PJ Party

Sep 7, 2016

The patient is admitted with a three-week history of fatigue and shortness of breath on exertion.

CXR shows bilateral infiltrates.

She has a long history of HIV but, for a variety of social reasons, has not been on ART and the CD4’s are now less than 50.

PJP and CAP therapy are started, and she gets a bronchoscopy: all negative, including the PJP DFA.

So the antibiotics are simplified to CAP therapy (ceftriaxone and doxycycline), and the patient worsens, so they call me.

Of course, they want to "broaden coverage" to vancomycin and zosin. Why? Because that is what is done, despite an extensive workup that fails to find a process or a culture that would be amenable to vancomycin or zosin. The response is always broader coverage. Not make a diagnosis or control the source or realize it is the natural history of the process. Nope. Broaden coverage.

Other labs of note: the LDH is in the mid 300’s and the 1–3-beta-D-glucan is off the wall positive, which they were crediting perhaps to the zosin.

I asked the patient about fungal risks, and outside of a childhood in the Midwest, nothing.

I figured this had to be PJP. With that LDH, that beta-d-glucan, combined with the CXR and that clinical presentation, really, what else could it be? Histoplasmosis? Perhaps. Lymphoma? Maybe.

So I called the lab. This has to be PJP. Could you take another look-see at the DFA?

They did.

And it was.

That is the advantage of being old, er, I mean experienced. I have far too many false-negative PJP tests from back in the day.

My dad told me many years ago that when the tests do not support the clinical diagnosis, the tests are wrong. Not always true, of course, but a good rule of thumb.

Part of the reason she decompensated was probably rebound from stopping the steroids, and she was markedly better back on prednisone.

Except.

In 48 hours, her platelets fell from 215 to < 5. Whoa.

I tend to think of marrow suppression from antibiotics as a non-specific finding that is slow to occur and usually think of hapten mediated disease from drugs or HIV when platelets fall precipitously.

She is fairly malnourished, so I wonder if this is due to trimethoprim exacerbating a folate deficiency?

Two patients had severe thrombocytopenia while taking trimethoprim-sulfamethoxazole. The mechanism is uncertain but probably is related to drug interference with folate metabolism. Recovery can usually be expected upon withdrawal of the medication and institution of folic acid therapy.

Folate levels are pending.

Rationalization

Clin Microbiol Infect. 2015 Apr;21(4):379.e1–10. doi: 10.1016/j.cmi.2014.11.025. Epub 2014 Dec 4. Diagnosis of Pneumocystis pneumonia: evaluation of four serologic biomarkers.

http://www.ncbi.nlm.nih.gov/pubmed/25630458

J Clin Microbiol. 2011 May;49(5):1872–8. doi: 10.1128/JCM.02390–10. Epub 2011 Mar 2. Multicenter, prospective clinical evaluation of respiratory samples from subjects at risk for Pneumocystis jirovecii infection by use of a commercial real-time PCR assay.

http://www.ncbi.nlm.nih.gov/pubmed/21367988

South Med J. 1983 Apr;76(4):503. Thrombocytopenia secondary to trimethoprim-sulfamethoxazole.

http://www.ncbi.nlm.nih.gov/pubmed/6836368

A Medical-Skeptical Classic.

https://www.sciencebasedmedicine.org/a-medical-skeptical-classic/

POLL RESULTS

When in doubt

• broaden coverage 8%
• change to a new antibiotic 2%
• give a big gun, strong, powerful antibiotic 8%
• do random stuff because Dunning-Kruger Rules 23%
• Google it 46%
• Other Answers 13%
• Get an ID consult.
• think real hard, try to remember what you were supposed to learn in ID class, then call Dr. Crislip and prepare to be humble.
• reconsider diagnosis

I Wish the Monkey Preferred Bananas

Sep 12, 2016

I am glad I am not an addict. Well, a drug addict. I have enough trouble resisting ice cream and maple bars. I cannot imagine having the monkey on my back of heroin, cocaine, or tobacco.

So I have mostly pity for those that cannot kick a habit even as they know it is destroying their lives. There but for the grace Flying Spaghetti Monster and all that.

The patient is a heroin user. First, he gets tricuspid valve endocarditis with MRSA.

He keeps using and develops an Enterobacter in his blood.

Repeat cultures are negative, so maybe, hopefully, it is a transient bacteremia from the water or heroin. But it is treated.

But the call of heroin is too much, and he continues to use.

Now there is a yeast in the blood, a new vegetation on the tricuspid valve, and the yeast is identified as C. dubliniensis.

Great.

I have seen a smattering of C. albicans tricuspid valve endocarditis as a complication of central lines. It is a known nosocomial complication:

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.

I have even cured a pair of Candida endocarditis over the years in patients whom/who were deemed too high risk to take to the OR. But I do not remember seeing a case of C. dubliniensis fungemia.

Although perhaps I have as in the old days, it was misidentified as C. albicans about 2% of the time. Still not that common.

In all, 368 isolates were identified as C. dubliniensis; 67.1% came from respiratory specimens, 11.7% from oral swabs, 9.2% from urine, 3.8% from blood, 2.7% from vaginal swabs and 5.4% from other sources.

If you are interested, C. dubliniensis is germ tube positive but, unlike other Candida, cannot grow at 42 C, which is 111.2 F. Do not think I will recommend fever therapy. And why would a Candida need to be able to grow at 111.2? Preparing for global warming?

There are a smattering of diseases due to C. dubliniensis, including a few endocarditides in the Pubmeds, but if you extrapolate from C. albicans, I would imagine the outcome is grim. Of course, the surgeons are not enthusiastic about replacing the valve.

He responded to amphotericin B , and if he can get drug treatment, always difficult when you are unemployed, homeless, and uninsured, then just maybe…

I just keep thinking that dead people can’t turn their lives around.

In the end, he left AMA never to be seen again.

Rationalization

Non-albicans Candida spp. causing fungaemia: pathogenicity and antifungal resistance.

http://www.sciencedirect.com/science/article/pii/S019567010191151X

Clin Cardiol. 2009 Dec;32(12):E48–54. doi: 10.1002/clc.20498. Endocarditis complicating central venous catheter bloodstream infections: a unique form of health care associated endocarditis.

http://www.ncbi.nlm.nih.gov/pubmed/20014189

PLoS One. 2012;7(3):e32952. doi: 10.1371/journal.pone.0032952. Epub 2012 Mar 2. Candida dubliniensis: an appraisal of its clinical significance as a bloodstream pathogen.

http://www.ncbi.nlm.nih.gov/pubmed/22396802

POLL RESULTS

The monkey on my back is

• Peter Tork. Don't ask. 29%
• fried batter of any kind 29%
• The Great British Baking Show 13%
• a literal monkey. I have become an organ grinder in lieu of participating in the ABIM MOC 4%
• a new tat. Better than a wing tattoo. 4%
• Other Answers 21%
• Mathematics. And the tolerance curve is exponential.
• Chocolate
• Chap stick. Just can't break that habit.
• reality.
• Scotch

What To Do

Sep 14, 2016

To treat, or not to treat- that is the question:

Whether ’tis nobler in the hospital to suffer

The slings and arrows of outrageous po antibiotics

Or to use IV against a sea of MRSA,

And by opposing end them.

S. aureus pays my mortgage. It is probably the most common organism for which I get a consult and often the most difficult to treat correctly. Sometimes the issues are susceptibilities, but more often, the issues are psychosocial.

The patient is a recalcitrant heroin user admitted to the hospital 6 weeks ago with MRSA in the blood, 2 sets drawn 5 minutes apart.

He received antibiotics, and the fever disappeared immediately. Repeat BC were negative, as was the TTE. He did have what was thought to be a leg cellulitis. I never saw it as it was at Outside Hospital.

Still, there are two reasons to treat S. aureus bacteremia (SAB): treat the infection and treat any potential metastatic focus such as an occult endocarditis or osteomyelitis. No surprise that S. aureus worships the supernatural.

S. aureus, unlike most other organisms, has a nasty predilection for causing metastatic foci, and that is the reason SAB gets 2–4–6 weeks of iv antibiotics, depending on the clinical scenario. Although it is the minority of patients who have a complication of their uncomplicated SAB, it is a large minority, which is why the guidelines suggest

For adults with uncomplicated bacteremia(defined as patients with positive blood culture results and the following: exclusion of endocarditis; no implanted prostheses; follow-up blood cultures performed on specimens obtained 2–4 days after the initial set that do not grow MRSA; defervescence within 72 h of initiating effective therapy; and no evidence of metastatic sites of infection), vancomycin (A-II) or daptomycin 6 mg/kg/dose IV once daily (AI) for at least 2 weeks. For complicated bacteremia (defined as patients with positive blood culture results who do not meet criteria for uncomplicated bacteremia), 4–6 weeks of therapy is recommended, depending on the extent of infection.

It had been decided to treat this patient with 4 weeks, but after 3 days, he left against medical advice. He returned briefly two weeks later and had negative blood cultures and again left after two days of antibiotics.

And now, he has returned again, and I was consulted with the question as to whether or not to continue his therapy.

It was an uncomplicated bacteremia, and he has done clinically well, and he has not been adherent with the compliance of his treatment plan. Or is it compliant with his adherence? I am slow with the new nomenclature.

Oral antibiotics? Don’t like to do it, but there is are studies that support oral treatment of SAB.

Patients were included if cultures showed the presence of bacteremia or deep-seated infections with Staphylococcus aureus (104 patients)…an oral regimen containing a fluoroquinolone plus rifampicin may be effective for treating staphylococcal infections,

As if there are any quinolone susceptible MRSA anymore. Linezolid?

Linezolid was associated with outcomes that were not inferior to those of vancomycin in patients with secondary S. aureus bacteraemia.

Giving homeless, uninsured heroin addicts expensive, or even cheap, oral therapy is just setting them up for failure. At least I know if they are getting their iv antibiotics. Assuming they followup and don’t disappear with a picc or use it to shoot up. It’s happened.

I decided that the proof is in the pudding that he was asymptomatic for 6 weeks for any recurrent or metastatic infection and needed no further antibiotics.

And as I was finishing my dictation, he left against medical advice again. All the Hamlet-like hand wringing and the decision was made for me.

Rationalization

Clinical Practice Guidelines by the Infectious Diseases Society of America for the Treatment of Methicillin-Resistant Staphylococcus aureus Infections in Adults and Children.

http://cid.oxfordjournals.org/content/52/3/e18.full

A Randomized Clinical Trial to Compare Fleroxacin-Rifampicin with Flucloxacillin or Vancomycin for the Treatment of Staphylococcal Infection.

http://cid.oxfordjournals.org/content/39/9/1285.short

Linezolid versus vancomycin for Staphylococcus aureus bacteraemia: pooled analysis of randomized studies.

http://jac.oxfordjournals.org/content/56/5/923.full

Absolut Dunning–Kruger

Sep 19, 2016

It is a sign of advancing age that issues that used to not bother me in my youth really gripes my cookies these days. I have less tolerance because, as I have noted before, it has never been easier to find the answer to any question.

Does anyone note the year? 2016? And that there is this thing called the internet with Google and PubMed? And pagers? And cell phones? It is so easy to get the right information so that patients get the correct care. And do people bother?

Doesn’t appear to the case.

This will perhaps be a surprise to large swaths of the medical community, but there is more to infectious diseases that picking an antibiotic off the culture and susceptibility report. The name of the beast, like S. aureus, has implications. It has implications for the cause of the infection or the appropriate therapy or both.

Hell, I don’t think I could remove a gallbladder, treat breast cancer, deliver a baby, or dialyze a patient. But everyone who can log on to the computer thinks they know what they are doing when it comes to treating infections. Oh, look, the Enterococcus in all those blood cultures is sensitive to vancomycin, here is a po prescription. Been there, seen that.

Dunning-Kruger rules:

The Dunning–Kruger effect is a cognitive bias in which low-ability individuals suffer from illusory superiority, mistakenly assessing their ability as much higher than it really is…

Here are some pearls for that, if taken to heart, may prevent your ID doc from rolling her eyes as she reads the chart AND improves patient care. While rules are made to be broken, it is just not to be broken by you.

Never. Ever. Never. Ever treat S. aureus in the blood culture as a contaminant. That’s a big never with a side of ever. Even if ‘just’ one bottle is positive. For S. aureus, there is no ‘just.’

Never. Ever. Never. Ever treat S. aureus bacteremia with oral antibiotics. Note the never here is cleverly combined with the ever to give a sense of an absolute.

Only treat MSSA with anti-staphylococcal beta-lactams. The top 10 treatment options are cefazolin, oxacillin, cefazolin, oxacillin, cefazolin, oxacillin, cefazolin, oxacillin, cefazolin, or oxacillin. On rare occasions, you can give cefazolin or oxacillin. Cephalexin is the oral option.

If you prefer a 'Never. Ever. Never. Ever' to an 'only': Never. Ever. Never. Ever use vancomycin, tmp/sulfa, clindamycin, doxycycline, or a quinolone to treat MSSA. They lead to markedly inferior outcomes. Allergies, notwithstanding, of course, although most of the alleged beta-lactam allergies aren’t if you take a careful history.

For MRSA? All options stink on ice. But for bloodstream infections? Never. Ever. Never. Ever use TMP/sulfa, clindamycin (the beloved choice of surgical house-staff), doxycycline, or a quinolone. Yes, I know there is a big ’S’ next to the antibiotic. Sometimes it stands for ‘Sucks.’

Education, like the above, is obviously not the solution as this is not new information. UpToDate should be called NeverReadByMe. While medical information is easily available on the net if you search, it is not to be found on pages concerning what the cast of MASH looks like now. Boy, will you be shocked at #5.

I think the solution lies in the EMR. First, for MSSA, all antibiotic choices need to be suppressed except for cefazolin. The second is if a provider tries to give any of the Never Evers, the keyboard delivers a painful shock to the prescriber.

Me bitter much? But I suffer from the second half of Dunning-Kruger:

Their research also suggests corollaries: high-ability individuals may underestimate their relative competence and may erroneously assume that tasks which are easy for them are also easy for others.

Got No Idea

Sep 21, 2016

I assume everyone has different goals that drive their medical career. Me? I like to understand my patients disease, and I require intellectual novelty. I get bored really easily, and it makes me glad that humans are not telepathic. If my mind could be read as some people drone on and on…

Some cases I just can’t figure out, and I take it personally. It is the job of an internist to make a diagnosis after all. Most of the time, patients get better with no diagnosis, but I really hate the occasional death with no unifying diagnosis.

Sometimes all the parts are there, but I just can’t coherently arrange them, a jigsaw puzzle with random pieces.

The patient comes in with a rapidly progressive lower extremity cellulitis after missing a vein in the foot injecting heroin. She is otherwise normal.

While it was the foot that had the trauma, the foot it spared. The infection started mid-calf, where she doesn’t inject and spread up to the thigh.

She had a cough and chest pain, and the lung CT shows classic septic emboli, TNTWTC (too numerous to want to count) peripheral cavitating abscesses.

She starts developing a clinical compartment syndrome and goes to the OR. No necrotizing infection, just lots of edema.

Here is where it gets annoying.

The blood cultures grow S. anginosus, of which I can find no cases infecting the right side of the heart. S. viridans endocarditis can occur on the right side of the heart, but it is very rare. I have seen one I can remember in 30 plus years, and we know how good my memory is.

And the TEE confirms it: the valves are pristine, and no shunt.

And the cultures of the leg have heavy growth of Fusobacterium necrophorum. She is a needle licker, so ok.

Fusobacterium does cause head and neck infections, soft tissue infections, and Lemierre’s syndrome, but there are no cases of deep extremity infections I can find in adults, just a few in captive wallabies. Yes, you read that right.

With that CT and the Fusobacterium in the leg, we went looking for infected clot and found none. Not in the legs, not in the abdomen, not in the head and neck.

Maybe there had been a clot in the leg, and it disintegrated like the asteroid in Armageddon, with similar results. I have no medical iridium layer with which to prove an asteroid hit. But then why no Fusobacterium in the blood cultures? And S. anginosus as a cause of septic thrombophlebitis is also rare.

I like to say that your spouse lies, your kids lie, politicians lie, the government lies, but the cultures always tell the truth if you understand what they are saying. I need a Rosetta stone for this one.

So annoying. But at least she is getting better.

Rationalization

J Pediatr Surg. 1998 Aug;33(8):1279–82. Superficial suppurative thrombophlebitis in children, caused by anaerobic bacteria.

http://www.ncbi.nlm.nih.gov/pubmed/9722004

Res Vet Sci. 1984 May;36(3):382–4. Aetiological agents of necrobacillosis in captive wallabies.

http://www.ncbi.nlm.nih.gov/pubmed/6463385

Ann Acad Med Singapore. 2013 Jan;42(1):52–4. Lemierre’s syndrome: an unusual cause of calf abscess.

http://www.annals.edu.sg/pdf/42VolNo1Jan2013/V42N1p52.pdf

Got No Idea

Sep 27, 2016

When you have been in medicine for three decades, you can remember how things were back in the day and compare them with how things are today, and marvel at the advances. And then proceed to bore almost to death some helpless intern who cannot escape. I am the Grandpa Simpson of my hospital and damn proud of it.

Two diseases with which we have made little progress and still give me conniptions are TB and Lues.

There are a fair number of people, often older, who have latent TB as judged by an IGRA and who need biologics of one sort or another, and as a result, they have

an increased risk of TB reactivation (OR 4.68, 95% CI 1.18 to 18.60; NNTH = 681, 95% CI 143 to 14706) compared to control.

But then they do not tolerate INH in any of its dosings. So the options are rifampin or rifampin/PZA, but the latter has increased hepatitis.

The problem is that we do not know which patient with a positive IGRA has latent bacilli and which have cleared the organism. It would sure be nice to know, although it is probably most who harbor viable bacilli. Looking at tissues with PCR from 49 people with latent TB who died of something other than TB

Lung specimens from most subjects (36) were positive for M. tuberculosis, as were specimens from the spleen (from 35 subjects), kidney (from 34), and liver (from 33).

Unlike love, TB is forever. And like a psycho ex, you never know if it will return to ruin your day.

And syphilis? Don't get me started on syphilis. We have been plagued by the organism for 500 years, and we still cannot tell if the infection is gone after treatment.

Besides the ongoing problem of uveitis and other eye problems in FTA positive/RPR negative patients, which I have bloviated about before, there is the serofast state.

I saw a patient whose RPR went from 1:256 to 1:32 after 2 courses of therapy (one PCN, the other doxycycline, both at Outside Hospital) and there it has remained at 1:32 for 2 years despite the 2 courses of therapy and no risks for reacquisition.

A continuing challenge to determining the response to treatment of early syphilis is exemplified by the substantial proportion of patients who fail to achieve serological cure and remain serofast, defined as a <4 data-preserve-html-node="true"-fold (2 dilution) decline in nontreponemal antibody titers at 6_x0013_12 months or as persistently low titers after treatment.

Tell me about it. It was a 4 fold drop, so it was a cure, right? While you can tell the patient they are a likely cure, their partner is not always so sanguine. The blood test is still positive, after all. I always like it when the patient or family looks at me with an expression that suggests I am a total idjet.

I suggested another course of benzathine for late latent, but I am not optimistic the RPR will improve:

Despite retreatment with 2.4 million units benzathine PCN, 73% of patients with early syphilis who failed to achieve serological cure at 6 months after initial therapy remained serofast at 12 months. Patients with early syphilis who had higher nontreponemal titers at baseline and at 6 months (e1:32) were more likely to exhibit serological cure after retreatment than those with lower titers.

Like latent TB, it should would sure be nice if, after all these years, we could say for sure that the syphilis is dead and gone.

Two diseases that need some improved diagnostics. Maybe at a clinic in Shelbyville?

Rationalization

The Simpsons - Grandpa Simpsons I had an onion on my belt

https://www.youtube.com/watch?v=-o\_x0013\_7MmhqNfA"

Cochrane Database Syst Rev. 2011 Feb 16;(2):CD008794. doi: 10.1002/14651858.CD008794.pub2. Adverse effects of biologics: a network meta-analysis and Cochrane overview. http://www.ncbi.nlm.nih.gov/pubmed/21328309

Latent Mycobacterium tuberculosis Infection

http://www.nejm.org/doi/full/10.1056/NEJMra1405427 J Infect Dis. 2012 Oct;206(8):1194_x0013_205. Epub 2012 Jun 25. Extrapulmonary locations of mycobacterium tuberculosis DNA during latent infection.

http://www.ncbi.nlm.nih.gov/pubmed/22732919

Discordant.

http://boards.medscape.com/forums/?128@@.2a7cadca!comment=1

Clin Infect Dis. 2013 Feb 1; 56(3): 420_x0013_422. Published online 2012 Nov 1. doi: 10.1093/cid/cis918 Response to Therapy Following Retreatment of Serofast Early Syphilis Patients With Benzathine Penicillin

https://pubmed.ncbi.nlm.nih.gov/23118269/

POLL RESULTS

The disease that gives me the most grief is

• lues 4%
• tb 8%
• life. And Cobra is the cure 28%
• all non-infectious diseases 16%
• stickittothemaneosis 32%
• Other Answers 12%
• the flux.
• trumpamania
• stupid.

Relapsing Price Gouging

Sep 28, 2016

The patient has had four identical 3 day long illnesses separated by about a week of feeling fine.

Each episode had a fever, headache, myalgias, and severe malaise.

Workup was negative, but each evaluation was at the tail end of the three days.

Years ago, I had a patient with an identical syndrome, and I asked her, “How was your vacation at Black Butte”?

The look of shock on her face as she asked how I knew she had been at Black Butte was priceless.

The pattern of the disease is a relapsing fever, and in Oregon, it is Black Butte that has all the Borellia, the cause of relapsing fever, in the state. It is one of those factoids known to ID docs but few others.

Exposure sites were in forested areas, at varying elevations, in mountainous regions (Cascade, Rocky Mountain, San Bernardino, and Sierra Nevada ranges) of the United States and Canada and in limestone caves in central Texas. Only 13 counties accounted for approximately 50% of all cases.

Look at the map in the third reference to see if you are at risk and note the dark blotch in Oregon. That’s Black Butte. Gorgeous county for hiking and golf, we vacation nearby every summer. I have also seen cases from the smudge in Eastern Washington, where Spokane is.

It turns out the patient lives in Black Butte, is an avid outdoorsman, and usually comes home covered in ticks.

Ick.

I asked the lab to look at a prior CBC for spirochetes, but it was negative, probably as it was done on the last day of the illness. I wonder if we are missing the disease. I think I have seen fewer cases since the computer took over all the CBC’s and algorithms determine who gets a manual differential. It used to be the hematology tech who made the diagnosis when they looked at the slide for the differential.

I suppose I could wait for one more relapse but opted for a course of doxycycline.

His primary care physician had also recognized the pattern had given him a prescription for tetracycline.

$600.

Yep. You read that right. Six. Hundred. Dollars.

That didn’t seem right a medication that is not just generic, it's geriatric, about to reach its 70th birthday, although I always give doxycycline, so it is not like I am in the loop with this antibiotic.

I checked with the clinic pharmacist, who said that after tetracycline returned after a period of shortage, the price went up. Way up. As in, let's really make people hurt up.

I am all for a good profit but

tetracycline antibiotic…the cost increases not only exceeded 1,000% but topped 17,000%

is ridiculous.

The modern career arc: they start as Wells Fargo Account Managers. When all moral/ethical barriers are exhausted to pursue profit, move on to the pharmaceutical industry.

Rationalization

West J Med. 1980 Sep;133(3):203–9. Tick-borne relapsing fever in the Pacific Northwest: an underdiagnosed illness.

https://www.ncbi.nlm.nih.gov/pubmed/7415171

How Much? Some Generic Drug Prices Are Skyrocketing: Analysis

https://www.wsj.com/articles/BL-270B-469

The epidemiology of tick-borne relapsing fever in the united states

http://www.ajtmh.org/content/journals/10.4269/ajtmh.2002.66.753

Cluster Fungus

Oct 3, 2016

The last six weeks have seen 4 primary Cryptococcal pneumonias. Weird. I thought events came in three, not four.

The rule of three or power of three is a writing principle that suggests that things that come in threes are funnier, more satisfying, or more effective than other numbers of things.

You know what those Latins used to say:

Omne trium perfectum (everything that comes in threes is perfect).

Well, not celebrity deaths or infections.

2 were made after a biopsy for a hot lung lesion on PET, which is perhaps the most common way I get a referral for Cryptococcus. PET scans pick up a whole lot more than cancer.

All had some immune-suppressing disease or medication, positive serum antigens, and negative CSF antigens. So they are all going to get a course of fluconazole, a more straightforward issue than Cryptococcus in the normal host.

It is odd to see a cluster of Cryptococcus, and none of my partners have seen a blip. So perhaps a fluke.

Or not. Summertime, when it is dry and dusty, is when you find Cryptococcus in the air of the Great Pacific NW.

air samples were more likely to be a higher concentration in the summer than in the winter

So the timing is right. Likely another infection that is spreading/changing as a result of warming, and it was a warm, dry summer.

Although, with its propensity to be found on Douglas Firs, I still expect a post-Christmas outbreak one of these years.

Rationalization

Int J Infect Dis. 2014 Jan;18:101_x0013_3. doi: 10.1016/j.ijid.2013.08.009. Epub 2013 Sep 25. Pulmonary cryptococcosis and cryptococcal osteomyelitis mimicking primary and metastatic lung cancer in (18)F-FDG PET/CT.

https://pubmed.ncbi.nlm.nih.gov/24129292/

Pulmonary Cryptococcosis in the Immunocompetent PatientMany Questions, Some Answers. http://ofid.oxfordjournals.org/content/3/3/ofw167.full

Cryptococcus gattii, a tropical pathogen emerging in a temperate climate zone.

https://ams.confex.com/ams/AFAPURBBIO/techprogram/paper\_80027.htm

POLL RESULTS

What comes in perfect three's

• Hear no evil, speak no evil, see no evil
• 23%
• Lillard against Houston 0%
• Green Day 3%
• rock, paper, scissors 35%
• blind mice 35%
• Other Answers 3%
• Sneezes. Bad haircuts. Good neighbors.

Old Drugs Return

Oct 5, 2016

A couple of years back, I came across an antibiogram from 1990, my first year in practice. No MRSA. No VRE. No ESBL. No CRE. No LSMFT. An ID Garden of Eden with no antibiotic resistance. Few know that the infamous apple had also been sprayed with streptomycin and oxytetracycline, leading to the first resistant bacteria. There is such a thing as an original sin.

The Borg had it wrong; resistance is inevitable, and between severe allergies and antibiotic resistance, about the only way I have to kill some infections is to autoclave the patient, an intervention that, for some odd reason, they resist.

The patient has renal stones, a stent, an ESBL, anaphylaxis to beta-lactams, and medicare, aka no home antibiotic coverage.

She has been on nitrofurantoin suppression for several years (not by me) and now has a burning feeling in her fingertips and lips.

So add neuropathy from nitrofurantoin (not forgotten by me) to the list of adverse drug reactions.

But what to treat her cystitis/pyelonephritis with? There are two options for oral therapy. I opted for fosfomycin, a drug so old it comes on sachets, I imagine like the gold bubble gum I had as a kid. But with little recent use, there is also little resistance. For now.

An extended-spectrum β-lactamase–producing E. coli clinical strain identified in Pennsylvania, USA, showed high-level fosfomycin resistance caused by the fosA3 gene. The IncFII plasmid carrying this gene had a structure similar to those found in China, where fosfomycin resistance is commonly described.

Prolonged fosfomycin has been used for prostatitis, so until the stent comes out in a couple of weeks, it is fosfomycin or nursing home for iv therapy.

The other oral option? Cycloserine, but I have yet to give it a try.

Cycloserine is still licensed in some countries for the treatment of urinary infections. The data presented here suggest that it may play a role in the management of infections resistant to trimethoprim and third-generation cephalosporins.

There is not much to miss about the ’80s except those were the days we could still easily kill bacteria. We will never see its like again.

Rationalization

Obstet Gynecol. 2007 Aug;110(2 Pt 2):510–2. Nitrofurantoin neuropathy: a forgotten adverse effect.

https://www.ncbi.nlm.nih.gov/pubmed/17666646

Fosfomycin Resistance in Escherichia coli, Pennsylvania, USA.

http://wwwnc.cdc.gov/eid/article/21/11/15–0750\_article

Experience with Fosfomycin for Treatment of Urinary Tract Infections Due to Multidrug-Resistant Organisms.

http://aac.asm.org/content/56/11/5744.full

Chemioterapia. 1988 Apr;7(2):96–100. Fosfomycin versus ampicillin in the treatment of acute pyelonephritis.

https://www.ncbi.nlm.nih.gov/pubmed/3396118

Clin Infect Dis. 2015 Oct 1;61(7):1141–3. doi: 10.1093/cid/civ436. Epub 2015 Jun 10. Fosfomycin for Treatment of Prostatitis: New Tricks for Old Dogs.

https://www.ncbi.nlm.nih.gov/pubmed/26063723

Eur J Clin Microbiol Infect Dis. 2014 Jul;33(7):1169–72. doi: 10.1007/s10096–014–2051–9. Epub 2014 Jan 29. Cycloserine as an alternative urinary tract infection therapy: susceptibilities of 500 urinary pathogens to standard and alternative therapy antimicrobials.

https://www.ncbi.nlm.nih.gov/pubmed/24474246

Sequestration

Oct 10, 2016

I got a page to see a consult, and yes, I still use a pager. I can turn my pager off for the weekend, but I can't turn my cell phone off, and the last thing you want is for people to get in the habit of calling your cell. I was asked to see a patient with a lung sequestration.

I looked at the message and thought, what? A sequestration? Of the lung? Huh? A sequestration is a piece of dead infected bone in osteomyelitis.

So I went and saw the patient, who had been ill with fevers and pleuritic chest pain for about a month, but no shortness of breath and no productive cough. No other medical problems.

The next step was radiology to look at the CT with the radiologist. And then I understood.

On the CT was a round consolidation. It was a congenital extra lobe of lung not connected to the airway, and with its own blood supply, an artery you could see coming off the aorta.

Since it does not connect to the airway, it is a permanently atelectatic piece of lung, and if it gets infected, there is no way to cough up the pus.

Pulmonary sequestration are rare and usually a problem in pediatrics. There are two forms:

Intralobar sequestration (ILS) in which the lesion is located within a normal lobe and lacks its own visceral pleura.

Extralobar sequestration (ELS) in which the mass is located outside the normal lung and has its own visceral pleura

My patient's sequestration was extralobar.

But how do they get infected? It is suggested that bacteria migrate through the pores of Kohn, which I also had never heard of or have forgotten since medical school. Pores of Kohn, in case your knowledge of histology is as poor as mine, are discrete holes in walls of adjacent alveoli that allow spread of air and bacteria.

Or perhaps by way of the canals of Lambert.

Intralobar sequestration theories debate in defining the disease as either a congenital or acquired condition. Theories of the acquired aetiology state that chronic pulmonary infections of a lung tissue disconnected from the normal bronchial tree can cause hypertrophy of a regional systemic artery, hence the aberrant arterial supply. Despite being separated from the bronchopulmonary tree, infections may spread to the sequestered segment from adjacent aerated lung tissue via accessory inter-alveolar or broncho-alveolar connections, e.g. pores of Kohn, and canals of Lambert.

No way. That suggests bacteria get into the lower airway, don’t cause an infection, but then move into the sequestration by way of the pores and canals.

Maybe for infected intralobar sequestration, but I bet the source is hematogenous for extralobar sequestration infection.

Annoyingly for an ID doctor, none of the reviews mention the microbiology, and the case reports are odd organisms: Aspergillus and MTb.

On antibiotics, the fevers went away, and it was resected without incident.

Cultures were negative. Meh.

Rationalization

Int J Clin Exp Med. 2015 Nov 15;8(11):21822–5. eCollection 2015. Pulmonary sequestration: a case report and literature review.

https://www.ncbi.nlm.nih.gov/pubmed/26885149

J Clin Diagn Res. 2015 Dec;9(12):AC05–8. doi: 10.7860/JCDR/2015/16004.7006. Epub 2015 Dec 1. Pulmonary Sequestration: A 29 Patient Case Series and Review.

https://www.ncbi.nlm.nih.gov/pubmed/26816878

Odd Nodes

Oct 12, 2016

It is interesting noticing bias bubble to the top. We all have subconscious shortcuts that allow us to make judgments, sometimes good, sometimes bad, with inadequate information. I hope my time in the skeptical world has made me more self-aware of my biases, and sometimes they jump right in my face.

There is a measure on the Oregon ballot this November to tax some corporations. I have not paid a lot of attention yet as it will be a while before I have to cast my vote, but there have been numerous ads on TV, and last night they had back to back pro/con ads.

The first was a local microbrewer who was in favor of the tax. A beer maker likes it? It must be good. Next, there was a doctor, a past president of the Oregon Medical Association in a white coat, stethoscope wrapped around his neck. And I immediately thought, if the past President of the OMA is against it, it must be a good bill. I am viscerally against anything organized money medicine favors. And anytime a Doctor wraps themselves in medical authority to shill for non-medical issues, like cigarettes or taxes, they have to be in the wrong. I have no trust in any of my representative medical organizations except to trust they will do the wrong thing.

But you can trust me; I’m a doctor.

The patient is a 26-year-old female who has two weeks of sore throat, fevers to 104, and massive bilateral cervical lymphadenopathy.

Work up is negative: CBC and LFTs are normal, no CMV, toxoplasma, or EBV, but the CRAP is 120. A CT is worrisome for lymphoma, so one node is removed, and it shows necrotizing granuloma. AFB and fungal stains are negative. She is sent to me.

In ID, you get what you are exposed to, so I take a history looking for causes of granulomatous necrotizing lymphadenitis.

The biggest problem with the Great Pacific NW, besides doctors doing ads against corporate taxes, is there are few interesting infections.

A barista in Portland, she has been nowhere and done nothing to be exposed to TB and the barest of exposures to cats (Bartonella), sheep (Q fever), and Histoplasma (a trip to Montana).

And workup is negative for the above and more—nothing to suggest sarcoid or lupus, two non-ID causes of that pathology.

So I suspect this is my first case of Kikuchi’s, an idiopathic cause of histiocytic necrotizing lymphadenitis that usually goes away its own.

It is a rare disease, occurs more often in young women, and is a diagnosis of exclusion. But it fits, and she should get better with time. She did. There are case reports of treating with steroids and IVIG, but causality is always suspect in a self-limited disease.

And I wonder what part of my brain information about that disease had settled in; I doubt I have read about Kikuchi's in years. Weird how sometimes the oddest things will pop out of memory, and yet I can struggle to remember the word "fissure" when discussing a chest CT today.

Stupid brain.

Rationalization

Granulomatous Lymphadenitis as a Manifestation of Q Fever. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2873736/

Systemic lupus erythematosus and granulomatous lymphadenopathy. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3827830/

Histoplasmosis in Idaho and Montana, USA, 2012–2013.

http://wwwnc.cdc.gov/eid/article/21/6/14–1367\_article

Kikuchi-Fujimoto disease.

https://ojrd.biomedcentral.com/articles/10.1186/1750-1172-1-18

POLL RESULTS

I automatically mistrust

• my state medical association 3%
• the AMA 28%
• the ABIM 9%
• RNC 31%
• DNC 9%
• Other Answers 19%
• My judgment
• anyone who says, "trust me."
• the IRS
• my own better judgment.
• Anyone over 30. Oh wait; I'd better update that to anyone over 50.

Not a fan of going negative

Oct 17, 2016

The patient is a young middle-class female, no medical problems, no risk factors for infections, no nothing.

She has the abrupt onset of progressive hip pain but no fevers, chills, or other signs of infection.

A tap shows 82,000 WBC, all neutrophils, and crystal negative.

So a septic hip, right?

But after 5 days the cultures are negative.

I always figure that the whole purpose of white cells is to kill bacteria, so I expect negative cultures. But I am not a fan. Not a fan of not knowing what I am killing. Not a fan of no explanation for the infection. Not a fan of having to choose best guess for antibiotics.

Patients with and without an identified infectious agent have similar demographic, clinical, laboratory and radiographic characteristics.

But what is?

There are a few series using 16S of culture-negative arthritis.

Kids? Yep. Evidently, kids get a lot of Kingella infections.

Dogs? Yep.

Adult native joints? They found a hodgepodge of bacteria:

Our molecular method identified a broad spectrum of pathogenic bacteria including Staphylococcus aureus, Streptococcus pyogenes, Streptococcus agalactiae, Enterococcus faecalis, Salmonella enterica, Escherichia coli, Pseudomonas aeruginosa, and fastidious bacteria like Neisseria gonorrhoeae and Fusobacterium nucleatum.

And of course, all the one-off cases of weird bugs.

So not helpful. It could be anything, although if we dont grow S. aureus, I suspect S. aureus isn't there.

In PDX, the problem is 16S is it is a send out, and I will have an answer back on the last day of antibiotics. Anything with a 2-week turnaround is of little clinical utility.

Or maybe itis the first manifestation of a rheumatic disease:

At least 14% of patients diagnosed with septic arthritis with negative bacteriological results subsequently develop rheumatic disease. This pseudoseptic arthritis is indistinguishable from true septic arthritis.

I don't know. So for now, a course of cefazolin. And never did get a diagnosis.

Rationalization

Joint Bone Spine. 2012 Mar;79(2):156_x0013_9. doi: 10.1016/j.jbspin.2011.04.019. Epub 2011 Jul 5. Septic arthritis with negative bacteriological findings in adult native joints: a retrospective study of 74 cases.

https://www.ncbi.nlm.nih.gov/pubmed/21733734

Infection. 2014 Apr;42(2):385_x0013_91. doi: 10.1007/s15010_x0013_013_x0013_0567-z. Epub 2013 Dec 7. Septic arthritis: patients with or without isolated infectious agents have similar characteristics.

https://www.ncbi.nlm.nih.gov/pubmed/24318567

Aust Vet J. 2015 Jun;93(6):204_x0013_7. doi: 10.1111/avj.12329. Comparison of synovial fluid culture and 16S rRNA PCR in dogs with suspected septic arthritis.

https://www.ncbi.nlm.nih.gov/pubmed/26010926

J Clin Lab Anal. 2010;24(3):175_x0013_81. doi: 10.1002/jcla.20384. The usefulness of multiplex PCR for the identification of bacteria in joint infection.

https://www.ncbi.nlm.nih.gov/pubmed/20486199

J Infect. 2007 Dec;55(6):510_x0013_7. Epub 2007 Oct 29. Improved diagnosis specificity in bone and joint infections using molecular techniques.

https://www.ncbi.nlm.nih.gov/pubmed/18029022

POLL RESULTS

I hate negative

• cultures 11%
• politics 11%
• bank balances 36%
• temperatures 19%
• attitudes 14%
• Other Answers 8%
• Altitudes
• Donald Trump
• So that person that said "altitudes" is afraid of being high?

Increased Retention

Oct 20, 2016

The patients, pleural, plural, had a lap cholecystectomy 3 and 5 years ago, respectively.

Both did well.

Both presented this year with RUQ pain.

Both eventually had CT’s and both had thick-walled fluid collections in the RUQ, between the liver and diaphragm.

The five-year-old collections also had small calcifications. It was tapped and grew Lactobacillus.

The three-year-old collection had no stones that could be seen, and when tapped grew Klebsiella.

The first is definitely due to a retained stone, and I suspect it was the cause of the latter as well.

I have seen a smattering of infection from retained stones over the years; the last one was due to Actinomyces.

There are no reported cases of Lactobacillus and only two due to Klebsiella in the Pubmeds. What most of the case reports have in common is years between the dropped stone and the presentation of the abscess, often with a fistula.

I remember watching the Adams Family as a kid (the tv show, not the movie), and they had a character called Uncle Fester.

Fester. I did not think of what fester meant until years later in medical school.

These infections fester in humans and, of all things, prairie dogs.

Hopefully, the stones will come out with the drain, and antibiotics will sterilize the stones. If not, we will have to go in and remove them.

Rationalization

Stones Not Grass?

http://boards.medscape.com/forums?128@@.2a5d09c9!comment=1

World J Surg. 2005 Apr;29(4):437–40. Dropped gallstones during laparoscopic cholecystectomy: the consequences.

https://www.ncbi.nlm.nih.gov/pubmed/15770380

JSLS. 1998 Jul-Sep;2(3):263–8. The fate of retained gallstones following laparoscopic cholecystectomy in a prairie dog model.

https://www.ncbi.nlm.nih.gov/pubmed/9876751

Conflicts? Who Can tell.

Oct 31, 2016

I returned late last night from ID Weak thanks to a fuel spill on the runway. Worst conference ever. The only thing I will note is that it is nice that instead of old white men reading me PowerPoint slides in a monotone in overly air-conditioned rooms, now ow there are more diverse speakers reading me PowerPoint slides in a monotone in overly air-conditioned rooms.

Before I left, I received an invitation to a local grand rounds. The topic was dalbavancin and ceftaroline for soft tissue infections. And here I thought there was too much vancomycin/Zosin being used for cellulitis. Who the hell would use those drugs for soft tissue infections when all you need is cefazolin?

15% of cellulitis cases in which organisms are identified, most are due to ²-hemolytic Streptococcus and Staphylococcus aureus. There are no effective diagnostic modalities, and many clinical conditions appear similar. Treatment of primary and recurrent cellulitis should initially cover Streptococcus and methicillin-sensitive S. aureus, with expansion for methicillin-resistant S. aureus (MRSA) in cases of cellulitis associated with specific risk factors, such as athletes, children, men who have sex with men, prisoners, military recruits, residents of long-term care facilities, those with prior MRSA exposure, and intravenous drug users.

So I put the speaker's name into Dollars for Docs, a website that tracks how industry money is doled out to physicians.

413,057.

Dollars.

That's who gives those drugs for cellulitis.

It always annoys me when speakers flash their conflict of interest slides, often with a sneer as to the need.

But I want to know how much they made. Money always talks.

So for hoots and giggles, I entered the names of all the speakers (MD and US only) at the symposiums I went to at ID Weak.

For 46 speakers, the average payment was 15,936, but that was skewed by one who made $344,000 and another $123,000. 24 had zero. So some of us are really feeding at the trough.

Did I detect any bias as a result? I dont know. If it was there, it was hidden in the hypnotizing lectures. Hard to find bias in a gentle drone.

It is clear from the literature that there can be a malign effect of pharma money on both research and prescribing. It is equally clear that physicians deny they are affected. Some of this money is more legit: payment for expertise on vaccines or for other advice. Some, like being a peripatetic lecturer, perhaps not so much.

I do think that with all conflict slides, there needs to be a dollar amount for each entry and the reason: talks, research, or advisory.

Let me be the judge as to how conflicted the speaker may be.

Rationalization

JAMA. 2016 Jul 19;316(3):325_x0013_37. doi: 10.1001/jama.2016.8825. Cellulitis: A Review.

https://www.ncbi.nlm.nih.gov/pubmed/27434444

Following the Script: How Drug Reps Make Friends and Influence Doctors.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1876413/

The Influence of the Pharmaceutical Industry on Healthcare Practitioners Prescribing Habits.

http://ispub.com/IJAPA/7/1/10273

To Sell Their Drugs, Companies Increasingly Rely on Doctors. For $750 and Up, Physicians Tell Peers About Products; Talks Called Educational

http://www.wsj.com/articles/SB112138815452186385

The Drug Pushers. As America turns its health-care system over to the market, pharmaceutical reps are wielding more and more influence, and the line between them and doctors is beginning to blur

http://www.theatlantic.com/magazine/archive/2006/04/the-drug-pushers/304714/

POLL RESULTS

The soul has been sold when the take is more than

• $0 22%
• $100 22%
• $1000 11%
• $10,000 22%
• $100,000 11%
• Other Answers 11%
• the give
• today's price of a Forever stamp.

Good Bye Mr. Chips

Nov 2, 2016

The patient is an elderly male with 2-3 months of failure to thrive. No localizing symptoms, just the progressive blahs.

Eventually, he was sent in to see his MD, and one thing lead to another, and a huge liver abscess was found. It was about the size of a grapefruit. The lack of localizing symptoms sometimes amazes me, but as one review noted:

These abscesses are sometimes difficult to detect due to a difficult or non-existent symptomatology.

It was drained and had pure growth S. constellatus. The organism is part of the S. anginosus (formally known as S. milleri group) group (S. intermedius, S. anginosus, and S. constellatus). It is the Streptococcus that likes to form abscesses. However, it is less common with S. constellatus, with only 5 reported liver abscesses in the PubMeds.

What to do is simple enough. Drain and antibiotics. Why he as the infection is more puzzling. There appears to be no colonic or biliary pathology, although I had another patient with an S. intermedius liver abscess in the hospital at the same time that was due to a diverticular abscess.

Bad luck from flossing and brushing? That would be my usual go-to explanation, but he has full dentures. So I talked it over with the patient, and we concluded that some cases are just a mystery. But the seed was planted. The next day he remembered that just before the onset of his symptoms, he had been eating potato chips, which he likes to do without his teeth in. He lacerated his gum and developed a small abscess that he treated with manual decompression and mouth wash.

Bingo.

I have seen a few infections due to tortilla chips causing esophageal lacerations who, due to ETOH, did not chew appropriately. Those things are like ninja throwing stars.

This would be my first infection from potato chip trauma. And the first-ever reported.

Is nothing safe to eat?

Rationalization

Infez Med. 2012 Sep;20(3):145 54. Streptococcus anginosus group disseminated infection: case report and review of literature.

https://www.ncbi.nlm.nih.gov/pubmed/22992554

Rev Med Interne. 2003 Sep;24(9):627 9. [Multiple liver abscesses caused by Streptococcus constellatus in association with diverticulitis].

https://www.ncbi.nlm.nih.gov/pubmed/12951186

Rev Med Interne. 1994;15(11):715 9. [Parenchymatous abscess in Streptococcus anginosus (Streptococcus milleri) septicemia. Value of their systematic search, apropos of 4 cases].

https://www.ncbi.nlm.nih.gov/pubmed/7846385

Am J Gastroenterol. 1992 Jan;87(1):128 31. Tortilla corn chip-associated esophageal perforation: an unusual presentation of achalasia.

https://www.ncbi.nlm.nih.gov/pubmed/1728109

Let The Chips Fall Where They May.

http://boards.medscape.com/forums/?128@@.2a7d9776!comment=1

Not Quite an Explanation.

http://boards.medscape.com/forums/?128@@.2a05951d!comment=1

POLL RESULTS

The most dangerous food to eat is

• tortilla chips 5%
• beer 0%
• Big Mac 29%
• crow 25%
• raw anything 33%
• Other Answers 7%
• your words
• My mother in law's baklava
• anything not yet dead with teeth, claws, spines, toxins, and/or bigger than your head.
• Anything you can't identify.

The Attic is Full

Nov 8, 2016

“I consider that a man’s brain originally is like a little empty attic, and you have to stock it with such furniture as you choose. A fool takes in all the lumber of every sort that he comes across, so that the knowledge which might be useful to him gets crowded out, or at best is jumbled up with a lot of other things so that he has a difficulty in laying his hands upon it. Now the skillful workman is very careful indeed as to what he takes into his brain-attic. He will have nothing but the tools which may help him in doing his work, but of these he has a large assortment, and all in the most perfect order. It is a mistake to think that that little room has elastic walls and can distend to any extent. Depend upon it there comes a time when, for every addition of knowledge you forget something that you knew before. It is of the highest importance, therefore, not to have useless facts elbowing out the useful ones.”

― Arthur Conan Doyle, A Study in Scarlet

I have been writing this blog 2 or 3 times a week for over a decade. That’s a lot of cases. It is a good thing I have documented my career as if it were not for the blog, I would have no memory of my medical life.

The patient starts with three days of intractable hiccups. On the way home from an evaluation, he has a seizure, and an enhanced CT shows multiple ring enhancing lesions in the frontal lobe and brain stem. With CD4 at 70, a positive HIV, and a positive toxoplasmosis serology, it is almost certainly toxoplasmosis.

Does toxoplasmosis cause intractable hiccups? I didn’t know. So I Googled toxoplasmosis and hiccups. The fourth hit was me.

I guess I saw a case a decade ago, wrote it up, and proceeded to forget all about it. There are a pair of cases in the PubMeds, so this blog doubles the world's literature. See? There is more here than the occasional pathetic attempt at humor.

The other curiosity is a pair of pulmonary nodules. Is this toxoplasmosis as well? They are too small to biopsy, but I suspect so. In the bad old days of the AIDS epidemic, toxoplasmosis was a disseminated disease and could be found in any organ:

Nine autopsy cases of disseminated toxoplasmosis in New York are reported. Brain were involved in 9 cases, heart in 8, lung in 4, and pancreas, GI tract, thyroid, lymph nodes and urogenital organs were also involved.

And nodules are one of the pulmonary manifestations, albeit a less common manifestation.

For the ever so primitive CXR,

The films most often showed bilateralv interstitial infiltrates, predominantly in the bases of the lungs (21 patients). Other abnormalities included bilateral interstitial infiltrates associated with nodular densities (two patients), multiple nodular densities alone (four), nodular densities associated with pleural effusion (one patient), pleural effusion alone (two), bilateral white lung (two), and pneumothorax (one).

While in normal hosts

Tomographic findings were bilateral smooth septal and peribronchovascular thickening (100%), ground-glass opacities (100%), atelectasis (33%), random nodules (33%), lymph node enlargement (33%) and pleural effusion (66%).

As you may remember, pyrimethamine went up a wee bit in price a while back. A 60 day course is now about $45,000, up 2500% or $375 a tablet. So the patient is on clindamycin and sulfadiazine and doing fine without pharmaceutical induced bankruptcy.

Now that I have seen two cases, maybe I will remember that toxoplasmosis (and other brainstem masses) can cause hiccups, but if so, I will have to get rid of lyrics of pop songs from the ’80s to free up some room.

Rationalization

Zhonghua Bing Li Xue Za Zhi. 1994;23(3):166–9. [AIDS complicated with disseminated toxoplasmosis: a pathological study of 9 autopsy cases].

https://www.ncbi.nlm.nih.gov/pubmed/7954957

BMC Pulm Med. 2014 Nov 25;14:185. doi: 10.1186/1471–2466–14–185. Tomographic findings of acute pulmonary toxoplasmosis in immunocompetent patients.

https://www.ncbi.nlm.nih.gov/pubmed/25420956

Pulmonary Toxoplasmosis in Patients Infected with Human Immunodeficiency Virus: A French National Survey

http://cid.oxfordjournals.org/content/23/6/1249.full.pdf

POLL RESULTS

My brain is full of

• useful facts 6%
• old song lyrics 33%
• information acquired in high school only 2%
• nothing. I refill it every day from the internet 18%
• straw. If I only had a brain. 31%
• Other Answers 10%
• Everyone else's discarded notions.
• Random trivia -- mostly useless.
• good memories and troubling memories, both of which make me depressed to the point that senility is looking pretty good right now.
• Interesting factoids
• mixture of useful facts and garbage

Twists and Turns

Nov 10, 2016

I discussed a case of C. dubliniensis endocarditis back on 9/12. Some more twists and turns on the case.

The patients disease was community-acquired. I think. However, his girlfriend also had endocarditis with the MRSA. Not a surprise, Staphylococcus often runs in families.

But the girlfriend had a new fever while visiting him in the hospital and her blood cultures grew C. dubliniensis. It took a bit of investigation, but eventually, we discovered he was cheeking his narcotics, and they shared it. So I suspect that is how the Candida was transferred. In her case, the Candidemia was transient.

There are still no cases of infections as a complication of cheeking in the PubMeds, so the world's literature remains in this blog. All three Candida.

The patient finished up a 6 weeks course of lipid amphotericin and then was discharged on what would be a long course of oral fluconazole.

Two weeks out, he presented with a fainting spell. Well, a dozen fainting spells that were due to short runs of torsades.

Crap. I checked a fluconazole level, and it was therapeutic but likely boosting the methadone with resultant cardiac arrhythmia. There are a bunch of drug-drug interactions boosting methadone associated arrhythmias; fluconazole is one of them.

Tough call. If we stop the methadone, it is likely he would relapse the heroin, and if we stop the fluconazole, the Candida may return. Continue both, and he will die. 31 years and I have yet to kill a patient, but, as in this case, I have come close.

We stopped the fluconazole, and the torsades went away.

Over three months have gone by. He, and his girlfriend, remain both drug-free and Candida free.

It is nice to have a win every now and then.

Rationalization

I wish the monkey preferred bananas.

http://boards.medscape.com/forums/?128@@.2a80bb19!comment=1

Cheeky.

http://boards.medscape.com/forums/?128@@.2a577130!comment=1

Clin Pharmacol Ther. 1998 Jun;63(6):655–62. The effect of fluconazole on the clinical pharmacokinetics of methadone.

https://pubmed.ncbi.nlm.nih.gov/9663180/

EXCLI J. 2015 May 5;14:577–600. doi: 10.17179/excli2015–553. eCollection 2015. A systematic review of the cardiotoxicity of methadone.

https://www.ncbi.nlm.nih.gov/pubmed/26869865

Always Ask Why?

Nov 14, 2016

One man is born a hero, his brother a coward. Babies starve, politicians grow fat. Holy men are martyred, and junkies grow legion. Why? Why why why why why why? Luck! Blind, stupid, simple, doo-dah, clueless luck!

~Harvey Dent

Bugs require an explanation. If you have organism X in space Y, you need a reason. There is more to ID, believe it or not, than looking at a culture and sensitivity report and picking an antibiotic. Not that people act that way.

The patient, otherwise healthy, presents to Outside Hospital with fever after a ground-level fall. Blood cultures are obtained and grow Clostridium sordellii.

Call ID? Nope

Look for a reason? Nah.

Do a Pubmed to edumacate oneself? Heaven forbid.

Instead, he was sent home on a 10-day course of metronidazole.

Clostridium sordellii bacteremias are very unusual, with less than a dozen hits in the Pubmeds. The usual risks are trauma, childbirth, gynecological procedures, or intravenous drug use. He had none of the above.

It is one of those Clostridia that can result in an overwhelming sepsis with hemolysis and marked third spacing, as was seen after medical abortions early this century. It is associated with high mortality.

But not always, as in this case. He did relatively well, and perhaps his organism did not make the haemorrhagic toxin or the lethal factor.

Lethal factor. You have to respect an organism that makes a lethal factor.

He presented two months later with a WBC of 45,000 and on CT had a large tumor with a necrotic, gas-filled center. Otherwise, he was fine except for fatigue.

There is a similar report of

a case of C. sordellii bacteremia in a patient with rectum carcinoma and liver metastases.

and as one review points out

although the leukemoid reaction is a remarkable clinical feature of C. sordellii infection, nothing is known regarding the underlying mechanisms. Ras GTPases control cell differentiation and proliferation, and by their modification, LT may play a role in the characteristic leukemoid reaction, although this has yet to be investigated. The similar leukemoid reactions in C. difficile and C. novyi infections suggest that a common toxin may be responsible.

LT being the lethal toxin, so maybe the patient just got lucky.

When the mass was removed, the WBC rapidly fell. Unfortunately, no operative cultures were done.

So the cause of the bacteremia was likely the cancer, akin to what is seen more classically with C. septicum.

The source of the Clostridium species was a gastrointestinal site in 24 patients (52.2%). The most frequently identified Clostridium species was Clostridium perfringens (in 10 [21.7%] of patients), followed by Clostridium septicum (in 9 [19.6%]). Thirty-one patients (67.4%) were aged > or =65 years, 13 patients (28.3%) had diabetes mellitus, and underlying malignancy was present in 22 patients (47.8%).

Always ask why? In this case, a carcinosarcoma, i.e., mixed Mullerian tumor invading the small bowel wall.

Rationalization

J Clin Pathol. 2000 Sep;53(9):709–12. The clinical spectrum of Clostridium sordellii bacteraemia: two case reports and a review of the literature.

https://www.ncbi.nlm.nih.gov/pubmed/11041062

Clin Infect Dis. 1992 Dec;15(6):950–4. Clostridium sordellii bacteremia: case report and review.

https://www.ncbi.nlm.nih.gov/pubmed/1457666

Infection. 2009 Aug;37(4):368–9. doi: 10.1007/s15010–008–8192-y. Epub 2009 Apr 23. A rare case of Clostridium sordellii bacteremia in an immunocompromised patient.

https://www.ncbi.nlm.nih.gov/pubmed/19390781

Clostridium sordellii Infection: Epidemiology, Clinical Findings, and Current Perspectives on Diagnosis and Treatment.

http://cid.oxfordjournals.org/content/43/11/1436.long

Fatal Clostridium sordellii Infections after Medical Abortions N Engl J Med 2010; 363:1382–1383.

http://www.nejm.org/doi/full/10.1056/NEJMc1001014#t=article

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.

https://www.ncbi.nlm.nih.gov/pubmed/11438901

POLL RESULTS

The most important question is

• why 24%
• where 2%
• to ask not what you can do for your country 0%
• WTF 48%
• life, the universe, and everything 19%
• Other Answers 7%
• Is it happy hour yet
• Why not?
• where's my phone?

Recurrent Uncertainty

Nov 16, 2016

I think, of the common infectious diseases, cellulitis is the most straight forward.

Not that you suspect it from the way so many approach the disease, fretting about MRSA and Pseudomonas and giving vancomycin and piperacillin/tazobactam.

And don’t get me started on how often lymphedema is called cellulitis.

Here is a sort of semi-classic case of cellulitis with a twist or two.

The patient has the abrupt onset of rigors and fevers, followed within a day by diffuse erythroderma of the leg.

She is seen, admitted, and the infections melts away with antibiotics.

Over the next 6 years, it happens two more times, almost exactly the same except the infection alternates legs. Which is odd.

It should be group A Streptococcus. S. pyogenes is the main cause of cellulitis and recurrent cellulitis, diffuse erythroderma with fever, aka erysipelas.

But it isn’t.

Two of the three times, blood cultures were drawn and grew Group B Streptococcus. The patient wants to know why the recurrent infections. Got me.

It is odd both in its rarity and the fact there are zero risk factors for infection; she is as healthy as the proverbial horse and has no lymphedema.

Is there something wrong with the host? I would think, as I have mentioned before, that Group B bacteremia would be indicative of an antibody problem. Still, that hypothesis is neither backed up by the literature nor my experience of sending off SPEP’s and antibody levels.

I suspect colonization, but years between episodes?

Would decolonization work? Is it the spouse that is the source? Are suppressive antibiotics indicated?

Maybe, maybe and probably not.

Given the length of time between episodes purporting causation or lack of causation to any intervention would be laughable.

Sometimes when you tell a patient you really have no idea what to do, they look at you like you are an ignoramus maroon. I laid out all the uncertainties to the patient, and she seemed satisfied.

Rationalization

Streptococcus agalactiae in Relapsing Cellulitis.

http://cid.oxfordjournals.org/content/44/8/1141.full

Rev Med Suisse Romande. 1987 Dec;107(12):1047–50. [Recurrent erysipelas due to Streptococcus G].

https://www.ncbi.nlm.nih.gov/pubmed/3432834

Br J Dermatol. 2006 Nov;155(5):947–50. Oedema as a risk factor for multiple episodes of cellulitis/erysipelas of the lower leg: a series with community follow-up.

https://www.ncbi.nlm.nih.gov/pubmed/17034523?dopt=Abstract

Tolerating Uncertainty — The Next Medical Revolution?

http://www.nejm.org/doi/full/10.1056/NEJMp1606402#t=article

POLL RESULTS

I am uncomfortable with

• uncertainly 19%
• no diagnosis 6%
• a dark ally after seeing Zoro 0%
• hotel clerks named Norman 6%
• ventriloquist dummies that talk on their own 56%
• Other Answers 14%
• certainty
• Donald Trump
• failure to acknowledge the role of inflammation in all diseases
• most everything.
• bedbugs

True?

Nov 21, 2016

The consult was a diverticular abscess in an otherwise healthy male.

Cultures from the IR drainage were the usual: an alpha Streptococcus and an E. coli susceptible to everything but quinolones.

The patient was on 250 qid cephalexin.

Huh.

After 31 years in the biz, I have tonnes of facts in my head, many of which are of uncertain provenance. Especially in the pre-internet days, I was given pieces of information by my betters that I took at face value because it was impossible in the old days to validate everything I was told.

I feel it is my duty and responsibility as a consultant to be able to back up each and every recommendation I make with a reference and, if one is not available, to note that I am offering an opinion from my experience and I always note that the three most dangerous words in medicine are “in my experience.”

I have it in my mind that, outside of UTI’s, you should never use cephalexin for E. coli. Someone told me that back in the mists of time.

So is that true?

Well, there are some trials of cephalexin and UTI with success rates of 90%, but some old studies had a 60% relapse rate.

As best I can tell, there are no studies of cephalexin in the treatment of abdominal abscesses.

So I went with basic pharmacokinetics.

At 250 mg qid, the peak serum level of cephalexin is 9. Double that for 500 mg qid. And that is for the mythical 70 kg person. Most Americans have not seen 70 kg since 5th grade.

The lab tells me they do not test cephalexin against E. coli as the MIC’s are too high.

As best I can tell, the data suggests that cephalexin MIC’s average around 8, the MIC 50 is 32, and the MIC 90 is 64. I am not confident in those numbers as the data is as old as my ID career.

There is more cefazolin data, but one study suggests cefazolin is not a surrogate for cephalexin.

So should you use cephalexin for E. coli abscesses? I do not think so. I do not think you can get enough cephalexin into the patient and then into the abscess to kill off the E. coli.

So I switched to an oral third generation. And he did fine, probably because it was drained.

Rationalization

Int J Antimicrob Agents. 2000 Jan;13(3):183-7. Comparison of pivmecillinam and cephalexin in acute uncomplicated urinary tract infection.

https://www.ncbi.nlm.nih.gov/pubmed/10724022

Cephalexin-a new oral antibiotic.

http://pmj.bmj.com/content/46/533/157.long

Cefazolin and Enterobacteriaceae: Rationale for Revised Susceptibility Testing Breakpoints.

http://cid.oxfordjournals.org/content/52/7/917.full

Narrow-Spectrum Cephalosporin Susceptibility Testing of Escherichia coli with the BD Phoenix Automated System: Questionable Utility of Cephalothin as a Predictor of Cephalexin Susceptibility▿

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2168537/

Comparative in vitro activities of amoxicillin-clavulanic acid, cefuroxime, cephalexin, and cephalothin against trimethoprim-resistant Escherichia coli isolated from stools of children attending day-care centers.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC171996/

POLL RESULTS

All my facts

• can be backed up with a reference 21%
• were told to me by someone else 13%
• are irrelevant. We are now in a post-fact world 44%
• as valid as my feelings 13%
• come from Facebook and Twitter. 8%

Another Odd Bug in an Odd Place

Nov 23, 2016

The title sums up one aspect on the list of what makes ID fun, second only to making the diagnosis before anyone else. Yeah, I am that petty and competitive.

The patient is a mostly healthy middle-aged male who has a growing red, hot, tender bump on his abdomen.

Urgent care rightly suspects MRSA and gives TMP/Sulfa.

It doesn’t get better.

So the next visit, it is opened up, and doxycycline is given. It doesn't’ get better.

For whatever reason, the urgent care not only sends regular cultures but AFB and fungal. And there are a lot of partially acid-fast organisms on the stain that are identified as Gordonia bronchialis in the MALDI-TOFF

Huh?

I have never heard of it. Well, as is so often the case, I had. As if I can remember anything these days. So many many bugs, so little recall. There is a brief entry in the Compendium that I will now need to buff up.

These are in the family of Actinomycetes and include Gordonia, Rhodococcus, and Tsukamurella.

According to their newly proposed hiercharchic classification system for the actinomycete line, Gordonia is the type genus of Gordoniaceae (the Gordonia family) within the suborder Corynebacterineae. This suborder includes also the families Corynebacteriaceae, Dietziaceae, Mycobacteriaceae, Nocardiaceae, Tsukamurellaceae, and Williamsiaceae

And there are around 21 different Gordonia spp.

Oddly as I was sitting in the clinic dictating the case, I was asked if I had ever heard of Tsukamurella, which was in the sputa of another patient. I always find the clustering illusion creepy. I listen to Audible books as I drive around the city, and it is always disconcerting when I see a word on a sign just as the narrator says the same word. If I were less skeptical, I might think the universe is talking to me.

Gordonia is an environmental organism that causes a hodgepodge of diseases, including soft tissue infections in mostly immunoincompetent patients.

This case? No reason I can find. No immunosuppression, no trauma, no odd exposure outside of being a gardener but he is not a wallow in the mulch pile kind of gardener. So I have no reason for the infection.

Gordonia are usually resistant to TMP/Sulfa and often resistant to tetracycline. It is usually sensitive to amoxicillin-clavulanate, so that I may have finally found an indication for that antibiotic. And he got all better. A cure would be number three on the list.

Rationalization

Biology of the Metabolically Diverse Genus Gordonia.

http://aem.asm.org/content/70/6/3195.full

Rev Esp Quimioter. 2016 Jun;29(3):170-3. Epub 2016 Mar 26. Cutaneous abscess due to Gordonia bronchialis: case report and literature review.

https://www.ncbi.nlm.nih.gov/pubmed/27015823

POLL RESULTS

The best part of medicine is

• getting to know a wide variety of people but not having to have dinner with them 35%
• curing patients 10%
• being called Doctor 5%
• almost everything. Compared to the other jobs, what's not to like? 20%
• nothing. I wish I had done something else with my life 20%
• Other Answers 10%
• working in a reality-based universe, until you run into folks who clearly belong in retail sales or televangelism. Then it starts to suck.
• making mama proud

Antibiotic Anger

Nov 28, 2016

I do not suffer from road rage. I do spend a lot of time in the car going from hospital to hospital, but I listen to Audible as I drive. I am halfway through The Wheel of Time, a 15 volume epic, and listening to the trials and tribulations of Rand et al.' Thor (Wheel of Time joke) keeps me mellow. And Audible makes me a better driver since I don’t speed to prolong my time with a book.

But then I get to work and see the following in an H&P of a consult for a case of lower extremity cellulitis with zero unusual risks.

Will treat aggressively with vancomycin and cefepime.

For cellulitis. You know, classic erysipelas, diffuse erythroderma with fever. Due to S. pyogenes, S. pyogenes, Group A Streptococcus, S. pyogenes, Group A Streptococcus, and a smattering of Group G Streptococcus, Group B Streptococcus, MSSA, and S. lugdunensis.

What is not on that list? MRSA and gram-negative rods. Zero need for vancomycin or cefepime. None. Zip. Nada. Nil.

It is not an aggressive treatment.

It is

STUPID TREATMENT.

All they need is cefazolin.

Sorry, I shouted.

I have antibiotic anger issues. I want Hulk out at the sheer stupidity of what should be one of the more straight forward infections to treat. I want to channel my inner Lewis Black and let loose with an expletive-laced rant.

But I can’t. One must be civilized. There are proprieties to observe. Deep breath.

Cellulitis is easy to recognize:

Both erysipelas and cellulitis are manifested clinically by rapidly spreading areas of edema, redness, and heat, sometimes accompanied by lymphangitis and inflammation of the regional lymph nodes. The skin surface may resemble an orange peel (i.e., peau d’orange) because superficial cutaneous edema surrounds the hair follicles, which causes dimpling in the skin because they remain tethered to the underlying dermis. Vesicles, bullae, and cutaneous hemorrhage in the form of petechiae or ecchymoses may develop on the inflamed skin. Systemic manifestations are usually mild, but fever, tachycardia, confusion, hypotension, and leukocytosis are sometimes present and may even occur hours before the skin abnormalities appear. Vesicles and bullae filled with clear fluid are common. Petechiae and ecchymoses may develop in inflamed skin;

Or so I thought.

The microbiology simple:

that most of the infections arise from streptococci, often group A, but also from other groups, such as B, C, or G…. S. aureus less frequently causes cellulitis, often associated with previous penetrating trauma, including injection sites of illicit drug use… Many other infectious agents can produce cellulitis, but usually only in special circumstances.

Note the “only in special circumstances.”

Take a history instead of throwing unneeded antibiotics at the patient under the delusion you are doing something.

Sorry. Calm. Wipe spittle from chin. Quit glaring.

And the treatment?

For parenteral therapy, which is indicated for severely ill patients or for those unable to tolerate oral medications, reasonable choices include a penicillinase-resistant penicillin such as nafcillin, a first-generation cephalosporin such as cefazolin.

How hard is it?

Evidently very. If there is another common infection that is routinely treated like the physician slept through every ID lecture in medical school, I am unaware.

Expletive deleted.

I sometimes wonder if I am heading into a frontal lobe dementia since this sort of practice did not bother me back in the day. But the older I get...

I wish anytime vancomycin and either cefepime or piperacillin/tazobactam is given for cellulitis, the prescriber has to pay for the antibiotics. THAT would stop the stupidity real fast.

Rationalization

Practice Guidelines for the Diagnosis and Management of Skin and Soft-Tissue Infections. http://www.idsociety.org/uploadedFiles/IDSA/Guidelines-Patient\_Care/PDF\_Library/Skin%20and%20Soft%20Tissue.pdf

POLL RESULTS

When I see stupid practice for common illnesses

• I rage 18%
• I sigh 12%
• I make it a teaching moment 28%
• I despair 7%
• I wonder if people pay attention anymore 30%
• Other Answers 5%
• I tug my (imaginary) braid like Nynaeve.
• I struggle for composure while biting my lip. Ouch.
• I rant to others who don't really care
• all above but not at the same occasion
• All of the above
• Usually make a joke about it to my ID colleagues
• All of the above
• all of the above
• All of the above.
• all of the above
• Combination of all of the above, if that is even possible.

SFHP

Nov 30, 2016

The patient has end-stage liver disease (ESLD) and recurrent ascites. She requires a paracentesis every week to keep the fluid at a manageable level.

She is admitted for a TIPS, and a tap shows a jump in white cells to 350. Spontaneous bacterial peritonitis (SBP) is a worry, and two days later, the cultures grow?

Candida glabrata.

What?

SBP suggests either hematogenous seeding of the ascites or translocation of bacteria across intact bowel wall. Candida in the peritoneal fluid to my mind suggests a violation of bowel wall integrity, which is not evident on the exam or CT. A repeat paracentesis shows a mild jump in the WBC to 450.

Contamination? Her skin is normal, no diaper rash like issues. C. glabrata, as best I can tell, does not colonize normal skin.

Candida doesn’t cause SBP, does it? As seems to be the case of late, I have seen a prior case and written about it. Sigh. I wonder if I will remember this case in the future. But since 2010, there has been more in the literature about SFP.

SFP occurs in about 10% of peritoniti/peritnonitises in cirrhotics, half being C. albicans, and 3% being C. glabrata and a 60% mortality rate.

Repeat cultures were negative as, eventually, was the beta-d-glucan. Was it early disease or contamination? No way to know.

Hard not to treat with that kind of mortality rate, and she did will on micafungin; it eventually tested as resistant to fluconazole, and who wants to give an azole in ESLD?

Medicine also has a problem with unneeded h’s. Consider cirrhotics, ophthalmology, and Crohn’s. Waste of a perfectly good consonant that only serves to make writing more different.

Rationalization

J Clin Microbiol. 1998 Feb; 36(2): 421–426. PMCID: PMC104553 Nosocomial Candida glabrata Colonization: an Epidemiologic Study.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC104553/

World J Gastroenterol. 2016 Sep 14; 22(34): 7742–7747. Published online 2016 Sep 14. doi: 10.3748/wjg.v22.i34.7742 PMCID: PMC5016373 Spontaneous fungal peritonitis: Epidemiology, current evidence and future prospective

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5016373/

Fungal Peritonitis: Underestimated Disease in Critically Ill Patients with Liver Cirrhosis and Spontaneous Peritonitis.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0158389

Truth, big ’T’.

http://boards.medscape.com/forums/?128@@.29f8da03!comment=1

POLL RESULTS

The least reliable letter is

• h 12%
• q 19%
• j 8%
• any letter with an umlaut 35%
• U of O football letter of intent 19%
• Other Answers 8%
• The one that comes in the mail saying "you may be a winner"
• I. Am very unreliable. Reliably so. Almost inevitably so.

Late Relapse

Dec 5, 2016

The patient, an elderly male, had sustained enterococcal bacteremia.

He had the 4-star work up: CT and TEE, and no source was found. No abscess, no vegetation on the valves, no clot on the pacer.

There are cases of enterococcal pacer infections. I count two on PubMed. But there are cases of everything causing an infection, and Enterococcus is not high on the list, and taking out a pacer is not a simple procedure.

Since a sustained bacteremia defines endocarditis, or an endovascular infection, I opt to treat with 6 weeks of ampicillin and ceftriaxone.

He gets instantly better on antibiotics and finishes an uneventful course of antibiotics. Post-treatment blood cultures are negative. It looks like another cure.

You have, however, read the title and know this is not going to end up well.

Seven, yes seven, months later, he returns with a septic hip. Not only does the joint grow the same Enterococcus, so does multiple blood cultures. And again, the 4 star work up is negative. A negative CT and TEE. No changes of osteomyelitis around the hip.

The pacer must be infected, and it is removed and grows Enterococcus.

A month or three before the hip infection, he had a decline in his energy, no fevers, but night sweats. He didn’t seek care as he is uninsured and not a citizen.

7 months for a relapse? Not my record. I had one native valve endocarditis from Micrococcus that was a year between presentations. But looking in the PubMeds, I can’t find a record; 6 months has always been the cut off for relapse vrs reinfection,

Is the pacer infected? Always a difficult call when ECHO’s are negative. Treating and waiting for relapse is unsatisfying. Perhaps the diagnostic test of choice is a PET. As an example:

Sensitivity, specificity, positive predictive value, and negative predictive value for 18F­FDG PET/CT were 82%, 96%, 94%, and 87%, respectively. 18F­FDG PET/CT was false ­negative in all cases with infected NV.

And may pick up the occasional unexpected cancer.

But PET is also expensive and often not reimbursed for processes where it is of real value: infectious diseases.

Rationalization

BMJ Case Rep. 2014 Oct 7;2014. pii: bcr2014206907. doi: 10.1136/bcr-2014-206907. Large vegetation in a 60-year-old man with Enterococcus faecalis cardiac implantable electronic device infection.

https://www.ncbi.nlm.nih.gov/pubmed/25293687

J Nucl Med. 2016 Nov;57(11):1726­1732. Epub 2016 Jun 3. Diagnostic Accuracy of 18F­FDG PET/CT in Infective Endocarditis and Implantable Cardiac Electronic Device Infection: A Cross­Sectional Study.

https://www.ncbi.nlm.nih.gov/pubmed/27261514 1/3

Repeat Infective Endocarditis: Differentiating Relapse from Reinfection.

http://cid.oxfordjournals.org/content/41/3/406.long

Common and Not So Rare?

Dec 7, 2016

The patient presented as a fall due to urosepsis with a pan sensitive E. coli.

E. coli bacteremia is a common enough problem, at around 30-50/100,000 population, so the US has around 150,000 cases a year.

The nice thing about E. coli urosepsis is while it may kill the patient upfront (that’s not the nice part), it has little predilection for causing metastatic complications.

Unlike S. aureus, you do not need to worry about seeding of valves or a distant abscess. At least not usually.

You can probably guess where this is going.

I was called to see the patient because of refractory low back pain and leukocytosis. She has a long history of back pain, but she was quite clear on this; it was right after the fall that the pain became markedly worse.

Exam is unremarkable beyond midline back pain.

She had an unenhanced (due to renal dysfunction) MRI a few days prior that showed a variety of degenerative problems but no fracture, no infection, but mild bilateral psoas edema. Bilateral? Seemed odd.

So I called radiology. Is an unenhanced MRI enough to exclude fracture or infection? Yes to the former, no to the latter.

With an improved creatinine, an enhanced MRI was ordered. Lumbar osteomyelitis, discitis, and tiny epidural abscess.

I was both surprised and not surprised by the result. With no fracture, it was the only diagnosis to explain the pain.

But most of the UTI related spine infections I have seen have been in men, a complication of prostatic obstruction where I blame Batson’s plexus. As seems to be the case of late, I had a similar case a year ago I forgot all about until now. This is getting to be a habit, my memory of cases relying on googling to find my prior blog entries. What do the rest of you do?

There are other cases in the Pubmeds of E. coli spinal epidural abscesses, but I only need one hand to count them. Perhaps it is more common than reported, and this is a publication bias.

Once the diagnosis had been made, the course of action was the same as for every infection: drain the pus and kill the bug.

Rationalization

Population-based incidence and comparative demographics of community-associated and healthcare-associated Escherichia coli bloodstream infection in Auckland, New Zealand, 2005-2011.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3849480/

Clin Microbiol Infect. 2008 Nov;14(11):1041-7. doi: 10.1111/j.1469-0691.2008.02089.x. Incidence, risk factors and outcomes of Escherichia coli bloodstream infections in a large Canadian region.

https://www.ncbi.nlm.nih.gov/pubmed/19040476

Pattern Recognition.

http://boards.medscape.com/forums?128@@.2a7f967a!comment=1

POLL RESULTS

I

• remember all my cases with complete clarity 0%
• remember what I need, what is forgotten is unimportant 9%
• have no need of a memory, I have google 28%
• only remember all the bad outcomes and mistakes with embarrassing clarity 35%
• Maurice sums it up for me: https://www.youtube.com/watch?v=sISWPzEqHLQ 16%
• Other Answers 12%
• forget most everything, eventually, I hope. Otherwise, it's gonna be a dismal last few years on earth.
• what was the question?
• I remember that everything.... wait - what was I saying?

You Woke Me Up For That ?!?

Dec 12, 2016

I have basically been on call since 1990. Except for weekends and vacations, the beeper is on. It is one of the reasons I refuse to use my phone as my primary contact for work: I can turn off my beeper, but I cannot turn off my phone, and I do occasionally want to escape medicine.

I never mind getting called because I figure there really is no such thing as a stupid question. Someone needs help? They need help.

Except.

The beeper goes off at 1 am. It is the ER.

The patient was sent in to treat an MRDO, er, I mean MDRO (multi-drug resistant organism), in the urine.

No symptoms. No pyuria.

I said: don't treat asymptomatic bacteriuria.

The urine is dark.

That's not a symptom; it's a sign. Don't treat asymptomatic bacteriuria.

It's sensitive to nitrofurantoin.

I said: don't treat asymptomatic bacteriuria.

Her doc wants her treated.

I said: don't treat asymptomatic bacteriuria.

We left it at that. I think I said don't treat asymptomatic bacteriuria about a dozen times.

This is not new information, people. The guidelines are over a decade old.

Do not treat

• Premenopausal, nonpregnant women
• Diabetic women.
• Older persons living in the community.
• Elderly, institutionalized subjects.
• Persons with spinal cord injury.
• Catheterized patients while the catheter remains in situ

There are zero benefits. You increase cost, side effects, breed resistance, and in some populations, increase the frequency of symptomatic UTI.

Those asymptomatic bacteria are probably protective, and you have to wonder if messing with the bladder microbiome is a bad idea. Yes, the bladder is not sterile and has a complex microbiome. We can't grow it, and perhaps that microbiome is protective for infections similar to the gi microbiome. It is why I wonder if the solution to recurrent UTI is a urine transplant. You heard it here first, although I will leave it to others to turn my brilliant idea into reality. I am more a Mycroft than a Sherlock:

He is described as having abilities of deduction and knowledge exceeding even those of his brother, though their practical use is limited by his poor physique and dislike of fieldwork.

The guidelines (currently being updated) still suggest treating in pregnant females and before urologic procedures, but that is problematic. The data since suggests that treating is not of benefit in either case. It will be interesting to see the next version of the guidelines.

Urine stinks? Doesn't count.

Delirium in the elderly as a sign of UTI has remarkably little data to support it as a sign of infection.

Though the studies examined, conclude that there is an association between UTI and delirium, all of them had significant methodological flaws that likely led to biased results. Therefore, it is difficult to ascertain the degree to which urinary tract infections cause delirium.

If there is a population in whom treating asymptomatic bacteriuria of proven benefit, I can't find it.

So stop it. Let me sleep.

Rationalization

Infectious Diseases Society of America Guidelines for the Diagnosis and Treatment of Asymptomatic Bacteriuria in Adults.

http://cid.oxfordjournals.org/content/40/5/643.full.pdf+html

BMC Pregnancy Childbirth. 2016 Nov 2;16(1):336. Benefits and harms of screening for and treatment of asymptomatic bacteriuria in pregnancy: a systematic review

https://www.ncbi.nlm.nih.gov/pubmed/27806709

Is Preoperative Assessment and Treatment of Asymptomatic Bacteriuria Necessary for Reducing the Risk of Postoperative Symptomatic Urinary Tract Infections After Urologic Surgical Procedures?

https://www.ncbi.nlm.nih.gov/pubmed/27773650

Curr Opin Obstet Gynecol. 2016 Oct;28(5):407-12. doi: 10.1097/GCO.0000000000000298. The urinary microbiota: a paradigm shift for bladder disorders?

https://pubmed.ncbi.nlm.nih.gov/27379439/

J Gerontol Nurs. 2004 Jun;30(6):4-9. Urinary tract infections. Does the smell really tell?

https://www.ncbi.nlm.nih.gov/pubmed/15227931

Delirium, a Symptom of UTI in the Elderly: Fact or Fable? A Systematic Review.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3940475/

Outcome of treated and untreated asymptomatic bacteriuria in renal transplant recipients.

http://ndt.oxfordjournals.org/content/26/12/4109.short

Am J Transplant. 2016 Apr 18. doi: 10.1111/ajt.13829. Should asymptomatic bacteriuria be systematically treated in kidney transplant recipients? Results from a randomized controlled trial.

https://www.ncbi.nlm.nih.gov/pubmed/27088545

POLL RESULTS

I most resemble

• Sherlock 17%
• Mycroft 23%
• Watson 26%
• Lestrade 11%
• Moriarty 11%
• Other Answers 11%
• House, MD ;-)
• Alfred E. Newman
• Gabby Hayes, on a good day. Mr.Hyde, otherwise.

I don’t care what the literature says, it’s still a bad idea.

Dec 14, 2016

That title is heresy coming from me.

The patient is a middle-aged IDDM. He comes in with fevers and pleuritic chest pain.

Blood cultures grow MRSA, and the CT is consistent with septic emboli, although the TTE is negative for vegetations.

The next day, 24 hours into vancomycin therapy, he complains of blurry vision. An eye exam shows bilateral endophthalmitis that eventually has gram-positive cocci on the stain but is culture negative. Fevers persist, and a TEE shows pulmonic valve vegetation.

So two unusual complications of S. aureus bacteremia, both of which I have seen before. PV IE accounts for a mere 1-2% of endocarditis, this being perhaps the third from my storied career.

This is the second case of bilateral endophthalmitis complicating endocarditis I have seen. There are a smattering of cases on the PubMeds. However, the one report got it backward: Infective endocarditis complicating bilateral bacterial ophthalmitis: a case report and strongly suggests ophthalmologists do not know how to treat Group B streptococcal endocarditis:

administration of penicillin G, panipenem, cefotaxime and clindamycin

for three and a half months !?!?!?!

Fortunately, eye infections are relatively rare in endocarditis. That it manifested after several doses of vancomycin is no surprise as vancomycin levels in the eye are poor.

Vitreous vancomycin concentrations for the treatment of gram-positive endophthalmitis were nontherapeutic after intravenous administration but therapeutic after intravitreal administration.

In talking with the patient, he was not using the best technique, injecting his insulin through his clothes.

The literature actually suggests it is safe to do

It is safe and convenient to inject insulin through clothing.

Just as reusing needles is usually safe.

Five studies showed no association between infection at site of injection and reuse of needles (risk difference=-0.00; 95% confidence interval=-0.12-0.11; P=0.99); heterogeneity between these studies was substantial (I(2)=66%; P=0.02).

But that is probably more about what you can get away with than optimal care.

Heroin users have the worst technique: licking needles, using tap water, not cleaning the infection site, reusing needles and syringes, and using a product that is rich in bacteria.

They get their fair share of infections:

55% reported a lifetime history of at least one skin infection and 29% reported having an infection in the last year.

but given the frequency of heroin injection, infections are relatively quite rare. It is probably a bad idea to imitate the technique of an IVDA. Or an acupuncturist.

From an infection control perspective, there is no one intervention that decreases the chance of infection; it is the summation of multiple interventions.

So why push your luck? For once, I would ignore the literature. Don't inject through your clothing, either heroin or insulin.

Rationalization

Rare and Rarer.

http://boards.medscape.com/forums/?128@@.2a804ee3!comment=1

Vancomycin Concentration in the Vitreous After Intravenous and Intravitreal Administration for Postoperative Endophthalmitis.

http://jamanetwork.com/journals/jamaophthalmology/fullarticle/412229

Diabetes Care. 1997 Mar;20(3):244-7. The safety of injecting insulin through clothing.

https://www.ncbi.nlm.nih.gov/pubmed/9051365

Int J Nurs Stud. 2016 Aug;60:121-32. doi: 10.1016/j.ijnurstu.2016.04.010. Epub 2016 Apr 27. Safety of the reuse of needles for subcutaneous insulin injection: A systematic review and meta-analysis.

https://www.ncbi.nlm.nih.gov/pubmed/27297374

An investigation into the microflora of heroin.

http://jmm.microbiologyresearch.org/content/journal/jmm/10.1099/0022-1317-51-11-1001

Infect Control Hosp Epidemiol. 2008 Sep;29(9):859-65. doi: 10.1086/590260. Outbreak of invasive methicillin-resistant Staphylococcus aureus infection associated with acupuncture and joint injection.

https://www.ncbi.nlm.nih.gov/pubmed/18684094

I don't know what to do.

Dec 21, 2016

The buck has stopped with me for a long time. The problem is, the longer I practice medicine, the more I encounter problems about which I really have no idea what to do. The last couple of weeks have seen a series of cases that have me flummoxed. But everyone expects an answer from me.

For example.

The patient is a middle-aged male from SE Asia who was treated for abdominal TB in 2003. Sounds like streptomycin for 2 months and INH and Rifampin for 6 months. He moves to the US two years later.

He has been asymptomatic for the last 14 years. No constitutional or GI symptoms. He has a CT for renal stones that demonstrated enlarged intraabdominal lymph nodes.

The lymph nodes are biopsied. Caseating granulomas. AFB negative. Culture negative.

He was sent to me.

No reason or symptoms of other diseases.

The node was sent for 16S, negative.

Now what?

Assuming there is no other diagnosis to account for the pathology, and I cannot find one, the question with no answer that I can find is: how long will granulomas persist after treatment of tuberculosis?

There was no answer that I could find on the Googles or the Pubmeds, and the TB experts I asked didn’t know either.

To my mind, 13 years seems too long unless there is some residual infection. Granuloma implies infection, although perhaps the patient has resolved the infection on his own given the negative 16S.

So it is either watch and wait or another course of therapy. Being from the better safe than sorry, my inclination is to give another course of anti-tuberculous therapy.

I just wish I had some data to guide me.

And Tb continues to frustrate.

Rationalization

A clinicopathological classification of granulomatous disorders.

http://pmj.bmj.com/content/76/898/457.full

The Granuloma in Tuberculosis: Dynamics of a Host–Pathogen Collusion.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3538277/

Modeling the Mycobacterium tuberculosis Granuloma – the Critical Battlefield in Host Immunity and Disease.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3631743/

POLL RESULTS

The buck

• stops with me 21%
• stops with me, but is only worth 50 cents 29%
• is deer to me 25%
• is passed on after taking my share 14%
• is not accepted, but I take American Express 4%
• Other Answers 7%
• stopped with me. Then I quit paying the others' tabs. Screw it, I said. I'm not going down with this ship of fools. Malpractice? Too much to swallow.
• trampled over me and kept on running.

Leading in a cyst.

Dec 26, 2016

The patient has end-stage liver disease/cirrhosis and is admitted with fever and chills.

Blood cultures grow K. pneumoniae. Not a surprise.

Gram-negative bacteria were the predominant microorganisms of bacteremia (75.6%). Among them, Escherichia coli, Klebsiella pneumoniae and Aeromonas hydrophilia were the three most commonly detected microorganisms.

He rapidly defervesed, and no reason was found for the bacteremia: no UTI, no pneumonia, no SBP, no occult abscess on CT.

So he received a course of quinolone. Two weeks later, he was back with the same symptoms and the same organism in the blood.

This time the CT revealed an abscess where there was once a small, single renal cyst. So small, in fact, the first CT report did not mention it.

Cysts are common. 50% of adults over age 50 will have a cyst. Russell Westbrook is averaging 10.9 per game. Amazing.

Infected cysts are common enough in polycystic kidney disease, but there are less than 20 cases in the Pubmeds of solitary cysts becoming infected. I suspect it is more publication bias than a rarity, although I cannot remember that I have ever seen a case myself.

We drained the abscess percutaneously, there was a gram-negative rod that didn’t grow, and he did fine.

And you know the drill. Next time YOU have a case of bacteremia in a patient with a solitary renal cyst, YOU need to consider secondary seeding.

Not.

Rationalization

Liver. 1991 Dec;11(6):334-9. Bacteremia in patients with cirrhosis of the liver.

https://www.ncbi.nlm.nih.gov/pubmed/1779712

Arch Esp Urol. 1993 Jun;46(5):419-21. The infected solitary renal cyst. A case review and review of the literature.

https://www.ncbi.nlm.nih.gov/pubmed/8342979

Does it make a Diff?

Dec 28, 2016

The patient had abdominal surgery for a malignancy and had, in the passive voice, an inadvertent colon enterotomy that was repaired.

He is readmitted a week later for fevers, and abdominal pain and an abscess is found on CT. It is drained, enterotomy was re-repaired in the OR, and the cultures of the abscess grow E. coli, C. perfringens, and C. difficile.

The patient is doing fine clinically post-op, with no sepsis or diarrhea.

What to do.

Drainage is most of the cure for abscesses. The C. perfringens? There are a smattering of C. perfringens causing mono-microbial abdominal abscesses. But as part of the GI flora, it will occasionally show up in mixed cultures from abdominal abscesses. People sometimes freak, but C. perfringens usually causes either overwhelming infection or is a big fat nothing. In this case, it was the latter.

It was the C. difficile that was the puzzle. Does the patient need isolation?

In all but one case, C. difficile isolation was obtained as part of a polymicrobial flora. The isolates were frequently non-toxigenic and the extra-intestinal infections occurred without concomitant diarrhea or prior anti-microbial therapy.

and

Two patients had bacteremic infections, 4 had abdominal infections without any prior surgery, 7 had abdominal infections after surgery, 4 had perianal abscesses, 13 had wound infections, and 1 had C. difficile in a urinary catheter. In most cases (85%), C. difficile was isolated together with other microbes. Most (81%) patients developed the infection when hospitalized and many had severe comorbidities. Sixteen (52%) had diarrhea

My go-to treatment for intra-abdominal infections is ceftriaxone and metronidazole (actually, my go to treatment is source control; the antibiotics are there mostly to kill off any residual bacteria), so I figured no diarrhea, no isolation.

Of course, once the post-operative ileus resolved, there was diarrhea that was toxin positive. So then we isolated the patient, for all the good that does.

The rate of transmission of toxigenic, predominantly non-hypervirulent C. difficile was low and no outbreaks were recorded over a 10-year period after discontinuing contact precautions for patients with CDI who were not severely incontinent and who used dedicated toilets.

I am increasingly of the opinion that isolation is a waste of time for any organism that is part of the normal flora as long as good universal precautions are performed. Outside of outbreaks and some specialty units like burn centers, perhaps.

If hands are being washed, gowns are a waste of time and only add more trash to the landfills.

Besides, I look terrible in yellow.

Rationalization

Clin Microbiol Infect. 2001 Aug;7(8):453-7. Extra-intestinal infections caused by Clostridium difficile.

https://www.ncbi.nlm.nih.gov/pubmed/11591212

Clin Infect Dis. 2013 Sep;57(6):e148-53. doi: 10.1093/cid/cit392. Epub 2013 Jun 13. Extraintestinal Clostridium difficile infections.

https://www.ncbi.nlm.nih.gov/pubmed/23771984

Transmissibility of Clostridium difficile without contact isolation: results from a prospective observational study with 451 patients

https://academic.oup.com/cid/article-abstract/doi/10.1093/cid/ciw758/2525936/Transmissibility-of-Clostridium-difficile-without

Snuggle

Jan 2, 2017

I have been doing this blog since September 2006 and have yet to run out of curiosities. ID is the gift that keeps on giving.

I started my fellowship the year Petersdorf wrote his famous article that there were too many ID doctors being trained and not enough for them to do. That was in 1986 and probably stands as one of the worst predictions in medicine, although not even on the list of worst predictions ever. C, X, and Q live on. And I want my flying car. Now.

2017 looks to be a banner year for ID: climate change, war, decreased vaccinations, and the gutting of the affordable care act all promise a resurgence in infections from TB to diarrhea to measles. And who knows what awful viral disease will emerge, or re-emerge, this year.

Yes, it is good to be an ID doctor, although it has always been a bummer that such an endlessly interesting field is driven by the horrible pain and suffering of others.

The patient is an elderly female who had breast cancer with bilateral mastectomy and reconstructions. She is admitted with cellulitis of the surgical incision, but it is in an odd distribution. It is multifocal, with a half dozen bilateral quarter-sized erythroderma all in the middle third of the torso. The peripheral wounds are spared. It looks just like erysipelas and responds rapidly to antibiotics.

It is a puzzle as to why with no exposure I can find on the initial review of systems.

So I talk it over with the patient, explaining it sure looks like Group A Streptococcus, the same Streptococcus that causes strep throat, but it is in an odd place with an odd distribution.

And as I talk, you can see the light turn on. It turns out she had been taking care of her grandchildren, who had sore throats/URIs, and they liked to snuggle up to grandmother's chest, just where the erythroderma patches were.

There is no shortage of Group A streptococcal infections acquired from colonized health care workers, but this was the only case and more than two weeks after the last intervention, so I am inclined against nosocomial acquisition.

Viral upper respiratory infections facilitate the transmission of other bacterial infections, including the following pathogens that colonize the nose: S. pneumoniae, S. pyogenes, H. influenzae, and N. meningitidis . Thus, cloud adults have the potential to play a role in the transmission of other organisms and might be involved with some of the explosive outbreaks of infection occasionally seen in day-care centers, homeless shelters, the military, and hospitals. Further work is necessary to understand the importance of cloud adults in the transmission of hospital infections.

What could more in a cloud of bacteria than a child with URI?

I never grew an organism to prove it, but the story is just too good to ignore.

Rationalization

Surg Infect (Larchmt). 2013 Aug;14(4):385-8. doi: 10.1089/sur.2012.050. Epub 2013 Jul 16. Outbreak of infections caused by Group A Streptococcus after modified radical mastectomy.

https://www.ncbi.nlm.nih.gov/pubmed/23859674

Emerg Infect Dis. 2001 Mar-Apr;7(2):241-4. "Cloud" health-care workers.

https://www.ncbi.nlm.nih.gov/pubmed/11294715

POLL RESULTS

In 2017 I look forward to seeing

• small pox 5%
• measles 32%
• polio 7%
• dengue hemorrhagic fever 11%
• English sweating sickness 27%
• Other Answers 18%
• Contagious suicidal impulses.
• All of the above, but only infecting those who have posted anti-vax memes on social media.
• Mars Attacks remade as the documentary of the real thing. It can't happen soon enough. When I'm calling Yoooooouuuuuuu..
• Strangles
• all of the above

No Go

Jan 4, 2017

The patient was on high dose prednisone, 60 mg a day, for an underlying autoimmune problem. The prednisone did nothing for the underlying problem but did lead to a steroid myopathy and a cavitary pneumonia in the RLL.

The prednisone was weaned off, and the patient was treated with Augmentin. The infiltrate/cavity maybe improved, but not enough to avoid a bronchoscopy. The gram stain showed branching gram-positive rods, and the cultures grew Nocardia nova.

He was surprisingly asymptomatic from the Nocardia: no pneumonia symptoms at all.

Cavitary pneumonia and Nocardia, ok, they go together like peanut butter and jelly. But N. nova? Not so much.

There are but a smattering of cases of pneumonia due to N. nova.

He is also on cardiac medications and arrhythmia issues that make sulfa problematic. Or so the pharmacist says. I do not know about you, but I find the drug-drug interactions generated by the computer are unhelpful. I can find one unconvincing case of cardiac toxicity from the combination of Bactrim and amiodarone. There are fewer cases with clarithromycin.

Not that I have a lot of options. Susceptibilities suggest Bactrim, clarithromycin, and imipenem are it. He also has cutaneous burning from sulfa, so clarithromycin it is. However, I wonder if he really needs the antibiotic now that the prednisone is gone. I bet he would get better on his own. But I am too chicken to see what the natural history of the disease might be.

Rationalization

Nihon Kokyuki Gakkai Zasshi. 2001 Jul;39(7):492-7. [Pneumonia caused by Nocardia nova].

https://www.ncbi.nlm.nih.gov/pubmed/11579529

Pol Merkur Lekarski. 2014 Nov;37(221):285-8. Cardiac arrest and electrical storm due to recurrent torsades de pointes caused by concomitant clarithromycin, cotrimoxazole and amiodarone treatment.

https://www.ncbi.nlm.nih.gov/pubmed/25546990

Don't Go Here.

http://www.snopes.com/business/misxlate/nova.asp

Atypical

Jan 9, 2017

There are typical typicals. These are diseases we know that present typically. There are typical atypicals. That is to say, there are atypical diseases that we know present typically. But there are also atypical atypicals. There are atypical diseases that present atypically. And they are a pain to diagnose.

Donald Rumsfeld. Kind of.

The patient had a kidney transplant last year. Her husband had a URI, and shortly thereafter, she became ill. Fevers, chills/rigors, and a bad headache.

Besides the headache, the ROS was negative, as was the exam.

The WBC was normal, with a slight left shift and a minimal elevation of transaminases.

Work up of the fevers was initially negative, and after 48 hours, she looked much better. The headache had resolved, and she was feeling improved and ready to go home.

Then things got worse. Progressive SOB requiring intubation, increasing fever, his WBC climbed to 12K, and some hypotension. Pan scan showed some patchy infiltrates and perhaps a large gallbladder.

Acalculous cholecystitis with sepsis? But the HIDA was negative.

Then the CMV quantitative PCR came back. 1.3 million.

Every CMV I have ever seen has had either cytopenia and/or hepatitis. This was an atypical presentation. But perhaps typical:

Five cases of late and atypical CMV disease in heart (n = 1), liver (n = 1), and kidney (n = 3) transplant recipients occurred within a 4-month period in early 1999. These patients presented at a median of 25 months after organ transplantation (range, 6 months to 22 years). Atypical findings included absence of fever in 3 patients, elevated white blood cell counts in 4 patients, and normal platelet counts in 4 patients. Four patients were at risk for primary CMV infection, and 3 received ganciclovir prophylaxis for 3 months. One patients was treated for rejection, and 2 patients had induction muromonab-CD3 (Orthclone; Orthobiotech). Two of the patients had pulmonary CMV disease, but neither of these patients had hypoxia.

So here is my conclusion about transplant patients. Like the old days with syphilis, CMV can present typically and atypically, and no matter what the signs or symptoms, until the CMV studies are back, assume CMV.

Rationalization

Clin Infect Dis. 2001 Oct 1;33(7):E62-8. Epub 2001 Sep 5. Late and atypical cytomegalovirus disease in solid-organ transplant recipients.

https://www.ncbi.nlm.nih.gov/pubmed/11528587

Transplant Proc. 2004 Jul-Aug;36(6):1841-3. Late cytomegalovirus disease with atypical presentation in renal transplant patients: case reports.

https://www.ncbi.nlm.nih.gov/pubmed/15350493

Abscess Does Not Make the Heart Grow Fonder

Jan 11, 2017

Some diseases are like jumping out of an airplane without a parachute. You might think that aiming for the lake instead of the concrete will make a difference, but it won’t.

Drug addiction is like that. Unchecked/untreated, it is certain death, not if, but when. The only uncertainty is how. OD? Murder? Infection?

The patient is a polysubstance abuser who was admitted with MRSA bacteremia, MIC to vancomycin of 1.0, and a TEE shows not only endocarditis but a myocardial abscess.

A myocardial abscess is a surgical disease. I have treated one Group G Streptococcal myocardial ring abscesses successfully when the surgeons have declared that the patient was not a surgical candidate. I have never tried with S. aureus, much less MRSA,

A ring abscess is close to jumping out of a plane sans parachute.

The hospital mortality rate was 90 percent in the 10 patients who did not receive surgical treatment, as compared with 26.6 percent in the 30 operated-on patients (p<0.001). data-preserve-html-node="true"

He keeps leaving for a day or three to inject drugs, so the surgeons are loath to operate.

He is also completely resistant to any intervention and says he wants to keep using.

Sad. I have enough difficulty generating the willpower to resist the siren call of maple bars. I can’t imagine being hooked on heroin or cigarettes. There but for the grace of the flying spaghetti monster go I.

I suggested rifampin in addition to the vancomycin for (perhaps) some extra intra-pus killing as,

Vancomycin and ciprofloxacin levels were inadequate in most abscesses.

but I am not optimistic. He left again just before snowmageddon, never to be seen again.

Rationalization

Perivalvular Abscesses Associated With Endocarditis: Clinical Features and Diagnostic Accuracy of Two-Dimensional Echocardiography.

http://www.sciencedirect.com/science/article/pii/S0012369216474787

Am J Surg. 2011 Mar;201(3):348-52; discussion 352. doi: 10.1016/j.amjsurg.2010.09.010. Impact of evaluating antibiotic concentrations in abdominal abscesses percutaneously drained.

https://www.ncbi.nlm.nih.gov/pubmed/21367377

Have We Been Thinking About Willpower the Wrong Way for 30 Years?

https://hbr.org/2016/11/have-we-been-thinking-about-willpower-the-wrong-way-for-30-years

POLL RESULTS

I can't resist

• illegal drugs 0%
• maple bars 15%
• tobacco 0%
• legal drugs 9%
• beer 32%
• Other Answers 44%
• Reading RDCT
• Chocolate
• Cookies!
• chocolate
• salty crackers
• The Borg
• chocolate
• open-ended polls.
• horses noses
• Licorice
• salt

A minor spleen vent

Jan 17, 2017

To vent the spleen. I imagine putting a tube in the spleen to let off pressure. Odd phrase.

In European medicine from the Middle Ages until the nineteenth century, the spleen was thought to be the source of the "humours" that caused the emotion of anger. Therefore one could expel anger by "venting the spleen".

I don't suppose spleen-venting leads to Howell-Jolly bodies or an increased risk for purpura fulminans, so I will be safe to continue.

Both my colleagues were gone today, and I had a 9 consult day. I really do not have the energy I did when I was young. I turn 60 this spring, 420 in dog years, and I am starting to feel it. So rather than a well-documented case, and I have a couple of cool ones if the cultures pan out, I will wave my AARP (the sound of an old man belching) card and winge.

The patient came in with influenza, of which we have been having an English tonne of admissions and a smattering of deaths. He got better. Then he sat on the wards awaiting a transfer to his care facility, who wouldn't take him back because of low-grade fever.

Low-grade fever.

No. Look at the fever curve.

The patient has been afebrile since 1/10. He could have gone back to his facility 4 days ago.

Fever, like pregnancy, is a binary function. Either the patient is febrile or not; there is no such thing as a low-grade fever any more than a low-grade pregnancy.

Normal body temp goes as high as 100.4 with an average of 98.2, yes, ninety-eight point two:

Results. —Our findings conflicted with Wunderlich's in that 36.8°C (98.2°F) rather than 37.0°C (98.6°F) was the mean oral temperature of our subjects; 37.7°C (99.9°F) rather than 38.0°C (100.4°F) was the upper limit of the normal temperature range; maximum temperatures, like mean temperatures, varied with time of day; and men and women exhibited comparable thermal variability. Our data corroborated Wunderlich's in that mean temperature varied diurnally, with a 6 AM nadir, a 4 to 6 PM zenith, and a mean amplitude of variability of 0.5°C (0.9°F); women had slightly higher normal temperatures than men; and there was a trend toward higher temperatures among black than among white subjects.

Conclusions. —Thirty-seven degrees centigrade (98.6°F) should be abandoned as a concept relevant to clinical thermometry; 37.2°C (98.9°F) in the early morning and 37.7°C (99.9°F) overall should be regarded as the upper limit of the normal oral temperature range in healthy adults aged 40 years or younger, and several of Wunderlich's other cherished dictums should be revised.(JAMA. 1992;268:1578-1580)

Second only to considering antibiotics as 'big gun', 'strong', or 'powerful' is the idea of a low-grade fever. A sure sign, like an L on the forehead, that the speaker is Jon Snow.

Now I am going to put on the golf channel and fall asleep on the couch.

Rationalization

A Critical Appraisal of 98.6°F, the Upper Limit of the Normal Body Temperature, and Other Legacies of Carl Reinhold August Wunderlich. JAMA. 1992;268(12):1578-1580. doi:10.1001/jama.1992.03490120092034

https://jamanetwork.com/journals/jama/article-abstract/400116

POLL RESULTS

I measure my age

• in dog years 7%
• in cat years 7%
• in Mayfly years 7%
• in lost hairs 9%
• in lost opportunities. 65%
• Other Answers 5%
• In the number of non-healing corneal erosions I have seen in 32 y3ears.
• in chipped and lost teeth.

A-III: A contradiction in evidence

Jan 18, 2017

When I get a consult for recurrent UTI’s, I just want to stick my fingers in my ears and make noise. Recurrent cystitis is virtually never an ID problem, it is a structural problem, and if the urologist can’t fix the underlying mechanics, there is not a lot (and by not a lot, I mean nothing) that I have to offer.

I get called about Pseudomonas in the urine of a paraplegic. What antibiotic, duration of that antibiotic, and when can the patient have a pacemaker?

The what is easy. I look at the C&S, and cefepime would be the choice if a symptomatic UTI.

How long? Got me.

The guidelines say

Seven days is the recommended duration of antimicrobial treatment for patients with CA-UTI who have prompt resolution of symptoms (A-III), and 10–14 days of treatment is recommended for those with a delayed response (A-III), regardless of whether the patient remains catheterized or not.

Does she need treatment? I don't know. Her only symptoms were increases spasticity.

The guidelines say

In patients with spinal cord injury, increased spasticity, autonomic dysreflexia, or sense of unease are also compatible with CA-UTI (A-III).

Both of these recommendations are A-III.

A is Good evidence, and III is the source of the evidence:

evidence of respected authorities, based on clinical experience, descriptive studies, or reports of expert committees.

In other words, III is likely worthless biased garbage. If there is one thing I have learned in my time at SBM, A and III do not belong together. Ever. It is "in my experience" hidden in Roman numerals.

The expert committee is from 1992. 25 years ago. It would be safe there is little from that era concerning UTI’s that holds true today. Just what the 1992 report based its opinion on, I cannot say; after 25 years, it is still behind a paywall.

As best I can tell, there is not a lick of real data to support increased spasticity, autonomic dysreflexia, or sense of unease as indicative of a UTI. But we have trained patients and health care workers alike, to say it is so.

And when you think about how much money is spent on this problem, mostly breeding bacterial resistance, you would think there would at least some hard evidence to guide us. Nope. Maybe my google-fu is off.

When can a cardiac device be put in?

I don’t know.

Extrapolating from other conditions like hip replacement, the organisms in the bladder are never found in the joint infection, and gram-negative rods have little potential of seeding the pacer. So do it anytime?

That's my A-III opinion.

Rationalization

Frequency of Permanent Pacemaker or Implantable Cardioverter-Defibrillator Infection in Patients with Gram-Negative Bacteremia

https://pubmed.ncbi.nlm.nih.gov/16912947/

Orthop Relat Res. 2013 Dec;471(12):3822-9. doi: 10.1007/s11999-013-2868-z. Are antibiotics necessary in hip arthroplasty with asymptomatic bacteriuria? Seeding risk with/without treatment.

https://pubmed.ncbi.nlm.nih.gov/23430723/

The prevention and management of urinary tract infections among people with spinal cord injuries. National Institute on Disability and Rehabilitation Research Consensus Statement. January 27-29, 1992.

https://pubmed.ncbi.nlm.nih.gov/1500945/

POLL RESULTS

I think

• A-III is worthless 26%
• A-1 is delicious 30%
• A-OK is fine 13%
• Ayyyyyyyyyy is Fonzilicious 17%
• A+ makes the grade 13%

Alternative Facts

Jan 23, 2017

I thought I had a solution to all the hassles of medicine. Don’t want to go with standard treatments as they are too expensive or inconvenient? Use alternative facts. Here is some oral PCN VK for your MRSA endocarditis. Infection rates up, and we have to report it? Use alternative facts and say the rates are zero. Don’t know the right answer on the recertification exam? Use alternative facts, and any answer becomes the right answer.

It is so freeing not having to worry about reality. I can see why it is popular in the Integrative Medical Clinics. But, sadly, the euphoria did not last the day. It turns out that it is not a useful technique if you want to practice reality-based medicine. Nothing like an infection to bring you back to earth:

5 months ago, the patient, an otherwise healthy female except for HIV, viral load undetectable, and CD4 1100 for years, was treated for secondary syphilis with a 28-day course of doxycycline due to a penicillin allergy. The VDRL went from 1:64 to 1:1

Now she presents with 2 weeks of headache and bilateral scotomata. An ophthalmologic exam showed bilateral retinal edema. The patient had the 5-star workup, including an MRI and LP (very slight protein elevation), and no diagnosis was made except for the 1:1 VDRL and a 4 plus FTA.

Lues? Perhaps. The annoying thing about lues is proving active disease.

How to put it together? This is my just-so story.

Syphilis disseminates to the CNS at every stage.

Treponema pallidum was isolated from the CSF of 12 (30%) of 40 patients (95% CI, 17 to 46) with untreated primary and secondary syphilis.

The doxycycline cleared out all the syphilis except in the protected space of the eye:

Although tetracycline and doxycycline are used as alternative treatments for syphilis there is less experience with their use, and patients receiving these regimens should be closely monitored. The oral administration of tetracycline or doxycycline, which are less lipophilic than minocycline, results in a low concentration in the spinal fluid. There is little information on the ocular penetration of doxycycline. Oral minocycline penetrates well into the eye achieving vitreous levels of about 50% of the plasma levels.15 This patient still manifested neurosyphilis despite benzathine penicillin and doxycycline.

Where it progressed to cause illness.

She should have been treated with penicillin as the allergy history was unimpressive: some sort of rashy something as a child that was never specified, all according to her mother. No hives or laryngeal edema. The usual. Most penicillin allergies are not, and if the patient doesn’t report a true Type 1 reaction with careful questioning, I give penicillin with impunity.

I do have one superstition: I put the code cart outside the room with the first dose. If you do that, it will never be used.

So we gave her penicillin, and she did just fine. Vision improved.

And another example of an adverse event when reacting to the alternative fact of a penicillin allergy.

Among 507 patients, 95 (19%) reported beta-lactam allergy; preferred therapy was a beta-lactam in 72 (76%). When beta-lactam therapy was preferred, 25 (35%) did not receive preferred therapy due to their report of allergy even though 13 (52%) reported non-severe prior reactions. After adjustment for confounders, patients who did not receive preferred beta-lactam therapy were at greater risk of adverse events (adjusted odds ratio [aOR], 3.1; 95% confidence interval [CI], 1.28–7.89) compared with those without reported allergy.

Rationalization

Invasion of the Central Nervous System by Treponema pallidum: Implications for Diagnosis and Treatment.

http://annals.org/aim/article/702757/invasion-central-nervous-system-treponema-pallidum-implications-diagnosis-treatment

Postgrad Med J. 2006 Jan; 82(963): 36–39. doi: 10.1136/pgmj.2004.020875 PMCID: PMC2563717 Neurosyphilis with optic neuritis: an update.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2563717/

Impact of Reported Beta-Lactam Allergy on Inpatient Outcomes: A Multicenter Prospective Cohort Study Clin Infect Dis. 2016 Oct 1;63(7):904-910. doi: 10.1093/cid/ciw462. Epub 2016 Jul 11.

https://pubmed.ncbi.nlm.nih.gov/27402820/

Special Report: When a Patient Reports a Penicillin Allergy, You Should…

https://www.medscape.com/viewcollection/33964

POLL RESULTS

In medicine, I an wary of

• alternative facts 15%
• alternative medicines 44%
• alternative music 7%
• alternative explanations 4
• alternative blame 22%
• Other Answers 7%
• alternating current, especially 60HZ, at anything over about 35V.
• all

Drug Complications

Jan 25, 2017

It has been crazy busy. We have had 736 admissions in Oregon just from influenza. It is looking like a record year for flu.

When I started in practice in 1990, the metro area had a population of 1,523,741. Now? 2,389,228. And in that time, we have closed three hospitals and converted all the semi-private rooms (What a term. Semi-private. I'll get a semi-private room at the next hotel. Not.) to singles. More people, more illness, and fewer beds. Great combination. But lots of pathology.

The patient has both chronic lung disease and renal failure on dialysis. He has a pneumonia and grows out a mostly resistant Pseudomonas, so he is treated with a beta-lactam and inhaled tobramycin.

We don’t have much CF in my hospitals as all the patients go to the University, and that is the only indication I know for inhaled tobramycin, but I always thought it a great way, in theory, to kill gram negatives in the lung and spare the kidney and 8th nerve. Sometimes.

They called me after 12 days as they wanted to know how what to do with the current antibiotics now that repeat cultures have a Pseudomonas is resistant to everything.

No surprise, there is now a pan-resistant organism; use it and lose it. Unfortunately, not only are combination (double cover, double cover, double cover) antibiotics not more effective, combination/synergistic antibiotics breed resistance faster. Curiously, antagonistic combinations may slow resistance—evolution in action.

But the patient is clinically getting better, and given the underlying structural lung disease, I would expect a clinical cure but not a microbiologic cure.

Ignore the new cultures, I said. Oh, and check a tobramycin level. At 12 days in the trough is 3.8. As best we can tell, there is no 8th nerve damage. Yet. They stopped the tobramycin.

There are other cases in the literature of inhaled tobramycin leading to toxic blood levels in renal failure.

The pearl: As an intern, I had a patient go deaf on neomycin peritoneal irrigation, and I learned just because a drug is not given iv doesn’t mean that it isn’t absorbed and can’t cause toxicity.

Rationalization

Drug interactions and the evolution of antibiotic resistance.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2855488/

High tobramycin serum concentrations after tobramycin inhalation in a child with renal failure.

https://www.ncbi.nlm.nih.gov/pubmed/25006239

I've always thought my opinion was the right one. It's a small flaw I have." - Lily King

Jan 30, 2017

“Opinions are easy,” said Henry with a shrug. “So long as I know anything at all about a topic, I’m going to have an opinion. Sometimes that opinion is going to be wrong, but one of the great things about opinions is that you can change them. And if you share your opinions, you’re much more likely to come across someone who disagrees with you and can help you to be less wrong, which is why I give my opinions so freely. Maybe the oathkeepers are nothing like what I imagine them to be. Maybe the small number of them I’ve met aren’t representative of the whole. I don’t think it’s out of the question that I might meet an oathkeeper who’s spent decades studying all of the same things that I’ve thought of and stands ready to demolish me in a debate. So long as I don’t start thinking of my opinions as something sacred, there’s no harm in them. So no, there’s nothing that I can think of that I don’t have an opinion on.” ― Alexander Wales,

I remember when H1N1 hit in 2009, shortly after the MRSA 300 epidemic had peaked, I fretted about the combination of the two infections. To quote me

...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.

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.

It happened.

During the 2003–04 influenza season, 17 cases of Staphylococcus aureus community-acquired pneumonia (CAP) were reported from 9 states; 15 (88%) were associated with methicillin-resistant S. aureus (MRSA). The median age of patients was 21 years; 5 (29%) had underlying diseases, and 4 (24%) had risk factors for MRSA. Twelve (71%) had laboratory evidence of influenza virus infection. All but 1 patient, who died on arrival, were hospitalized. Death occurred in 5 (4 with MRSA). S. aureus isolates were available from 13 (76%) patients (11 MRSA)

But not to the degree that I worried about. We had a smattering of S. aureus pneumonias, but, fortunately, no deluge. Ick. A deluge of Staphylococcal sputum.

I was right, but was only off by 8 years. In the last month, I have seen about 8 cases of influenza and other URI’s followed by multifocal necrotizing Staphylococcal pneumonia, both MRSA and MSSA.

And they have been a son of a gun. If I were a superhero, S. aureus would be my Lex Luthor. Sadly, we really do not know what the best treatment for severe staphylococcal infections is.

I have come to the following opinions, and you know what they say about opinions, about treating S. aureus in the lung. Informed opinions, perhaps, but opinions none the less.

Vancomycin stinks on ice. It should be the last antibiotic used for S. aureus. I only want to use it for relatively trivial infections with good source control. That is neither pneumonia nor empyema.

Linezolid isn’t much better. Pick your study or meta-analysis, but saying linezolid is better than vancomycin is damning with faint praise.

What is the best therapy? Not therapy we can get away with most of the time but the best? Got me. I have the hint of a suspicion of an opinion that it is combination therapy. There are hints here and there in the literature, depending on the organ infection and the model used, that one is the loneliest number for killing S. aureus. Two is better than one, but which two? And for what infection? Daptomycin and nafcillin? Vancomycin and rifampin? An anti-staph antibiotic and clindamycin? An anti-staph antibiotic and rifampin? Linezolid and a carbapenem? Vancomycin and a beta-lactam?

Our data indicate that β-lactam antibiotics should be included in the treatment regimen as an adjunct antivirulence therapy for patients with MRSA infections. This would represent an important change to current clinical practice for the treatment of MRSA infection, with the potential to significantly improve patient outcomes in a safe, cost-effective manner.

My fav as of 1/20/17 at 8:08 pm? Ceftaroline and clindamycin >> rifampin. Kill the bug and mess with virulence factors like PVL.

Do I know it is best? Nope. And I am likely to have a different opinion in a year.

“My opinions may have changed, but not the fact that I'm right.” ― Ashleigh Brilliant

Maybe before I retire we will know.

Rationalization

Concurrent Epidemics of Skin and Soft Tissue Infection and Bloodstream Infection Due to Community-Associated Methicillin-Resistant Staphylococcus aureus.

https://academic.oup.com/cid/article/55/6/781/344436/Concurrent-Epidemics-of-Skin-and-Soft-Tissue

Bacterial and viral infections associated with influenza. A postinfluenza model of Staphylococcus aureus pneumonia Influenza Virus Primes Mice for Pneumonia From Staphylococcus aureus.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3071123/

Severe Community-acquired Pneumonia Due to Staphylococcus aureus, 2003–04 Influenza Season.

https://wwwnc.cdc.gov/eid/article/12/6/05-1141\_article

Eur J Clin Pharmacol. 2015 Jan;71(1):107-15. doi: 10.1007/s00228-014-1775-x. Epub 2014 Oct 30. Linezolid versus vancomycin for the treatment of suspected methicillin-resistant Staphylococcus aureus nosocomial pneumonia: a systematic review employing meta-analysis.

https://www.ncbi.nlm.nih.gov/pubmed/25355172

Redeploying β-Lactam Antibiotics as a Novel Antivirulence Strategy for the Treatment of Methicillin-Resistant Staphylococcus aureus Infections. https://www.ncbi.nlm.nih.gov/pubmed/28077586

Cushy Red Bumps

Feb 1, 2017

The patient is a young male who had a femoral neck fracture doing routine work in his birth county. No reason for the fracture was found or looked for.

He came to the Great Pacific NW, where he has worked in landscaping, suffering some spinal compression fractures. He also developed diabetes that became increasingly difficult to control, leading to his admission.

His exam? Hypertensive. Buffalo Hump. Abdominal striae. Peripheral muscle wasting. And red bumps all over his arms and legs.

Labs? A serum cortisol of 52 that did not suppress, an elevated ACTH, and a pituitary adenoma on MRI. Classic endogenous Cushing’s. I have never seen real Cushing’s, only iatrogenic disease.

But wait, you say, red bumps are not part of Cushing’s. Right you are.

Red bumps in the immunoincompetent are AFB, especially atypical mycobacteria, fungal, especially Cryptococcus, and Bartonella. Risk factors are mostly his work as a landscaper.

That put Cryptococcus at the top of the list. We sent off all the above tests, and only the serum Cryptococcal antigen came up positive, although the skin biopsy did not show Cryptococcus. CSF was negative.

Cushing’s and Cryptococcus? It happens. There are a few cases of pneumonia and a single case of disseminated disease.

I have now doubled the medical literature. There are also a smattering of other invasive fungal diseases with endogenous Cushing’s.

He improved on fluconazole and has his adenoma removed.

Rationalization

Korean J Intern Med. 2003 Sep;18(3):199-201. Disseminated cryptococcosis in a patient with pituitary Cushing's disease. <https: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/14619392>

Opportunistic Infections in Endogenous Cushing's Syndrome. <http: data-preserve-html-node="true"//citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.854.3224&rep=rep1&type=pdf>

Ann R Coll Surg Engl. 1969 Apr; 44(4): 180–181. PMCID: PMC2387613 The Basophil Adenomas of the Pituitary Body*,1 Harvey Cushing. <https: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pmc/articles/PMC2387613/.>

Annoyingly, I can find only the first two pages of the original on the web.

Back Pain

Feb 6, 2017

The patient has back pain, lumbar, that progresses over a month and a half. There is the usual conservative care that fails, including a steroid injection. You know, since this is an ID blog, that I am not presenting a case of a tumor or a herniated disc. It’s going to be bad if I want to write about it.

Eventually, he gets an MRI in the ER, and it shows discitis and osteomyelitis. History reveals no risks of note. He has an uneventful life so that I would expect a Staphylococcus or Streptococcus.

While in the hospital, he has progressive neurologic symptoms and so to the OR for an I&D. I am occasionally asked if I am the I&D doctor. Nope. That would be the surgeon. I am an internist.

The pathology shows?

Hyphae. Did not see that coming.

And the lab eventually calls it Aspergillus nidulans, which grows in all the samples.

All Aspergilluses/Aspergilli are not the same, and A. nidulans?

Interestingly, Aspergillus (Emericella) nidulans is the second most encountered mold in CGD patients, causing almost exclusively invasive infections in this specific host, and is characterized by its aggressive behavior.

Emericella is the name given for its sexual form, although why Aspergillus needs another name for sex is uncertain. I guess it is like an internet ‘nym for anonymity when logging on some websites?

The annoying aspect is the workup for CGD, as well as a suggestive history, are negative, with a normal granulocyte dihydrorhodamine fluorescence suggesting normal NADPH oxidase activity. I suppose it could be from the steroid injection, but those have been due to A. fumigatis. There have been no other cases, he had no herniation to account for the pain, and no other reason for a discitis found.

He was placed on voriconazole, and we will see.

Of interest, anidulafungin was derived from A. nidulans var. echinulatus strain A 32204. So could you use anidulafungin against A. nidulans? Yep.

All 13 A. nidulans strains were highly susceptible to anidulafungin, with a MEC of 0.031mg/L … In conclusion, chemical modification of the original echinocandin B moiety renders this natural product active against moulds, including A. nidulans.

Better living through chemistry.

Rationalization

J Infect Dis. 2012 Oct 1;206(7):1128-37. doi: 10.1093/infdis/jis473. Epub 2012 Jul 24. Aspergillus nidulans and chronic granulomatous disease: a unique host-pathogen interaction.

https://www.ncbi.nlm.nih.gov/pubmed/22829648

Int J Infect Dis. 2004 Mar;8(2):103-10. Osteomyelitis due to Aspergillus spp. in patients with chronic granulomatous disease: comparison of Aspergillus nidulans and Aspergillus fumigatus.

https://www.ncbi.nlm.nih.gov/pubmed/14732328

J Antimicrob Agents. 2009 Mar;33(3):285-6. doi: 10.1016/j.ijantimicag.2008.08.022. Epub 2008 Nov 20. Antifungal activity of anidulafungin, a product of Aspergillus nidulans, against Aspergillus nidulans.

https://www.ncbi.nlm.nih.gov/pubmed/19026523

Apeeling

Feb 8, 2017

The patient is a healthy female, no medical problems who has nightly high fevers for 5 days. She became progressively weak and was finally admitted to the hospital.

The evaluation was unsatisfactory.

ROS was significant for intermittent severe arthralgias in hands, feet, knees, shoulders, and hips but no red hot tender joints. And her thumbs, she said, felt like they had a layer of plastic over them.

When febrile, she had a red rash on the abdomen.

Labs had a slight decrease in the WBC and increased inflammatory markers with the ESR 60, CRP 33, Ferritin 602.

In the hospital, the arthralgias were less of an issue, and no process was identified, so she was discharged to home.

In the clinic several days later, she was about the same: nighttime fevers and severe arthralgias.

The curious finding was her fingertips and toes were peeling.

That’s weird.

The differential of isolated peeling fingers is narrow: exfoliative toxins from Staphylococcus and Streptococci, Kawasaki (she is much too old, no oral, conjunctival, or adenitis, but… it has occurred as old as age 68) and Stills.

It is kind of weird how just the fingers and toes are peeling. Why not the rest of the dermis? The skin is odd that way.

The other issue was the ferritin, kind of low for Stills:

Detection of ferritin values above 3000 micrograms/l should lead to the consideration of Still's disease when there is an acute febrile illness without evidence for bacterial or viral infections, serum ferritin being suitable for monitoring treatment.

But perhaps the disease needed to fester longer to raise the ferritin higher.

Rheumatology has never been my strong suit. Let’s just say that for my medicine boards, I might have had better scores on the Rheumatology section if I had simply answered every question ‘B.’ I have missed the diagnosis of Still’s twice in my career. I do not want to miss a third, so I sent her to Rheumatology to confirm or deny the diagnosis. They called it Stills.

*Celebratory Dance*

She improved on prednisone.

Rationalization

Diagnosis of “probable” Still's disease and its outcome.

https://scholar.google.com/scholar?q=still%27s+disease+peeling+&btnG=&hl=en&as\_sdt=0%2C38

Ann Rheum Dis. 1992 May;51(5):683-5. Evaluation of serum ferritin as a marker for adult Still's disease activity.

https://www.ncbi.nlm.nih.gov/pubmed/1616341

Arch Mal Coeur Vaiss. 2007 May;100(5):439-47. Kawasaki disease is also a disease of adults: report of six cases.

https://www.ncbi.nlm.nih.gov/pubmed/17646771

Autoimmun Rev. 2016 Mar;15(3):242-9. doi: 10.1016/j.autrev.2015.11.010. Epub 2015 Nov 26. Kawasaki disease in adults: Observations in France and literature review.

https://www.ncbi.nlm.nih.gov/pubmed/26631821

60%

Feb 13, 2017

The patient is a renal transplant who presents with fevers, delirium, and a consolidated pneumonia, and multiple pulmonary nodules.

Work up? WBC 28K. Blood & bronchoscopy stains and cultures negative. The beta-D-glucan is 210. Not as high as one would like for all the pulmonary nodules. Multiple pulmonary nodules suggest a hematogenous infection, and I would expect a very positive 1-3-beta D glucan.

There is the issue of the elevated WBC, which may make the 1-3-beta D glucan less reliable, probably as the WBC are eating up the glucan.

Compared with the testing of neutropenic patients, the serum GM or BG assay alone was less useful for the diagnosis of IPA in non-neutropenic patients.

Mmmmmmmmm. Beta-D-glucan. On antifungals and antibacterials, he has no improvement, and since we have no diagnosis, we biopsy a nodule.

Negative stains, so we, and by we I mean I, send the specimen off to the University of Washington for magic, aka 16S ribosome testing. While waiting, the biopsy starts growing a partially acid-fast something or other, which magic calls Nocardia farcinica.

He is getting better on TMP/sulfa and imipenem, awaiting final susceptibilities. Nocardia farcinica is sometimes TMP/sulfa resistant, but imipenem and quinolones are reliable. And his beta-D-glucan has fallen by half.

There are two cases on the Pubmeds of pulmonary Nocardia and an elevated beta-D-glucan. This is the third one reported on this blog, so I now have 60% of the world's reported Nocardia cases with an elevated beta-D-glucan.

Go me.

Rationalization

Pulmonary nocardiosis with elevation of serum beta-D-glucan in a patient with polymyositis. Hashizume Y, Takise A, Kawata T, Suzuki K, Endou K, Horie T. Nihon Kokyuki Gakkai Zasshi. 2011 Oct;49(10):750-5.

https://pubmed.ncbi.nlm.nih.gov/22117312/

A case of disseminated nocardiosis followed by pneumocystis pneumonia in a patient prescribed corticosteroid and cyclosporin A and having elevated blood (1-->3)-beta-D-glucan. Harada S, Hatakeyama S, Kitazawa T, Itoyama S, Ota Y, Koike K. Kansenshogaku Zasshi. 2009 Sep;83(5):538-43. Japanese.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7380859/

In Medicine You Can Never Know Enough.

http://boards.medscape.com/forums/?128@@.2a791f88!comment=1

More Fleas and Lice.

http://boards.medscape.com/forums/?128@@.2a7bce64!comment=1

Vague Unease

Feb 15, 2017

Several months after my Dad retired as a cardiologist, he became remarkably more energetic and rested. I commented that he must be getting a good night's sleep now that he wasn’t getting called all the time. He told me it wasn’t the calls that ruined his sleep but fretting about patients.

I can relate. Bedtime, in the dark and quiet, is a good time to perseverate about patients. That and existential angst are good ways to delay sleep.

I have had a bolus of patients the last few weeks whom either I can’t figure out or, as in this case, generate a vague unease that there is more going on than I can pinpoint—a case in point. And no, she is not talking to senior Russian officials throughout her hospitalization.

An elderly female at Outside Hospital has both influenza A and bacteremic Yersinia enterocolitica diarrhea. She receives a course of iv antibiotics and oseltamivir and is sent out on a second-generation cephalosporin.

Two days after stopping the oral antibiotics, she has fevers and chills and is admitted to my hospital with elevated WBC, and maybe an infiltrate on CXR. The patient is coughing but non-productive and looks modestly ill.

The only issue of note is a pacemaker.

She is placed on vancomycin and cefepime, and the next day, I get called.

What do we find?

She is still positive for flu by PCR. That is no surprise; the PCR can be positive for 14 days.

There is a gram-negative rod in the sputum, identified as Pseudomonas. Probably not the real deal, but she does get better on the antibiotics. I suspect true/true and unrelated but post influenza bacterial pneumonia is common, so I am hesitant to stop all antibiotics.

She gets better slowly, perhaps due to age. I fret about the pacer wires being infected after the bacteremia, but gram-negative rods just do not have a predilection for pacers. It is hard to justify the cost and risks of a TEE just because I am ill at ease, and there is nothing objective to suggest a pacer infection.

Then she develops ankle, knee, and neck pain, now a month out from the bacteremia. Inflammatory parameters are still way up, and there is now an effusion in the knees, but they are not red, hot, or tender. The neck is very tender to light percussion.

Post-infectious arthritis? Yersinia is one of the infections that can trigger arthritis, and as best I can tell from the literature, the spine can be involved.

Most of the 19 patients with polyarthritis had preceding fever and gastrointestinal symptoms. Fingers, knees and ankles were most often affected. Three patients had acute sacro-iliitis and some others back pain or severe myalgia.

Or is the disc infected? MRI can’t be done due to the pacemaker.

Time, bone scan, and HLA will tell.

But I just can’t shake the sense that all is not well.

Rationalization

Arthritis Associated with Yersinia Enterocolitica Infection.

http://www.tandfonline.com/doi/abs/10.3109/rhe1.1969.15.issue-1-4.32

Ten-year followup study of patients with yersinia arthritis.

http://onlinelibrary.wiley.com/doi/10.1002/art.1780310410/full

Reactive Arthritis of the Cervical Spine Due to Yersinia Enterocolitica in a Patient with Preexisting Ankylosing Spondylitis.

http://www.tandfonline.com/doi/abs/10.3109/03009749209095076

POLL RESULTS

At bedtime, I fret

• about patients 21%
• about my inevitable unpleasant death 9%
• about finally being caught 23%
• about my children's future 20%
• not at all and sleep like a baby 14%
• Other Answers 13%
• patients, death, and my child!
• about everything done, undone, planned, hypothetical, failed, lost, forgotten, remembered, hated, or loved. Essentially, anything possible to fret over.
• my exclusion at work because I am paraplegic
• about my future

SMP

Feb 28, 2017

Back from a week off. Miss me? Had a great time in San Antonio and Port Aransas. Except for the beer. No matter where I travel, they just can’t make beer like we have in the Great Pacific NW. Several times I tried a “West Coast-style IPA.” Um, nope.

The first day back is always painful, and it is depressing how fast vacations fade in memory. At least ID still has the ability to thrill and amaze.

The patient is a young female, no medical problems, who presents with an acute abdomen and fever. She is started on antibiotics after a CT that shows no specific pathology. After several days she continues to have fevers, leukocytosis, and abdominal pain, so an exploratory laparotomy is performed.

Diffuse peritonitis, no reason found. The gram stain shows WBCs, but no organisms, and the cultures are negative. Pathology showed peritonitis.

The symptoms persist, so they call me.

H&P yields nothing of note, so I figure this is a Group A Streptococcus. I have seen a pair of cases of SBP with no ascites from this organism, so I gave therapy directed against Group A Streptococcus with a beta-lactam and clindamycin. I wasn’t happy with the negative gram stain, but she had been on antibiotics, and S. pyogenes can cause a marked inflammatory response.

And she did not get better. Repeat studies showed abscesses that were drained, and only WBCs were seen on gram stain.

What doesn’t grow and isn’t seen on standard stains? Spirochetes, Myco- and Urea- plasmas, and Chlamydia and searching the PubMeds there are a smattering of cases of SBP from all the above. So pending the molecular testing, I started treatment with azithromycin betting on Ureaplasma or Chlamydia, and she improved. Slowly.

True true and unrelated? Perhaps. But the 16S did eventually come back positive for M. hominis. The problem is M. hominis is often resistant to doxycycline, macrolides (especially azithromycin), and quinolones, although from the Dark Ages (1984):

in vitro clindamycin would appear to be highly active against pregnancy-associated strains of M. hominis.

She was changed to doxycycline.

There are about a dozen cases of M. hominis causing peritonitis on the Pubmeds, all but one, a post-myomectomy infection, in various transplant patients. There is no suggestion of any immunodeficiency in my patient.

This would be the world's first reported case of SBP without ascites due to M. hominis in a normal host. But it will not be the last. As molecular methods for diagnosis become more widespread, I suspect we will see more cases like this.

She slowly improved.

Rationalization

Br J Surg. 2010 Jan;97(1):104-8. doi: 10.1002/bjs.6822. Diagnosis and treatment of spontaneous group A streptococcal peritonitis

https://www.ncbi.nlm.nih.gov/pubmed/20013929.

BMC Infect Dis. 2014 Mar 28;14:171. doi: 10.1186/1471-2334-14-171. Antimicrobial susceptibility patterns of Ureaplasma species and Mycoplasma hominis in pregnant women.

https://www.ncbi.nlm.nih.gov/pubmed/24679107

Am J Obstet Gynecol. 1984 Jul 1;149 (5):477-80. In vitro activity of clindamycin against strains of Chlamydia trachomatis, Mycoplasma hominis, and Ureaplasma urealyticum isolated from pregnant women.

https://www.ncbi.nlm.nih.gov/pubmed/6742014

POLL RESULTS

When I travel, when compared to home, I am most disappointed with

• the beer 20%
• the mattress 24%
• the sales tax 0%
• the water 24%
• the local news 22%
• Other Answers 10%
• The air
• wine
• the food
• the toilet paper.

How Long is Enough?

Mar 1, 2017

The patient is a refractory IVDA, mostly abusing heroin. I note that the computer often transcribes it as heroine abuse. Poor Wonder Woman.

She is seen at another hospital 3 months ago with MSSA bacteremia and a vegetation on the tricuspid valve. She gets three days of antibiotics before leaving AMA. She presents to another hospital 10 days later with MSSA in the blood and then leaves after 10 days.

Seven weeks pass, and she shows up in my hospital with a fever and a WBC of 36K.

Blood cultures are negative, the fever and WBC revert to normal in 24 hours, and there is still a .5 cm vegetation of the TV.

Now what?

There were no stigmata of endocarditis outside of the ECHO, which will be positive for years.

Usually, MSSA endocarditis is treated for 6 weeks. At least in the US guidelines.

I just discovered that the British suggest

Intravenous therapy for 4 weeks is recommended for staphylococcal NVE, which should be extended to ≥6 weeks in patients with intracardiac prostheses, secondary lung abscesses and osteomyelitis.

Two weeks is a big difference in the length of therapy, and I cannot find a discussion as to why the difference.

And can you get away with less than 4 weeks? Perhaps.

S aureus IE in IDUs often involves the tricuspid valve. Cure rates for right-sided S aureus IE in IDUs are high (>85%) and may be achieved with relatively short courses of either parenteral or oral treatment (2-4 weeks).

So was the 10 days enough to cure her? Perhaps. And perhaps the fevers were due to “cotton fever,” the injection of various pyrogens in heroin and its adulterants. The negative cultures? Perhaps they just missed the bug; there are always sampling issues with cultures. She denied taking antibiotics after leaving the hospital.

What I want to do is nothing. What I feel we should do is give a definitive course of therapy and put it to rest. Two weeks. Of?

There are several animal and human studies from the old days using two weeks of aminoglycosides and a beta-lactam. The aminoglycoside has become passe for native valve right-sided IE, but I am not so sure. I do not doubt that the aminoglycosides are toxic, I am not entirely certain aminoglycosides are without added benefit for shortening the course of therapy.

The guidelines point to

Of the 37 patients who completed 2-week treatment with cloxacillin, 34 (92%) were cured, and 3 (8%) needed prolonged treatment to cure the infection. Of the 34 patients who completed 2-week treatment with cloxacillin plus gentamicin, 32 (94%) were cured and 2 (6%) required treatment for 4 weeks.

as the one comparator study, but there is no way with those few patients anyone can tell if there is any real difference in the two groups. If you are a fan of trends, and I am not, the combination group was slightly better.

As is often the case with guidelines, when you read the original references, the data to support the recommendations is thin gruel. With no definitive study, I am left interpreting a messy and incomplete literature and apply it to a messy and incomplete clinical case.

How to do the most good, the least harm, before she leaves AMA again. I am inclined towards the beta-lactam and tobramycin approach, but it is one of those cases where no matter what I do, I will be unsatisfied.

Rationalization

Ann Intern Med. 1994 Dec 1;121(11):873-6. Short-course antibiotic therapy for right-sided endocarditis caused by Staphylococcus aureus in injection drug users.

https://www.ncbi.nlm.nih.gov/pubmed/7978701

Guidelines for the diagnosis and antibiotic treatment of endocarditis in adults: a report of the Working Party of the British Society for Antimicrobial Chemotherapy.

https://academic.oup.com/jac/article/67/2/269/701537/Guidelines-for-the-diagnosis-and-antibiotic

Infective Endocarditis in Adults: Diagnosis, Antimicrobial Therapy, and Management of Complications A Scientific Statement for Healthcare Professionals From the American Heart Association.

http://www.idsociety.org/uploadedFiles/IDSA/Guidelines-Patient\_Care/IDSA\_Practice\_Guidelines/Fever\_and\_Infections/AHA%20Infective%20Endo.pdf

Ann Intern Med. 1996 Dec 15;125(12):969-74. Effectiveness of cloxacillin with and without gentamicin in short-term therapy for right-sided Staphylococcus aureus endocarditis. A randomized, controlled trial.

https://www.ncbi.nlm.nih.gov/pubmed/8967707

Ann Intern Med. 1988 Oct 15;109(8):619-24. Right-sided Staphylococcus aureus endocarditis in intravenous drug abusers: two-week combination therapy.

https://www.ncbi.nlm.nih.gov/pubmed/3421575

Influenza Vaccine and Health Care Workers. More than one way to skin a literature.

Mar 6, 2017

I usually keep my SBM and ID worlds separate, but issues with the influenza vaccine pop up in both worlds. So this is a cross-post from SBM, with a slight addition. Enjoy. Or not.

I work in a teaching hospital. That means there are often residents and medical students involved in the care of patients. So when I have a consult, not only do I have to give my assessment and plan, I try and justify that assessment and plan with the literature.

But the literature is often less than clear-cut.

There are those consults where my conclusion has the force and authority of the 10 commandments. Perhaps a bad metaphor. Some consults, like the treatment of MSSA endocarditis, result in an assessment and plan that is big 'T' Truth.

Others? Like how to treat MRSA endocarditis? Lots of depends (no incontinence jokes, please) that requires an interpretation of a less than straightforward literature. These are times that I have to offer my best synthesis of the data. But my opinion is likely better than most.

Sometimes I have little to guide me. I have a weird bug in a weird place, and no literature outside of a few case reports. All I have is the bacterial antibiotic sensitivity pattern and hope.

And sometimes I got nothing. I get asked a question that has no real answer, such as is the fever from infection? I don’t really know, and I let the house staff know that my opinion is just that, an opinion informed by experience and bias, not evidence. And oddly, others often defer to my advice—kind of scary. One of the few advantages of being old and gray, it gives the illusion of wisdom. I often say being a sub-specialist is being ignorant with style and authoritah.

But I need to be explicit when my opinion is just my opinion.

Sometimes papers are opinion wrapped in data, which is nice, as that is just what this blog is. Still, the medical literature, I think, tends to be read with the assumption that the journal articles are written are without bias, the opposite of a blog. Not always.

Take Influenza Vaccination of Healthcare Workers: Critical Analysis of the Evidence for Patient Benefit Underpinning Policies of Enforcement.

They reviewed the studies to date on the benefits of health care worker influenza vaccination and conclude:

The four cRCTs underpinning policies of enforced HCW influenza vaccination attribute implausibly large reductions in patient risk to HCW vaccination, casting serious doubts on their validity. The impression that unvaccinated HCWs place their patients at great influenza peril is exaggerated. Instead, the HCW-attributable risk and vaccine-preventable fraction both remain unknown and the NNV to achieve patient benefit still requires better understanding. Although current scientific data are inadequate to support the ethical implementation of enforced HCW influenza vaccination, they do not refute approaches to support voluntary vaccination or other more broadly protective practices, such as staying home or masking when acutely ill.

The studies, all done in long-term care facilities (aka nursing homes), are admittedly relatively weak tea when taken in isolation from the rest of the vaccination literature. But it is the data we have.

They did not include Influenza vaccination of healthcare workers in acute-care hospitals: a case-control study of its effect on hospital-acquired influenza among patients from 2012, probably as it wasn't an RCT. The only study in hospitals, it demonstrated benefit from HCW flu vaccination:

The median proportion of vaccinated HCW in these units was 11.5% for cases vs. 36.1% for the controls (P = 0.11); 2 (20%) cases and 21 (48%) controls were vaccinated against influenza in the current season (P = 0.16). The proportion of ≥ 35% vaccinated HCW in short-stay units appeared to protect against HAI among patients (odds ratio = 0.07; 95% confidence interval 0.005-0.98), independently of patient age, influenza season and potential influenza source in the units.

CONCLUSIONS: Our observational study indicates a shielding effect of more than 35% of vaccinated HCW on HAI among patients in acute-care units.

The authors of the review do declare their bias behind the review upfront:

The ethical premise for mandatory HCW influenza vaccination critically hinges upon the valid demonstration of patient benefit substantial enough to justify infringement of the personal rights of HCWs who would otherwise choose not to receive influenza vaccine each year.

What, I wonder, is substantial enough?

So I start with an entirely different premise/bias for my take on the literature. I approach the problem from a patient safety perspective and start with the issue of patient harm. What is the result of hospital-acquired influenza?

Answer?

Death.

"Characteristics of patients with hospital-acquired influenza A (H1N1)pdm09 virus admitted to the intensive care unit":

influenza A (H1N1)pdm09 infection (odds ratio: 1.63; 95% confidence interval: 1.37-1.99)…CONCLUSION: Influenza A (H1N1)pdm09 infection acquired in the hospital is an independent factor for death in critically ill patients admitted to the ICU.

And:

in children with severe viral respiratory infection, hospital acquisition of infection is associated with increased mortality even after adjusting for chronic medical conditions that predispose to an increased risk of complications from viral illness.

And:

Influenza virus pneumonia (3 patients) and attributable mortality (2 patients) during active infection was observed in patients with lymphocytopenia at onset.

Although others have demonstrated less influenza mortality in retrospective studies, all have the patient morbidity of a week or two of influenza.

Killing patients by giving them influenza is, to my mind, a bad thing. What is an insubstantial number of deaths from flu acquired from HCW's such that no vaccination is required? For me? Zero.

Hospital-acquired influenza does happen, although rarely:

The overall incidence of hospital-acquired respiratory viral infection was 3.9 (95% confidence interval, 3.7-4.1) cases per 1,000 admitted patients. Rhinovirus was the most common virus (30.3%), followed by influenza virus (17.6%) and parainfluenza virus (15.6%).

Of course, knowing the influenza is acquired in the hospital is one thing; knowing if the patient acquired influenza from a health care worker is quite another. Often, we do not know just where the patient acquires her influenza:

Unobservable transmission was the main cause of HA-ILI transmission suggesting that symptom-based control measures alone might not prevent hospital outbreaks.

And more exposure is worse the less:

Hospitalization in double-occupancy rooms and the risk of hospital-acquired influenza were assessed prospectively. The incidence was 2.0 for 100 patient-days in double- vs. 0.7 in single-occupancy rooms (p 0.028).

So hospital-acquired influenza is rare, difficult to determine the source, can be fatal, results in morbidity, and is hard to control.

And I will note there is often an odd disconnect between morbidity and mortality from hospital-acquired infections and taking responsibility for that morbidity and mortality. I suspect it is part of why infection control and prevention guidelines are sometimes forgotten or ignored. There is an institutional responsibility (in my institutions, we 'deep dive' into every infection) but not personal responsibility, as would occur if a patient had a fatal overdose or a doctor put a chest tube trocar through the heart. If we could only know who passed on the organism that caused infection and when it occurred, guilt would be so much simpler. So who gave the patient the influenza that killed her? We never know, and it takes the edge off of the responsibility for some.

In my own experience, and I am not immune to the dangers of anecdotes, in my 27 years, we have had one influenza outbreak that we could credit to a HCW, unvaccinated, who came down with symptoms in the middle of his 12-hour shift. No one died, although there was significant morbidity. And to the best of my memory, we have never had a death from nosocomial influenza in my hospitals.

And:

Nearly half of HCWs with influenza were afebrile prior to their diagnosis. HCWs with respiratory symptoms but no fever may pose a risk of influenza transmission to patients and coworkers.

Making waiting for symptoms to intervene problematic.

As a health care provider, the dominant ethical imperative is to protect my patients. It is the first law: A robot, er, I mean, health care worker may not injure a human being or, through inaction, allow a human being to come to harm.

I wonder. Is there a relatively effective way to prevent the spread of influenza? I would suggest the flu vaccine. I have written buckets on the flu vaccine at SBM, so my summary. All the data points in the same direction: the flu vaccine decreases the chance of acquiring the flu, and if a HCW does not get the flu, they are not going to pass it to their patients. And kill them. Plus, a vaccinated HCW is potentially one less vector in the community, adding to herd immunity, such as it is with flu. It is a consistent finding in medicine, be it the Pneumococcus, H.influenza b, or HPV, that when vectors are vaccinated, infections in at-risk, unvaccinated populations declines. I can see no reason why this would not be as true for influenza.

Is the bang worth the buck? That is a question I cannot answer. What is one life worth? We do many things in the hospital to prevent complications that have a low probability of occurring but have a high morbidity and mortality. And if I have learned one thing in 30 plus years of infection control, there is no one intervention that will prevent infections; it is the summation of many interventions.

I do think our primary moral imperative is to not kill our patients with vaccine-preventable illnesses, and that is the more important ethical imperative, not HCW autonomy.

But that is me.

It would be interesting to come up with a series of vignettes, like the Trolley Problem, to see where most people stand with the ethics of HCW vaccination.

Rationalization

Influenza Vaccination of Healthcare Workers: Critical Analysis of the Evidence for Patient Benefit Underpinning Policies of Enforcement

https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0163586

BMC Infect Dis. 2012 Feb 1;12:30. doi: 10.1186/1471-2334-12-30.

Influenza vaccination of healthcare workers in acute-care hospitals: a case-control study of its effect on hospital-acquired influenza among patients

https://pubmed.ncbi.nlm.nih.gov/22292886/

J Hosp Infect. 2017 Feb;95(2):200-206. doi: 10.1016/j.jhin.2016.12.017. Epub 2016 Dec 30.

Characteristics of patients with hospital-acquired influenza A (H1N1)pdm09 virus admitted to the intensive care unit

https://pubmed.ncbi.nlm.nih.gov/28153560/

Am J Infect Control. 2017 May 1;45(5):e45-e47. doi: 10.1016/j.ajic.2017.01.009. Epub 2017 Feb 15.Laboratory-based surveillance of hospital-acquired respiratory virus infection in a tertiary care hospital

https://pubmed.ncbi.nlm.nih.gov/28214160/

Clin Microbiol Infect. 2016 May;22(5):461.e7-9. doi: 10.1016/j.cmi.2016.01.010. Epub 2016 Jan 22. Hospitalization in double-occupancy rooms and the risk of hospital-acquired influenza: a prospective cohort study

https://pubmed.ncbi.nlm.nih.gov/26806256/

Influenza Among Afebrile and Vaccinated Healthcare Workers Clinical Infectious Diseases, Volume 60, Issue 11, 1 June 2015, Pages 1591–1595,

https://doi.org/10.1093/cid/civ163

Parotitis

Mar 9, 2017

The patient is a mid 70-year-old male who presents from Outside Hospital for an ID consultation. He had initially been admitted with parotitis and was not improving.

When I saw him, he had a markedly swollen left parotid gland with no abscess on CT. ENT had cultured the duct, and it grew MRSA. And Candida. And Streptococcus salivarious.

Most parotitis in the adult is due to S. aureus, so he was placed on vancomycin and didn’t get better. In fact, he got worse, going into respiratory failure requiring intubation.

He was modestly febrile, a normal WBC, and his sputum cultures grew nothing. Over the next week, while on HAP coverage, his pulmonary function worsened while his CXR was consistent with ARDS.

The respiratory panel was negative, except for Coronavirus.

Well, Coronavirus is a cause of pneumonia, but does Coronavirus cause parotitis? Not that I can find in humans (it does in rats), but there is only one study using molecular methods to evaluate the etiology of parotitis.

Viruses were detected in 52 (51.5%) of samples: one virus (25 EBV, 8 PIV3, 4 adenovirus, 4 PIV2, 1 PIV1, 1 InVA, and 1 enterovirus) was detected in 44 patients (84.6%), two viruses in 7 patients, and three viruses in one patient.

I didn't think the parotitis was due to massive head scourge, which

...Is caused by invasion of the body by exopathogenic wind-heat toxin from the mouth and nose. This pathogen mixing with phlegm turns into fire to obstruct the Shaoyang and Yangming Channels, leading to lump due to accumulation of heat in the parotid region. Therefore, the principle of treatment should be to eliminate stagnated heat from the Shaoyang and Yangming Channels.

Ten days in, I wondered. Mumps? Mumps is booming in the US, with over 5000 cases last year, and given his age, maybe he escaped the illness growing up. But does mumps cause pneumonia? Maybe. I found one case In the adult:

A 38-year-old male with swollen parotid glands was admitted to our hospital with dyspnea on effort. Positive serum IgM antibody for mumps supported a diagnosis of mumps. Computed tomography (CT) scan showed a ground-glass appearance in both lower lungs. On the third day of hospitalization, bronchoalveolar lavage demonstrated an elevation of both the total cell (2.0 x 10(6)/cc) and the lymphocyte count (83%), as well as a decrease of the CD 4+/CD 8+ ratio (0.4). Bronchial biopsy specimens revealed infiltration of lymphocytes in both the bronchiolar walls and the alveolar septa. These data were suggestive of mumps pneumonia.

And a smattering of congenital cases.

So I sent of mumps serology, and the IgM came back way positive. Huh.

As best I can tell, there is no cross-reactivity between Coronavirus and mumps, either with serology or PCR, and they are very different viruses.

So do I have mumps with pneumonia? Or mump and pneumonia. Hickam or Occam?

It is not clear-cut to me, having seen only one other case of mumps in my career, so I called the peds ID folks. It turned out they had never seen a case of mumps.

That, unfortunately, will be changing.

Rationalization

Hum Vaccin Immunother. 2015;11(1):282-7. doi: 10.4161/hv.36165. Epub 2014 Nov 1. Viral etiology of mumps-like illnesses in suspected mumps cases reported in Catalonia, Spain.

https://www.ncbi.nlm.nih.gov/pubmed/25483547

Nihon Kokyuki Gakkai Zasshi. 2000 Dec;38(12):932-6. [A case of mumps pneumonia complicated with acute respiratory failure].

https://www.ncbi.nlm.nih.gov/pubmed/11244731

Sialodacryoadenitis and Coronavirus Infection in Rats.

http://www.petmd.com/exotic/conditions/respiratory/c\_ex\_rt\_sialodacryoadenitis\_coronavirus#

Complications. Not as rare as I would have thought.

Mar 13, 2017

I know so much, yet I know so little. The patient is an elderly female who has routine cataract surgery. She has no other medical problems, and the surgery goes smoothly.

Ten days post-op has the abrupt onset of a painful red eye and a loss of vision.

Despite the usual ophthalmologic care, she eventually requires enucleation.

And all the cultures, including samples from the orbit, grow Aspergillus fumigatis.

Now what?

I expected to find few cases of Aspergillus infection complicating cataract surgery, but there were 39 hits, with enough cases to warrant a review. No great insights. As would be expected, once a mold gets into the eye, the outcome is not good no matter what is done.

The infection is now gone, the patient is immunologically normal, but there were positive cultures in areas in close proximity to the brain. It makes me nervous, although the risk of extension from the orbit into the brain is low. I think.

I opted for oral voriconazole. Bad choice. With the medication, she had severe hallucinations. Antibiotics, like any medication, can cause alterations in mental status. I have not needed to give much voriconazole in my career, and hallucinations were not on my list of side effects. It is now.

As part of a prospective natural history cohort study of voriconazole toxicity, we describe the characteristics of 12 of 72 voriconazole-treated patients who experienced hallucinations from March 2006 through November 2007. Hallucinations associated with voriconazole use are not uncommon. Doctors should be aware of this complication, and the recipients of the drug should be reassured that the hallucinations are an effect of the drug.

17% is a lot and occurs with the iv and po formulations. Like my patient, the toxicity can occur with the first dose, perhaps linked to CYP2C19 and CYP2C9 polymorphisms to increase serum levels.

Now what? Amphotericin or a 'fungin? Or nothing? I have seen far too many orbital fungi invade the CNS, albeit in at risk patients, to feel sanguine about doing nothing. I still think Murphy was an optimist.

Though orbital aspergillosis is commonly seen in immunocompromised patients, it should be suspected in young immunocompetent individuals presenting with proptosis of insidious onset and infiltrating lesions involving the paranasal sinuses. Definitive diagnosis is achieved by histopathological and microbiological evaluation. Systemic steroids should be avoided prior to definitive diagnosis. Prolonged systemic antifungal therapy with an option of additional debulking of lesions provides good disease control with improved survival.

She had an uneventful course of lipid amphotericin.

Rationalization

Mycopathologia. 2015 Dec;180(5-6):291-7. doi: 10.1007/s11046-015-9932-z. Epub 2015 Aug 29. Risk of Fungal Endophthalmitis Associated with Cataract Surgery: A Mini-Review.

https://www.ncbi.nlm.nih.gov/pubmed/26318595

Am J Ophthalmol. 2006 Sep;142(3):509-11. Early onset endophthalmitis caused by Aspergillus species following cataract surgery.

https://www.ncbi.nlm.nih.gov/pubmed/16935607

Neurology. 2016 Mar 8;86(10):963-71. doi: 10.1212/WNL.0000000000002455. Epub 2016 Feb 17. Antibiotic-associated encephalopathy.

https://www.ncbi.nlm.nih.gov/pubmed/26888997

Drug Metab Pharmacokinet. 2013;28(5):439-41. Epub 2013 Apr 2. A case-report of unpredictable and massive voriconazole intoxication in a patient with extensive CYP2C19 and CYP2C9 polymorphisms.

https://www.ncbi.nlm.nih.gov/pubmed/23545593

Clin Infect Dis. 2008 Jul 1;47(1):e7-e10. doi: 10.1086/588844. Hallucinations during voriconazole therapy.

https://www.ncbi.nlm.nih.gov/pubmed/18491963\

Br J Ophthalmol. 2014 Oct;98(10):1379-84. doi: 10.1136/bjophthalmol-2013-303763. Epub 2014 May 13. Orbital aspergillosis in immunocompetent patients.

https://www.ncbi.nlm.nih.gov/pubmed/24825845

Un Well

Mar 20, 2017

One of the great joys in ID is the little things. Or maybe it is the little joys from great things. Nope. Doesn’t work. But cases occasionally result in a frisson of excitement when everything falls into place as it should.

The patient is immuno-incompetent, on low dose prednisone and methotrexate. He has an infected knee (coagulase-negative Staphylococcus) removed and was discharged. 10 days later, he returns with a red, hot, swollen knee.

It was tapped, a gram-negative rod was seen, and so the knee was debrided, which also grew a gram-negative rod.

Achromobacter.

Not common. Usually, I see Acromobacter in diabetic feet, and there are less than half a dozen cases of septic arthritis on the Pubmeds.

But the better question is why. What was the exposure?

Achromobacter is found in water and decomposing organic material. And crude oil sludge. And the GI tracts of earthworms. So I asked around looking for a reason, not too worried about exposure to crude oil sludge or earthworm intestines. And sure enough, his home is on well water, not city water. There is a case report of Achromobacter sepsis from well water.

He suffered from a perfect storm: compromised immune system, surgical trauma, and an exposure. It is just so nice when a case comes together.

Being on well water is common outside of the city limits of Portland, and once or twice a year, I see a surgical infection with an odd gram-negative, and the patient is on well or similar water. I have yet to get the confirming environmental culture.

There are a remarkable number of infections that have been traced back to well water on Pubmed, and people will often have unexpected water exposures. I still like the Aeromonas colitis from holy water the best. I have suggested to our SSI team that perhaps we should ask patients what their water source is and warn them if is not city water.

On the way to the Oregon coast, there is a pair of drinking fountains where you will always see people filling jugs, thinking they are getting clean, natural, spring water. But probably not sterile.

The autochthonous microbial flora consists of psychrotrophic and of distinctly oligocarbophilic, mainly gram-negative bacteria such as Achromobacter, Flavobacteria, Pseudomonas as well as gram-positive Arthrobacter-species.

The water may look clear, but it is teeming with bacteria, MMMMMM. Bacteria.

Rationalization

Springerplus. 2016 Nov 9;5(1):1946. eCollection 2016. Isolation and characterisation of crude oil sludge degrading bacteria.

https://www.ncbi.nlm.nih.gov/pubmed/27933233

Chemosphere. 2017 Feb;168:1194-1202. doi: 10.1016/j.chemosphere.2016.10.079. Epub 2016 Oct 31. Responses of earthworms and microbial communities in their guts to Triclosan.

https://www.ncbi.nlm.nih.gov/pubmed/27810239

J Clin Microbiol. 1988 Mar;26(3):598-9. Achromobacter xylosoxidans (Alcaligenes xylosoxidans subsp. xylosoxidans) bacteremia associated with a well-water source: case report and review of the literature.

https://www.ncbi.nlm.nih.gov/pubmed/3281982

Ann Ist Super Sanita. 1976;12(2-3):93-112. Microbiological characteristics of natural mineral water.

https://www.ncbi.nlm.nih.gov/pubmed/829205

A Cryptic Case of Acute Colitis.

http://www.medscape.com/viewarticle/764743

Misleading Packaging

Mar 22, 2017

The patient has decades of homelessness, mental illness, and substance abuse.

He has rigors, fevers, and altered mental status shortly after injecting drugs. He is admitted to the hospital with sepsis/sirs. Eventually, his blood cultures are positive for E. coli and Proteus mirabilis. Not the typical organisms associated with heroin.

I suspect, living on the street, that he used water of uncertain provenance. It would not be the first time I had a patient use toilet water to mix their drugs. Toilet water, tap water, puddle water, saliva, Willamette river water, and seltzer have been some of the fluids used to mix drugs. The oddest was a meth user whose dealer gave him a vial of brown liquid to mix his drug. He did. And was the first and only positive blood cultures for Mucormycosis I have ever seen.

So I asked. Nope. Tap water.

And then he volunteered, “I shot up shit.”

I thought at first he was being colloquial about some bad heroin. Nope.

He found a bag on the street with what looked like black tar heroin in a dog poop bag. So he injected it.

I can see making the mistake. Dog poo and black tar heroin look the same, and he tells me heroin is occasionally distributed in dog poo bags. Not a bad idea as it would be unlikely to be inspected closely unless, I suppose, you were carrying the bag around without a dog.

But the Proteus puzzled me. E. coli is part of the go tract of dogs, but Proteus? Yep. Dogs and humans often share the same microbiology, both normal and pathogenic.

That shared microbiology is one of the reasons I am less than thrilled with pet therapy. Would you let a human go room to room in the hospital to be rubbed all over by patients, occasionally licking patients after licking his own butt? I don’t think so. I always cringe when a see a dog licking a human on the face. Ew. But that’s me.

The patient did fine with antibiotics, and I hope he will be more circumspect about packaging in the future.

Rationalization

J Med Microbiol. 2014 Nov;63(Pt 11):1561-7. doi: 10.1099/jmm.0.081539-0. Epub 2014 Sep 3. Phenotypic and molecular characterization of antimicrobial resistance in Proteus mirabilis isolates from dogs.

https://www.ncbi.nlm.nih.gov/pubmed/25187600

Anim Health Res Rev. 2012 Jun;13(1):78-88. doi: 10.1017/S1466252312000059. Epub 2012 May 30. Current state of knowledge: the canine gastrointestinal microbiome.

https://www.ncbi.nlm.nih.gov/pubmed/22647637

J Hosp Infect. 2009 Jul;72(3):268-9. doi: 10.1016/j.jhin.2009.02.019. Epub 2009 Mar 28. Contamination of pet therapy dogs with MRSA and Clostridium difficile.

https://www.ncbi.nlm.nih.gov/pubmed/19329224

Clin Infect Dis. 2012 Mar;54(6):e55-7. doi: 10.1093/cid/cir975. Epub 2012 Jan 11. Life-threatening respiratory pasteurellosis associated with palliative pet care.

https://www.ncbi.nlm.nih.gov/pubmed/22238163

Odd Name

Mar 27, 2017

The patient is billed as a postherpetic neuralgia.

She awoke in the middle of the night with severe arm pain. In the ER it was diagnosed as rashless zoster.

Maybe. It happens. Zoster sine herpete can have all sorts of neurologic manifestations without, obviously, a rash. But how to prove it?

Talking with the patient, I am not so sure it is VZV.

The pain is in three dermatomes, and there is more than pain: she has paresthesias and weakness, neither of which are typical of zoster.

And she is on a biologic for Crohn's. One, and by one I mean me, would think there should have been an exuberant rash on a biologic, not zoster sine herpete.

I suspect it was mononeuritis multiplex (a painful, asymmetrical, asynchronous sensory and motor peripheral neuropathy involving isolated damage to at least 2 separate nerve areas), a disease whose name I hate. It should at least be called polyneuritis multiplex since it involves more than one nerve. I can't find the word origin.

But why?

It turns out the TNF inhibitors are associated with mononeuritis multiplex like processes.

The annoying thing, and this happens to me all the time, is I do a search at work and find an article, in this case, a review of biologics and mononeuritis multiplex. I do what I think is the exact same search at home and? Different results. The review is nowhere to be found. Drives me nuts. But there are case reports. So I am sticking with my diagnosis.

I sent her to neurology for further diagnostic testing who confirmed the diagnosis.

Rationalization

Neurological Disease Produced by Varicella Zoster Virus Reactivation Without Rash.

https://link.springer.com/chapter/10.1007/82\_2009\_3

Open Forum Infect Dis. 2016 Sep 28;3(4):ofw205. eCollection 2016. Risk of Herpes Zoster in Individuals on Biologics, Disease-Modifying Antirheumatic Drugs, and/or Corticosteroids for Autoimmune Diseases: A Systematic Review and Meta-Analysis.

https://www.ncbi.nlm.nih.gov/pubmed/27942537

J Neurol Sci. 2015 Feb 15;349(1-2):246-8. doi: 10.1016/j.jns.2015.01.003. Epub 2015 Jan 9. Multifocal-motor-neuropathy-like disease associated with Infliximab treatment in a patient with Crohn's disease.

https://www.ncbi.nlm.nih.gov/pubmed/25592414

Anaerobic Odd Bugs

Mar 29, 2017

I will turn 60 this spring and will be irremediably old. No way to avoid it, I am soon to be 420 in dog years. And I find as I get older, it is the little things that annoy the hell out of me.

I am sure most people reading this have, at one time or another, received a form as part of credentialing to vouch for the skills and personality of a colleague.

You check the boxes. Skills are fine, I know of nothing that would prevent her from practicing medicine. But this form ended with the question, would I send a family member to this doctor?

What the hell does that have to do with anything? Such a question either implies that I do know something to prevent her from practicing medicine, and I just lied, or I have different referral standards for patients and family. Either is insulting. So I left it blank; although I should have commented that while I would send my mother-in-law to the doctor, I would not send my mother and let them figure out what I meant.

As to cases? Two odd bugs for no good reason. A 20 something female, no medical problems comes in with sepsis and MOSF.

Blood cultures grow?

Bifidobacterium.

She gets the full evaluation, and no reason for a bacteremia is found. Most of the cases are associated with probiotic use in preterm infants, of which she did not partake. Probiotics or preterm infants.

Bifidobacterium species bacteremia seems to be a rare event, but its true incidence could be underestimated. Indeed, Bifidobacterium species could be considered as nonpathogenic bacteria, as these anaerobic, nonsporulating, gram-positive rods are part of the physiological oral, vaginal, and intestinal flora. Besides bacteremia, urinary, pleuropulmonary, obstetric, and gynecologic infections and dental caries have been reported…Bacteremia due to Bifidobacterium species is an emerging entity the role of probiotics should be better investigated in cases occurring in adults, as already studied in preterm infants.

She got all better on antibiotics.

The other is a middle aged, otherwise healthy female who has a month of fevers, chills, and failure to thrive. CBC and comp were negative, but eventually, a CT as part of the FUO evaluation showed a liver abscess. It was drained and grew?

Parvimonas micra

Yeah, I had heard of that one.

Parvimonas micra, formally known by the ‘illegitimate names’ of Peptostreptococcus micros or Micromonas micros is an anaerobic gram-positive coccus in the mouth. The derivation of the name is

L. adj. parvus, little, small; L. fem. n. monas, a unit, monad;

And a micra is a millionth of a meter. So it is one tiny microbe, probably with feelings of inadequacy.

As with all organisms, there are a smattering of cases of this bug causing disease in one organ or another, including a liver abscess. It can be killed with the usual antibiotics.

Among Gram-positive anaerobes, Actinomyces spp., Parvimonas micra and Propionibacterium spp. were universally susceptible to β-lactams

With occasional metronidazole resistance.

Why the liver abscess? No idea. Probably bad luck after flossing and brushing:

They found that P. micra was one of the most frequently identified periodontopathogens in peripheral blood. It was still present in the bloodstream, in some cases, 30 min after the dental procedure.

But source control and antibiotics worked its usual magic. Well, science, not magic.

Rationalization

Clin Infect Dis. 2015 Aug 1;61(3):482-4. doi: 10.1093/cid/civ347. Epub 2015 Apr 28. Bifidobacterium species bacteremia: risk factors in adults and infants. https://academic.oup.com/cid/article-lookup/doi/10.1093/cid/civ347

Proposal of Parvimonas gen. nov. and Quatrionicoccus gen. nov. as replacements for the illegitimate, prokaryotic, generic names Micromonas Murdoch and Shah 2000 and Quadricoccus Maszenan et al. 2002, respectively http://ijs.microbiologyresearch.org/content/journal/ijsem/10.1099/ijs.0.64338-0#tab2

Anaerobe. 2014 Aug;28:120-5. doi: 10.1016/j.anaerobe.2014.05.015. Epub 2014 Jun 9. Antimicrobial susceptibility of clinical isolates of anaerobic bacteria in Ontario, 2010-2011. https://www.ncbi.nlm.nih.gov/pubmed/24923267

Gram-positive anaerobic cocci – commensals and opportunistic pathogens. http://onlinelibrary.wiley.com/doi/10.1111/1574-6976.12005/full

POLL RESULTS

I measure the passage of time

• in years 9%
• in dog years 0%
• in mayfly years 0%
• in empty beer bottles 22%
• in dollops of regret and bitterness 47%
• Other Answers 22%
• in failing organ systems and cognitive faculties. Or something like that. I can't remember the specifics of it all.
• the number of name changes to microorganisms
• In number of one-night-stand...
• In brain cells I will never recover.
• moments.
• In leaps and bounds.

Horrible Complication

Apr 3, 2017

I have taken care of a lot of endocarditis in my 30 plus years, but the last few years have seen a bumper crop, mirroring the trend in the US and overseas.

These results show that IE incidence has increased in the United States over the past decade. With regard to the microbiology of IE, there has been a significant rise in the incidence of Streptococcus IE since the 2007 guideline revisions

I am seeing mostly young injection drug users and more females.

Our findings suggest that the demographics of inpatients hospitalized with IDU-IE are shifting to reflect younger PWID who are more likely to be white and female than previously reported.

Endocarditis has been a growth industry.

As far as I can tell, there is no direct link to the opiate overuse crisis in the US, as most do not seem to be addicts due to chronic pain. Just the standard bad decisions and poor social networks that have sucked in and killed so many young addicts over the years. But that could just be confirmation bias as I do not tend to ask detailed questions about how they came to be addicts.

As a result of the boom in endocarditis, I have had the awful opportunity to witness some complications I just as soon never have seen.

The patient is one of many right-sided endocarditis this year, one of many with a large tricuspid vegetation and one of many intubated because of respiratory failure from a breathtakingly large number of septic emboli exacerbated by leaving AMA during the first course of antibiotics.

That tells you how severe addiction is. You tell a patient that untreated their disease is 100% fatal, and they still leave. I am glad I do not have that monkey on my back.

The patient, who by all criteria was responding to antibiotics, starts to have a massive pulmonary hemorrhage that doesn’t stop, and in a very short period of time, she dies. Awful.

I have had one patient die of pulmonary hemorrhage from a TB related Rasmussen's aneurysm, but this is my first for endocarditis. And I hope my last. I find these particularly horrific as there is little that can be done to stop the bleeding until you get them to the angiography suite to embolize the aneurysm.

There are a few, maybe a dozen cases all told, of pulmonary mycotic aneurysms in right-sided endocarditis.

Like cerebral mycotic aneurysms, they may be more common than we suspect as they are rarely symptomatic:

During the postmortem study of pulmonary lesions in intravenous drug addicts, three patients were found to have bilateral multiple mycotic aneurysms of the peripheral pulmonary arteries in association with embolic pneumonia. Two of these patients had infective tricuspid endocarditis, and one had hemoptysis. This report draws attention to the occurrence of mycotic aneurysms in this unusual location and suggests that these pulmonary lesions may be more common than currently believed.

Another time bomb to worry about with endocarditis.

Rationalization

Increasing Infectious Endocarditis Admissions Among Young People Who Inject Drugs.

https://doi.org/10.1093/ofid/ofw157

J Am Coll Cardiol. 2015 May 19;65(19):2070-6. doi: 10.1016/j.jacc.2015.03.518. Trends in infective endocarditis incidence, microbiology, and valve replacement in the United States from 2000 to 2011.

https://pubmed.ncbi.nlm.nih.gov/25975469/

BMJ Case Rep. 2010 Aug 24;2010. pii: bcr1020092404. doi: 10.1136/bcr.10.2009.2404. Massive haemoptysis in an intravenous drug user with infective tricuspid valve endocarditis.

https://www.ncbi.nlm.nih.gov/pubmed/22767369

Am J Med. 1984 Jun;76(6):1124-31. Mycotic aneurysms of the pulmonary arteries in intravenous drug addicts. Report of three cases and review of the literature.

https://www.ncbi.nlm.nih.gov/pubmed/6547273

Rasmussen's Aneurysm.

http://www.nejm.org/doi/full/10.1056/NEJMicm050783#t=article

Doesn't Lack a Bacillis

Apr 5, 2017

The patient is an elderly male with a bioprosthetic valve. He presents with a stroke but no fevers, chills, or other signs and symptoms of infection.

As part of the ER evaluation, blood cultures are done. Both bottles in two sets start growing a gram-positive rod at 48 hours.

A miracle occurs: repeat blood cultures are drawn before antibiotics are given. Amazing. ID docs love us our repeat blood cultures; it is the sustained bacteremia that is the sine qua non of endocarditis. But I so rarely get the cultures I want.

And sure enough, the repeat blood culture also grows a gram-positive rod at 48 hours. Eventually, the MALDI-TOF called it a 50% chance Lactobacillus casei and a 50% chance of L. paracasei. But there is only a 10% chance of that.

ECHO failed to find a vegetation, but it is prosthetic valve endocarditis of which there are just a few dozen cases in the Pubmeds. How to treat with documented hives to penicillin pending sensitivities? I opted for a carbapenem, and it eventually came back with an MIC to penicillin of 0.05 and, as is often the case, resistant to vancomycin. It was also sensitive to clindamycin, but I can’t see using clindamycin for prosthetic valve endocarditis.

And why this bug? No idea. His dentition is fine (Lactobacilli are part of the oral flora), does not take probiotics, and, wisely, does not like yogurt. So bad luck strikes again. He clinically did well on the meropenem, although he did well clinically before the diagnosis.

Ended up a cure.

Rationalization

Eur J Clin Microbiol Infect Dis. 2005 Jan;24(1):31-40. Pathogenic relevance of Lactobacillus: a retrospective review of over 200 cases.

https://www.ncbi.nlm.nih.gov/pubmed/15599646

Ecology of Lactobacilli in the Oral Cavity: A Review of Literature.

https://pdfs.semanticscholar.org/9441/9574b4bcad25f1655d4c3e6da96f090083ca.pdf

Clin Infect Dis. 2015 May 15;60 Suppl 2:S98-107. doi: 10.1093/cid/civ072. Lactobacillus species: taxonomic complexity and controversial susceptibilities.

https://www.ncbi.nlm.nih.gov/pubmed/25922408

Naked Gun 50/50 Chance of Living

https://www.youtube.com/watch?v=DDoncJckows

Tattoo You

Apr 10, 2017

I am old and rarely relevant. Much of popular culture eludes me. I do not understand body art, I suppose, because I have seen too many old tattoos. As the skin ages and sags, the tattoo of a rose will wither and become a long stem. No way these tats are going to look good as they age into the ’50s and beyond. But people are a slave to fashion.

I was making rounds when one of the hospitals saw me. I was waiting for a friend, she said, can I ask you a question?

Start me up, I replied.

The patient had a tattoo a week prior to admission and now has cellulitis and isn’t responding to antibiotics. Can you take a quick look?

The patient looked ill, was febrile, hypotensive, and had very tender erythroderma and pustules downstream of the tattoo (which looked fine) extending all over the chest wall.

It looked like necrotizing fasciitis and septic, but not toxic, shock.

I’m worried about you. I said

And we called the surgeon, who took him to the OR, where necrotizing fasciitis was indeed found. No use in crying, nothing heals like cold steel, and he was prevented from going to heaven. Now he looks tops.

Cultures grew MRSA.

BTW: see what I did there?

Needles are bad, including tattoo needles. And there are 243 hits on Pubmed for “tattoo infection.” I was impressed, finding hits for hepatitis, atypical mycobacteria, Group A streptococci, gram-negative rods, and, yes, MRSA.

The tattoo material isn’t always as sterile as I would want:

Published bacteriological surveys showed that opened as well as unopened tattoo ink bottles frequently contained clinically relevant levels of bacteria indicating that the manufactured tattoo product itself may be a source of infection. In our bacteriological survey, two of 39 colorants were contaminated with aerobic mesophilic bacteria.

And sentences like

CA-MRSA among 44 recipients of tattoos from 13 unlicensed tattooists in three states; use of nonsterile equipment and suboptimal infection-control practices were identified as potential causes of the infections.

give me the wiggins. Who goes to unlicensed tattooists? Probably people who have ‘love’ and ‘hate’ on their knuckles and a tear in the corner of one eye.

Years ago, I had a patient with his arm completely tattooed that had to be split right down the middle because of infection. The arm, not the patient. Ruined the art, although he had a nice repair job later.

I notified the state, and so far, he is the only case associated with the tattoo parlor in question. So probably a fluke.

But I am not getting my tat any time soon.

Rationalization

Dtsch Arztebl Int. 2016 Oct 7;113(40):665-671. doi: 10.3238/arztebl.2016.0665. The Risk of Bacterial Infection After Tattooing.

https://www.ncbi.nlm.nih.gov/pubmed/27788747

MMWR Morb Mortal Wkly Rep. 2006 Jun 23;55(24):677-9. Methicillin-resistant Staphylococcus aureus skin infections among tattoo recipients--Ohio, Kentucky, and Vermont, 2004-2005.

https://www.ncbi.nlm.nih.gov/pubmed/16791134

The More I Explain, the More Likely I Will Be Wrong

Apr 12, 2017

The patient is admitted with a headache, followed by decreased mental status, followed by a seizure.

Otherwise healthy, he had been on a recent course of Augmentin for sinusitis. CT shows a 3.5 cm abscess in the brain and mastoiditis.

Take a second. Hold your finger 3.5 cm apart. That’s about one and a half inches. Hold it next to your head. That’s big. A ping pong ball is 4 cm across. So there was almost a ping pong ball of pus in his brain.

Brain volume is 1260 cm3, and his abscess is 180 cm3, 15% of his brain. It is an old myth that we use 10% of our brain. Sadly, we use 100% and look at the result. Losing 15% from an abscess is bad.

So they drain thick green pus and call me. I pontificate at length how we will grow an alpha streptococcus from the intermedius group, although if you do molecular methods, there are often far more organisms present than grown. And the gram stain comes back with gpc in chains, and I get the smug satisfaction from thinking I called it. I love predicting the cultures.

Data mining discriminated 2 distinct bacterial populations in brain abscess from dental and sinusal origin. In addition, of the 80 detected bacterial species, we identified 44 bacteria that had never been found in brain abscess specimens, including 22 uncultured bacteria.

and for my patient, with a sinus etiology, I expected

Sinusitis or dental defect was associated with Streptococcus species, Prevotella species, Peptostreptococcus species, Streptococcus intermedius, Campylobacter species, Fusobacterium species, other anaerobes, M. faucium, and uncultured bacteria

Nope. S. pneumoniae. Which in the above study was only seen with otitis media.

There are several dozen brain abscess cases with this beast, usually as complications of otitis, sinusitis, and metastatic infection from pneumonia and endocarditis.

I see a community-acquired bacterial brain abscess perhaps every couple of years; if I have seen an S. pneumonaie, I can’t remember it.

He did quite well, and the organism was sensitive to penicillin, so the prior amoxicillin didn’t select for resistance.

Rationalization

Metagenomic Analysis of Brain Abscesses Identifies Specific Bacterial Associations

https://academic.oup.com/cid/article-lookup/doi/10.1093/cid/cir797

Feeling Ranty Today: Hidden Messages

Apr 17, 2017

The last couple of days have been weirdly slow. When I was young, I would fret when there were no consults. Now? I am of an age where I really do not want to work like I did when I was 30.

So instead, I will take this opportunity to look for hidden messages in the medical literature. There are messages if you know what to look for.

It is known in the ID community that infectious disease consultation improves outcomes for a variety of diseases. But what is the hidden message in some of these studies?

First, cryptococcal meningitis:

The patients with an ID consult had a higher fungal burden but a lower 90-day mortality compared to patients without ID involvement (27% vs 45%, p<0.001), data-preserve-html-node="true" with an adjusted hazard ratio of not receiving an ID consult of 4.1.

where

One hundred (68%) patients with an ID consult and 47 (32%) patients without an ID consult were included in subsequent analyses.

Second, one of many concerning S. aureus bacteremia:

Out of 599 SAB episodes, 162 (27%) were followed by an IDC…In patients with SAB, all-cause mortality was significantly lower in patients who had an IDC, because of the higher proportion of patients receiving effective initial antibiotics.

And we end with

The strongest evidence for a clinical benefit is found in the context of Staphylococcus aureus bacteremia (SAB), where in-hospital- and day-30 mortality was significantly and consistently reduced by about 40% in patients that were evaluated and treated in cooperation with an ID physician…Of note, informal or curbside consultations do not seem to be equivalent to a formal ID consultation with bedside patient evaluation. Studies in other patient groups (solid organ transplant recipients or intensive care unit patients) or in the context of other infections (infective endocarditis, pneumonia, other bloodstream infections) also revealed positive effects of ID consultations.

What is the hidden message in these studies? That there are a god awful number of physicians flailing about taking care of infections for which evidently they do not know a burro from a burrow.

32% of patients with cryptococcal meningitis were getting incompetent treatment by a non-ID doc. 73% of S. aureus bacteremia were being screwed up by a non-ID doc. The patients DIED. You can’t suggest that the care was fine. Care sucked. People did not know what they were doing. Big time. And it showed in the worst possible way: mortality.

What in hell is going on in those hospitals? What kind of dumb ass thinks they can take care of complex and/or rare diseases without getting help from someone who actually knows what they are doing? In the Cryptococcal study, they do not mention who the double O health care providers were.

And what kind of health care system lets it happen? Well, I know the answer to the last question—the US health care system.

It's horrific. No one would treat leukemia without an oncologist or deliver a baby without ob-gyn involvement, but too many docs seem to feel comfortable in their Dunning-Kruger ignorance treating diseases for which they are Jon Snow.

And people die.

I wonder how many hospital deaths from infectious diseases have physician ignorance as to the real cause.

I would also be curious if this phenomenon occurs more often in University rather than community hospitals. I am always amused when someone wants a second opinion and asks to go to the University. Doctors there are on service, what, 3 or 4 months a year? I have been seeing patients every month for 27 plus years, or 6.75 in University years. And my patient care experience is direct, not filtered through med student to resident to fellow to attending. If I needed a second opinion, I would head to our cross-town rivals in the community.

Want to improve outcomes and quality with patients across a wide variety of diseases? Mandate ID involvement either directly or through stewardship programs. In this century, no patient in the hospital should be on an antibiotic without some degree of ID oversight. Unless, of course, you lack for patients for autopsy conference.

Rationalization

Clin Infect Dis. 2016 Dec 7. pii: ciw786. Impact of Infectious Diseases Consultation on Mortality of Cryptococcal infection in Patients without HIV.

https://www.ncbi.nlm.nih.gov/pubmed/27927865

Eur J Clin Microbiol Infect Dis. 2012 Sep;31(9):2421-8. doi: 10.1007/s10096-012-1585-y. Epub 2012 Mar 3. Formal infectious diseases consultation is associated with decreased mortality in Staphylococcus aureus bacteraemia.

https://www.ncbi.nlm.nih.gov/pubmed/22382823

Z Evid Fortbild Qual Gesundhwes. 2015;109(7):500-10. doi: 10.1016/j.zefq.2015.09.008. Epub 2015 Oct 17. [Impact of an infectious diseases consultation service on the quality of care and the survival of patients with infectious diseases].

https://www.ncbi.nlm.nih.gov/pubmed/26593765

Improving Outcomes with ID Consultation: Three More Papers For the Collection.

https://blogs.jwatch.org/hiv-id-observations/index.php/improving-outcomes-id-consultation-three-papers-collection/2017/02/26/

This (great) blog suggests anyone can do what an ID doc can do:

the basics of ID clinical practice are available to everyone.

Sorry. Wrong. Not only do we have clinical experience in infections that non-ID docs can never come close to obtaining, we know more. I have 8 gigs of papers I have downloaded and reviewed for the Puscast in the last 12 years, 16,500 papers. And when I went completely digital, I recycled two stacks of papers as tall as me. And that doesn’t include the papers reviewed for this blog and general patient care. ID docs have seen more, done more, and know more about infections, and it shows inpatient care. When it comes to infections, we are pros from Dover. You are Captain Peterson. Deal.

Thus endeth the rant.

POLL RESULTS

I

• know as much as any arrogant ID doc thanks to the Sanford Guide 10%
• don't get ID consults because they are know it all jerks 3%
• just give vancomycin and zosin knowing all will be well 21%
• think Dunning and Kruger doesn't apply to me 21%
• send my patients to the integrative medicine clinic. Getting acupuncture and energy therapy will make it all better. 31%
• Other Answers 14%
• Definitely will get ID consult ;)
• 've got nothing.

Three Rarities. One Patient.

Apr 19, 2017

The patient has a CNS tumor for which he is being weaned off high dose dexamethasone. He gets progressive shortness of breath and is admitted to the ICU.

Work up is significant for unilateral diffuse interstitial infiltrates on CT, an LDH of 1300 and a 1-3 beta-d-glucan greater than 500.

No bronchoscopy (refused) and no sputum production.

So PJP? It happens on steroids, more importantly, as the steroids are weaned. There is a lot of Sturm und Drang over PJP risk with steroids. Long term use of at least 30 mg a day seems to be the worry point, but for what it is worth (virtually nothing), the only PJP I have ever seen from steroids as the only risk was 25 years ago in a brain tumor patient on dexamethasone. It happens.

Pay attention to the second sentence:

One-third of PJP cases occur in non-HIV patients, and have a higher morbidity and mortality. Most immunocompromised patients typically exhibit PJP during a corticosteroid taper.

I was troubled by the unilaterality on CT, a PJP presentation I had never seen. That happens as well, along with a hodgepodge of other X-ray findings:

Atypical patterns were observed in 32% of cases and consisted of: unilateral involvement in 11% of cases, apical involvement in 6%, pleural effusion in 9%, hilar and/or mediastinal lymph nodes in 4%, parenchymal nodules in 6% and finally pneumatocele in 12% of cases.

And then, to make it even odder, he developed TTP to the trimethoprim-sulfamethoxazole. Never saw that from trimethoprim-sulfamethoxazole either.

Clindamycin/primaquine, and a month later, the LDH was fine, the 1-3-beta-D-glucan was negative, and the CXR cleared.

So PJP, in all its atypicality, it was.

Rationalization

BMJ Case Rep. 2015 Aug 26;2015. pii: bcr2015210117. doi: 10.1136/bcr-2015-210117. Fatal Pneumocystis jirovecii pneumonia in a HIV-negative adult.

https://www.ncbi.nlm.nih.gov/pubmed/26311008

Severe Pneumocystis Jirovecii Pneumonia Presenting As Unilateral Parenchymal Infiltrates In A Non-HIV Patient With Malignancy.

http://www.atsjournals.org/doi/abs/10.1164/ajrccm-conference.2012.185.1\_MeetingAbstracts.A5468

Radiol Med. 1994 Jun;87(6):763-7. Atypical radiological images in Pneumocystis carinii infection in HIV-positive patients

https://www.ncbi.nlm.nih.gov/pubmed/8041929).

Am J Hematol. 2007 Jul;82(7):679-81. Thrombotic thrombocytopenic purpura induced by trimethoprim-sulfamethoxazole in a Jehovah's Witness.

https://www.ncbi.nlm.nih.gov/pubmed/17266059

Soaked and Sodden Infections

Apr 24, 2017

I am a native of the great Pacific NW. Rain and clouds are part of my DNA, but this winter/spring seems to be All the Summer in a Day.

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. A thousand forests had been crushed under the rain and grown up a thousand times to be crushed again. And this was the way life was forever in Portland.

Or so it seems.

To me, water is all about the infections it carries. The patient is middle-aged, diabetic, and has chronic renal failure. He has altered mental status, diarrhea, and a fuzzy right lower lobe infiltrate. Gram stain has WBC but no organisms.

CAP, HAP, or VAP? It’s all crap. I just can’t think of pneumonia that way. I think of pneumonia in terms of the germs, the risk factors, and their presentation.

No dense consolidation, negative Gram stain. That’s the bugs that can’t be grown: Legionella, Chlamydia, Mycoplasma, Q fever, and viral. Those kinds of pathogens.

Is the altered MS and diarrhea helpful? Not really. While it may point to Legionella, all infections can lead to delirium, and TNF, the mediator of fevers, causes diarrhea.

However, those with LP had higher body temperatures (39.0°C vs. 37.5°C; p < 0.001), a higher incidence of relative bradycardia (45.5%vs. 0%; p < 0.001), diarrhea (15.4%vs. 0%; p= 0.053), and lower platelet counts (178.5 × 10(3)/mm(3)vs. 233.7 × 10(3)/mm(3); p= 0.026). Radiological findings showed that the major abnormality, lobar consolidation, was indistinguishable between LP and PP.

That is why we have diagnostics. And it was Legionella on the PCR. We see maybe a case or two a year of Legionella in my hospitals despite its association with rain.

Using negative binomial model a 1-cm increase in rainfall was associated with a 2.6% (RR 1.026, 95% CI 1.012-1.040) increase in legionellosis incidence.

Probably as it is warm, humid weather that spreads Legionella, and we are cold and dank. Or we were.

It is interesting that Oregon has had more Legionella each year, whether, due more to testing or the world getting warmer, I do not know. And there is always the home water supply as well.

In our study, Legionella spp. were isolated in 22.6% of domestic hot water samples, with a mean number of legionellae in positive samples of 1.17 x 103 CFU/L (geometric mean); the highest concentration was 8.7 x 104. In previous studies in Finland and Germany, the occurrence of legionellae was similar (30% and 26%, respectively) as well as the contaminating concentration. In an Italian study of hot water samples taken from swimming pool showers, 27% were positive for Legionella spp. and 46% for P. aeruginosa, findings in line with results of our study on domestic water plants. According to a survey in Germany, L. pneumophila is by far the most abundant species in potable and environmental water samples, as >75% of positive samples were contaminated by L. pneumophila.

Like so many common and uncommon pathogens, in the end, an unsatisfactory explanation as to why.

Rationalization

Epidemiol Infect. 2007 Jul;135(5):811-7. Epub 2006 Nov 23. Increased rainfall is associated with increased risk for legionellosis.

https://www.ncbi.nlm.nih.gov/pubmed/17121693

BMJ Open. 2013 Mar 5;3(3). pii: e002428. doi: 10.1136/bmjopen-2012-002428. Meteorological factors and risk of community-acquired Legionnaires' disease in Switzerland: an epidemiological study.

https://www.ncbi.nlm.nih.gov/pubmed/23468470

J Microbiol Immunol Infect. 2010 Jun;43(3):215-21. doi: 10.1016/S1684-1182(10)60034-5. Comparisons of clinical characters in patients with pneumococcal and Legionella pneumonia.

https://www.ncbi.nlm.nih.gov/pubmed/21291849

Legionella Infection Risk from Domestic Hot Water.

https://wwwnc.cdc.gov/eid/article/10/3/02-0707\_article

Prosthetic Valve Zit

Apr 26, 2017

The patient had the abrupt onset of fevers and chills two weeks ago. Work up finally led to a TEE where a large vegetation was found on the bioprosthetic valve with a ring abscess. Blood cultures were negative.

The valve was replaced, gram stain had gram-positive rods, and the cultures grew P. acnes.

That is the second P. acnes PVIE I have seen, the last back in 2013.

Both male. One was 6 months after replacement, the other was about 2 years after replacement. Both were bioprosthetic valves.

The most recent had the valve replaced using a minimally invasive technique, going in using a mini-thoracotomy. The first case did as well. I kind of remember the patient unhappy that he was going to get a median sternotomy.

A search of PubMeds finds no association of endocarditis, P. acnes, or otherwise, with minimally invasive surgery over and above the risk from having a prosthetic valve. I have to wonder, given the organism's niche of the hair follicles of (furry) men, if it was dragged in through the incision. It could just as well have made it to the valve hematogenously.

A rare cause of endocarditis, P. acnes tend to present with advanced disease and ring abscess, no surprise given the tendency for this organism to fester for months and years with minimal inflammatory response.

Remarkably, the Cleveland Clinic had 24 cases in a 9 year period; that’s a couple a year. As is so often the case, the article is behind a paywall, and it is not worth $35.95 of my, or my hospital's, money to see if any of the patients had a minimally invasive valve replacement.

The medical literature should be free or at least like iTunes, 99 cents a paper. $35.95. Puh-leaze.

Rationalization

A Connecticut Yankee.

http://boards.medscape.com/forums/?128@@.2a5ad057!comment=1

Clin Microbiol Infect. 2017 Jan 3. pii: S1198-743X(16)30658-9. doi: 10.1016/j.cmi.2016.12.026. [Epub ahead of print] Propionibacterium acnes endocarditis: a case series.

https://pubmed.ncbi.nlm.nih.gov/28057559/

J Clin Microbiol. 2007 January; 45(1): 259–261. Published online 2006 October 25. doi: 10.1128/JCM.01598–06 PMCID: PMC1828954 Propionibacterium acnes as a Cause of Prosthetic Valve Aortic Root Abscess.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1828954/

POLL RESULTS

The medical literature

• should be free 63%
• should be 99 cents 21%
• should cost whatever the market will tolerate 6%
• should cost by the word 0%
• should cost by the impact factor 3%
• Other Answers 7%
• Should be kept as a trade secret.
• five cents
• Should automatically upload to wiki
• should be obtainable to those with a "growing media empire" by tweeting to #icanhazpdf

Firstest with the Rightest

May 9, 2017

How to win a battle? "Getting there firstest with the mostest" ~Nathan Bedford Forrest.

Back from a 5-day vacation in Las Vagus, home of the 10th cranial nerve. The heat was so nice after 6 months of Oregon dank. The hikes in the Vegas area are fantastic: Red Rock Canyon and Valley of Fire. But back to work.

Everyone, or at least I hope everyone, has some aspect of medicine that adds an extra frisson of joy to their day. For me, it is getting to the diagnosis before anyone else, including the lab. Yeah, I am that petty/competitive. All of medicine provides ample positive reinforcement, and at the end of the day, there is always the satisfaction of knowing that someone's life was made a wee bit better because of our jobs.

But for me? I want to be the first to put it all together. It doesn't often happen, but when it does, it makes me feel like Principal Snyder:

These are moments you want to savor. You wish time would stop so that you could live them over and over again.

and

I have a nearly physical sensation of pleasure at the thought of making a diagnosis. I'd describe myself as tingly.

The best is making the diagnosis with as little information as possible. And really, so much of a textbook case can be distilled into just a few pertinent points.

The hospitalist says he has a consult for the next day when the organism in the blood is identified, but I am heading out the door for Vegas, whose motto is what happens in Vegas goes home to your significant other. So I say, I'll see him now.

22-year-old male.

Fevers and sore throat.

Admitted with pleuritic chest pain and septoid, aka SIRS.

Gram-negatives growing anaerobically.

Only one thing it can be. I called the lab: Tell me it is Fusobacterium

They look at the gram stain, and they couldn't. Maybe, but it didn't look classic.

Well, it has to be.

And it was.

Lemierre's. It has been a while since I saw a case. Interestingly there was no clot or abscess in the neck, but I figure it went downstream, hence the chest pain. No abscess was found elsewhere.

His symptoms melted away on metronidazole.

For you youngsters who read this blog. Always call the diagnosis if you can, before all the information is back. And do it with Authoritah. No one will remember if you are wrong, but they will always remember when you were right. It will build you a reputation. Babe Ruth not only led the league in home runs but strikeouts.

Rationalization

World J Clin Cases. 2017 Mar 16;5(3):112-118. doi: 10.12998/wjcc.v5.i3.112. Pulmonary embolism and internal jugular vein thrombosis as evocative clues of Lemierre's syndrome: A case report and review of the literature.

https://www.ncbi.nlm.nih.gov/pubmed/28352635

Anaerobe. 2016 Dec;42:89-97. doi: 10.1016/j.anaerobe.2016.09.006. Epub 2016 Sep 28. The role of Fusobacterium necrophorum in pharyngotonsillitis - A review.

https://www.ncbi.nlm.nih.gov/pubmed/27693542

POLL RESULTS

I gain the most satisfaction in medicine from

• making the diagnosis 53%
• helping people understand their disease 28%
• getting an insurance company to approve an MRI 3%
• yelling at house staff 3%
• calling myself Doctor at the BMW dealership. 9%
• Other Answers 3%
• not having to testify in court, for the defense, in the malpractice trial.

Famata is not Famata

May 10, 2017

I checked my email just before I started to write this entry. There is an invitation from the telavancin folks for a dinner lecture.

At the most expensive steak house in the city.

And I looked up the speaker on Dollars for Docs. Over $636,000 in the last three years. Whoa.

Who thinks that’s OK? Who thinks this is an unbiased lecture? Who goes to stuff like this? I got no idea. I would have to purge both my stomach and brain if I attended such an event. I am a paid blogger but will have to write for over 1826 months, or 152 years, to hit that number. I guess I will be blogging for a while.

Anyway, back to clinical medicine. The patient is on CAPD and comes in with abdominal pain, fevers, and cloudy CAPD fluid.

And it grows a Candida.

C. lusitaniae. Odd, but whatever. Then the blood cultures grow a yeast. C. famata.

Now what? I do not have a concordance of cultures, which always annoys me. The MALDI-TOV called it, but not with a great deal of enthusiasm. 94% probable.

Yeasts can be difficult to identify, and being called C. famata when it isn’t is an issue:

Among 53 strains collected during the SENTRY and ARTEMIS surveillance programs and previously identified as C. famata (includes all submitted strains with this identification) by a variety of commercial methods (Vitek, MicroScan, API, and AuxaColor), DNA sequencing methods demonstrated that 19 strains were C. guilliermondii, 14 were C. parapsilosis, 5 were C. lusitaniae, 4 were C. albicans, and 3 were C. tropicalis, and five isolates belonged to other Candida species (two C. fermentati and one each C. intermedia, C. pelliculosa, and Pichia fabianni). Additionally, three misidentified C. famata strains were correctly identified as Kodomaea ohmeri, Debaryomyces nepalensis, and Debaryomyces fabryi using intergenic transcribed spacer (ITS) and/or intergenic spacer (IGS) sequencing. The Vitek 2 system identified three isolates with high confidence to be C. famata and another 15 with low confidence between C. famata and C. guilliermondii or C. parapsilosis, displaying only 56.6% agreement with DNA sequencing results. Matrix-assisted laser desorption ionization–time of flight (MALDI-TOF) results displayed 81.1% agreement with DNA sequencing. One strain each of C. metapsilosis, C. fermentati, and C. intermedia demonstrated a low score for identification (<2.0) data-preserve-html-node="true" in the MALDI Biotyper. K. ohmeri, D. nepalensis, and D. fabryi identified by DNA sequencing in this study were not in the current database for the MALDI Biotyper.

It makes a difference as C. famata, if that what it really was, is resistant to fluconazole. We pulled the CAPD catheter, and the patient did fine on fluconazole. Eventually, the reference lab called them both C. lusitaniae, long after completing a course of therapy.

Take home? Candida famata might not be Candida famata.

And no drug company paid me to say that.

Rationalization

Candida guilliermondii and Other Species of Candida Misidentified as Candida famata: Assessment by Vitek 2, DNA Sequencing Analysis, and Matrix-Assisted Laser Desorption Ionization–Time of Flight Mass Spectrometry in Two Global Antifungal Surveillance Programs. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3536252/

POLL RESULTS

I

• deserve anything I get because I have Doctor privilege 0%
• have never taken a thing from big pharma 30%
• prefer denial. Take what I can, deny it means anything 15%
• don't get enough reimbursement, so letting pharma subsidize me through high drug costs is fine with me 0%
• am too jaded to care 36%
• Other Answers 18%
• I wish Big Pharma would offer *me* something.
• am not a doctor.
• I've done it in the past but have not for many years now, and don't plan to go back.
• Work in long term care and am lucky to get a pack of crackers.

Pictures are worth 1000 words

May 15, 2017

The patient came in with urosepsis and had this CT:

![A picture containing text, dark, tableware, ceramic ware

Description automatically generated](Aspose.Words.008a338b-8827-4faa-8ea2-26bdfe5d0381.001.png)

That’s gas.

It has been a while since I have seen a case of emphysematous cystitis/pyelonephritis. I always want to call it pneumocystis, but that name is taken,

The cultures of the urine and the nephrectomy both grew E. coli.

While there are cases where the patient is treated medically, usually the best treatment is removal. The patient has diabetes, the usual risk for emphysematous urinary tract infection.

I wonder about the diabetes. In part, it makes the patient more immunosuppressed, but is the organism using the extra glucose of diabetes for fermentation in a dead kidney to make all the extra gas?

Under anaerobic conditions and in the absence of alternative electron acceptors Escherichia coli converts sugars to a mixture of products by fermentation. The major soluble products are acetate, ethanol, acetate and formate with smaller amounts of succinate. In addition the gaseous products hydrogen and carbon dioxide are produced in substantial amounts.

That’s substantial gas. I wonder how flammable it is?

And look at the (your) left clavicle. There’s gas in the marrow as well.

![A picture containing dark

Description automatically generated](Aspose.Words.008a338b-8827-4faa-8ea2-26bdfe5d0381.002.png)

The blood culture were negative, but the area progressed on antibiotics to a septic joint/osteomyelitis that required debridement.

I could find no cases of metastatic gas from E. coli quite like it. E. coli has so little propensity for causing metastatic infection after bacteremia that, as a rule, I don’t worry about it.

Time, drainage, and antibiotics eventually cured the infection.

Rationalization

Indian J Surg. 2013 Jun;75(Suppl 1):272-4. doi: 10.1007/s12262-012-0690-6. Epub 2012 Jul 6. Emphysematous Pyelonephritis-a Rare Surgical Emergency Presenting to the Physician: A Case Report and Literature Review.

https://www.ncbi.nlm.nih.gov/pubmed/24426588

Int Urol Nephrol. 2014 Jan;46(1):223-7. doi: 10.1007/s11255-013-0446-7. Epub 2013 Apr 17. Medical therapy alone can be sufficient for bilateral emphysematous pyelonephritis: report of a new case and review of previous experiences.

https://www.ncbi.nlm.nih.gov/pubmed/23591724

FEMS Microbiol Rev. 1989 Sep;5(3):223-34. The fermentation pathways of Escherichia coli.

https://www.ncbi.nlm.nih.gov/pubmed/2698228

Expert Opinion

May 17, 2017

Life is so strange

Duration unknown

When you don't know

Your duration

Something could change

It's unknown

And then you won't know

Duration unknown

Missing Persons. Kind of. Yeah, I know I have used this quote before. But the situation is unchanged. Still.

I often get asked for the duration of antibiotics. Sometimes I know, sometimes I don’t. Either way, I have to come up with an answer.

When there is no data, we get expert opinion: biased advice based on inappropriate extrapolations from other studies filtered through the lens of experience. And when it comes to deciding on therapy, the three most dangerous words in medicine remain ‘in my experience.’

I was asked yet again how long to treat a coagulase-negative Staphylococcus central line infection. It was the real deal, both sets positive, and the PICC line set was positive before the peripheral set.

The PICC was pulled, the fevers abated, the repeat blood cultures were negative, and the patient has no endovascular devices.

Expert opinion in Up To Date suggests 5-7 days, where other Up To Date experts suggest no antibiotics if the patient does clinically well after pulling the line.

As an expert, my opinion falls in the latter camp. I figure that the patient's antibiotics for the septoid state are sufficient if there is no endovascular hardware.

As noted before, the IDSA guidelines say for coagulase-negative Staphylococcal bacteremia:

For uncomplicated CRBSI, treat with antibiotics for 5–7 days if the catheter is removed (B-III) ... Alternatively, patients with uncomplicated CRBSI can be observed without antibiotics if they have no intravascular or orthopedic hardware, the catheter is removed, and additional blood cultures (performed on samples collected when the patient is not receiving antibiotics) are obtained after catheter withdrawal to confirm the absence of bacteremia (C-III).

Although the guidelines give it a B III and C III, the text says

There are no compelling data to support specific recommendations for the duration of therapy for device-related infection.

Writers of guidelines get the privilege of disguising opinion as fact and obscuring that fact with categories of evidence I at least can never remember. Which one is not evidence-based medicine? Oh, yeah, III.

Level III: Opinions of respected authorities, based on clinical experience, descriptive studies, or reports of expert committees.

For other bloodstream infections from far more pathogenic organisms, 3-5 days is probably enough with good source control. I am increasingly of a mind that bacteremia (outside of S. aureus and Candida alibicans) is unimportant in determining the length of therapy.

For most bugs, one shot of antibiotics is probably enough to sterilize the blood. The question is not the bacteremia but is the source controlled/controllable and what the risk is of a metastatic infection.

Since I am a respected authority (!?!) with clinical experience, I suggested no further antibiotics.

The patient did fine.

Slow Motion

May 22, 2017

The patient is a female, otherwise healthy, about my age, with a week of sore throat, then fevers and rigors, then severe hip pain, then anterior pleuritic chest pain.

The admitting diagnosis was sepsis and viral pericarditis based on the pain and a small pericardial effusion. She was started on colchicine for the pericarditis.

The blood grew gpc in pairs and chains, and I was betting on another case of Lemierre's. Not all Lemierre's is due to Fusobacterium, and I ordered a CT of the chest and neck.

The MRI of the hip showed a bursitis, which was tapped then I&D’s and, like blood, grew Group A Streptococcus. There are Lemierre's cases from group A strep, but the CT did not confirm septic emboli. Now the small pericardial effusion was very large and turbid.

So it was off to the OR for a window for purulent pericarditis. There was tamponade physiology in the OR, and gram stain showed lots of WBC, but nothing grew.

A bunch of take-home points.

First, Occam rules. No way would a patient have both bacteremic pharyngitis AND viral pericarditis. Everything needs to be tied up in a nice neat razor.

Group A Streptococcus is an uncommon cause of Lemierre's but an equally uncommon cause of purulent pericarditis, with the majority of cases in kids. The smattering of cases I have seen have been due to S. aureus or the Pneumococcus.

Thirdly, how did the Streptococcus get to the pericardium? Hematogenously? Probably. But the lymphatics of the pharynx connect to the pericardium and has been suggested as part of the pathophysiology of rheumatic fever. I think it is a bit of a stretch and never quite bought that explanation, but head and neck anatomy was not my best class in med school.

Finally, what puzzled me most was the relatively slow progression of her bacterial pericarditis; it evolved over several days from pain to ECHO to CT to OR, with tamponade physiology taking 4 or 5 days to develop. Was it the colchicine? Colchicine stops WBC in their tracks with gout. Why not with purulent pericarditis? There are cases of colchicine being given for septic arthritis, but they do not comment as to whether colchicine was helpful. I can find no reports of colchicine being used, accidentally or deliberately, for any other infection. But it seems a reasonable hypothesis.

Nothing heals like I&D and antibiotics, and she did just fine.

Rationalization

Lancet Infect Dis. 2007 Mar;7(3):233. Lemierre syndrome caused by Streptococcus pyogenes in an elderly man. \https://www.ncbi.nlm.nih.gov/pubmed/17317605

Med J Aust. 2017 Feb 20;206(3):113-114. Streptococcus pyogenes pericarditis in a healthy adult: a common organism in an uncommon site.

https://www.ncbi.nlm.nih.gov/pubmed/28208036

Lymphology. 1995 Dec;28(4):208-17. The lymphatic drainage of the parietal pericardium in man.

https://www.ncbi.nlm.nih.gov/pubmed/8771014

Nail Freak

May 24, 2017

I always loved Sherlock Holmes, his ability to see a small detail and recognize its significance. I am no Sherlock Holmes, but sometimes you can do that in medicine, and it might freak out the patient.

I am seeing an elderly female for S. aureus bacteremia. I am looking at the fingernails for emboli and note that about a third of the way up each nail is a groove. Beau’s lines. I see Beau’s lines all the time in chemo patients. The nails are like tree rings and represent times of stress, like chemotherapy or infection. They were even found on Otzi.

One of his fingernails (of the two found) shows three Beau's lines indicating he was sick three times in the six months before he died. The last incident, two months before he died, lasted about two weeks.

I knew she had no chemotherapy, so I asked if she a severe infection about a month ago.

It freaked her out.

“How did you know I had pneumonia last month?” she asked. “I am totally wiggins that you know I had pneumonia. How did you know that?”

She didn’t strike me as a BTVS fan, but I didn't ask.

I explained to her about Beau’s lines, but she still thought it was freaky I could do that. I can see how people can be impressed by a psychic's cold reading, given how people react when I call some oddity with only minimal information.

My favorite was early in my career when I was asked to see an FUO.

The patient's fever began 3 weeks ago. Her temperature was 102°F, and she had shaking chills, headache, myalgia, and lassitude that lasted about 5 days and then resolved. After a 5-day hiatus, the symptoms returned, identical to the first episode, lasted for another 5 days, and then remitted for 5 days before recurring yet again. The headache was associated with photophobia and a slightly stiff neck.

Now I know that Black Butte is the epicenter for relapsing fever in Oregon and a popular vacation spot. So after hearing her history of relapsing fevers, rather than an open-ended question about recent travel, I asked, "So, how was your vacation in Black Butte?" The look of shock on her face when she said, "How did you know I was in Black Butte?" was one of the more satisfying responses I have had in my career.

I have done similar things in the past, more often with a miss than a hit, but when it is a hit, it is oddly satisfying. It is often the little things in life that are particularly delightful.

Rationalization

West J Med. 1980 Sep; 133(3): 203–209. PMCID: PMC1272260 Tick-borne Relapsing Fever in the Pacific Northwest: An Underdiagnosed Illness?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1272260/

Intern Med. 2015;54(17):2281. doi: 10.2169/internalmedicine.54.5166. Epub 2015 Sep 1. Beau's Lines and Mees' Lines Formations after Chemotherapy.

https://www.ncbi.nlm.nih.gov/pubmed/26328664

Biomedica. 2013 Oct-Dec;33(4):500-2. Beau's lines secondary to acute illness in an elderly woman.

https://www.ncbi.nlm.nih.gov/pubmed/24658448

Otzi

https://en.wikipedia.org/wiki/Ötzi

Wiggins

an uneasy feeling; a sense of foreboding badness. Originally coined by Joss Whedon, on his cult TV show Buffy the Vampire Slayer.

https://www.urbandictionary.com/define.php?term=wiggins

Weird PJI. Part One

May 31, 2017

The patient returned from a walk, sat down for a rest, and when he stood up, his 10-year-old prosthetic knee was swollen, hot, and painful.

This was at the end of a three-month stay in urban Colombia, where he had no unusual exposures. He also has no other medical problems, healthy as the proverbial horse.

He returned to the US and eventually had his knee tapped, there were 45,000 cells, but the gram stain and cultures were negative.

Because the cultures were negative, he was told the knee was not infected. Still, he eventually ended up in the care of an orthopedic surgeon who also tapped the knee, with similar results, but this time took the patient for I&D.

It was grossly infected and loose, so it was removed.

Gram stain: pus but no organisms. ID was consulted.

I figured with a negative gram stain and an 8-month course, if it were something he picked up in Columbia, it would be either Salmonella or Brucella. Maybe TB; I have seen one prosthesis infected with TB.

Nope.

Listeria monocytogenes.

I guess that is my second case, although I do not remember the first. Thank goodness for this blog; it serves as a replacement for a memory I do not have.

Armed with an organism, I re-took a history looking for a reason. Nada. He also never had diarrhea or a febrile illness that could have been the initial infection.

He did eat a lot of cheese, and soft cheeses are a classic US risk for Listeria, but other foods can contain Listeria as well.

So as is so often the case, I have to blame bad luck. He did fine on a course of antibiotics and is awaiting a new knee. And maybe healthy as a horse is not the best metaphor when it comes to Listeria.

No significant differences were obtained in the incidence of L. monocytogenes in whole cured meat products (e.g., raw ham) and minced cured meat products (e.g., dry fermented sausage), 14.92 and 11.69%, respectively. Lower incidence rates of L. monocytogenes were obtained for raw, cured meat products using beef or horse meat, 4.65 and 5.88%, respectively, A high incidence rate of L. monocytogenes was noted for the mayonnaise based salads (21.28% (186/874)) as well as for prepared meals (11.70% (92/786)), the latter especially due to contamination of vegetarian meals.

Rationalization

Fetid Dingos’ Kidneys.

http://boards.medscape.com/forums/?128@@.2a7b4c5b!comment=1

Healthy as a Horse?

http://www.doctorramey.com/healthy-as-a-horse/

J Med Microbiol. 2009 Jan;58(Pt 1):138-41. doi: 10.1099/jmm.0.004234-0. Chronic prosthetic joint infection caused by Listeria monocytogenes.

https://www.researchgate.net/publication/23655564\_Chronic\_prosthetic\_joint\_infection\_caused\_by\_Listeria\_monocytogenes

J Food Prot. 2011 Jun;74(6):949-53. doi: 10.4315/0362-028X.JFP-10-536. Multistate outbreak of Listeria monocytogenes associated with Mexican-style cheese made from pasteurized milk among pregnant, Hispanic women.

https://pubmed.ncbi.nlm.nih.gov/21669072/

Int J Food Microbiol. 1999 Dec 1;53(1):75-80. Incidence of Listeria monocytogenes in different types of meat products on the Belgian retail market.

https://www.ncbi.nlm.nih.gov/pubmed/10598117

https://pubmed.ncbi.nlm.nih.gov/21669072/

Weird PJI 2: Electric Boogaloo

Jun 5, 2017

The patient had a hip replaced several weeks ago. She is otherwise healthy with no co-morbidities. The wound opens up, and it starts to drain clot, and she develops a fever. She is taken to the OR, where a large infected hematoma that extends into the hip is found.

Washout and poly-exchange, what you do when your parrot dies, I suppose.

The gram stain shows mostly blood, gram-negative rods, and a smattering of WBC.

So I figure it will be an E. coli or some such.

Nope.

All the cultures grow Bacteroides thetaiotaomicron.

I don’t think I have ever seen a Bacteroides prosthetic joint infection. It happens. Every bug eventually shows up in every organ. And as best I can tell, there is nothing particularly compelling to set this bug apart from others.

One review suggests

Many patients with osteomyelitis due to anaerobic bacteria have evidence of an anaerobic infection elsewhere in the body that is the source of the organisms involved in the osteomyelitis.

Although she had nothing to suggest this was a metastatic infection. I presume it was due to a hematoma in close proximity to, um, well, you know. The butt.

With the bioavailability of metronidazole approaching 100%, I could see no compelling reason to treat with iv, and he did quite well on oral. The big question is whether, for this organism, chronic suppression is a good idea, as neurotoxicity is a potential long term problem. I don't know, but I lean that way.

Rationalization

Breakin' 2: Electric Boogaloo.

https://en.wikipedia.org/wiki/Breakin%27\_2:\_Electric\_Boogaloo

Anaerobe. 2004 Oct;10(5):255-9. Antimicrobial susceptibilities of Bacteroides fragilis and Bacteroides thetaiotaomicron strains isolated from clinical specimens and human intestinal microbiota.

https://www.ncbi.nlm.nih.gov/pubmed/16701525

J Bone Jt Infect. 2017 Mar 19;2(3):122-126. doi: 10.7150/jbji.17129. eCollection 2017. Clinical and Microbiological Characteristics of Bacteroides Prosthetic Joint Infections.

https://www.ncbi.nlm.nih.gov/pubmed/28540148

Probably Not Relevant But Fun to Think About

Jun 7, 2017

The patient had a perforated diverticulitis 8 months ago, treated with partial colon resection and antibiotics.

5 months later, she represents with fevers and has a right upper quadrant abscess that is drained and grows E. coli, resistant to quinolones.

It is treated with percutaneous drainage and Augmentin and is apparently a cure.

Nope.

Two months later, it recurs and is drained again. Same E. coli as last time. This time I am called.

There are a couple of issues. One, it does not appear that the abscess is being fed by an ongoing leak.

So why is the infection not getting better? Response to infection depends on the host, the organism's virulence, and the efficacy of the antibiotic.

Augmentin is in the guidelines as an option, but a mere B-2. Most antibiotics work fine if the host is normal and the drainage is adequate, although I fret about the pharmacokinetics of oral agents like Augmentin.

But I wonder if the issue is the host as she has hemochromatosis.

Iron is an important growth factor for bacteria, and we aggressively sequester iron from pathogens. Giving iron to bacteria is like putting me in a Baskin Robbins. For bacteria, extra iron is hog heaven.

Most of the literature suggests patients with hemochromatosis have increased severity of infections, not refractory disease or abscess, although there was a pair of Yersinia liver abscesses.

I doubt the hemochromatosis had anything to do with the relapsing infection, but still fun to think about. It could have tipped the balance in favor of the E. coli. Sometimes it is the little things that give the bacteria an advantage. And not much I can do about it.

And I sent her out on iv ceftriaxone. Maybe the third time will be the charm.

It was.

Rationalization

Association of hemochromatosis with infectious diseases: expanding spectrum.

http://www.sciencedirect.com/science/article/pii/S1201971207000811

Scand J Gastroenterol. 2001 Feb;36(2):220-4. Yersinia enterocolitica infection with multiple liver abscesses uncovering a primary hemochromatosis.

https://www.ncbi.nlm.nih.gov/pubmed/11252417

Third Time to be a Charm?

Jun 12, 2017

The patient has had a bad year: perforated gastric ulcer with enterocutaneous fistula. He has been on TPN for the last several months. One of his multiple hospitalizations was complicated by a myocardial infarction and the need for a pacemaker.

Now he has had a month of intermittent fevers and two episodes of transient (2-3 days each) of pleuritic chest pain.

Blood cultures grow yeast. C. glabrata.

A workup ensues. TEE with a small vegetation on the tricuspid valve. Neither the central line nor the pacer system grows yeast, and at the time of pacer extraction, the vegetation is gone. Gone downstream, I suppose. The 1-3 beta D glucan is greater than 500 five days after all the hardware is out.

Candida endocarditis? Probably.

Endocarditis complicating central lines and pacers is an increasing issue, right up there with heroin use.

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%

Curable without surgery? Maybe. I have cured a pair of tricuspid endocarditis due to Candida in patients deemed too high risk for surgery. I have failed in more. And there are a smattering of medical cures reported, no doubt representing a severe case of publication bias.

With kidneys that do not tolerate amphotericin, I will treat it with micafungin, follow the beta-D glucan and see if I can cure my third. It may be the charm.

It was.

Rationalization

Clin Cardiol. 2009 Dec;32(12):E48-54. doi: 10.1002/clc.20498. Endocarditis complicating central venous catheter bloodstream infections: a unique form of health care associated endocarditis.

https://www.ncbi.nlm.nih.gov/pubmed/20014189

Mycoses. 2015 Nov;58(11):637-41. doi: 10.1111/myc.12391. Epub 2015 Sep 25. Candida and cardiovascular implantable electronic devices: a case of lead and native aortic valve endocarditis and literature review.

https://www.ncbi.nlm.nih.gov/pubmed/26403965

Antimicrob Agents Chemother. 2012 Aug; 56(8): 4552–4553.doi: 10.1128/AAC.00515-12 PMCID: PMC3421621 Anidulafungin for Candida glabrata Infective Endocarditis.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3421621/

Source?

Jun 14, 2017

The patient is an injection drug user, heroin, who comes in with multiple abscesses due to MRSA. Nothing unusual there. But one of the blood cultures grows Acinetobacter baumannii.

Now, where did that Acinetobacter from? The patient uses tap water to cook the black tar heroin but filters it through cotton balls.

Is it from the water? Probably. I had a patient years ago who came in with recurrent Acinetobacter bacteremia, and she shot up using either water from the Culligan dispenser in her youth hostel or the lady's room at a local burger franchise. I never did test either water source, but she stopped having bacteremia when informed of my suspicion.

As best I can tell from the city water reports, there is not Acinetobacter in Portland water when tested. This is not Flint, after all, but who can say what is the tap of her old downtown hotel.

Is it the cotton balls? The classic organism to cause cotton fever is Pantoea (formally Enterobacter). Pantoea is in the cotton bolls because it is part of the stink bug stool microbiome, and some stink bugs live in cotton bolls.

Previously, we demonstrated that Pantoea sp. strain Sc 1 is a causal agent of an emerging disease of immature green cotton bolls in southeastern Cotton Belt states and is vectored by boll-piercing insects such as stink bugs.

So some heroin users filter the dissolved heroin through stink bug stool.

But stink bugs do not have Acinetobacter in their colon.

But it appears that Acinetobacter is also found in cotton:

Acinetobacter baumannii and Arthrobacter spp. were present in cotton stems but not in cotton roots...

and Acinetobacter is found in the colon of cotton bollworms and grasshoppers

We compared the bacterial communities in the larval midgut of field and laboratory populations of a polyphagous pest, the cotton bollworm (Helicoverpa armigera), using denaturing gradient gel electrophoresis (DGGE) of amplified 16S rDNA sequences and 16S library sequence analysis. DGGE profiles and 16S rDNA library sequence analysis indicated similar patterns of midgut microbial community structure and diversity: specific bacterial types existed in both populations, and a more diverse microbial community was observed in caterpillars obtained from the field. The laboratory population harbored a rather simple gut microflora consisting mostly of phylotypes belonging to Enterococcus (84%). For the field population, phylotypes belonging to Enterococcus (28%) and Lactococcus (11%), as well as Flavobacterium (10%), Acinetobacter (19%), and Stenotrophomonas (10%) were dominant members.

and

The grasshopper was found to harbour Acinetobacter baumannii and Klebsiella pneumoniae. Red pumpkin beetle, blue pumpkin beetle and tiger beetle harboured, respectively, Pseudomonas spp., Enterobacter cloacae and Staphylococcus spp., whereas the red cotton bug was found to contain Bacillus spp., in their whole body homogenates.

So maybe the cotton balls, maybe the water as the source. The patient did fine with a short course of antibiotics.

The things you can discover with Google and curiosity.

Rationalization

Arch Intern Med. 1993 Oct 25;153(20):2381-2. Enterobacter agglomerans--associated cotton fever.

https://pubmed.ncbi.nlm.nih.gov/8215743/

I Don't Cotton to That.

http://boards.medscape.com/forums/?128@@.2a064487!comment=1

Plant and Soil June 1995, Volume 173, Issue 2, pp 337–342 Survey of indigenous bacterial endophytes from cotton and sweet corn

https://doi.org/10.1007/BF00011472

Microbial communities in the larval midgut of laboratory and field populations of cotton bollworm (Helicoverpa armigera) http://www.nrcresearchpress.com/doi/abs/10.1139/w06-064#.WUAk8LkkuUk

Genome Sequence of Pantoea sp. Strain Sc 1, an Opportunistic Cotton Pathogen

http://jb.asm.org/content/194/11/3019.full

Cellulolytic activity of microbial flora of agricultural insects [2008].

http://agris.fao.org/agris-search/search.do?recordID=PK2008000299

Dilemmata

Jun 19, 2017

The patient is an elderly male who presented with altered mental status and fever. He had an RRT (rapid response team, which is a noun, but the acronym is a verb), which delayed his spinal tap until day two of admission, which had 800 WBC, mostly monocytes and a protein of 600, with a normal glucose. During this time, he was on lotsa antibiotics.

He had a patch of what appears to be shingles on his arm, so we suspected VZV, and thanks to the magic of the PCR panel, we had an answer by the end of the workday. VZV it was.

Encephalitis and cerebellar ataxia are the most common CNS complications of VZV. His labs were towards the extreme end of the spectrum for this disease:

The CSF findings are usually abnormal with elevated opening pressure, a mild-to-moderate lymphocytic pleocytosis (usually <100 data-preserve-html-node="true" cells/μL), mildly elevated protein (50–100 mg/dL), and normal glucose levels.

But no other reason was evident, such as a vasculitis.

Unfortunately, the creatinine rose. Was this acyclovir nephrotoxicity due to drug crystals precipitating out in the kidneys? I have seen this but once before and with oral acyclovir.

Here is the confusing part: there were no crystals in the urine, but there were eosinophils.

I could find one case of AIN from acyclovir on the PubMeds, and he had had all sorts of other nephrotoxic insults: cephalosporins, vancomycin, contrast, hypotension.

And the only other options, foscarnet, and cidofovir are nephrotoxic as well.

Rock, meet hard place. Hard place, rock.

I am betting against AIN from acyclovir and will hang tough.

His kidney did fine.

Rationalization

Varicella-Zoster Virus: Atypical Presentations and Unusual Complications

https://academic.oup.com/jid/article/186/Supplement\_1/S91/838964/Varicella-Zoster-Virus-Atypical-Presentations-and

Nephron. 1990;56(4):436-8. Acyclovir-induced acute tubulo-interstitial nephritis.

https://www.ncbi.nlm.nih.gov/pubmed/2080005

The Benefit of Being Around A Long Time

Jun 21, 2017

There are advantages to being 420 in dog years. If you include my fellowship, I am heading into the 32nd year of clinical ID. 50 weeks a year, a low ball, 10 new consults a week, that's like 16,000 unique patients I have seen. Curbsides are probably one hundred times that number. It has made me a better diagnostician, and if you have ever had the misfortune of reading notes from early in your practice, you know what I am talking about.

It is why I am always amused when a patient asks for a second opinion and wants to go to the University. The average academic doc is on service, what, 4 months a year? And all the clinical care filtered through medical students, residents, and fellows. They have dog years kind of experience. If I had a disease no one could figure out, I wouldn’t go to an academic center to get a diagnosis.

I am not necessarily any better at knowing what to do for patients. That’s why I read the literature. And a quick check shows I have 16,500 articles, almost 8 gigs, that I have read just for my ID puscasts, and that’s since 2006 when I went all digital. I still remember recycling all the papers I read from 1986 to 2006, three filing cabinets worth.

But what is curious as a result of all that patient care and reading is how, over the years, I can arrive at a diagnosis with increasing rapidity. And it is not conscious. The diagnosis often just burbles up out of who knows where. Not always the right diagnosis, mind you, but still. ID is more than coming up with an endless differential and testing for everything, no matter how far fetched. You have to commit to A diagnosis.

The patient had three months of fevers, sweats, weight loss, severe arthralgias and myalgias, a WBC of 25K, and a markedly elevated CRaP after a year in Western Europe. After an extensive work-up, they called me.

About 60 seconds in, I thought, ‘It’s Stills.’

Still, I went through the routine. No risks for anything odd, nothing of note on exam, and all the diagnosis studies negative.

So when I was done, I hunted down the resident and said, ‘It’s Stills.

While I dictate all my consults, my typed note in EPIC said, in its entirely:

Note dictated.

Still's.

The ferritin was 3000, so confirmatory, as best you can confirm Still’s.

So fun. There is nothing like being right.

That is the good thing about have been around forever: I have seen a remarkable number of cases, and they seem to be filed somewhere for comparison to current cases and rapid matching. I sometimes think the average consult anymore takes about 3 minutes to get to the likely diagnosis. The rest of the time is doing the complete H&P to make sure I haven't missed anything important that would disconfirm the diagnosis or lead me elsewhere.

Perhaps more importantly, there are all the cases I have missed. I have mentioned before how I completely missed a pair of Still’s early in my career, and like all failures, it has a disproportionate effect on my practice.

And here is a piece of advice for you youngsters. Patients with chronic undiagnosed diseases worry they have cancer. And they will never ask. And even if you give them a diagnosis of, say, Stills, they still worry about cancer. I always make a point, when I can, to say there is nothing to suggest cancer. And the statement is always met with great relief and often with tears.

It is often as important to tell the patient what they don’t have as what they do.

Rationalization

More of my adventures with Still's.

Apeeling.

http://boards.medscape.com/forums/?128@@.2a813a9a!comment=1

Ghost in the Machine

http://boards.medscape.com/forums/?128@@.2a358c9d!comment=1

POLL RESULTS

If I had an undiagnosed illness, I would go to

• an ID doc 58%
• the Mayo 9%
• my local University 12%
• a naturopath. At least I would get the diagnosis of Lyme no matter what. 5%
• a medical psychic 7%
• Other Answers 9%
• Med school. To diagnose it myself.
• A bar. A really rough bar. If my undiagnosed disease is infectious, alcohol should kill it. If it needs surgery, I can just insult a drunk.
• nearest bar

Idle Speculation While Work is Slow

Jun 26, 2017

It has been weirdly slow all over the city for infectious diseases. Maybe it’s all global warming, as August is classically the slow month for me. There was one August I had a total of one paying consult. It was back before the Affordable Care Act when about a quarter of my consults had no insurance. Back then, it worried me. Now? I don’t mind the lazy days of summer.

Summer is S. aureus season, and we have finally finally finally had some hot weather, and people are sweating with the heat. Staph, I presume, enjoys a warm, sweaty skin fold from which to launch an attack. It is why there is

… some seasonal variation in the occurrence of S. aureus infection appears to exist, particularly an association of warm-weather months with S. aureus skin and soft-tissue infections.

The patient in question had a fractured hip replacement 3 months ago, back in the middle of the cold, wet, dreary, dark winter. He did well except for the need to drain a hematoma a couple of weeks post-op. Now he has increasing pain in his hip and at I&D has S. aureus.

The curious thing is he has a pea-sized arterial-venous malformation on his lower lip that bleeds from time to time and tntc cherry angiomata on his skin.

He tells me with direct questioning that he had lots of nose bleeds as a child, but not as an adult.

Is this some variation of hereditary hemorrhagic telangiectasia (HHT)? Or is the arterial-venous malformation on his lip a red herring?

The question I cannot find a definitive answer to is: are cherry angiomata associated with HHT? As best I can tell, the answer is no, they are not. The AVM I have seen with HHT (a grand total of two cases) look different than this AVM and look different than cherry angiomata.

While classically associated with brain abscess, HHT patients get more osteoarticular and other infections, although no prosthetic joint infections have been reported in PubMed.

I have seen the odd chronic bleeding lesion in other patients that I think are the source of S. aureus bacteremia. If not HHT, then it could still be from the lip. So maybe.

When things are slow, I tend to go down rat holes such as these.

Rationalization

Seasonality of staphylococcal infections. http://www.sciencedirect.com/science/article/pii/S1198743X14610880

Infez Med. 2014 Mar;22(1):50-6. Extra-cerebral severe infections associated with haemorrhagic hereditary telangiectasia (Rendu-Osler-Weber Disease): five cases and a review of the literature.

https://www.ncbi.nlm.nih.gov/pubmed/24651092

Eur J Clin Microbiol Infect Dis. 2017 Jun 3. doi: 10.1007/s10096-017-3023-7. Prevalence of in patients operated for cerebral abscess: a retrospective cohort analysis.

https://www.ncbi.nlm.nih.gov/pubmed/28578477

POLL RESULTS

When work is slow

• I search odd questions on PubMed 8%
• I search odd questions on Google 42%
• I go home and watch golf 4%
• I invent work to keep busy 13%
• work is never slow 21%
• Other Answers 13%
• I search odd questions on TVTropes
• I'm retired. There is no such thing as work. I do what I want when I want.
• I start watching laboratory/hospital politics.

Doing Nuthin'

Jun 28, 2017

Man, is it slow. I'm not complaining, mind you. I am of an age where slow is better. But I like to work when I am at work. Going to the hospital when there is little clinical work (there is always no end of administrative work to catch up on) is mentally like putting the car in neutral and pushing down the gas pedal.

So some graphs. I like my numbers as graphs. A picture worth 999 words and all that.

This is the WBC of a patient in the ICU, otherwise stable recovering from encephalitis.

![A picture containing shoji

Description automatically generated](Aspose.Words.008a338b-8827-4faa-8ea2-26bdfe5d0381.003.png)

WBC's never bounce up this fast in a stable patient, and I told them, too late, to ignore it. It is a spurious lab value especially given equally odd changes in the platelets, MCV and Hgb. I suspect the CBC was from a different patient. But the ICU team makes rounds early, and this jump from 3.5 to 26 lead to a pan culture. Money wasted. The next days WBC returned to baseline.

![Chart, line chart

Description automatically generated](Aspose.Words.008a338b-8827-4faa-8ea2-26bdfe5d0381.004.png)

New interns are starting this week. A piece of advice for the newbies. With every lab, ask yourself does this value make sense for the patient. Laboratory values have an undeserved cachet.

The same patient also had an interesting fever curve:

![Chart, scatter chart

Description automatically generated](Aspose.Words.008a338b-8827-4faa-8ea2-26bdfe5d0381.005.png)

A slow rise to several days of a continuous fever. Again, the patient is stable and nonfocal.

When I see this pattern, a continuous fever, I think drug or central. The patient is not on any medications typically associated with a drug fever, so central?

Doesn't have the usual risks:

The combination of negative cultures; absence of infiltrate on chest radiographs; diagnosis of subarachnoid hemorrhage, intraventricular hemorrhage, or tumor; and onset of fever within 72 hours of admission predicted central fever with a probability of .90.

I can't find a case of presumptive central fever after VZV encephalitis, and there does not appear to be a VZV vasculitis or a stroke to cause a central fever. So I suggested, again, to do nothing as the patient was stable. As my wife will attest, I excel at doing nothing. And for whatever reason, the fevers subsided.

![Chart, scatter chart

Description automatically generated](Aspose.Words.008a338b-8827-4faa-8ea2-26bdfe5d0381.006.png)

So when I have nothing to do, I do nothing. It seems to work well.

Rationalization

JAMA Neurol. 2013 Dec;70(12):1499-504. doi: 10.1001/jamaneurol.2013.4354. Indicators of central fever in the neurologic intensive care unit.

https://www.ncbi.nlm.nih.gov/pubmed/24100963

J Neurol Neurosurg Psychiatry. 2007 Nov;78(11):1278-80. Non-infectious fever in the neurological intensive care unit: incidence, causes and predictors.

https://www.ncbi.nlm.nih.gov/pubmed/17940175

Look

Jul 3, 2017

For the last year, I have had an unhealthy obsession with cable news. I have noticed that pundits often start their bloviating with ‘Look’ or ‘Well, look.’ It is starting to bug me. They should say 'Listen."

Look. The patient is a young male with no medical problems who presents with severe chest pain, “like I was stabbed.”

One thing, as it often does, led to another, and eventually, a CT showed an infection in the sternal-manubrium joint, a biopsy of which grew MSSA.

Look, the history reveals nary a risk for anything. He is just this guy, you know, with a spontaneous septic pseudo-joint.

When was the last time you had to consider anything in the sternum outside of trauma? Never. The last time for me was as a second-year resident in the ER. Look, this very stoned patient took an ambulance into the ER in the middle of the night in the middle of a Minnesota snowstorm because he found a big lump in his chest. It was his xiphoid process.

Look, that’s why it is called dope. Marijuana does not make anyone smarter.

Look. Infections of the SM joint are rare as hens' teeth:

This case illustrates an unusually rapid development of septic arthritis involving a fibrocartilaginous joint in an otherwise healthy young man. Nine other cases have been described in the literature and are reviewed.

Look. Maybe less rare.

Contrary to the well-known phrase, 'As rare as hens' teeth,' the researchers say they have found a naturally occurring mutant chicken called Talpid that has a complete set of ivories.

The team, based at the Universities of Manchester and Wisconsin, have also managed to induce teeth growth in normal chickens -- activating genes that have lain dormant for 80 million years.

He has done quite well on a course of cefazolin.

Look. If it weren’t for random badness, I wouldn’t have a practice. As the Drunkard’s Walk points, randomness is under-appreciated by most people. It pays my mortgage.

Look. Look. Look. Look. Look.

I think I am ready to be a CNN pundit. My only fear is the potential for a faux-pummeling from a New York real estate magnate. It’s worth it.

Rationalization

Ann Thorac Surg. 2007 Mar;83(3):1190-4. Septic arthritis of the manubriosternal joint.

https://www.ncbi.nlm.nih.gov/pubmed/17307494

Hens' Teeth Not So Rare After All.

https://www.sciencedaily.com/releases/2006/02/060223083601.htm

The Drunkard's Walk: How Randomness Rules Our Lives.

https://www.amazon.com/Drunkards-Walk-Randomness-Rules-Lives/dp/0307275175

POLL RESULTS

Look

• Look? 8%
• Look! 21%
• Look :) 21%
• Look :( 13%
• Look $ 25%
• Other Answers 13%
• so.
• Saturday Evening Post.

That's A Curbside ?!?

Jul 10, 2017

I get asked for a lot of curbside advice. I have been at an actual curbside only two times that I can remember. Usually, I am sitting at the computer, so perhaps it should be modernized to PC consult. Most of the time, the questions are reasonable, and I know who is asking the questions, and I trust their abilities.

Interns on the first month on the wards? Maybe not so much.

I remember early in my practice being asked by a new intern, how long should you treat a bladder infection?

Three days for uncomplicated cystitis. But I started asking questions, and I discovered: Pseudomonas. Very resistant. In the urine and blood. Of a patient with a new kidney transplant. In the ICU.

So I learned early that depending on who is asking the question, there might be a lot more not being said.

Recently another curbside. The patient was being discharged in a couple of hours. Are two weeks enough for Listeria?

Say what? And I quickly found out.

Lymphoma. On steroids. Presented with diarrhea and weakness. It grew in the blood and a chronic pleural effusion. Not the stool, and a spinal tap hadn't been done.

I think the intern was using a Nutri-Matic machine, which had provided me question that was almost, but not quite, entirely unlike what a curbside should be.

I just laughed. You seriously think that is a curbside question?

It became a consult.

No good risks for her to acquire Listeria, no raw milk, or other dietary indiscretions. But the world, and all we eat, has a variably thick patina of stool, so who knows the source. It is why I only eat deep-fried food.

The diarrhea was probably the primary infection. Listeria is a known cause of colitis, although it is not on the PCR panel, and the lab doesn't have the wherewithal to isolate it. It requires cold enrichment and other techniques to grow.

The question is where to go with the pleural fluid. The patient has a chronic effusion from CHF, and it grew Listeria, but she has no symptoms, and the fluid parameters were not impressive by Light's criteria. Not like Pneumococcal empyema, yet Listeria tends to have a slower course with changes on the LP. Why not in the pleural fluid as well? The smattering of cases of Listeria empyema suggests a chest tube or VATS as the way to go. But now, 8 days in and doing well?

Where is the risk/benefit? A longer course of antibiotics? A chest tube on general principles? Sample the fluid to see if infected?

I don't know. I hate it when they call me late in the course of an infection.

Rationalization

J Vet Med B Infect Dis Vet Public Health. 2002 Dec;49(10):502-6. Optimization of a culture technique for the isolation of Listeria monocytogenes from faecal samples.

https://www.ncbi.nlm.nih.gov/pubmed/12485361

Ann Agric Environ Med. 2012;19(1):69-74. Validation of direct plating of a stool sample as a method for Listeria monocytogenes detection.

https://www.ncbi.nlm.nih.gov/pubmed/22462448

A Rare Case of Empyema Thoracis Caused by Listeria moncytogenes.

http://www.atsjournals.org/doi/abs/10.1164/ajrccm-conference.2017.195.1\_MeetingAbstracts.A4055

POLL RESULTS

I get my curbsides

• at the curb 0%
• in the cafeteria 27%
• at the computer 7%
• in the hall 33%
• I don't get cubsides 33%

Smug

Jul 12, 2017

Those whom the Gods wish to destroy first they make smug.

I am, quelle surprise, one smug SOB. The problem with being smug is that reality has a way of catching up with you. It is why I sometimes hate reality despite having to live in it.

The patient is admitted with DKA and S. aureus bacteremia and bacteriuria. I bet 90% of my service this month and a quarter of my consults are due to S. aureus in one manifestation or another. If I were a superhero S. aureus would be my arch nemesis, the Lex Luthor to my Superman. I was a DC guy growing up.

I know S. aureus like I know no other organism. And with overweening smugness, I forget that when it comes to S. aureus, and all infections, we are all Jon Snow.

I do my usual history and physical, and the predominant complaint is weakness such that there is difficulty standing and walking.

Exam shows that she cannot lift her legs up. Her thighs are not doing what they are asked. I ask multiple times: is it pain, or you just cant do it. No pain. Not in the back, the legs, or the abdomen. Weakness.

OK. This has to be an epidural abscess. The lack of the classic triad didn't bother me.

Back pain (present in about three quarters of patients), fever (documented in almost half of patients), and neurologic deficit (detected in about one third of patients) are the three most common symptoms. However, this classic clinical triad of back pain, fever, and neurologic deficit is present only in a minority of patients.

I have long thought, neither confirmed nor denied as best I can tell in the literature, that epidural abscess pain occurs more when the infection starts in the disc, but if the organisms bypass the disc and go straight to the epidural space, there will not be pain.

Plus, there was S. aureus in the urine; that always increases the worry about infection in and along the spine.

In septic conditions, especially without IDUC, SABU may indicate SAB with foci of infection in the urinary tract or the vertebral column.

So I ordered the MRI, putting as the indication the smug certainty of an epidural abscess.

Nope.

Huge abscess in the lower pole of the kidney extending into the iliopsoas. She couldn't lift her leg because the iliopsoas was a pocket of pus. Another cold abscess by S. aureus: no rubor, dolor, calor, just tumor.

The abscess was drained, and the patient did well.

But I hate stumbling into the diagnosis, getting the right test for the wrong reason. I would rather be smug after being right.

Rationalization

Spinal Epidural Abscess

http://www.nejm.org/doi/full/10.1056/NEJMra055111

J Infect. 2009 Jul;59(1):37-41. doi: 10.1016/j.jinf.2009.05.002. Epub 2009 May 23. The clinical significance of concurrent Staphylococcus aureus bacteriuria in patients with S. aureus bacteremia.

https://www.ncbi.nlm.nih.gov/pubmed/19539997

POLL RESULTS

I was always a smug fan of

• DC 8%
• Marvel 20%
• Mad 20%
• the Sunday comics 20%
• Archie 12%
• Other Answers 20%
• cheese
• Bloom County
• Garfield
• Danica Patrick
• The Lancet.

Would you like cheese with this whine?

Jul 17, 2017

I switched antibiotics when your back was turned! Ha ha, you fool! You fell victim to one of the classic blunders! The most famous of which is "never get involved in a land war in Asia," but only slightly less well-known is this: "Never go in against a cefazolin when DEATH is on the line!"

The Princess Bride. Kind of.

I have probably whined about this before, but if so, I do not remember. In the last decade, I have easily written 1.5 million words, and I have reached the stage of my life where it is a challenge to remember my children’s names, much less a blog entry from years ago.

ID is unique as a speciality as everyone seems happy to $%^&* with your orders. No one alters the oncologists chemo orders or screws around with the nephrologist's dialysis plan, but every Dunning-Kruger acolyte feels quite happy &^Y_& with my antibiotic orders.

The MSSA bacteremia, big renal/ileo-psoas abscess I discussed a couple of days ago? For a while, the antibiotic was changed to ceftriaxone as

sensitive to PCN, cephs, will transition to CFTX for easier dosing.

Actually sensitive to oxacillin/nafcillin, which are a PCN, but is not PCN.

Here is a rule: don’t opt for convenience over efficacy. It rhymes with rulelish. Never

We found that ceftriaxone had a higher rate of treatment failure than cefazolin for parenteral treatment of MSSA bacteremia

and

Empirical treatment with cloxacillin or cefazolin (n = 131) was associated with lower 30-day mortality as compared with cefuroxime (n = 98, p 0.058), ceftriaxone or cefotaxime (n = 194, p 0.008) and beta-lactam-beta-lactamase combinations (n = 61, p 0.013), with adjusted odds ratios (OR) for death ranging from 1.98 to 2.68.

I 'discussed' the issues of altering my plans with the involved physicians. Don't think they will do that again. Don’t mess with my antibiotics. I know what I am doing. You don’t.

Rationalization

Cefazolin Versus Ceftriaxone for the Treatment of Methicillin-Susceptible Staphylococcus aureus (MSSA) Bacteremia in a Tertiary-Care VA Medical Center

https://doi.org/10.1093/ofid/ofy089

Clin Microbiol Infect. 2011 Oct;17(10):1581-6. doi: 10.1111/j.1469-0691.2010.03425.x. Epub 2010 Dec 14. Are all beta-lactams similarly effective in the treatment of methicillin-sensitive Staphylococcus aureus bacteraemia?

https://pubmed.ncbi.nlm.nih.gov/21073629/

POLL RESULTS

When people mess, yeah mess, that's the word, with my orders I get

• pissed 30%
• irritated 13%
• annoyed 17%
• apoplectic 15%
• enraged 13%
• Other Answers 13%
• Dangerous, just like Hannibal Lecter ;)
• educated
• literary
• a conniption fit.
• smug
• all of the above.

Blame the Medications First

Jul 24, 2017

When patients ask why they have a particular infection, often the only answer I have is bad luck. And often they reply that it is so typical, that if there is going to be bad luck, it is going to happen to them. No one has ever said, that’s odd. I tend to be lucky. It is unusual for me to have bad luck.

Me? Good luck dominates. I have been lucky all my life. I work in the best hospital system with the best providers on the planet. Period. I can honestly say I have never had a bad day at work since I graduated medical school. That is not to say that awful things have not happened. Awful things always happen. That’s life. But awful events do not make for a bad day.

Work is also a constant reminder for my future, the inevitable decline and death. People like to share life lessons at the end, and I long ago learned that there is one sentence that has never been spoken by any human ever in the history of the world:

Doc, I wish I had spent more time at work.

But since I turned 60 this year, with the knowledge that I likely on the last quarter mile lap of the mile race of life, I have had a real shift in attitude. I am letting go of most of the responsibilities that have defined the last 34 years of medicine: meetings, lectures, etc. Time for my younger partners to take over. And it is wonderful.

Last week I spent a long weekend in Northeast Oregon. A nice hotel in La Grande above a wine bar. Hiked Mt Howard, Anthony Lakes, boated down Hells Canyon (saw bear, bighorn sheep, deer), wandered Baker City and Joseph, went to the Oregon Trail Museum, watched the sunset over the hills at the wine bar, then finishing up every night at a pub with great beer. An amazing area of the state.

And today? For the first time, I kind of resented having to go to work. Sitting in traffic, I thought, screw this. Why am I working? Oh yeah. Health care,. Fortunately, once I got to work and started seeing patients, the fun that is ID kicked in. Not quite as fun as the 5 days with my wife, but still. I still get the same frisson of joy with the puzzles, big and small, that come my way.

The patient is admitted with the fevers and ascites and gets a course of antibiotics for presumptive SBP. A week in, he gets new fevers, leukocytosis, and loose stools.

The C. difficile assay read

Positive for Clostridium difficile antigen (GDH) but negative for the toxins by enzyme immunoassay This is an inconclusive result for determination of active Clostridium difficile infection.

So a PCR was sent, was positive, and he was started on metronidazole. And improved. So C. difficile, right?

But he had also been on rifaximin for a week, which is an effective treatment for C. difficile. And what to make of the indeterminate test?

Looking at the medication list, I noted he has been on cholestyramine for the last week, which is very potent at binding C. difficile toxin. Is this a false negative toxin assay because of the cholestyramine?

Maybe. It is hypothesized in one review and given that

Cholestyramine and colestipol were tested for binding of Clostridium difficile cytotoxin with use of batch absorption and column chromatography. The toxin was bound by both resins and could not be eluted from cholestyramine with either an ionic of a pH gradient… Cholestyramine and vancomycin were also tested for therapeutic efficacy in the hamster model of clindamycin-induced cecitis. Both compounds delayed death and reduced levels of cytotoxin in stool

a reasonable explanation, but it has never proven as clinically relevant.

And he was also getting the rifaxamin and cholestyramine at the same time.

So. Partially treated C. difficile due to rifaximin inactivation by cholestyramine (nothing on PubMed) and a false negative assay due to the same medication? We have a cardiologist who, when he ran noon report, always started every differential diagnosis with medications. It should be infection, but medications should always be number two.

That’s my story, and I am sticking to it.

Now I am heading back to La Grande. I wish.

Rationalization

Rifaximin Is Effective for the Treatment of Clostridium difficile—Associated Diarrhea: Results of an Open-Label Pilot Study.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3216319/

New advances in the treatment of Clostridium difficile infection (CDI).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2621401/

Evaluation of a new enzyme immunoassay for Clostridium difficile toxin A.

http://jcp.bmj.com/content/jclinpath/50/12/996.full.pdf

J Infect Dis. 1980 Jan;141(1):92-7. Binding of Clostridium difficile cytotoxin and vancomycin by anion-exchange resins.

https://www.ncbi.nlm.nih.gov/pubmed/7365273

A Gamble That Paid Off

Jul 26, 2017

The patient had a liver abscess for no good reason beyond a prior cholecystectomy. A drain was placed, and it grew Pseudomonas aeruginosa and E. coli.

The former organism is not high on my list of liver abscess etiologies, but we see this, both following procedures and community-acquired from underlying biliary issues.

Both organisms were pansensitive, so she was sent home on oral ciprofloxacin and metronidazole and did well for the next 2-ish weeks. Then she developed severe arthralgias, presumptively from the ciprofloxacin.

Quinolones are great drugs for killing organisms, but their toxicities are impressive: tendon rupture, arthralgias, AAA rupture, retinal detachment, altered mental status, renal failure, qt prolongation, C. difficile, and MRSA. I avoid them if I can, but often they are the only oral option.

Repeat imaging showed there was still a 1 cm abscess where radiology could not safely place a drain.

Well, I said, we have two options. We can admit you to the hospital, get a PICC in, and, since you have Medicare, you will have to go to a nursing home for a month to get your antibiotics.

Or we can gamble.

There is an old drug that your organisms are probably sensitive to, although I can’t prove it as the culture was discarded. There are minimal studies using it outside the prostate, but it looks like it works when combined with other antibiotics. Maybe we have taken care of the infection with the current antibiotics and what remains in the abscess on CT is dead. So I am not sure it will work or if you even need more antibiotics, but we can take a shot.

The patient did not want to go to a nursing home and took the gamble. I substituted fosfomycin for the ciprofloxacin.

It has a broad spectrum of activity against a wide range of Gram-positive and Gram-negative bacteria. It is highly active against Gram-positive pathogens such as Staphylococcus aureus and Enterococcus, and against Gram-negative bacteria such as Pseudomonas aeruginosa and Klebsiella pneumoniae… Intravenous fosfomycin has been administered in combination with other antibiotics for the treatment of nosocomial infections due to multidrug-resistant (MDR) Gram-positive and Gram-negative bacteria. Fosfomycin has good distribution into tissues, achieving clinically relevant concentrations in serum, kidneys, bladder wall, prostate, lungs, inflamed tissues, bone, cerebrospinal fluid, abscess fluid, and heart valves.

And a month later? AlthoughI can’t say for sure it wasn’t the natural history of a sterile collection, the abscess was all gone. Better than a month in the nursing home and less cost.

Rationalization

Scand J Infect Dis. 2011 Dec;43(11-12):877-82. doi: 10.3109/00365548.2011.599332. Epub 2011 Aug 26. Pyogenic liver abscess caused by Pseudomonas aeruginosa: clinical analysis of 20 cases.

https://www.ncbi.nlm.nih.gov/pubmed/21867474

Infect Dis Ther. 2017 Jun;6(2):233-243. doi: 10.1007/s40121-017-0150-5. Epub 2017 Mar 11. Fosfomycin and Comparator Activity Against Select Enterobacteriaceae, Pseudomonas, and Enterococcus Urinary Tract Infection Isolates from the United States in 2012.

https://www.ncbi.nlm.nih.gov/pubmed/28285420

Int J Infect Dis. 2011 Nov;15(11):e732-9. doi: 10.1016/j.ijid.2011.07.007. Epub 2011 Sep 25. The revival of fosfomycin.

https://www.ncbi.nlm.nih.gov/pubmed/21945848

Does Two a Hodgepodge Make?

Jul 31, 2017

No great insights today, but a hodgepodge of curiosities. But it is the curiosities that give me that frisson of joy. Or anger.

I have a patient with cryptococcal meningitis, so I sent the prescription into the pharmacy for the 5 flucytosine. I warned her of sticker shock, but the insurance should cover it. Two weeks cost $3900. In India, flucytosine is 2 dollars a tab.

The same day I saw a case of Old World Leishmaniasis. He had done a little research about miltefosine and found the current cost for a course of the drug is $59,000. Miltefosine is a lot cheaper in India.

To save some money, the insurance companies should buy the patient a round trip ticket to the UK or India and get the medications there. Or better yet, send me to pick it up. Even first-class tickets and a three-star hotel would cost less than the drug.

Oh well, I can dream. On to some clinical medicine.

It is always weird how I go for years, never having heard of a disease, then I see two cases in a month.

The patient has a knee replacement that is complicated post-operative blisters around the wound, leading to a Group C streptococcal knee infection.

The next patient, two weeks later at a hospital 35 miles away (I cover a lot of turf on my job), has ankle surgery complicated by large blisters that led to an Enterobacter infection.

Both had fracture blisters, the first diagnosed by a dermatologist who should know what she is doing. I have never heard of fracture blisters. You? Probably.

Fracture blisters are a relatively uncommon complication of fractures in locations of the body, such as the ankle, wrist elbow and foot, where skin adheres tightly to bone with little subcutaneous fat cushioning. The blister that results resembles that of a second degree burn.

As best I can tell, the literature focuses on fracture blisters resulting from trauma, not a complication of surgery. Not that surgery isn’t trauma. In a few cases, the blisters delayed surgery and led to wound infections.

As I think back on it, I think I have seen a smattering of other post-op fracture blisters cases that led to infection, but I have shrugged my shoulder, assuming the blisters were a reaction to the surgical scrub. Maybe not.

So it would appear this blog entry has the entire world's medical literature (and my blog is literature: a body of artistic writings of a country or period characterized by beauty of expression and form and by the universality of intellectual and emotional appeal. Yep. That’s me.) of fracture blisters as a risk for postoperative orthopedic infections.

You read it here first.

Rationalization

Costs of medicines in current use for the treatment of leishmaniasis

http://www.who.int/leishmaniasis/research/978\_92\_4\_12\_949\_6\_Annex6.pdf

West J Emerg Med. 2011 Feb; 12(1): 131–133. PMCID: PMC3088393 Fracture Blisters.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3088393/

More Myths

Aug 2, 2017

They, whoever they are, have long asserted that half of all that is learned in medical school will be found later not to be true. Sure. We learn, things change, medicine advances. Except in the world of alternative medicine, of course, which is as resistant to change as it is data.

One of the interesting variations on the theme is medical myths, ideas that everyone thinks are true but either are disproven or have almost no data to support them. Like alternative medicine, only based on reality.

I thought I knew all the important myths: normal temperature is 98.6, atelectasis causes fevers, gotta double cover Pseudomonas, anaerobes are important in acute aspiration, to name a few. I added one this week.

I had a relative with acute diverticulitis who was bemoaning having to forego her nightly glass of wine for fear of a disulfiram reaction with the metronidazole.

I learned that as a medical student: metronidazole plus alcohol could lead to a degree of vomiting that, if pointed in the right direction, might allow one to levitate.

Like many factoids learned early in my career, I never went back to look at the original literature. So out of curiosity, I went looking to see what the risk really was, mostly since I wanted to have a cocktail with my wife, and oh, and I oversharing?

And that literature is a sorry sack of garbage.

The warning against simultaneous use of alcohol and metronidazole appear to be based on laboratory experiments and individual case histories in which the reported reactions are equally likely to have been caused by ethanol alone or by adverse effects of metronidazole. Recent research does not confirm a clinically relevant interaction between ethanol and metronidazole.

The warning is evidently based on animal studies and on a whopping 10 human case reports. On review of these case reports found

…no convincing evidence that this reaction exists. Six case reports involving eight patients were evaluated. CONCLUSIONS: Four of the eight cases were serious, including one death, but the authors of all the reports presumed the metronidazole-ethanol reaction to be an established pharmacologic fact. None provided evidence that could justify their conclusions.

And one challenge trial found

Metronidazole did not raise blood acetaldehyde or have any objective or subjective adverse effects when used together with ethanol.

“Beer is proof God loves us and wants us to be happy.” Ben Franklin. That’s a myth as well. Franklin never wrote it. He actually said it about wine.

We hear of the conversion of water into wine at the marriage in Cana, as of a miracle. But this conversion is, through the goodness of God, made every day before our eyes. Behold the rain which descends from heaven upon our vineyards, and which incorporates itself with the grapes to be changed into WINE; a constant proof that God loves us, and loves to see us happy!

But the concept is true. For 50 years, we have denied patients a dram happiness while on metronidazole based on virtually nothing.

It is time to stop. Quit telling patients alternative facts unless, of course, you get them from a phone call from the leader of the Boy Scouts.

Did I convince my wife? Of course not. Duh.

Je vous renvoie à ce que disoit madame Cornuel, qu’il n’y avoit point de héros pour les valets de chambre, et point de pères de l’Église parmi ses contemporains.

But I mentioned this to a colleague who was eventually on metronidazole and had a drink with no ill consequences.

That’s my N of 1, and I am sticking to it.

Cheers.

Rationalization

In honor of Betteridge's law of headlines: "Any headline that ends in a question mark can be answered by the word no

Tidsskr Nor Laegeforen. 2014 Sep 16;134(17):1661-3. doi: 10.4045/tidsskr.14.0081. eCollection 2014 Sep 16. [Is combining metronidazole and alcohol really hazardous?].

https://www.ncbi.nlm.nih.gov/pubmed/25223673.

Ann Pharmacother. 2000 Feb;34(2):255-7. Do ethanol and metronidazole interact to produce a disulfiram-like reaction?

https://www.ncbi.nlm.nih.gov/pubmed/10676835

Ann Pharmacother. 2002 Jun;36(6):971-4. Lack of disulfiram-like reaction with metronidazole and ethanol. https://www.ncbi.nlm.nih.gov/pubmed/12022894

Translation: “I refer to what Madame Cornuel said, that there were no heroes to valets, nor to the Fathers of the Church among their contemporaries.”

Progressive Primary?

Aug 7, 2017

“TB or not TB, that is the congestion. Consumption be done about it? Of cough, of cough. But it takes a lung, lung time.” Woody Allen

The patient presents to the ER with a month of consumption: fevers, malaise, weight loss, mild shortness of breath, and a nonproductive cough.

She has been on infliximab for a decade with good control of her primary disease.

CXR leads to a CT that shows this:

![A picture containing text

Description automatically generated](Aspose.Words.008a338b-8827-4faa-8ea2-26bdfe5d0381.007.png)

Which is named after these:

![A pile of coffee beans

Description automatically generated with low confidence](Aspose.Words.008a338b-8827-4faa-8ea2-26bdfe5d0381.008.png)

Most of the time, I am not a fan of food related disease descriptors, but the CT lesions do have the size and shape of a millet seed. That is as good an x-ray of miliary TB as I have ever seen.

I hate miliary TB, dating back to my first consult in practice, the diagnosis of which was made post mortem. The evaluation of miliary TB is simple. Get as many cultures cooking that you can (lung, bone marrow, blood) and then start PIER, no wait, RIPE, asap, which we did. The bronch was 3+ AFB, an impressive mycobacterial load for miliary disease, which has a negative sputum like as not.

She had tested negative for latent Tb before the biologic was started, which is the odd part. It is well known that people on TNF alpha inhibitors will reactivate TB, often miliary, but most do it after the first three doses.

There were 70 reported cases of tuberculosis after treatment with infliximab for a median of 12 weeks. In 48 patients, tuberculosis developed after three or fewer infusions.

and

The median interval from the start of treatment with infliximab until the development of tuberculosis was 12 weeks (range, 1 to 52).

A decade later is most unusual, and I wonder if this is progressive primary TB, although she has nothing that even vaguely resembles a TB exposure.

This is the second such case of miliary TB a decade into infliximab where I suspect, mostly based on time lag and a prior negative evaluation for latent TB, of progressive primary Tb. I can find no cases quite like them on the PubMeds.

I was talking the case over with the house staff, and one asked if it makes any difference.

Well, no. But it is fun to think about.

She has been getting slowly better on IEPR.

Rationalization

Tuberculosis Associated with Infliximab, a Tumor Necrosis Factor α–Neutralizing Agent.

http://www.nejm.org/doi/full/10.1056/NEJMoa011110#t=article

Progressive Primary Tuberculosis in the Adult and Its Differentiation from Lymphomas and Mycotic Infections David T. Smith† N Engl J Med 1949; 241:198-202August 4, 1949

http://www.nejm.org/doi/full/10.1056/NEJM194908042410503

Infliximab Therapy Leading to Pulmonary Tuberculosis in a Patient With Negative Interferon γ Release Assay (IGRA)-Based QuantiFERON Gold Test

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5507378/

Z Gastroenterol. 2013 Oct;51(10):1177-83. doi: 10.1055/s-0033-1350372. Epub 2013 Oct 11. Development of miliary tuberculosis under infliximab in a patient with spondyloarthritis and suspected Crohn's disease.

https://www.ncbi.nlm.nih.gov/pubmed/24122379

Mysteries

Aug 14, 2017

The patient was a mystery, and I always learn a few things investigating a mystery, even if I have no final answer. The patient is a young male admitted with MOSF and sepsis. No past medical history, no risks for anything unusual. The two characteristics of note were a diffuse erythroderma that eventually peeled and low calcium. So toxic shock syndrome, right?

Except nary a S. aureus nor a Streptococcus of any kind to be found. We even went so far as to look for Yersinia pseudotuberculosis as the beast can cause TSS, although most of the cases have been in the far East, not the great Pacific NW.

Far East scarlet-like fever (FESLF) is a severe inflammatory disease that occurs sporadically and in outbreaks in Russia and Japan. Far East scarlet-like fever is caused by Yersinia pseudotubuclosis infection, an organism that typically causes self-limiting gastroenteritis in Europe. Studies suggest the ability of Far Eastern strains to produce superantigen toxin Y pseudotuberculosis-derived mitogen A is integral to FESLF pathogenesis

We did treat with IVIG pending workup, with little effect. And there were two other outliers: he had meningitis by LP, not a feature of TSS, and hyperlipidemia on admission with triglycerides of 1500, also not part of TSS.

It was noted by those smarter than me (yes, they exist but are few and far between) that this is the presentation of Hemophagocytic Lymphohistiocytosis syndrome, a disease I had never seen before.

In 19 patients (68%), hypertriglyceridemia was noted on diagnosis or during the disease period (mean: 242 mg/dL). Furthermore, the triglyceride (TG) level decreased with the treatment-related amelioration of HLH (mean level before and after treatment: 297 and 136 mg/dL, respectively, p=0.0001).

The ferritin was also off the wall, part of Hemophagocytic lymphohistiocytosis syndrome, but no sign in the bone marrow or periphery of hemophagocytosis.

I wondered about Kawasaki's despite the advanced age. No way to prove or disprove the diagnosis, and it is the wrong season. Curiously, Kawasaki's is associated with the weather:

...a common seasonal increase in KD cases is associated with a large scale shift in the Asia-North Pacific wind pattern. This involves the wintertime development of a “duct” that sweeps from Asia to the western North Pacific and an associated trans-Pacific transport across the North Pacific from Japan to Hawaii and southern California.

As part of the workup, he had an Interleukin 2 Receptor (CD25), Soluble, which returned 4 times normal at 4790. I never heard of that test. Evidently

Twenty-two articles describe sIL-2r as a sensitive diagnostic marker for HLH

but it also goes up with Kawasaki's.

serum soluble IL-2 receptor can be a potent marker of disease activity and therapeutic effects in patients with Kawasaki disease

And it is elevated in a variety of other diseases as well, so it has the specificity of a sed rate. There were a tonne of other diseases were considered, from Stills to Leptospirosis, but nothing ever came to fruition. Every idea had at least one aspect that didn't fit.

No diagnosis was ever made, but I suspect Kawasaki's, and we will see if coronary artery aneurysms develop in the weeks to come.

Rationalization

Open Forum Infect Dis. 2015 Dec 17;3(1):ofv202. doi: 10.1093/ofid/ofv202. eCollection 2016 Jan. Far East Scarlet-Like Fever: A Review of the Epidemiology, Symptomatology, and Role of Superantigenic Toxin: Yersinia pseudotuberculosis-Derived Mitogen A.

https://www.ncbi.nlm.nih.gov/pubmed/26819960

Intern Med. 2009;48(10):775-81. Epub 2009 May 15. Analysis of triglyceride value in the diagnosis and treatment response of secondary hemophagocytic syndrome.

https://www.ncbi.nlm.nih.gov/pubmed/19443971

Sci Rep. 2011;1:152. doi: 10.1038/srep00152. Epub 2011 Nov 10. Association of Kawasaki disease with tropospheric wind patterns.

https://www.ncbi.nlm.nih.gov/pubmed/22355668

Ann Hematol. 2017 Aug;96(8):1241-1251. doi: 10.1007/s00277-017-2993-y. Epub 2017 May 12. Clinical utility of soluble interleukin-2 receptor in hemophagocytic syndromes: a systematic scoping review.

https://www.ncbi.nlm.nih.gov/pubmed/28497365

Ann Clin Biochem. 2017 Mar;54(2):209-213. doi: 10.1177/0004563216677583. Epub 2017 Jan 12. The serum concentration of soluble interleukin-2 receptor in patients with Kawasaki disease.

https://www.ncbi.nlm.nih.gov/pubmed/28081636

Roman Names

Aug 28, 2017

While I do have the best job in the world, vacation is better. A week in Bend. Hiking, biking, golfing, eating, drinking, complete with seeing totality.

And today? In all my years, I have never had a patient tell me at the end, doc, I wish I had spent more time at work. Why am I doing this? Oh yeah. Two kids in higher education.

But it really is a great job, one of the few where you get to cure people once and forever.

The patient has a long history of back pain, not incapacitating, but interfering with life. He has tried the usual interventions with only small success. What gives him the most relief is steroid injections, of which he has had four.

The fourth, though, is different. A month after initial improvement, the pain returned, and then over the next 6 months progressed and became incapacitating. He was referred to a neurosurgeon who got an MRI that showed changes classic for infection.

I wanted to blame the injection, except the changes were one level removed from any injection site. Odd. But I see the occasional spontaneous discitis from S. aureus or oral Streptococci. My whole practice is based on bad things happening for no damn good reason.

So there was a biopsy, and it grew?

Candida.

lusitaniae.

Huh?

So I went back looking for a reason. None. No IVDA, no procedures, no acupuncture, no nothing. The steroids were not from a compounding pharmacy.

So no good reason. Although the one case in the PubMeds was after a discogram. Does that procedure have a mirror ball?

The claim to fame for this beast is that it can be amphotericin resistant, which it wasn't. This one was pan-sensitive. Debridement and a long course of fluconazole led to marked improvement of the pain.

But where did the name come from? Torpedoed luxury liners? Kind of. The closest I can get is:

Dietrichson called this species Candida parapsilosis var. obtusa in 1954. In 1959 van Uen and do Carmo-Sousa named it C. lusitaniae. It was first isolated from the alimentary canals of warm-blooded animals in Portugal.

and

... Lusitania, an ancient Roman province on the west of Iberian Peninsula, the region that is now southern Portugal and Extremadura (Spain).

The real truth remains behind a 50-year-old paywall. So, like S. lugdunensis, Rome lives on in our pathogen's names.

Now we need a Candida asterix.

Rationalization

Origin of the Names of Species of Candida

http://www.antimicrobe.org/h04c.files/history/candida-history.asp

Spine J. 2011 Oct;11(10):e1-6. doi: 10.1016/j.spinee.2011.09.004. Candida lusitaniae discitis after discogram in an immunocompetent patient.

https://www.ncbi.nlm.nih.gov/pubmed/22005083

NSAIDS: Anti-inflammatory is a bad thing

Aug 30, 2017

The patient is a young male, no medical problems, who has a day and a half of progressive fevers, rigors, diffuse myalgias, and left thigh pain.

He had been backpacking in the great Pacific NW, in the remaining wilderness that is not on fire. Man, has it been smokey in the valley this year as the West goes up in flames. It is more like Victorian London that hipster Portland.

While hiking, he had a few bug bites but no other trauma of any kind. Except for the hiking, I suppose. I did enough backpacking in my youth to know the pain in the legs from a long trek with a heavy pack.

As he got sicker, he treated the symptoms with NSAIDs, but the leg pain became unbearable, and he was admitted with sepsis/myositis when the CT in the ER showed fluid in the thigh.

A trip to the OR showed pus in the thigh, but no necrosis and they called me for antibiotics.

Exam and labs had nothing unique for infection except he had red cheeks that spared the skin around the eyes and lips, a scarlet fever-like distribution.

I said this was going to be Group A Streptococcus and treated accordingly: beta-lactam and clindamycin. The next day the blood and wound grew Group A Streptococcus. It sure is nice to be right.

Two things about this case made me call a Group A Streptococcus. First was the red cheeks that spared the lips. The rash did not spread to palms and soles, and the hyperemia of his conjunctiva was minimal at best. So not the best Scarlet fever presentation, more of a forme fruste version. But close enough.

But I wondered. Why spare the lips? Why circumoral pallor with Scarlet fever. Or, as it was almost called, Pansy fever?

No clue. Like what is the pathology behind the strawberry tongue, the medical literature is silent. If anyone has an explanation, feel free to let me know.

The other was the NSAID use. Inflammation is usually beneficial, and you should anti-inflame with caution. I am pretty much convinced that NSAIDs make Group A Streptococcal infections worser. Yes. Worser.

In total, these findings support the notion that in GAS soft tissue infections, nonselective NSAIDs shift the host/pathogen interaction in favor of the pathogen, and suggest that once infection is established, even a brief exposure to such NSAIDs limits antibiotic efficacy and contributes to worse outcome.

and

Use of nonselective NSAIDs, either alone or as adjuncts to antibiotic therapy, for GAS soft tissue infection may contribute to worse outcomes.

and

The results supported the concept that ibuprofen use in GAS soft tissue infections might induce the development of severe necrotizing infections and increase mortality rate.

I am a believer, and I have the confirmation bias to support it. It seems every severe S. pyogenes infection I remember was on NSAIDs prior to admission.

The patient did fine.

Rationalization

Curr Opin Infect Dis. 2015 Jun;28(3):231-9. doi: 10.1097/QCO.0000000000000160. The roles of injury and nonsteroidal anti-inflammatory drugs in the development and outcomes of severe group A streptococcal soft tissue infections.

https://www.ncbi.nlm.nih.gov/pubmed/25918957

J Infect Dis. 2014 May 1;209(9):1429-35. doi: 10.1093/infdis/jit594. Epub 2013 Nov 11. Effects of selective and nonselective nonsteroidal anti-inflammatory drugs on antibiotic efficacy of experimental group A streptococcal myonecrosis.

https://www.ncbi.nlm.nih.gov/pubmed/24218498

J Microbiol Immunol Infect. 2011 Dec;44(6):418-23. doi: 10.1016/j.jmii.2011.04.012. Epub 2011 Jun 22. Ibuprofen worsens Streptococcus pyogenes soft tissue infections in mice.

https://www.ncbi.nlm.nih.gov/pubmed/21697021