the etiology of the abscess. So far cultures and work up are negative for Strep, staph, EBV, CMV, HIV and GC. How GC gets in the throat I still have not figured out. So what is the cause?

Two papers this month have suggested that Fusobacterium necrophorum is the primary cause of peritonsillar abscess and it causes 10% of pharyngitis in the adolescent population. Fusobacterium necrophorum usually causes Lemmier's disease, septic thrombophlebitis of the internal jugular or post anginal sepsis.

Our micro lab would be unable to grow this organism outside of blood cultures as it is an anaerobe; most labs can't grow It could be a reason to not treat pharyngitis with macrolides as Fusobacterium is resistant. So besides the usual suspects, I am making sure I kill Fusobacterium.

But I suspect that is what he has. Maybe we should call it Fuso voice?

Rationalization

J Voice. 2006 Dec;20(4):616-22. Epub 2005 Dec 19. "Hot potato voice" in peritonsillitis: a misnomer.

Expand the pharyngitis paradigm for adolescents and young adults. Centor RM. Ann Intern Med. 2009 Dec 1;151(11):812-5.PMID: 19949147

Fusobacterium necrophorum: most prevalent pathogen in peritonsillar abscess in Denmark.Ehlers Klug T, Rusan M, Fuursted K, Ovesen T. Clin Infect Dis. 2009 Nov 15;49(10):1467-72.PMID: 19842975

Ick

Dec 15, 2009

Or maybe ech. Ick is that stuff that grows on guppies.

Patient presents with chemotherapy-induced neutropenia and fevers. That is common enough.

But he has these painful lesions on his left arm and hand, including the palm and the middle of the middle finger.

The middle of the lesions is black-blue, surrounded with erythema and are, as mentioned, very painful.

The rest of his exam is negative. No murmur, no nothing.

His blood cultures are growing MSSA.

So are these emboli from endocarditis? They do not look like it. And they have the wrong distribution, not being at the extreme periphery of the body. And how do you have a vegetation with emboli when your platelets are 10K? Even if they were 401K, with the current economy they would be about half their prior value.

Here is my theory, completely unsubstantiated by the medical literature. Since the vegetation of endocarditis is due to layers of platelets and thrombin, if you are thrombocytopenic or on Coumadin, you should not form a vegetation. Someone like to do a study for me and prove this? I would, but WWF is on tonight.

His ECHO is negative, and I wonder if these skin lesions are ecthyma gangrenosum. Ecthyma usually occurs with Pseudomonas bacteremia in the neutropenic, although other organisms can also cause ecthyma. The bacteria come to a stop in the capillaries, multiple and thrombose/necrose the local skin. Hence the central black of EG. A biopsy of ecthyma shows necrosis with surrounding bacteria.

There is one case of MRSA causing ecthyma, but I wonder if these lesions we see on occasion with endocarditis are not embolic events but ecthyma. Or maybe Osler's and ecthyma are the same manifestation in different hosts, one neutropenic and the other with white cells.

The other name, btw, for S. aureus is coagulase positive Staphylococcus. It makes one potent coagulase that clots blood in no time. It makes some pathophysiological sense that S. aureus could cause local clot and necrosis.

Interestingly, there is not a lot on the histopathology of Oslers.

"The pathogenesis of Osler's nodes and Janeway lesions remains a mystery despite vigorous debate over the last 113 years."

and

"The histologic findings in Osier's nodes and Janeway lesions have been reported rarely; we found descriptions of only 10 such cases, mostly from the late nineteenth- and twentieth-century French literature."

So nobody nodes the troubles we have seen. So much sound and fury on rounds, pontificating on the fine points of Osler and Janeway, and based on a molehill of data.

I suppose it makes no real difference, but I find these fine points interesting.

Rationalization

Ecthyma-gangrenosum-like lesions associated with methicillin-resistant Staphylococcus aureus infection.Int J Infect Dis. 2009 Jul;13(4):e173-5. Epub 2008 Nov 21. PMID: 19027336

Janeway lesions and Osier's nodes: A review of histopathologic findings Australas J Dermatol. 2007 Nov;48(4):251-5. .

Passive Voice

Dec 17, 2009

I like to read op notes, and it is amusing how in many notes there does not seem to be anyone doing the operation. It is all in the passive voice: the abdomen was entered (by whom?), the vein was transected (divine intervention?), the spleen was removed (transported out by Mr. Scott?). I guess there is no 'I' in surgery. I am glad I am not a surgeon, my ego is too ginormous to be confined to the passive voice.

Two patients, different hospitals, had fevers and WBC of 40K.

Both recently had their spleens out during surgery: one inadvertently, the other advertently when it was involved with tumor.

Patients without spleens often bump their white cells into the 20 or 30 K range in the immediate post-operative period, but 40K means probable infection.

Patients without spleens are prone to some infections that are worser than in those who still have their spleens, and it tends to be due to encapsulated organisms: S. pneumo, H. flu, Salmonella. Or do they?

There was an interesting report in the Annals last month that looked at the risk of infection in patients with their spleens out and the biggest risk of infection was in the first 90 days after the spleen was removed. Like these two patients.

Also of interest in this study is that

"encapsulated bacteria, such as pneumococci, meningococci, and Haemophilus influenzae, were rarely encountered in the splenectomized cohort."

They had E. coli (23%) followed by S. aureus (16%) as the top two organisms, just like normal folk.

One patient maybe has liver abscesses, there is too much coagulopathy to get a biopsy.

The other? CT was ordered. Blood cultures were obtained. The blood is growing S. aureus as is an intra-abdominal fluid collection.

I was consulted.

I gave antibiotics. Yeah. I stood at the bedside and pushed the cefazolin in myself. No passive voice for me.

Rationalization

Risk for Hospital Contact With Infection in Patients With Splenectomy A Population-Based Cohort Study. Ann Intern Med. 2009;151:546-555.

Mai? Oui? Peut etre?

Dec 19, 2009

I often get asked questions for which there are no answers. For example. A young, at least by my standards, since I am 364 in dog years, female has a colonoscopy as part of screening for cancer.

Her ileum is inflamed so a biopsy is done. It shows granulomatous ileitis consistent with Crohn's disease. She has no symptoms of Crohn's or anything else for that matter.

This is a serendipitous finding during screening. So the GI doc sends off stool AFB cultures, looking for MTB and instead finds Mycobacterium avium aka, MAI.

Now what? I don't know.

MAI is everywhere. If you culture your tap water, you will grow MAI and other mycobacteria.

"MAI isolation rates from water supply systems were 8 of 25 (32%) samples in the United States."

It is a common organism in your water and when you shower you are probably inhaling the organism, the alleged source of MAI pneumonia.

Now the mantra of all skeptics is association is not causation, even though it is well known cause and effect that declining pirate populations are causing increase in mean global temperature.

When I see granuloma, I think infection, and there is a long-standing association between M. avium spp paratuberculosis and Crohn's.

There is a nice review in the Lancet Infectious Diseases

"This systematic review assesses the evidence for an association between Mycobacterium avium subspecies paratuberculosis (MAP) and Crohn's disease. We analyzed 28 case-control studies comparing MAP in patients with Crohn's disease with individuals free of inflammatory bowel disease (IBD) or patients with ulcerative colitis. Compared with individuals free of IBD, the pooled odds ratio (OR) from studies using PCR in tissue samples was 7.01 (95% CI 3.95-12.4) and was 1.72 (1.02-2.90) in studies using ELISA in serum. ORs were similar for comparisons with ulcerative colitis patients (PCR, 4.13 [1.57-10.9]; ELISA, 1.88 [1.26-2.81]). The association of MAP with Crohn's disease seems to be specific, but its role in the aetiology of Crohn's disease remains to be defined."

But my personal favorite was "three unrelated individuals who lived on the same block along a street in a Midwestern American city and developed Crohn's disease within four years of each other in the 1960s. A common tap water pipe supplied their homes" that grew MAI.

What to do? Watch and wait, I suppose. Treat? With what and for how long? No data. If I treat now will I abort the development of Crohn's? No data. Will this go away on its own? No data.

Once upon a time I read, but for the life of me I cannot remember where, that if you have no data to guide therapy, the odds are you will do more harm than good. So I tend to not try experimental therapies with one exception. My personal theory is beer kills MAI, so I only shower in Bud Light.

Infections are the one true cause of all disease, all others are posers.

Rationalization

Pirates and global warming.

Lancet Infect Dis. 2007 Sep;7(9):607-13. Mycobacterium avium subspecies paratuberculosis and Crohn's disease: a systematic review and meta-analysis.

Gut Pathog. 2009 Sep 23;1(1):17. Possible transmission of Mycobacterium avium subspecies paratuberculosis through potable water: lessons from an urban cluster of Crohn's disease.

J Clin Microbiol. 1993 December; 31(12): 3227-3230 Isolation of Mycobacterium avium complex from water in the United States, Finland, Zaire, and Kenya.

POLL RESULTS

The One True Cause of All Disease is

1. Infection 43% (23)

2. Genetic 19% (10)

3. Toxins 9% (5)

4. Subluxations 2% (1)

5. Blocked chi 17% (9)

6. Other Answers 11% (6)

7. Insufficient nitric oxide

8. WITCHES

9. The Flying Spaghetti Monster

10. Demons.

11. life

Kobayashi Maru

Dec 21, 2009

There are no win situations in medicine. On occasion, the choice is to decide what the least bad option is. There is a rock and hard place. Choose. MRSA bacteremia. A standard consult. And a consult everyone should consider, since the self-serving ID literature shows that patients who get an ID consult for their S. aureus bacteremia have better outcomes.

"All 4 standards of care (removal of intramuscular foci of infection, obtaining follow-up blood culture samples, use of parenteral beta-lac tam therapy when possible, and administration of >/=28 days of therapy for complicated infections) were adhered to more frequently with routine consultation (40% vs. 74%; P <.001). data-preserve-html-node="true" Treatment failure (microbiological failure, recurrent bacterial, late metastatic infection, or death) occurred less often during the intervention year (17% vs. 12%)."

Go me.

The problem with this case is several pieces of endovascular hardware. An old mechanical valve and a relatively new fem-pop bypasses.

No stigmata of either endocarditis or graft infection, ECHO negative and the usual post-op fluid around the graft.

Graft infected, valve infected, both infected. I can't tell.

I can't cure either if they are infected, but there are TNTC co-morbid conditions that make a valve replacement problematic and graft surgery will likely lead to amputations.

OR or no OR. That is the question. The problem is that I can't see into the future, so I can't predict which path is more likely to do the most harm. Probably both.

I like what one recent review said

"The current literature suggests that MRSA-infected graft preservation should only be attempted with minor graft involvement. The high proportion of amputations (24 percent) was likely due to the prevalence of MRSA and the excision of the graft in a population with already threatened limbs. Despite the success of irrigation and debridement in group 3 MRSA-infected grafts in our sample, it is probably imprudent to treat this virulent organism with local measures alone."

Imprudent. So understated.

In the meantime, its vancomycin, gentamicin and rifampin while we look for an unsatisfactory solution.

And I do not get to reprogram the computer to win.

Rationalization

Clin Infect Dis. 2008 Apr 1;46(7):1000-8. Impact of routine infectious diseases service consultation on the evaluation, management, and outcomes of Staphylococcus aureus bacteremia.

POLL RESULTS

1. The correct solution is

2. Evacuate the ship and then crash it into the Klingons. 24% (12)

3. It’s a trap. Do nothing. 14% (7)

4. Bypass the Klingon shields. 14% (7)

5. Trick the computer into fighting itself. 36% (18)

6. Destroy the Kobayashi Maru. 8% (4)

7. Other Answers 4% (2)

8. Increase nitric oxide levels!

9. Isn't Kobayahi Maru a baseball player... either that or some form of Japanese BBQ

Big MAC Attack

Dec 29, 2009

The patient is a middle-aged male who presented with fevers and three months of wasting. His HIV was elevated and his CD4's were in the 20s. He was, as best as could be told, OI free, and was started on HAART.

His viral load fell to zero and his CD4's popped up into the low two hundreds. At satisfying response, but clinically the patient worsened.

Head, neck and groin lymph nodes exploded, figuratively speaking. But the size of the lymphadenopathy was in the extra-large egg size, they were painful and the fevers returned.

Biopsy showed lots of AFB that were identified as MAC and he was given a short course of prednisone and a long course of antibiotics, again with improvement followed by a marked worsening of symptoms when the prednisone was stopped.

As IRIS (Immune Reconstitution Inflammatory Syndrome) goes, this is more severe than usual. IRIS is when the immune system comes back and attacks a preexisting infection that, due to a lack of an immune response, is asymptomatic. Any and all OI's have been reported to cause IRIS: MAI, Cryptococcus, toxoplasmosis, CMV, etc.

"The incidence of non-tuberculous mycobacterial immune reconstitution syndrome was 3.5% among patients initiating highly active antiretroviral therapy (HAART) with a baseline CD4+ cell count of <100 data-preserve-html-node="true" cells/μL. Three main clinical presentations were peripheral lymphadenitis (in 17 patients)"

It was initially referred to as IRS, but the feds came down hard on the IDSA, threatening them with being audited, so they added the I, as florists have little clout.

IRIS is not uncommon

"the percentage of patients developing IRIS and the timing of IRIS onset following HAART initiation have been surprisingly similar. For patients with an underlying OI, between 15 and 45% of patients developed IRIS with the majority of cases presenting within 60 days of initiating antiretroviral therapy.13,15,16,19,20 When all patients receiving HAART were analyzed, between 15 and 25% of patients developed IRIS, with most cases again occurring in the first 3 months of therapy."

But usually not so severe.

Steroids can help, "Prednisone was associated with clinical responses in 8 (89%) of 9 patients with evaluable cases," although when he relapsed and we checked a cortisol, it was a whopping 1.6. Cosyntropin test is pending.

MAI is a common cause of HIV associated Addisons in HIV, usually due to adrenal invasion, but it can be more subtle. A proportion of HIV patients develop cortisol resistance, a kind of Type II Addisons. These patients have normal cortisol and slightly high ACTH, unlike this patient.

I remember years ago, an AIDS patient transferred to Oregon where his family lived, so he could die. He had been in the Mass General for two months with progressive wasting and when I saw him he was as tan as if he had spent a month in Jamaica. His ACTH was off the wall and his cortisol unmeasurable. With replacement steroids he lived another year. I have not been so impressed with the cases from the Mass General since.

Rationalization

Immune reconstitution inflammatory syndrome: more answers, more questions. Shelburne SA, Montes M, Hamill RJ. J Antimicrob Chemother. 2006 Feb;57(2):167-70. Epub 2005 Dec 14

Clin Infect Dis. 2005 Nov 15;41(10):1483-97. Epub 2005 Oct 12. Nontuberculous mycobacterial immune reconstitution syndrome in HIV-infected patients: spectrum of disease and long-term follow-up. Phillips P, Bonner S, Gataric N, Bai T, Wilcox P, Hogg R, O'Shaughnessy M, Montaner J.

Glucocorticoid resistance and the immune function in the immunodeficiency syndrome. Norbiato G, Bevilacqua M, Vago T, Clerici M. Ann N Y Acad Sci. 1998 May 1;840:835-47. Review.

POLL RESULTS

As we approach the New Years, its

1. Go Ducks. 14% (3)

2. Go Oregon. 5% (1)

3. Ducks all the way. 14% (3)

4. How did Pasadena get a Rose Bowl? Portland is the Rose City. 24% (5)

5. Do not even think of mentioning Ohio in "Other' answers, even if I was born in Cleveland. 14% (3)

6. Other Answers 29% (6)

7. having grown up 10 minutes away from the rose bowl I argue against number 4 and for number 2 and the latter part of 4

8. In the spirit of mocking our Rose Bowl opponents, I move that Oregon change it's state motto to, “The Duck-Eye State”;.

9. It's (still) great to be a Florida Gator!

10. Go Cowboys!

11. go bucks

One Darn Thing After Another

Dec 31, 2009

Medicine is dangerous. We do dangerous things to people and most of the time we get away with it. This century at my hospitals we have aggressively introduced "bundles," collections of best practices, for ventilators and catheters and surgery. The consistent application of these practices have driven hospital acquired infections into the toilet.

Unfortunately, as I make a living, or used to, from hospital-acquired infections. Now I see at best one ventilator-associated pneumonia or line infection a year. Tops.

Soon I will be standing on a street corner with a poorly lettered sign "Well do ID for food" or "Why lie? I need to give a cephalosporin."

However, there is still the occasional complication to keep a chicken on the table.

Patient has a central line (IJ) placed for sepsis and has a pneumothorax. Needs a chest tube. Patient, after transfer to the floor, decides to go to the gift shop and unhooks themselves.

Break the seal and the, slurp, bacteria are sucked into the pleural space.

A large, round, abscess forms, full of MRSA and strep. That requires a VATs and another chest tube. It is quite the sequence of events to get to an ID consult. Line to pneumo to chest tube to gift shop (the big problem) to infection to VATS to me. Better than a triple play. Infections from chest tubes are rare, despite the fact that all tubes are two-way streets.

The question was what to treat with (vancomycin as it was MRSA with an MIC of 1.0) and how long (until better).

And it you are using bundles, stop it. I have a kid soon-to-be starting college, and I do NOT want to have to sell a kidney to pay for it.

Rationalization

Infect Control Hosp Epidemiol. 2006 Feb;27(2):195-7. Epub 2006 Feb 8. Chest tube-related empyema due to methicillin-resistant Staphylococcus aureus: could the chest tube be coated with antiseptics? Torres HA, Hanna HA, Graviss L, Chaiban G, Hachem R, Chemaly RF, Girgawy E, Raad II.

J Trauma. 1997 Nov;43(5):764-71. Posttraumatic empyema thoracis: a 24-year experience at a major trauma center. Mandal AK, Thadepalli H, Mandal AK, Chettipalli U.

Hippy Newb Beer

Jan 2, 2010

Ducks just lost. Crap. A couple of years ago Dr. John Bartlett was giving a talk about bird influenza and he noted that migrating birds were probably going to be the vector by which bird flu makes it to the US, particularly ducks, since they tend not to die from bird flu.

"No one can stop the Ducks" he said, unaware of the U of O mascot.

Sigh.

The last case of the year and the decade was a 90-year-old female who presented with right foot pain over her "bunion."

The ER did an I&D and expressed 'pus' although it was not sent for culture or gram stain, and she was placed on vancomycin. For 5 days the foot remained red and painful and swollen over the first metatarsal. So they called me.

She had two weeks of exquisite pain in her bunion, no trauma, fever, chills, etc.

Plain film showed nothing, MRI had bone edema, perhaps osteomyelitis, but no bone erosion.

Her toe had rubor, dolor, calor and tumor with a white pasty pus coming out of the incision. The black line that was drawn around the redness showed no improvement.

People do not respond to antibiotics for three reasons.

1) Pus needs draining. The best antibiotic is cold steel in the hands of a surgeon.

2) The bug is resistant.

3) Wrong diagnosis.

Her creatinine as up to 1.8 (from 1.1), her uric acid was 12 and the pus, when sent to the lab, showed no WBC and all urate crystals.

Gout. Podagra. I guess vancomycin doesn't treat gout. I have been fooled by gout many times, especially when it is in odd joints. I once saw a patient with polyarticular small joint arthritis, and I went through the differential with my resident not once mentioning gout. She nodded, but, on her own, sent the joints off for crystals, which were positive. I now send off every joint fluid for crystals as well as the usual infectious disease diagnostics. No one (except for the hospitalist who picked up the patient on day 5) thought about gout.

I like this quote from the Wikipedia entry on gout from 30 AD.

"Again thick urine, the sediment from which is white, indicates that pain and disease are to be apprehended in the region of joints or viscera. … Joint troubles in the hands and feet are very frequent and persistent, such as occur in cases of podagra and cheiragra. These seldom attack eunuchs or boys before coition with a woman, or women except those in whom the menses have become suppressed. Upon the commencement of pain blood should be let; for when this is carried out at once in the first stages it ensures health, often for a year, sometimes for always. Some also, when they have washed themselves out by drinking asses' milk, evade this disease in perpetuity; some have obtained lifelong security by refraining from wine, mead and venery for a whole year; indeed this course should be adopted especially after the primary attack, even although it has subsided."

I will NOT drink asses' milk nor avoid venery should I get the gout.

I have never seen a case of gout with "urate milk": so many crystals in the joint the fluid looks like, well, milk, I expect it will take a long time to get better. Even with simple gout

"MSU crystals disappeared from the synovial fluid of all 18 joints after reduction of SUA to normal levels. The time required for disappearance ranged from 3 to 33 months"

Rationalization

Ann Rheum Dis. 2007 Aug;66(8):1056-8. Epub 2007 Jan 12. Time required for the disappearance of urate crystals from synovial fluid after successful hypouricaemic treatment relates to the duration of gout.

Pascual E, Sivera F.

J Rheumatol. 1997 Dec;24(12):2389-93. Acute gouty synovitis associated with "urate milk." Fam AG, Reis MD, Szalai JP.

Book Review

Jan 4, 2010

It is the seasonal slowdown and I will soon be standing on a street corner with a sign "will do ID for food." It is always quiet this time of year, and I suppose I could pull a case out of the files, but instead I will do a book recommendation.

Back in high school I read Earth Abides, by George R. Stewart. I remembered it as a good book, but have been wary of re-reading books I loved as youth. All too often they have not stood the test of time. I tried to re-read Dune when I was about 26 and, blech. Maybe at 52 I should retry Dune. By chance Earth Abides was recommended as an audible pick on one of the TWIT podcasts, and I decided to re-read it.

Great book. It takes place from 1949 on, when the world's population has been wiped out by a plague, and is how the earth and the few remaining humans adapt.

Infections play several key roles, or as I call them, plot devices, in the novel. Humanity is done in by a "super measles." See, the MMR is important. Syphilis, pharyngitis, the common cold, and typhoid play supporting, yet important, roles in the book. I will not give any spoilers. From the vantage point of 50 years later, the author gets almost all the epidemiology and infectious diseases right.

I would also recommend that you sign up for Audible and listen to it. There are deals where you can get your first book free. The reader, Jonathan Davis, has a reading style more than does the book justice.

We saw Avatar this weekend, and while I thought the movie was great, it suffered from no infectious diseases, a lack that even 3D digital could not overcome.

Poll Results

My favorite plague book is

1. The Earth Abides 12% (3)

2. The Plague 35% (9)

3. I am Legend 19% (5)

4. Mandel, Douglas and Bennett 12% (3)

5. Other Answers 23% (6)

6. A Man of Faith: The Spiritual Journey of George W Bush. David Aikman. I haven't recovered yet.

7. World War Z

8. the white plague

9. WH Mcneill,"Plagues and Peoples"

10. The Andromeda Strain

Coke Adds Life?

Jan 6, 2010

The patient was admitted in November with severe sore throat, fevers, and a white cell count of zero. Extensive work up of the leukopenia yielded nothing. Time and/or G-CSF lead to improvement of both her symptoms and her white count, so she was discharged.

Four weeks later it is dejà vu all over again.

Fevers, 1 poly and 1 band on her differential and a severe sore throat.

Work up again is negative except for the fact she spends most of her free time using cocaine.

Is cocaine the cause of the low white cell count? Kinda sorta.

Cocaine is.. what?

Contaminated? Makes it sound like the product was made with the intent of purity that somehow went awry.

Adulterated? Cut? Spiked? With levamisole.

Levamisole is

"an antimicrobial belonging to the class of imidazothiazole derivatives, this agent has been reported recently in a high proportion of seized cocaine throughout North America and Europe. Historically, the primary therapeutic uses of levamisole have been as treatment for rheumatoid arthritis and various cancers, and as an anti helminthic agent in both humans and animals."

It can be 30% to 70% of the coke by weight and is a well-described cause of neutropenia. Of course, there are many other substances in cocaine to increase its bulk, mostly caffeine and anesthetics.

Why does levamisole cause neutropenia? No one knows.

"Instances of the reaction emerged with the use of levamisole as a treatment for rheumatoid arthritis in the late 1970s and early 1980s, providing clues to a possible cause and genetic predisposition. The incidence of agranulocytosis among patients with rheumatoid arthritis was determined to be as high as 20%, although reports varied.7 Several small studies involving patients with rheumatoid arthritis and related disorders reported a strong association between the development of agranulocytosis and the presence of HLA-B27."

"Anti-neutrophil antibodies found in patients who develop neutropenia after levamisole use have been postulated as a potential cause for the neutropenia. ANCA has also been implicated in drug-induced neutropenia."

And she is ANCA positive.

Most of the cases have occurred on the West Coast of the US and Canada.

So. Does Coke add life? Well, not really. I prefer a Diet Rite with a cap full of vanilla extract. And it is Watsons that is the best vanilla. I think I will have one now.

Rationalization

CMAJ. 2010 Jan 12;182(1):57-9. Epub 2009 Dec 7. Cocaine adulterant linked to neutropenia. Matthew O. Wiens PharmD, Wai Kon Son MD, Colin Ross PhD, Michael Hayden MD PhD, Bruce Carleton PharmD

Harm Reduct J. 2009 Nov 17;6:30. Levamisole tainted cocaine causing severe neutropenia in Alberta and British Columbia. Knowles L, Buxton JA, Skuridina N, Achebe I, Legatt D, Fan S, Yan Zhu N, Talbot J.

Truth, big T.

Jan 9, 2010

The Greeks had their geometrical theorems to derive truth, at least geometrical truths. Two parallel live will never meet unless properly introduced. There are other systems that have fundamental facts from which all truth and understanding are developed.

All truth, for an infectious disease doc, in the end, comes from the cultures. The cultures do not lie, although they can mislead.

Patient has known ESLD from ETOH with ascites. Bili 4.0, Albumin 2.1, Coags OK at baseline. Comes in with acute abdominal pain and fevers and ends up in the ER with bowel obstruction from some odd tumor, which is resected with an end to end nastymosis.

Post op is initially stable except for copious peritoneal fluid leaking from the wound.

Then, sepsis occurs. The blood grows E. coli and the peritoneal tap grows Candida and enterococcus.

This is not what one would expect with SBP. Candida is a rare cause of, well, SFP, and the same can be said for enterococcus. The only reason these two organisms are in the peritoneal fluid together is a hole in the nastymosis.

Holes are two-way streets, and I suppose these organisms could have gained access to the peritoneal space from the abdominal wound, but not as likely.

Every now and then I see a CAPD peritonitis from a Bacteroides or mixed cultures. Then you know the CAPD catheter eroded into the bowel. The only explanation for those bugs there is a hole in the bowel.

I will not know if there is a hole in the bowel; other factors have led to a different clinical course.

I can only suspect the truth in this case since I do not get a definitive e-lap. The question is not what is the bug. The question should always be why that bug there. The answer will often lead to the etiology of the disease. That will give you the truth.

Rationalization

Scand J Infect Dis. 2004;36(9):649-55. Clinical significance of untreated Candida species isolated from ascites in cirrhotic patients. Choi SH, Soo Kim Y, Chung JW, Choo EJ, Kwak YG, Lee YS, Kim MN, Woo JH, Ryu J, Kim NJ.

Eur J Clin Microbiol Infect Dis. 2009 Jan;28(1):21-6. Epub 2008 Jul 9. Enterococcus: not an innocent bystander in cirrhotic patients with spontaneous bacterial peritonitis. Lee JH, Yoon JH, Kim BH, Chung GE, Myung SJ, Kim W, Kim YJ, Kim EC, Lee HS.

POLL RESULTS

I get my truth from

Cultures. 23% (12)

Fox news. 8% (4)

Oprah. 4% (2)

the first hit on Google. 37% (19)

truth is relative, so I ask my Uncle. 15% (8)

Other Answers 13% (7)

the magic 8 ball

The Flying Spaghetti Monster.

Harrison's Principles of Internal Medicine

All that glitters

Jan 12, 2010

Fever. Almost all my patients have a fever, at least at the beginning. Sometimes I am asked to figure out why the fever.

Patient is an elderly female who had a steroid injection in her C spine for pain. Three days after the injection: fevers to 101 sweats, diffuse muscle pain, and progressive weakness in the arms and legs. Symptoms persist for over a month.

No bowel or bladder dysfunction. The husband tells me that she can no longer get off a chair without help, which she could do before the injection.

The exam was odd for the epidural abscess I supposed she had.

No neck tenderness to percussion, normal reflexes and she was weak, but in a 'can't do it cause it hurts' kind of way not in an 'I can't do it' kind of way. She could generate muscle tension, but could not raise her legs or do the chicken (those that have attended a wedding in the Midwest will understand).

Labs? An increased WBC and a sed rate >100. Epidural. Has to be. Odd features, but what else would tie it all together? Maybe endocarditis, but no murmur or emboli.

So it’s Friday afternoon, last consult of the day, and I told the hospitalist that it was probably an atypical epidural, get an MRI.

As I finished the dictation, I ended with a throwaway thought that I didn't really believe. "If this isn't an epidural, it’s the most acute case of PMR I have ever seen."

I don't know where that thought came from.

So off I went for a weekend of golf and errands and I come back on Monday and what do you know: MRI was negative and, after excluding every other disease, it is thought that yes, it’s PMR.

The heck. Sure surprised me. But clinically, and especially the exam, it was in retrospect more like PMR than an epidural abscess. Although it all occurred just after the injection, it was the old true-true and unrelated. All that glitter is not gold and all causes of fever are not infectious. Unfortunately.

Rheumatology tells me that Polymyalgia Rheumatica can be acute in its presentation, which was a surprise to me. I had always considered it a disease with an indolent progression. How often it presents this way, I cannot find.

Itchy Red Bumps

Jan 15, 2010

Patient had three months of itchy red bumps. But you probably guessed that. I am not a fan of seeing derm patients. I hate making rash decisions.

Thank you thank you, I will be here all week, do not forget to tip your waitress.

These red bumps have been going on for 3 months and she has had multiple treatments for mur-sa to no avail. They occur on her left arm and her neck.

Otherwise she is healthy.

On exam, and I am terrible at describing skin diseases, were what appeared to be follicular rash in various stages of evolution. One was red, scaly and about the size of a dime.

It sure looked fungal to me. But why?

So I started asking. Pets? 4 cats. Any with a problem? Yep. One of the cats is losing its hair from a skin condition. She holds the cat in her left arm and it licks her neck as she combs out the diseased hair. And her granddaughter was recently diagnosed with ringworm after a visit.

It is not that unusual for infections to spread back and forth from humans and their pets. S. aureus, C. difficile, and even E. coli causing UTIs have been reported. It is why I am leery of pets in the hospital, even as a 'therapy' animal (ADA excluded. Even I would not forbid a seeing eye dog). And I point out that pets lick their rears, then you let them lick your face?

Cutaneous fungal infections and sporotrichosis are known to come from cats. I bet this was spread from cat to my patient and her granddaughter. That it is found where she holds the cat and where the vermin licks her is icing on the metaphorical cake. It could be Tinea, Microsporum or even Malassezia which is found in cats: Malassezia pachydermatis was isolated from 52%, M. furfur from 38%, and M. sympodialis from 9.5% of cats. There was one case of a hedgehog that was the source of cutaneous fungal infections in humans and dogs.

I suggested an antifungal for the patient and autoclave for the cat. You can't be too careful and it tenderizes the meat nicely. Cat. The other white meat.

Rationalization

Mycoses. 2007 Nov;50(6):491-5. Dermatophytoses in cats and humans in central Italy: epidemiological aspects.

Vet Dermatol. 2006 Oct;17(5):327-31. Isolation of Microsporum canis from the hair coat of pet dogs and cats belonging to owners diagnosed with M. canis tinea corporis.

POLL RESULTS

From a purely microbial perspective, the most repulsive creature is

1. a dog. 14% (10)

2. a cat. 26% (18)

3. a dung beetle. 10% (7)

4. a vulture. 28% (19)

5. my ex. 13% (9)

6. Other Answers 9% (6)

7. a toddler.

8. Rush Limbaugh

9. Aspergillus

10. Anopheles gambiae, and its relatives - who not only leave an itchy bite, but are the predominant carriers of Plasmodium falciparum.

11. A toddler

12. human

My liver quivers.

Jan 17, 2010

"My liver quiver my blood pressure high. Yet I don't want no doctor." ~Reggae Fever by Bob Marley.

Much as I like Mr. Marley, I can't see a liver quivering, at least not from Reggae fever, which is due, I think, to Tb acquired from hotboxing too much ganja. If your liver quivers see a doctor.

Patient is a middle-aged male who comes in with fevers and right upper quadrant pain.

Elevated white count and LFT's, as well as a UTI. The latter is odd for a middle-aged male.

Culture of the urine grows K. pneumoniae and a CT shows a ten centimeter (pronounced cent-a-meter, not saunt-a-meter, at least outside of France. I mean, do you ask for 50 saunts to buy a Snickers?) abscess and it, too, grows Klebsiella pneumoniae.

Lab tells me it is thick and mucoid, like snot on a plate. That is the K. pneumoniae that is associated with liver abscesses, endophthalmitis and more. It may just make your liver quiver after all.

There are several genotypes of K. pneumoniae, and the K1 is the one associated with metastatic complications. This organism is one of dem dare emerging pathogens. The mucoid capsule makes the beast resistant to phagocytosis and allows it to cause abscesses, although as is often the case, it is the confluence of multiple virulence factors that lead to increased invasion.

Did it start in the urine or go to the urine? I don't know. Drainage, antibiotics and time and he should get better. And he did.

Rationalization

Clin Infect Dis. 2007 Aug 1;45(3):284-93. Epub 2007 Jun 19. Klebsiella pneumoniae genotype K1: an emerging pathogen that causes septic ocular or central nervous system complications from pyogenic liver abscess.

Diagn Microbiol Infect Dis. 2008 Sep;62(1):1-6. Epub 2008 May 16. Comparison of prevalence of virulence factors for Klebsiella pneumoniae liver abscesses between isolates with capsular K1/K2 and non-K1/K2 serotypes. Yu WL, Ko WC, Cheng KC, Lee CC, Lai CC, Chuang YC.

POLL RESULTS

As for me, I want a doctor when

1. My liver quivers. 9% (3)

2. My colons rollin'. 9% (3)

3. My eyes fries. 22% (7)

4. My brain sprains. 25% (8)

5. My bones groan. 22% (7)

6. Other Answers 13% (4)

7. My prostate is prostrate.

Lend me your ears.

Jan 19, 2010

The patient is a 24-year-old student, so an adult. She has Graves and, since the US ranks 37th in the world for health care, has access to medical care. Not. She has been on her Grave's medications intermittently for cost reasons.

She has the sudden onset of ear pain. No other symptoms and it progresses to the worst pain she has ever had, so she comes to the ER.

She has no other history of note.

CT and exam have the ocular findings of Graves and otitis media with mastoiditis.

Odd things: fever to 40, which matches her respiratory rate, and she is hypotensive. How much is untreated hyperthyroidism and how much infection? Can't say for sure.

Work up reveals nothing else of note but the next day her blood cultures are positive for S. pneumoniae. No meningitis, abscess, subdural empyema or pneumonia. No history to suggest an immunodeficiency and her HIV is negative.

I do not think of acute otitis media as a source of bacteremia.

Grave's, it will be noted, is not associated with any infectious complications, so it is a disease of no interest.

In my world otitis media is usually Wegener's. Adults rarely get acute otitis media (AOM) with an incidence of 0.25%. So far every AOM in the adult I have seen (maybe 3) have turned out to be Wegener's.

Kids get AOM all the time and get treated for it whether they have AOM or not. Kids do get bacteremia with AOM, maybe 3% of the time. 24 isn’t a kid. Well, to me anyone under 35 is a kid. They are letting children into Medical School if you ask me.

Adults? I can't find any cases of AOM with bacteremia that did not have a concomitant complication elsewhere. Odd. Welcome to my world.

Rationalization

Pediatrics. 1991 Jan;87(1):48-53. Bacteremia with otitis media. Schutzman SA, Petrycki S, Fleisher GR.

Purulent otitis media in adults. Arch Intern Med 1992 Nov;152(11):2301-4.

POLL RESULTS

They are still children to me if they are

1. less than 18 years old. 19% (10)

2. less than 21 years old. 31% (17)

3. less than 30 years old. 26% (14)

4. less than 40 years old. 0% (0)

5. everyone seems to be a child to me. 20% (11)

6. Other Answers 4% (2)

7. Fans of reality TV shows.

8. Pre-pubescent.

Little things

Jan 21, 2010

I have been doing ID for about 25 years, half a lifetime and yet I seem to know less and less. A day does not go by that I do not learn something new, even about diseases I would think I know like the back of my hand. Hmmm. Back of hand. Where did the scar some from? Has that mole always been there? Squirrel......

I'm back. Patient is a middle-aged male who was admitted 2 weeks ago with pneumonia. No microbiologic diagnosis was made and he was sent home on a quinolone, as is everyone.

10 days later he has profuse watery diarrhea leading to dehydration and is readmitted to the hospital and, due to respiratory compromise, requires intubation.

He had not been having any respiratory symptoms at home and seemed to be improving until the diarrhea hit

CT for pulmonary embolism was negative, but he did have patchy bilateral infiltrates. C. diff was positive. No surprise. Nothing drives C. diff like a quinolone. Quinolones are probably the worst antibiotic for causing secondary infections like C. diff and MRSA. Bad for the local environment.

But interestingly, this time (but not last) he has a Legionella antigen sent and it was positive. Now what?

With Legionella it is always fun to try and hunt down a source. Rates go up after thundershowers, and there have been outbreaks associated with fountains, showers, public aquariums and nuclear cooling towers. Homer developed cutaneous Legionella after plugging a leak at the plant. My patient had no good water exposure that could be determined, and we do not see a lot of Legionella in the great Pacific Northwest, despite all the rain. Probably as it is not humid enough, although we do get a burst after thunderstorms, perhaps due to the fact I harangue the housestaff to order more tests.

You cannot use the urinary antigen to determine how the patient is responding to therapy. I discovered today that the Legionella urinary antigen (and who knew Legionella could urinate?) can be positive for weeks after the onset of disease and in one case it was positive for almost a year, which suggests a false positive to me. Or the patient was a cooling tower.

Rationalization

J Clin Microbiol. 1984 Oct;20(4):605-7. Onset and duration of urinary antigen excretion in Legionnaires’ disease. Kohler RB, Winn WC Jr, Wheat LJ.

Finger Infection?

Jan 23, 2010

Last spring the patient smashed the middle finger of his left hand, breaking the bones and requiring a wire to hold it all together. I do not know about you, but I probably could not drive if I didn’t have ready access to that digit.

He did well at first, then developed a pin tract infection that required debridement and a course of antibiotics. Cultures were negative, but he gets a variety of iv and po antibiotics.

I get called by the surgeon because upon the unwrapping of the finger it was blistered and blistered even as they watched and while on antibiotics.

Cultures again were negative and they called me. Patient had no symptoms of infection.

I saw him the next day in clinic and the finger looked bad, but not infected. The bandage was wet and all the skin from the blisters was dead and white. It looked like a finger on a corpse. But it was not hot, oozing clear fluid, and I do not think it was infected.

Years ago I say a patient for a chronic facial cellulitis. Remembering that bacterial cellulitis is never ever never never ever ever chronic, I took a history. He had a bug bite. The usual invisible bug no one sees, he put on a dab of triple antibiotic cream on it. It spread a little. He added more antibiotic cream. It got bigger. He added more. This continued until he looked like two-face, with one half of his face red and swollen. He was having a topical dermatitis reaction to the antibiotic cream.

I saw a similar case years later, this time due to tea tree oil being slowly applied in ever-enlarging swaths to the expanding redness of an ear and face.

Both triple antibiotic cream and tea tree oil can cause an allergic reaction that looks like cellulitis.

This patient, I think, was having a reaction to the Betadine being used to clean the finger. He was not happy with my conclusion, but that made the most clinical sense. I love it when a patient looks at me with total disbelief in what I tell them. I stopped the topical Betadine and I expect he will get better. He did.

Rationalization

Dermatol Surg. 2004 Apr;30(4 Pt 1):521-4. From road rash to top allergen in a flash: bacitracin.

Australas J Dermatol. 2007 May;48(2):83-7. Allergy to tea tree oil: retrospective review of 41 cases with positive patch tests over 4.5 years.

POLL RESULTS

Bacterial cellulitis

1. is never chronic. 20% (10)

2. never ever chronic. 28% (14)

3. Yes. It can be chronic. I have seen it. No wonder that patient thought you were a bozo. 24% (12)

4. No. You haven't, you are just fooling yourself. 2% (1)

5. Exactly what is this cellul that gets an itis anyway? 26% (13)

6. Other Answers 0% (0)

Microcosm

Jan 26, 2010

There are broad themes in my practice. The bugs change names (I presume microbiologists get drunk and change the names as a prank. I can just seem them sitting in a bar somewhere saying, "No, no, wait. Call it Stenotrophomonas" and then collapsing in laughter, beer squirting out their nose. Or is that just me?), the antibiotics come and go, new diseases are discovered, old diseases evolve, and through it all there is antibiotic resistance.

Resistance, to paraphrase the Borg, is inevitable. The consult today was a microcosm of the last ten years of my practice.

First is the ever-popular Methicillin-resistant Staphylococcus aureus (MRSA). A while back the patient had an 82-day course of vancomycin (NOT my doing, let me tell you) for a diabetic foot bone infection. This time the patient is admitted after an arrest (cardiac not legal) and develops MRSA pneumonia.

The vancomycin MIC was 1.0, and he was placed on vancomycin. After a week the patient was not better, and repeat cultures demonstrated that the MIC of the organism went to 2.0.

This slight increase in the MIC is, I think, due to what is called heteroresistant MRSA. What happens is that patients who have often had a long course of vancomycin select for a mutant strain that are occasionally kicked out daughter cells (they are, oddly, never referred to as sons) with decreased susceptibility to vancomycin due alternations in the cell wall that, among other things, make the cell wall thick and shaggy. Heteroresistance may be the first step down the path to full vancomycin resistance. Heteroresistance is hard to test for, so it is only a supposition.

Fortunately, the bug responded to linezolid, and, except for uber-tight isolation, the MRSA seems to not be a problem.

And then.

Just before discharge the patient has a worsening pulmonary function and a new infiltrate, and a bronch is done that grows an ESBL E. coli and a Burkholdia cepacia. It used to be Pseudomonas cepatia, but for too many tequila shots

I do not think either organisms are actually causing disease and everything improved in less than a day and so I suspect it was all mucous plugging. The bacteria were picked up from the tracheostomy on the way down.

But ESBL's are bad. ESBL stands of extended spectrum beta lacamase and they chew up every beta lactam but the carbapenems.

"Extended spectrum -lactamases (ESBLs) are plasmid mediated, TEM and SHV derived enzymes, first isolated in Western Europe in mid 1980s, most commonly in Klebsiella spp., followed by Escherichia coli. These enzymes are capable of hydrolyzing broad spectrum cephalosporins and monobactams but inactive against cephamycins and imipenem. In addition, ESBL producing organisms exhibit coresistance to many other classes of antibiotics resulting in limitation of therapeutic option."

Kind of limits treatment options, and since people don't usually start with carbapenems with acute infections, there may be increased mortality from these organisms.

More worrisome is this resistance is on a plasmid, so it has the ability to spread through the population like grass through a goose. ESBL's are rare. Now. But 19 years ago MRSA was rare, less than 2% of isolates. So I bet a nickel that in 10 years we have more than 50% ESBL's. Any takers? Given reimbursement trends, in a decade I may welsh on the bet.

The third issue is the Burkholdia, which is seen mostly in cystic fibrosis patients and patients who have been on antibiotics for a long time. It is an organism associated with medical care and frequent name changes. Of interest, according to the Wikipedia, the font of all wisdom (not Helvetica as some would say)

"B.cepacia was discovered by Walter Burkholder in 1949 as the culprit of onion skin rot."

It’s why I keep rotting onions out of the ICU.

Three issues in my professional life this decade: MRSA, ESBL and odd organisms with changing names. All in one patient, Infectious Diseases writ small.

Rationalization

J Clin Microbiol. 2009 Jun;47(6):1640-4. Epub 2009 Apr 15. Vancomycin MIC plus heteroresistance and outcome of methicillin-resistant Staphylococcus aureus bacteremia: trends over 11 years. Musta AC, Riederer K, Shemes S, Chase P, Jose J, Johnson LB, Khatib R.

J Antimicrob Chemother. 2010 Feb;65(2):333-41. Epub 2009 Dec 3. Bacteraemia due to extended-spectrum beta-lactamase-producing Escherichia coli (ESBL-EC) in cancer patients: clinical features, risk factors, molecular epidemiology and outcome. Gudiol C, Calatayud L, Garcia-Vidal C, Lora-Tamayo J, Cisnal M, Duarte R, Arnan M, Marin M, Carratalà J, Gudiol F.

POLL RESULTS

Microbiologists change organism names

1. to honor their dead. 7% (4)

2. to justify their jobs. 15% (8)

3. to annoy ID docs 6% (3)

4. because they can't hold their liquor 15% (8)

5. because they are afraid that we will otherwise notice that they still haven't figured out a way to classify streptococci. 50% (27)

6. Other Answers 7% (4)

7. to honor Heraclitus

8. because they discover new things about bacterias

9. Because they are perfectionists and the perfect name is always changing.

Return of the Bad Old Days

Jan 28, 2010

It was like the old days, the bad days, the days before HAART.

Patient has not received health care for three years since he lost his job and his insurance and has not been on his HAART. I do not even pretend to know how to fix the problems with health care, but I cannot understand why we have people die in this country from lack of health care. I see a one or two people a year die from delaying care due to lack of insurance.

I sometimes think the problem is that people are looking for reform that will lead to a good health care system, rather than looking for the least bad solution. Any solution will be bad, it is a matter of deciding which bad features you can live with. Like death panels. I so want to be on a death panel. In my mind the least bad solution would include basic health care for everyone and god-awful amounts of money spent on ID docs relative to everyone else. But I would settle for the former feature.

Anyway, the patient’s HIV progressed, as it is wont to do when you can’t afford the medications, which runs 1 to 2 grand a month.

He has two to three weeks of progressive SOB, minimal cough and fever. He hits the ER with a pO2 of 69 and diffuse, bilateral infiltrates, and a CD4 of 38.

PJP right? Well, there are two outliers.

One. His LDH is normal. I have never seen severe PJP with a normal LDH. While there is some variation, the worser the PJP the higher the LDH. A normal LDH excludes PJP.

The other was massive adenopathy on the CT and CXR. PJP does not cause adenopathy. Or pleural effusions. Or cavities (expect patients on inhaled pentamidine).

So off to bronch, and there are yeast on the biopsy. His Cryptococcal antigen is > 1:2024 in the blood. He doesn’t have pneumonia so much as miliary Cryptococcus and the diffuse infiltrates are due to hematogenous spread of the yeast. I bet if we were to do a liver biopsy or bone marrow biopsy, we would find more yeast than human cells.

It is also worrisome that he has so little inflammatory response. No fever at all. In the old days when you had patients like this and they received therapy, once the yeast died and spilled their antigens, patients would have a dramatic reaction, sort of a Jarisch Herxheimer response and herniate or go into multi-organ system failure.

Should I give him steroids along with the Ampho B and 5FC? Little good data, and although I am tempted, I will not yield to the temptation.

I expect to see more Cryptococcus since the outbreak of Cryptococcus neoformans var. gattii in Vancouver Island is slowly spreading south, thanks to the lousy work of homeland security.

BTW: if you are having trouble sleeping, the 2010 IDSA guidelines for Cryptococcus are available. Much better than any purple dinosaur. Or is it a butterfly?

Rationalization

Clin Infect Dis. 2009 Aug 15;49(4):591-5. Dexamethasone in Cryptococcus gattii central nervous system infection. Phillips P, Chapman K, Sharp M, Harrison P, Vortel J, Steiner T, Bowie W.

POLL RESULTS

As a physician, I know the solution to ALL problems. The cure for the health care 'system' is

1. tax and spend 22% (10)

2. free markets. 11% (5)

3. there is no health care problem as long as I get paid. 4% (2)

4. a virulent plague. 51% (23)

5. global warming. 0% (0)

6. Other Answers 11% (5)

7. more nitric oxide

8. perhaps a combo - virulent plague AND tax and spend

9. 42

10. smallpox

The Real Deal?

Jan 31, 2010

Blood cultures drive. Me. Crazy.

This week I had two patients with positive blood cultures.

The first came in with an acute MI and a ruptured chordae. At admit he had a fever and all four bottles, drawn at the same time, grew Streptococcus parasanguinis. Valve was replaced and subsequent cultures, all on antibiotics, are negative. TEE was negative and the mitral valve, at least, was negative for infection in the OR. The aortic valve was not seen.

The second came in with acute lobar pneumonia and the sputum grew H. influenza, but all the blood cultures grew Staphylococcus hominis, a coagulase-negative Staphylococcus. Subsequent cultures were negative (on antibiotics) and workup for an endovascular infection is negative including TEE.

So why the positive blood cultures? 4/4 contaminant? Transient bacteremia? Endocarditis beyond my ability to diagnose clinically? Another source?

I don't know. It would have been so much nicer to have repeat blood cultures before antibiotics were started, but the patients were too unstable.

There are no human cases of S. parasanguinis in humans; it does cause mastitis in sheep.

S. hominis causes the occasional endocarditis and she had a recent central line, a port for chemotherapy that was removed a month ago, so she is at risk for an endovascular infection. S. hominis is also found in French cheeses and dry fermented sausages.

Neither patient had contact with sheep, sausages, or brie.

If the first case, because there is a new valve in place, I elected to give him a course of antibiotics.

In the second, I elected to stop and see what happened.

Maybe I should have done it the other way around. But that’s why I don't get the big bucks.

I hate blood cultures.

Update: It worked. Neither had a recurrence of the bacteremia. Lucky them. And me.

Rationalization

Clin Cardiol. 2009 Dec;32(12):E48-54. Endocarditis complicating central venous catheter bloodstream infections: a unique form of health care associated endocarditis. Chrissoheris MP, Libertin C, Ali RG, Ghantous A, Bekui A, Donohue T.

Fungus Ball

Feb 2, 2010

Patient is admitted with nausea and right flank pain. It has been progressive for about a week, but it was a fever that brought her to the ER.

Several months earlier she had a gram-negative kidney infection and it was serendipitously discovered that she had ureteral obstruction that lead to a stent placement.

She has diabetes and baseline mild renal insufficiency with a creatinine that hovers above 2.0.

Now she has Candida albicans in the urine, Candida in the blood, an increase in the kidney size and a new obstruction of the renal pelvis with a fungus ball.

This is one of the many cases where no matter what you do, it may not work.

Echinocandins will not work at all as the urinary levels are sub-homeopathic. I know there was the series in CID of Candida UTIs treated with caspofungin, but that just goes to show the importance of a placebo comparator in the treatment of a self-limited disease.

Amphotericin will drive the creatinine even higher. Fluconazole is not a bad drug, but with a low CrCl she is not going to get much drug into her urine.

And then there is that plastic, to which Candida sticks better than a burr to a wool sock. They don’t call me Dr. Metaphor for nothing. Well, they don’t call me Dr. Metaphor. I spent two years of my life as fellow (before gender change?) trying unsuccessfully to figure out why Candida was so sticky. When I germinated Candida in the plastic test tube, we routinely lost a log or more of organisms as they stuck to the test tube.

And there is the fungus ball, that needs to be removed to be cured, but she has other comorbidities that make surgery problematic. Maybe we could remove it with a percutaneous nephrostomy, but that is plastic as well.

It is one of those cases where the question is what is the least bad solution. Every choice has the opportunity of ending up bad.

For now it’s high dose fluconazole and a probable nephrostomy with an amphotericin wash out.

There are not that many case reports in the literature of fungal balls in the kidney.

The IDSA guidelines are apparently based on little more than anecdotes, based on four references, mostly in neonates, as is so often the case with yeasts:

Fungus balls can occur anywhere in the urinary collecting system. Aggressive surgical debridement is central to successful treatment in most nonneonatal cases. Systemic treatment with AmB-d (with or without flucytosine) or fluconazole has been used most often. If a percutaneous device provides direct access to the renal pelvis, ureters, or bladder, local irrigation with AmB-d at a dosage of 50 mg/L of sterile water should be considered as an adjunct to systemic antifungal therapy, but the optimal dose and duration of AmB-d irrigation have not been defined . Other methods to facilitate the breakdown and passage of fungus balls include intermittent saline irrigation, debulking of the fungal mass through a percutaneous device, and irrigation with streptokinase.

For all the fretting we do about it, apparently it is not all that common.

Eventually the infection was eradicated, but not without a percutaneous nephrostomy.

Rationalization

Actas Urol Esp. 1990 Jul-Aug;14(4):314-8. Systemic candidiasis and ureteral fungus ball. Ketoconazole and irrigating solutions in the management of urinary candidiasis. Martínez Bengoechea J, Allepuz Losa C, Gil Sanz MJ, Minguez Pemán J, Rioja Sanz LA.

POLL RESULTS

Candida balls

1. are a good substitute for popcorn balls at Halloween. 11% (3)

2. are an outdated dance of the upper-class molds. 36% (10)

3. should be treated with orchiectomy. 36% (10)

4. tend to slice if hit with the club face open. 4% (1)

5. is one courageous fun guy. Hey. You try for 5 bad puns about a yeast infection. Ain't easy. 7% (2)

6. Other Answers 7% (2)

7. Is what you get when you go out on a really cold day.

Louie Louie, oh no me gotta go

Feb 4, 2010

The Kingsman were a Portland band that made a hit of the song Louie, Louie. Supposedly there were smutty lyrics, but who could tell since the recording was so muddled. Since doing ID for a living, I always hear it as Lues, Lues. It is an ode to a spirochete. That’s why me gotta go now.

The patient has long-standing HIV and no CD4 cells. None. Like the patent a week or so ago, no job leads to no insurance leads to no health care leads to HIV progression.

He has had this rash, and I am not certain what it is. It is moderately itchy, flat, kind of hyperpigmented and some areas are verrucous. I have not seen anything quite like it.

It does not look like KS or Bacillary angiomatosis, the two most common skin lesions.

I would have thought it was Norwegian scabies except we find no scabies on exam, and now I have started to itch.

The FTA is positive as is the RPR, but only 1:4. I am suspicious that the skin lesions are due to syphilis. He denies ever getting treated for syphilis and could this be an RPR that has burned out? Been treated? Or falsely low due to a bankrupt immune system?

We are going to get a skin biopsy and an LP before starting penicillin.

Pinta (Treponema pallidum carateum), more than a bean and a ship, and Yaws (Treponema pallidum pertenue) also cause skin conditions that can be verrucous.

When I was a kid, one of the burger joints in our neighborhood was called Yaws. I have since wondered what was in the burgers and why they went out of business.

Patient was lost to follow-up and the skin biopsy was non-diagnostic.

Rationalization

Br J Dermatol. 2005 Jun;152(6):1343-5. Extensive annular verrucous late secondary syphilis. Pournaras CC, Masouye I, Piletta P, Piguet V, Saurat JH, French LE.

Migratory Plastic

Feb 5, 2010

Birds migrate. Wildebeests migrate. Salmon migrate. Medical devices should stay put.

I have, over the years, seen various medical devices move. I have seen two VP shunts migrate into the colon and the patient present with gram-negative meningitis. There is a case out of Africa where the mother thought there was a worm in the child's rectum and yanked it out, pulling out the shunt as well. Maybe that’s apocryphal, as I can't find the reference, but I remember reading it once upon a time. Really.

Pacemakers love to erode out of the pocket site to cause infections, especially in thin people. There are benefits to having increased bulk.

The patient I saw recently presented with acute pelvic pain with no other past medical problems. Evaluation demonstrated that there was a pelvic abscess, not that unusual, but the US showed that the IUD, which had been in for many years, and migrated through the uterus and into the bowel.

My gaster was flabbered, but a Pubmed reveals over 200 references of IUD's migrating to cause various complications, depending on which route they take. So IUD migration is rare but not unheard of.

In the OR abscess was found to be a uterine-cecal abscess due to the IUD migration. The abscess grew pure S. anginosus, one of the abscess forming streptococci, and should improve with antibiotics. The classic 'odd' infection with long-standing IUDs is actinomycosis, but I have not seen one of these since I was a fellow.

The oddest thing I have seen causing a colonic perforation was a square plastic bag tie like you use on the bread bag. I never did discover how it had been inadvertently (I assume) eaten. The oddest cause of esophageal perforation was a young man who did not chew his tortilla well enough thanks to an excess of beer and it lacerated his esophagus. I always chew my Doritos very carefully.

Plastic and metal just doesn’t like to stay put.

This kind of entry begs for anecdotes. Top my stories in the comments if you can.

Rationalization

Yonsei Med J. 2009 Aug 31;50(4):555-9. Epub 2009 Aug 19. Clinical features of abdominopelvic actinomycosis: report of twenty cases and literature review.

Pediatr Surg Int. 2007 Jun;23(6):575-80. Epub 2007 Mar 27. Trans-anal protrusion of ventriculo-peritoneal shunt catheter with silent bowel perforation: report of ten cases in children.

PMID: 17387494

SMALL BOWEL PERFORATION DUE TO A PLASTIC BREAD BAG CLIP: THE CASE FOR CLIP REDESIGN. ANZ Journal of Surgery Volume 75 Issue 5, Pages 360 - 362

Gastrointestinal Endoscopy Volume 38, Issue 1, January 1992, Page 100. Esophageal hematoma and tear from a taco shell impaction.

Using the Untried and the Unproven

Feb 9, 2010

I am an early adopter. My basement is littered with old technology that I neither use nor part with. Do I need an iPad? I doubt it, although with a bluetooth keyboard it may be a good replacement for my netbook. Do I want one? You bet. Like I want all new tech. Will I get one? Probably not in this economy, or at least until my netbook breaks. Anyone want to play soccer with a netbook? Of course as an iPod developer I really do need one for testing, right? I am practicing for the inevitable conversation with my wife.

I have to be careful not to let the enthusiasm for the new not spill into the practice of medicine, since the new often turns out to have unforeseen complications. I let others use new antibiotics and see if widespread use kills people. I never used trovafloxacin and have yet to give telithromycin. I try to be neither the first to try the new nor the last to abandon the old.

And yet.

My other bad habit is to reason from physiology to try interventions when I have no data to suggest they will work. I usually do not give in to the urge, but this week I did.

The patient is a relatively new quad with a neurogenic bladder and Foley who has had increasingly frequent UTIs with progressively resistant Pseudomonas. I am asked what can be done to prevent future infections.

And the answer is nothing. History and physical fail to find a single potentially reversible cause for the UTI.'s

However. People get UTIs from their bowel flora. Thanks to repeated antibiotics and prolonged hospitalizations, he is probably colonized with pathogenic flora rather than normal flora. If we reconstitute his bowel flora, maybe we can decrease his UTIs.

I am not, as a rule, proponents for probiotic pills. They are not regulated and posters at IDSA have shown that what is in the probiotic is not always what is in the pill and not infrequently the organisms in the pills are dead. VRE has also been isolated in probiotic pills; like much of the supplement industry, it is an unreliable product.

The literature to support probiotics to prevent UTIs is in females and is not encouraging. The systemic reviews suggest the studies are lousy and the efficacy problematic. No data in paraplegic males. But, perhaps, there is biologic plausibility with the probiotic organisms crowding out the pathogenic ones.

There is, however, success in treating antibiotic associated diarrhea by using yogurt high in bacteria. One of the local products is used in my hospitals in all patients on antibiotics and we have seen a marked decrease in C. difficile disease and testing. I reasonable surrogate of efficacy.

I hope that by altering his flora away from pathogenic gram-negative rods he may quit having recurrent UTIs. When he goes home, I told him to eat the 'natural' yogurt filled with bacteria; the one that most resembles poo. I bet they do not want that for a motto: "Eat out yogurt, it’s the closest to stool."

If it works or doesn't work, causality will be suspect. Never trust experience in a therapeutic ‘N’ of one.

Rationalization

BMJ. 2007 Jul 14;335(7610):80. Epub 2007 Jun 29. Use of probiotic Lactobacillus preparation to prevent diarrhoea associated with antibiotics: randomized double-blind placebo-controlled trial. Hickson M, D'Souza AL, Muthu N, Rogers TR, Want S, Rajkumar C, Bulpitt CJ.

Milliways

Feb 12, 2010

The patient has three impossible clinical characteristics.

One, he has recurrent leg cellulitis. Not that unusual in the obese you say. Well, yes, it was group A streptococcus. Most recurrent cellulitis is due to group A streptococcus, and the rest is from S. pyogenes. I know. Same thing. Joke. But three times in the last year he has had the abrupt onset of rubor, dolor, calor, and tumor of one of his legs and each time his blood cultures have grown a progressively resistant Pseudomonas aeruginosa. That bug is not supposed to cause non-necrotic cellulitis, much less recurrent disease. That’s not supposed to happen.

He has no immunodeficiency, no diabetes and he does not put his leg in any water outside his own shower. He has no abscess or osteomyelitis and, as best as can be told given the limitations of diagnostic studies in patients over 500 pounds, he has no other source for the bacteremia. That’s not supposed to happen.

He was placed on ceftriaxone and he improved over the next two days before the cultures showed it to be resistant to all beta-lactams. That's not supposed to happen.

Various permutations of his disease and organism yield nothing on Pubmed (and evidently "pubmed.com expired on 02/05/2010 and is pending renewal or deletion'). I do NOT want to have to learn a new URL for a search. No way am I going to Bing,

I was talking with my boss today, and we are both of the opinion that we are seeing more odd things than we used to. Probably because we have banished ventilator associated pneumonias and line infections (mostly) to the dustbin of history. AIDS and the diabetic foot are rarely in the hospital. So all I am left with is the strange things that I cannot figure out. Like this case. Cool. Interesting. And impossible.

Still, I had three impossible things happen today. So I am off to have breakfast at Milliways.

Rationalization

J Infect. 2010 Mar;60(3):191-9. Epub 2009 Dec 22. Recurrent bacteraemia: A 10-year regional population-based study of clinical and microbiological risk factors.Jensen US, Knudsen JD, Ostergaard C, Gradel KO, Frimodt-Møller N, Schønheyder HC.

POLL RESULTS

At Milliways I will have

1. a sandwich prepared by Chef Dent. 3% (1)

2. a pangalactic gargleblaster 44% (14)

3. a liquid that is almost, but not quite, entirely unlike tea. 13% (4)

4. a NowWhattian boghog. 3% (1)

5. a pint of bitter and peanuts. 19% (6)

6. Other Answers 19% (6)

7. Gin and tonic with a steak from a sentient cow, while watching Hotblack Desiado.

8. to 'Bing' the menu!

9. nachos (carnitas)

10. Large pizza with anchovies

Purpura

Feb 16, 2010

Purpura is bad. Not as bad as the movie Purpura Rain, but bad. It is one of the few things that cause me to bubble sort the order I see patients, having them rise to the top of the to-do list. I was just leaving the hospital this weekend when the ER called.

Patient had been in the day before for a cellulitis of both breasts. Labs were normal, so she was sent out on clindamycin. Bilateral infections are odd and usually not due to infections. She was back in, worse, and now she has cellulitis of the both breasts with purpura. And her ears have purpura. And there is a patch of purpura on her flank.

No trauma or injury or exposure to anything but cocaine and heroin.

She is afebrile and nontoxic and her labs are normal, including the platelets, except for a lowish WBC (2.9).

Purpura means meningococcus or gonococcus in normal people, and in the asplenic pneumococcus, Yersinia and Capnocytophaga. All bad. Other diseases, noninfectious and so less interesting, cause purpura as well, such as TTP, but she is not thrombocytopenic.

Next day, despite antibiotics, she has new purpura and her cultures are all negative and will remain so.

So why the purpura?

I wonder if it is due to the cocaine. There are a smattering of cases of TTP and purpura from cocaine.

On the other hand, I recently had a case of levamisole contaminated coke leading to severe neutropenia. Well, adulterated not contaminated. Contaminated makes it sound as if it was inadvertently put in the coke, when they put the levamisole into the cocaine advertently. There are two cases levamisole causing ear purpura, which is an odd place to have purpura.

Coke? Levamisole? Both? Neither? I bet both.

I am going to go out on a limb here and say that drugs is not a healthy lifestyle. And I need a lifestyle myself; all I seem to have is a life. No style. Maybe a lifestyle coach....

It turned out to be vasculitis from Lupus.

Rationalization

Pediatr Dermatol. 1997 Nov-Dec;14(6):477-9. Ear lobe bilateral necrosis by levamisole-induced occlusive vasculitis in a pediatric patient. Menni S, Pistritto G, Gianotti R, Ghio L, Edefonti A.

Br Med J. 1978 February 18; 1(6110): 408. Cutaneous necrotizing vasculitis induced by levamisole. M A Scheinberg, J B Bezerra, F A Almeida, and L A Silveira

Cocaine-induced microangiopathic hemolytic anemia and thrombocytopenia simulating thrombotic thrombocytopenia purpura. Keung YK, Morgan D, Cobos E. Ann Hematol. 1996 Mar;72(3):155-6. No abstract available.

Clin Nephrol. 1995 May;43(5):348-9. Schoenlein-Henoch purpura with necrotizing vasculitis after cocaine snorting. Chevalier X, Rostoker G, Larget-Piet B, Gherardi R.

My Least Favorite Nun

Feb 18, 2010

The patient came in with seizures and new onset right arm weakness. MRI shows edema and TNTC (well, not really. I suppose they could be counted, but once you get past a half-dozen or so, what is the point, really, of counting) cysts.

I have taken care of this patient for the last year when she presented with seizures and was diagnosed with cysticercosis. She has had two rounds of anti-helminth therapy, for all the good it has done her, and her pork tape worms continue to die and cause edema.

When I last saw her in October, her brain MRI was normal (except for the cysts and scattered calcifications) and she had no brain edema, so she has been off the steroids for 4 months. No one in the family is a carrier and she has not returned to SE Asia to be re-exposed.

It is problematic as to whether she should get further therapy. The problem with cysticercosis is not the worms, which cause zero reaction, but the death of the organisms, which is what causes edema and damage as the cysts and the organisms lose their structural integrity. Like the Congress, if you think about it. Treat the infection, the worms die, and the edema gets worse.

It is curious why the worm causes no reaction, a benign Mr. Mind. The cyst pushes the brain aside, but it doesn’t kill neurons. I can find little in the literature as to why there is no response to the cysts until the organisms dies. The organism has been studied in mice and sheep, but men are neither mice nor sheep. We are devo.

One study that compared the disease in mice and sheep suggested

"The vigorous cellular response observed in the livers of sheep contrasts sharply with the lack of lymphocyte infiltration reported in mice indicating that small animal models may not be appropriate to study cellular responses to cysticercosis in large animals and man."

This is not the first time there is species variation in response to infections and there is no study I can find that looks at the immune response, or lack thereof, to cysticercosis in our close relatives of the primates.

The problem with the steroids is, of course, Cushings and ongoing long-term prednisone are apparently in the cards for her. The literature suggests that methotrexate may be a reasonable alternative to controlling the inflammatory response to the dying organisms, but methotrexate is not without its problems as well. What to do?

How do you solve a problem like cysticercosis?

Rationalization

J Parasitol. 2001 Jun;87(3):587-90. Cellular immune response and Th1/Th2 cytokines in human neurocysticercosis: lack of immune suppression.

Parasitol Res. 2000 Jun;86(6):500-3. Cellular immune responses in human neurocysticercosis. Grewal JS, Kaur S, Bhatti G, Sawhney IM, Ganguly NK, Mahajan RC, Malla N.

Clin Infect Dis. 2007 Feb 15;44(4):549-53. Epub 2007 Jan 8. Methotrexate as a corticosteroid-sparing agent in complicated neurocysticercosis. Mitre E, Talaat KR, Sperling MR, Nash TE.

POLL RESULTS

For me, TNTC is

1. 1 11% (5)

2. 5 11% (5)

3. the number of fingers on my hands. Then I run out of numbers, 24% (11)

4. I'm an internist. I count everything. 24% (11)

5. Texas Nature Tourism Council. 11% (5)

6. Other Answers 18% (8)

7. Tell Nurse To Count.

8. the number of things that more nitric oxide is good for.

9. more than 50

10. 20 I take my shoes off to count

11. I like your sense of humour - I think.

12. too numerous to count

13. above 15

Make a grown man cry

Feb 19, 2010

To treat or not to treat, that is the question.

Elderly male with cancer is admitted with shortness of breath. Work up show mucous plugging and white out of the lung that improves with a bronch. Cultures grow small numbers of a hodgepodge of organisms except it did not grow what was in the blood, but there are no white cells in the bronch fluid. But he has:

1/2 blood cultures with S. viridans.

1. A month of fevers (100.5) and chills (chilly not rigors) and weight loss.

2. Abnormal ECHO with a non-mobile vegetation.

3. Splinter hemorrhage on the thumb.

4. WBC of 25.

Endocarditis, right?

But.

1. Big cancers can cause fevers and weight loss and leukocytosis.

2. Not a sustained bacteremia.

3. Also grew coagulase-negative staphylococcus in the other set of blood cultures.

4. Has no teeth.

5. The vegetation looks more sclerosis than endocarditis.

6. The splinter looks traumatic

7. Underlying lung disease precludes a TEE.

Should he be treated? I suppose. It is better to treat an endocarditis he doesn't have than not treat one he does have.

Perhaps I put too much emphasis on his lack of teeth for the reason I doubt he has endocarditis. The presumption is that bleeding around the teeth is the defect that allows oral streptococci to sneak into the blood stream and then to the valve. No teeth, no endocarditis.

There are 6 or so cases on Pubmed of S. viridans endocarditis in edentulous patients and having no teeth is protective:

"No association was seen with pulmonary, gastrointestinal, cardiac, or genitourinary procedures or with surgery. Edentulous patients had a lower risk of IE from dental flora than patients who had teeth but did not floss. Daily flossing was associated with a borderline decreased IE risk...

We repeated the oral hygiene analyses considering only cases infected with dental flora (106 cases and their matched controls) and observed an increased risk associated with having teeth compared with being edentulous: adjusted OR=7.02 (95% CI 1.25 to 39.6), P=0.03 (Table 3). Ninety-three percent of edentulous subjects had complete dental prostheses; edentulousness was associated with decreased risk (adjusted OR=0.11 [95% CI 0.02 to 0.71], P=0.02) compared with having teeth and not flossing."

Clean teeth and healthy gums are the best protection, but I hate flossing. Makes me think of the movie Marathon Man. So I munch on dog chews instead, despite the salmonella risk.

While taking the history he brought up costs of care, that he and his wife have multiple medical problems, that he worked his entire life in construction and that they live on social security and can't pay their medical bills, as which point he broke down crying saying, "I don't ever want to be known as a deadbeat."

I could rant. I won't. But it breaks my heart how much suffering and death there is in this country that doesn’t need to occur. At least I sleep better knowing that our congressman and senators have good health care. Whew. A relief there, I can tell you.

Rationalization

Circulation. 2000 Dec 5;102(23):2842-8. Risk factors for infective endocarditis: oral hygiene and nondental exposures.

The King’s Evil

Feb 21, 2010

There are idioms in medical speak that annoy me for mostly irrational reasons. Well, completely irrational reasons. One is the phase "It's X until proven otherwise." Of course it is otherwise if you find an alternative diagnosis. Duh. I know the phrase is meant to emphasize that a particular diagnosis is most likely or important. It is just so self-evident, the equivalent of observing that you always find a missing object in the last place you look. As if you kept looking after you find it.

The patient is a young female from Tibet who has had several months of a large, painless neck and submandibular adenopathy. No other constitutional symptoms. She has been in the US for only a couple of years. The nodes have not improved with cephalexin. On exam she has boggy, robins egg sized, slightly tender lymph nodes on the right size of her neck. Labs were normal and CT demonstrated what we already knew from exam, but did add that the lungs were clear and that the lymphadenopathy was localized.

It makes me want to use the idiom I dislike so much, but it had to be Tb. There are other things in the differential, sure, and my dictation rambled on about toxoplasmosis and lymphoma. I ended by saying this has to be Tb. On Friday the lab called, three weeks after the lymph node was removed, to say that the cultures were growing MTb. Whew. Of interest, no organisms were seen on stain but she was quantiferon positive. Since she had active Tb, at least as far as I was concerned, I did not place a PPD. As a medical student my resident told me to put a PPD on a patient with AFB in his sputum, and like a dutiful fool, I did as I was told. With a geared up immune system, his whole forearm reacted and his skin sloughed off, requiring skin grafting. I have been hesitant to use a PPD on anyone with active Tb since, although this sort of severe reaction is rare.

Why is it called scrofula? It means "little pigs," from Latin, scrofa "breeding sow." The connection may be because the glands associated with the disease resemble the body of a sow, or because pigs were thought to be prone to it. " Oh-kay. If you say so. I don't see pigs.

And why is it called the King’s Evil? From the ever-helpful Wikipedia

"In the Middle Ages it was believed that "royal touch," the touch of the sovereign of England or France, could cure diseases due to the divine right of sovereigns. Scrofula was therefore also known as the King's Evil. The kings were thought to have received this power due to their succession from Edward the Confessor, who, according to some legends, received it from Saint Remigius. From 1633, the Book of Common Prayer of the Anglican Church contained a ceremony for this, and it was traditional for the monarch (king or queen) to present to the touched person a coin — usually an Angel, a gold coin the value of which varied from about 6 shillings to about 10 shillings. King Henry IV of France is reported as often touching and healing as many as 1,500 individuals at a time. (I assume they mean consecutively).

Queen Anne touched the infant (later Doctor) Samuel Johnson in 1712, but King George I put an end to the practice as being "too Catholic." The kings of France continued the custom until Louis XV stopped it in the 1700s, though it was briefly revived to universal derision in 1825.”

Therapeutic touch has a longer history of being useless than I had thought.

Tibetan immigrants have a very high risk for active Tb and drug resistance. In Canada,

"..culture-positive TB was diagnosed in 24 patients (13%, 4,571 per 100,000), 12 patients had at least one drug resistance (50% of cases), and 4 patients were resistant to at least isoniazid and rifampin (multidrug resistant, 17% of cases). "

And, in ‘it sure is cold, oh yeah sure don’t cha know let’s go ice fishin', 98% of Tibetans were PPD positive.

Susceptibilities are pending but I expect a cure.

And allow me to rant: wack out a lymph node, at least consider infections before you plop the whole thing into formalin. At least once a year I get to see a patient with granulomas on the pathology and nothing sent to micro. AAAAAAARRRRRRRGGGGGGGHHHHHHHHHHHHHHHHH.

Rationalization

Tuberculosis among Tibetan refugee claimants in Toronto: 1998 to 2000. Marras TK, Wilson J, Wang EE, Avendano M, Yang JW. Chest. 2003 Sep;124(3):915-21.

Tuberculosis among Tibetan immigrants from India and Nepal in Minnesota, 1992-1995. Truong DH, Hedemark LL, Mickman JK, Mosher LB, Dietrich SE, Lowry PW. JAMA. 1997 Mar 5;277(9):735-8.

Oh No.

Feb 23, 2010

When I check my clinic schedule for the day, I usually see one or two words to describe why the patient is there. A couple words always give me a sinking feeling as they are sensitive and specific for an unsatisfying patient-doctor interaction. Not 100%. But close.

One is fatigue. It is rare, despite my best efforts, to find a treatable diagnosis for patients with fatigue.

Another is Lyme. It is especially true if they already have the 'diagnosis' made by a naturopath after sending the serology to one of many unreliable labs in the US, some of which, as best I can tell (confirmation bias?) have never had a negative test.

The last is parasites.

Patients in this group can be subdivided into three groups.

1) Those who have traveled to an area where worms and parasites are common and they are worried that they may have acquired an infestation. Most docs have not needed to learn the life cycle and presentation of parasites, and so send the patient on to me to determine whether parasites is a reasonable diagnosis. Most of the time it is not, but occasionally I have diagnosed a schistosomiasis, cutaneous larva migrans or a gnathostomiasis. I have yet to see a Botfly larva, and hope never to. Gives me the willies.

2) Those who misidentify environmental worms as originating from themselves. I once had a patient who had an earthworm fall out of their pocket and into the toilet after gardening and they thought the worm came from them. The US is reasonably worm free, so passing a worm is unusual in the adult, but I have seen the occasional ascariasis, usually in an immigrant.

3) Deluded people.

These are divided into classic delusions of parasitism and its modern cousin Morgellon's. The most disgusting thing I have seen in my career was a gentleman who was eating a raw garlic clove every 15 minutes to keep the parasites at bay. I asked where the parasite was and he said in his nose; he pulled them out every day. He then took out a large jar of dried boogers, the 'proof' of his parasitism, and dumped them on the exam table. Proudest moment of my life was when I did not scream or vomit. However, I could not eat garlic for a year, and perhaps explains my subsequent conversion to a vampire.

What these patients have in common and what makes it difficult in the clinic is that they are convinced they have a disease that they do not. No amount of information will convince some patients that they do not have chronic Candida or Lyme or a parasite. I like to help people and having an adversarial relationship with my patients is not what I went into medicine for. It is such a joy to have a patient look at you with an expression that says, "You are full of crap." I know I should not take it personally, but after one such interaction I had a rather awful review on one of the rate a doc sites.

Fortunately, the patient this week fell into category 1, worried about parasites after travel, but none of the symptoms were likely due to parasites and the exposure history was not impressive for worm risk.

We had a good visit and I think she left reassured that she did not have a worm. But it will not prevent that sense of dread the next time I see 'parasite' on the schedule.

Rationalization

Clin Microbiol Rev. 2009 Oct;22(4):690-732. Delusional infestation. Freudenmann RW, Lepping P.

The bugs are more complicated than we suspect.

Feb 26, 2010

My son says my job is easy. All I ever seem to say is get cultures and start vancomycin. How hard is that? He asks.

I have trouble generating a coherent argument, since much of my job consists of trying to kill MRSA.

Not this week. This week I got to try to kill yeast. The patient has a new prosthetic valve and extensive arterial grafting to repair a huge aortic dissection. Now it is not just yeast, but Candida parapsilosis. It is not the living Velcro that is Candida albicans, which likes to stick to plastic like peanut butter to the roof of my mouth. But I still need to worry about the extensive clot and artificial material the yeast may land on and set up shop.

And how to treat it?

The more we look at organisms in detail the more complex classification becomes. It used to be simple. A smattering of germs. But it turns out that organisms that appear to be superficially the same are often different genetically. The histoplasmosis in the US is not the same as the histoplasmosis in Africa. The coccidioidomycosis in California is not the same as the coccidioidomycosis in S. America. Hmm. Here is an observation I do not think anyone has made before. If organisms are separated by geography, over time they may change into different species. I wonder if that has been noticed by others?

Candida parapsilosis looks like one yeast, but it isn't. It is three bugs: Candida metapsilosis, C. orthopsilosis and C. parapsilosis. I wonder what, if any, environmental pressures lead to the three subspecies. The pressure can be minor. There was a talk at the last IDSO where the speaker presented data showing that each tooth evolves its own flora over time and that the flora of, for example, the canines on opposite sides of the mouth are more alike than the flora of the teeth next to the canines. Each tooth is its own Galápagos island, the bacteria a finch. Perhaps there is something in the GI tract that lead to the different strains of C. parapsilosis, maybe an origin in the feces? Groan if you must.

And they have slightly different susceptibilities:

"All echinocandins showed lower MICs (mean MICs 0.05-0.71 mg/L) and the highest killing rates (-0.06 to -0.05 CFU/mL/h) for C. metapsilosis and C. orthopsilosis than for C. parapsilosis (mean MICs 0.59-1.68 mg/L). Micafungin and anidulafungin killing rates were greater than that of caspofungin. None of the echinocandins had fungicidal activity against C. parapsilosis."

and

"Fluconazole was fungistatic at > or =1x MIC (0.5-2 microg/mL) against C. parapsilosis and at > or =2x MIC (4-8 microg/mL) against C. orthopsilosis and C. metapsilosis isolates. Voriconazole inhibited C. parapsilosis at > or =1x MIC (0.015-0.12 microg/mL), but the other 2 species were inhibited only at 4 to 8x MIC (0.25-0.5 microg/mL). Against C. orthopsilosis and C. metapsilosis, posaconazole was fungistatic close to the MIC (0.03-0.06 and 0.015-0.03 microg/mL, respectively). Against C. orthopsilosis and C. metapsilosis, fluconazole and voriconazole, but not posaconazole, seem to be less active in vitro than against C. parapsilosis."

They all die from amphotericin B but not the best choice in acute renal failure.

It will take weeks to get the answer back from a reference lab as to which parapsilosis it really is. In the meantime, what to treat acutely and what to give for lifetime suppression?

It is NOT vancomycin, that's for sure. Ha. Take that, son.

Time for a little self-aggrandizement: my iPhone/iTouch Infectious Disease application is now available on iTunes. We are one step closer to the Omega Point.

Rationalization

Antimicrob Agents Chemother. 2010 Feb 9. In Vitro Fungicidal Activity of Echinocandins against Candida metapsilosis, C. orthopsilosis and C. parapsilosis by Time Killing Studies. PMID: 20145083

Diagn Microbiol Infect Dis. 2009 Jul;64(3):283-8. Epub 2009 Apr 25. In vitro efficacy of 5 antifungal agents against Candida parapsilosis, Candida orthopsilosis, and Candida metapsilosis as determined by time-kill methodology. PMID: 19394787

Horse, Donkey, Zebra or Unicorn?

Feb 27, 2010

Common things are common. That is one of the rules of medicine. As the old saw goes, when you hear hoofbeats, think of horses, not zebras. This is true if you are a primary care provider, but it is not so true of ID. I get sent all the weird cases and the unknowns. I not only hunt zebras, I hunt unicorns, so I can bathe in their tears.

Most docs will see one case of endocarditis in a career, if that. It is a rare disease. Because of its rarity and the nonspecific manifestations of subacute disease, it is not unusual for the diagnosis to fester along for a month or two before the diagnosis is made. BTW, it wasn't until I was in medical school did I recognize the significance of the name Uncle Fester from the Addams Family. One day, out of nowhere, I thought, Uncle Fester. Fester. I get it. Better late than never.

Like the patient this week, who has been low grade ill for the last 6 to 8 weeks with fatigue, malaise, and a general decline in function. But no dramatic fevers or physical findings until she presented to the hospital short of breath and all her blood cultures grew S. mitis, a mouth streptococcus. ECHO has an aortic valve vegetation.

Examination, besides a murmur, is not impressive, except for leg pain. Her thigh is painful and an ultrasound shows an aneurysm, confirmed by MRI. The MRI also demonstrated retrograde flow of contrast, showing artery had eroded into the vein to cause an AVM (atrial-venous malformation).

Common things are common, as I said, but for all the fretting we do about mycotic aneurysms in endocarditis, this is the first I have seen this century and the first ever in the leg. And I see a case of endocarditis at least once a month. Being the only ID doc at 4 hospitals, I am the final common pathway for a lot of weirdness.

Mycotic aneurysms are commonly reported in the literature from endocarditis, and, while unusual, are seen on occasion in the arteries of the leg.

But AVMs as a manifestation of endocarditis is not common, I can find two reported cases.

For now we are going to treat with antibiotics and time. You do not want to put a coil into an infected space and surgery has the same problem.

Not quite a unicorn, but close.

Rationalization

Vasc Endovascular Surg. 2008 Jun-Jul;42(3):293-5. Epub 2008 Mar 3. Endovascular management of an arteriovenous fistula and concomitant pseudoaneurysm in an intravenous drug abuser. PMID: 18316363

Nippon Kyobu Geka Gakkai Zasshi. 1991 Jan;39(1):120-3. [Successful management of mycotic abdominal arteriovenous fistula complicated with infective endocarditis--a case report]

Poll Results

In my practice

1. Common things are common. 30% (13)

2. Common things are uncommon. 5% (2)

3. Uncommon things are common. 27% (12)

4. Uncommon things are uncommon. 23% (10)

5. Other Answers 16% (7)

6. In primary care, they are all anxious, depressed, or both.

7. All things are unique

8. Uncommon things are commonly uncommon.

9. meh

Frankly

Mar 2, 2010

Twice today I heard the phase "frank pus." Who is Frank? And how does frank pus differ from plain old pus? There is frank bleeding, which is contrasted with occult bleeding. But is there occult pus? I don't think so. This has nothing to do with the case at hand, I am just a grumpy old man who likes to complain.

Over the weekend a patient was admitted quite ill. It started with a sore throat, then went to fevers and rigors for which he took ibuprofen (an NSAID). He then went into progressive multi-organ system failure and admitted to the ICU with multi-lobar pneumonia.

Not an uncommon presentation, but the cultures grew S. pyogenes aka Group A Streptococcus.

This is not a common cause of community-acquired pneumonia. I think this is maybe the second I have seen in 25 years, although my memory is not as good as it once was. Patients do not do well with invasive Group A strep disease with mortality rates around 40%.

"We identified 323 patients with invasive group A streptococcal infections, for an annual incidence of 1.5 cases per 100,000 population. The rates were highest in young children and the elderly. Fifty-six percent of the patients had underlying chronic illness. Risk factors for disease included infection with the human immunodeficiency virus, cancer, diabetes, alcohol abuse, and chickenpox. The most common clinical presentations were soft-tissue infection (48 percent), bacteremia with no septic focus (14 percent), and pneumonia (11 percent). Necrotizing fasciitis occurred in 6 percent of patients, and toxic shock in 13 percent. The mortality rate was 15 percent overall, but it was 29 percent among those over 64 years of age (P<0.001) data-preserve-html-node="true" and 81 percent among those with toxic shock (P<0.001)." data-preserve-html-node="true"

It is also a cause of secondary bacterial pneumonia after influenza H1N1.

I wonder about the NSAID use. There has been a long debate about whether NSAIDs may increase the risk of Group A Streptococcus necrotizing fasciitis, although a review of literature will lead the reader wondering. Could the NSAID delay seeking care because it modifies symptoms or tip the host immune system in favor of the organism? If you blunt the immune response, can it make the infection worse? To quote Medicine

"Case reports and retrospective studies suggest that the application of NSAIDs to relieve these nonspecific symptoms can delay diagnosis and treatment of GAS necrotizing fasciitis. However, prospective studies do not support a risk of developing GAS necrotizing fasciitis as a result of NSAID therapy, or a worsening of established streptococcal infection."

But I still wonder if NSAIDs can cause more harm than good in some patients with infections. It is always a complex balance between the host immune system and the virulence of the organism, and sometimes it may take a pill of ibuprofen to break the immune system's back.

Rationalization

Eur J Clin Microbiol Infect Dis. 1999 Jul;18(7):506-9. Review of 17 cases of pneumonia caused by Streptococcus pyogenes. Barnham M, Weightman N, Anderson A, Pagan F, Chapman S. PMID: 10482030

N Engl J Med. 1996 Aug 22;335(8):547-54. Invasive group A streptococcal infections in Ontario, Canada. Ontario Group A Streptococcal Study Group.Davies HD, McGeer A, Schwartz B, Green K, Cann D, Simor AE, Low DE. PMID: 8684408

Assessing the relationship between the use of nonsteroidal anti-inflammatory drugs and necrotizing fasciitis caused by group A streptococcus. Aronoff DM, Bloch KC. Medicine (Baltimore). 2003 Jul;82(4):225-35. Review.

An appeeling case

Mar 3, 2010

The patient is a middle-aged Native American male with a progressive sore throat and hoarseness. At its worst he could not talk, and he is still a little hoarse (I keep thinking of the movie Top Secret), maybe, maybe not, a hot potato voice. He also has had fevers and chills. He is seen in the ER, has a negative rapid strep, and is sent home.

No significant past medical history, a touch of diabetes, a whiff of hypertension. No exposure to anything odd, he has been nowhere and done nothing. Like me, but more so.

On admission he is febrile and has a WBC of 12 but the rest of exam, including his throat, is negative except for his fingers.

On his fingers, and just his fingers, the skin is peeling off. Just like when I was a kid and would let glue dry on my fingers and pull it off (the glue, not the finger) in one big piece. Nowhere else is the skin peeling.

Cultures are negative in the hospital, but he is two weeks into the illness. CT of the neck, looking for evil, shows only thickened vocal cords and on antibiotics he gets better very fast.

He says, on questioning, that his legs also became red and swollen a few days before admission, but this lasted only a few days. No rash anywhere else.

What did he have?

I don't know. I wonder if it is Scarlet Fever (Rhett Butler suffered from this but not Ashley, never Ashley), since the peeling of the finger tips is supposed to be what happens with scarlet fever. He otherwise kind of fits clinically, but I never got to see him early on to see if he had a strawberry tongue or sandpaper rash.

Maybe it is Arcanobacterium haemolyticum, which causes a similar syndrome and would account for the negative rapid strep screen.

He is getting better and I am trying to minimize testing as he has no insurance. I sent him home on amoxicillin, but like so many cases, the final diagnosis seems to lie just beyond my grasp.

Rationalization

Scarlet Fever http://emedicine.medscape.com/article/785981-overview

Arcanobacterium Haemolyticum http://emedicine.medscape.com/article/1054547-overview

[Nick and Hillary arrive at the Potato Farm. Shetland pony is coughing]

Nick Rivers: What's wrong with him?

Wagon Driver: Oh, he caught a cold last week and he's just a little hoarse.

Nick Rivers: Is this the potato farm?

Albert Potato, Resistance Member: Yes, I'm Albert Potato

~Top Secret

Poll Results

I prefer

1. Top Secret 11% (8)

2. Police Squad 9% (7)

3. Airplane! 50% (38)

4. Hot Shots 12% (9)

5. Kentucky Fried Movie 9% (7)

6. Other Answers 9% (7)

7. Police Academy

8. The Life of Brian

9. anything with Johnny Depp

10. Fried Green Tomatoes

11. National Lampoons vacation movies

12. criminal minds. Fascinating!

13. blazing saddles

Poly want a microbial

Mar 9, 2010

I have mentioned in the past that heroin in not a good lifestyle. I have also mentioned in the past that I need a lifestyle, I seem to be limited to having a life. Heroin is rich in bacteria and yeast and the use of needles for any reason increases the chance of being a staph carrier. Put them all together and that spells endocarditis, even if you are as bad a speller as I am.

The patient comes in with classic right sided endocarditis: fevers, pleuritic chest pain, numerous "cannon ball" infiltrates and cavities on the CAT scan, and blood cultures 3/3 for methicillin susceptible S. aureus. Easy enough. ECHO shows no vegetation, but given the number of lesions in her lungs, I figure that the vegetation broke up like it was attacked by Harry Stamper et. al. and showered downstream.

She was put on nafcillin and that should be the end of it. Except.

Even though the cultures were positive, the lab still continued to incubate the blood cultures. I didn't know they did that. It is like continuing to look for your glasses after you find them, kind of, well, not really, as sometimes people have polymicrobial infections and bugs grow at different rates. Still, it is not typical for other organisms to pop up later in the cultures.

So after three days of incubation the blood cultures start to grow yeast, and all blood cultures from over three days grow C. parapsilosis. So it is a polymicrobial endocarditis.

Certainly, the vegetation of endocarditis is fertile soil for subsequent infections, so, while odd, is not unheard of.

"The polymicrobial endocarditis is rare: 1-3%. It is being observed with increasing frequency among drug users; a predominance of tricuspid valve involvement exists. We report a case of dual etiology infective endocarditis (IE) - Candida tropicalis and Staphylococcus aureus."

Preexisting clot from central venous catheters probably accounts for the odd bugs that cause hospital acquired endocarditis. Yeast and coagulase-negative staphylococci usually can't stick to valves unless there is pre-existing clot.

My personal record is three valves with vegetations and three organisms in all the blood cultures. I cured the patient with a course of antibiotics. The record, and I cannot for the life of me find the reference, is on order of 10 or 11 organisms in a German drug user. Or so I remember. The Google and Pubmed failed me.

Candida endocarditis is an absolute indication for valve replacement, although I have cured a pair in my day in patients who were "not surgical candidates."

Don't let my surgeons know, or they may ask me to repeat that miracle.

Rationalization

Endocarditis complicating central venous catheter bloodstream infections: a unique form of health care associated endocarditis. Chrissoheris MP, Libertin C, Ali RG, Ghantous A, Bekui A, Donohue T. Clin Cardiol. 2009 Dec;32(12):E48-54. PMID: 20014189

A "true" polymicrobial endocarditis: Candida tropicalis and Staphylococcus aureus--to a drug user. Case presentation and literature review. Popescu GA, Prazuck T, Poisson D, Picu C. Rom J Intern Med. 2005;43(1-2):157-61. PMID: 16739876

Herpes for Reals?

Mar 11, 2010

As long as the pulmonologist is taking the time and the risk to do a bronchoscopy, they might as well send the specimen for everything they can. It is a (slightly) risky procedure and, I suppose, costly, so it is better to order all the tests than re-bronch the patient at a later date. Seems not unreasonable to me. Problem is, when you send the test for everything, anything might pop up in the results, whether or not you were expecting it. Don't take a temperature if you do not want to deal with a fever.

Elderly female with a long history of smoking and its sequela: COPD etc. She is admitted to Outside Hospital and eventually requires a trach for ventilator dependence. There is a bronch done for mucous plugging and mucous was successfully unplugged. Mucous unplugged. Isn’t that an MTV show? The airway was red and irritated, not unlike me after an August day working in the back yard. As long as they were in there, they sent off everything and the PCR came back positive for Herpes simplex, HSV-1. Patient had no fevers and no new infiltrates, but no positive culture should ever go untreated, so she was started on i.v. acyclovir. And then she was sent to me.

Is the HSV the real deal? Probably not in this otherwise Immunocompetent patient. She was otherwise stable and had no new infiltrates nor signs of infection. The problem is herpes reactivates all the time.

"Methods. Twenty‐five HSV‐2–seropositive and 18 HSV‐1–seropositive healthy adults collected anogenital and oral swabs, respectively, 4 times per day for 60 days. Swabs were assayed for HSV, using a quantitative polymerase chain reaction assay.

Results. Twenty‐four percent of anogenital reactivations and 21% of oral reactivations lasted 6 h, and 49% of anogenital reactivations and 39% of oral reactivations lasted 12 h. Lesions were reported in only 3 (7%) of 44 anogenital reactivations and 1 (8%) of 13 oral reactivations lasting 12 h. The median HSV DNA levels at initial and last detection were 103.5 and 103.3 copies/mL, respectively, during anogenital reactivation and 103.7 and 103.0 copies/mL, respectively, during oral reactivation.

Conclusions. This high frequency of short subclinical HSV reactivation in immunocompetent hosts strongly suggests that the peripheral mucosal immune system plays a critical role in clearing HSV reactivations."

Somehow I do not think I would have been a participant in that study.

But if you have HSV, you are probably shedding wee bits of HSV all the time. Get sick, the amount of shedding goes up and when you have a test as sensitive as PCR, you get positive results. Is HSV causing disease? Tough question. Like CMV, finding HSV in a bronch is a bad prognostic finding, but it may be more of a marker of severity of disease than the cause of morbidity and mortality.

"Critically ill patients in whom HSV-1 from BAL is isolated, have about 40% chance of dying, mainly because of severe underlying disease and comorbidity, which may predispose to endogenous reactivation of the virus. There is no clinical evidence for direct cardiorespiratory pathogenicity and beneficial effects of antiviral therapy. HSV-1 isolated from lung secretions may thus be a marker rather than a mediator of severe illness."

So most of the time I ignore the HSV in a bronch, but always with a little worry in the back of my mind. Occasionally HSV can cause real disease in ostensibly normal people, and I would not want to miss it.

Oh yeah. I stopped the acyclovir. Sometimes I think I am the only person who gets to ignore cultures and stop antibiotics. Patient is doing fine.

Rationalization

The Journal of Infectious Diseases 2008;198:1141–1149 Rapidly Cleared Episodes of Herpes Simplex Virus Reactivation in Immunocompetent Adults. Clin Microbiol Infect. 2006 Nov;12(11):1050-9.

Herpes simplex virus type 1 and respiratory disease in critically ill patients: Real pathogen or innocent bystander? Simoons-Smit AM, Kraan EM, Beishuizen A, Strack van Schijndel RJ, Vandenbroucke-Grauls CM. PMID: 17002604

J Clin Virol. 2004 May;30(1):68-72. Respiratory herpes simplex virus type 1 infection/colonisation in the critically ill: marker or mediator? PMID: 15072757

Poll Results

In my community

1. There is no Outside Hospital. 7% (2)

2. There are only Outside Hospitals. 7% (2)

3. I work at Outside Hospital. 25% (7)

4. All hospitals are Outside to those looking in. Deep. 46% (13)

5. I don't get it. Everyone does need a cath. 14% (4)

6. Other Answers 0% (0)

Complications. I hate complications

Mar 13, 2010

ID is cool in so many ways. Cure is one of the ways. I get to cure people, get rid of their infection completely and totally, for now and maybe forever. Not always, nothing is 100% in medicine. There are diseases I can't cure, either due to the organisms or the host. There are unexpected complications and rare expected complications of diseases that can make cure problematic.

Usually we get lucky and avoid the complications by careful monitoring, but not always. The worst are the complications that can occur and we can do nothing to prevent. You know that eventually the asteroid will hit, but since there is not a damn thing you can do about it, you go about your day as if it is never going to happen. Eventually everything happens. And I hate it when the asteroid hits. I take it personal. My (metaphorical) mass should be able to deflect any incoming.

Patient is an elderly male with S. mutans in all his blood cultures and a small vegetations on his prosthetic mitral valve. He has been sick maybe 6 weeks and exam is unimpressive for stigmata of endocarditis. No emboli. Good. When they do not have emboli up front, it is rare for the patient to get emboli later.

The MIC of the organism is 0.01 so he is on penicillin and gentamicin, all systems are stable after 5 days, and he is ready for discharge.

Then.

Big, multiple, emboli to the brain, one of which hemorrhages. He went, in the space of a few hours, from ready to go home with an excellent chance of cure to fatal strokes.

Crap. I know there is nothing to be done to prevent this, but still. Crap.

I know prosthetic valve endocarditis is often fatal, with or without surgery. I know emboli can occur late. I had one patient who had a fatal CNS emboli from endocarditis the day after completion of therapy, after the "things look good, think we may have a cure, here are the things we need to do in the future" talk. The knowledge that the outcome could be awful somehow doesn't help when the 'could' becomes 'is'.

Unfortunately, there is nothing to be done to prevent emboli except valve replacement, and usually the patient has a higher change of surgical complications given underlying comorbidities.

Treating with aspirin after the diagnosis is made doesn't help:

" In endocarditis patients already receiving antibiotic treatment, the addition of aspirin does not appear to reduce the risk of embolic events and is likely associated with an increased risk of bleeding. Aspirin is not indicated in the early management of patients with IE."

and

"In patients with endocarditis, long-term daily use of aspirin does not reduce the risk of embolic events but may be associated with a higher risk of bleeding. In the acute phase of endocarditis, aspirin should be used with caution."

although being on other antiplatelet agents prior to endocarditis may prevent emboli:

"Embolic events occurred significantly less often among those who had received prior, continuous daily antiplatelet therapy (aspirin, dipyridamole, clopidogrel, ticlopidine, or any of combination of these agents) (12.0% of patients who had received therapy vs. 27.8% patients who had not receive therapy."

Yes, I know aspirin was in all three studies. Whoever said medical research is clear-cut. You want clear-cut, be a NW logger.

I suppose what I need is a psychic. Seriously. If those frauds, er, I mean psychics could really predict the future, why don't they save a few lives and predict who will get endocarditis and put the patient on expectant aspirin? Where is Miss Cleo when you really need her? A psychic would almost be better than being helpless.

Rationalization

J Am Coll Cardiol. 2003 Sep 3;42(5):775-80. A randomized trial of aspirin on the risk of embolic events in patients with infective endocarditis. Chan KL, Dumesnil JG, Cujec B, Sanfilippo AJ, Jue J, Turek MA, Robinson TI, Moher D; Investigators of the Multicenter Aspirin Study in Infective Endocarditis.

Clin Infect Dis. 2008 Jan 1;46(1):37-41. Effect of long-term aspirin use on embolic events in infective endocarditis. Chan KL, Tam J, Dumesnil JG, Cujec B, Sanfilippo AJ, Jue J, Turek M, Robinson T, Williams K. PMID: 18171211

Clin Infect Dis. 2007 May 1;44(9):1180-6. Epub 2007 Mar 14. Impact of prior antiplatelet therapy on risk of embolism in infective endocarditis. Anavekar NS, Tleyjeh IM, Anavekar NS, Mirzoyev Z, Steckelberg JM, Haddad C, Khandaker MH, Wilson WR, Chandrasekaran K, Baddour LM. PMID: 17407036

Grumpy Old Fart

Mar 14, 2010

I am on call this weekend. We cover for 4 docs on the weekend, so the usual constant flow of questions that marks my day can be increased many fold. And there is a characteristic about many of the calls that brings out the grumpy old fart in me.

It is the lack of organization when people call me about a case and the inability to get to the point about why they are calling. Sure. We are all busy. But if you are going to call someone with a question, shouldn’t you be prepared to present the information in an organized fashion? Like I was trained to do as a resident, the 6 minute case presentation. Instead, people wander from the chief complaint to the labs to the history to the X-rays almost, it seems, to demonstrate that the concept of Brownian motion can apply to medical thought.

And you would think that if someone answers your page almost immediately (and I answer almost all pages as soon as the pager goes off) that you would have the database in your brain, or even in front of you, so that when I ask a question like "what is the white count?" you have the answer readily available.

Bah, humbug. Back in the day.

It does seem like having the patient organized in your head for presentation is a lost art. Not in residents. They are well prepared for me. Many are aware that I will ask for a name, a room, and then limit them to a five-word question they want answered. It is amazing how often the reason for a consult can be summarized in five words medical students you expect to ramble. They are learning. It's the newer attendings. Where is the focus?

Whippersnappers.

And as long as I am on the topic, here is another issue that fries my bacon.

So the resident presents a case and we talk about it. Then at some point we stand up to go and see the patient and it is my habit to continue to discuss the case as we walk, blathering on with teaching points. Now here is the deal. I walk kind of briskly. The longer you are at work, the longer you are at work. Walking slowly only keeps you at work longer. Here's the thing. Even though I am talking away about some topic, no one EVER attempts to keep up with me. I have to stop and wait until they catch up. After a few times, I point it out and then it is not a problem. They keep up. When I was a student, I would have kept up with my attending. Period.

Young punks.

The Same but Different

Mar 16, 2010

The patient comes to clinic with the question as to whether or not she had Lyme. I see Lyme on the clinic chart, I never know if it is going to be the real deal, someone who wants information, or a "chronic Lyme."

She had one, maybe two, tick bites, and a rash that could have been ECM. The rash was in a place that was awkward for her to see.

She was treated a week after the bite with doxycycline then amoxicillin.

Then, 5 months later, has Lyme serologies.

The ELISA is positive, but the Western blot has a few bands positive and is considered negative. The western blot was positive for IgG at bands 45 and 41, the IgM is positive for band 23, the interpretation is negative.

Did she have Lyme?

Here is the clincher. The tick bite was while hiking in Europe. Is it different in Europe, and I'm not talking Tilia cordata?

Borrelia burgdorferi sensu lato (I prefer sunsu cappichino) is the main cause of Lyme disease in the United States, but Borrelia afzelii, Borrelia garinii, and B. valaisiana cause European Lyme. They evolved separately over 150 million years, at least since the Atlantic opened up. They are not the same organisms. So would a test made in the US against US Lyme be useful for European Lyme?

"The identity of the predicted amino acid sequences was 43 to 62% among Borrelia burgdorferi sensu stricto, B. afzelii, and B. garinii."

and they respond differently to serologic testing

"Among individual borrelial proteins from different species, sequence heterogeneity varies up to 40%, and their use as antigens may affect the sensitivity of the assays."

And, not unsurprisingly, they may each have a different clinical manifestation.

"It was suggested that different species possess different organotropisms and may preferentially cause distinct clinical manifestations of Lyme disease. Molecular analyses revealed a strong association of B. afzelii with the late cutaneous manifestation acrodermatitis chronica atrophicans, whereas B. garinii was predominantly identified in clinical samples from patients with neuroborreliosis. PCR-based analyses of samples from European patients with Lyme arthritis had given controversial results, but B. burgdorferi sensu stricto appears to be the major pathogen."

As best I can tell from the literature, it is probably a negative, even for European Lyme. Not enough good bands. True in music, true in ID.

"Among the sera with a preferential reactivity to B. burgdorferi sensu stricto (n = 23), the 12-kDa, 16-kDa, OspC, 58-kDa, and 66-kDa antigen bands were found to have a higher discriminative power with B. burgdorferi sensu stricto than with the other species. Sera with a preferential reactivity to B. garinii (n = 17) had greater reactivities to the 16-kDa, 18-kDa, 20-kDa, OspC, OspD, 30-kDa, OspA, 45-kDa, and 60-kDa antigen bands. Sera with a preferential reactivity to B. afzelii (n = 43) had greater reactivities to the 12-kDa, 14-kDa, 16-kDa, 18-kDa, OspC, and 45-kDa antigen bands."

But then, that’s self-evident. Either way she has had sufficient treatment and is heading back to Europe in a few months. I told her to get her serologies repeated if she were interested; I could find no reputable lab that runs serology for European Borrelia.

Rationalization

J Clin Microbiol. 2002 February; 40(2): 453–460. Species-Specific Serodiagnosis of Lyme Arthritis and Neuroborreliosis Due to Borrelia burgdorferi Sensu Stricto, B. afzelii, and B. garinii by Using Decorin Binding Protein A

Z Rheumatol. 2003 Apr;62(2):148-54. [Heterogeneity of Borrelia burgdorferi: etiopathogenetic relevance and clinical implications].

Not everything is infections.

Mar 18, 2010

An attending back in my training days once said that the ID doc has to be the second-best subspecialist in the hospital. Since infections can affect any organ, ID docs have to know a little about all the subspecialties. Not that I am the second-best cardiologist or pulmonologist by any means. But I have to keep an eye out for other processes that can mimic the interesting, er I mean, infectious diseases. I made a couple non ID diagnoses this week, which is made all the more fun by the people I work with.

I work with a bunch of real smart hospitalists. It is hard to come up with a diagnosis that they did not consider, but like all docs sometime we walk down blind alleys and are unaware of it until someone else takes a fresh look at the case. I am certainly not immune to walking down the wrong diagnostic path. I write this blog more or less every other day and discuss the diagnostic and therapeutic cases where I have a diagnosis. If I were to write about the cases where I could not make the diagnosis or made the wrong one, I would be able to post BID.

The first case was an almost elderly female who had every other day fevers accompanied with a lethargic delirium. She was nearly unresponsive during her fevers and non-focally ill on days she was not febrile. She is diabetic and had a history of brain tumor treated with radiation and she had the deluxe fever work up by the hospitalist and me. Only thing abnormal was a protein in the CSF of 145, which the neurologist said was due to radiation effect. Everything came up blank. No infection. So I sent off an ESR. It was 100. Temporal arteritis? US was negative and she is soon to have a biopsy (I hope, there are other issues in the case that have delayed diagnostic biopsy, the world is often less than perfect) but given the neurologic findings she got 40 of prednisone and the next day was neurologically normal and fever free.

Yeah, I know. No biopsy, no diagnosis. Know biopsy, know diagnosis.

But temporal arteritis is the leading diagnosis and may the cause of the increased protein in the CSF.

The other was a recalcitrant alcoholic who came in with fevers and delirium tremens. After a prolonged stay, she continued to have intermittent fevers and an increased WBC with a left shift. Her exam and labs were consistent with the ravages of alcoholism with cirrhosis. CT and CXR failed to find a reason for the leukocytosis and left shift, so they called me.

There were myelocytes, metamyelocytes, a smattering of blasts, nucleated reds and smudge cells. It was more than a left shift, it was AML. The hospitalist, who is one of the best, in my opinion, was chagrined that the AML was missed. There is always a slight, friendly, competition to make the diagnosis amongst internists in the hospital. This time it was my turn, the next time someone will make a diagnosis I missed. That’s medicine.

I am on vacation next week. Spring break. So you will have to go a week without the wonder that is rubor dolor calor tumor. Lest you think my house can be burgled, in these tough economic times I will be home, on a rocking chair on my front porch, unshaven, with a bottle of whiskey in one hand and a shotgun in the other, muttering about the government. Try me.

See you in a week.

I'm Baaaaaaaaaaaaak.

Mar 29, 2010

Why even bother with a vacation? The first day back is usually such an inundation of deferred work that it would have been easier to have stayed home. However, I played a lot of golf with the kids, ate good meals with my long-suffering wife, and walked on the Oregon coast. Well, the beach at the Oregon coast. I cannot as of yet walk on the ocean. I always tell myself and the residents that I have never had a patient tell me at the end of their life "Doc, I sure wish I had spent more time at work." It is good to get away, despite the pain of the return. Douglas MacArthur had it easy.

All sorts of interesting cases came in while I was gone. I assume the patients were just waiting for me to leave so they could be admitted and give my partner the great diagnoses. Patients can be so sneaky that way.

One is an elderly female with protracted nausea and vomiting for four days. She comes into the hospital dehydrated. Yes, dehydrated. Not volume short. I just pissed off a nephrologist, and I feel good about it. Her WBC was 40,000 on admit and she had a sepsis work up. Blood cultures were positive. Trying to find a source of sepsis was unsatisfactory, maybe a tip of an appendix inflamed, maybe a touch of sigmoid thickening suggesting diverticulitis.

After a few days her prosthetic knee became increasingly red, painful, hot, and swollen, the rubor, dolor, calor, and tumor of which I am so fond. Rest of the exam, including the abdominal exam, is negative. Tap of the knee had 50,000 PMN's, but a negative gram stain, cultures pending. On antibiotics her infection parameters have normalized and the only culture is the blood which grew, Clostridium perfringens.

What?

A Pubmed reveals fewer than 40 cases of infected joints from all Clostridium species, so it is a rare cause of joint infections, < 1%.

"Although a hematogenous route has been reported, most cases were associated with a traumatic, penetrating injury. C. perfringens was the most common infecting species. In most instances, Clostridium was the sole pathogenic factor; however, 5 polymicrobial infections were reported. The knee was the most frequent joint involved, and in no case reviewed was a joint in the foot implicated."

And that’s for native joints, infections of prosthetic joints are rarer yet. Cut off a hand and you could count the number. Unless you have only one hand.

Most of the time when C. perfringens is in the blood cultures of ostensibly normal people, it is either causing overwhelming death (rare) or is real but causing no disease, (more often). In hosts with underlying diseases (cancer, liver disease, etc.) Clostridium bacteremia is an ominous finding with high mortality. There have been cases of Clostridium joint infection associated with contaminated cadaver grafts, which she never had.

So I assume gi inflammation to blood to joint. What will happen to the joint is uncertain. The few cases suggest the joint will not be salvageable. We will see.

"When addressed early, the treatment of clostridial septic arthritis has produced satisfactory results. With the exception of immunocompromised persons, successful results were obtained in all cases. A review of the literature has revealed that the treatment of choice seems to be IV penicillin and open arthrotomy performed somewhat soon after the time of onset. With prompt diagnosis and proper management, a good functional result can be expected."

It was salvaged. The heck.

Rationalization

Clin Infect Dis. 2000 Mar;30(3):590-4. Polymicrobial septic arthritis due to Clostridium species: case report and review. PMID: 10722451

Clin Infect Dis. 2001 Aug 1;33(3):349-53. Epub 2001 Jun 22. Clinical features of clostridial bacteremia: a review from a rural area. PMID: 11438901

Poll Results

When I return from vacation, I am

1. recharged. 20% (8)

2. Depressed. 35% (14)

3. in love with the cabin boy. 5% (2)

4. pregnant. 10% (4)

5. having this itching that just doesn’t go away. 18% (7)

6. Other Answers 13% (5)

7. in need of retraining.

8. recharged until I am back in the office, then I get depressed.

9. Exhausted

Dog or Cat?

Mar 31, 2010

Do you prefer John, Paul, George or Ringo? Apple? Windows? Linux? Are you a dog person? A cat person?

We define ourselves in part by our preferences.

The patient is a 90 yo male with lymphoma on therapy. He also has an aortic bioprosthesis. He comes in septic, but not neutropenic, and has the usual ICU care thrown at him and survives.

On day three his blood cultures are positive for a small gram-negative rod. One day four his artificial knee swells up and becomes exquisitely painful. There are 12,752 WBC on the knee tap. About 12,750 too many. Gram stain is negative.

Next day the organism in the blood is identified as Pasteurella species.

I call the lab and they tell me the machine is calling it 50:50 either P. multocida or P. canis. And there is only a 10% chance of that. Thank you, Lt. Drebin.

I talk to the patient and he tells me his dog leaves him alone, but his vermin, er, I mean cat, scratches him not infrequently. He shows me some fresh claw marks on the arm.

There are many Pasteurellae: P. aerogenes; P. avium; P. bettyae; P. caballi; P. canis; P. dagmatis; P. gallinarum; P. langaaensis; P. mairii; P. multocida; P. pneumotropica; P. skyensis; P. stomatis; P. testudinis; P. trehalosi; P. volantium. They can be found in cats and dogs and rabbits and cattle and chickens. Oh my.

P. multocida is common from cat bites but people do not think of Pasteurella from other animal bites.

P. canis is found in... Hmmmmm. Canis. Sounds Latin. It must be found in cans or maybe canes. Patient has no exposure to cans or canes. Kind of confusing.

"Pasteurella species were the most frequent isolates from both dog bites (50 percent) and cat bites (75 percent). Pasteurella canis was the most common isolate of dog bites, and Past. multocida subspecies multocida and septica were the most common isolates of cat bites."

Lab does further testing and Sherlock calls it P. canis. Can't blame the other white meat for this infection.

The knee is going to be debrided, cultures are negative so far, but he had been on antibiotics. His TEE is negative as are repeat blood cultures, so I feel moderately good this is 'only' a prosthetic joint infection. He is heading for a long course of therapy for the joint infection. The dog, in the end, is going to be his most expensive possession.

I remember when my son’s Hamster escaped in January, fell down a heating duct and died on the heating unit, filling the house with the smell of roasting/rotting hamster whenever the heat kicked on. I was annoyed when it cost $400 to get the heating unit cleaned, not including the repairman’s vomit, which he took care of gratis. If my dog cost me tens of thousands of dollars, I would not be a happy camper.

There are 4 cases of Pasteurella prosthetic joint infections on Pubmed so you do not even need a thumb to count them all on one hand and all were due to multocida.

Rationalization

Pasteurella http://microbewiki.kenyon.edu/index.php/Pasteurella

N Engl J Med. 1999 Jan 14;340(2):85-92. Bacteriologic analysis of infected dog and cat bites. Emergency Medicine Animal Bite Infection Study Group. Talan DA, Citron DM, Abrahamian FM, Moran GJ, Goldstein EJ.\

J Arthroplasty. 2004 Jun;19(4):525-7. Prosthetic joint infection with Pasteurella multocida following cat scratch: a report of 2 cases. Mehta H, Mackie I.

Poll Results

I am a

1. cat person. 32% (75)

2. dog person. 36% (85)

3. ferret person. 1% (3)

4. My uniqueness cannot be defined by mere pets. 18% (43)

5. Multiple personality person. Want to meet my goth cowgirl? 8% (19)

6. Other Answers 4% (9)

7. all animal person

8. dogs, cats, llama, horse, donkey,lambs,geese, ducks, chickens, guinea, alpaca, rabbits, goats

9. animals...should have been a vet

10. Rabbit

11. all animals

12. Kid person. Oldest of 11 and have 8 of my own. Should have had more.

13. icelandic horse

More Gray

Apr 2, 2010

Given the nature of my writing 'style' and tone, I thought about an April Fool’s entry, but I figured no one would be able to tell the difference.

The patient is an elderly male with about a week of fevers to 100.8, shakes but not teeth chattering rigors, some new night sweats and 48 hours of 10/10 low back pain.

He goes to Outside Hospital, has one set of blood cultures (but no cath) and is started on antibiotics.

His blood cultures then grow both coagulase-negative Staphylococcus and S. viridans.

His ESR is 65, his WBC is 13.

He has a defibrillator and the TEE, while showing no vegetation, maybe, maybe not, is a touch shaggy. Maybe. Nothing definitive.

He is on warfarin and Plavix. Patients on antiplatelet therapy may have fewer emboli when they develop endocarditis, although this finding is not confirmed in all studies.

"Embolic events occurred significantly less often among those who had received prior, continuous daily antiplatelet therapy (12.0% of patients who had received therapy vs. 27.8% patients who had not receive therapy; P<.001)." data-preserve-html-node="true"

And I have always wondered if, since vegetations are platelets and thrombin, if anticoagulation render the ECHO's less sensitive for endocarditis. That could be a study for a budding cardiologist out there.

He has no teeth. No original parts at least, his dentures are at the bedside. It is very rare to get a strep endocarditis in patients with no teeth, as the source is supposed to be bleeding around the teeth/gums.

Repeat blood cultures are negative, but he is on antibiotics.

His back pain is gone after a week on antibiotics. I can't get an MRI because of the pacer, something about a moving magnetic field inducing a current in a wire. Supposed to be bad if the wire ends in the heart.

I wanted to get a bone scan, but there is a technetium shortage in the US. Who knew? Bacteremia, esp. S. aureus bacteremia, often presents as severe back pain even if there is no discitis.

So what do I treat and why? The literature for salvaging pacer systems is grim: Ah canna work miracles, Captain. But the literature is primarily pacers infected with staph. I can usually kill strep.

I don't want to stop the antibiotics if the system is involved, as giving the bug a chance to settle in would be a disaster. Or maybe the bacteria are contaminants.

So since it is my job to make a firm decision based on inadequate data. So I am going to treat him with a healthy course of antibiotics IV. And get a bone scan with the radioactivity is available. And enjoy the gray.

Addendum: he was cured without taking out the pacer, so it was probably not infected.

Rationalization

Int J Cardiol. 2009 Sep 11;137(1):e13-4. Epub 2008 Aug 5. Streptococcus oralis endocarditis presenting as infective discitis in an edentulous patient. Renton BJ, Clague JE, Cooke RP. PMID: 18684532

Chronic antiplatelet therapy and mortality among patients with infective endocarditis. Pepin J, Tremblay V, Bechard D, Rodier F, Walker C, Dufresne D, Lafontaine A, Li N, Lacroix C, Lanthier L.Clin Microbiol Infect. 2009 Feb;15(2):193-9. Epub 2009 Jan 22.PMID: 19196260

Impact of prior antiplatelet therapy on risk of embolism in infective endocarditis. Anavekar NS, Tleyjeh IM, Anavekar NS, Mirzoyev Z, Steckelberg JM, Haddad C, Khandaker MH, Wilson WR, Chandrasekaran K, Baddour LM. Clin Infect Dis. 2007 May 1;44(9):1180-6. Epub 2007 Mar 14.PMID: 1740703

Easter

Apr 4, 2010

It is Easter. Everything has an infectious association, and Easter is no different. You may not think about it, but the traditions associated with each holiday have the potential to spread infections. Life is good.

Chickens, of course, are associated with Salmonella and Campylobacter, but chickens carry alpha strep as well and there are the occasional infection after being pecked by chicken, albeit a rooster. Don’t let the chick peck you.

Baby ducks are not the much better. In addition to Salmonella, Erysipelothrix rhusiopathiae is found in ducks and can be transferred to humans. Avian flu, if it ever gets to the US, may get here by way of migrating ducks as the virus is not as lethal for ducks. No one can stop the ducks. Except Ohio State.

Bunnies? Besides a source of tularemia, they are carriers of P. multocida. That is one reason that rabbit is dynamite and why we have rabbit for our Easter dinner. The kids are never expecting the Easter bunny as a result, and I don’t have to worry about chocolate, which is a known source of Salmonella.

Rationalization

J AAPOS. 2006 Dec;10(6):579-80. Subclinical endophthalmitis following a rooster attack.

Cephalic tetanus as a result of rooster pecking: an unusual case. Kara CO, Cetin CB, Yalçin N. Scand J Infect Dis. 2002;34(1):64-6. PMID: 118741

Fatal case of brain abscess caused by rooster pecking. Berkowitz FE, Jacobs DW. Pediatr Infect Dis J. 1987 Oct;6(10):941-2. PMID: 3696828

Vet Microbiol. 2010 Jan 27;140(3-4):405-17. Epub 2009 Aug 8. Erysipelothrix rhusiopathiae.

Outbreak of Salmonella napoli infection caused by contaminated chocolate bars. Gill ON, Sockett PN, Bartlett CL, Vaile MS, Rowe B, Gilbert RJ, Dulake C, Murrell HC, Salmaso S. Lancet. 1983 Mar 12;1(8324):574-7. PMID: 6131266

International outbreak of Salmonella Eastbourne infection traced to contaminated chocolate. Craven PC, Mackel DC, Baine WB, Barker WH, Gangarosa EJ. Lancet. 1975 Apr 5;1(7910):788-92. PMID: 48010

Fly Like an Eagle

Apr 6, 2010

Streptococcus pyogenes can be one wicked bug. A couple of times a year it tries, and sometimes succeeds, in killing people. It killed Jim Henson, as the most famous example.

Group A strep can kill in three ways: Toxic shock syndrome, necrotizing fasciitis and, less often, old-fashioned septic shock.

It always seems to hit the young who, with a brisk immune system, have a dramatic response to bacteremia. The patient last week has the old-fashioned strep throat that got way out of control with bacteremia and multi-organ system failure. CT of the neck showed a phlegmon in the neck. Part of the reason she became so ill, not unsurprisingly, was no insurance, so there was an almost fatal delay in seeking health care.

What is the best therapy for group A strep? Probably penicillin, but strep are prone to the Eagle effect, where the organism makes inexplicably popular pop music.

The Eagle effect is where at high inoculum S. pyogenes is unaffected by penicillin but is killed by clindamycin. The effect appears relevant in animals, but men are not mice. Tell me about the Eagle effect, George.

"We investigated the relative efficacies of penicillin, clindamycin, and erythromycin in a mouse model of myositis due to Streptococcus pyogenes. Penicillin was ineffective unless given at the time of bacterial injection, and treatment delays of 2 h reduced its efficacy such that survival was no better than that of untreated control animals (P less than .05). Survival of erythromycin-treated mice was greater than that of both penicillin-treated mice and untreated controls, but only if treatment was begun within 2 h. Mice receiving clindamycin, however, had survival rates of 100%, 100%, 80%, and 70% even if treatment was delayed 0, 2, 6, and 16.5 h, respectively. Thus, clindamycin demonstrated superior efficacy to penicillin among all the various treatment groups (P less than .05). Our results corroborate the failure of penicillin in this model of streptococcal infection and suggest that, unlike penicillin, the efficacy of clindamycin is not adversely altered by the "Eagle effect."

I am, as you may know, reasonably convinced of the importance of the immunomodulatory effects of macrolides on improving the outcomes of sepsis. So I did not object to the clindamycin, which, yes, I know, is a lincosamide. Thank you very much, Lindsay.

While she improved with time and 'double coverage,' the WBC remained elevated and repeat CT of the chest showed my multiple peripheral emboli in the lung and thrombosis of the subclavian vein. Septic thrombosis of the great vessels? Not really reported for Group A strep, and upper extremity DVT is not uncommon.

"204 patients underwent venous duplex scans for clinical suspicion of DVT. About half (103 patients) had both upper- and lower-extremity scans, 24 patients had upper-extremity scans, and 77 had lower-extremity scans...DVT was confirmed in 39 patients. The incidence of upper-extremity DVT was higher than that of lower-extremity DVT (17% vs 11%; P = .11)."

A TEE shows a tricuspid valve something, not really a classic vegetation, but, given the CT finding which looks for all the world like septic emboli, I feel since safe > sorry, I will treat her for endocarditis. At least S. pyogenes endocarditis is reported on the TV, albeit as rare as a Blazers championship.

"Group A streptococcus is an uncommon cause of infective endocarditis. We report five probable cases during a 10-year period (1980-1989) from a 750-bed community-teaching hospital. None of the patients were drug abusers. Group A streptococcus is the cause of infective endocarditis in between 0 and 5% cases in reported series. Since the introduction of penicillin 69 cases of group A streptococcus endocarditis has been reported in the literature. Clinical details of 14 patients, none of whom were drug abusers, are available. Included are our five cases. Eight patients had no underlying valve lesions. The overall mortality was 21% but only 15% for patients treated approximately. Among the 25 reported IV drugs abusers with group A streptococcus endocarditis and known valve involvement, right-sided heart valves were involved in 19 and left sided in six. The overall mortality was 9%."

Another straight forward case, n'es pas?

Rationalization

Here is the classic reference from 1949 THE EFFECT OF THE SIZE OF THE INOCULUM AND THE AGE OF THE INFECTION ON THE CURATIVE DOSE OF PENICILLIN IN EXPERIMENTAL INFECTIONS WITH STREPTOCOCCI, PNEUMOCOCCI, AND TREPONEMA PALLIDUM by Harry Eagle http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2135933/

SCCM 2009: Upper-Extremity DVT as Prevalent as Lower-Extremity DVT in ICU Patients

Group A streptococcus endocarditis: report of five cases and review of literature.

My secret

Apr 8, 2010

The patient could be one of any number I have seen over the years. Big abscess. In the brain, the liver, the pleura, the peritoneal cavity. And what they have in common is that the person who is best at draining them cannot or will not drain the pus. I can't drain it as there is no straight shot on the CT or I can't drain it because the patient is too ill, too infected, too sick, to go to the OR. So they turn to me and say, hey, tubby, cure this with antibiotics.

I have found over the years that internists are as interchangeable as Lego. A cardiologist is a cardiologist. You get the same opinion from each one. ID docs? Pulmonologists? The same. We all respond to the same case in the same way. Not so surgeons. Some will operate, some will not. If the patient has a belly full of pus and is on the trauma service, they are off to the OR. In another institution, with a different surgeon on an identical case, nothing can induce them to take an ill patient to the OR. And I do not know the right answer. It is not as if there is a lot of literature on when a patient should or should not go to the OR.

Certainly, a trip to the OR should be considered for

"patients with clinical deterioration or lack of clinical improvement with a likely intra-abdominal cause...The decision to perform an on-demand relaparotomy was made by the multidisciplinary medical team. To guide the decision for reoperation, the following definitions of deterioration and lack of improvement were specified in the protocol.

Deterioration after the previous operation was considered if there was an increase of more than 4 points in the Multiple Organ Dysfunction Score20 or prespecified surgical emergencies (i.e., abdominal compartment syndrome; intra-abdominal bleeding with persistent decrease in hemoglobin despite replacement and hemodynamic instability; burst abdomen; perforation of visceral organs; anastomotic leakage; intra-abdominal abscess that cannot be drained percutaneously; ischemia/necrosis of a visceral organ.

Lack of improvement of clinical signs of persistent sepsis was considered if the Multiple Organ Dysfunction Score was unchanged (±2 points) for at least 48 hours following the index laparotomy or the previous relaparotomy. Abscess detected at CT imaging with positive fine-needle aspiration results (Gram stain with evidence of bacterial involvement) that could not be drained percutaneously was another reason for relaparotomy."

Seems easy enough. But I know that I can't treat any infection over about 2 cm. That’s cent-a-meter, not saunt-a-meter.

Abscess is a perfect storm of conditions that ensure antibiotics will not/cannot work.

Abscesses

• have no blood supply, so antibiotic delivery is decreased.

• are round, and therefore have the least surface area to volume. It would sure be better if they were long, narrow sheets. It would make it easier to deliver antibiotics.

• can be filled with beta-lactamases, more than you can deliver with a dose of unisin. My personal spelling and editorial comment, not a typo.

• can be inhospitable to antibiotic function: aminoglycosides do not work in the pus environment.

• do not contain actively growing organisms. Most of the bugs are in stationary phase and can't be killed with most antibiotics. They only die when they are reproducing. I am glad I do not share that characteristic with bacteria.

So what is the best antibiotic that overcomes those issues? A scalpel or a big, fat drain in IR. But no drainage, no cure. Know drainage, know cure.

My secret? Antibiotics do not do diddley for most abscesses. So quit asking me to do the impossible and cure abscess without drainage.

Rationalization

JAMA. 2007 Aug 22;298(8):865-72. Comparison of on-demand vs. planned relaparotomy strategy in patients with severe peritonitis: a randomized trial.

POLL RESULTS

The least interchangeable in medicine is

1. internal medicine. 6% (2)

2. general surgery. 6% (2)

3. directory of nursing. 15% (5)

4. CEO of the hospital. 18% (6)

5. me. I am unique and wisdom and experience is irreplaceable. 48% (16)

6. Other Answers 6% (2)

A quick overreaction

Apr 10, 2010

Patient has surgery and 3 weeks later has a red, hot area over the incision. The surgeon opens it up, cultures it, packs it, and starts cephalexin. But, surprise, surprise, it grows MRSA, so she is started on DS Bactrim 2 bid.

Over the next 48 hours, it all gets worse.

Fevers to 104, rigors, headache, a slight rash on the back and neck. It persists and the patient gets weaker. After 5 days she goes to the ER and is admitted. Now the WBC is 1.5, the creatinine 1.8 and sodium is 120.

Exam: wound looks great. The slight rash as mentioned. Normal eyes, palms, tongue, soles, calcium.

The admitting diagnosis is uncontrolled MRSA infection and she is started on vancomycin and a quinolone.

Next day I am called.

I think she transitioned from a wound infection, which has resolved, into a whopping Bactrim reaction. It is more what she didn't have, the normal eyes, palms, soles and tongue that make it not toxic shock syndrome but drug reaction. This kind of reaction is more common in AIDS patients, but occasionally non-AIDS patients can overreact to Bactrim. I asked if she had prior sensitization due to a prior treatment of a UTI, but she does not remember.

I expect she will be ill until the drug is out of her system, about 4 half-lives. I'll know on Monday if I was wrong or not. She was probably under-dosed for the MRSA and overdosed for a drug reaction.

And indeed by Monday she was all better.

The Names Keep Changing

Apr 16, 2010

I have been quite ill the last six days and today is the first time in almost a week where I didn't feel like passing out after walking fifty yards. A bad case of stickittothemaneosis, methinks, and the worst case I have had this century. Still, I have a miracle cure that ensures that every self-limited disease I contract will get better: I sit in my lazy boy until I am all better. That lazy boy, let me tell you, is more better than any homeopathic remedy, as it is 100% effective in getting me well and back to work. And I like work, except for that whole getting up early for meetings part.

The patient is an elderly female with severe aortic stenosis. For the last month, she has had fevers and chills and progressive failure to thrive.

She has many non-contributory diseases of aging, and her blood cultures are all positive for streptococci. 4 sets over 2 days, so she has the sine qua non of endocarditis, sustained bacteremia. Doesn't matter what the ECHO shows (negative) or the exam (no emboli). It is endocarditis, and I do not need to prove otherwise, so do not ask me to.

But what is the strep, you ask? Should I tell you? Or lead you on, a sort of strep tease? OK. I'll tell you. It was Streptococcus infantarius.

What is that?

Streptococci are a pain. The more genetic evaluation they do of streptococci, the more they split the organism’s classification. At the present rate of analysis, I expect in a decade each culture will be given its own name. Patient has four out of four cultures for Streptococcus William Barney Christopherson. The Third.

And, by the way, who says microbiologist don't have a sense of humor. Or that mind is at the level of a 12-year-old boy. There is a renamed S. bovis (Biotype II/2), a colonic organism, that is now called Streptococcus gallolyticus subspecies pasteurianus.

Really.

So S. infantarius used to be the artist formerly known as S. bovis II/1. The organism is associated with cancer as well, but not colon cancers like S. gallolyticus.

"The association of colon tumors with S. gallolyticus was 48.5% (51 of 105) versus 11% (3 of 28) for S. infantarius (P < 0.0003). Nevertheless, for noncolonic cancer the association was 6% (6 of 105) for S. gallolyticus versus 57% (16 of 28) for S. infantarius (P < 0.0001). Of these 16 noncolonic cancers associated with S. infantarius, 12 (75%) were of the digestive tract (fundamentally pancreas and biliary tract), 9 of them appearing as cholangitis."

The name changes, the bug is the same, but an understanding of their associations improve, and so much of ID is understanding associations, in my case loose associations.

The patient? The noncontributory factors to her infection were more important to her he quality of life, and she went to hospice with no work up her potential cancer.

Rationalization

J Clin Microbiol. 2008 Apr;46(4):1570. Epub 2008 Feb 6. Association between Streptococcus infantarius (formerly S. bovis II/1) bacteremia and noncolonic cancer. Corredoira J, Alonso MP, Coira A, Varela J.

J Clin Microbiol. 2010 Jun;48(6):2247-9. Epub 2010 Mar 31. Streptococcus gallolyticus subspecies pasteurianus (biotype II/2), a newly reported cause of adult meningitis. Sturt AS, Yang L, Sandhu K, Pei Z, Cassai N, Blaser MJ.

Lady Windermere

Apr 19, 2010

Another weekend of call is behind me and I have a week of work and, I hope, Trailblazer victories, in front of me.

One of the consults this weekend was what to do about Mycobacterium avium intracellulare, MAI, in the lung.

The patient is an 80ish, thin, small, Caucasian female with a long history of lung disease for no good reason. No smoking, no asthma, no environmental exposures to lead to COPD, but she has COPD, and bronchiectasis, as well. MAI is often a disease of elderly, thin, Caucasian females.

"NTM lung disease has been recognized in disproportionately increased numbers in postmenopausal women. Among these patients, slender body habitus and thoracic cage abnormalities, such as pectus excavatum and scoliosis, are commonly described. Notably, no long-term prospective clinical studies exist to corroborate that low weight is an independent risk factor for NTM lung disease."

Why thin females?

"However, based on the findings of a limited number of experimental studies, we hypothesize that decreased leptin, increased adiponectin, and/or decreased estrogen in older women with slender body habitus may account for their increased susceptibility to NTM infections."

Maybe, maybe not, but the paper is an interesting hypothesis. But I don't know enough to know if they are blowing smoke, albeit with a low FEV1.

She has a chronic cough and intermittent steroid use, but nothing else of note.

Her CXR is curious, with patchy, subtle, infiltrates and multiple small, indistinct nodules.

Her sputum has MAI and has for most of this century. What to do about it, I am asked.

I reply, probably nothing.

Treatment of MAI pneumonia in the normal person is often a waste of time, with cost and toxicity and little benefit. It seems all too often that the elderly do not tolerate MAI therapy well at all, and I cannot remember ever making a patient better with the treatment. I have made then ill and significantly poorer.

Since it is nice to do more good than harm, I suggest, as her symptoms are stable and the CXR is without change, to continue to ignore the MAI.

Lady Windermere was a character in Oscar Wilde's play Lady Windermere's Fan. It was hypothesized that since Victorian females did not cough, they would collect the sputum in the airway (ick) and therefore be predisposed to getting pneumonia, such as MAI. However, the grumpy stickler (not me, but I would agree) suggests it is a bad literary fit:

"The condition has been named Lady Windermere syndrome, as the name is based on the aphorism, 'ladies don't spit.' A lady, as described in literature, is a woman of good social standing and has a polite and refined disposition. Ladies are assumed to be fastidious, and as spitting is socially unacceptable, they voluntarily suppress their cough and infected secretions are retained in the lungs. The name, Lady Windermere, comes from Oscar Wilde's play, Lady Windemere's Fan, written in 1892, and is a witty dramatization of manners and morals in Victorian upper-class society. The fastidious behavior is illustrated by Lady Windermere's remark, "How do you do, Lord Darlington? No, I can't shake hands with you. My hands are all wet with these roses."

“However, Lady Windermere was a vivacious 21-year-old girl, who was married for two years and had never coughed or showed any other illness. Although the name Lady Windermere is rather inappropriate and hence has not come into general use, NMIs must be considered in elderly women with unexplained respiratory symptoms and a tree-in-bud appearance on HRCT.”

Rationalization

Slender, Older Women Appear to Be More Susceptible to Nontuberculous Mycobacterial Lung Disease GENDER MEDICINE/VOL. 7, NO. 1, 2010

POLL RESULTS

The NBA champion will be

1. Portland 0% (0)

2. The Blazers 0% (0)

3. The Trailblazers 4% (1)

4. The Portland Trailblazers 0% (0)

5. Crislip is deeply deluded on this and other topics. 85% (22)

6. Other Answers 12% (3)

7. Rip City

8. Who watches basketball when MLB season has started???

9. Who's playing?

He Read the Textbook

Apr 20, 2010

HA. Blazers 1 Suns 0. HA.

Most patients do not bother to read the textbooks before they come to the hospital or clinic. As a result, the history and physical can be missing key aspects that would make the diagnosis easy. There is the usual presentation of common diseases, the unusual presentation of common diseases, the usual presentation of an uncommon disease and, what I seem to write about, the uncommon presentation of an uncommon disease.

Yesterday I had a common presentation of a common disease, but a disease I have not seen this century.

Young male was in the brush of Namibia and Zimbabwe this spring. He was covered at the end of the day with ticks. Ick. Blood suckers. Gives me the willies just to write about it.

Most of the tick bites leave nothing behind, but one bite gets red and tender and forms a half cm necrotic eschar. Simultaneously he develops fevers, headache, deep bone pain and arthralgias. He also has regional adenopathy. No rash. CBC and LFT's are normal and his malaria smear is negative.

Tick bite fever. Rickettsia africae.

It’s like he reads CID:

"26.6% of those reporting flu-like symptoms, had ATBF diagnosed. More than 80% of the patients had fever, headache, and/or myalgia, whereas specific clinical features such as inoculation eschars, lymphadenitis, cutaneous rash, and aphthous stomatitis were seen in < or = 50% of patients. Game hunting, travel to southern Africa, and travel during November through April were found to be independent risk factors. Our study suggests that ATBF is not uncommon in travelers to rural sub-Saharan Africa and that many cases have a nonspecific presentation."

He responded rapidly to doxycycline and was mostly better in 24 hours. ID docs call rickettsial illnesses a doxycycline deficient state.

R. africae is not just in Africa. It is also found in the West Indies.

"In Africa, the tropical bont tick, Amblyomma variegatum, is commonly infected with R. africae and is likely the major vector of the organism. This tick was introduced from Africa (Senegal) into the West Indies (Guadeloupe) in the early 1800s but has only spread widely and become endemic on many islands in the last 30 years. This spread was probably due to an increase in the between-island movement of livestock, major hosts of A. variegatum, and the introduction and spread of the cattle egret (Bubulcus ibis), a host of the immature stages of A. variegatum. Recent studies have demonstrated R. africae infections in A. variegatum, persons, and animals in the West Indies."

I bet it came to the West Indies as part of the slave trade, although it is not specifically mentioned in the article. The slave trade led to some interesting disease epidemiology in the Caribbean. Most of the population of Haiti is from Africa by way of the slave trade. The Hepatitis B in Haiti is mostly types A1 (44%), also found in East Africa, and A5 (20%) also found in the Bight of Benin, a former African slave hub. Hepatitis B A1 and A5 came to Haiti with the slaves in the 1800s.

However, Hepatitis B types E and A5 now dominate in Africa. When they look at the difference between the strains of A5 in Haiti and Africa, they diverged about 270 years ago, the beginning of the slave trade. Type E, however, by genetic analysis, has been in Africa for less than 200 years. Where did it come from and how did it spread so rapidly? They postulate the mass inoculation programs of the late 1800/early 1900s, where 90,000 people would be injected using a single syringe, was a potential source for the rapid spread for the Hepatitis B type E in Africa.

Yet another instance where infections shed light on human history, or is it the other way around?

Rationalization

Kelly PJ. Rickettsia africae in the West Indies. Emerg Infect Dis. 2006 Feb. http://dx.doi.org/10.3201/eid1202.050903

Clin Infect Dis. 2003 Jun 1;36(11):1411-7. Epub 2003 May 19. African tick bite fever in travelers to rural sub-Equatorial Africa.

The Real Monas

Apr 22, 2010

The patient is a middle-aged female who comes in with chemotherapy-induced neutropenia and fevers. Not that uncommon. But, unlike most patients, she has focal symptoms. She has a collection of a half-dozen tender, purple-red pustules with surrounding ecthyma.

Her WBC is normal the next day, and the fevers are gone, and cultures of one of the lesions grows Pseudomonas aeruginosa. Where did that come from?

So I take the usual exposure history and she had been in a public hot tub about a week before the chemo. She did not do anything out of the ordinary in the hot tub, just relaxed with a relative. As she remembers it, the hot tub was adequately stinky with disinfecting chemicals.

Still, the most common source for a Pseudomonas infection would be a water source, and the classic infection from hot tubes is a folliculitis. The hot water opens the follicles, the contaminated water gets in, and then is sealed in place as the patient gets out of the hot tub and cools off.

Her problem, or so I hypothesize, is the neutropenia allowed the infection to get worser than usual. Her blood cultures were negative so I do not think this was hematogenous and the lesions do not look like ecthyma gangrenosum, the other classic skin disease of this beast.

The other infections I have seen from Pseudomonas related to hot tubs is one case of Pseudomonas pyelonephritis with bacteremia and another of Pseudomonas endometritis. Both occurred shortly after sex in the hot tub. And that is not the only case:

"We report a case of a previously healthy 38-year-old male with acute prostatitis and concurrent Pseudomonas aeruginosa urosepsis. Pulsed-field gel electrophoresis analysis confirmed that the source of the organism was the patient's newly purchased hot tub, which was filled with water from a stream...Sexual activity and the use of nonpotable water were likely risk factors for infection."

You have to be careful of what you do in hot tubs.

"Hot tub use has been linked to P. aeruginosa folliculitis and more-serious infections, including pneumonia and those involving the urinary tract (cystitis, prostatitis, and urosepsis)."

It is a hardy beast, and will grow rapidly in hot tubs.

"Superchlorination or the draining, cleaning, disinfection, and refilling of whirlpools markedly reduced densities of P. aeruginosa in whirlpool water, but the bacterial populations were rapidly reestablished (fewer than 10(3) cells per ml) when disinfectant concentrations decreased below recommended levels (chlorine, 3.0 ppm [3.0 micrograms/ml]; bromine, 6.0 ppm). P. aeruginosa in the water was replenished from various sources, such as hoses used to fill the whirlpool and the biofilm in the filter and piping of the whirlpool systems. Daily monitoring and adjustment of chemical characteristics (regardless of bather load) were essential for controlling densities of P. aeruginosa."

Make sure that that hot tub is clean.

Rationalization

MMWR Morb Mortal Wkly Rep. 2000 Dec 8;49(48):1087-91. Pseudomonas dermatitis/folliculitis associated with pools and hot tubs--Colorado and Maine, 1999-2000. Centers for Disease Control and Prevention (CDC).

J Clin Microbiol. 2009 May; 47(5): 1607–1608. Pseudomonas aeruginosa Acute Prostatitis and Urosepsis after Sexual Relations in a Hot Tub

J Clin Microbiol. 1988 Sep;26(9):1650-4. Incidence and persistence of Pseudomonas aeruginosa in whirlpools. Price D, Ahearn DG.

When to operate

Apr 24, 2010

One interpretation of quantum mechanics is the many worlds theory, which to quote the ever-helpful Wikipedia, "In layman's terms, there is a very large—perhaps infinite—number of universes, and everything that could possibly have happened in our past, but didn't, has occurred in the past of some other universe or universes."

Quantum mechanics makes my brain hurt. But medicine would be a lot easier if we had the ability to see what happened in alternate realities. It would make decisions easier since we would know the consequences of making alternative choices.

The patient came in septic: multi-organ system failure and a WBC of 50,000. Evaluation led to the diagnosis of C. difficile colitis and he was started on both IV and oral treatment for the C. difficile. The CT did not show toxic megacolon, but an extraordinarily thick, inflamed colon.

He doesn't get better and I am consulted. I suggest, give the severity of his disease, that he needs a colectomy. Is that the right decision? I think so, and we are all agreed and he has a colectomy. He does get better, although as I left for the weekend his WBC is still 50,000. Would he have improved without the colectomy? I do not know, but wish I could have surfed the quantum waveform down alternate realities to see what might have otherwise happened.

What are the criteria for surgery for C. difficile ?

"Early diagnosis and treatment with subtotal colectomy and end ileostomy is critical in reducing the mortality associated with fulminant colitis. Patients who have a history of inflammatory bowel disease (IBD), recent surgery, prior treatment with intravenous immunoglobulin (IVIG), vasopressor requirements, leukocytosis, or increased lactate should have early surgical consultation and operative intervention."

Other studies have suggested

"Independent predictors of mortality included the following: (1) age of 70 years or older, (2) severe leukocytosis or leukopenia (white blood cell count >or=35 000/microL or <4000 data-preserve-html-node="true"/microL) or bandemia (neutrophil bands >or=10%), and (3) cardiorespiratory failure (intubation or vasopressors)."

He had two out of three, so I think I made the right decision.

A day later one of the pharmacists at another hospital had a quote he attributed to Dr. Maki "You can live without a colon, but you can't live long with a bad colon.

The problem may be a mutant C. difficile strain, as

"recent outbreaks of C. difficile infection carry deletion mutations in the tcdC inhibitory gene that have been associated with an increase by more than a factor of 10 in the production of toxins that mediate colonic tissue injury and inflammation in C. difficile infection."

So the bug just pumps the toxin into the environment at an increased rate to kill off the colon.

I have also wondered, as an aside, with the C. difficile toxin, and other bacterial toxins, what function the toxins really evolved for. I can't see how causing diarrhea in patients leads to an increase in organism survival, since diarrhea leads to isolation and fatal antibiotics. I assume, perhaps incorrectly, that these toxins have an alternative purpose and the causation of disease is a side effect of that function.

Maybe "the patient is both alive and dead, irrespective of whether he had surgery but the "alive" and "dead" patients are in different branches of the universe, both of which are equally real, but which cannot interact with each other.

But if I can choose my alternative reality, I do not want a universe without shrimp.

Rationalization

Arch Surg. 2009 May;144(5):433-9; discussion 439-40. Fulminant Clostridium difficile colitis: patterns of care and predictors of mortality. Sailhamer EA, Carson K, Chang Y, Zacharias N, Spaniolas K, Tabbara M, Alam HB, DeMoya MA, Velmahos GC.

Am J Surg. 2010 Jul;200(1):131-5. Epub 2010 Apr 21.Surgical aspects of fulminant Clostridium difficile colitis. Butala P, Divino CM.

Clostridium difficile — More Difficult Than Ever Ciarán P. Kelly, M.D., and J. Thomas LaMont, M.D. N Engl J Med 2008; 359:1932-1940 October 30, 2008

Insect Poo, Insect Puke

Apr 26, 2010

The patient is elderly, demented, diabetic and evidently just wants to be left alone. Chronic stasis and lack of wound care can be a bad combination, and at some point, we are not sure when, his hyperkeratotic leg broke down and became infected. And necrotic. And then the flies came.

When the ambulance drivers finally opened the door, it was noted that the room smelled of rot and the leg was teaming with maggots.

I haven't seen maggots for a while.

As a fellow in one of the hospitals I rotated to had a breakdown of the air conditioning system, and in the hot Los Angeles summer, they opened the windows for a day. It makes you wonder how funky hospitals were in the era before good ventilation and central air. The odors of vomit, stool, melena and necrosis are bad enough in a modern hospital room with 6 air exchanges a minute.

Anyway. A week after the failure of the air conditioning they had a mini-outbreak of maggots in the ICU, where flies had laid eggs in the snot of patients in the vent. Icky, and not very aesthetic, but harmless.

In my first year of practice, I took care of a street person who had been hit about the head and bled between his scalp and skull, and then lay under a bush for a week. The maggots entered the laceration on his scalp and filled the clot in his subgaleal space. In the OR his head looked like he had been sleeping in a bowel of rice, he had so many maggots.

But this is my first maggot infestation this century.

Maggots are good for wounds. I always thought it was due to simple ingestion; the maggots eat only the dead tissue, leaving good meat behind. It turns out, maggots are more sophisticated than that.

"Maggots may contribute to wound healing by removing cell debris and non-viable tissue,19 inhibiting the pro-inflammatory responses of phagocytes and promoting tissue remodelling. The molecules involved in these actions are believed to be contained in the excretions/secretions (ES) of the maggots. Interestingly, clinical observations have indicated that maggot therapy is more effective in patients with wounds infected with Gram-positive bacteria, such as Staphylococcus aureus, than those infected with Gram-negative bacteria, such as Pseudomonas aeruginosa. Additionally, more maggots are needed to accomplish healing of wounds infected with the latter bacterium...

...As little as 0.2 microg of maggot excretions/secretions (ES) prevented S. aureus biofilm formation and 2 microg of ES rapidly degraded biofilms. In contrast, ES initially promoted P. aeruginosa biofilm formation, but after 10 h the biofilms collapsed."

That’s a job I want: collector of maggot excretions/secretions.

I have never prescribed maggots, evidently green bottle blowfly Lucilia sericata is what is used and can be purchased with a doctor’s prescription. 500 to 1000 sterile maggots only $150. Anti-emetics extra.

Rationalization

J Antimicrob Chemother. 2008 Jan;61(1):117-22. Epub 2007 Oct 26. Maggot excretions/secretions are differentially effective against biofilms of Staphylococcus aureus and Pseudomonas aeruginosa. van der Plas MJ, Jukema GN, Wai SW, Dogterom-Ballering HC, Lagendijk EL, van Gulpen C, van Dissel JT, Bloemberg GV, Nibbering PH.

All About Maggot Therapy

Any Bug, Any Place

Apr 29, 2010

That’s the thing about infectious diseases. Any bug can show up in any site at any time. Many a CV has grown as a result. Sure, some bugs are more common than others, and if you play the odds most of the time you will be right. But not always, which is why you get cultures.

The patient is an elderyish male who has had an artificial hip for years. For the last week, he has had increasing pain in the hip and a decrease in his mental status. He evidently lives in squalor (a suburb of Portland) and by report had a layer of stool in the environment, although human or cat could not be determined. Really. He had that many cats.

His hip is tapped and is filled with pus. Initially the gram stain is gram-positive cocci in chains, and if you were a betting man, you would bet on a group b or a viridans streptococcus. And you would lose the bet.

All the cultures grew Peptostreptococcus, An anaerobic streptococcus. This is maybe the third Peptostreptococcus infection I have seen in a joint that I can remember, and my memory is not what it used to be. I have only two kids and ask me if I can get their names straight. Nope. And for some reason it pisses them off. Yet another reason not to have kids when you are older.

Peptostreptococcus is a colon and skin bug and it is a rare cause of invasive disease. There are a smattering of human cases where it is the only organism; it is more often part of mixed infections. There are fewer than a dozen cases of joint infections reported, a couple of which suggested it was due to a dental procedure, although my patient has no teeth, and no skin breakdown to suggest a cutaneous route of infection.

I suppose we should look in his colon for a source, although there is no data to support a colonoscopy, he is due for screening.

Peptostreptococcus also causes infections in the feet of neonatal pigs. So if your baby pig is limping...

There is, by the way, a study that suggests prophylaxis of joints for dental procedures is a waste of time. Finally. It is not an uncommon question, and I never had data upon which to render an opinion.

“Background. The actual risk of prosthetic joint infection as a result of dental procedures and the role of antibiotic prophylaxis have not been defined.

Methods. To examine the association between dental procedures with or without antibiotic prophylaxis and prosthetic hip or knee infection, a prospective, single‐center, case‐control study for the period 2001–2006 was performed at a 1200‐bed tertiary care hospital in Rochester, Minnesota. Case patients were patients hospitalized with total hip or knee infection. Control subjects were patients who underwent a total hip or knee arthroplasty but without a prosthetic joint infection who were hospitalized during the same period on the same orthopedic floor. Data regarding demographic features and potential risk factors were collected. Logistic regression was used to assess the association of variables with the odds of infection.

Results. A total of 339 case patients and 339 control subjects were enrolled in the study. There was no increased risk of prosthetic hip or knee infection for patients undergoing a high‐risk or low‐risk dental procedure who were not administered antibiotic prophylaxis (adjusted odds ratio [OR], 0.8; 95% confidence interval [CI], 0.4–1.6), compared with the risk for patients not undergoing a dental procedure (adjusted OR, 0.6; 95% CI, 0.4–1.1) respectively. Antibiotic prophylaxis in high‐risk or low‐risk dental procedures did not decrease the risk of subsequent total hip or knee infection (adjusted OR, 0.9 [95% CI, 0.5–1.6] and 1.2 [95% CI, 0.7–2.2], respectively).

Conclusions. Dental procedures were not risk factors for subsequent total hip or knee infection. The use of antibiotic prophylaxis prior to dental procedures did not decrease the risk of subsequent total hip or knee infection.”

So when asked, I can say the data doesn’t support it, although the data is not perfect. What to do for neonatal pigs that need dental work, however, I remain uncertain.

Rationalization

Clinical Infectious Diseases 2010;50:8–16. Dental Procedures as Risk Factors for Prosthetic Hip or Knee Infection: A Hospital Based Prospective Case‐Control Study

Rip, Tear, and Fever

Apr 30, 2010

I am currently an old arrogant sob and not short of breath. It is part of my charm, nest pas? So I have a patient with a fever. I do the usual fever work up and find nothing. She has a few afebrile days, then spikes another temperature, gets tachycardic and tachypneic and is transferred back to the hospital where they work her up and find no cause of her fever. Or do they?

She had initially been at the other hospital for a dissecting aortic aneurysm that had been wrapped, and as part of the work up this time they did a CT that demonstrated an extension of the dissection, but the surgical powers that be thought it do not warrant an intervention.

Aneurisms can cause fevers for, oh, I suppose four reasons. The clot can become infected and the classic organism is Salmonella. The repair can become infected and that is always a worry as infected aortic grafts are a disaster. In this case there were no unusual fluid collections or,, more ominous, air in the graft repair, so I think the patient dodged that bullet. Rarely, as it dissects, the aneurysm can cause cholesterol emboli which can cause fevers, but she had no emboli on exam.

Finally, a dissection can cause fever. When I was a young arrogant sob, my first year in practice, I saw a patient with 2 weeks of fevers and a new aortic insufficiency murmur. I ordered blood cultures and waited. The murmur worsened on antibiotics and the fevers persisted. So, after 5 days, I ordered an ECHO. No endocarditis, but an aortic dissection that led to both the murmur and the fevers. The patient was repaired and suffered no harm from the slight delay in diagnosis.

Turns out that dissection can cause a fever and there are maybe 22 cases in the literature. Later, I presented the case to the person who first described dissection as a cause of fever and he missed it. So I didn’t feel so bad, although my threshold for ECHO in endocarditis is lower.

So I think, or I presume, that the fevers are due to the extension of the dissection. The fevers went away, as fevers often do, and there was never another cause found. That’s my story and I am sticking to it.

Rationalization

JAMA. 1976 Oct 11;236(15):1725-7. Dissecting aortic aneurysm manifested as fever of unknown origin. Mackowiak PA, Lipscomb KM, Mills LJ, Smith JW.

Miliary

May 2, 2010

Certain words will lead to quick associations. ID is all about disease associations.

If you say Central Valley to an ID doc, he will say coccidioidomycosis.

If you say cat, she will say Pasteurella, although I am more likely to say Power. The Greatest.

If you say potato, they will say botulism, not po-tah-toe. At least so I would hope.

And if you say miliary, you should hear TB in reply.

The patient is a middle-aged Hispanic male who presents with small bowel obstruction and a miliary pattern on CT and CXR that is as textbook as you will ever see.

He is from Mexico, and remembers no Tb exposure. His sputum smears for TB are negative, but maybe 25% of sputums are negative in miliary Tb. Miliary Tb is an infection of the vascular tree, not the alveoli, so the Tb does not have ready access to the airway and thence to the sputum. So he is off to the OR as they think he has cancer with lung mets causing the obstruction. A big, inflammatory mass in found at the ileocecal junction. Sure sounds like Tb.

But the pathology shows a yeast consistent with Histoplasma and the histoplasma antigen is sky high. Histoplasma can mimic adenocarcinoma in the immunodeficient and many things can cause a miliary pattern. The differential diagnosis of miliary Tb is vast, but the causes include any fungus that disseminates homogeneously, like histoplasma, Tb, and varicella pneumonia.

So what looks like Tb and smells like Tb and acts like Tb is not Tb.

He is tolerating amphotericin B constant infusion. I tend to give constant infusion ampho as it is less toxic and no worse than standard or lipid ampho if you dose it high enough, or so I hope. And talk about cost. Lipid ampho costs a fortune (two to 300 dollars a vial) and he is both uninsured and is not here legally. There is one trial of regular vrs ampho for the treatment of Histoplasma that gives a slight edge to lipid ampho, although they gave 0.7 mg/kg regular ampho and I am giving 0.8 mg/kg. Maybe more is better if given slowly, and he is getting better.

He improved and once changed to po after a long course of amphotericin, he vanished.

Rationalization

Ann Diagn Pathol. 2003 Feb;7(1):14-9. Colonic histoplasmosis in acquired immunodeficiency syndrome mimicking carcinoma. PMID: 12616469

Safety and efficacy of liposomal amphotericin B compared with conventional amphotericin B for induction therapy of histoplasmosis in patients with AIDS. Ann Intern Med. 2002 Jul 16;137(2):105-9. PMID: 12118965

Poll Results

If I say cat, you say

1. Pasteurella. 24% (12)

2. Power. 12% (6)

3. The other white meat. 20% (10)

4. LOL 14% (7)

5. cat [-nbsuvet] [file...] 12% (6)

6. Other Answers 16% (8)

7. Toxoplasmosis

8. bad luck

9. Peking Moon

10. the best use of which is for anatomy lessons for undergrads...

11. cmv

12. Toxoplasmosis

13. toxoplasmosis

Batting 126

May 4, 2010

The patient is a middle-aged male who is admitted with community-acquired pneumonia (CAP). Nothing special at first, he is placed on ceftriaxone and azithromycin, but over the first 24 hours things do not go well.

He has rapid progression of his infiltrates, goes into respiratory failure and ends up on a vent, in the ICU and now on zosin and vancomycin. He continues to decline, and his WBC goes to 35,000. So they call me.

His bronch shows lots of PMN's but no organisms so this is more typical of an atypical pneumonia and not typical of a typical pneumonia. Typically typical pneumonias have organisms on gram strain, while typically atypical does not. You would be impressed with how fast I can say that.

About the only thing I sometimes have to offer is the endless series of questions that ID docs ask in an attempt to find an exposure for a weird illness.

His mother is at the bedside, so I start asking the usual questions.

Turns out he is back after a week of a tour of the southern California theme parks. Any water exposures on the trip? Hot tubes, saunas or swimming pools?

Oh yes, he loves hot tubes and will stay in them for hours.

Bingo. This has to be Legionella, a water-borne illness that is surprisingly rare in the rain drenched Pacific Northwest. I bet I see no more than a case a year. Legionella is associated with a wide vary of odd water exposures: shower heads, fountains, cooling towers, and hot tubs.

His urine Legionella antigen is positive and he improves rapidly when azithromycin restarted. He looks. He shoots. He scores. One of the things I like to do is commit to a diagnosis. ID docs can generate a long differential diagnosis and send off innumerable tests and then sit back and wait for the diagnosis to be handed to them. But if you call a good diagnosis before the tests returns, everyone remembers and no one remembers when you called it wrong. Babe Ruth also led the league in strikeouts but that is not what he is famous for.

The other interesting thing about this case was the docs involved were following the protocols. We drum into everyone’s head that the data demonstrates that when docs follow guidelines, outcomes improve. Yet, in this case they followed the protocols for CAP then changing to CAP in the ICU and as a result they dropped the azithromycin. This time the protocol failed since the protocols do take into account when the patient has a relatively unusual illness.

It is a truism in medicine: no good deed ever goes unpunished.

Rationalization

Hot tub legionellosis. Tolentino A, Ahkee S, Ramirez J. J Ky Med Assoc. 1996 Sep;94(9):393-4. PMID: 8855593

Hot tub legionellosis. Legionnaires' disease and Pontiac fever after a point-source exposure to Legionella pneumophila. Thomas DL, Mundy LM, Tucker PC. Arch Intern Med. 1993 Nov 22;153(22):2597-9. PMID: 8239853

Picky Picky

May 6, 2010

To state the obvious, infections can make people real sick, real fast.

The patient is a young male with chronic medical problems that require prednisone and a lack of insurance that precludes appropriate follow-up. He has the onset of a severe frontal headache, fevers, and decreased mental status.

Ominous.

He comes to the ER, or rather is brought in, and he has a stiff neck, a WBC of 26K, no brain pathology on the unenhanced CT and an LP with 11 PMN's but a normal glucose and protein. One of each class of antibiotics is given after blood cultures and he is admitted around midnight.

Overnight he continues to be febrile, tenuous blood pressure, and within 12 hours his blood cultures have gram-positive cocci in chains. And he develops progressive bilateral proptosis with periorbital rubor, dolor, calor, tumor. ID is consulted first thing in the am.

Proptosis is bad, with mucor the worst cause, so off to MRI, which confirms the proptosis, but is interesting for what it does not show. No abscess, no cavernous vein thrombosis, no subdural empyema. Just sphenoid sinusitis which was noted on the CT. There can be cavernous vein thrombosis from sphenoid sinusitis with proptosis, be it wasn't there.

The cultures grew Group A streptococcus aka S. pyogenes. An ECHO obtained for reasons that elude me as I write (I think it was the fact he had a heart; Nick Chopper would have been spared the test) this showed a floppy vegetation on the tricuspid valve. Now that Sony is no longer making floppies, I suppose we will have to call it a USB or an SD vegetation.

Because of the sinus opacification, ENT looked up his nose and he had no nasal septum. Usually that is from cocaine use, but it turned out, once extubated, that he is a compulsive nose picker, and picked his entire nasal septum away. I postulate that is the source of his group A streptococcus.

With time and antibiotics, he got better and everything resolved.

There is only one case of complications from rhinotillexomania (a word I bet you never, ever, see again in your professional career, although imagine the Scrabble score) in the literature, more mild nose picking, such as you see around you in rush-hour traffic, may increase the risk of S. aureus carriage.

"Among ENT patients, nose pickers were significantly more likely than non-nose pickers to carry S. aureus (37 [53.6%] of 69 vs. 60 [35.5%] of 169 patients; relative risk, 1.51 [95% confidence interval, 1.03-2.19]). Among healthy volunteers, there was a statistically significant positive correlation between the self-perceived frequency of nose picking and both the frequency of positive culture results (R=0.31; P=.004) and the load of S. aureus present in the nose (R=0.32; P=.003)."

Kindergartners beware.

This is not the most impressive case of compulsive picking I have seen. I had a patient years ago with cranial osteomyelitis from picking off a section of scalp down to bone about the size of a small plate.

In medicine you get to see the most curious human behaviors.

Rationalization

AJNR Am J Neuroradiol. 1997 Nov-Dec;18(10):1949-50. Self-induced ethmoidectomy from rhinotillexomania. PMID: 9403460

Infect Control Hosp Epidemiol. 2006 Aug;27(8):863-7. Epub 2006 Jul 20. Nose picking and nasal carriage of Staphylococcus aureus. PMID: 16874648

Measles. What is old is new again.

May 8, 2010

There was a recent measles outbreak in British Columbia, a couple of hundred miles to the north. I assume that, like its failure with Cryptococcus gattii, the border patrol failed to prevent this organism from crossing the border and I will soon see cases of measles in Portland. I have always wanted to see a real live Koplik spot.

I had assumed I would never see a case of measles, but thanks to Dr. Wakefield's report in Lancet, since discredited and withdrawn, there had been a marked decline in MMR vaccination in the not so Great Britain, and they have had a resurgence of measles and mumps. In honor of Lend-Lease, they were kind enough to export both infections to the US. I have seen a case of mumps.

Although no study has found a link between vaccinations and autism (except for one that showed the MMR to be protective), there remains a fear of vaccines, especially in the higher socioeconomic groups. In the 2008 San Diego outbreak

"Substantial rates of intentional under vaccination occurred in public charter and private schools, as well as public schools in upper-socioeconomic areas."

Some private schools are an all you can eat smorgasbord of preventable infections in the non-immune, an outbreak waiting to happen.

Measles and the mumps are coming back. If you see a case and are asked, where did measles come from, you might answer not so Great Britain? Or maybe cows.

The thing about infections is, unlike much of modern medicine, they have a history. Much of medicine treats first-world problems, complications of not dying from infections and poor nutrition. Most people in the past did not get to live long enough to get heart disease or glioma or Alzheimer’s. They got et or died of trauma (getting et is, I suppose, a form of trauma) and they died of infections.

So how long have we had measles and where did it come from? Modern molecular biology and epidemiology can give hints.

Measles requires a minimum population to persist, so it wasn't until people started gathering into large groups was it possible for measles to become endemic.

"MeV (Measles Virus) infection can confer lifelong immunity, and there is no animal reservoir or evidence of latent or common persistent infection except for subacute sclerosing panencephalitis (SSPE). Therefore, maintenance of MeV in a population requires constant supply of susceptible individuals. If the population is too small to establish continuous transmission, the virus can be eliminated. Mathematical analyses have shown that a naïve population of 250,000-500,000 is needed to maintain MeV. This is approximately the population of the earliest urban civilizations in ancient Middle Eastern river valleys around 3000-2500 BCE."

The current strain of measles, using the molecular clock, has only been around for 60 years.

"Molecular clock analysis can estimate the age of ancestors in evolutionary history by phylogenetic patterns. The basic approach to estimating molecular dates is to measure the genetic distance between species and use a calibration rate (the number of genetic changes expected per unit time) to convert the genetic distance to time. Pomeroy et al. showed that "Time to the Most Recent Common Ancestor" (TMRCA: the age of the sampled genetic diversity) of the current MeV circulating worldwide is recent, i.e., within the last century (around 1943)."

The measles virus is related to the Rinderpest virus (RPV) of cattle. It is also related to dolphin and porpoise morbillivirus, canine distemper virus, phocid distemper virus, and peste des petits ruminants virus. It is interesting how these viruses have cousins in other animals. When did measles jump from cows to people? Or do we blame Flipper? Using the molecular clock, it is estimated that

"divergence between MeV and RPV occurred around the 11th to 12th centuries."

And ancient records of disease description, always questionable, supports measles as a new disease, either from a common ancestor that infected cows and people, or it jumped from cows to people.

"An increasing number of descriptions of measles in the 11th and 12th centuries may reflect the emergence of MeV in human populations at that time. Linguistic evidence suggests that the disease was recognized before the Germanic migrations but after the fragmentation of the Roman Empire, i.e., between 5th and 7th centuries. This age is still within 95% credible intervals of our results."

This is yet another example of why ID is, and always shall be, the coolyest subspecialty in medicine. And the most dispiriting.

Rationalization

Pediatr Infect Dis J. 2010 May;29(5):397-400. Lack of association between measles-mumps-rubella vaccination and autism in children: a case-control study. Mrozek-Budzyn D, Kiełtyka A, Majewska R.

Measles Outbreak in a Highly Vaccinated Population, San Diego, 2008: Role of the Intentionally Undervaccinate. Pediatrics Vol. 125 No. 4 April 1, 2010. pp. 747 -755

Origin of measles virus: divergence from rinderpest virus between the 11th and 12th centuries. Yuki Furuse, Akira Suzuki and Hitoshi Oshitani Virology Journal 2010, 7:52

Out, damned spot! out, I say!

May 10, 2010

I am, not unsurprisingly, a big proponent of hand washing and hand hygiene. While we have only been aware of the importance of hand hygiene for 160 years, the last 10 years have seen a renewed interest in clean hands. For years, the issue preventing compliance with the adherence, or is it adherence with the compliance, of hand washing was time. To wash hands appropriately at each and every opportunity would mean that some providers would spend most of their work day scrubbing their hands rather than providing patient care.

The big change was alcohol foam. Five seconds using the foam is better than 30 seconds at the sink, and certainly more practical. It took me a while to become accustomed to the appropriate use of the foam. I thought it was to be used like cheese whiz, and I was squirting the foam into my mouth. And as a kid ‘to urinate’ was ‘to whiz,’ so just what is cheese whiz? Maybe it’s why it is one of the few foods I have never eaten. Along with raw oysters.

The results of using the alcohol foam was amazing. Even at 20% adherence with the product, the infection rates fell by half at every one of my hospitals. Then over the next decade the use of hand hygiene foam and hand washing has steadily climbed to 90% and as the rates have gone up, the infection rate steadily fell. It has been amazing to watch.

But better hand hygiene may have unexpected side effects.

Turns out washing hands may have psychologic effects that make the washer feel better about decisions, not that it worked all that well for Lady MacBeth.

"A couple of researchers at the University of Michigan conducted a study asking students to choose between two objects out of several they had ranked. When students washed their hands after making the choice, they seemed to experience less cognitive dissonance, while students who did not wash their hands behaved as if they needed to justify their choices to themselves."

"The authors think this indicates that physical cleanliness may have a broader impact on individual psychology than previously thought—washing has been linked before to absolution of moral guilt, but less so to self-perception...hand-washing somehow dispensed with the need to justify a choice."

Every day we have to make important decisions about patient care, and even if we make a wrong decision, as we walk out of the room and wash our hands, perhaps we inadvertently reinforce the wrong decisions in the name of infection control.

I doubt it. But.

There have been several reports that demonstrate that humans who are toxoplasma seropositive are at increased risk for car accidents. If I ever have a fender bender, I am going to get tested and, if positive, use it as an excuse to weasel out of the consequences of my actions.

It wasn't my fault, yer honor, it was the toxoplasma.

Similarly, if I ever get sued for malpractice for making a bad decision, I can blame the hand hygiene policy of my hospitals for the mistake.

I would have made a better decision, yer honor, but I had to wash my hands.

Think it will work?

Rationalization

Hand washing dispels the decision demons http://arstechnica.com/science/news/2010/05/hand-washing-dispels-the-decision-de mons.ars

Poll Results

I have never eaten

Cheez Whiz. 5% (2)

Raw Oysters. Snot on a shell. 30% (13)

Cat. The other white meat. 44% (19)

Horse. 2% (1)

Tongue. It would taste me while I tasted it. 14% (6)

Other Answers 5% (2)

all of the above. Plus Vegemite.

All of the above -- except tongue.

N-Rays

May 12, 2010

Humans are excellent pattern recognition machines. If there is a pattern, someone will find it. Problem is, if there is no pattern, people will find one anyway. Seeing a pattern where none exists is one of the many ways we fool ourselves and a reason why 'alternative' medicine persists. We see what we want to see, what we expect to see, whether it is there or not. One of the things that makes a good skeptic, in medicine and in life, is trying to keep in mind that just because I see a Mother Teresa in the cinnamon roll doesn’t mean her likeness is really there. I always wonder is it really there? Or am I seeing N-Rays?

"In 1903, Blondlot, a distinguished physicist who was one of 8 physicists who were corresponding members of the French Academy of Science announced his discovery while working at the University of Nancy attempting to polarize X-rays. He had perceived changes in the brightness of an electric spark in a spark gap placed in an X-ray beam which he photographed and he later attributed to the novel form of radiation, naming it the N-ray for the University of Nancy. Blondlot, Augustin Charpentier, Arsène d'Arsonval and approximately 120 other scientists in 300 published articles claimed to be able to detect N-rays emanating from most substances, including the human body with the peculiar exception that they were not emitted by green wood and some treated metals.

The "discovery" excited international interest and many physicists worked to replicate the effects. However, the notable physicists Lord Kelvin, William Crookes, Otto Lummer and Heinrich Rubens failed to do so. Following his own failure, self-described as "wasting a whole morning," American physicist Robert Wood, who had a reputation as a popular "debunker" in the period, was prevailed upon by the journal Nature to travel to Blondlot's laboratory in France to investigate further. Wood suggested that Rubens go since he had been the most embarrassed when the Kaiser asked him to repeat the French experiments and then after two weeks he had to report his failure to do so. Rubens, however, felt it would look better if Wood went since Blondlot had been most polite in answering his many questions.\

In the darkened room, Wood secretly removed an essential prism from the experimental apparatus, yet the experimenters still said that they observed N-rays. He also secretly replaced a large file that was supposed to be giving off N-rays with an inert piece of wood, yet the N-rays were still "observed." His report on these investigations, published in Nature, suggested that N-rays were a purely subjective phenomenon, with the scientists involved having recorded data that matched their expectations."

I often get called to see complex, or perhaps more accurately, uncertain cases, and get to the final arbitrator as to what to do. I get to make decisions based on contradictory data. Like the case this week.

Patient has two weeks of malaise and weakness, but never takes her temperature.

She has mitral stenosis from rheumatic heart disease.

1/2 blood cultures has S. viridans and she has been having a lot of dental work, for which she always takes antibiotics.

WBC is elevated and she gets better on antibiotics.

She has a funky CT with what looks like a kidney infection, maybe a bleed, maybe an embolic event.

Do you see endocarditis? I do.

But.

TEE is negative for a vegetation.

No other emboli on exam.

UA has no pyuria, but 5-10 RBC.

But the ECHO could be negative as she is on Coumadin for atrial fibrillation and maybe the thrombus moved downstream to the kidney

It is not a sustained bacteremia and transient bacteremia is the norm for dental manipulation of all kinds, including brushing.

So am I seeing a bunny in the clouds? Is there a pattern here, or I am I just talking myself into a diagnosis she doesn't really have?

On TV they usually get the diagnosis by the end of the hour; I am left with uncertainty. And that seems to be the norm in ID.

In the end it is better to treat her for a disease, she doesn't have than to not treat her for one she does; the next emboli could be to the brain. So I recommended a course of antibiotics for endocarditis.

But there is always that little voice, not suppressed by the Thorazine, that says,' Oh no. Wrong diagnosis. You are seeing N-rays.'

Rationalization

http://en.wikipedia.org/wiki/N_ray

http://www.skepdic.com/blondlot.html

Poll results

My favorite delusion:

There are N Rays. 5% (2)

That scoop of ice cream doesn’t have any calories. 31% (13)

Homeopathy works. 7% (3)

Health care in the US has no problems and is second to none. 14% (6)

Things were better back in the day. 43% (18)

Other Answers 0% (0)

Epiphanies

May 16, 2010

Amongst my many jobs is Infection Control. For twenty years I have chaired Infection Control for both the Legacy Health, a collection of 5 hospitals in the Portland-Vancouver area as well as for Portland Adventist Medical Center.

When I started back in the last century, I thought that hospital acquired infections were part of the price of taking care of ill and compromised patients. Sure, we can minimize infections, but wound infection, ventilator pneumonias and line infections are going to happen. You can't do the things we do to people and NOT get an infection.

Right?

Wrong.

What both administrations in Portland have in common is a commitment to patient safety and over the last decade they have committed considerable time and money to the application of proven procedures to decrease infections.

The first intervention was the use of alcohol foam instead of hand washing. The foam is now ubiquitous in the hospitals. Even when the use of the foam was 20%, the overall infection rate in the hospitals fell by half. Then, over the next decade, the hand hygiene compliance rate has steadily increased to around 90% and there was a corresponding steady decrease in infections.

But that is not the only intervention my hospitals have implemented.

Surgical check lists, bundles to prevent ventilatory pneumonias, to prevent intravenous catheter-related infections, to prevent urinary tract infections.

Many interventions and the results have been amazing. At Legacy we have dropped our infections rates by 40% and as a result over the last several years, over 200 lives were saved and 570 infections prevented. At Legacy it is estimated the interventions have saved 8 million dollars.

A few of the hospitals have gone a year without a ventilator-associated pneumonia or a catheter-related bloodstream infection.

I used to think that infections were inevitable, but no longer. There is the occasional patient who will get an infection: the badly burned, the multiple trauma. We had a wound infection in a 400 lb patient who literally had dirt tattooed in the palms and soles and a hemoglobin H1c of 15 who required emergency surgery. I was not surprised that patient developed a post-op infection. But even the trauma ICU had a marked decrease in infections with good infection control compliance.

But the experience of Legacy and Adventist suggests that aggressive adherence to proven infection control works and that the majority of health care associated infections need not happen. I have three epiphanies in my life: my first great meal, my first great Bordeaux, and when I realized that most infections in the hospital need not happen.

This has a real decrease in infections, not just playing with numbers. These hospitals look at every hospital acquired infection as an improvement opportunity and do not sweep data under the rug.

I also know personally that the numbers are real. I used to derive a significant portion of my income from hospital-acquired infections. There are many reasons that my income has declined 60% over the last decade, not the least of which being large numbers of patients that used to make up my practice (HAIs, AIDS) have disappeared. I feel like Phillip Morris making stop smoking ads.

It was not easy making these changes; it took years of committed work. People are like oil tankers and change course slowly. And some are filled with toxic waste. The other interesting aspect of instituting the policies and procedures has been who fought against the changes the hardest. Docs. Not all of them, just a small subset. There is a curious subset of MD's who feel that the data does not apply to them. They do not need to follow IC procedures, use full barriers when placing a line, or even wash their hands. And I do not get it. I cannot figure out why some docs are so recalcitrant about doing the right thing.

Perhaps those who comment can say why.

Rationalization

How Legacy Reduced Infections 40 Percent

http://www.thelundreport.org/resource/how_legacy_reduced_infections_40_percent

My My Mi

May 19, 2010

When I was a resident, we had to draw our own blood, do our own blood gasses and, on a bad night, place our own Foley's. Wait. That doesn't sound right. We had to draw blood from our patients ourselves. There. That sounds better.

And, not only did we have to walk bare foot through the snow (not uphill, I did my residency in Minneapolis, where the word 'hill' need never be used), but we diagnosed myocardial infarctions with serial CPK's and LDH isoenzymes. So what do I do with the fancy, schmancy troponin? Got me.

68 yo male comes in with 2 weeks of decline, then 36 hours of fevers and rigors. Real rigors, the get under the electric blanket set to 10 and a quilt kind of bone-chilling shake that only comes with bacteremia. He comes to the ER and has a fever work up that includes troponin's. I do not know why they checked the troponins, perhaps the hypotension that leads to his trip to the ICU. Should troponin's should be done routinely on the way to the ICU? Got me. His blood cultures are growing Group B Streptococcus and his troponin is 4.0.

They tell me the latter is abnormal; I know about the former.

So why the elevated troponin?

Option one: he had an MI. Infections are a prothombotic state, and myocardial infarctions are associated with acute infections like pneumonia.

Option two: his bacteremia was over two days, so an endovascular infection, i.e., I.E., is a worry. Group B strep is not on my top ten reasons as an etiology of endocarditis, but it does occur. Every bug can cause endocarditis. He could have left sided disease and flipped an embolus down a coronary artery, a surprisingly rare complication. Or, since he has a pacemaker, he has right sided disease and a myocardial abscess. You want to give a rabbit endocarditis, besides making it a junkie, you can put a wire across a valve and give the animal a bolus of bacteria. Instant endocarditis.

Option three: troponins go up in sepsis. Sometimes due to MI, sometimes due to sepsis and is a bad prognostic sign:

"Of 103 patient admissions, 52 (50.5%) had 1 or more elevated troponin measurements, and 49 (94.2%) had medical charts available for review. Troponin elevation was adjudicated as myocardial infarction (MI) in 53.1% of patients, sepsis in 18.4%, renal failure in 12.2%, and other causes in 16.3%. Overall ICU mortality was 16.0%; 2.0% for patients with no troponin elevation, 23.1% in patients with MI, and 39.1% in patients with troponin elevation not due to MI."

This finding is supported by several studies.

And acutely elevated troponins may not be due to thrombus:

"We found no differences in coagulation parameters analyzed with rotational thrombelastometry between cTnI-positive and -negative patients with SIRS, severe sepsis, and septic shock. These findings suggest that pathophysiological mechanisms other than thrombus-associated myocardial damage might play a major role, including reversible myocardial membrane leakage and/or cytokine mediated apoptosis in these patients."

And I, for one, will never argue with the results of rotational thrombelastometry, always important so you do not get uneven wear on your thrombelastometry. Because if you have to replace one thrombelastometry due to uneven wear, you have to buy a set of 4.

Rationalization

Clin Infect Dis. 2008 Jul 15;47(2):182-7. Acute myocardial infarction in hospitalized patients with community-acquired pneumonia. Ramirez J, Aliberti S, Mirsaeidi M, Peyrani P, Filardo G, Amir A, Moffett B, Gordon J, Blasi F, Bordon J.

J Crit Care. 2010 Jun;25(2):322-8. Epub 2009 Sep 24. Etiology of troponin elevation in critically ill patients. Lim W, Whitlock R, Khera V, Devereaux PJ, Tkaczyk A, Heels-Ansdell D, Jacka M, Cook D.

PLoS One. 2010; 5(2): e9017. Elevated Cardiac Troponin I in Sepsis and Septic Shock: No Evidence for Thrombus Associated Myocardial Necrosis

POLL RESULTS

The test I least understand is

1. CRP (since it is C ReActive Protein, it should be CRAP). 12% (6)

2. Troponin. 4% (2)

3. Any rheumatologic test. 24% (12)

4. Those damn name changes microbiologists foist upon us. 35% (17)

5. The ABIM recerts. Why do they cost so much, yet teach so little? 22% (11)

6. Other Answers 2% (1)

It all comes together after the fact.

May 22, 2010

I am asked to see a patient with WBC of 45K

He has had bladder cancer removed and a Neo-bladder constructed. He is admitted with nausea and vomiting and every time he eats it worsens. He as some mild abdominal/back and ultrasound shows bilateral obstruction, nephrostomy tubes are placed and cultures of urine and blood grow Candida. OK. Post obstructive urosepsis with Candida. Not a big mystery.

Patient is started in fluconazole and does fine clinically. The WBC is 25 at this time.

Then he has a single fever, and this time the blood cultures grow Enterococcus and the urine culture is negative. WBC is 31K. Ampicillin is started and I am called the next day.

Where is the Enterococcus coming from? Nothing on exam except mild abdominal pain that increases with eating. Must be coming from the GI tract somewhere. TIme to look.

CT of the abdomen shows the kidneys to be OK, but the wall of the small bowel, about 10 cm from the cecum, is markedly thickened to about 2 cm. Odd. Is this ischemic bowel? Weird place, but could be an operative complication. Radiology says maybe, but it also looks like lymphoma. I am betting on ischemia since it would explain the leukocytosis better. No reason to suspect lymphoma.

Over the next week the patients WBC slowly increases to 50K with no left shift, no fever, and continued mild abdominal pain. I am convinced it has to be bowel ischemia given the CT, the WBC, and the risk factors of HTN, smoking, combined with no readily available alternative explanation for the symptom complex. An angiogram, however, shows a wide open abdominal vascular tree and there is nothing to suggest an emboli. Now I am less sure it is ischemic bowel, but what else could account for the symptom complex and lab findings. TB? Another infection? I am puzzled.

The surgeons are understandably hesitant to take the patient to the OR given the poor nutritional state, but an e-lap was finally done and they found the small bowel encased in recurrent bladder tumor. Poor thing.

But then it comes together.

Bladder cancer is one of those cancer that can produce G-CSF. That is probably what is driving the leukocytosis and was a marker of recurrence, although the WBC was normal at initial diagnosis. I knew that bladder cancer makes G-CSF before the operative results, but I assumed that Enterococcus and the Candida came from the GI tract due to a vascular induced breakdown of GI continuity, not due to recurrence of the cancer. I didn't have cancer in the differential. It just didn't click. That happens sometimes. You stare at a case for days and not see the pattern, and then, something falls into place and the lady at the mirror becomes a skull. And then all you can see is the skull, it is so obvious, how did I not see it before?

Arrrggghhhh. Medicine. No matter how Zahphod Beeblebrox I think I am, there is always a case waiting at the Frogstar to throw me into the total perspective vortex.

I served with Zahphod Beeblebrox, I knew Zahphod Beeblebroxy, Zahphod Beeblebroxy was a friend of mine. Doctor, you are no Zahphod Beeblebrox.

And neither am I.

I should probably check a G-CSF level just to be complete, but I hate getting tests that will make no difference in patient care, as much as my curiosity itch needs scratching.

Rationalization

Urology. 2009 Apr;73(4):928.e17-9. Epub 2008 Aug 21. Paraneoplastic leukemoid reaction as marker for transitional cell carcinoma recurrence.

Hinyokika Kiyo. 2008 Dec;54(12):775-8. Urinary bladder cancer producing granulocyte-colony stimulating factor: a case report and review of the literature. PMID: 19175000

Uncertainty

May 23, 2010

I have this shtick I use when I bemoan the escalating use of antibiotics when there is no microbiologic diagnosis. What if oncology was practiced the same way? The patient may have lymphoma, so let's give CHOP, and what if they have lung cancer, so let's add Adriamycin and it might be testicular, even though it's a female, so let's add cis-platinum to be safe, and on and on. Spiraling empiricism.

I remain a little jealous of my heme-onc colleagues as they always have a pathologic diagnosis in hand before embarking on therapy. In ID you have to weigh the risks and benefits of a diagnostic procedure vrs trying empiric therapy. In oncology, the decision is virtually always in favor of the diagnostic procedure that makes the diagnosis. Cancer is not treated empirically.

The patient is an elderly male with the new diagnosis of AML, acute myelocytic leukemia, and has had one episode of chemotherapy. He is admitted for neutropenic fever and I am asked to see him when his fever does not resolve.

He has three features on evaluation. A progressive cough over three months that predates his AML diagnosis, an LDH of 800, and bilateral interstitial infiltrates on CXR that look for all the world like PJP (Pneumocystis. And never say PJP pneumonia. The final 'P' stands for pneumonia. It is like saying PIN number).

So it's PJP, right? No. There are fewer than a dozen cases of PJP in patients with AML, and all were associated with chemo. So on the basis of epidemiology, the odds are against PJP.

This would have to be a community-acquired PJP, an even odder manifestation of the disease in the absence of AIDS. But only PJP and fibrosing pulmonary processes will lead to an LDH that high from a pulmonary process.

So off to bronch with BAL, but no biopsy. The pulmonologist was worried about the platelets of 8000. Wimp.

All the bronchi results were negative, no PJP, no nothin', but since the BAL for PJP in non-AIDS patients has a significant false negative rate, we treated him for PJP and I will be damned if he didn't get all better.

PJP? Any ID doc worth his salt substitute knows the worst way to make a diagnosis is by response to therapy, yet short of an open lung biopsy, I have no good way to confirm the diagnosis. Maybe in retrospect I should have looked into a PJP PCR and a beta d glucan; two tests I am not in the habit of ordering. Old dogs and new tricks.

So I am stuck with a course of therapy and a sense of dissatisfaction.

Rationalization

Serum Indicators for the Diagnosis of Pneumocystis Pneumonia. Sadatomo Tasaka, MD, FCCP; Naoki Hasegawa, MD; Seiki Kobayashi, MD; Wakako Yamada, MD; Tomoyasu Nishimura, MD; Tsutomu Takeuchi, MD; Akitoshi Ishizaka, MD. CHEST.2007;131(4):1173-1180

Infection. 2009 Jun;37(3):261-5. Epub 2008 Dec 5. Detection of Pneumocystis jirovecii by two staining methods and two quantitative PCR assays. Rohner P, Jacomo V, Studer R, Schrenzel J, Graf JD.

Lying liars and their lying lies.

May 25, 2010

There is an infamous hoax from last century called The Protocols of the (Learned) Elders of Zion, an anti-Semitic text purporting to describe a plan to achieve global domination by the Jewish people. Despite the fact that the Protocols are a work of fiction, there have been and are folks who believe it to be real, from Hitler on down (on up? Can one be lower than Hitler? And have I already committed a breach of Godwins law?).

Inventing what appears to be legitimate information is a useful propaganda device not limited to anti-Semites. Having people appear evil or uncaring using their own words is far more effective than calling them evil and uncaring.

There are a lot of people in the community who suffer from a variety of complaints that I cannot diagnose, and, as people do not like uncertainty about their health, they will find someone who can give them a diagnosis, and not infrequently they will come upon chronic Lyme disease.

I do not think that the data supports the concept of chronic Lyme disease, and being a Tool of the Medical Industrial Complex (TMIC), that is just what you would expect me to say. But despite the paucity of data to support chronic Lyme, there is a contingent of patients and doctors who feel that the disease is real.

In the battle to win the hearts and minds of those who do not buy into chronic Lyme, those in favor of the syndrome have several options.

1). They could argue with the science. That would be a losing technique as the totality of the published literature is against them.

2) You demonize the opposition. If the speaker is an evil TMIC, then whatever message the speaker has is evil as well. You are more likely to dismiss the message if you can dismiss the messenger. Certainly, anything Jrjnv Kndfvmit says is automatically nonsense since Kndfvmit is a moron. It is a simple mental shortcut.

But doctors still have a degree of respect, deserved or not, in society. I think mostly deserved. Most of the people I work with are caring, compassionate people who work hard for the betterment of their patients. Not all. But most.

So you can call me and mine a TMIC, but it will not stick most of the time. I'm made of rubber, you are made of glue, what bounces off of me, sticks to you.

What would be better is to find examples of the opposition being a TMIC and display it for all the world to see. What if you can't find examples?

That is where you become a lying liar with lying lies. The nice thing about the Internet era is it is easy to transmit information. What often seems to be lacking is the ability for people to take just a little bit of time to fact check the information they get. They do not. Hoaxes propagate endlessly on the interwebs, ranging from Captain Kangaroo’s war record to Nigerian money transfers. All easy to fact check, but many do not. It is easier to believe what you read, especially if it supports your prior convictions.

PalMD, a co-blogger over at Science-Based Medicine, received an open letter from the IDSA about Lyme disease and he thought it smelled funny, and not Ha Ha funny. More like boiling melana funny. PalMD has a good nose, and a quick email to the IDSA confirmed the letter is a hoax. I am sure that many will get a copy of this letter and be angered at their suffering being called delusional. If I thought I had chronic Lyme and read the tripe that follows, it would fry my bacon. Most will not bother to check the legitimacy of the letter. It is, in a word, crap.

What follows is a hoax, lying lies from a lying liar.

Open Letter to the Mental Health Community from the Infectious Diseases Society of America May 24, 2010 Delusional Chronic Lyme Syndrome (DCLS) affects tens of thousands of new victims every year. This debilitating mental illness is destroying the emotional and financial livelihood of families across our country. As the Infectious Diseases Society of America (IDSA), we see firsthand the damage inflicted by this illness. Its sufferers frequently seek medical help from our member's practices; however, we are powerless to cure its underlying roots, as this mental illness exists well outside our domain knowledge of pathogens and human infection. Therefore, we are strenuously imploring the mental health community to take up research action in earnest. After our Lyme disease treatment review panel concluded last month, it is now indisputably self-evident that DCLS has reached epidemic proportions and its yearly growth rate is alarming. The historical duration, demographic breadth, and geographical extent of this mass psychogenic illness is a fascinating and unprecedented event in the history of our country, perhaps in the history of mankind. It has persisted for four decades, affects all ages, and exhibits an intriguing geographic clustering phenomenon. The intensity of its delusions drives sufferers to such extremes as self-mutilation via catheterization and sometimes suicide. Currently, there is no formal diagnostic classification or treatment regimen for DCLS. Meanwhile, this is empowering opportunistic medical doctors to prescribe improper and costly pharmaceutical treatment. This only furthers delays patients from seeking out the mental health professionals they so desperately need. Unfortunately, general awareness within the mental health field is virtually nonexistent. As president of the IDSA, I bear some responsibility for this ignorance, by not encouraging more cross-discipline pollination of our medical information. As this crisis has illuminated, the IDSA has not been true to its stated core value to "promote collaboration and cooperation among other professional colleagues." In response, I passionately pledge to our members and public constituents to reverse this myopic trend within our esteemed organization. IDSA member, Dr. Gary Wormser, has been a tireless crusader in promoting awareness of this emerging illness. I owe him immense gratitude for keeping true to his values as a physician in the face of sometimes caustic opposition to his fresh ideas. We beseech mental health researchers to carry on the torch ignited by Dr. Wormser and create pervasive, national recognition for this destructive disorder. By doing so, you will bring hope and compassion to those afflicted by this strange and insidious illness. To actualize this crucial transfer of information, the IDSA will be hosting free workshops on DCLS for mental health professionals at our upcoming annual meeting. This meeting will be hosted on October 21st through 24th, 2010 in Vancouver, Canada. We look forward to bringing the mental health community up-to-date on all relevant research and known data for DCLS. For more information, please contact the DCLS workshop coordinator at (xxx) 299-0200. Sincerely, Richard J. Whitley, MD

If only those were real HTML tags.

POLL RESULTS

To me, Jrjnv Kndfvmit is

1. Rush 34% (17)

2. Ann 12% (6)

3. Michael 14% (7)

4. Al 8% (4)

5. Bill 8% (4)

6. Other Answers 24% (12)

7. BP

8. Dr. Crislip

9. given celebrity

10. Bucket Head

Don't just peat, repeat

May 27, 2010

I have been busy the last few days, but no fasinomas. No curiosities or infections that are metaphors for human existence. Just run-of-the-mill, bread and butter, infectious diseases cases.

A strep endocarditis on a bicuspid valve, a cellulitis or two, a mycoplasma pneumonia (this one was tricky due to the underlying disease that confused the presentation), the ICU fevers that no one can figure out, least of all me. All things I have written about before and, contrary to the impression that the 'humor' in this blog may suggest, I try not to repeat myself.

So rather than discuss a case, I am going to complain about a problem that Drives. Me. Crazy.

Let's take a representative case from this week. So I guess I am going to discuss a case after all. It's an elderly female who has a new pacer system and a new aortic valve. Although not febrile, her WBC is not coming down post-op, hovering at 21K. So they get blood cultures.

And after a day one bottle of the one and only set has gram-positive cocci in clusters.

So what do you do? Patient is otherwise totally stable.

You could start by ignoring it, but hard to do with all the new hardware.

If you are like most docs, you will get the call of the positive blood cultures and the first words out of your mouth or out of your pen will be vancomycin and soon, too soon, before I am called, vancomycin is coursing through the patient’s veins.

What is wrong with that?

You. Didn't. Get. More. Blood. Cultures.

The world would be a better place if, upon awakening, more people asked themselves, how can I make Mark Crislip’s life better today? And the answer is simple. Repeat blood cultures. The first response to positive blood cultures, especially if they demonstrate something round, purple and in clumps or chains, is repeat the cultures.

The way to separate real from contaminant and endovascular from non-endovascular is repeat blood cultures.

The sine qua non of endocarditis/pacer infection is a sustained bacteremia, multiple positive blood cultures over time.

Now I, and more importantly my patient, is stuck. With one of two bottles positive and vancomycin flooding her system like the rage virus, killing all in its way (yes I know vanco kills nothing, but I am going for a zombie metaphor here, so cut me some slack), I have no other reliable way to decide whether to ignore the cultures or commit her to vanc/rif/gent for 6 weeks. Of course she can, and will, get a TEE, but do I trust a negative study? And a TEE is more costly and dangerous than a set of blood cultures, unless you use diamond-encrusted gold syringes and only draw blood from the left ventricle.

Somehow, with all the fancy-schmancy EMRs, I need to figure out a way for it to be impossible to order vancomycin for positive blood cultures without first getting another set of blood cultures.

So do yourself, your patents, and more importantly your ID doc a favor. Have your first response to staph and strep in the blood NOT be antibiotics but recheck the blood cultures.

And why you are at it, reform health care and stop global warming.

Sigh.

Curbside

Jun 1, 2010

I get lots of curbsides. People have the odd case they "just want to run by me." Run little case, run, you are free, free.

I never mind the curbsides since most of the time it is one of the hospitalists who needs a touch of reassurance or guidance. There was a poster at the meetings years ago where an ID consultant answered the curbside question and then went and looked at the case. He decided he had given the wrong advice about half the time because important information was left out of the presentation.

I remember I was called years ago by a new intern who asked me how long to treat a urinary tract infection. I said three days. Then I paused and considered. Odd question. Who is the patient and what did they grow?

Diabetic renal transplant patient with MRSA in the urine and blood. A horse of a different color, is it not?

But that was an intern at the start of the year, not a hardened, knowledgeable hospitalist, who has a case of (well, is taking care of a case) of a 38-year-old smoking male presenting with fevers, cough, slight hemoptysis and a LLL infiltrate in CXR.

Community acquired pneumonia, but the oddity is blood and sputum grew N. meningiditis. We see this.

There have been a little over half a hundred cases of N. meningiditis causing CAP, and I have seen a pair (gram-negative pair?) in my day.

"Fifty-eight cases of meningococcal pneumonia were included in this review. Fifty cases previously described in the literature from 1974 through 1998 and 8 new cases were included in this series. The median age of patients was 57.5 years, and pleuritic chest pain was described in 21 (53.9%) of 39 cases. Blood cultures were positive in 42 (79.3%) of 53 cases for which results were mentioned. Despite the presence of bacteremia, patients did not develop the syndrome of meningococcemia with its associated complications. Serogroup Y meningococci were most commonly recovered and accounted for 44.2% of identified isolates. Therapy has dramatically changed over the past 25 years; prior to 1991, penicillin antibiotics were most often used. Since 1991, 12 (80%) of 15 patients received cephalosporin antibiotics. Only 5 (8.62%) of 58 patients died. Secondary cases of meningococcal infections following exposure to patients with meningococcal pneumonia were noted in 2 instances."

In this series they mention that a complement deficiency was not noted; but it should be checked when the patient is all better. There are two inborn reasons people are predisposed to invasive meningococcal disease: terminal complement deficiency (often a bored, yes bored, question) and, as I have written about before, polymorphisms in snot.

It is also curious that patients do not have the purpura fulminans syndrome that is the tip-off to place patients in isolation, so we are going to have to dispense some prophylactic antibiotics. The rule is that the HCW has to spend more than four hours in the room with the patient, and since there has never ever been a physician in the history of medicine to spend four hours with a patient, I suspect no docs will be getting Cipro. Would you believe it? Some people think I am a cynic.

Rationalization

Clin Infect Dis. 2000 Jan;30(1):87-94. Meningococcal pneumonia: characterization and review of cases seen over the past 25 years.

Limitations

Jun 3, 2010

There are three limitations in treating infections.

The first is resistance of the bacteria limits choices. Take MRSA. Please. I often have few options to kill that beast under the best of circumstances and I am rarely called under the best of circumstances. The patient has MRSA, sensitive to vancomycin, TMP/Sulfa, linazolid and daptomycin, the last two costing a pound of flesh and the first male son. But someone has to pay for pizza at conference. Tomatoes do not grow in trees, you know.

The second is allergies. The patient has hives to vancomycin.

The third is the tissue that is infected. In this case it is bone, a chronic Brodies abscess. A Brodies is a spontaneous Staphylococcal abscess of long bone. Not many antibiotics penetrate well into bone, limiting efficacy.

The fourth is no insurance. The patient is unemployed and has no money. A course of the available antibiotics will bankrupt him many times over. Linazolid is around $1000 a week, and that had better buy some pretty damn good pizza. I certainly do not have the hubris to know what is needed to fix the health care 'system,' but anything has to be better than what we have now.

The fifth is I do not know how to count, but 5 out of 4 Americans do not understand statistics.

But there may be an option that is both effective and not all that expensive: tmp-sulfa plus rifampin po for 8 weeks. There have been two studies last year that show efficacy.

"the efficacy and safety of a combination of rifampicin and linezolid (RLC) with those of a combination of rifampicin and cotrimoxazole (RCC) in the treatment of BJI. Between February 2002 and December 2006, 56 adult patients (RLC, n = 28; RCC, n = 28), including 36 with infected orthopaedic devices (RLC, n = 18; RCC, n = 18) and 20 with chronic osteomyelitis (RLC, n = 10; RCC, n = 10), were found to be eligible for inclusion in this study. Patients who discontinued antibiotic therapy within 4 weeks of commencing treatment were considered to represent cases of treatment failure and were excluded. Rates of occurrence of adverse effects were similar in the two groups, at 42.9% in the RLC group and 46.4% in the RCC group (p = 1.00), and led to treatment discontinuation in four (14.3%) RLC and six (21.4%) RCC patients. Cure rates were found to be similar in the two groups (RLC, 89.3%, RCC, 78.6%; p = 0.47). Prolonged oral RLC and RCC therapy were found to be equally effective in treating patients with BJI caused by resistant GPC, including patients with infected orthopaedic devices. However, the lower cost of cotrimoxazole compared with linezolid renders RCC an attractive treatment alternative to RLC. Further larger clinical studies are warranted to confirm these preliminary results."

and

"Consecutive nonaxial Staphylococcus aureus chronic osteomyelitis cases were included in a comparative trial after debridement. Fifty patients were randomized: group A (n = 22) was treated with cloxacillin for 6 weeks intravenously plus 2 weeks orally (p.o.), and group B (n = 28) was treated with rifampin-cotrimoxazole for 8 weeks p.o. During follow-up (10 years), five relapses occurred: two (10%) in group A and three (11%) in group B. Foreign-body maintenance was associated with relapse (P = 0.016). Oral rifampin-cotrimoxazole treatment showed outcomes comparable to those for intravenous cloxacillin treatment."

He has been debrided and I will give tmp-sulfa and rifampin a shot. 80% cure rate seems pretty good and he can afford the care.

As best I can tell with osteomyelitis, it worked.

Rationalization

Efficacy and tolerance of rifampicin-linezolid compared with rifampicin-cotrimoxazole combinations in prolonged oral therapy for bone and joint infections. Nguyen S, Pasquet A, Legout L, Beltrand E, Dubreuil L, Migaud H, Yazdanpanah Y, Senneville E. Clin Microbiol Infect. 2009 Dec;15(12):1163-9. Epub 2009 May 4. PMID: 19438638

Long-term follow-up trial of oral rifampin-cotrimoxazole combination versus intravenous cloxacillin in treatment of chronic staphylococcal osteomyelitis. Euba G, Murillo O, Fernández-Sabé N, Mascaró J, Cabo J, Pérez A, Tubau F, Verdaguer R, Gudiol F, Ariza J. Antimicrob Agents Chemother. 2009 Jun;53(6):2672-6. Epub 2009 Mar 23. PMID: 19307354

Turbulence

Jun 6, 2010

Call weekend. Blech. And there is someone who always feels the need to call me at 7 a.m. with a question about a UTI. I bet occurs every weekend I am on call. I don't mind the question, but us old geezers need sleep and I have never seen a UTI that cannot wait until later in the day after coffee and a shower. Grump grump grump and get off my lawn.

Not much going on in terms of odd cases, but there is always something of interest even with the more common cases. Well, common for me. Two cases of endocarditis this week. One is a dialysis patient who had Enterococcus in the blood two months ago. It was thought due to a catheter infection, although after the catheter was removed, confirmatory line cultures were not done. After a short course of antibiotics he Enterococcus with constitutional symptoms (fever and chills, not the quartering of soldiers in time of peace) and 1/3 blood cultures were positive for enterococcus. His TTE was negative two months ago for a vegetation but he has known severe AI that was seen on the ECHO.

He had no stigmata of endocarditis and this time I obtained a TEE. A negative TTE isn’t worth crap in the diagnosis of endocarditis, but they are cheaper and easier on the patient. With my uber-sensitive gag reflex, I wouldn't want a TTE probe stuffed down my throat. There was a 1.5 cm vegetation on, well, on what? Not the aortic valve with the known pathology, but the posterior leaflet of the mitral valve. Why there?

Endocarditis occurs on platelet/thrombin and platelet/thombin are found where there is turbulence. The regurgitant jet of the AI smacked against the posterior leaflet of the mitral valve and lead to platelet/thrombin deposition and the Enterococcus subsequently found a home. Bacteria, with the exception of S. aureus, do not stick to endothelial cells, and the Teflon like coating due to the endothelial cells prevents most infections from sticking to valves or elsewhere. But a little turbulence leads to clot and then an infection.

I wonder if a bad airline flight would have similar consequences.

I find these little pathophysiologic pearls interesting. It explains why the infections occur in some places and not others.

It also explains how the piddley doses of antibiotics work for the prophylaxis of endocarditis, if antibiotics do work for prophylaxis and I am not so certain that the do. Antibiotics like amoxicillin mess with the cell walls of bacteria and make them less sticky. No stick, no infection.

Rationalization

J Clin Invest. 1981 Nov;68(5):1381-4.Bacterial adhesion in the pathogenesis of infective endocarditis. Effect of subinhibitory antibiotic concentrations on streptococcal adhesion in vitro and the development of endocarditis in rabbits. Scheld WM, Zak O, Vosbeck K, Sande MA.

J Clin Invest. 1981 Nov;68(5):1381-4.Bacterial adhesion in the pathogenesis of infective endocarditis. Effect of subinhibitory antibiotic concentrations on streptococcal adhesion in vitro and the development of endocarditis in rabbits. Scheld WM, Zak O, Vosbeck K, Sande MA.

A Blast from the Past?

Jun 7, 2010

It has been slow at work for the last few weeks. Between the lack of new cases and Medicare no longer paying for consults, I may soon be at the freeway off-ramp with a sign that says, "Will do ID for food." At least each of my kids has at least one extra kidney to help pay for college.

No cases to write about, at least with an interesting explanation. Certainly, there are the fevers with no answers and the occasional prosthetic joint infection, but I have a deficiency of well-defined fascinomas to thrill and amaze my readers. So instead I will discuss a case where I think I know what is going on, but I am awaiting proof.

Patient is in her 60's and is admitted for a month of constant right sided abdominal pain with nausea and vomiting after eating where, at best, she can eat a few bites before giving up. Not a problem I have yet to experience.

No fevers or chills; she is a smoker but nothing else noted on admission.

The CT shows a huge gallbladder with air in it, inflammation in the duodenal area, and numerous lesions in her liver that are called probable mets but less likely infection.

The powers that be all feel it is most likely cancer, perhaps biliary, and she is sent off for biopsy. Of interest is totally a normal liver panel and a minimally elevated WBC. Odd for cancer or infection.

The liver biopsy shows not cancer (yeah) but infection/abscess and the cultures grow Methicillin-resistant Staphylococcus aureus, MRSA. That is odd as well. Most liver abscess are a mixture of Streptococci and anaerobes. MRSA is reported in ye olde pubb med as a cause of liver abscess in fewer than a dozen cases.

As best I can tell she has none of the standard reasons for S. aureus in a deep organ. Her lack of fevers and other signs of infection is not all that unusual for S. aureus, an organism that every now and then causes a 'cold' abscess that mimics tumor.

I am, as I have mentioned, an old geezer. I was there at the start of the H2 blocker era. I only survived the severe dyspepsia of call as a resident thanks to cimetidine. Back in the day a perforated ulcer was a common reason for admission. Now days everyone and their mother is on either a PPI or an H2 blocker and I see a perforated ulcer once a decade.

I think she perf'd (a Shakespearean term. Thou cast perf'd yonder viscous) a duodenal ulcer. It would account for the CT findings as well as the history. When I went in to take a history (I returned it when I was finished) she volunteered that her pain was right where she had ulcer pain all her life and the pain was just like her ulcer pain, although this time the ulcer medicine she took for the pain didn't work.

We will see if the subsequent evaluation supports or denies my suspicion. Unfortunately, all too often a great diagnosis is ruined by reality.

Addendum: Patient finally went to the OR and had a gastro-colonic fistula, reason uncertain. Close enough, I give myself partial credit, as my fragile ego demands it.

Rationalization

Hong Kong Med J. 2010 Jun;16(3):227-9. A community-acquired methicillin-resistant Staphylococcus aureus liver abscess. Wong VW, Cheung YS, Wong J, Lee KF, Lai PB.

Poll Results

I would not have survived my residency without

Cimetidine. 15% (4)

Thorazine. 27% (7)

Fluoxetine. 15% (4)

sildenafil 8% (2)

ciprofloxicin 8% (2)

Other Answers 27% (7)

Diet Coke

soothing liaisons

my wife

my wife

Caffeine

red wine

Lisinopril

Sunburn in PDX? No way.

Jun 9, 2010

"It had been raining for seven years; thousands upon thousands of days compounded and filled from one end to the other with rain, with the drum and gush of water, with the sweet crystal fall of showers and the concussion of storms so heavy they were tidal waves come over the islands."

I have an affinity for All Summer in a Day by Ray Bradbury. It describes what this winter/spring has been like. So when someone comes with a sunburn looking like a boiled lobster but has not left the state in months, it gets my attention.

It began with foot pain, followed by the rapid onset of rubor, dolor, calor, and tumor that went up the entire leg in a day. He was admitted and started on TNTC antibiotics before the blood cultures were obtained (arrrrrrrgggggggghhhhhhhhhhhh). I am called 36 hours later.

Here is what I find.

He was febrile on admit, but no longer.

Leg looks like cellulitis with one big blister.

He has a fading erythroderma that involves the palms and soles, and the family said that 2 days ago he was bright red all over.

He has bright red conjunctiva.

His tongue is, maybe, looking kind of like a strawberry, but not the best strawberry tongue I have seen. It did not, however, taste like a strawberry. Just kidding.

His CBC, lytes, creatine and calcium are all normal now, but on admit there was only moderate leukocytosis.

The leg "looks" like an infection from Group A streptococcus, as if I can tell the difference between Staphlococcal and Streptococcal cellulitis.

The sunburn rash? In Oregon? Where the sun is seen less frequently than a cicada? It looks like a toxic shock rash, but he is neither toxic nor shocky and none of his labs support TSS.

Scarlet fever? In adults that is a disease that is gone with the wind. There have been five cases of scarlet fever with cellulitis, so it seems unlikely and the rash isn't right.

It is not Staphylococcal scalded skin syndrome as he does not have the skin fragility aka Nikolsky's sign.

I assume it is all due to a streptococcal toxin:

"Three streptococcal pyrogenic exotoxins (SPE), formerly known as Erythrogenic toxin, are recognized: types A, B, C. These toxins act as superantigens by a mechanism similar to those described for staphylococci. As antigens, they do not require processing by antigen presenting cells. Rather, they stimulate T cells by binding class II MHC molecules directly and nonspecifically. With superantigens about 20% of T cells may be stimulated (vs 1/10,000 T cells stimulated by conventional antigens) resulting in massive detrimental cytokine release. SPE A and SPE C are encoded by lysogenic phages; the gene for SPE B is located on the bacterial chromosome.

The erythrogenic toxin is so named for its association with scarlet fever which occurs when the toxin is disseminated in the blood. Re-emergence in the late 1980s of exotoxin-producing strains of S. pyogenes has been associated with a toxic shock-like syndrome."

That is my story and I am sticking to it. It is my job to make the occasional rash decision.

Rationalization

New Microbiol. 2004 Apr;27(2):203-6. Toxic scarlet fever complicating cellulitis: early clinical diagnosis is crucial to prevent a fatal outcome.

Lau SK, Woo PC, Yuen KY.

Nikolsky’s sign

Streptococcus pyogenes and Streptococcal Disease

ALL SUMMER IN A DAY Story

Groin Pull- the reason for the abscess

Jun 11, 2010

Groin pull. It sounds fun, but it isn't. Many people get the groin pull. Slip in water, dive for a basketball, lift a heavy barrel, stumble getting out of a car. Ouch. You strain your iliopsoas, or as they call it in the meat section of the store, the pork loin.

Skeletal muscle is hard to infect. The animal model that gives even me the willies is to smack a rabbit leg with a hammer. Otherwise skeletal muscle cannot get infected. The groin pull is the moral equivalent of smacking a rabbit with a hammer. It is hypothesized, but never proven, that there is then a little blood in the muscle. That just doesn’t sound fun.

Once there is blood and, if you are unlucky and develop a little bacteremia, then you get seeding of the clot and an iliopsoas abscess.

These are often initially missed since it is rare and the pain is thought to be coming from kidneys or back or just muscle strain.

I have seen two iliopsoas abscesses this month, both after a muscle strain and both with a complication I have never seen before. Both eroded into the sacroiliac joint to cause pelvic osteomyelitis. One was discovered later in the course of illness when the CT was done (or performed? I hate the use of that term for tests) to see if the infections were cured and the antibiotics could be stopped. The other? It too was discovered later when the patient relapsed with pain and fever after stopping antibiotics for MSSA bacteremia.

Both started as a groin pull complicating a fall.

The sacroiliac joint is not a real joint,

"In reality, only the anterior third of the interface between the sacrum and ilium is a true synovial joint; the rest of the junction is comprised of an intricate set of ligamentous connections."

And so there is nothing to debride or washout like a regular joint, and since it is not a real joint, most orthopods (my spell checker thinks orthopods should be arthropods) will not go near it. Although 90% of SI infections will get better without debridement, one of the patients probably needs the SI joint cleaned out so I have to find a surgeon who will tackle it, probably getting a groin pull himself.

There are numerous reports of the combination of SI infections with iliopsoas abscess. All the organisms found in the index of a microbiology text are represented. Every bug will infect every organ at one time or another, and it allows the Curriculum Vitae to grow. Most of the literature suggests it starts as an SI infection that goes to the iliopsoas, but the history in both my patients suggests the other way around. But I have no way to prove it. Gravity suggests the joint comes first and it tracks down. But I suppose both are possible.

Rationalization

Sacroiliac Joint Pain: A Comprehensive Review of Anatomy, Diagnosis, and Treatment. A & A November 2005 vol. 101 no. 5 1440-1453.

Semin Arthritis Rheum. 1996 Dec;26(3):592-604. Septic sacroiliitis. Zimmermann B 3rd, Mikolich DJ, Lally EV.

Surg Today. 2002;32(5):443-5. Psoas abscess as a complication of pyogenic sacroiliitis: report of a case. Gorgulu S, Komurcu M, Silit E, Kocak I.

Poll Results

Medical procedures should be

1. performed. 26% (9)

2. achieved. 0% (0)

3. conducted. 9% (3)

4. avoided. 40% (14)

5. done by someone other than me. 20% (7)

6. Other Answers 6% (2)

7. rationed

Evolution in action: Strep Pneumoniae resistance over time

Jun 13, 2010

Some cases are not brain surgery. And with all due respect to my neurosurgical colleagues, who do amazing work, brain surgery really should not epitomize medical difficulty, don't you think? Brain surgery isn't rocket science after all.

Patient comes in with rapid onset of severe headache followed by decreased mental status. The LP has 24,000 PMN's, a glucose < 10, a protein of 710 and gram-positive cocci on the gram stain.

S. pneumoniae meningitis, he is put on vancomycin and ceftriaxone pending sensitivities.

First question is why meningitis? Probably sinusitis; his mastoid is filled with more than a gobbet of pus.

Second question is best therapy. Turns out that the organism is sensitive to penicillin.

It has been interesting what has happened with S. pneumoniae this last decade.

There are, as I am sure you are aware, over 90 strains of S. pneumoniae. Some strains more commonly cause disease and these strains, due to the pressure of antibiotic therapy, are also the strains that are more likely to have resistance to penicillin. Use and lose it, that’s my motto. And I am going to be a little sloppy here, lumping penicillin intermediate and resistant strains together.

The conjugated vaccine for S. pneumoniae used in kids targets the most common strains, also the more commonly resistant strains of S. pneumoniae. For those keeping score they are types 6A, 6B, 9V, 14, 19A, 19F, 23F. Hey. BINGO.

Giving the vaccine to kids has resulted in a marked decline in invasive disease in kids due to these strains and, since kids are the mucous producing vector, there was also a decrease in invasive disease in adults with these strains as well. Cool. Vaccinate the kids and adults are protected.

And since the common strains are the resistant strains, there has been a decrease in the antibiotic resistance strains as well.

When an ecological niche opens up, it will be filled, and the serotypes not covered by the vaccine are increasing in incidence. And, to add insult to injury, these stains are also increasing in resistance. We really need a 90-valent conjugate vaccine, but it would probably come in syringe the size of a can of pop, or as I call it, soda pop.

Resistance is inevitable, so sayith the Borg.

The third question is how long to treat. Here is an infectious disease secret. The duration of therapy is usually a multiple of 7 because we have 7 days in the week, or is 10, because we have 10 fingers. I bet in societies that use fingers and toes to count, patients get 20 days of therapy. If I lose a hand, antibiotic use will fall by half in my hospital. There are no studies as to the duration of therapy in bacterial meningitis, so the patient will probably get 10 days.

Rationalization

The Lancet Infectious Diseases, Volume 8, Issue 12, Pages 785 - 795, December 2008. Impact of conjugate pneumococcal vaccines on antibiotic resistance

Poll Results

Difficulty is best epitomized by

1. brain surgery. 0% (0)

2. rocket science. 3% (1)

3. nephrology. Loop of Henle? More mysterious than quantum mechanics. 28% (8)

4. quantum mechanics. More mysterious than the fact that Don Henley and the Eagles have the second best-selling album ever. 41% (12)

5. Whatever it is I do. As Barbie said, "Medicine is hard." 24% (7)

6. Other Answers 3% (1)

7. Immunology

Idiopathic Low CD4

Jun 15, 2010

The patient initially presented with a chronic ulcer on his cheek. He had a variety of empiric antibiotics that did not result in improvement, so it was biopsied and it grew Cryptococcus neoformans.

His serum antigen was negative and he was placed on fluconazole and it faded away.

His HIV is negative but his CD4's were about 150. He presented years ago and during that time his CD4's have been stable at 150 and several attempts to diagnose an underlying reason have been for naught.

He has the annoying idiopathic low CD4 count syndrome. I say annoying, as all idiopathic diseases are annoying. I want a reason for the disease, and idiopathic just doesn’t cut it.

This syndrome has all the manifestations of AIDS with neither the virus nor, often, the progression. They get the same opportunistic diseases: Cryptococcus, PJP, MAI, CMV, PML, FBI, CIA, LSMFT (how many readers are old enough to remember what the last collection of letters means).

Is it due to excess destruction from an autoimmune disease? Is it due to an undiagnosed infection that whacked the CD4 precursors, a Soprano virus of some sort? Or are they born that way? No one knows.

As the most recent review says, it is a

"poorly understood syndrome of idiopathic CD4 lymphocytopenia...Little research has tried to systematically dissect this probably heterogeneic syndrome after its initial description in 1992. Numerous cases presenting with opportunistic infections have been reported. Disturbed differentiation of stem cell precursors may contribute to CD4 lymphocytopenia. Because infections and lymphoma may also cause CD4 lymphocytopenia, the distinction between cause and effect may evolve only during follow-up."

At least one patient has a genetic defect, although the abstract makes my brain hurt.

"The hypothesis that the cellular immune defect may be due to biochemical failures of the CD3-TCR pathway is investigated here in a patient associating a severe selective CD4(+) lymphocytopenia with an increased CD8(+) T cell count discovered in the course of a cryptococcal meningitis. A 40% reduction of T cell proliferation to CD3-TCR stimulation is observed only in the CD4(+) subpopulation. The early CD3-induced protein tyrosine phosphorylations are conserved in both CD4(+) and CD8(+) subsets, and the levels of the T cell protein tyrosine kinases p56(Lck), p59(Fyn) and ZAP-70 are normal. However, we find a 50% reduction of p56(Lck) kinase activity in the patient's T cells compared to a healthy control donor. p59(Fyn) activity does not appear to be altered. Nevertheless, we do not find any genetic abnormality of p56(Lck). These results thus suggest that a defect of an unknown protein regulating p56(Lck) activity takes place in this patient's T cells. Taken together, these findings reveal p56(Lck) alteration in ICL and confirm the critical role of this kinase in the maintenance of the peripheral CD4(+) T cell subpopulation."

Well, duh.

An interesting thing about my patient is his son had his CD4 cells measured and they have consistently been in the 400's, about half normal. So I would presume Mom had all the necessary genes, Dad had none and their offspring has half the genes needed to make CD4 cells.

It’s all in the family

Rationalization

Curr Opin Rheumatol. 2006 Jul;18(4):389-95.Idiopathic CD4 lymphocytopenia.Walker UA, Warnatz K.

Rinsho Shinkeigaku. 2000 Mar;40(3):249-53.[CNS cryptococcosis with idiopathic CD4+ T lymphocytopenia].[Article in Japanese]Watanabe H, Inukai A, Doyu M, Sobue G.

Int Immunol. 2000 Apr;12(4):449-57. Defective p56Lck activity in T cells from an adult patient with idiopathic CD4+ lymphocytopenia.Hubert P, Bergeron F, Ferreira V, Seligmann M, Oksenhendler E, Debre P, Autran B.

Cellulitis and Fevers: More and Less Than Expected

Jun 18, 2010

The patient is not so elderly (about my age) and presents with the sudden onset of rubor, dolor, calor, tumor of the leg. No surprise. Cellulitis is not an uncommon (or is common, I do not not like double negatives) disease and she is admitted for IV antibiotics. Over the next 6 hours, the rubor rapidly progresses to her mid thigh and she is put on many an antibiotic, and after 24 hours or so it stabilizes.

One of my unvalidated rules of thumb (rule of thumbs?) is that, given that it takes four doses or so of antibiotic to get to sort of steady state, cellulitis can worsen for the first 24 hours, it then stabilizes the second 24, and starts to get better in the third 24. Anyone disagree?

After a day all her blood cultures grow Streptococcus dysgalactiae subsp. equisimilis.

What is that?, you ask. Well, if you lived in Finland, you would know that Streptococcus dysgalactiae subsp. equisimilis more commonly causes bacteremic cellulitis than Group A strep,

"Beta‐Hemolytic streptococci were isolated from 26 (29%) of 90 patients, 2 isolates of which were blood‐culture positive for group G streptococci, and 24 patients had culture‐positive skin lesions. Group G Streptococcus (Streptococcus dysgalactiae subsp. equisimilis) was found most often and was isolated from 22% of patient samples of either skin lesions or blood, followed by group A Streptococcus, which was found in 7% of patients."

I would not be surprised if similar microbiology were occurring in the US as I have seen more Streptococcus dysgalactiae subsp. equisimilis of late, although it just may be confirmation bias.

So I stopped all her antibiotics and placed her on ceftriaxone (hives to penicillin. I used to get hives to bee stings, is that why they are called hives?) and she did well except for continued refractory fever. Her temp never fell below 38.5 and got as high as 40.1. He leg looked great and the rest of her infection parameters were on the mend.

Here is another unsubstantiated pearl. You get two today, well on the way to a full necklace.

Continuous fever can be a hint that it is drug fever, but I freely admit there is no data to support the contention. Feel free to do a study, just credit me in the acknowledgements. With infections, fevers always fall to normal and then spike again. Drug fever can, but not always, be continuous. I find very little on searching for 'continuous fever’ on Pubmed. Drug fever can have any pattern, so this unsubstantiated pearl is nowhere near 100%. I changed her from IV ceftriaxone to po doxycycline and within 48 hours all the fever was gone.

I did not do the one diagnostic maneuver that would have clinched the diagnosis: I did not rechallange with ceftriaxone. It would be safe, since drug fever is not an allergic response. But I hate it when reality falsifies a good diagnosis.

Rationalization

Clin Infect Dis. 2008 Mar 15;46(6):855-61. Acute bacterial, nonnecrotizing cellulitis in Finland: microbiological findings. Siljander T, Karppelin M, Vähäkuopus S, Syrjänen J, Toropainen M, Kere J, Vuento R, Jussila T, Vuopio-Varkila J.

Can You Prove a Negative? Nope.

Jun 20, 2010

It is probably easier to prove a diagnosis than to disprove one. After enough data is in you can say with certainly that, for example, the patient has endocarditis: the right symptoms, positive blood cultures, big vegetation on a valve. Piece of cake. But can I say the patient doesn't have endocarditis? I cannot disprove the existence of Santa, only that there is no reliable information to support his existence (I assume this blog is not being read by 7-year-olds and I just dashed some child’s dreams to bits, or to bytes).

I get a call to see a patient to rule on whether or not the patient has endocarditis.

Middle-aged male had lymphoma with radiation and chemotherapy as a teen. He has had progressive symptoms of poor cardiac output for the last year. No fevers. No chills. No weight loss. No constitutional symptoms whatsoever. Exam has no stigmata of endocarditis and his labs only have a slight increase in the WBC, but he is without a spleen. No risk factors for endocarditis, no unusual exposures to suggest uncultureable organisms.

So why did they want me to comment on endocarditis?

The reason for his SOB was progressive aortic and mitral stenosis.

In the OR, at the time of aortic and mitral valve replacement, it was noted that there was calcium and scarring, but no vegetation. However, the pathology showed "inflammation" and I was called.

Pathology did indeed show WBC, but tissue gram stain showed no organisms.

Here is the confounder. Mediastinal radiation, which he had for his Hodgkins, leads to long-term coronary artery disease and valve dysfunction/scarring. Of patients with a history of mediastinal radiation,

"1/25 patients had abnormal valvular or subvalvular structures. Valvular stenosis was not found but aortic, mitral and tricuspid regurgitations were found in 1/25, 9/25 and 22/25, respectively."

There is no shortage of clinical studies demonstrating long-term damage to heart valves from radiation therapy for cancer, but I cannot find pathologic studies. Most of the time patients do not need to have their valve removed.

So is the inflammation just long-term radiation damage? Is the valve infected? Since the damage from radiation injury does increase the risk for endocarditis, I have to fret.

I do not think he has endocarditis based on the information I have, but there is that nagging doubt, since I can't prove negative.

Rationalization

BMC Cancer. 2008 May 20;8:141. Cardiac damage after treatment of childhood cancer: a long-term follow-up. Velensek V, Mazic U, Krzisnik C, Demsar D, Jazbec J, Jereb B.

Ann Oncol. 1990 Sep;1(5):355-63. Late cardiac effects after mantle radiotherapy in patients with Hodgkin's disease. Gustavsson A, Eskilsson J, Landberg T, Svahn-Tapper G, White T, Wollmer P, Akerman M.

Classical Gas. Gangrene.

Jun 21, 2010

I really do not remember why I wanted to be a doctor, I barely remember by kids’ names, much less my motivations from 35 years ago. But I am glad I did, as medicine, and especially infectious diseases, is so much fun.

People are drawn into their specialty for a variety of reasons, and I cannot speak as to whether the cardiologist or the OB-Gyn or the radiologist still finds as much joy in their job today as they did when they were starting out. But I sure do. In fact, it becomes more fun with each passing year. There are a lot of great things about being an ID doc, but what I like the most is figuring things out, and it is the most fun when I figure it out before I get the tests back to prove the diagnosis. I get that frisson of joy every time, and it keeps me coming back for more, like Baskin Robbins chocolate chip.

I had a call on Friday morning from the OR. The surgeon said he had an elderly man who was being debrided for two areas of gas producing infection. One on his right buttock, the other on the left arm. CT showed a probable large cecal cancer.

This has to be Clostridium septicum or maybe Clostridium perfringens. I said. Clostridium septicum is the bug that likes to invade colon cancers and then disseminate to cause myonecrosis.

"Associated malignancy was found in four (80%) of the patients with Clostridium septicum infection. Two infections were related to colorectal cancer, two to haematological malignancies and one to radiation-induced recto-urethral fistula. Those patients who had colorectal cancer presented with septicaemia and vague abdominal symptoms."

I'll see him in the ICU post op. So I get to the ICU and imagine my disappointment when the tissue gram stain has gram-negative rods. Crap. C. septicum is a gram-positive rod. So I do the usual H&P and as I hang up from my dictation, micro calls the ICU to let us know that the blood cultures are positive, and not only positive, but foamy. Foamy, she said, the media almost squirts out of the bottle and is usually due to Clostridia and there are gram-positive rods in the blood. She also reviewed the tissue gram stain and she thinks it is more likely gram positive as well.

Hot damn. Maybe I hit the rusty, contaminated nail on the metatarsal head after all.

I get back today, and, yep, it’s C. septicum. I couldn't have had more pleasure if you had directly stimulated the happy centers of my brain with an electrode.

My first and only post mortem consult was a lady who died of overwhelming sepsis and while they were preparing the body to be moved, a cellulitis popped out of her right buttock and over the next hours marched across her flank. Her blood grew C. septicum and she had a cecal cancer at autopsy.

I once had a case in a patient who developed C. septicum after chemo for lymphoma, presumably the chemo lead to necrosis of bowel wall lymphoma and allowed subsequent invasion. He refused antibiotics and did well after 24 hours of sepsis physiology. He recovered without antibiotics, something I would not want to try, since the first example had a more typical clinical course.

The bug is sensitive to all antibiotics and once I knew it was a mono-microbial infection I changed the patient to penicillin. He is doing very well.

I miss my predictions more often than I get them right, reality often ruins a good diagnosis. But anticipation of the next unexpected problem is part of what keeps me coming to work. That and the mortgage.

Rationalization

ANZ J Surg. 2001 Nov;71(11):647-9. Clostridium septicum and malignancy. Chew SS, Lubowski DZ.

POLL RESULTS

I continue in my chosen field of practice after all these years because

1. It is endlessly fun. 38% (18)

2. I am trapped by a mortgage and 2 ex-spouses, and that lazy kid in grad school. 9% (4)

3. I need something to do while I am waiting to die. 30% (14)

4. I like helping patients. 9% (4)

5. The money and the prestige. I am not an ID doc. 13% (6)

6. Other Answers 2% (1)

7. I have to do something with this head-full of lab trivia that I possess.

Beta-lactam Side Effect - Sometimes an STD

Jun 23, 2010

Antibiotics are relatively safe as drugs go, especially the beta-lactams. I still have a predilection for killing bacteria with a beta-lactam if I can. Antibiotic use is, at some level, a matter of habit and, for a variety of reasons, I have never used much beta-lactam/inhibitor combinations. In part due to habit, in part a mistrust of the pharmacokinetics of two agents and in part cost. Combination antibiotics are less expensive in my institutions, so rather than unisin I give cefazolin and metronidazole and instead of zosin I lean towards a third-generation cephalosporin and metronidazole.

However, the decerebrate drug of choice is often zosin and the question at hand today was whether or not the thrombocytopenia in the patient is due to piperacillin/tazobactam.

Patient was admitted and found to have a gallbladder with air in it and was started on piperacillin/tazobactam. And had the usual collection of diagnostic and therapeutic interventions to help the gallbladder drain, and in the process the evil humors were stirred up and he becomes septoid. His blood cultures are growing several gram-negative rods including a Pseudomonas, but 5 days into his antibiotic course his platelets fell from 210 to 20K. He does not have DIC by other labs.

I suppose it could be due to the piperacillin/tazobactam.

Beta-lactams can be directly marrow suppressing, by mechanisms that elude me. There is not much literature on the effects of beta-lactams on the marrow.

Other antibiotics can mess with human enzymatic pathways to cause marrow suppression, but last I checked human cells to not have a peptidoglycan cell wall upon which the piperacillin could act. Unless it is an invasion of the body snatchers scenario. I would think pods would be susceptible to cell wall active agents.

The other mechanism is immune mediated, and perhaps they are one and the same. It is presumed that the penicillin acts as a hapten, binding to the platelet or other cells and the platelet is destroyed as an innocent bystander.

"using a fluorescent antiglobulin technique with paraformaldehyde-fixed cells, demonstrated a complement-fixing IgG penicillin antibody reacting with the patient's granulocytes and platelets in the presence of the drug."

It seems a bit quick to be due to direct suppression and if he had been primed with prior penicillin exposure, then perhaps it could be immunologic. As best can be determined, he has not prior penicillin exposure.

Reactions to penicillins, allergic and otherwise, are unusual. The most curious is people who get reactions to penicillins after being exposed to their sexual partners.

"In two cases contact (to penicillin) was by sexual intercourse with a partner who was receiving penicillin."

I never ask my home antibiotic patients if their sexual partner is allergic to penicillin and perhaps I should. And as I think about, enough patients over the years have been unable to wait until they get home that maybe it should be a warning on the wall, right next to the hand washing sign.

Rationalization

BMC Clinical Pharmacology 2003, 3:2 Piperacillin induced bone marrow suppression: a case report Ashish Kumar, Gourdas Choudhuri and Rakesh Aggarwal.

Transfusion. 1984 Sep-Oct;24(5):395-8. Red cell and platelet-bound IgG penicillin antibodies in a patient with thrombocytopenia. Salamon DJ, Nusbacher J, Stroupe T, Wilson JH, Hanrahan JB.

Clin Exp Allergy. 1996 Mar;26(3):335-40. Anaphylaxis to penicillins after non-therapeutic exposure: an immunological investigation. Blanca M, Garcia J, Vega JM, Miranda A, Carmona MJ, Mayorga C, Moreno F, Juarez C.

Red Bump Disease

Jun 25, 2010

I am not, obviously, a dermatologist. I don’t do them fancy, schamncy Latin terms to describe rashes. I am just a simple man, with a simple vocabulary. Erythema whatsis whosis? Got me.

The patient is a kidney transplant patient on cyclosporin and steroids and for the last two months he has had fevers, malaise, red bumps on his extremities, and a CT with small nodules in the lungs.

He has the red bumps on the cool areas of his body: arms, legs, face. He comes to me in search of a diagnosis.

I have a differential for what I call red bump disease, which is usually seen in HIV patients. But transplant patient are a form of acquired mild AIDS with the same differential diagnosis.

Now I have an advantage: he had a skin biopsy that shows necrotizing granulomas and the strains are negative for AFB and fungi. So all I need to do is go through the differential diagnosis and take an exposure history.

Any water exposures or environmental exposures? Nope. Makes AFB less likely. M. marinum likes to grow in cool places, but he is AFB negative on the skin biopsy so AFB is down the list.

Any recent travel? Nope. Distant travel to the Midwest and SW. Cocci and histo are on the list, but histo and cocci are not usually a cause of necrotizing granulomas.

Cryptococcus is coming to the Pacific Northwest and is a cause of red bump disease, but it is usually seen on the stains. Still, I will order a serum cryptococcal antigen.

I so want to ask a direct question since necrotizing granulomas for an ID doc means Ted Nugents disease, but instead ask the open-ended: Any pets or animal exposure? Yep. 2 cats. Bingo. Wait. Bingo is a dog. What is the name for a cat? Chan Marshall. My favorite cat.

Red bump disease, immunocompromised patient, cats, necrotizing granulomas. Has to be cat scratch disease, Bartonella henselae. Just has to be. I know I have to generate a differential, but in the end I like to settle on a disease. It’s no fun if you can't come to a diagnosis after the H&P.

I will see. I sent off the serology, as well as studies for Cryptococcus, histo and cocci, and AFB cultures are cooking on the biopsy. I will let you know.

To be continued...

Rationalization

Transplantation. 1999 Jan 27;67(2):296-8. Bacillary angiomatosis in a renal transplant recipient. Cline MS, Cummings OW, Goldman M, Filo RS, Pescovitz MD.

Starts as one diagnosis. Turns out to be another

Jun 27, 2010

Bitch Bitch Bitch. This call weekend was a first. Four hospitals, a slew (as in large number, not the past tense of slay) of follow-ups, and 4 consults and no one, not a one, of the patients who required an ID intervention, had insurance. So I made not a farthing this weekend, but did have to pay for gas, so the weekend is a net financial loss. About 1 in 6 patients I see have no insurance, but it is unusual to have them clustered into one weekend. Soon I will be standing in a street corner with a sign "Will do Infectious Diseases for Food."

On the bright side, I saw some cool cases.

One was a middle-aged female who I was asked to see because she is neutropenic with an upper lobe pneumonia with early cavitation on CT. Seems straight forward. She has been in the hospital for 5 days with no diagnosis. She has an absolute neutrophil count of 1.0 and she has not had chemo. Her ESR is 95. Nothing else. Curious. Chart indicates no past medical history of interest. So I go in the room.

History as it unfolds.

Several months of fatigue and a 30-pound weight loss, and fevers for a week.

Painful oral and vaginal ulcers.

Bing Bing Bing. I do not know what part of my brain processes data and spits out ideas, but I have it. That’s it. I have a diagnosis. But I am complete, so I go through the routine.

ID history: no travel, pets, diet or exposure history to suggest any of this is due to an infectious disease. No past medical history.

So time for direct questions.

Any eye pain? Yes. My right eye sometimes gets red and painful for several days. With light? Yes. And my left eye acts up as well, but not as bad.

Any red bumps on the skin? Yes. She shows me red bumps on her arms and chest.

I go through the rest of the ROS, but I am convinced I have a diagnosis. Behcets.

The classic triad is aphthous ulcers, genital ulcers and uveitis.

But what about the leukopenia? Google to the fescue, since I hope to lawn something. Ugh.

"A case is described of Behcet’s syndrome in which the active phases of the disease were associated with a profound neutropenia in contrast to the expected finding of normal or raised neutrophil count."

Not many cases, Helen Kimble's killer could count them, but they do exist. The pneumonia? That may be a complication of the neutropenia, as lung involvement with Behcet's is rarer than neutropenia.

"Both patients developed fever, cough and pleuritic chest pain during follow-up by our outpatient clinic. Chest X-rays and computed tomographies developed ground glass opacity, peripheral nodular opacities and consolidations...Both cases were diagnosed as having organizing pneumonia." Those union folks get everywhere."

Bronch is pending for this afternoon to make sure the lung process is not something evil.

I am putting my money, if I had any, on Behcet's.

And so it was.

Rationalization

Postgrad Med J. 1981 July; 57(669): 448–449. Behçet's syndrome and neutropenia R. C. F. Leonard and R. B. Thompson

Clin Exp Rheumatol. 2007 Jul-Aug;25(4 Suppl 45):S103-6. Cryptogenic organizing pneumonia in two patients with Behçet's disease. Nanke Y, Kobashigawa T, Yamada T, Kamatani N, Kotake S.

Behcet Disease

A New Cellulitis Mimic

Jun 29, 2010

I have a lot of cases with a potential diagnosis on the back burner, but not much going to today to write about. I did get a call from the ER.

Elderly female with recurrent cellulitis of the leg. She is on her third episode in the last year and someone (not me) has her on outpatient vancomycin. She has been on therapy for 5 days, improving, when she develops are red, hot swollen shoulder.

At least, that is what the ER doc tells me on the phone. I cover 4 hospitals and field a lot of questions on the phone before I can get in to see the patient. The ER doc tells me she is in the ER with new onset of right shoulder cellulitis. He assures me it is newly red, hot, swollen and tender.

Odd, I say, to get a cellulitis on antibiotics, especially on vancomycin. Are you sure it's infected? No trauma, no bite, no other reason?

No, he assures me. Its red and hot and new and nothing else. It's cellulitis.

No fevers and WBC is normal.

Huh. The only thing I can think of is that it is a metastatic infection from endocarditis or other bacteremic disease. Get some blood cultures and I will see her later. I am puzzled but will, I hope, figure it out when I can take a history.

There are many things that mimic cellulitis. I refer the house staff to the Annals review of the topic, although in this case nothing seems to fit.

Couple of hours later I get a call from the hospitalist. He has a diagnosis. It's sunburn on top of a recent tetanus booster. But, he says, it is definitely sunburn. When he can examine her entire skin, he can clearly see the burn lines.

I really laughed when I heard the solution. I always ask for odd reasons, but I never considered sunburn as a mimic for cellulitis. I guess that’s what you get for living in Portland. Sun-related illness, especially this year, is not in the differential.

Rationalization

Narrative Review: Diseases That Masquerade as Infectious Cellulitis Ann Intern Med. 4 January 2005;142(1):47-55

Shopping at the GAP

Jul 1, 2010

There is the acute illness of the patient and then there is the underlying disease that leads to the acute illness. There is the tree, and the dirt in which it grows. Most of the time we focus on the acute disease, but always keep an eye out for the underlying undiagnosed problem.

The patient is a 53-year male who presents with fevers, rigors and increasing problems with swallowing. He comes to the ER and a CT shows epiglottitis. That’s odd in an older person, but odder still he had the same problem 10 years ago and required a trach. He has the scar to prove it.

Otherwise his past history is unimpressive.

Recurrent epiglottis in the adult is rare as hen’s teeth. Some are anatomic, due to a vallecular cyst, the term, evidently, for an epiglottic cyst. Others are due to an immunoglobulin defect.

"When recurrent acute epiglottitis occurs in adults, it is important to investigate the immune system because a quantitative or a specific antibody deficiency could be found. It also follows that these patients will be successfully treated either by immunization or antibody replacement."

10 years between episodes makes a cyst more likely, but at the time of the consult I have a bit more information.

He has gram-positive cocci in pairs in his blood, his anion gap is 3, and his total protein is elevated and his HIV is negative. His CT of the neck doesn’t show an abscess or a cyst.

Multiple myeloma should be the underlying problem and the organism should be S. pneumoniae. Both of which turned out to be true a few days later.

Not much gives a low anion gap, and the only one of interest is a gammaglobulinopathy like multiple myeloma or Waldenströms. I learned that my first month as an intern, when I had a patient with an anion gap of zero and the SPEP demonstrated Waldenströms. Haven't seen a case since, but I have found a number of myelomas by calculating the gap. Also, as a pearl for you youngsters out there in the blogosphere: S. pneumoniaein the blood, especially if there are no classic predisposing factors, should suggest an HIV and/or an SPEP. More often than not you will find another diagnosis and you will get the fun of putting it all together.

Rationalization

Ann Allergy Asthma Immunol. 2002 May;88(5):513-7. Recurrent acute epiglottitis in adults: defective antibody response. Gagnon R, Bédard PM, Côté L, Lavoie A, Hébert J.

Otolaryngol Head Neck Surg. 2008 Mar;138(3):321-7. Adult vallecular cyst: thirteen-year experience. Berger G, Averbuch E, Zilka K, Berger R, Ophir D.

Vitamin D-iarrhea

Jul 4, 2010

Patient has had diarrhea since overseas travel, now with 6 months of bloating, cramping and loose stools.

Work up has consistently demonstrated Dientamoeba fragilis in the stool.

For them what are not connoisseurs of poo and its pathogens, Dientamoeba fragilis is a parasite of humans and animals (humans are not, for the purpose of this blog, an animal) and causes the symptoms found in this patient. It is more common in areas that are not noted for investing in public sewer systems. It is often a colonizer (or colon-izer. That is a mark of a wackaloon when they make word play like dis-ease, so I needs be careful) in patients from endemic areas, so determining its pathogenicity can be problematic. This patient has lots of parasites and lots of diarrhea, so the diagnosis is not uncertain.

She has had two courses of metronidazole with no effect, so she has been sent to me. Of interest, she has been diarrhea free for the last week. It is similar to when the toothache vanishes when you visit the dentist. However, her primary recently checked her vitamin D levels and found, like so many here in the sun-free Pacific NW, she was very deficient. She had noticed that the diarrhea was worse when she had milk products, perhaps some infection induced lactose intolerance, so she was inadvertently decreasing her vitamin D intake by avoiding dairy. Within several days of starting vitamin D, her diarrhea resolves and a repeat stool has no parasites.

True, true and unrelated? I do not know. A constant mantra of the skeptic is association is not causation. Vitamin D is an important immunomodulator and required for bowel integrity.

"Vitamin D deficiency may compromise the mucosal barrier, leading to increased susceptibility to mucosal damage and increased risk of IBD."

And vitamin D deficiency increases the risk of C. difficile severity and relapse.

That is all I can find of the topic of infectious diarrhea and vitamin D. But vitamin D deficiency is an important risk for everything from viral URI to TB, so maybe the supplementation is what leads to resolution. Or maybe I am just seeing the natural history of the disease.

Rationalization

Am J Physiol Gastrointest Liver Physiol. 2008 Jan;294(1):G208-16. Epub 2007 Oct 25. Novel role of the vitamin D receptor in maintaining the integrity of the intestinal mucosal barrier. Kong J, Zhang Z, Musch MW, Ning G, Sun J, Hart J, Bissonnette M, Li YC.

Epidemiol Infect. 2010 Sep;138(9):1322-7. Epub 2010 Jan 8. Healthcare costs of Staphylococcus aureus and Clostridium difficile infections in veterans: role of vitamin D deficiency. Youssef D, Bailey B, El Abbassi A, Copeland R, Adebonojo L, Manning T, Peiris AN.

Miss the diagnosis once, shame on me, miss it twice, Fool me — you can't get fooled again.

Jul 6, 2010

Years ago I saw a patient who presented with fevers, severe polyarticular arthritis, rash on a Friday afternoon in clinic and I didn't have a clue what she had. I just knew she was sick, so I admitted her. When I returned on Monday the hospitalist said she had Stills, duh, and we sent her home on prednisone all better.

Totally missed the diagnosis, and I vowed not to miss it again. And just a few months later I, well, er, missed it again. Crap. Haven't missed it since. At least I don't think so.

This morning I was the discussant for a case at morning report, and I went though the discussion as the case was presented and in the end totally missed the diagnosis. This time it was not Stills, but it was similar to a case I had three years ago. One of the reasons I write this blog and do the podcasts, besides an overweening ego, is that the process helps cement information into my own increasingly fragile memory. I have trouble remembering to my kids’ names and I only have two.

The patient I saw was 24 yo female presents psychotic: agitated, violent, yelling, refractory to sedation with antipsychotics.

Otherwise nothing in her history to suggest a medical reason for a psychotic break.

I get called as the work up shows a mild increase in cells and protein in the CSF. We do the mongo evaluation for a reason for psychosis and come up with nothing. Eventually she is transferred to another hospital and they find the reason for her psychosis: a teratoma.

Huh?

Turns out teratomas, and some other tumors such as small cell, result in anti-NMDA-receptor antibodies which cause a limbic encephalitis. The NMDA receptor, a glutamate receptor, is the predominant molecular device for controlling synaptic plasticity and memory function. Find out more than you want to know about the NMDA receptor on the Wikipedia.

There is a cross reactivity of antibodies produced by the immune system against ectopic brain tissues, such as those found in teratoma, resulting in limbic encephalitis. Cut out the tumor, cure the encephalitis. You can measure anti-NMDA-receptor antibodies and my patient was anti-NMDA-receptor antibody positive, as well as the patient presented today. I had never heard of the syndrome until three years ago, although it is rare.

The key, clinically, is the aggressive, violent nature of the psychosis, far more than is seen with schizophrenia.

So there. I have written about it. Next time I will not miss the diagnosis and neither will you.

Riiiiiigggghhhhhht.

Rationalization

J Clin Psychiatry. 2010 Apr;71(4):504. Acute psychosis associated with anti-NMDA-receptor antibodies and bilateral ovarian teratomas: a case report. Fawcett RG.

http://www.youtube.com/watch?v=eKgPY1adc0A

A Pres-ing diagnosis

Jul 8, 2010

I have been an MD for more than half my life and I routinely come across diseases I have never heard of. Disease is infinite, my brain and experience are finite.

The patient is a young kidney transplant who is admitted with headache, altered mental status, unilateral 6th nerve palsy progressing over three days. She also has decreased hearing and vision.

No fevers, normal WBC, no exposures for odd infectious diseases.

Spinal tap has 85 cells, mostly lymphocytes and a protein of 95 and a normal glucose.

MRI show no mass, no inflammation, but the radiologist calls it bilateral symmetrical edema that worsens over three days as does the patient.

Pick an infectious disease, any infectious disease, the tests come back negative.

The radiologist also gave a diagnosis, at least a tentative one based on the MRI: PRES, short for posterior reversible encephalopathy syndrome. Patients present with edema from hypertension or preeclampsia and the get headache, confusion, seizures and visual loss. That's my patient.

This patient has neither hypertension nor preeclampsia, but a Pubmed shows that PRES can also be caused by tacrolimus, which she is on. We stopped that tacrolimus and she has improved a wee bit.

"Posterior reversible encephalopathy syndrome (PRES) is a serious complication of immunosuppressive therapy use following solid organ or stem cell transplants. Clinical findings including headache, mental status changes, focal neurological deficits, and/or visual disturbances. Associated with these are characteristic imaging features of subcortical white matter lesions on computed tomography (CT) or magnetic resonance imaging (MRI). The changes in the subcortical white matter are secondary to potentially reversible vasogenic edema, although conversion to irreversible cytotoxic edema has been described. These imaging findings predominate in the territory of the posterior cerebral artery. Many studies have shown that the neurotoxicity associated with tacrolimus may occur at therapeutic levels. In most cases of PRES, the symptom complex is reversible by reducing the dosage or withholding the drug for a few days. While PRES is an uncommon complication, it is associated with significant morbidity and mortality if it is not expeditiously recognized."

So a reasonable diagnosis, although I can't locate any information on the spinal tap in patients with PRES.

Rationalization

Emerg Radiol. 2009 Nov;16(6):493-6. Epub 2008 Dec 19. PRES (posterior reversible encephalopathy syndrome), a rare complication of tacrolimus therapy.

Addendum from a reader, snipergirl

Try this article: http://www3.interscience.wiley.com/cgi-bin/fulltext/118828913/HTMLSTART

"CSF cultures were sterile in all patients. CSF white cell counts ranged from 0 to 0·002 × 109/l (reference 0–0·01 × 109/l) while CSF protein ranged from 0·1 to 0·57 g/l (reference 0·15–0·55 g/l)."

An ID lullaby

Jul 10, 2010

The patient is an elderlyish male who has a week of fevers, chills, weight loss and malaise. But then don’t all my patients. Most of my presentations have the generic fever and chills; the body has a limited way of responding to infections.

He is admitted to the hospital and then it gets interesting.

His past medical history is of interest: pacemaker, diastolic heart failure, diet controlled diabetes.

He has a dog, has a cabin down the Columbia gorge where he likes to chop wood and clear brush, but it has been a month since he was last there.

His CBC and comp are WNL (we never looked) and his blood cultures are negative.

His CXR shows nodular infiltrates and his CT shows numerous round lesions that could be tumor, could be infection.

My first worry was this was Cryptococcus since it is a cause of round pneumonia and Cryptococcus slowly coming south from Vancouver following the fungal Schlieffen Plan. Negative blood cultures make a pacer infection less likely, and his TEE is pristine.

So maybe it is tumor, so we do a biopsy of one of the lung lesions: it's infection, no tumor, no organisms seen. He slowly improves on ceftriaxone and he is discharged on an empiric and arbitrary course of IV antibiotics pending final cultures.

Four days later, the lab calls. The lung biopsy is growing a small gram-negative rod on chocolate only, Mmmmmmm. Chocolate. Where was I? Oh, yeah. Something is growing and they think it is Francisella tularensis, which the state lab subsequently confirms. Damn. Tularemia. Never even considered it, even though in retrospect he had the risk factors present in all prior 3 cases I have seen in my career: a place in the gorge and a liking for woodpiles and yard work. I presume the woodpile is a place for the vectors of tularemia: rodents and rabbits, who piss on the wood and pass it on to the patient when they stacking and cutting wood or otherwise mucking about in the yard.

"Results. We identified 15 patients with tularemia; 11 of these cases were primary pneumonic tularemia. Francisella tularensis type A was isolated from blood and lung tissue of the one man who died. Patients were more likely than controls to have used a lawn mower or brush cutter in the two weeks before the illness (odds ratio, 9.2; 95 percent confidence interval, 1.6 to 68.0) and during the summer (odds ratio, undefined; 95 percent confidence interval, 1.8 to ). Lawn mowing and brush cutting remained significant risk factors after adjustment for other potentially confounding variables. Only one patient reported being exposed to a rabbit while cutting brush. Of 40 trapped animals, 1 striped skunk and 1 Norway rat were seropositive for antibodies against F. tularensis.

Conclusions. Study of this outbreak of primary pneumonic tularemia implicates lawn mowing and brush cutting as risk factors for this infection."

Tularemia is a rare disease in the US and even rarer in Oregon and primary pneumonia with multiple oval infiltrates is also odd, with oval opacities accounting for 8% of chest X-ray findings. The usual upper limit of the incubation period is 14 days; he was a month from his last potential exposure. So an unusual manifestation of an unusual disease. My usual.

I changed him to doxycycline and he continues to improve.

Now sing along with me:

"Over in the gorge Many many months ago, Me Mither killed a rabbit In the mower it did go.

It aerosolized the bunny In the good ould Toro way, Sending bacteria into the air To be sucked into the lung to stay. Chorus: Too-ra-loo-ra-le-mia, Too-ra-loo-ra-li, Too-ra-loo-ra-le-mia, now you are going to die! Too-ra-loo-ra-le-mia, Too-ra-loo-ra-li, Too-ra-loo-ra-le-mia, that's an ID lullaby."

Rationalization

An Outbreak of Primary Pneumonic Tularemia on Martha's Vineyard Katherine A. Feldman, D.V.M., M.P.H., Russell E. Enscore, M.S., Sarah L. Lathrop, D.V.M., Ph.D., Bela T. Matyas, M.D., M.P.H., Michael McGuill, D.V.M., M.P.H., Martin E. Schriefer, Ph.D., Donna Stiles-Enos, R.N., David T. Dennis, M.D., M.P.H., Lyle R. Petersen, M.D., M.P.H., and Edward B. Hayes, M.D. N Engl J Med 2001; 345:1601-1606November 29, 2001DOI: 10.1056/NEJMoa011374

AJR Am J Roentgenol. 1978 Aug;131(2):277-81. Radiographic spectrum of pleuropulmonary tularemia. Rubin SA.

An Irish Lullaby

A Strep I had not heard of. Which one? I am not telling in the title. Call it a strep tease.

Jul 13, 2010

So many bugs, so little time to see them all. There are still germs I have yet to see (P. knowlesi), some I hope never to see (smallpox) and some I have never heard of.

Twenty-five-year-old male presents with sudden onset of severe back pain and fevers.

He is too young to have any medical problems that are not self induced: he uses meth (snorts, not injects).

MRI shows discitis and osteomyelitis.

Exam is unimpressive except for back tenderness and what we call meth teeth: the uniquely poor dentition that accompanies methamphetamine use, although a mild case as meth teeth goes, and the dentition can really go with meth teeth. Google it of you want to see some awful dentition. And these people often have significant others who, one supposes, kisses them.

"Dental patients who abuse methamphetamine can present with poor oral hygiene, xerostomia, rampant caries ('Meth mouth'), and excessive tooth wear" and is due to a combination of teeth grinding, poor dental care and meth induced decreased saliva flow.”

Seem a reasonable source for the infection, as he grew S. gordonii from both the blood and back biopsy. S. gordonii is a mouth strep that I had never heard of before. S. sanguis is now divided into S. sanguis sensu stricto and S. gordonii and the fictional S. gordonii stricto commissioneri.

No surprise that I had never heard of it as S. gordonii is a relatively rare cause of endocarditis even amongst the viridans streptococci:

"...the most common species identified were Streptococcus sanguis sensu stricto (31.9%), S. oralis (29.8%) and S. gordonii (12.7%)."

There are no reported cases of discitis, so this is the first, although it is probably because most of the time the lab may not go past 'viridans strep' in the identification. Only the ID doc want to know the name of the organism down to the exact name.

Work up shows no endocarditis, as best as one can demonstrate the absence of disease, and he is being treated with a course of beta lactam.

Rationalization

Oral Dis. 2009 Jan;15(1):27-37. Epub 2008 Sep 25. Methamphetamine abuse and dentistry. Hamamoto DT, Rhodus NL.

J Med Microbiol. 1993 Sep;39(3):179-82. Identity of viridans streptococci isolated from cases of infective endocarditis. Douglas CW, Heath J, Hampton KK, Preston FE.

Streptococcus gordonii

Weird Rashes

Jul 14, 2010

I was asked to see a weird rash today as a curbside. For you non-medical folks, a curbside is "an informal and unofficial consultation obtained from a health professional by either a layperson or a fellow health care professional." It is where you get all the liability and none of the reimbursement. A formal consult requires a tuxedo complete with a cummerbund. We really do not wear enough cummerbunds in the U.S.

First the patient falls and injures her ankle. To relieve the pain she has been rubbing an as of yet unknown ointment, brought from the old country, Ukraine, on her leg. It has become red, hot and tender and she has developed a similar patch on the opposite knee. The family is going to bring in the ointment later today.

No fevers or leucocytosis, she is brought in and admitted for what looks like a cellulitis. She is started on vancomycin and while on the antibiotics, develops a rash on her upper legs and trunk.

Here is what I think is going on.

The leg looks like a contact dermatitis, dark red, like old hamburger, with a well-demarcated cut off. The opposite leg has a similar lesion right where you rest your leg when you cross them. I think she transferred the unknown ointment to the opposite leg when she crossed her legs. Metastatic contact dermatitis.

The other rash, on the upper leg and chest, is probably from the vancomycin, not quite a red man syndrome, but it itches and worsens with each infusion.

I did what I do best: suggested they stop the antibiotics and we will see if she improves.

Topical dermatitis is common from triple antibiotic ointments

"The frequency of allergic contact dermatitis proved by patch testing to neomycin and bacitracin is five (5.3%) of 94 and four (2%) of 198."

And I have also seen a severe case on the face from tree tee oil.

The family is going to bring in the ointment and we will place a small schmear on her forearm and see if she reacts there as well.

They did, she did, and stopping everything got her all better.

Rationalization

Arch Dermatol. 1992 Mar;128(3):365-7. Frequency of postoperative allergic contact dermatitis to topical antibiotics. Gette MT, Marks JG Jr, Maloney ME.

Australas J Dermatol. 2007 May;48(2):83-7. Allergy to tea tree oil: retrospective review of 41 cases with positive patch tests over 4.5 years. Rutherford T, Nixon R, Tam M, Tate B.

Can I Ignore A Positive Blood Culture?

Jul 19, 2010

Back from a short vacation at the Oregon coast. No infections there for four days. But I did not win Powerball. Again. So back to the daily grind. The consult today was positive blood cultures. A homeless person is admitted with fevers, which occurred for three days. Each day he gets a set of blood cultures.

Cultures from day one. Nothing.

From day two. Nothing.

From day three. Both sets are positive for MSSA. So I am called.

He has no significant history except: homeless, alcoholic, and a pacemaker.

Oh. And lice. Lots of lice. He has thickened , excoriated skin on his neck, arms and legs. With blisters and crusting. It looks like what we called in the day, Norwegian scabies, an infestation so severe it looks like psoriasis. Now it is called crusted scabies, thanks to the all-powerful Norwegian lobby, whose tentacles reach into the very heart of the US healthcare system. It is no wonder that the snakes on the caduceus have just eaten tyttebærsyltetøy.

It was first described in Norway in 1848, where it was thought to be a variant of leprosy. That's bad scabies, and I itch as I write this. Treatment is ivermectin and a topical agent. None of the areas of infestation on my patient appear to be secondarily infected.

Still. There are case reports of S. aureus bacteremia due to crusted scabies. Scabies and staphylococcal impetigo go together like peanut butter and jelly, but not half as tasty.

The incidence of active impetigo, group A streptococcal (GAS) impetigo, Staphylococcus aureus impetigo and scabies was 122, 80, 64 and 51 cases per 100 child-years respectively. Impetigo was strongly associated with scabies infestation.

So both Staph bacteremia and skin infections are increased with scabies. I assume, but cannot find data to support the idea that patients with scabies are more likely to be heavily colonized with S. aureus, given the propensity of S. aureus to colonize other chronic skin conditions.

So it is conceivable that the S. aureus in the blood cultures is a contaminant, especially since it was the third of three sets that were positive and there are no stigmata of infection anywhere else.

Even I, the great and powerful Oz, cannot ignore a S. aureus in the blood as much as I want to in this case. So I will recommend treatment. But what? Homeless, alcoholic, non-compliant with his adherence and non-adherent with his compliance, he has no IV access and no social support. Perfect. Health care is the US is second to none. It's because we are 23rd.

Rationalization

Permethrin and Ivermectin for Scabies Bart J. Currie, F.R.A.C.P., and James S. McCarthy, F.R.A.C.P. N Engl J Med 2010; 362:717-725February 25, 2010

J Am Geriatr Soc. 2009 Sep;57(9):1713-4. A case report of crusted scabies with methicillin-resistant Staphylococcus aureus bacteremia. Lin S, Farber J, Lado L.

PLoS Negl Trop Dis. 2009 Jun 23;3(6):e467. High burden of impetigo and scabies in a tropical country. Steer AC, Jenney AW, Kado J, Batzloff MR, La Vincente S, Waqatakirewa L, Mulholland EK, Carapetis JR.

Am I Feeling Lucky Today? Am I? TVIE.

Jul 22, 2010

I have sympathy for drug users. I have never been one myself, but there for the grace... If I had lived a few decades earlier, I suspect I would be a two pack a day smoker and look like Henry the VIII. Coke or heroin? I am sure that once started, I would never stop. I have enough trouble skipping the maple bars in the cafeteria. So I am never surprised, only saddened, when one of the IVDA's I have treated for endocarditis relapses.

Young female had tricuspid endocarditis due to MSSA a year ago that developed a ring abscess and a protracted course that eventually resulted in a tricuspid valve replacement with a bioprosthesis.

She presented this week with fevers, rigors and all the blood cultures with MSSA.

ECHO shows the valve covered in vegetation, but no ring abscess.

So what to do? The surgeon is willing to re-operate, which is nice, as not all surgeons will operate under these circumstances. I always figure that where there is life there is a chance to turn your life around. Death seems such an exorbitant price to pay for yielding to temptation. The surgeon is worried from a mechanical perspective. Evidently, the sewing ring on the right side is more tenuous than in the mitral or aortic position and he worries that while he may be able to take the valve out, there may not be anything left to sew a new valve into, much less put the heart back together. So I am tasked with curing a prosthetic valve infection medically. Lucky me.

There is a distinct lack of literature on tricuspid prosthetic valve endocarditis, and I am not surprised as the best I can remember this is the only case I have ever seen. It would probably be difficult to amass a series of this disease in one city, much less one institution of a disease this rare. As a rule, right sided endocarditis is a somewhat less virulent disease than left-sided disease and more likely to be cured medically with shorter courses of antibiotics. Why? A mystery. Lower oxygen tensions? Less pressure? Different antibiotic pharmacokinetics? The right side is different than the left, but how that difference translates to endocarditis outcomes is a curiosity.

Right sided prosthetic valve endocarditis may be less virulent as well, he says whistling in the dark while the wolves howl for blood. I found one case of MRSA TVIE that was cured with linezolid of all things, so if a drug as half-assed as linazolid can cure endocarditis, maybe the all powerful nafcillin, gentamicin and rifampin has a chance. Maybe.

Postscript. Blind pigs and truffles, I cured her. Of the infection. IVDA? We will see.

Rationalization

Successful treatment of right-sided prosthetic valve endocarditis due to methicillin-resistant teicoplanin-heteroresistant Staphylococcus aureus with linezolid. Souli M, Pontikis K, Chryssouli Z, Galani I, Giamarellou H. Eur J Clin Microbiol Infect Dis. 2005 Nov;24(11):760-2.

The Evil Betty

Jul 23, 2010

The patient is a middle-aged male who, for a variety of reasons, stopped taking his HIV medications several years ago. He now comes in with several months of shortness of breath, chronic non-productive cough, and failure to thrive.

Otherwise his past medical history is unrevealing; his HIV was not notable for prior opportunistic infections.

He has a cat, lived for a while in the upper Midwest years ago, smokes, but has recently been nowhere and done nothing, kind of like me. I have zero infectious disease risk factors, although I would like to be at risk for Campylobacter from eating rare pigeon in Paris.

His labs have a pancytopenia, his CD4 is 18. Comp and LDH is normal.

His CXR: a LLL consolidated infiltrate and the makings of another in the right mid lung. CT shows bilateral infiltrates with early necrosis in the center of the right infiltrate.

A chronic, consolidated, perhaps necrotic pneumonia in an AIDS patient.

In house (as opposed to out house) he only coughs up small amounts, despite trying, and to my relief as after 30 years I still want to puke when someone coughs up a gobbet of sputum. Some nurses know this and delight in trying to show me sputum. Bacterial cultures negative, cryptococcal antigen negative, PJP negative, histoplasma and coccidioidomycosis negative. Three AFB are thrice negative times three. One cannot be two careful with TB. I crack me up.

At this point I am betting an invasive mold, probably Aspergillus, so when he is off to bronch I ask for a biopsy as well and the biopsy showed Bronchiolitis obliterans organizing pneumonia (BOOP). “Boop-boop-be-doop-boop!"

Organizing pneumonia. A pathologic diagnosis that mimics pneumonia that can occur after a variety lung trauma (he has none) and can be idiopathic (which he appears to have).

Is BOOP a manifestation of AIDS? You bet.

About a dozen or so cases in the literature. Like Catcher in the Rye. Literature. In HIV BOOP can present as lobar infiltrates such as occurred in this patient.

He is restarted on his HAART and will need steroids for the BOOP. I do not expect he will do well.

Rationalization

Acta Vet Scand. 2010 Jun 22;52:45. Screening for several potential pathogens in feral pigeons (Columba livia) in Madrid. Vázquez B, Esperón F, Neves E, López J, Ballesteros C, Muñoz MJ.

Imaging in Bronchiolitis Obliterans Organizing Pneumonia

J Infect. 2004 Aug;49(2):159-64. Bronchiolitis obliterans organizing pneumonia as a manifestation of AIDS: case report and literature review. Khater FJ, Moorman JP, Myers JW, Youngberg G, Sarubbi FA.

A Turbulent Mouth

Jul 28, 2010

Turbulence. Bad. Turbulence in the heart leads to platelet/thrombin deposition. Bacteria do not care much for endothelial cells. But platelet/thrombin is a hospitable environment where they can stick and grow.

Patient is young and has had a life long history of a murmur. Of late he was been seeing a cardiologist who has been treating him with a beta blocker, but the medication made him fatigued. About three weeks ago the fatigue ratcheted up, and included fevers, chills and drenching sweats. He became so fatigued that he was unable to work, and his cardiologist got an ECHO and, goodness, gracious, great balls of fire, he had a 2 x 1.5 cm vegetation on this mitral valve.

He has a 4/6 murmur but no other stigmata of endocarditis.

His blood cultures grew S. oralis. Hmm. With that name it must be a found in the toes. I often put my foot in my mouth, so that is probably how the organism got its name. He as several rotten teeth, so there is a reasonable source for the endocarditis.

The turbulence? I used to call it IHSS, now it is called nonsense, no, bullsh.. no HOCUM (Hypertrophic Obstructive Cardiomyopathy). I guess cardiologists like to change names as frequently as microbiologists.

Endocarditis is a known complication of HOCUM, but is no longer on the list of underlying diseases that require prophylaxis. I had assumed endocarditis was a relatively common complication of HOCUM and it was a matter of chance that I had never taken care of a case. Turns out that endocarditis is relatively rare in HOCUM and there are fewer than 40 cases in the literature.

"It is a rare condition and the estimated cumulative 10 year probability of developing endocarditis in patients with obstruction is < 5%." or "1.4 per 1000 person/year in all patients and it increases to 3.8 per 1000 person/year in patients with left ventricular outflow obstruction."

The turbulence leads to specific alterations in the mitral valve of most patients:

"It is clear from morphological studies that systolic anterior motion of the anterior mitral valve leaflet is relevant to the pathogenesis of endocarditis. Examination of excised mitral valves has indicated that vegetations are located most commonly on the septal aspect of the anterior mitral valve leaflet."

As was the case in this patient.

His S. oralis is sensitive to penicillin, so I expect a cure of his endocarditis before he gets his valve replacement.

Rationalization

Platelets. 1997;8(5):285-94. The role of platelets in infective endocarditis. Ford I, Douglas CW.

Heart. 2002 June; 87(6): e8. Mitral valve endocarditis in hypertrophic cardiomyopathy: case report and literature review. G Morgan-Hughes and J Motwani

Eur J Echocardiogr (2006) 7 (6): 468-470. Infective endocarditis complicating hypertrophic obstructive cardiomyopathy

There Will Be Blood. Then an Abscess.

Jul 29, 2010

It is hard to infect muscle in normal people. The rare times you see a muscle abscess is after some sort of trauma. A young male has a 'groin pull' from diving for a basketball or lifting a heavy object, then develops fevers, pain and evaluation will show an abscess in the iliopsoas or iliacus or paraspinous muscles. The presumption is trauma causes some bleeding into the muscle, then there is a transient bacteremia (which is more common than people suspect) that unluckily goes to the blood in the muscle. Hematoma is the fertile soil in which the bacteria, usually S. aureus, can grow.

This patient is different. She has S. aureus in her blood and has extensive abscess in all those muscle groups as well as her SI joint. It is an impressive amount of pus.

It is the trauma that is interesting. Leading up to her infection, she had been having a week of daily or twice daily chiropractic manipulation to realign her pelvis and spine that was out of wack from a knee injury.

I hypothesize that the chiropractic manipulation led to the bleeding that was subsequently seeded by the S. aureus.

There are maybe a couple dozen cases of epidural hematomas from chiropractic manipulation, most reported in the cervical and thoracic spine, where they can cause more clinical symptoms.

"Posttraumatic spinal epidural hematoma is an unusual pathology. The authors report the case of a 64-year-old woman who experienced thoracic epidural hematoma during a session of spinal manipulation therapy (SMT). In the literature, such an event has been reported previously only twice. This case represents the first spinal epidural hematoma occurring after a chiropractic manipulation in the lumbar region. Surgical evacuation of the spinal hematoma resulted in complete recovery in the patient. Complications of SMT are reviewed, and the etiology and features of spinal epidural hematoma are discussed."

I am not surprised manipulation can cause a bleed if you are unlucky.

"A passive hanging (no drop) gives about 686 Newton’s of force around the neck for a 70 kg human. In chiropractic, “the mean force of all manual applications (is) 264 Newton’s and the mean force duration (is) 145 milliseconds (8).” So a chiropractic manipulation, for a short period of time, can provide 38% the force of a hanging... Chiropractors often have their patients relax just before the coup de grace, I mean manipulation, helping to maximize the chance of injury despite having less force applied to the spine than a noose and gravity."

There are only a couple of lumbar bleeds reported, probably as they are more likely to be silent. There is only one case in the literature similar to mine, most other reports deal with patients who received chiropractic by mistake for their misdiagnosed back infection.

"Paraspinal infection is a rare condition. Modes of infection include transcutaneous infection of the deep tissue by needles or catheters, surgery, blunt trauma, and hematogenous spread from distant sites. Chiropractic manipulation is a noninvasive procedure but is sometimes associated with vascular or neurologic insults resulting in hematoma or cerebrovascular accidents. We report a paraspinal muscle abscess in a healthy young man 7 days after Chinese Kong Fu practitioner manipulation for back pain without definite infection sources. The local paraspinal tenderness as demonstrated by the patient should be considered to be a sign of infection. Paraspinal infection often subjects to delayed diagnosis and this delay may be disastrous. In the management of low back pain or treating spinal disorders, physicians should be aware of the possibility of such a condition, particularly in patients whose back pain has been managed with chiropractic manipulation to avoid misdiagnosis."

I found that patients do not often volunteer receiving infection and trauma inducing 'alternative' therapies (acupuncture and chiropractic) unless asked directly; they did not think it germane to the problem. I have seen multiple infections for acupuncture, this is my first probably from chiropractic.

Rationalization

Chiropractic and Stroke: Evaluation of One Paper

Acta Anaesthesiol Sin. 1998 Jun;36(2):107-10. Paraspinal muscle abscess after Chinese Kong Fu practitioner manipulation--a case report. Sun HL, Cheng CY.

J Spinal Disord. 1999 Dec;12(6):534-6. Thoracic epidural hematoma after spinal manipulation therapy. Ruelle A, Datti R, Pisani R.

Adverse Drug Reaction?

Jul 31, 2010

Pregnant patients give me the willies. They shouldn't. But when I get called to the Ob floor for a consult, I get this vague sense of unease.

The patient is pregnant and has the sudden onset of severe abdominal pain, starting RLQ and then moving so that she hurts all over.

Rest of her history is negative and exam shows her to be afebrile and to be very sensitive to touch. She is painful everywhere, but especially her abdomen and back.

She gets the work up for an intra-abdominal catastrophe, and is negative. Only a normal child in the uterus. CBC, Comp, UA all negative. They call me.

I do my usual history and physical and also find nothing. Repeat labs are still normal. She needs IV Dilaudid to control the pain, she has no history of drug seeking and looks like she is in lots of pain. She had nothing like this with her first pregnancy.

I am baffled. First time ever in my life. Is this what it is like to not make a diagnosis? I looked at her med list and see that she is on nitrofurantoin daily for UTI prophylaxis.

Nitrofurantoin is a potentially nasty drug. It can cause hypersensitivity pneumonitis, pulmonary fibrosis, and retroperitoneal fibrosis. Maybe she is having an odd complication to the Macrobid.

Pubmed provides one hint.

"Med Clin (Barc). 1985 Apr 13;84(14):588-9. [Acute abdomen and nitrofurantoin]". Nitrofurantoin can also cause neuropathy and the onset of adverse reactions can be abrupt.

"The latter form (Macrodantin) is reported to engender less gastrointestinal intolerance but it can produce the same adverse effects as the conventional form--liver damage, acute and chronic pulmonary reactions, peripheral neuropathy, blood dyscrasias and allergic reactions--and does so just as rapidly and floridly; one such case is reported here."

We stopped the drug and she improved. Causality? Who knows. I am oddly disinclined to rechallange the patient to see if the symptoms recur.

Anyone Spanish speakers out there who has old copies of Med Clin (Barc) can you please let me know what the reference says?

Rationalization

Br Med J (Clin Res Ed). 1982 May 15; 284(6327): 1440–1442. Adverse reactions to nitrofurantoin in the United Kingdom, Sweden, and Holland. R G Penn and J P Griffin

Med J Aust. 1986 Nov 3;145(9):476-7. Macrodantin: a cautionary tale. Davey R.

25 Years Ain't Never Seen This Bug Before

Aug 3, 2010

As an ID fellow last century, I devoted two years to investigating the interaction of Candida and endothelial cells. Talk about the Peter Principle in action. If there was ever a more incompetent lab rat than me, speak now. Two years and nothin'. However, I did develop an appreciation for Candida species and its clinical manifestations, as my boss at time was, as is, one of the premier Candida experts in the US.

One of the many things I discovered is that there are an amazing number of Candida species. One individual seemed to spend his time in the wilds of South America, culturing this water collection and that decaying pile of wood and finding new Candida species. He found lots of new Candida. Good gig if you can get it.

Patient I saw had a perforated viscous and a yeast in his abdominal fluid, along with the usual hodgepodge of bacteria. Not much of a surprise, and he also had a yeast in his blood. A bit more unusual, as fungemia is more often a late manifestation of a GI perforation, not with the acute event. It was also odd that the blood cultures were positive within 18 hours, since that is usually more indicative of line infections. Oh well, patients have a nasty habit of not bothering to read the textbook so they know how to present.

The next day things were both more and less clear. The peritoneal fluid grew C. albicans, but the blood grew C. kefyr. I had vaguely heard of the latter. I called the lab, and they said, nope, no kefyr in the peritoneum. We looked. I work with a good lab. So I figured that C. kefyr. had to come from his central line, which had been in 10 days prior to the perforation. So we pulled the line and cultured the tip and...nothing. Culture negative. So I am no certain where the kefyr came from.

C. kefyr accounts for < 0.01% of fungemia in clinical studies.

"6082 bloodstream infection (BSI) isolates of Candida spp. collected from 250 medical centres in 32 nations over a 10-year period from 1992 through 2001. The species included 3401 C. albicans, 984 C. glabrata, 796 C. parapsilosis, 585 C. tropicalis, 153 C. krusei, 67 C. lusitaniae, 48 C. guilliermondii, 10 C. famata, 10 C. kefyr, six C. pelliculosa, five C. rugosa, four C. lipolytica, three C. dubliniensis, three C. inconspicua, two C. sake and one isolate each of C. lambica, C. norvegensis and C. zeylanoides."

I had not heard of nine of these Candida. According to the literature and the ever-helpful Dr. Fungus, C. kefyr is susceptible to all the standard antifungals. It is also found in milk, cheese and, Zimbabwean naturally fermented milk. MMmmmmm. Fermented milk.

There are them what drink raw milk; I do not think that is such a good idea.

"A total of 436 milk samples from non-infected and 80 from infected quarters were investigated: 24.5% of the samples collected from non-infected and 55% of those collected from infected quarters were positive. Normal milk yielded not fewer than 16 different species and among them many potentially pathogenic yeast species such as C. parapsilosis, C. guilliermondii, C. tropicalis, C. glabrata and T. asahii, all five able to grow at 40 ° C. In contrast, the yeasts isolated from infected quarters were from 3 species: C. kefyr, C. catenulata and C. lambica, which were also among the yeasts species recovered from normal milk. Among the three species, only one i.e., Candida kefyr is able to grow above 40 ° C and from there can be considered as potentially pathogenic, even if bacterial association is necessary to cause mastitis."

Me? I like pasteurization.

Rationalization

J Hosp Infect. 2002 Apr;50(4):243-60. Non-albicans Candida spp. causing fungaemia: pathogenicity and antifungal resistance. Krcmery V, Barnes AJ.

MYCOPATHOLOGIA Volume 135, Number 2 (1996), 99-102 Isolation of yeasts from bovine milk in Belgium P. E. Lagneau, K. Lebtahi and Danielle Swinne

Dr. Fungus

IVDA. A Bad Lifestyle Except For the Fungi

Aug 7, 2010

I just have a life, I am in need of a lifestyle. I need a style, a good style, a cool style. Not a style associated with sepsis and death.

Patient is a young male with one of those not so good lifestyles: IVDA. IntraVenous Drug Abuser. I know the preferred term is IVDU. User, not abuser, but injecting drugs always seems a wee bit self-abusive to me.

He tries to die: fevers, acute respiratory failure and cardiovascular collapse within an hour after IV meth. But, thanks to the power of modern medicine, he survives and thanks to his youth recovers rapidly.

He tells us that his meth dealer was also kind enough to throw in a vial of water with which to mix his drug for injection. How nice. Buy your drugs, get free water. Homeopathy in reverse. The provenance of the water is uncertain, but I bet it is the source of his positive blood cultures. Meth, as I have discussed in prior entries, is apparently not a hospitable environment to support the growth of bacteria, unlike heroin which, when cultured, grows more organisms that your stool. No one, however, has reported on the microbiology of meth, so perhaps I am wrong in that observation.

Certainly, if you google on how to make meth, the process looks to be bactericidal.

"Of the various syntheses only two are applicable to home chemists, utilizing easily available ephedrine or pseudoephedrine as a precursor. 1) Reduction With Hydroiodic Acid and Red Phosphorus or 2) Lithium-Ammonia Reduction of Ephedrine to Methamphetamine"

The first being the matchbook method, the latter being the Nazi method. Not something that appears to result in a good culture media, much less something to inject directly into the blood. But it seems that meth doesn't have the odd infections associated with it that heroin does.

Another fun fact about meth production is that some cook meth in a lava lamp. Who thinks of these things? Who looks at a lava lamp and thinks, "what a good place to cook my meth." I guess I am not that creative. Occasionally I see a news report of a fire in a remote trailer house from an exploding lava lamp. Wonder what they were doing? Who knows what they could do with an Easy Bake Oven.

His blood grew Bacillus spp., Candida parapsilosis and mucormycosis. Whoa. That’s strong water, more powerful than any homeopathic nostrum. This is the first time I have seen mucor in a blood culture, he must have had quite an initial inoculum for us to catch it.

Now what to do. He is now asymptomatic and nonfocal.

Bacillus can cause endophthalmitis the IVDA, er IVDU.

Candida can cause all sorts of complications in heroin users, from endophthalmitis to endocarditis, although it is more often than not Candida albicans.

Cerebral mucormycosis is a known complication of heroin use as well.

None of the above have yet to be seen in meth users.

So treat? I did. He had anti-bacillus therapy in the hospital and was sent home on a course of posaconazole. Maybe a waste of drug as he did not need, but safe is better than sorry.

Rationalization

Br J Ophthalmol. 1990 Jan;74(1):26-9. Bacillus-induced endophthalmitis: new series of 10 cases and review of the literature. Hemady R, Zaltas M, Paton B, Foster CS, Baker AS.

Chest. 1978 Apr;73(4):546-9. Successful medical therapy for endocarditis due to Candida parapsilosis. A clinical and epidemiologic study. Mayrer AR, Brown A, Weintraub RA, Ragni M, Postic B.

Surg Neurol. 1987 Dec;28(6):468-72. Primary phycomycosis of the brain in heroin addicts. Kasantikul V, Shuangshoti S, Taecholarn C.

Size Matters?

Aug 9, 2010

No, this is not about spam email. The patient I saw with the CROCK, no HOCUM, with the S. oralis endocarditis (A Turbulent Mouth) was back to the ER at Outside Hospital with progressive heart failure. No fever, no chills, no sweats. Progressive peripheral edema and PND.

Exam is without change, maybe the murmur is a wee bit louder, but no emboli. His labs were unchanged, all normal. The cardiologist re-echoed him and the vegetation is now "a lot bigger" and he is transferred in to my hospital. What's a lot? An empty piece of ground? I couldn't reach the cardiologist to get a number and the dictated report is pending. Still, a lot is more than a little, and significantly more than a skosh, a tad, a jot, a smidgen and bit.

I see him and he is looking the same, maybe a bit more heart failure. He is 12 days into his therapy. What to make of the bigger vegetation? Most of the time I wish we had never invented the ECHO. It often gets ordered for the indication that the patient has a heart (Nick Chopper being the one person safe from this indication), or, if we are lucky, to 'rule out endocarditis' in a patient with no clinical stigmata of the disease.

Now refractory heart failure is a reason to replace the valve sooner rather than later, and an ECHO to look at valve function is a good idea, but it is probably a waste of time to worry over much about the change in the vegetation size. Although the bigger the vegetation, the more likely the embolization, vegetations normally wax and wane during treatment for endocarditis. They may get bigger, they may shrink, and they persist long after the infection is cured.

Examples from what is a minimalist literature:

"Forty-one vegetations were identified in 32 patients on initial echocardiograms. At the end of treatment, 29 vegetations were still present; 59% had no significant change in size and 52% appeared to be denser in consistency."

There is some correlation with treatment and the vegetation:

"Treatment with different kinds of antibiotics corresponded with significant differences in vegetation size; vancomycin-associated treatment was related to a 45% reduction, ampicillin to a 19% reduction, penicillin to a 5% reduction, penicillase-resistant drugs to a 15% increase, and cephalosporin to a 40% increase in vegetation size. Multivariate analysis showed that penicillin, cephalosporin, and penicillase-resistant drug treatments were associated with an increased embolic risk, vancomycin treatment with abscess formation, and cephalosporin medication with increased mortality"

Given that what a piece of crap vancomycin is I was surprised to see it lead to more vegetation reduction than a beta-lactam. Vegetations increasing in size is not that uncommon:

"The vegetations grew during medical therapy (even when the patients were apyrexic) in 29% of cases, and even after a 40-day course of anti infectious therapy in 2 cases."

As a fellow I was called by the OR. The surgeon had worn her mask to lunch and in the middle of the case a broccoli floweret fell out of the mask and into the operative field. While that remains the largest vegetation I have ever seen, it proved to be of little importance to the patient, who did well. I was just glad she had not been eating corn on the cob.

Rationalization

Am Heart J. 1994 Dec;128(6 Pt 1):1200-9. Natural history of vegetations during successful medical treatment of endocarditis. Vuille C, Nidorf M, Weyman AE, Picard MH.

Clin Cardiol. 1997 Feb;20(2):132-40. Effect of antibiotic treatment on vegetation size and complication rate in infective endocarditis. Rohmann S, Erhel R, Darius H, Makowski T, Meyer J.

Arch Mal Coeur Vaiss. 1982 Sep;75(9):1061-8. [Outcome of echocardiographic vegetations in bacterial endocarditis during and after anti-infective therapy]. Roudaut R, Billès MA, Ginestes J, Randazzo W, Videau P, Dallocchio M, Bricaud H.

Not where you expect it to be

Aug 13, 2010

I have always hated the phrase "expect the unexpected." Obviously if you could expect it, it would not be unexpected and since it is unexpected, how can you expect it?

The patient is an elderly female with minimal medical problems who comes in with multi-organ system failure from an apparent intraabdominal catastrophe. She has free air, a WBC of 35K and is whisked off to the OR where she has extensive dusky small bowel. The surgeon did Dopplers and found the vascularity of the small bowel to be fine and he judged the bowel to be viable, so she was sewn back up and sent to the ICU, with the anticipation that she would need another exploration in a day or two.

In the ER she had complained of diarrhea, and although she had been on no recent antibiotics, the ER sent a C. difficile assay which came back positive, which was not expected, which lead to an ID consult which led to a stroll down Pubmed.

When I saw her, I put her on oral vancomycin for the C. difficile and antibiotics for generic abdominal sepsis and I'll be damned if she did not slowly get better.

Unfortunately for us, but not for her, she did not get a pan-endoscopy which would have proven the diagnosis. So how do I put it together?

C. difficile is in the food supply. It can be found in ground meat and fast food salads. So I assume she inadvertently ate some C. difficile. As if anyone would eat it advertently. Some C. difficile may well be a food-borne illness.

It multiplied in her gut and caused C. difficile disease, which can occur without the classic risk factors, as demonstrated in the Netherlands:

Among 31 patients with toxin-positive stool samples for whom information was available, 20 (65%) had not been admitted to a healthcare institution in the year before, 13 (42%) had not used antibiotics during the 6 months before, and eight (26%) had neither risk factor.

And small bowel disease? That occurs and is a particularly fulminant form of C. difficile.

The literature contains an increasing number of reports describing infections of the small bowel with fulminant clinical courses and high mortality rates of 60-83%.

I would wonder if the relative lack of bacteria in the small bowel allows the organism to multiply with particular abandon.

Time and antibiotics and she slowly improved.

Take home?

Look for C. difficile in the outpatient setting without risk factors, in what looks like small bowel ischemia, and only eat fried food. My theory is that all physicians die of diseases in their subspecialty. I am destined to die of an infection, so I do not have to worry about vascular disease. I am glad I did not go into Ob. Oh. And the unexpected? Nothing you can do about it. But you expect that.

Rationalization

Clin Infect Dis. 2010 Sep 1;51(5):577-82. Clostridium difficile in food and domestic animals: a new foodborne pathogen? Gould LH, Limbago B.

Clin Microbiol Infect. 2009 Dec;15(12):1087-92. Epub 2009 Jul 16. Clinical and microbiological characteristics of community-onset Clostridium difficile infection in The Netherlands. Bauer MP, Veenendaal D, Verhoef L, Bloembergen P, van Dissel JT, Kuijper EJ.

Int J Colorectal Dis. 2011 Feb;26(2):245-51. Epub 2010 Jul 14. Clostridium difficile infection of the small bowel--two case reports with a literature survey. Holmer C, Zurbuchen U, Siegmund B, Reichelt U, Buhr HJ, Ritz JP.

POLL RESULTS

My favorite deep-fried food

1. french fries 59% (24)

2. ice cream 7% (3)

3. Twinkies 5% (2)

4. snickers bars 5% (2)

5. I just infect the fat straight 7% (3)

6. Other Answers 17% (7)

7. chocolate burrito

8. dough

9. doughnuts

10. Tempura

11. o rings

12. oreo cookies

13. seafood

Lue Lue

Aug 15, 2010

Syphilis is still around, and evidently one of the risks is having sex. Go figure. People often have no symptoms with primary disease and the chancre can occur in places the patient does not routinely examine.

As a result, it may be the symptoms for secondary disease that bring the patient into the hospital: fevers, rashes, hepatitis, hair loss to name a few. Most would not relate a painless ulver months ago with a fever today. I have seen many whose primary symptom is ocular. The patient is admitted with fevers and sweats of a week duration, and a spotty rash on the palms and soles. Few diseases cause palmer rashes; what it is about the palms that are refractory to rashes I do not know.

Patient has a VDRL of 1:8 and a positive FTA. He also has HIV, so the question is when to LP an HIV patient? When there are neurologic symptoms (duh), CD4 < 350 or serum RPR >= 1:32.

The estimated prevalence of neurosyphilis among non-HIV patients with untreated latent syphilis and serum VDRL < 1:16 was below 6.2%.

There are several studies about when to LP in the HIV, and it is CD4 < 100 or VDRL > 1:32. His CD4 cells were less than 100, so he had an LP that was normal, and he received his benzathine penicillin and several hours later he had fevers, rigors, chills, and transiently dropped his blood pressure.

Appears that despite a lack of immune system he was able to mount a Jarisch-Herxheimer reaction: the massive kill off the syphilis leading to an acute inflammatory response. Have to remember the JH reaction, as some will mistake it for a drug reaction.

The other curiosity was he has been on weekly azithromycin for MAI prophylaxis, but had enough Treponema (I loved that song, the Lady from Treponema) to have a JH reaction, so I presume azithromycin resistance.

Azithromycin treatment failures in syphilis were first noted in San Francisco in 2002 and result from an A-->G mutation at position 2058 of the 23S rRNA gene of T. pallidum. This mutation confers resistance by precluding macrolide binding to the bacterial 50S ribosomal subunit, of which 23S rRNA is a structural component. Azithromycin resistance has also been identified in T. pallidum specimens from elsewhere in the United States, Ireland, and Canada, and the number of resistant specimens has increased with time.

Lue Lue.

Me gotta go now.

Rationalization

Sex Transm Dis. 2007 Mar;34(3):141-4. HIV and syphilis: when to perform a lumbar puncture. Libois A, De Wit S, Poll B, Garcia F, Florence E, Del Rio A, Sanchez P, Negredo E, Vandenbruaene M, Gatell JM, Clumeck N.

Clin Infect Dis. 2009 Mar 15;48(6):816-21. Lumbar puncture in HIV-infected patients with syphilis and no neurologic symptoms. Ghanem KG, Moore RD, Rompalo AM, Erbelding EJ, Zenilman JM, Gebo KA.

Sex Transm Infect. 2010 Feb;86(1):39-40. Epub 2009 Oct 16. Usefulness of routine lumbar puncture in non-HIV patients with latent syphilis of unknown duration. Choe PG, Song JS, Song KH, Jeon JH, Park WB, Park KU, Park SW, Kim NJ, Oh MD, Kim HB.

Curr Opin Infect Dis. 2008 Feb;21(1):83-91. Azithromycin resistance in Treponema pallidum. Katz KA, Klausner JD.

Politicians are Immune

Aug 18, 2010

Everyone gets back pain at one time or another. The spine often has to support more weight than it should and activity often leads to aches and pains. If you have a spine, eventually you will get back pain.

My patient had an achy, breaky back that just didn't go away. It wasn't horrible, maybe a three out of 10, but it persisted and annoyed the otherwise healthy patient, so for the first time in three quarters of a century, he seeks health care and gets the best that medical technology has to offer.

He has no fevers, chills or other symptoms, and as his work up progresses, his pain subsides. But, once started, a work up progresses despite the resolution of symptoms, and I'll be darned if the MRI didn’t show discitis and osteomyelitis. So a biopsy was done, the path showed osteo and the cultures grew Peptostreptococcus. And he was sent to me, on IV penicillin for a few days, and he is symptom free. No tenderness, normal range of motion.

There are 5 cases of Peptostreptococcus discitis and osteomyelitis in the literature; stick Peptostreptococcus and discitis in Pubmed and you can find them.

I am not certain why he developed this organism, but much of my practice is based on people having unusual organisms for no good reason. And why so few symptoms? Most, if not all, patients with discitis are incapacitated by the pain.

Peptostreptococcus is a relatively indolent organism, so perhaps he just didn't develop enough of an inflammatory response to hurt.

And maybe he was controlling the infection on his own. Once upon a time I had an IVDA who had months of back pain he self treated with heroin. Eventually he came in to the ER and was admitted with vertebral collapse and what looked to be osteomyelitis on the MRI. His WBC was normal as was his ESR and in the OR there was nothing but fibrosis. Cultures and biopsy was negative. I presume he cured the infection on his own; a clinical course we never get a chance to see in the antibiotic era. I can't find references from the old days where osteomyelitis cured itself.

This patient will get a course of antibiotics as for the time being I can treat infections.

Rationalization

AJNR Am J Neuroradiol. 2005 May;26(5):1008-11. Resolution of an aggressive idiopathic diskitis. Smith AB, Kane AG, Sholes AH, Freeman JH.

Follow the Culture

Aug 19, 2010

Sometimes it's the history that leads to a diagnosis.

Sometimes it's the physical, or the labs, or the X-rays.

But the cultures. The cultures never lie. Well, sometimes they kind of lie. When they do lie, you still have the diagnosis of a factitious illness; I haven't seen a Munchausen in years and if I find that the history, physical, labs and and X-rays are not supporting the culture results, then everything else is wrong. Go with the cultures, Luke.

Patient has been on Continuous ambulatory peritoneal dialysis (CAPD) for a year without issue and then develops fevers, severe abdominal pain and the fluid changes from clear to white with chocolate milk swirls. No Nesquick for me tonight.

CAPD peritonitis. Not uncommon. Usually a coag negative Staphylococcus, the patient is given intraperitoneal vancomycin and admitted.

The cultures start dribbling in. First an E. coli, then a B. fragilis, and then a few days later a C. glabrata. Clinically the patient only marginally improved on antibiotics and continued to have abdominal pain and an increasing cell count in the CAPD fluid.

Why is the peritonitis not better? It has to be some sort of abdominal disaster. The Bacteroides and the Candida say there has to be a leaky colon. There can’t be any other reason for those bugs in that space. Listen to the cultures.

CAPD patients also have a much higher rate of badness in the abdomen, and clues to the badness are polymicrobial cultures or finding B. fragilis in the fluid. Occasionally intraperitoneal catheters erode into bowel to cause all sorts of havoc.

"The experience at University Hospitals of Cleveland suggests that abdominal catastrophe occurs in approximately 10% of all patients treated with PD, and is associated with high mortality."

So off to the OR and they found toxic megacolon of the cecum, although the why of the megacolon is pending. I have seen a few C. difficile's isolated to the cecum with no diarrhea and only megacolon as the presentation, but that has not been reported in the literature, so take it with a grain of salt substitute. Well, not reported in humans. It can be hell on Syrian hamster colonies.

Rationalization

Perit Dial Int ABDOMINAL CATASTROPHE REVISITED: THE RISK AND OUTCOME.OF ENTERIC PERITONEAL CONTAMINATION 2002 May-Jun vol. 22 no. 3 323-334

Lab Anim Sci. 1991 Dec;41(6):553-8. Clostridium difficile typhlitis associated with cecal mucosal hyperplasia in Syrian hamsters. Ryden EB, Lipman NS, Taylor NS, Rose R, Fox JG.

Draining Pus

Aug 21, 2010

Patient is an elderly female who had the misfortune of having an infected artificial hip. Over the last several years she has had multiple attempts at cure with removal of the prosthesis, debridements, and she had an open wound for many months that slowly closed.

Her cultures have grown a hodgepodge of organisms and she has been on a gallimaufry of antibiotics, but the infection remained in the bones of what used to be a hip joint.

But then, as I say, the chronic draining wound finally closed over and she went of vacation. While on vacation she developed fevers and marked erythema over her hip and was admitted to one of my hospitals (not that I own them, but I do have a sense of possession that makes them my hospitals) and I was called to see her.

She has no new complaints, the hip, being a Girdlestone, always hurts and is no worse. The tissues over the hip are red and boggy. The plain film shows osteomyelitis and her CRP and ESR have the same value as the national debt.

She has an incurable infection, short of complete leg removal, and the surgeon is understandably unwilling to operate, but like all ID docs I want source control and cultures, so while we are contemplating open vrs CT guided aspiration, the pus makes our decision for us: it finds the weak spot in the incision and gushes into the bed. Nurses say it was at least a quart.

Now what to do.

Over the years I have seen a number of chronic, incurable osteomyelitises of the hip or other sites where definitive debridement was worse than the disease. As long as there was a chronic draining sinus, the patient did fine. If the drainage stopped, either due to normal healing or some idiot ID doc giving antibiotics, the infection would build up and, since it could not drain into the environment, the patient went septic instead.

I think these infections are often best treated with no treatment. Keep the pus draining and avoid antibiotics unless there is an acute infection. In the old days, the pre-antibiotic days, that is what chronic osteomyelitis would do and patients would often live relatively normal lives, in equilibrium with their infection.

The best approach to chronic osteomyelitis is debridement and antibiotics, she can't be debrided and antibiotics have been used in her for years with no resolution of infection.

Sometimes it is best to do nothing, and with increasing antibiotic resistance, that may be the only option in the future.

Usually I tell people, we need to be draining pus, now I say let the pus be free. Fly away free, pus, fly away.

POLL RESULTS

Doing nothing is key when

1. Approaching incurable infections. 14% (7)

2. You are in the Congress. 18% (9)

3. You are a spouse and there are chores. 6% (3)

4. You are a teen and there are chores. 8% (4)

5. Doing nothing is doing something. Ohmmmmmmmmmm. 49% (25)

6. Other Answers 6% (3)

7. state legislature

8. They're asking for volunteers.

9. DNR, of course.

What's My Line? Infection

Aug 23, 2010

You learn early in medicine that you have to be very, very careful. Even little interventions can go south with amazing rapidity and lead to significant morbidity and mortality. As an intern I took care of an elderly female who had an IV placed that became infected, the infection seeded her aortic valve which blew out and she died. Crap. Death from a piddley IV.

These days, thanks to application of many best practice bundles, we do not see many infections from intravenous catheters, but there are patients that need long-term central lines for chemotherapy or nutrition, as with this patient.

All central catheters eventually fail: either they break or they get infected. My patient presents with fevers for 11 days, rigors and mild shortness of breath. She grows, in all her blood cultures, two different coagulase-negative Staphylococci. She gets progressively septic over the next day: hypotensive, tachycardic, tachypneic and febrile despite vancomycin and pulling her CVP.

The TTE shows maybe a bicuspid aortic valve, and a TEE confirms a bicuspid aortic valve and a big vegetation. And her vitals worsen and she starts requiring more pressors. It isn’t the infection, coagulase-negative staphylococci rarely makes people that sick, although early in my career I had a patient die of septic shock from coagulase-negative staphylococcus. I have noted over the years that bicuspid aortic valves do not tolerate the stress of endocarditis all that well and tend to fall apart quickly when infected, an observation sort of supported by the literature.

"...patients with infective endocarditis in a bicuspid aortic valve were younger and had a higher incidence of periannular complications. Although a worse prognosis has been reported previously, we found that infective endocarditis in a native bicuspid aortic valve is not likely to increase the risk of death in comparison with infective endocarditis in native tricuspid aortic valve."

With worsening vitals, she is off to the OR where they find not only a bicuspid valve, a big vegetation, an annular abscess, but a 1 x 2 cm hole in the septum.

Whoa. That’s a lot of damage for what is an 11-day history of fevers, and her valve grows a third coagulase negative staph, at least to judge from antibiotic susceptibilities, one of which is an MRSE with an MIC to Vanco of 2.0.

Polymicrobial endocarditis is not that rare, the record, which I cannot locate, is somewhere around a Baker’s dozen of organisms in a German heroin user, if my memory is correct. My Google-fu fails me searching for the case. Endocarditis is a good substrate upon which to develop endocarditis: Big vegetations have little vegetations upon their backs to bite them, and little vegetations have lesser vegetations, and so ad infinitum. Three bacteria on three valves is my record, tied with this patient, although three different coagulase-negative staphylococci is odd and maybe a pubmed record.

Endocarditis is an increasingly recognized (hey, look, a case of endocarditis) complication of central lines.

"From October 1, 1998 until December 31, 2006, 24 patients were identified with inpatient mortality of 20.8%. Nine cases were nosocomial and 15 were non-nosocomial. The most common comorbidities were diabetes mellitus (45.8%), chronic kidney disease (58.4%), prior valvular abnormalities (37.5%), and multiple prior hospitalizations (65.2%). There were 13 external lines, 9 tunneled lines, and 2 implantable ports. Responsible microorganisms included Staphylococcus aureus in 54.6%, coagulase-negative staphylococci in 37.5%, Candida species (spp.) in 16.6%, and enterococci in 12.5%. Five cases were polymicrobial. The line tip was within the right atrium (RA) in 37.5%, the superior vena cava (SVC)-RA junction in 20.8%, the SVC in 33.3%, and the pulmonary artery in 4.2%of patients.Sites of endocardial involvement were the aortic valve in 6 patients,mitral valve in 7 patients, tricuspid valve in 6 patients, right atrial wall in 11 patients,and pacemaker wire in 2 patients. Isolated right-sided involvement occurred in 50% of cases, isolated left-sided in 33.4%, and bilateral involvement in 16.6%. Transesophageal echocardiography (TEE) was necessary for diagnosis in 10 cases (41.6%)."

That's a nasty group of infections and locations.

The patient is getting better, slowly, post-op, but an impressive amount of damage from such usually wimpy organisms.

Rationalization

Tex Heart Inst J. 2009; 36(2): 111–116. Impact of Bicuspid Aortic Valve on Complications and Death in Infective Endocarditis of Native Aortic Valves

http://onlinelibrary.wiley.com/doi/10.1002/clc.20498/pdf

http://en.wikipedia.org/wiki/The_Siphonaptera

It's Been A Long Time

Aug 25, 2010

Middle-aged male with a year and a half of cachexia/consumption. About a year ago, he had an episode of high fevers and slight abdominal pain that lasted for about a day. The pain went away, but it started his decline: decreasing energy, appetite, and mood. He lost 30 lbs. on an already thin frame.

Totally non-focal, he spent many days abed with malaise and apathy that was thought to be depression. Like many a male, he was taken to the doctors by his wife instead of going under his own power.

It is remarkable how often the reason males go to the ER or office is "because my wife/girlfriend made me." Most men would be dead if not for our women folk.

They find an anemia, but the rest of the labs are normal, so the next step is colonoscopy as he has no focally on exam or ROS and they find an extrinsic mass pushing in on his colon as well as a few tics.

CT shows a large mass that looks like a tumor, so it is biopsied and, as you can guess since this is an ID blog and not an oncology blog, no cancer but chronic infection. So off to see me.

My history and physical: no abdominal symptoms at all. Some occasional rigors and sweats that were felt to be unimportant/due to depression by the patient.

CT looked like tumor, so I was betting on actinomycosis. Unfortunately, bacteria do not grow in formalin, so he had a repeat biopsy: no cancer, pus, growing a variety of anaerobes.

So has he had a festering asymptomatic abscess for 18 months, perhaps from a popping tic or perhaps a bone? History suggests that this is indeed the case, and I try to never ignore the history.

There are reports of silent abscess, but a year and a half is well well beyond the norm. Years ago I saw a K. pneumoniae periheptatic abscess that was a year in the diagnosis and once saw a perforated appendix in a mute/brain-damaged patient who may have had the abscess for months, at least long enough to get an immune complex glomerular nephritis from the infection, so a delay in the diagnosis is not totally unheard of. But still. A year and a half?

He is improving on antibiotics, but given the size of the mass, it probably deserves an e-lap, both for debulking/drainage of the infection and to look for an etiology of the perf. I still have trouble believing this has been present for 18 months.

Rationalization

AJR Am J Roentgenol. 1983 Jul;141(1):21-5. The silent abdominal abscess: role of the radiologist. Goldman R, Hunter TB, Haber K.

Mystery Case 1

Aug 31, 2010

The last week has been busy, but none with dénouements to write about. I tend to write about the cases for which I have an answer, but I am not House, or even Condo, and a lot of the time I do not end up with an answer. Most of the time it is because the answer doesn’t matter: a self-limited disease with no therapeutic interventions or long-term sequelae. The unfortunate truth is that most infections improve with little or no medical intervention required, or some diseases get better and we do not have a diagnosis.

Patient in a middle-aged male with fevers to 40. Pulse of 80. Hmm. Faget's. For every degree your temperature goes up, your pulse should go up 10. In the US, it’s beta blockers that lead to Faget's, but the classic reasons are typhoid, brucella, yellow fever, tularemia, and Legionella.

He has a RLL infiltrate that is more patchy than consolidated, low WBC and platelets, non-productive cough and minimal pulmonary symptoms, and lots of diarrhea.

He has been traveling lately, and I ask him if he has been in humid, thundershower weather, and yes he has, about a week before the onset of his symptoms.

I tell the residents that a lobar community acquired pneumonia with a low WBC, minimal cough and recent humid weather (a risk for Legionella) with Faget's on the vitals has to be, it just HAS to be, Legionella.

So I bet him a Hostess cupcake the urinary Legionella antigen (Legionella urinary antigen sounds like it is the Legionella that is urinating) will be positive.

The Legionella antigen was negative. Crap. It turns out that there are no Hostess Cupcakes at the local store, so I gave the team a box of Little Debbie cupcakes. The resident make a point of getting a picture of me handing him the box, as if he were receiving an award.

Oh well, my motto is 'Frequently in error, never in doubt.' It still could be Legionella as there are Legionella that are not picked up by the urine antigen assay. I try to not let reality intrude upon a good clinical diagnosis.

And the thunderstorm? It was in India. He has been slow to defervese as happens with intracellular infections like Legionella and typhoid fever.

From 1902:

"All of us have been taken in at least once in our lives by cases of typhoid with abrupt invasion, add all the signs and symptoms of pneumonia, but very few of the textbooks lay any stress upon this important point."

More recent studies suggest this could be S. typhi:

"High fever, toxaemia, constipation during first week of fever, complicated by encephalopathy and perforation during third week of fever are the typical manifestations of typhoid fever. However, the classical presentation of typhoid fever has considerably changed now. AIM: To study atypical presentations of typhoid fever....All culture-positive adult patients of typhoid fever admitted over a period of seven years were studied RESULTS: Thirty-two adult patients were admitted. Fifteen (46.9%) patients presented with atypical manifestations. Atypical manifestations observed were burning micturition with normal urine examination (n= 5, 15.6%) diarrhoea in first week (6.2%), encephalopathy in first week (3.1%), isolated hepatomegaly (6.2%), pneumonitis (3.1%) and bone marrow depression (6.2%)."

Typhoid? Legionella? Something else? No risks based on extensive history.

Blood cultures are negative so far, so I suppose I will have to await serology, and the problem is that convalescent serology never gets sent.

You got a better idea?

PS: Never had a diagnosis.

Rationalization

Br Med J. 1902 November 22; 2(2186): 1682. Pneumonia and Typhoid Fever

Dutta TK, Beeresha, Ghotekar LH. Atypical manifestations of typhoid fever. J Postgrad Med 2001;47:248

Mystery Case 2

Sep 2, 2010

Another day of mysteries.

The patient is a young female, no significant past medical history except arthritis, who presents with a headache and not just any headache. This one has been going on for two months and during this time she had numerous lumbar punctures with the same thing. 150 WBCs, protein of 120, and a normal glucose. She has had an extensive work up at another hospital with every test you can list with no answer. She comes to the ER of my hospital and is admitted with more of the same: a bad headache and an abnormal spinal tap.

As mentioned, no significant past medical history, exposure history equally negative: she has been nowhere, done nothing; a life as dull as mine.

Exam is also negative except for stiff neck and mild photophobia.

Labs are negative for the basics and the tests done here and at the other hospital have made ARUP a good investment. Pick a test for a viral, bacterial, spirochetsial, or fungal etiology and it has been sent and negative.

One of the causes of aseptic meningitis is drug and NSAIDs are a well-described etiology. It turns out that she slathers on lots of topical NSAIDs for chronic joint pain (DJD) and we thought we had the first case of topical NSAID's causing meningitis but unfortunately stopping the NSAID's did nothing.

So I reason that maybe the issue is not the infection, but the host. Although there is nothing in the history to suggest an immundefiency, I send off quantitative immunoglobulins and IgG subtypes, and what the heck, not only are the IgG and IgM seriously depressed, the IgA level is 5x normal.

Just back today is the immunofixation that shows it to be a monoclonal spike so I have (well, I did have a little help from hematology) stumbled upon an IgA myeloma.

So how does that explain the meningitis?

It doesn't, really. Myeloma meningitis is rare and this case does not fit the clinical syndrome, plus there is no myeloma cells seen on prior CSF cytology. Enterovirus can cause chronic meningitis in patients with agammaglobulinemias and myeloma but the PCR is negative and the lab tells me the test we use gets damn near all the enteroviri. Like the plural of Elvis.

Diagnosis? She is going to get a large volume tap to look again for malignancy and I will send viral cultures. Again.

An empirical course of IgG? Nothing an ID doc hates more than a trial of therapy when there is no diagnosis.

Your turn. I am 0 for two and on the next entry you will see I am 0 for three.

Rationalization

Cancer. 2008 Apr 1;112(7):1562-7. Myelomatous meningitis. Chamberlain MC, Glantz M.

J Clin Immunol. 1992 Jul;12(4):266-70. Chronic enteroviral meningoencephalitis in agammaglobulinemia: case report and literature review. Misbah SA, Spickett GP, Ryba PC, Hockaday JM, Kroll JS, Sherwood C, Kurtz JB, Moxon ER, Chapel HM.

Common, Critical, or Cool

Sep 5, 2010

After you see a patient, you generate a differential diagnosis, a list of things that the patient may have. In addition, I like to generate three separate lists: what the patient probably has, what I do not want to miss (the disease that could kill or maim the patient), and the cool case: the odd or unusual disease I have yet seen. Most of the time it isn't a cool diagnosis, but that doesn't stop me from looking. I want to find a great case.

Patient is a youngest male with progressively severe right shoulder pain. No fevers, chills, sweats or other trauma to the shoulder. He does use black tar heroin, however.

Exam shows the right shoulder and trapezius muscles are swollen and exquisitely tender. His WBC is only 13 K. The CK is 800.

CT shows the trapezius group is now a large necrotic collection of dead muscle.

So what is it? Radiology tells me that there are often anomalous veins from the arm that bypass the subclavian and go by way of the back. So presumptively there was an injection of black tar heroin that went by way of the anomalous veins and stopped in the trapezius.

I think he needs an aggressive debridement, and he is off to surgery, but can I predict the organism?

The usual cause of necrotizing myositis is group A streptococci. But he is not toxic enough; people with Group A as a cause are usually trying to die.

Mixed synergistic myositis does not occur in normal people, so I doubt that.

Black tar heroin is associated with a variety of Clostridia: sordelli, perfringens, and septicum. That’s the disease I do not want to miss. Unlikely, but I have recently seen a cold metastatic Clostridia infection, so it is not out of the question.

MRSA is a newish cause of myositis, especially those strains that make the Panton-Valentine leukocidin, a protein that liquefies human tissues like water on Elphaba and can also cause a relatively cold abscess.

So I bet either Clostridia or MRSA.

At surgery they find necrotic muscles and the cultures grow MRSA. Clindamycin resistant, so no use in trying to suppress toxin production.

Kind of common, kind of critical, and kind of cool. I guess this was a three in one, an ID trinity.

Rationalization

PLoS One. 2009; 4(7): e6387. Staphylococcus aureus Panton-Valentine Leukocidin Contributes to Inflammation and Muscle Tissue Injury.

J Med Microbiol. 2006 Jan;55(Pt 1):123-5. Community-acquired methicillin-resistant Staphylococcus aureus pyomyositis in an intravenous drug user. Fowler A, Mackay A.

LANGENBECK'S ARCHIVES OF SURGERY Volume 392, Number 6 (2007), 761-765. Severe pyomyositis caused by Panton–Valentine leucocidin-positive methicillin-sensitive Staphylococcus aureus complicating a pilonidal cyst. Udo Lorenz, Marianne Abele-Horn, Dieter Bussen and Arnulf Thiede

Fe Man

Sep 8, 2010

Middle-aged male with a day of fevers, teeth chattering rigors, and a drenching sweat. He says he gets these on occasion over the years, but they never last, so he ignores them. This time, however, he develops severe shoulder pain. So severe he cannot move his shoulder, so off to the ER where a tap shows WBCs but no organisms. He is admitted and I am called.

PMH: diabetes for 5 years and hemochromatosis (an iron overload state) for life. No history of trauma or joint problems.

Exam is negative except for the painful, hot, swollen shoulder.

So he has a septic joint, but with what and why?

Iron is an important growth factor for bacteria and there is an argument that we have evolved to be, or at least tolerate, iron deficiency to protect against a wide range of infections.

"Several thousand years ago, human culture changed profoundly with the agrarian revolution, when humans turned to agriculture. Their diet became iron deficient and new epidemic infections emerged due to crowding and lifestyle changes. There is convincing evidence that iron deficiency protects against many infectious diseases such as malaria, plague, and tuberculosis as shown by diverse medical, historical, and anthropologic studies. Thus, this change of diet increased the frequency of iron deficiency, and epidemic infections exerted a selection pressure under which the iron deficiency phenotype survived better."

To make it even more complicated, hereditary hemochromatosis patients have decreased iron levels inside macrophages, a compensatory mutation that may help counteract the increased risk of infection from increased blood iron.

"The mystery surrounding the apparent lack of iron within the macrophages of individuals with hereditary hemochromatosis, a condition of excessive uptake of dietary iron, has yet to be fully explained. We have suggested that iron deficiency of macrophages in people with hereditary hemochromatosis mutations is associated with increased resistance to infection by Yersinia and other intracellular pathogens, a selection pressure resulting in unusually high current population frequencies of hereditary hemochromatosis mutations. Such selection pressure has been called Epidemic Pathogenic Selection (EPS). In support of the theory of EPS, a considerable number of virulent species of bacteria multiply mainly in iron-rich macrophages of their mammalian hosts. Among these fastidious pathogens are strains of Chlamydia, Coxiella, Francisella, Legionella, Mycobacterium, Salmonella and Yersinia. Iron deficiency of macrophages of persons with hereditary hemochromatosis gene mutations may result in increased resistance to members of these bacterial pathogens."

Patients with hemochromatosis do have an increased risk for infection, although Vibrio and TB are the more commonly noted pathogens. Given the negative gram stain I was expecting a gram-negative organism because they are often not seen against the background of pink white cells; instead he grows S. sanguis from the joint only.

Mouth bugs get in the blood all the time, and most of the time they have nowhere to go. In this case they found the shoulder. Perhaps it is less the iron overload state and related to the arthropathy of hemachromatosis; bacteria love to go to damaged joints. Or his diabetes was the reason. The etiology of most diseases is multifactorial and rarely as simple as one would like, and it is made more difficult by looking for iron under 'Fe.' I have the same issue with sodium (Na), gold (Au), potassium (K) and silver (Ag). Can't ever find them in the dictionary.

He was debrided and will get a course of antibiotics.

Rationalization

J Clin Gastroenterol. 2009 Oct;43(9):890-3. Hemochromatosis and Vibrio vulnificus wound infections. Barton JC, Acton RT.

Int J Infect Dis. 2007 Nov;11(6):482-7. Epub 2007 Jun 27. Association of hemochromatosis with infectious diseases: expanding spectrum. Khan FA, Fisher MA, Khakoo RA.

Nutrition. 2007 Jul-Aug;23(7-8):603-14. Epub 2007 Jun 20. Nutritional iron deficiency: an evolutionary perspective. Denic S, Agarwal MM.

Biometals. 2004 Apr;17(2):135-9. Hemochromatosis and the enigma of misplaced iron: implications for infectious disease and survival. Moalem S, Weinberg ED, Percy ME.

Postscript

That’s it. Another year of bugs and drugs. You can read my continuing adventures as a Puswhisperer in real time over at Medscape.

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