Puswhisperer 11

Urosepsis

Sep 5, 2018

The patient is elderly and was found to have trouble walking at the store and appeared confused.

He was taken to the ER, where an evaluation started.

One thing, as one thing is wont to do, led to another, and he was admitted, and both sets of blood cultures and urine grew Staphylococcus.

epidermidis.

Urosepsis from coagulase-negative staphylococcus? Sure. Why not? I have seen a case or three over the years.

The patient has had some burning and frequency for the prior month, so he has been symptomatic.

Looking for other cases, I find only one, and it is not on Pubmed. As I have mentioned over the years, we really need a case report database in ID to collect all the odd cases we see in ID.

He has no endovascular hardware and no recent soft tissue infections, but he does have many senile keratoses he picks at (as would I), which could be a source for seeding the urinary system.

I suggested evaluating the collecting system, as there is no way someone will get bacteremic with coagulase-negative staphylococcus without obstruction, and he had hydronephrosis from a small stone.

It was removed, and he did fine with a course of cephalexin.

Note: For regular readers, there will be a break in the blog for a couple of weeks while I hike the National Parks of the West, knees permitting. See you at the end of September. Or lose you to a summer love.

Rationalization

A WOLF IN SHEEP’S CLOTHING: A CASE OF SEPSIS CAUSED BY COAGULASE-NEGATIVE STAPHYLOCOCCI. https://www.shmabstracts.com/abstract/a-wolf-in-sheeps-clothing-a-case-of-sepsis-caused-by-coagulase-negative-staphylococci/

Back. And Annoyed.

Sep 25, 2018

…it is a tale. Told by the CID, full of sound and fury, Signifying nothing.

Macbeth

I took two weeks off to hike in the Great Pacific NW with my wife. Mt. Rainier, North Cascades, Glacier, Yellowstone, Grand Tetons, and Craters of the Moon. Stupendous.

As much as I love work, vacation is better. As I like to tell residents, no one on their death bed has ever said, “Doc, I wish I had spent more time at work.”

The first day back is always a bit chaotic, getting caught up with all the little things that accumulated while gone. It takes time to get back into the rhythm of clinical medicine. But the song remains the same, at least for stewardship.

Uncomplicated cellulitis. Simple right?

The guidelines are not rocket science. Or brain surgery. Treat strep and MSSA. Cefazolin is a good choice for the likely microbiology.

Typical cases of cellulitis without systemic signs of infection should receive an antimicrobial agent that is active against streptococci. For cellulitis with systemic signs of infection, systemic antibiotics are indicated.

For 5-7 days.

Then why, oh why, does do they keep giving vancomycin and zosin? For days on end?

It has been noted that

…we and others have described frequent treatment with antibiotics that have activity against aerobic gram-negative bacilli or anaerobic species. In addition, industry-sponsored clinical trials of new antimicrobial agents involving cellulitis and abscess have utilized treatment regimens with a spectrum of activity beyond typical gram-positive organisms.

Read that second sentence again.

In addition, industry-sponsored clinical trials of new antimicrobial agents involving cellulitis and abscess have utilized treatment regimens with a spectrum of activity beyond typical gram-positive organisms.

And who publishes those studies that exacerbate the inappropriate use of antibiotics? Ironically it is Clinical Infectious Diseases in a so-called “major article”: A Comparison of the Efficacy and Safety of Intravenous Followed by Oral Delafloxacin With Vancomycin Plus Aztreonam for the Treatment of Acute Bacterial Skin and Skin Structure Infections: A Phase 3, Multinational, Double-Blind, Randomized Study.

Major. You keep using that word. I do not think it means what you think it means.

Vancomycin and Aztreonam for cellulitis? Who does that? Who compares two expensive, inferior, toxic

Treatment-emergent adverse events leading to study drug discontinuation was higher in the vancomycin + aztreonam group

drugs to a new expensive (about 1500 for 20 tabs) quinolone?

I know new antibiotics need to be tested but don’t compare it to antibiotics I would call stupi… er, I mean, inappropriate for most cellulitis.

They included cellulitis/erysipelas, wound infection, major cutaneous abscess, and burn infections as if these were all the same kind of infection. Nope.

And I had to laugh when I read

Based on currently available data, delafloxacin does not appear to be associated with an increased risk of AEs associated with other fluoroquinolones.

Riiiigggggtttttttt. When I was a fellow, I remember being told by the rep that amikacin would not only be less toxic, but it would not breed resistance. Yeah, that worked out well.

Future observation as the drug is more widely used in the clinic will be prudent.

That’s a great idea. Let’s use it wisely instead of amoxicillin and/or cephalexin and see if we can rupture a few tendons or induce torsades.

Actions have consequences. I can just see the delafloxacin reps passing out the paper and increasing the use of unneeded combination therapy for cellulitis or prescribing an unneeded and expensive quinolone.

In my opinion, this study is counter-productive to what the IDSA, and ID docs in general, are trying to do with antibiotic stewardship.

Thank you, CID.

Sad.

Rationalization

Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections: 2014 Update by the Infectious Diseases Society of America https://academic.oup.com/cid/article/59/2/e10/2895845

Decreased Antibiotic Utilization After Implementation of a Guideline for Inpatient Cellulitis and Cutaneous Abscess https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/227576

Add Another to my Bucket List

Sep 27, 2018

The patient has progressive hip/pelvic pain. She has severe osteoporosis and has suffered many pathologic fractures over the years.

This pain was different, persistent, and she eventually gets a CT that shows sacroiliac joint destruction and a mass of some sort in the adjacent muscle.

Biopsy: negative gram stain, culture-negative, but pus.

So it is biopsied again and this time sent for “everything.” Everything doesn’t grow, but Mycobacterium abscessus does.

Mycobacterium abscessus is a bad bug, so whatcha going to do? Hard to kill and aggressive. When the first hit is Mycobacterium abscessus: a new antibiotic nightmare, you know you are in trouble. As if I don’t have enough antibiotic nightmares.

There has been a lot of press of late of the organism in CF, but what about extrapulmonary disease. It is, as is often the case, a group: M. abscessus sensu stricto, Mycobacterium massiliense, and Mycobacterium bolletii. Final identification is still pending, but it is sensitive to tigecycline, amikacin, imipenem, and clofazimine. What a group of antibiotics to choose from.

So I had another first; I actually ordered tigecycline. Never had the need before to give that antibiotic.

I am lucky that I have atypical mycobacterial experts at the local University helping me out. At 427 in dog years, I am far too old to try and become an expert in M. abscessus since, at the current rate, I will be long in my grave before I see the next one. I will let them guide me.

The more curious question is, why does she have this infection?

M. abscessus is found in water, but she has no odd water exposures, living in urban Portland with no travel in 25 years.

There are a few cases after gastric banding, and she did have a gastrectomy for gastric ulcers 20 years ago. That’s it. Seems a stretch as a risk.

As best I can tell, no good reasons for this pelvic infection.

So now it is debridement and a long course of multiple iv and po antibiotics.

Rationalization

J Antimicrob Chemother. 2012 Apr;67(4):810-8. doi: 10.1093/jac/dkr578. Epub 2012 Jan 30. Mycobacterium abscessus: a new antibiotic nightmare. https://www.ncbi.nlm.nih.gov/pubmed/22290346

Emerg Infect Dis. 2015 Sep; 21(9): 1638–1646. doi: 10.3201/2109.141634 Mycobacterium abscessus Complex Infections in Humans https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4550155/

Mycobacterium abscessus Complex Infections: A Retrospective Cohort Study. https://academic.oup.com/ofid/article/5/2/ofy022/4848653

Emerg Infect Dis. 2014 Oct;20(10):1612-9. doi: 10.3201/eid2010.140077. Rapidly growing mycobacteria associated with laparoscopic gastric banding, Australia, 2005-2011. https://www.ncbi.nlm.nih.gov/pubmed/25279450

And the Fever Persisted

Oct 2, 2018

The patient is an IVDA, heroin, who comes in with fevers due to MRSA bacteremia and a lung abscess.

She was started on Vancomycin.

And the fever persisted.

Repeat blood cultures were negative, as was the ECHO.

Review of systems and exam was negative.

So I suggested patience. It takes time for MRSA to respond to vancomycin.

And the fever persisted.

Review of systems and exam was negative.

So we changed to ceftaroline. I think vancomycin stinks on ice for the treatment of MRSA and look for any reason to change. And it could be drug fever.

And the fever persisted.

Review of systems and exam was negative.

So we did the pan CT.

Empyema and an abscesses, never mentioned by the patient, in the arm and the back.

They were drained.

And the fever persisted.

Review of systems and exam was negative.

So after 11 days, the CT was repeated.

New empyema and a large abscess in the buttock, not present before.

They were drained.

And the fever resolved.

Here is what annoys me no end about gram-positive bacteremia and persistent fevers. Patients often have a metastatic infection, but

…signs and symptoms guiding the attending physician in the diagnostic workup were present in only a minority of cases (41%).

Or 59% of the time, you have no clue from the H&P why the fever persists.

My whole raison d’être is the careful and complete H&P. And for persisting fever with gram-positive bacteremia, more often than not, it does not matter. You just have to go looking with a CT (or PET/CT if you practice in the Netherlands) and ECHO,

as only a minority of foci were accompanied by guiding signs or symptoms, the number of foci revealed by symptom-guided CT, ultrasound, and magnetic resonance imaging remained low.

Such an unsatisfactory approach to ID.

Tomorrow I head for ID Weak in San Francisco. I dread it. I get no credit for the 500 plus hours a year of CME I do for blogging, podcasting, and updating my app. The AMA and ACP, when asked, say nope. I need ‘official’ CME, which means sitting in a cold room listening to people read me Powerpoint slides about topics I either don’t care about or already know. Yeah. Such a waste of time.

How to stay engaged. I am thinking of live blogging on Tumblr (https://pusware.tumblr.com/) and Twitter (@idfactoid). I don’t know if I can do it. ID Weak is just so boring I may not be able to pull it off and, instead, work on being a Supreme Court nominee. Lots of bars in the bay area, and I do like beer. Just not THAT much.

Rationalization

Medicine (Baltimore). 2012 Mar;91(2):86-94. doi: 10.1097/MD.0b013e31824d7ed2. Metastatic infectious disease and clinical outcome in Staphylococcus aureus and Streptococcus species bacteremia. https://www.ncbi.nlm.nih.gov/pubmed/22391470

J Nucl Med. 2010 Aug;51(8):1234-40. doi: 10.2967/jnumed.109.072371. Epub 2010 Jul 21. 18F-FDG PET/CT for detection of metastatic infection in gram-positive bacteremia. https://www.ncbi.nlm.nih.gov/pubmed/20660384

J Nucl Med. 2017 Sep;58(9):1504-1510. doi: 10.2967/jnumed.117.191981. Epub 2017 Mar 23. 18F-FDG PET/CT Optimizes Treatment in Staphylococcus Aureus Bacteremia and Is Associated with Reduced Mortality. https://www.ncbi.nlm.nih.gov/pubmed/28336786

POLL RESULTS For persistent fevers with gram-positive bacteremia I

• rely on my H&P for a reason 14%
• rely on CT for a reason 22%
• rely on autopsy for a reason 19%
• rely on my ID consultant for a reason 43%
• give up 3%

  Back to Real Learnin’

  Oct 9, 2018

I spent the last 5 days in San Francisco at ID Weak. Every time I go to that meeting, it is worse than the one before.

Lots of time and money spent to learn very little. You really do have a choice between two kinds of talks: stuff I already know or stuff I don’t care about.

There is information to be gleaned, but it is few and far between and comes at great expense in both time and money. It is the most inefficient way to learn every devised.

I suppose if you never read a paper or surf the web, or are a first-year fellow, ID Weak could be of value. But 5 days and 3 grand to learn less than a dozen bits of information, only one of which will actually change my practice? What a waste. But I need legit CME/MOC, so I got 18.25 hours, compared to the 500 hours a year I do with blogs and podcasts and apps, none of which I get credit for.

I get more bitter with time.

Now hows about some real learnin’ with a whinging old man?

The patient is a young male, just moved here from S. America to go to college, who has fevers to 104, severe myalgias, headache, a transient rash, and diarrhea. His major complaint was the diarrhea.

He came to the ER and was found to have a pancytopenia, with platelets less than 10,000 and a transaminitis with LFTs in the low thousands, and was admitted.

He had a petechial rash on exam and developed a bleed under the blood pressure cuff—hint hint.

There is the usual differential diagnosis for fever in a traveler, but we figured it was likely dengue. It was the liver that took the greatest hit. His SGOT reached 7,000, the INR increased, and he became encephalopathic. He was put on the liver transplant list but got lucky and improved before any liver became available.

His dengue serology was strongly positive for both IgG and IgM, and eventually, the PCR came back positive for dengue as well. Evaluation for all the other potential pathogens were negative.

I have seen maybe a half dozen dengue cases in the Great Pacific NW, all acute first infection. This is my first case of severe dengue/dengue hemorrhagic fever.

Some things I learned about dengue that you might already know:

IgM goes up with each reinfection. So the IgG and IgM both being very positive is consistent with an infection with a second strain, a risk for severe dengue.

Severe diarrhea can be the presenting symptom.

And a severe transaminitis is not that unusual, causing acute liver failure in 8% of adults in endemic areas.

This will likely/hopefully be my first and last case of DHF. Global warming will have to get a wee bit worse before dengue settles in Oregon, but I will not be surprised when it does. We are primed with the mosquitos but not quite yet with the climate.

Rationalization

Dengue in a changing climate. https://www.sciencedirect.com/science/article/pii/S0013935116303127

Differentiating secondary from primary dengue using IgG to IgM ratio in early dengue: an observational hospital based clinico-serological study from North India https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-016-2053-6

Wien Klin Wochenschr. 2004;116 Suppl 4:58-60. Imported Dengue fever presenting with febrile diarrhoea: report of two cases. https://www.ncbi.nlm.nih.gov/pubmed/15683045

World J Clin Cases. 2015 Feb 16; 3(2): 125–131. Published online 2015 Feb 16. doi: 10.12998/wjcc.v3.i2.125 Dengue and its effects on liver. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4317605/

Here I Go Again

Oct 10, 2018

After I wrote this, I thought, damn, here I go complaining again. So here I go again.

I have asked this question before, but what is the allure of Augmentin? Why do people use it when they do not need it. Two cases in point in the last week: a Streptococcal infection. A pan-sensitive E. coli. The first, of course, never makes a beta-lactamase and the latter was ampicillin sensitive, not making a beta-lactamase. It was right there at the top of the sensitivity panel, the first antibiotic alphabetically.

But both were given Augmentin, which, in a word, is stupid. And I see this all the time. The only time to give Augmentin is when you do not like the patient and want to give them diarrhea.

What weird sway does Augmentin have that results in this behavior?

I suspect that many do not think of antibiotics as molecules that kill bacteria. Rather, they are strong, big gun, powerful potions that kill demons like Pseudomonas and Mursa.

It sure as h e double toothpicks doesn’t appear to be due to understanding infectious diseases.

And I suspect few look at a culture and sensitivity report with understanding.

The patient has a complicated abdominal abscess that grows with E. coli and S. anginosus. The E. coli is ceftriaxone resistant, cefoxitin, piperacillin-tazobactam, and cefepime sensitive, so likely ESBL. The patient had 6 days of piperacillin-tazobactam, then was “narrowed” to cefepime, but was not improving, and there are issues concerning proper source control despite a drain.

What is the best treatment? Besides source control? Probably not cefepime.

There was a trend towards increased mortality in the cefepime group (hazard ratio, 2.87; 95% CI, .88–9.41), which enhances the existing literature suggesting that cefepime may be suboptimal for invasive ESBL infections. and

cefepime definitive therapy is inferior to carbapenem therapy in treating patients with so-called cefepime-susceptible ESBL-producer bacteremia. And not Zosin. Among patients with E coli or K pneumoniae bloodstream infection and ceftriaxone resistance, definitive treatment with piperacillin-tazobactam compared with meropenem did not result in a non-inferior 30-day mortality. These findings do not support use of piperacillin-tazobactam in this setting.

and

PTZ appears inferior to carbapenems for the treatment of ESBL bacteremia. For patients at high risk of invasive ESBL infections, early carbapenem therapy should be considered. The answer is carbapenems. Which she is now on.

I know this is an abscess, not a bacteremia. Yet. But philosophically, if an antibiotic is preferred for the worst of cases, why not give it for less severe infections? Give the best, not what you can get away with most of the time.

And I again wonder as I watch others flail about treating infectious diseases: what would happen if cancer was approached like infectious diseases.

Rationalization

Cefepime Therapy for Cefepime-Susceptible Extended-Spectrum β-Lactamase-Producing Enterobacteriaceae Bacteremia https://www.ncbi.nlm.nih.gov/pubmed/27419191

Cefepime therapy for monomicrobial bacteremia caused by cefepime-susceptible extended-spectrum beta-lactamase-producing Enterobacteriaceae: MIC matters https://www.ncbi.nlm.nih.gov/pubmed/23090931

Effect of Piperacillin-Tazobactam vs Meropenem on 30-Day Mortality for Patients With E coli or Klebsiella pneumoniae Bloodstream Infection and Ceftriaxone Resistance: A Randomized Clinical Trial. https://www.ncbi.nlm.nih.gov/pubmed/30208454

Carbapenem therapy is associated with improved survival compared with piperacillin-tazobactam for patients with extended-spectrum β-lactamase bacteremia. https://www.ncbi.nlm.nih.gov/pubmed/25586681

POLL RESULTS I give Augmentin because

• it is two drugs, and two are better than one 10%
• it augments the treatment of infection for goodness sake 23%
• many of my patients have constipation 32%
• beta lactamases are a Chinese hoax 19% they provide great pizza 13%
• Other Answers 3%
• I’m a frickin psychiatrist. I don’t know any better. They shouldn’t expect me to fill in for the med guys.

  Act II. Scene II.

  Oct 15, 2018

O Krusei, Krusei! wherefore art thou Krusei? Deny thy father, and refuse thy name; Or, if thou wilt not, be but sworn my love, And I’ll no longer be a Pichia. Krusei. [Aside.] Shall I hear more, or shall I speak at this? Jul. ’Tis but thy name that is my enemy; Thou art thyself though, not a Candida. What’s Candida? it is nor hand, nor foot, Nor arm, nor face, nor any other part Belonging to a yeast. O! be some other name: What’s in a name? that which we call a rose By any other name would smell as sweet; So Krusei would, were he not Krusei call’d, Retain that dear perfection which he owes Without that title. Krusei, doff thy name; And for that name, which is no part of thee, Take all myself.

The patient presents with a red hot knee. She has been treated as an outpatient with a month of micafungin for C. krusei endocarditis. Now with a septic arthritis, the knee grows a Klebsiella and C. krusei and the blood cultures remain positive for C. krusei. ECHO has a vegetation on the tricuspid valve.

The surgeons are not particularly enthusiastic about replacing the valve.

So what to do?

Got me. It is not like there is a lot of literature to guide us/me. I find zero hits on both the Googles and the Pubmeds for endocarditis from this yeast.

Echinocandins such as micafungin are the current drugs of choice for treatment of C. krusei infections, but echinocandin-resistant strains with point mutations in the FKS1 gene have been reported

A single dose of amphotericin B tripled the creatinine. One of those whose kidneys seem ultrasensitive to amphotericin.

An azole? C. krusei is famous for being fluconazole resistant. For this beast the MIC to fluconazole is 8, but to voriconazole and posaconazole is it 0.1.

Maybe a loooong course of an azole and see if the beta D Glucan (currently > 500) falls? That is what I suggested. It will be months before we know.

But what is C. krusei really? Some sort of Pokeman perhaps?

C. krusei is the same species as Pichia kudriavzevii, a yeast that is regarded as non-pathogenic and has important applications in biotechnology and food industries. We examined the genomes of 20 clinical isolates (‘C. krusei’) and 12 environmental isolates (‘P. kudriavzevii’) and find that there is no genetic distinction between them. The environmental isolates have similar levels of drug resistance to the clinical isolates.

It has also been called Issatchenkia orientalis, and Candida glycerinogenes.

As they note

C. krusei (family Pichiaceae), C. albicans (family Debaryomycetaceae) and C. glabrata (family Saccharomycetaceae) are as distantly related to each other as humans are to sea-squirts [33] and it is rather misleading that they are all named Candida (which simply means that a sexual cycle has not been observed in any of them). Apart from C. krusei, the only other known pathogens in family Pichiaceae are the rare species Pichia norvegensis (also called Candida norvegensis) and Pichia cactophila (also called Candida inconspicua).

Who cares? I do. Microorganisms are like humans in fantasy novels. If you know their true name, then you have power over them, from knowing their source to how to kill them.

Or so I hope.

Rationalization

Population genomics shows no distinction between pathogenic Candida krusei and environmental Pichia kudriavzevii: One species, four names https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1007138

J Heart Valve Dis. 2017 Mar;26(2):208-210. (1→3)-β-D-Glucan Assay in Monitoring Response to Anti-Fungal Therapy in Fungal Endocarditis. https://www.ncbi.nlm.nih.gov/pubmed/28820552

Medicine (Baltimore). 2011 Jul;90(4):237-49. doi: 10.1097/MD.0b013e3182259d38. The role of fluconazole in the treatment of Candida endocarditis: a meta-analysis. https://www.ncbi.nlm.nih.gov/pubmed/21694646

Why So Long

Oct 17, 2018

The patient is at a University Hospital in another state for E. coli urosepsis and wants to come home. She is on iv antibiotics for a planned 14-day course. As is often the case in the elderly Medicare patient, arranging outpatient iv antibiotics is challenging.

So I called the doctor who is sending the patient my way to double-check the plan.

It was the intern, who said they got an ID consult who said 14 days.

Is it a complicated urosepsis? Pyelonephritis or abscess or something?

No.

So why the 14 days?

It is what ID told us to do.

Did they leave a reference?

No.

I have come to the conclusion that most of the time, bacteremia does not matter once appropriate antibiotics are started. Except, of course, for S. aureus and maybe Candida. Most of the common causes of bacteremia have almost zero risk of causing a metastatic complication, and the first dose of antibiotic probably sterilizes the blood.

Part of the reason repeat blood cultures are a waste of time for gram-negative and streptococcal infections. The bugs are dead and gone.

Treating infection is all about the source control.

One of the problems with being the sole ID doctor for the last 28 years is I have to be careful that I don’t do what I do because I do it. So for every recommendation, I try to leave a reference or three from the PubMeds. The house staff seems to like it, and it helps if there are disagreements as to the direction of care. Evidence almost always rules.

I always quote the following when I am asked about the duration of antibiotics for bacteremia.

"Twenty-four eligible trials were identified, including one trial focusing exclusively on bacteremia, zero in catheter related bloodstream infection, three in intra-abdominal infection, six in pyelonephritis, 13 in pneumonia and one in skin and soft tissue infection. Thirteen studies reported on 227 patients with bacteremia allocated to ‘shorter’ or ‘longer’ durations of treatment. Outcome data were available for 155 bacteremic patients: neonatal bacteremia (n=66), intra- abdominal infection (40), pyelonephritis (9), and pneumonia (40). Among bacteremic patients receiving shorter (5-7 days) versus longer (7-21 days) antibiotic therapy, no significant difference was detected with respect to rates of clinical cure (45/52 versus 47/49, risk ratio 0.88, 95% confidence interval [CI] 0.77-1.01), microbiologic cure (28/28 versus 30/32, risk ratio 1.05, 95% CI 0.91-1.21), and survival (15/17 versus 26/29, risk ratio 0.97, 95% CI 0.76-1.23)

and

Short courses of antibiotic therapy (8 days) yield similar clinical outcomes as prolonged courses of antibiotic therapy for Enterobacteriaceae bacteremia…

At one of the ID Weak sessions, they mentioned a study that suggested 7 days was sufficient for Enterobacteriaceae bacteremia, but I can’t find the abstract.

And the antibiotic doesn’t have to be iv.

And that doesn’t include the STOP-IT trial and the cholangitis literature that suggest four and three days suffice.

All the data points in the same directions. Less is better—5 to 7 days antibiotics for most uncomplicated Enterobacteriaceae bacteremias.

I cannot understand why anyone in 2018 would suggest 14 days of iv therapy for an uncomplicated E. coli bacteremia. Unless, of course, they don’t bother with keeping up with the literature, which at a University Teaching Hospital would be suboptimal.

I suggested to the intern that in the future that he request a reference from his consultants to justify their recommendations. It is the least a consultant should do.

In the meantime, I suppose they are relying on alternative approaches:

Eminence based medicine—The more senior the colleague, the less importance he or she placed on the need for anything as mundane as evidence Experience, it seems, is worth any amount of evidence. These colleagues have a touching faith in clinical experience, which has been defined as “making the same mistakes with increasing confidence over an impressive number of years.”7 The eminent physician’s white hair and balding pate are called the “halo” effect. Vehemence based medicine—The substitution of volume for evidence is an effective technique for brow beating your more timorous colleagues and for convincing relatives of your ability.

Eloquence based medicine—The year round suntan, carnation in the button hole, silk tie, Armani suit, and tongue should all be equally smooth Sartorial elegance and verbal eloquence are powerful substitutes for evidence.

Providence based medicine—If the caring practitioner has no idea of what to do next, the decision may be best left in the hands of the Almighty. Too many clinicians, unfortunately, are unable to resist giving God a hand with the decision making.

Diffidence based medicine—Some doctors see a problem and look for an answer Others merely see a problem. The diffident doctor may do nothing from a sense of despair. This, of course, may be better than doing something merely because it hurts the doctor’s pride to do nothing

Rationalization

Follow-up Blood Cultures in Gram-Negative Bacteremia: Are They Needed? https://academic.oup.com/cid/article-abstract/65/11/1776/4036391?redirectedFrom=fulltext

Duration of antibiotic therapy for bacteremia: a systematic review and meta-analysis https://ccforum.biomedcentral.com/articles/10.1186/cc10545

Clin Infect Dis. 2018 Jan 6;66(2):172-177. doi: 10.1093/cid/cix767. Comparing the Outcomes of Adults With Enterobacteriaceae Bacteremia Receiving Short-Course Versus Prolonged-Course Antibiotic Therapy in a Multicenter, Propensity Score-Matched Cohort. https://www.ncbi.nlm.nih.gov/pubmed/29190320

Retrospective analysis comparing oral stepdown therapy for enterobacteriaceae bloodstream infections: fluoroquinolones versus β-lactams https://www.ijaaonline.com/article/S0924-8579(17)30441-7/fulltext

Evaluation of Oral Ciprofloxacin and Intravenous Antibiotics in the Treatment of Gram-Negative Bacteremia https://idsa.confex.com/idsa/2018/webprogram/Paper72489.html

Gastrointest Endosc. 2002 Apr;55(4):518-22. Duration of antibiotic therapy for cholangitis after successful endoscopic drainage of the biliary tract. https://www.ncbi.nlm.nih.gov/pubmed/11923764

Seven alternatives to evidence based medicine. https://www.bmj.com/content/319/7225/1618

POLL RESULTS

The magic number is

• 3 3%
• 5 21%
• 7 53%
• 10 8%
• 14 5%
• Other Answers 11%
• 42
• 42
• 42, base 10.

  Eau de toilette

  Oct 22, 2018

The patient is a young former heroin user who presents with 6 months of progressive malaise, night sweats, weight loss, then shortness of breath to the point where she was admitted. She quit cold turkey 6 months ago.

ECHO shows a 2 cm vegetation, and the next day, all the blood cultures are growing gram-positive cocci in pairs and chains.

With 6 months of symptoms, I rambled on about viridans Strep, Abiotrophia, blah blah blah.

Nope.

E. faecalis.

Obviously didn’t see that coming.

I have seen one other Enterococcal endocarditis in a young adult, also a prior IVDA.

So I went through the reasons for Enterococcal bacteremia, and she had none of them. But then, when mentioned that it is a colonic bug, her s.o. mentioned that she used toilet water to mix her heroin. Clean toilet water. But toilet water nonetheless.

And bingo was her name-o.

I have seen/heard about E. coli, Serratia, and Pseudomonas endocarditis from toilet water

Pseudomonas aeruginosa is another organism that has been noted to preferentially attack right-side, previously undamaged heart valves in IDUs. A high correlation between the use of the street drugs pentazocine and tripelennamine and pseudomonas endocarditis has been noted [57]. This may be due to the preparation of these drugs, as they are said to be often dissolved in tap or toilet water and injected without prior boiling. Pseudomonas species are hardy organisms that can survive in sinks and drains, a characteristic that may account for this association.

But I can find no cases of Enterococcus endocarditis from eau de toilette searching either the Googles or the Pubmeds. Yet another first for this blog.

A week into therapy, she had abrupt onset of left upper quadrant pain, and a CT showed 2/3 of the spleen is now gone. A repeat ECHO showed no more vegetation. Finding subclinical splenic or renal emboli is not uncommon; having a big one like this is less common.

Well, at least the vegetation went to a (relatively) benign area. She never developed Howell-Jolly bodies, so I presume there is adequate splenic function. But we vaccinated her all the same, just in case.

And why does splenic lose an ‘e’ from spleen? Since the word origin is

c. 1300, from Old French esplen, from Latin splen, from Greek splen

Or maybe I should ask why the extra ‘e’ in spleen.

In the end, she did just fine. At least as far as the infection goes. Long term, there is the issue about when to fix the mitral regurgitation.

The presence of mitral insufficiency in patients with left ventricular dysfunction is independently associated with adverse outcomes, including death and hospitalization for heart failure. This has potentially important clinical implications for the assessment and management of patients with heart failure.

But that’s not an ID issue.

Rationalization

Right-Side Endocarditis in Injection Drug Users: Review of Proposed Mechanisms of Pathogenesis Jennifer A. Frontera Jeremy D. Gradon Clinical Infectious Diseases, Volume 30, Issue 2, 1 February 2000, Pages 374–379, https://academic.oup.com/cid/article/30/2/374/381830

Splenic septic emboli in endocarditis https://www.researchgate.net/publication/20931455\_Splenic\_septic\_emboli\_in\_endocarditis

Mitral insufficiency and morbidity and mortality in left ventricular dysfunction https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2651385/

What Are You Going to Do?

Remembrance of Things Past

Oct 29, 2018

Memories light the corners of my mind Misty water-colored memories of the way we were Scattered pictures of the smiles we left behind Smiles we gave to one another for the way we were

Seriously? I don’t think Barbara ever had medical training. There are some scattered smiles, but most of my vivid memories from my clinical training years are neither misty nor water-colored. More like sharp, stark black and white photographs of a murder scene. Not that I have ever killed anyone. It’s a simile.

My second rotation as a medical student was medicine, and on one of my first call nights, I went to use the restroom around 3 am. The door only partially opened, then stopped. I gave it a shove and looked down to see the body of a 40 something man on the floor.

A code was called, but he had been long dead from a drug overdose. After all was said and done, we had to get the body off the floor and onto a gurney. I got the arms, and as he gave a heave, the arms compressed the chest, forcing air out the lungs with a loud moan. I yelped and let go. Fortunately, the body had enough momentum to reach the gurney.

To this day, when I open the door of the hospital restrooms, I do it cautiously, remembering the event. So far, I have not encountered a corpse, but you never know. I do not think memory reaches the level of PTSD, but it did make an impression on me.

The patient is admitted with an MI. An iv had been placed in the field 5 days ago, and now the patient has fevers, chills, and pain the old iv site.

All the blood cultures grow MSSA, and an ultrasound shows extensive clot in the arm.

Time, cefazolin, and anticoagulation get him all better.

I remember a similar case as an intern whose outcome was not so good. She had a peripheral iv placed in the field, became bacteremic from septic thrombophlebitis, seeded her mitral valve, blew out the valve, coded, and died, all in 48 hours. It was equally parts impressive and horrible.

I learned early in medicine that even the most trivial intervention can kill and that S. aureus is one vicious bacteria. And always look at the old iv sites, not just the current ones. That may be the issue.

We identified 34 PIV-related infections (7.6%) in a cohort of 445 patients with SAB. Peripheral intravenous catheter-related SAB was associated with significantly longer bacteremia duration and thrombophlebitis at old PIV sites rather than current PIVs.

Rationalization

Peripheral Intravenous Catheter Placement Is an Underrecognized Source of Staphylococcus aureus Bloodstream Infection. Not by me. https://academic.oup.com/ofid/article/3/2/ofw072/2399348

POLL RESULTS

My memories of training

• are buried where I can find them 8%
• are drowned in beer 14%
• are lost in syphilitic dementia 14%
• are seen through rose-colored glasses 11%
• are crowded out by subsequent horrors 53%

  Just Don’t Do It

  Nov 6, 2018

Getting old is becoming a patient. I had arthroscopic surgery last week to repair medial and lateral meniscus tears and remove a loose body. A knee I injured walking on a putting green.

Man, getting old stinks. You fall apart at the slightest touch.

The surgery went just fine, although I am walking ever so slowly.

I still find anesthesia weird. This was my 5th general over the years and I always try to see the anesthesia coming. I never do. I figure propofol is the closest you can get to dying/dead without actually expiring. One moment you are looking at the OR light, then nothing until someone is talking to you in recovery. I suspect that is exactly what a v-fib arrest is like. Minding your business and then oblivion. Of course, I am in no hurry to find out if that is true.

Some days I feel like the anti-Nike, getting people to stop whatever it is they are doing.

Last week I saw a pair of consults, both essentially the same.

Both had S. aureus bacteremia (SAB) at outside hospital. One from a central line, another from cellulitis. Both being MSSA, they were treated for two weeks by ID at outside hospital. Which was reasonable; both were low risk for endocarditis or other complications and two weeks is the minimum duration of iv antibiotics everyone anyone should receive for SAB.

I always tell housestaff that when they are 98 years old, demented and dying in the ICU, even if they don’t remember their name, their last words should be “Two weeks minimum iv for SAB.” Or maybe that should be their last words before propofol. Same thing.

Both relapsed and were admitted to my system.

Both were treated with ceftriaxone.

Let me say: Just don’t do it.

I was always taught not to give ceftriaxone for MSSA since most (95%) is protein bound and the free levels of ceftriaxone are near at the mic. I am not certain that is true when you run the numbers with ceftriaxone; at 16 hours the free levels in serum at still about 1.5. But tissue levels can be a fraction of serum; for vegetations somewhere around a third.

My take over the years is that if you have good source control, like a washed out joint or a drained abscess, then ceftriaxone will likely be fine. If you have a serious infection, like bacteremia or poor source control, stick with an anti-staphylococcal beta-lactam.

The literature can be read either way, bad studies with small numbers suggesting ceftriaxone is or isn’t effective for S. aureus, depending on the infection evaluated. But I have always seen the glass as half empty and have never used any second or third generation cephalosporin for SAB.

There is the suggestion that ceftriaxone is becoming less effective over time:

While all MSSA isolates exhibited cefazolin susceptibilities within the “susceptible” zone range, there have been a proportion of isolates with ceftriaxone susceptibilities falling in “intermediate” zones, ranging from 2.6% in 2011 to 8.3% in 2016.

And when it comes to bacteremia, I’ll stick with an anti-staphylococcal beta-lactam:

…treatment of MSSA bacteraemia with cefazolin is not significantly different from treatment with cloxacillin, while treatment with other beta-lactams, including second and third generation cephalosporins, might be associated with higher mortality.

and a recent study out the VA showed that

Out of 71 patients, 38 received treatment with cefazolin and 33 with ceftriaxone. The overall rate of treatment failure was 40.8%, with significantly more failures among patients receiving ceftriaxone (54.5% versus 28.9%; P = .029).

Avoiding ceftriaxone seems the safer, if less convenient, choice.

Rationalization

Value of antibiotic levels in serum and cardiac vegetations for predicting antibacterial effect of ceftriaxone in experimental Escherichia coli endocarditis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC175004/?page=4

Continued in vitro cefazolin susceptibility in methicillin-susceptible Staphylococcus aureus. https://ann-clinmicrob.biomedcentral.com/articles/10.1186/s12941-018-0257-x

Are all beta-lactams similarly effective in the treatment of methicillin-sensitive Staphylococcus aureus bacteremia? https://www.sciencedirect.com/science/article/pii/S1198743X14618814

A Comparison of Cefazolin Versus Ceftriaxone for the Treatment of Methicillin-Susceptible Staphylococcus aureus Bacteremia in a Tertiary Care VA Medical Center https://academic.oup.com/ofid/article/5/5/ofy089/4999397

Stepping in the Haze

Nov 7, 2018

The patient, a diabetic, has a heel ulcer that does not heal. Eventually, osteomyelitis is found both clinically and radiographically. He is taken to the OR for debridement, and dead bone is removed and sent for culture. And then they sent for me.

The culture from the bone grew Proteus mirabilis and Pasturella canis.

So my first question was: do you have a dog?

Yes.

Has it ever licked your feet?

Ew. No.

Are you barefoot much at home?

All the time.

Good enough. I have seen a few cases of Pasturella acquired, I think, from walking barefoot in a house with vermin, er, I mean cats and dogs. Otherwise, his foot had not been in anything except Portland city water.

Pasturella canis is found in dog mouths. And in cats, rabbits, horses, sheep, cattle, ferrets, deer, and California sea lions, none of which she was exposed to.

Usually Pasturella canis causes human disease by way of trauma: bites and scratches. There are less than a dozen cases of this organism causing human osteomyelitis, mostly reports in children.

I think of all creatures like PigPen in Charlie Brown: they exist in a haze of shedding skin, bacteria, and more. So it is a reasonable hypothesis that he acquired the Pasturella by stepping in dog shed.

How about the Proteus? It is found in soil and water in the environment and is part of the normal flora of the human gut.

Humans and dogs have a similar microbiome. And dogs get Proteus UTI’s, which suggests GI carriage, since

In contrast to healthy dogs, P. mirabilis was also isolated in high numbers from the faeces of dogs suffering from recurrent urinary tract infections.

E. coli gets around, spreading from humans to pets and back:

E. coli clones, including ExPEC, can be extensively shared among human and animal household members in the absence of sexual contact and in patterns suggesting host-to-host transmission.

So why not Proteus? But as best I can tell, no one as described P. mirabilis as a colonizer of healthy dogs.

As much as I would like to, I can’t blame the dog for the Proteus.

Rationalization

Ann Lab Med. 2016 Nov; 36(6): 617–619. Published online 2016 Aug 24. doi: [10.3343/alm.2016.36.6.617 Identification of Pasteurella canis in a Soft Tissue Infection Caused by a Dog Bite: The First Report in Korea https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5011120/

Similarity of the dog and human gut microbiomes in gene content and response to diet. https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-018-0450-3

Isolation and characterisation of dog uropathogenic Proteus mirabilis strains. https://www.sciencedirect.com/science/article/pii/0378113595001336

Clin Infect Dis. 2006 Nov 15;43(10):e101-8. Epub 2006 Oct 10. Sharing of virulent Escherichia coli clones among household members of a woman with acute cystitis. https://www.ncbi.nlm.nih.gov/pubmed/17051483

The Pleural of Tb

Two of Four

Nov 14, 2018

No. Not a Borg.

The patient had a renal transplant 8 years ago and has been doing fine on her immunosuppression. About two years she had spine surgery, which resolved her sciatica. But shortly there after knee pain started and has progressed for the last year and half.

The knee is tapped and has 1000 PMN’s. Not impressive. But, for reasons that are not clear, rather than the usual 5 days the culture was held for 2 weeks. It is, by the way, a native joint. And at 10 days it starts to grow P. acnes.

In the meantime an MRI us done which show destruction and cystic changes of the knee.

Ortho sends the patient to me with the question, “Is it real.”

Got me. I have seen all sorts of P. acnes infections over the years, but never in a native joint.

Talking with the patient reveal she had no trauma or infection or habits that put undue stress on her knee to cause what was thought to be bad DJD.

Looking the knee it had dolor and tumor, but no rubor or calor. Hence the title of the entry.

So when in doubt, PubMed. Yep. Around 18 cases of P. acnes native joint infections:

Fourteen cases showed few signs of acute infection, slow culture growth, and delayed diagnosis. In 3 cases an early culture was dismissed as a contaminant. Six cases were reported as caused by recent arthrocentesis. Fifteen cases were cured with antibiotics, although 5 of these 15 also required surgical intervention. Two patients were diagnosed while undergoing surgery for osteoarthritis…Propionibacterium as a cause of septic arthritis in native joints demonstrates few signs of acute infection, presents with prolonged course, and is often misdiagnosed or unsuspected…Consider Propionibacterium septic arthritis in atypical osteoarthritis prior to arthroplasty.

P. acnes keeps showing up in all these odd places if you look for it: valves, central lines, herniated discs. And that is the problem. You have to look for it. It takes a while to grow and, more annoyingly, rarely causes the rubor, dolor, calor, and tumor that usually leads clinicians to suspect infection. We were lucky to get 2 of 4.

How it got there, I do not know, but I suspect a combination of very bad luck and dental hygiene.

Many of the bacteremia after dental procedures studies find P. acnes and it is often blown off as contaminant. I wonder. And I wonder if its commensal status, where it is mostly ignored by the host immune system, is a virulence factor. It is mostly pays it no attention, allowing it to go places it doesn’t belong. It is the Invisible Boy of pathogens. I suppose i should be happy it is not the Spleen of pathogens.

And now how do I prove she doesn’t have an infected knee? I can’t.

But clinically it all points to the P. acnes being the real deal.

So it’s I&D and a long course of antibiotics.

Rationalization

Infect Dis Rep. 2017 Oct 2; 9(3): 7185. Published online 2017 Oct 2. doi: [10.4081/idr.2017.7185] Native join Propionibacterium septic arthritis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5641666/

The Advantage of Screwing Up

Nov 19, 2018

The patient is a young male from rural SE Asia who has been in the US for 20 years, returning home just once a year ago.

He has had a non-focal fever of unknown origin for the last three months, night sweats, and a 30 lb weight loss. As part of the workup, he was put in what one resident called the donut of truth. It showed a belly full of enlarged lymph nodes.

One was biopsied and showed necrotizing granuloma. There was no lymphoma, and special stains were negative. So as best I can tell, they decided to watch for a while and see what happened.

The article asks the question: Necrotizing granulomatous inflammation: what does it mean if your special stains are negative?

The answer? Consult an ID doctor.

After a month, he was eventually admitted to the hospital when I was called. The only other thing of note in the history was a very positive Quantiferon with admit labs but no TB exposure, and he said he was PPD negative when he arrived in the US.

There is a differential for necrotizing granulomatous lymphadenitis, but practically speaking, it was a diagnosis of one: TB.

The ‘nice’ thing about having practiced ID for over 32 years is that in that time, I have screwed up many times, and there is no better teacher than error.

As a fellow, I saw a patient with abdominal lymphadenopathy due to TB. Not that I made the diagnosis; it wasn’t even in the differential of my note. Isolated abdominal tuberculosis lymphadenopathy is a rare manifestation of an unusual form of TB. And one report suggested,

Asians developed the majority of ileocecal and mesenteric lymph node disease

My second consult in practice was a patient who became neutropenic from tmp/sulfa and eventually died of miliary TB. Pre-mortem, as part of his evaluation, he had a liver biopsy that had necrotizing granulomas that were special stain negative. I had no clue what it meant as he had zero TB risks. But he grew MTB from all his specimens a month later.

As I think back on it, TB and I have always had issues, and if I have screwed up and missed a diagnosis, it would be on a case of TB. Are there 24 AFB in a case? You come for the ID, and you stay for the measurement puns.

So it had to be TB.

Unlike 1990, there is now PCR for diagnosis, so I sent the node, which was positive. Then, after almost 6 weeks, it is also growing MTB.

Miss a case of abdominal tuberculous lymphadenopathy or tuberculous necrotizing granulomas once; you will not miss the second.

The patient did fine on RIPE.

It is just a shame that the best way to learn is from mistakes.

Well, for some of us.

Rationalization

Mod Pathol. 2012 Jan;25 Suppl 1:S31-8. doi: 10.1038/modpathol.2011.155. Necrotizing granulomatous inflammation: what does it mean if your special stains are negative? https://www.ncbi.nlm.nih.gov/pubmed/22214968

AJR Am J Roentgenol. 1999 Mar;172(3):619-23. Tuberculosis versus lymphomas in the abdominal lymph nodes: evaluation with contrast-enhanced CT. https://www.ncbi.nlm.nih.gov/pubmed/10063847

J Infect Dis. 1988 Oct;158(4):687-92. Clinical features of abdominal tuberculosis. https://www.ncbi.nlm.nih.gov/pubmed/3171223

Mod Pathol. 2012 Jan;25 Suppl 1:S31-8. doi: 10.1038/modpathol.2011.155. Necrotizing granulomatous inflammation: what does it mean if your special stains are negative? https://www.ncbi.nlm.nih.gov/pubmed/22214968

AJR Am J Roentgenol. 1999 Mar;172(3):619-23. Tuberculosis versus lymphomas in the abdominal lymph nodes: evaluation with contrast-enhanced CT. https://www.ncbi.nlm.nih.gov/pubmed/10063847

J Infect Dis. 1988 Oct;158(4):687-92. Clinical features of abdominal tuberculosis. https://www.ncbi.nlm.nih.gov/pubmed/3171223

POLL RESULTS I learn the most from

• my mistakes 47%
• your mistakes 21%
• mistake free experience 3%
• the ramblings of specialists 16%
• Public television fundraising special 8% Other Answers 5%
• my mistakes, that are bleeding obvious to my wife.
• Donald J. Trump

  Truth and Gas

  Nov 26, 2018

A 30-something patient is admitted for symptomatic kidney stones with obstruction, which are stented, and a large perinephric, gas-containing fluid collection. He had K. pneumoniae in the urine several months back, but now the urine culture is negative.

The collection next to the kidney was drained and grew Kleibsiella, which has been associated with various gas-forming infections. As I have mentioned in the past, the end result of all organic energy production is gas. Everything makes gas.

But it also grew Actinomyces turicensis, the third one I have seen this year (see the references for the other two).

This organism has not been described to cause gas that I can find, although there is no reason to suppose it doesn’t. And it has never been associated with UTI/renal infections. Its home is the GI tract.

So, I said, this is not a perinephric abscess but due to a bowel leak. And that was proved with a little dye, where a connection with the jejunum was found. That is odd, and the why’s and wherefore’s of the leak are under investigation.

As I always say, the government will lie. The president will lie. Your parents, spouse, and children will lie. But the cultures will always tell the truth if you know what they are saying. And this time, they said ‘bowel leak’ with a weird Slavic accent.

But I had an interesting conversation with the radiologist while reviewing the CT. He told me he had called the same leak, also because of the gas.

Most of the gas he sees is iatrogenic, and he is of the opinion that most of the other gas is due to holes in body parts to allow gas in. He thinks that any large amount of gas is due to a connection with the outside world. Gas from organisms is rare and overrated.

Which is an interesting idea. As far I can tell from the Googles and the Pubmeds, no one has ever evaluated how often gas is from bacteria and how often it is from a hole in the bowel. I see gas, and I think gas-producing organisms. He sees gas, and he sees perforation.

And I wonder, is it one, the other or both. And how could you ever tell?

Rationalization

Mazel Tov http://boards.medscape.com/forums/?128@@.2a82da31!comment=1

Other reports? Czech. http://boards.medscape.com/forums/?128@@.2a82fd5c!comment=1

POLL RESULTS

Gas in an abscess usually comes from

• bacteria 38%
• a connection to the outside world 11%
• seltzer water 11%
• the local gas company 5%
• fermentation 32%
• Other Answers 3%
• Jumpin’ Jack Flash.

  Almost, but not quite, entirely unlike pyomyositis

  ID: Finally Getting Modern

  Dec 11, 2018

The patient, a middle-aged female with no prior medical problems, has 10 days of fevers, diffuse abdominal pain, and progressive bloating. She finally comes to the ER, where a CT shows multiple large fluid collections.

Radiology thinks it looks more like some sort of cancer but is surprised when nothing but pus on the grams stain of the subphrenic/perihepatic collection. But no organisms are seen, and none grew. There are 4 separate collections into which drains are placed, but the fluid is so thick it doesn’t flow.

History reveals no unusual exposures or risks for infections, and a repeat CT shows there is also an abscess in the liver that had been hidden amongst the subphrenic/perihepatic collection.

On ceftriaxone and metronidazole, she got better.

ID has long been the most old-fashioned of specialties. Do a history and physical, get some cultures, and hope something grows on agar plates, a technology that is even older than me. We are so last century.

Except. The one thing I learned at the otherwise useless ID Weak was the Karius test, which looks for microbial cell-free DNA in a blood draw, and it can identify over 1000 pathogens. I thought I would likely order it for culture-negative endocarditis or FUO, but I thought this might be an interesting way to make the diagnosis. I wondered if it was another Mycoplasma SBP, as it was similar to the case I had before.

The only downside is that the lab tells me it costs $2020. Get it? 20:20. Perfect vision? So funny. I would have charged $666, but that’s just me.

And it came back positive for Fusobacterium nucleatum. Interesting. Fusobacterium are a cause of liver abscesses, but does it explain all the uber-thick abscesses in the abdomen?

Google to the rescue.

Women get SBP with no pre-existing ascites. Usually, it is due to Group A Streptococcus (I have seen a pair in my day). There are cases of S. pneumoniae, nonenteric Salmonella spp, Neisseria meningitidis, and F. necrophorum.

So I wonder if this was primary peritonitis from Fusobacterium nucleatum with a secondary liver abscess. It would account for the diffuse abdominal pain at presentation and the weird multiple, large, thick abscesses.

That’s my story, and, as usual, I’m sticking to it.

Time and antibiotics, and she got all better.

Oh. And no Lemierre’s. In case you were wondering.

Rationalization

Can J Surg. 2008 Apr; 51(2): E40–E41. PMCID: PMC2386325 PMID: 18377740 Primary peritonitis in a young healthy woman: an unusual case https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2386325/

SMP http://boards.medscape.com/forums/?128@@.2a814845!comment=1

LDH

Dec 13, 2018

The patient has been managed (not by me) as an outpatient for HIV complicated by disseminated Histoplasmosis. There are a variety of psycho-social issues that ensure spotty follow-up and compliance. He is never really therapeutic on his itraconazole and, after three months, shows up in one of my hospitals, pancytopenic and febrile.

Work-up finds a sky-high urine Histoplasma antigen, and eventually, both the blood and bone marrow grow Histoplasma.

He is started on amphotericin B and does mostly fine. But how to know?

After 2.5 weeks, the urine Histoplasma antigen is unchanged. Usually, to diagnose the disease, a urinary antigen is all that is needed, and it takes time for the antigen to clear, especially given what was likely a huge fungal burden in this patient.

Three infections will lead to a sky-high LDH: PJP, Histoplasmosis:

The mean LDH level for patients with histoplasmosis was 1068 +/- 197 IU/L; for PCP, it was 375 +/- 23. An LDH level of more than 450 IU/L was 9.33 times more likely to be associated with a diagnosis of histoplasmosis than with PCP

and disseminated toxoplasmosis:

All 9 patients had extreme elevations of their serum lactic dehydrogenase (LDH) concentrations (median, 10,222 IU per liter; range, 2868 to 16,000.

On admission, his LDH was 1400.

You can follow the LDH in PJP as a marker of response to therapy:

Serial determinations of LDH during treatment for PCP showed that 27 of 36 (75%) of the survivors had gradual decreases of LDH, whereas 9 of 12 (75%) nonsurvivors had rising values during treatment.

But I could find no articles where serial LDH were used to follow response.

That didn’t stop me, and his repeat LDH was 45.

So I take that as a good thing, a marker of a good response to amphotericin B. I hope.

But if there is a fellow in Indiana looking for a quick study, hows about trending LDH in Histoplasmosis as a marker of response to therapy?

Rationalization

Am J Clin Pathol. 2018 Mar 7;149(4):362-368. doi: 10.1093/ajcp/aqx169. Histoplasma Urinary Antigen Testing Obviates the Need for Coincident Serum Antigen Testing. https://www.ncbi.nlm.nih.gov/pubmed/29462251

J Vet Intern Med. 2016 Jul;30(4):1065-73. doi: 10.1111/jvim.13962. Epub 2016 May 9. Antigen Concentrations as an Indicator of Clinical Remission and Disease Relapse in Cats with Histoplasmosis. https://www.ncbi.nlm.nih.gov/pubmed/27158815

Antimicrob Agents Chemother. 2002 Jan;46(1):248-50. Antigen clearance during treatment of disseminated histoplasmosis with itraconazole versus fluconazole in patients with AIDS. https://www.ncbi.nlm.nih.gov/pubmed/11751146

Antimicrob Agents Chemother. 2001 Aug;45(8):2354-7. Clearance of fungal burden during treatment of disseminated histoplasmosis with liposomal amphotericin B versus itraconazole. https://www.ncbi.nlm.nih.gov/pubmed/11451696

AIDS Read. 2002 Jul;12(7):317-21. Serum LDH level as a clue to the diagnosis of histoplasmosis. https://www.ncbi.nlm.nih.gov/pubmed/12161854

Extreme Elevations of Serum Lactic Dehydrogenase Differentiating Pulmonary Toxoplasmosis from Pneumocystis Pneumonia https://www.nejm.org/doi/full/10.1056/NEJM199204303261815

Am Rev Respir Dis. 1988 Apr;137(4):796-800. Serum lactate dehydrogenase levels and Pneumocystis carinii pneumonia. Diagnostic and prognostic significance. https://www.ncbi.nlm.nih.gov/pubmed/3258483

So Many Things I Don’t Know

Dec 18, 2018

Follow the mentor’s spirit, not the mentor’s footsteps.

Dr. Kiyoshi Shiga

Just because it’s an infection, it doesn’t mean I know anything about it. Like most doctors, I know the most about what I do—inpatient infectious diseases. But there are diseases I never take care of: Sore throat. Otitis media. Paronychia. Shigella.

The patient is an HIV patient, CD4 100, homeless, with 8 weeks of profuse watery diarrhea due to Shigella sonnei. It is resistant to ampicillin, tmp/sulfa, azithromycin and quinolones. They want me to weigh in on the treatment. He had an extensive and negative evaluation for other causes of diarrhea,

Got me. In 32 years of ID, I don’t think I have ever been asked to treat a case of Shigella.

I know antibiotic resistance is common in MSM, but that’s about it.

I never had it on my list of infections in HIV, and that seems to be confirmed in a search: a few cases here and there of diarrhea, some bacteremias, but no real association with HIV.

How to treat? It is sensitive to ceftriaxone (for now), but Shigella is an intracellular organism, and ceftriaxone gets lousy intracellular levels.

Neomycin and Rifaximin have been studied and failed, probably due to low intracellular levels.

So I had no good ideas. Push ahead with the ceftriaxone and expect a slow response was the best I could offer.

And there was something else I didn’t understand. The lab report said no Shiga toxins was detected, so no E. coli. Wait. Shouldn’t Shigella make Shiga toxin?

Nope.

Shiga toxin is named after Dr. Kiyoshi Shiga, the discoverer of Shigella dysenteriae. I suppose it is an honor to have the cause of bloody diarrhea named after you. I prefer an IPA named after me. They are made by Shiga toxin–producing Escherichia coli and Shigella dysenteriae serotype 1. But not, as a rule, by other Shigella, although there have been some cases of toxin 1–producing Shigella sonnei.

But you probably knew that.

And the patient did slowly improve.

Rationalization

Emerg Infect Dis. 2017 Feb; 23(2): 332–335. doi: 10.3201/eid2302.161203 doi: 10.3201/eid2302.161203 Increasing Antibiotic Resistance in Shigella spp. from Infected New York City Residents, New York, USAIncreasing Antibiotic Resistance in Shigella spp. from Infected New York City Residents, New York, USA https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5324786/

J Clin Microbiol. 1989 Feb;27(2):353-5. Chronic Shigella flexneri infection preceding development of acquired immunodeficiency syndrome https://www.ncbi.nlm.nih.gov/pubmed/2644299

Cell Microbiol. 2006 Feb;8(2):177-84. Intracellular survival of Shigella. https://www.ncbi.nlm.nih.gov/pubmed/16441429

Emerg Infect Dis. 2016 Apr; 22(4): 679–686. doi: 10.3201/eid2204.151825Shiga Toxin 1–Producing Shigella sonnei Infections, California, United States, 2014–2015 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4806944/

Dr. Kiyoshi Shiga: Discoverer of the Dysentery Bacillus. https://academic.oup.com/cid/article/29/5/1303/344334

Outbreak of Dysentery Associated with Ceftriaxone-Resistant Shigella sonnei: First Report of Plasmid-Mediated CMY-2-Type AmpC β-Lactamase Resistance in S. sonnei. https://jcm.asm.org/content/43/6/2608.short

POLL RESULTS

In my honor, I want

• a statue 2%
• a toxin named after me 11%
• a germ named after me 27%
• a road named after me 2%
• my name spelled right on my tombstone 51% Other Answers 7%
• to give apologies to everybody. I was a horrible person, mostly.
• to be remembered as kind and respectful

  Cold

  Huge

  Dec 27, 2018

I often see in the note something to the effect “ID Consultation appreciated.” It seems de rigueur this century to acknowledge consultations in that manner. But do they really? I suspect my recommendations are not appreciated every time. They are like flossing, an unpleasant pain. Maybe not a good metaphor. And sometimes, they say my recommendations are appreciated even before I write my note. Now that is the definition of false confidence. I so want to write something completely inappropriate for my recommendation, but I do have some self-control. Or do I?.

The patient was admitted with cellulitis in an extremity noted for chronic lymphedema. The cellulitis rapidly resolved. Too rapidly, if you ask me, the extremity was totally normal when I saw it, but the fevers, tachycardia, and tachypnea did not. So I was asked to comment on her ongoing SIRS.

Work-up found nothing infectious. I said stop the antibiotic, clindamycin, and in 24 hours, the fever went away. Drug fever from the clindamycin? Maybe. The natural history of what was really causing the fever? I don’t know. Perhaps. I saw the patient 8 days in, and everything looked normal at that point.

The tachycardia and dyspnea? On CT, the patient had a ginormous liver cyst, larger than my ego. It had pushed the heart to the side, and much of the right lower lung was compressed. It/they were amazingly large.

Was that the cause of the dyspnea? I think so. I found two cases.

We present a woman case of 93 years old who was diagnoses of giant simple hepatic cyst presented as dyspnea. The management of this patient was with percutaneous aspiration and fenol alcohol.

They were not infected, BTW.

I know the answer is not an infection, but it is too cool nonetheless. Maybe I should have sent this into the NEJM for images in medicine, but this way, at least the case gets published.

As it was Christmas and he was otherwise stable, the patient went home to have IR drainage as an outpatient.

It was drained later with marked improvement of dyspnea.

Rationalization

An Med Interna. 2007 Mar;24(3):135-7. [Giant simple hepatic cysts as dyspnea symptom in a 93-year-old patient]. https://www.ncbi.nlm.nih.gov/pubmed/17590136

American Journal of Respiratory and Critical Care Medicine 2017;195:A5500 Giant Hepatic Cyst Causing Hypercapnic Respiratory Failure. https://www.atsjournals.org/doi/abs/10.1164/ajrccm-conference.2017.195.1\_MeetingAbstracts.A5500

Slow Joint

Jan 3, 2019

A new year. And a new infection, at least for me.

The patient had a prosthetic hip placed 8 years ago for avascular necrosis. He did well until about a year and a half ago when there was slowly progressive hip pain.

One thing led to another, as often happens with one thing and another, and a CT showed inflammation/pus around the joint. It was tapped and grew?

Salmonella spp., pan-sensitive, should you want to treat it with a goat-god.

That is an odd one.

Looking back in the medical record, he had a case of Salmonella gastroenteritis about 18 months ago, roughly the time of the joint pain. No bacteremia.

Salmonella is a rare cause of prosthetic joint infection, maybe 2 dozen cases in the PubMeds. Most seem to be fairly acute, so a year and a half of festering seems unique.

I always want to know the source of infections, but I only have hints with no solid reason.

He lives the rural life with some exposure to chickens and goats, and he has a dog and dog food, both of which could be a source of infection:

Gastrointestinal diseases are the most prevalent clinical presentations of salmonella in human and dogs; however, the majority of infected animals or humans is asymptomatic and may shed the pathogen through feces for a period of 6 weeks and transmit the pathogen to other animals or individual.

Unfortunately, it was so long ago I shall never know.

The was a cool article in Emerging Infectious Diseases this month where they used whole-genome sequencing and found certain genome patterns of Salmonella enterica were associated with specific animals and could predict the source of the outbreak. It is a shame my Android can’t do machine learning Random Forest classification to figure it out. Or maybe it can. Much of medical research is increasingly like magic to me.

As best as can be found, the patient is immunologically normal and will be treated with a two-stage joint exchange and a course of antibiotics. He did fine.

Rationalization

J Med Life. 2015; 8(Spec Iss 4): 1–5. Review of bacterial and viral zoonotic infections transmitted by dogs https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5319273/

BMC Infect Dis. 2014; 14: 633. Published online 2014 Nov 26. doi: 10.1186/s12879-014-0633-x Prosthetic joint infection due to Salmonellaspecies: a case series https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4258011/

Human Salmonella Infantis Infections Linked to Dry Dog Food https://www.cdc.gov/salmonella/dog-food-05-12/pet-owners-info.html

Zoonotic Source Attribution of Salmonella enterica Serotype Typhimurium Using Genomic Surveillance Data, United States. https://doi.org/10.3201/eid2501.180835

Busy Busy

Jan 8, 2019

Work is either up or down. One day nothing, then a day like today with 7 consults. 3 consults from one hospitalist who apologized for the work. I always find it odd that people apologize for giving me work that I love to do and pays my bills. It is always good to get a consult. I have never had a bad one.

And really, they usually are not that hard. As I have said, me find bug, me kill bug, me go home. I know ID docs love to brag about how much they do and all the time it takes, but between you and me? Commenting on how long a consult takes? Most of the time, it is not a good thing:

Talking about how many hours you work is not impressive. Far from being an indication of industrious achievements or alpha status, it should be seen as a professionally embarrassing sign that, quite frankly, you have nothing else to boast about.

It was a long day, but it wasn’t that long. I have time to do this, for example.

The patient presents with back pain, slowly progressive, over about 3 months, that finally results in an MRI when he can’t get out of bed. Well, he didn’t have the MRI in his bed, he came into the ER and had his MRI in radiology.

Discitis.

Of course, the ER started antibiotics right away. Crap. Why do people do that? You have a process that has been going on for months. What is the hurry? Got me. But it happens all the time. Too much ‘don’t just stand there, do something’ in medicine and not enough ‘don’t just do something, stand there’ if you ask me, and since you are reading this, you are asking.

We get a biopsy anyway; I doubt there is enough ceftriaxone and vancomycin in the disk to mess with the cultures. And five days later, it grows..

Scant Finegolia magna

It happens. I think. Except I can’t find a case on Pubmed or Google Scholar. A couple Peptostreptococcus micros (Finegoldia used to be Peptostreptococcus) but no S. magna or F. magna.

So can I believe it? It would not be the first time I reported a case for which I can find no others.

Or is it contaminant, the biopsy site not being all that far from the rectum and from a patient who has been on his back, and not in a shower, for at least a week? Maybe the prior antibiotics really did screw up the cultures.

So, given the allergies, I opted for vancomycin more for the usual beasts and po metronidazole for the F. magna just to play it safe. It felt unsatisfactory.

After writing the order, well, entering it into Epic. I still say dial the phone, but at least I still have a functional black bakelite phone at home that I can dial. My Grandmother ‘rented’ it from AT&T for probably 45 years or more, so she likely paid out more than its weight in gold. When she died, I got the phone.

But I digress.

After entering the order, the pharmacy called to tell me they changed it from 500 mg q 12 to q 8.

Nope. Change it back.

Metronidazole is mostly a q 12 drug it probably a q 24 hour drug (with 1 gram), staying well above the MIC for most anaerobes. The q 8 dosing is of historical interest, and since drug toxicity is cumulative,

… we found a higher incidence of peripheral neuropathy in patients receiving >42 g total (>4 weeks) of metronidazole compared with those patients receiving ≤42 g total…

Q 12 dosing allows longer courses with fewer potential side effects. And it is cheaper.

Although I still say the three most dangerous words in medicine are “in my experience”, I have been giving metronidazole q 12 since I learned about it 28 years ago (except, I will admit, for brain abscess) and in my experience, I have not had a treatment failure. Yes, I am well aware of all the issues with that last paragraph.

What I need to do is get the q 8 option off of EPIC. Yeah, like that will happen. The three most common words from EPIC? “Can’t do it.”

Rationalization

Boasting about how many hours you work is a sign of failure. https://qz.com/work/1486863/boasting-about-how-many-hours-you-work-is-a-sign-of-failure/

Eur J Clin Microbiol Infect Dis. 2014 Aug;33(8):1355-64. doi: 10.1007/s10096-014-2073-3. Epub 2014 Feb 28. Bone and joint infections due to anaerobic bacteria: an analysis of 61 cases and review of the literature. https://www.ncbi.nlm.nih.gov/pubmed/24577953

The Secret History Of: The 700 series Bakelite telephone. https://www.independent.co.uk/property/interiors/the-secret-history-of-the-700-series-bakelite-telephone-2003428.html

Pharmacokinetics of Metronidazole as Determined by Bioassay https://aac.asm.org/content/6/6/691.short

J Chemother. 2007 Aug;19(4):410-6. Metronidazole single versus multiple daily dosing in serious intraabdominal/pelvic and diabetic foot infections. https://www.ncbi.nlm.nih.gov/pubmed/17855185

Once Daily Dosing of Ceftriaxone and Metronidazole in Children With Perforated Appendicitis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4869771/

Int J Antimicrob Agents. 2018 Mar;51(3):319-325. doi: 10.1016/j.ijantimicag.2017.08.033. Epub 2017 Sep 5. Clinical relevance of metronidazole and peripheral neuropathy: a systematic review of the literature. https://www.ncbi.nlm.nih.gov/pubmed/28887203

Frugal for Infection

Jan 10, 2019

The patient, an elderly male, has three months of slowly progressive back pain, low-grade fever, sweats, and malaise. He gets an MRI that shows discitis and vertebral body collapse.

Three months ago, he had urosepsis and was treated with the usual course of antibiotics.

Exam is negative except for back pain.

So we get blood cultures, and they are negative, as is the biopsy of the discitis.

So is it the urosepsis organism that is the cause of the discitis?

You probably want to know what it was first.

Aerococccus urinae.

Yeah. Me too. I thought it was the likely cause:

Aerococccus urinae (AU) is a pathogen mainly identified in male urinary tract infections and responsible for bacteremia and endocarditis. To the best of our knowledge, there are only five patients with osteomyelitis due to AU described in the literature. All of them had urinary tract disease or systemic conditions such as diabetes, and two were associated with an endocarditis.

This would be the fifth time I have written about Aerococcus, one of which was also a discitis. One of the nice things about this blog is it is a diary of all the odd infections I have seen.

He was started on antibiotics and, about a week in, had acute chest pain/coronary event that required transfer to the ICU. Part of the workup included an echo, and it showed a vegetation on the aortic valve.

I did not initially order an echo as the blood cultures were negative, and he had no stigmata of disease. And, as he was heading for a 6-week course of antibiotics, it would not change therapy.

I went back and re-listened to his heart. I could hear no murmur, although I did give some of my hearing to Led Zeppelin in my youth. I know AI can be hard to hear, but in this case, I couldn’t even pretend to hear it.

And I remember being told as a fellow all those years ago that the longer a patient has Streptococcal endocarditis, the more likely the blood cultures will be negative. But I can’t find a reference, so is that another truism that isn’t?

As a rule, I do not order tests if 1) there is no clinical indication, and 2) it will not alter therapy.

Most of my patients have some sort of deductible and have to pay 10% or more of anything I order. I was in overnight last year for small bowel obstruction; my bill came to $10,000, of which I paid 10%. I wasn’t happy to do it, but like most doctors writing a $1000 check isn’t that painful. 40% of Americans can’t even cover a 400 dollar emergency. I know what I order is a drop in the bucket of their hospitalization but if I am going to contribute to my patients eventual bankruptcy, I want every penny I spend of their money to matter.

I digress. Some bugs in the blood, for example S. aureus or S. mitis, mean endocarditis is likely. There was a great table in the green edition of Mandell that showed the odds that a Streptococcus in the blood meant endocarditis. It disappeared in subsequent editions. I think. Does anyone even spend 449 dollars on a textbook in the era of the internet? Been years since I bought one.

And how about A. urinae? Probably. My best ballpark guess from the literature is around 40% of cases of A. urinea bacteremia have underlying endocarditis. And knowing that would make a long-term difference.

Rationalization

Infection. 2018 Jun;46(3):419-421. doi: 10.1007/s15010-017-1106-0. Epub 2018 Feb 16. Spondylodiscitis due to Aerococcus urinae and literature review. https://pubmed.ncbi.nlm.nih.gov/29453766/

Urine and the Heart. http://boards.medscape.com/forums/?128@@.2a7da214!comment=1

Significance http://boards.medscape.com/forums/?128@@.2a7d45b7!comment=1

Odd bacteria in bad places. http://boards.medscape.com/forums/?128@@.2a5c5bfe!comment=1

What’s in a name? A rose by any other name would smell as sweet. http://boards.medscape.com/forums/?128@@.29f6e4f1!comment=1

POLL RESULTS

When ordering tests

• I order what I want when I want, patient cost be damned 8%
• I remember I am spending my patients money and try to be careful 76%
• it never crossed my mind how much the patients pay 8%
• I look up what to do in Mandell 4%
• I just click on order sets, who has time to cognate 4%

  Longer?

  Jan 21, 2019

The patient has multiple medical problems: elderly, IDDM, dialysis, recent transurethral treatment of bladder cancer. She is admitted with fevers, altered mental status, hypotensive.

I am called when the urine, but not the blood, grows an ESBL E. coli. She responded rapidly to meropenem, having been symptomatic with the same ESBL in her urine two other times in the last 6 months.

I am asked how long to treat, with what, and how to prevent a fourth recurrence.

I don’t know. I mean, I do. It is a complicated UTI with no pyelonephritis.

But there are issues.

For example, what are antibiotic levels in the bladder of someone with almost complete anuria? Usually, it is the urine levels that kill the bacteria. If no urine is made, then what is the antibiotic concentration in bladder sweat? No one has ever looked, as best I can tell.

Because of this, should I give IV therapy? Probably, as my oral options are limited.

Is ESBL or MRDO a reason to give a more prolonged course of therapy? Most people are hesitant to give shorter courses for more resistant organisms. Again, I can find no data to suggest MDRO need longer courses of antibiotics; MRSA may be the one exception. But a carbapenem or quinolone should kill a susceptible MDRO just as easily as a non-MRDO.

Are ESBL more virulent? Maybe, maybe not. It is organism-dependent. I find reports going both ways for E. coli:

EPE acquired during travel have seemingly low pathogenicity, possibly indicating a low risk of clinical infection.

or

that the aquatic environment is a potential reservoir of E. coli variants that combine ESBL-genes, a high level of multi-drug resistance, and virulence factors

The problem is less likely virulence of the E. coli and more likely that she is colonized with this strain, and there is not much to be done about that:

A significant proportion of ESBL and CRE carriers remain colonized up to 1 year in the healthcare setting. While short-term decolonization therapy reduces carriage during therapy, its longer-term effects are unclear.

Except, perhaps, a stool transplant.

We report a case in which fecal microbiota transplantation (FMT) utilized for relapsing Clostridium difficile colitis successfully eradicated colonization with several multidrug-resistant organisms (MDROs). FMT may have an additive benefit of reducing MDRO carriage and should be further investigated as a potential measure to eradicate additional potentially virulent organisms beyond C. difficile.

And yes, I know it is not an indication for a stool transplant, but it is being studied.

So the real answers to the questions I was asked? A big gallic shrug.

I will probably go with 10 days of ertapenem. I gotta recommend something; it’s my job.

Rationalization

Frequent acquisition of low-virulence strains of ESBL-producing Escherichia coli in travellers. https://academic.oup.com/jac/article/71/12/3548/2631294

Extended-Spectrum β-Lactamase–Producing Escherichia coli From Retail Chicken Meat and Humans: Comparison of Strains, Plasmids, Resistance Genes, and Virulence Factors. https://academic.oup.com/cid/article/56/4/478/351651

Pathogenic Escherichia coli producing Extended-Spectrum β-Lactamases isolated from surface water and wastewater https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4585870/

Natural history and decolonization strategies for ESBL/carbapenem-resistant Enterobacteriaceae carriage: systematic review and meta-analysis https://academic.oup.com/jac/article/71/10/2729/2388093

Fecal Microbiota Transplantation and Successful Resolution of Multidrug-Resistant-Organism Colonization https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4432040/

Donor feces infusion for eradication of Extended Spectrum beta‐Lactamase producing Escherichia coli in a patient with end stage renal disease https://onlinelibrary.wiley.com/doi/full/10.1111/1469-0691.12683

Heavy Metal MoM

Jan 17, 2019

The patient, as is the case of many of those I take care of, is a homeless meth and heroin user. Not heroine, as so often appears in the note. Heroin. For the last month, he has had progressive pain in his hip, to the point where he could no longer walk, and so to the ER.

A few years back he had a metal hip replacement after a traumatic fracture, so the first step was a CT.

Holy cannoli. Huge, almost as large as my ego, abscesses in the iliopsoas as well two abscesses in the gluteal muscles.

The pus was tapped and it was full of MSSA.

Unbeknownst to me, metal joints have issues. As the metal wears, it flakes off to cause metallosis

…defined as aseptic fibrosis, local necrosis or loosening of a device secondary to metallic corrosion and release of wear debris…

and can lead to large pseudotumors:

Asymptomatic pseudotumours have been identified on ultrasound and MRI scanning in 27%–32% of patients with MoM hip replacements…

And of course, they can go on to get bigly infected. The title of on series says it all:

The Relationship between the Presence of Metallosis and Massive Infection in Metal-on-Metal Hip Replacements

And redos that aren’t infected have a higher risk of becoming so.

The Orthopedist had seen a few in training and noted they were particularly difficult to treat as the metallosis leads to tissue necrosis, is impossible to debride completely as the metal is too diffuse, and the metal serves as a diffuse foreign body.

The patient also had elevated chromium and cobalt levels which are associated with neurological damage, hypothyroidism and/or cardiomyopathy.

I also tried to find the effect of cobalt and chromium on S. aureus, but found little of interest or, to be honest, understanding.

Long term these patients do not do well due to a lack of source control, so we will see.

He did OK. We cured the infection and he received a new hip after a long, complicated course but was eventually lost to follow-up .

Rationalization

Metal-on-Metal Hip Arthroplasty: A Review of Adverse Reactions and Patient Management https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4598667/

[The Relationship between the Presence of Metallosis and Massive Infection in Metal-on-Metal Hip Replacement] https://journals.sagepub.com/doi/abs/10.1177/112070001002000216

[Pseudotumor with superimposed periprosthetic infection following metal-on-metal total hip arthroplasty: a case report] https://journals.lww.com/jbjsjournal/Citation/2010/07070/Pseudotumor\_with\_Superimposed\_Periprosthetic.14.aspx

Systemic toxicity related to metal hip prostheses. Clin Toxicol (Phila). 2014 Sep-Oct;52(8):837-47. Epub 2014 Aug 16. https://www.ncbi.nlm.nih.gov/pubmed/25132471

Can is not Ought

Jan 21, 2019

Just because you can do something doesn’t necessarily mean you should do it.

I think that every time someone brings their fur-covered infection vector into the hospital.

Contamination of pet therapy dogs with MRSA and Clostridium difficile

Contamination? As if dogs are not supposed to have these bacteria. Also Brucella, Bacillis anthracis, B. zoohelcum, Campylobacter, Capnocytophaga canimorsis, Cryptosporidia, Corynebacterium ulcerans, Enterohemorrhagic Escherichia coli O157-H7, Erysipeloid, Giardiasis, Leptospira, Lyme, Pasteurella, Rabies, Rocky Mountain spotted fever, Salmonella, S. canis, Toxocara, Tularemia, West Nile encephalitis, and Yersinia.

Just what I want in my hospital.

The patient is 99 years old, slightly demented, but otherwise with no health issues. A year ago, he had a toe amputated, and now there is an occasional sinus track down to the metatarsal and chronic osteomyelitis. Further surgery is not an option, and no cultures were obtained.

I am asked about treatment.

I figured I could treat the chronic osteomyelitis but should I?

This gets to the natural history of chronic osteomyelitis. In the pre-antibiotic era (and parts of the developing world), chronic osteomyelitis is more of an inconvenience depending on location -of the osteomyelitis, not the part of the world- than a life or limb threatening infection.

Chronic osteomyelitis may present as a recurrent or intermittent disease, with periods of quiescence of variable duration. Relapses of the disease several decades after the acute episode are well known. Late reactivation of osteomyelitis up to 80 years after the primary illness had been cured have been reported. In a series of 12 patients with a minimum latent period of 20 years, no definite predisposing factor was identified, and both haematogenous and post-traumatic infections seemed equally to be involved.

It has always been my understanding that sepsis virtually never happens from chronic draining osteomyelitis, and if there is a counterexample in Pubmed or Google, I can’t find it.

Chronic osteomyelitis should fester (a reference I didn’t ‘get’ until well into my twenties) on and off with minimal impact on quality of life. I also figure as long as the infection has an ‘out,’ it will not cause problems. I suspect, and I learned this the hard way early in my career, that antibiotics might heal the sinus but at the risk of sepsis.

We observed that sinus persisted in the presence of sequestrum. Once the sequestrum was resorbed or was extracted, the sinus healed. However, at times, the sinus, stopped draining even in the presence of sequestrum for a few days, which usually caused exacerbation of infection leading to septicaemia.

And, without debridement, there is no chance of cure.

I explained all of the above, and it was elected to do nothing unless the infection became a problem.

As we slide into the post-antibiotic era, it would be nice to know the natural history of common diseases to prepare. Fortunately, the environmental catastrophes of global warming will likely render this problem less on an issue as the bugs are already disappearing.

Or is that the wrong kind of bug?

Rationalization

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

A history of osteomyelitis from the Journal of Bone and Joint Surgery https://online.boneandjoint.org.uk/doi/full/10.1302/0301-620X.89B5.19170

Natural course of hematogenous pyogenic osteomyelitis (a retrospective study of 110 cases). http://www.jpgmonline.com/article.asp?issn=0022-3859;year=1991;volume=37;issue=2;spage=69;epage=75;aulast=Kharbanda

Pathophysiology of chronic bacterial osteomyelitis. Why do antibiotics fail so often? https://pmj.bmj.com/content/76/898/479

Climate-driven declines in arthropod abundance restructure a rainforest food web https://www.pnas.org/content/115/44/E10397

BMC Vet Res. 2018 Nov 13;14(1):343. doi: 10.1186/s12917-018-1676-9.Isolation of Streptococcus agalactiae in a female llama (Lama glama) in South Tyrol (Italy). https://www.ncbi.nlm.nih.gov/pubmed/30424747

Therapy llamas, alpacas bring joy to patients at Oregon hospitals https://www.cbsnews.com/news/therapy-llamas-alpacas-bring-joy-to-patients-at-oregon-hospitals/

I Was Right From the Start

Jan 29, 2019

While I love doing ID, I am of an age (497 in dog years) where I want to see more of the world/US before the inevitable decline and dirt nap. The title of Fred Allen’s autobiography, Treadmill to Oblivion, is increasingly applicable to life.

So I hopped off the treadmill last week for a long weekend in Tucson. Fantastic place to visit and hike, except they have ways to go before they match PDX in food and beer. But they are a lot cleaner. The one thing I can say about Portland when I visit other cities is that Portland is, for a major metropolitan area, squalor central. Piles of garbage and litter, most of which come from the homeless. They do not seem all that interested in recycling. So if you want great food, drink, and hikes, just remember it comes with a large order of filth.

Plus, we have measles, thanks to some of the worst vaccination rates in the US.

Welcome to Portland.

The patient is a young, otherwise healthy female who comes in with abdominal pain and fevers 6 weeks after delivery. In the time before admission, she had a case of cellulitis, treated with Augmentin and Bactrim. Sigh. I was not involved. And an IUD was placed.

The evaluation shows the usual signs of infection and a distended, tender abdomen. The IUD was removed, and a culture of the cervix grew Group A Streptococcus.

CT abdomen showed a large amount of abdominal fluid and several large rim enhancing fluid collections.

One collection was tapped and showed pus, but gram stain and cultures were negative.

At first, I thought it was all Group A Streptococci. I have seen 2 or 3 cases of SBP in normal females from this beast:

GAS primary peritonitis should be considered in particular in young, previously healthy women who present with peritonitis but lack radiological findings of an infectious focus. The treatment of choice is immediate antibiotic therapy. Surgical intervention is difficult to avoid since the diagnosis of GAS peritonitis is usually not confirmed until other causes of secondary peritonitis have been excluded.

So I treated her with a beta-lactam and clindamycin, and she did not get better.

Distention and abdominal pain persisted, and CT showed no resolution, despite a drain, of the collections.

I was puzzled. Group A Streptococcus should be nuked by the therapy, and there was no improvement. I wondered about other causes. I did have that case of M. hominis a few years back, but to make that diagnosis, I needed tissue, and I had no tissue.

I added treatment for Mycoplasma/Ureaplasma but still no improvement. Abdominal pain and bloating, and leukocytosis persisted.

So we went for an exploratory lap to make a diagnosis and source control.

Lots of pus and necrosis but gram stain and cultures are negative.

But the magic comes through again.

16S ribosome finds?

Group A Streptococcus.

I was right from the start but didn’t know it.

I sure wish I had access to molecular testing that is cheap and accessible. So often, it is the uncertain cases that drives testing and treatments the patient may not need.

So much hinges on an accurate diagnosis, and so often I can’t get it as I have to rely on cultures, which is so last century. Someday there will be a microbiological tricorder. But likely around the time Portland gets cleaned up, aka long after I am dead.

Rationalization

Group A Streptococci: A rare and often misdiagnosed cause of spontaneous bacterial peritonitis in adults https://www.ncbi.nlm.nih.gov/pmc/articles/PMC434795/

SMP http://boards.medscape.com/forums/?128@@.2a814845!comment=1

Rules are made to be broken

Jan 31, 2019

My eldest is getting close to the end of time on my insurance, and as such, is taking care of all his medical issues while he is still on my dime.

He was slightly irked because his doctor was 30 minutes late for his 1 o’clock appointment. He would never do that to a client.

I explained that it is hard to keep to a schedule in medicine as patients often have issues that need to be addressed, and it takes more than the allotted time.

Yeah, he said, but I saw him walk into the office at 1:20 with his lunch.

The lesson for the day: always use the back door.

The patient was at Outside Hospital for Enterococcal line sepsis; the CVC in for short gut.

The line was pulled, an appropriate workup was done, and she was treated with a standard antibiotic course. Looking over the care, I would not have done anything differently.

A week after stopping the antibiotics, she returns the fever and eye pain.

Blood cultures again grew Enterococcus faecalis, a workup showed a vegetation on the mitral valve. Ophthalmology did their usual treatment of the endophthalmitis—needles in the eye. I mean, Ewwww. Gives me the willies.

Gram stain and cultures were negative from the eye and started treatment for Enterococcal endocarditis.

This raised a couple of questions.

How often does an Enterococcal line infection lead to endocarditis? Not often. Zero out of 69 in one series. And can you imagine a hospital, in this case, General Infirmary Leeds, Leeds, UK, that could have that many Enterococcal line infections in three years? That is almost 2 a month! I doubt I see one a year. I’m not going to get my CVC placed in that institution.

And how often does Enterococcus go to the eye? Even less, with fewer than a half dozen cases I can find on the Googles and Pubmeds.

And there is very little on antibiotic penetration into the vitreous, with more rabbit studies than human.

So she was treated with intraocular and intravenous antibiotics, and as best I can tell, iv antibiotics will do little for the eye. It is the intravitreal antibiotics that will do the heavy lifting.

10 days later, she returns with back pain, right over the kidney, and she thinks she is passing a kidney stone.

Nope. There is a destructive lesion in the body of a thoracic vertebrae, completely sparing the disc space. That’s tumor. Tumor always goes to the bone, and infection always goes to the disc.

Except here. On the last day of incubation, the vitreal cultures grew Candida albicans for which we had been trying, unsuccessfully, to contact the patient. Fortunately, ophthalmology pays little attention to cultures as they always inject cefepime/vancomycin/voriconazole.

The 1-3 beta D glucan was > 500, so I suspect the Candida is more widespread than just the eye. Like in the spine.

Fungal cultures are still pending on the back biopsy, but I suspect it is Candida, a violation of a fundamental law of infectious diseases.

Vertebral osteomyelitis is most commonly due to pyogenic or granulomatous infection and typically results in the combined involvement of the intervertebral disc and adjacent vertebral bodies. Non-infective causes include the related conditions of chronic recurrent multifocal osteomyelitis (CRMO) and SAPHO (synovitis, acne, pustulosis, hyperostosis, and osteitis) syndrome. Occasionally, these conditions may present purely within the vertebral body, resulting in various combinations of vertebral marrow oedema and sclerosis, destructive lesions of the vertebral body and pathological vertebral collapse, thus mimicking neoplastic disease.

But laws are made to be broken, especially by Candida and TB:

Similar to tuberculosis, fungal spondylodiscitis tends to involve the anterior vertebral body, has a predilection for paraspinal encroachment, and tends to spare the intervertebral disc due to a lack of proteolytic enzymes.

And 20% of Candida vertebral osteomyelitis does not have disk involvement. A fine point of which I was unaware. And looking back at an earlier CT from the last admission, there was a very subtle paraspinal thickening that was evident with the retrospectoscope.

So an antifungal is added to the mix, and we will see.

Rationalization

Enterococcal intravascular catheter-related bloodstream infection: management and outcome of 61 consecutive case. https://academic.oup.com/jac/article/50/4/577/761671

Case Rep Ophthalmol Med. 2013;2013:174869. doi: 10.1155/2013/174869. Epub 2013 Jul 1. Enterococcus faecalis Endogenous Endophthalmitis from Valvular Endocarditis. https://www.ncbi.nlm.nih.gov/pubmed/23936701

Clin Radiol. 2004 Oct;59(10):881-91. Vertebral osteomyelitis without disc involvement. https://www.ncbi.nlm.nih.gov/pubmed/15451346

Candida Osteomyelitis: Analysis of 207 Pediatric and Adult Cases (1970–2011) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3657498/

A Beginning?

Feb 5, 2019

I have noticed we have an issue that has paralleled the opiate addiction problem. In one chart after another, I see that the patient uses heroine. Wonder Woman? Captain Marvel. Buffy? They never specify. But I worry.

The patient is admitted to Outside Hospital with fevers and a cough and is diagnosed with influenza, H1N1. She does mostly fine and is discharged but continues to worsen with progressive shortness of breath and productive cough.

She comes to my hospital and is re-admitted. CXR and chest CT shows a consolidative, multilobar, somewhat nodular pneumonia.

Her past medical history is significant for HIV, well-controlled for years with a normal CD4 count.

Bacteria cultures and gram stain are negative.

CD4, 1400 two months ago, is now 210.

Cultures grow Aspergillus, however, and the BAL index is 6.

So it is likely Aspergillus as a complication of flu. This happens:

Two systematic reviews of invasive aspergillosis complicated by Influenza infection reported 68 and 57 total cases. One review of immunocompetent and immunocompromised patients with Influenza and IPA reported Influenza A in 93% of cases, with the majority of these having H1N1.

I am not certain what to make of the CD4; the viral load is still suppressed, and influenza should do nothing to the CD4 counts.

Following influenza infection or vaccination, most patients did not have a significant increase in HIV viral load or decrease in CD4 cell count.

But where did the Aspergillus come from? I bet marijuana; she is a regular smoker.

Molds, like Aspergillus and Mucormycosis, like to grow in dead organic material, which pretty much defines marijuana.

I wonder as legalization spreads, if we will see more invasive fungal infections. Best I can tell, marijuana production seems more mom and pop than industrial, but that too will change.

She slowly improved on voriconazole.

Rationalization

Diagn Microbiol Infect Dis.PMCID: PMC5970059 Invasive pulmonary aspergillosis and Influenza co-infection in immunocompetent hosts: case reports and review of the literature. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5970059/

Comparison of the effects of acute Influenza infection and Influenza vaccination on HIV viral load and CD4 cell counts. https://www.sciencedirect.com/science/article/pii/S1386653202000471

Mediterr J Hematol Infect Dis. 2011; 3(1): e2011005. Published online 2011 Jan 14. doi: 10.4084/MJHID.2011.005 PMCID: PMC3103256 PMID: 21625309 Too Many Mouldy Joints Marijuana and Chronic Pulmonary Aspergillosis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3103256/

Appl Microbiol. 1971 May; 21(5): 854859. Growth of Aspergillus repens in Flue-Cured Tobacco https://www.ncbi.nlm.nih.gov/pmc/articles/PMC377296/

Poll Results

My favorite Heroine

• Wonder Woman 39%
• Batgirl 4%
• Buffy 18%
• Opiate Gal 18%
• Meth Maid 4% Other Answers 18%
• Catwoman (Michelle Pfeiffer)
• Suzy Creamcheese
• Robin (with Batman)

  Crossing Lines

  Feb 7, 2019

I have never bothered with the AMA. Any group with the judgment to lose 10 million to Sunbeam isn’t going to use my dues to pay for their stupidity.

And their cheesiness continues. I keep getting ‘invoices’ from the AMA for dues renewal. I think they hope my office manager will just assume I am a member and pay the dues. The problem is, they send it to me, and I toss it in recycling.

Several times over the years, I have written them to take me off their invoice list, I have no intentions of joining, and besides, I like Kitchen Aid.

But they keep on sending these old-school phishing letters. So tawdry.

The patient is a male who, in the 9th decade of this life, perforated his appendix. We do not see a lot of appendicitis in the very elderly. I suspect most people take care of that entry in the bucket list at an earlier age.

Cultures of the peri-appendiceal grew the usual: E.coli and B. fragilis, but no Fusobacterium, much to my disappointment since

Local infection with Fusobacterium nucleatum/necrophorum is responsible for the majority of cases of acute appendicitis.

He has a remarkably un-rocky course, likely as this was the first medical problem of his life.

He did have some post-op shortness of breath, and a CXR showed a loculated right pleural effusion that was tapped and showed pus.

Cultures grew Actinomyces israelii ?!?.

Once the fluid was removed, the CXR was clear, so anot pneumonia. How did that get there?

It turns out empyema as a complication of appendicitis is a thing, with a half dozen cases on the PubMeds, mostly in children.

Acute appendicitis is the most common abdominal surgical emergency. Atypical presentations lead to a late diagnosis with a higher complication rate. Given its rarity, we report a case of a thoracic empyema due to subphrenic appendicitis.

Somehow, the bacteria ‘translocates’ to the pleural space, but as best I can tell, there is no direct anatomical link from the appendix to the pleura. Translocates is medicine for ’no clue what happens. Although

The pleural membranes are semipermeable. A small amount of fluid continuously seeps out of the blood vessels through the parietal pleura. The visceral pleura absorbs fluid, which then drains into the lymphatic system and returns to the blood.

So I suppose a little Actinomyces could hitch a ride. The other way to get empyema is the wandering appendicolith:

A retained appendicolith is a complication that occurs when the appendicolith is expulsed from the appendix as a result of perforation or failure of removal during surgery. An ectopic appendicolith can migrate to a variety of ectopic locations, acting as a nidus for abscess. Clinical presentation may be delayed by days, weeks or even months after surgery. We present and discuss an unusual case of empyema caused by migration of an appendicolith into the chest cavity.

Now that is cool.

And of course, there are a few cases of Actinomyces israelii causing appendicitis:

We report the rare case of a retrocecal appendicitis in an adult caused by an Actinomyces israelii mixed infection.

I bet the A. israelii was in the pus, but we didn’t look for it, and by the time the empyema was diagnosed, the cultures for the appendiceal pus had been tossed. It then ‘translocated’ to the pleural space—wink wink.

With standard empyema drainage and long-term penicillin, he has done quite well.

Rationalization

World J Emerg Surg. 2014; 9: 6. Published online 2014 Jan 15. doi: 10.1186/1749-7922-9-6 PMCID: PMC3896723 PMID: 24428909 Acute appendicitis in the elderly: risk factors for perforation

Gut. 2011 Jan;60(1):34-40. doi: 10.1136/gut.2009.191320. Epub 2009 Nov 18. Acute appendicitis is characterized by local invasion with Fusobacterium nucleatum/necrophorum.

Tuberk Toraks. 2013;61(1):54-6. Thoracic empyema due to bacterial translocation in acute appendicitis. https://www.ncbi.nlm.nih.gov/pubmed/23581268

Acta Gastroenterol Latinoam. 2010 Sep;40(3):276-7. [Thoracic empyema due to subphrenic appendicitis: an infrequent presentation]. https://www.ncbi.nlm.nih.gov/pubmed/21053489

Zentralbl Chir. 2001 Aug;126(8):632-4. [Acute retrocecal appendicitis caused by an Actinomyces israelii mixed infection]. https://www.ncbi.nlm.nih.gov/pubmed/11519006

Pediatr Radiol. 2015 Jul;45(7):1091-4. doi: 10.1007/s00247-014-3247-y. Epub 2014 Dec 6. The ‘wandering appendicolith’. https://www.ncbi.nlm.nih.gov/pubmed/25480435

Another Actinomyces

Feb 11, 2019

I bitch all the time that aspiration pneumonitis is not not not not the same as an aspiration pneumonia. But everyone, and I mean everyone, continues to treat the former like the latter. Drives me nuts. Since

Prophylactic antimicrobial therapy for patients with acute aspiration pneumonitis does not offer clinical benefit and may generate antibiotic selective pressures that result in the need for escalation of antibiotic therapy among those who develop aspiration pneumonia.

Perhaps there is something wrong with my messaging……….Nah.

This patient at least had the courtesy to read the textbook, with poor dentition and frequent loss of consciousness due to alcohol abuse. He comes in with a month of fevers, weight loss, a productive cough, and a necrotic lobar pneumonia with empyema.

Now that’s an aspiration pneumonia.

He goes to VATS and grows a bit of S. mitis, a smidgeon of Peptostreptococcus, and a whole lot of Actinomyces meyeri.

Never saw that last one before, but Google to the rescue:

Actinomyces meyeri is an uncommon cause of actinomycosis. We present a patient with pneumonia and empyema due to A. meyeri. The patient underwent open thoracotomy with decortication and was discharged home on a twelve-month course of oral penicillin. Review of the English literature revealed thirty-two cases of infection due to A. meyeri. The majority of patients were male, and a significant number had poor dental hygiene and a history of alcoholism. More than other Actinomyces species, A. meyeri causes pulmonary infection and has a predilection for dissemination.

My patient exactly.

One series suggests it is more common than A. israelii as a cause of actinomycosis:

A. meyeri was more common than A. israelii (33% versus 8%; P < 0.05)…particularly thoracic infections.

The organism is also associated with brain abscess.

And it may not need the prolonged course of antibiotics that we give for A. israelii.

We still have no idea how long to treat empyemas, but given the complexity of the infection, it will be longer rather than shorter.

Rationalization

Prophylactic Antimicrobial Therapy for Acute Aspiration Pneumonitis Clinical Infectious Diseases, Volume 67, Issue 4, 1 August 2018, Pages 513–518, https://doi.org/10.1093/cid/ciy120

Actinomyces meyeri infection: Case report and review of the literature https://www.sciencedirect.com/science/article/abs/pii/S0163445312000461

Emerging role of Actinomyces meyeri in brain abscesses: A case report and literature review https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5554978/

A rare case of Actinomyces meyeri empyema: Still a challenging entity to manage https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5573790/

Am J Med Sci. 2016 Jul;352(1):53-62. doi: 10.1016/j.amjms.2016.03.003. Epub 2016 Mar 18. Actinomyces meyeri, a Common Agent of Actinomycosis. https://www.ncbi.nlm.nih.gov/pubmed/27432035

Can That Be Chronic?

Feb 14, 2019

The patient, a young female… well, young by my standards. I’ll be 62 this spring, and most of my middle-aged patients seem young, and the house staff? When did they let children, barely out of diapers, become physicians?

Anyway. The middle-aged female started to have abdominal pain six months ago. The diagnosis of acute diverticulitis was made clinically, and she was placed on oral antibiotics.

Several studies of late suggest that tincture of time is just as effective as antibiotics for acute diverticulosis. For example

Observational treatment without antibiotics did not prolong recovery and can be considered appropriate in patients with uncomplicated diverticulitis.

It would appear the natural history of diverticulitis in many is benign, at least in the modern era. And it makes me wonder: what happened to diverticulitis in the 1920s?

Apparently, diverticulitis was not considered a real disease as late as 1917:

In 1917, when last reviewing the subject, I wrote: “Diverticulitis is a condition that has now passed out of the realm of doubt and uncertainty into that of proved and accepted fact…This last statement is not as yet true of all clinicians, some of whom are still apparently unaware of the condition, and not a few of its frequency and clinical importance. Not until a morbid condition is described in all the ordinary students text-boos of medicine and surgery can it be said to have attained complete recognition, and this is not yet the case with diverticulitis.”

And diverticulitis was mostly a disease treated by surgeons. I can not glean from the old discussions how many patients were observed and how many went to the OR. I hope it was the former.

And in 1920, they were curious: who needs surgery and who needs conservative therapy?

We have a similar problem today: who needs antibiotics, who needs surgery, who needs nothing? It is often difficult to apply group data to the individual in front of you with abdominal pain.

In this case, despite antibiotics, the symptoms did not abate.

So a CT was done, confirming the clinical diagnosis of diverticulitis of the transverse colon, and the antibiotics were changed. And changed again because she does not get better. The pain and gi complaints were unremitting.

Finally, after 6 months, the patient was sent to me. They really did not want to operate as there are various co-morbidities that make a trip to the OR dangerous, and GI, the referring service, did not want to do an endoscopy. Maybe they should have as

Early colonoscopy detected other significant pathology, which accounted for the clinical presentation in 17% of patients with persistent acute diverticulitis.

And the risk of perforation, or ‘colonic blowout,’ is uncertain but real:

Rather, excluding instances where electrocautery is used, we feel it is due to instrument trauma. Less commonly, excessive air insufflation can result in serosal laceration and mucosal rupture, whereas diverticular blowout is probably limited to the setting of acute diverticulitis.

I’ve had some meals that resulted in a colonic blowout.

Repeat CT showed ongoing mild to moderate diverticulitis but no abscess or perforation.

So can diverticulitis be chronic?

I suppose. There are cases of chronic diverticulitis that present with pain and obstruction and seem to more to do with scarring than ongoing infection. It is an unsatisfying collection of papers.

And is that really the diagnosis? A lack of confirming studies hampers me.

For the short term, I tried iv antibiotics, reasoning that the oral agents failed less because they do not work and more they were difficult to dose due to obesity or resistant organisms.

And it didn’t work, so is there IBD or some other process lurking in the colon that needs a diagnosis?

It’s back to GI or surgery for an educational if unsatisfactory case.

Rationalization

Br J Surg. 2017 Jan;104(1):52-61. doi: 10.1002/bjs.10309. Epub 2016 Sep 30. Randomized clinical trial of observational versus antibiotic treatment for a first episode of CT-proven uncomplicated acute diverticulitis.

World J Gastrointest Surg. 2015 Nov 27;7(11):313-8. doi: 10.4240/wjgs.v7.i11.313. Natural history Of uncomplicated sigmoid diverticulitis

Discussion on Diverticulosis. 1920

Chronic Diverticulitis: Clinical, Radiographic, and Pathologic Findings. DOI:10.2214/AJR.07.3597

Chronic diverticulitis vs. colorectal cancer: findings on CT colonography. https://www.ncbi.nlm.nih.gov/pubmed/22366853

World J Gastroenterol. 2008 May 7; 14(17): 2763 2766. Published online 2008 May 7. doi: 10.3748/wjg.14.2763 Role of colonoscopy in patients with persistent acute diverticulitis

Dig Dis Sci. 1984 May;29(5):427-31. Diverticular rupture during colonoscopy. Fact or fancy?

Poll Results

Colonic blowout is

• a complication of endoscopy 8%
• a Minnesota Vikings game 4%
• a POTUS speech 58%
• Ann Colter on any topic 23%
• lunch at Chipolte 8%

  Wondering

  Feb 19, 2019

I remember in High School when I wrote for the Grantonian (class of 75), all articles had to have who, what, where, when, why, and how answered somewhere in the story. The same principle applies to a successful ID consult, although on occasion, the answers can be a little fanciful.

But patients have curious findings that beg for an explanation, and understanding the who, what, where, when, why, and how leads down interesting paths.

The patient has had years of recalcitrant colo-vaginal fistula and recurrent pelvic abscess.

Recently she developed itchy/tender reddish bumps on a few of her fingers. I did not see them that time, but she was on a course of antibiotics for a pelvic abscess and the bumps resolved.

After several months, with the recurrence of the primary issues, the bumps returned.

This time I saw them.

They looked kind of sort of like the few Osler’s nodes I have seen.

So I wondered. Can Osler’s nodes occur outside of endocarditis?

Not that I can find. As best I can tell, these lesions only occur with endocarditis.

Osler’s nodes are rare with SBE. The patients I see are diagnosed promptly based on blood cultures. Most of the time, patients with endocarditis are not ill long enough to start have embolic phenomena, much less immune-complex diseases. No one festers with endocarditis for months and months anymore.

Most of what I see with endocarditis are hemorrhagic, non-tender lesions in the extremities, what are classically called Janeways, but I tend to call embolic events. You can see them in any number of places, and I never saw the point in differentiating a conjunctival lesion from a Roth spot from an emboli on CT from a lesion on the finger. Emboli are emboli are emboli.

Osler’s, I was always told, are immunologic, a form of immune-complex small vessel vasculitis. Note the term ‘I was always told.’ I don’t think I ever bothered to look it up. Until today.

The literature on Osler’s nodes is less than satisfying, but it is safe to say the bulk of the literature suggests it is not immune-complex, but due to micro-emboli resulting in dermal abscesses:

• Histologic examination of an Osler’s node from one of the patients with S. aureus endocarditis showed a microabscess in the papillary dermis together with microemboli in nearby dermal arterioles. Workers previously have interpreted similar histologic findings as consistent with perivasculitis resulting from an immunologic reaction to the pathogenic organism. The present findings support Osler’s original contention that the skin lesions that bear his name are “in all of probability caused by minute emboli.”*

and

Osler’s nodes and Janeway lesions are the result of minute septic emboli that cause dermal microabscesses to form. The argument that these lesions are the result of small-vessel vasculitis originated at a time well before highly sophisticated immunologic methods were available and was based on morphologic criteria alone. Thus, this etiologic theory is highly suspect. The cause of Osler’s nodes and Janeway lesions in patients with infectious endocarditis should not be confused with the immunologically based glomerulonephritis, which also can occur in these patients. The time has come to stop attributing Osler’s nodes and Janeway lesions to vasculitis.

And occasionally, the organism in the blood of an endocarditis patient are grown from an Osler’s node.

So Osler’s likely isn’t immune complex. Or is it?

I have seen immune-complex glomerular nephritis from chronic, non-endocarditis infection. I remember one case from a chronic perforated appendix in a mute patient, and the renal disease completely resolved with treatment of the peri-appendiceal abscess.

In my patient’s case, there is zero reason to suspect endocarditis or a rheumatologic problem. It is curious that these lesions get better with antibiotics/treatment of her abscess/fistula and relapse along with her disease.

I know. The bumps on her fingers should be biopsied. Dermatology is not my strong suit; I hate making rash decisions. There are a variety of logistical reasons why a derm consult has not yet occurred. You know how the practice of medicine can be in the US. Sucks eggs.

After I wandered the literature of Osler’s nodes, I began to wonder if these are indeed immune complex but more akin to a rheumatoid nodule than an Osler’s. They are not acting like polyarteritis nodosa or other, more fulminant, vasculitis.

So I also wonder if Osler’s nodes actually come in two flavors: microemboli and immune-complex. It is not as if these two pathophysiologies are mutually exclusive. The literature is very either/or.

It is not an idea that will be ever be falsified. I doubt we will ever have a sufficiency of patients with Osler’s node to do a series to answer the who, what, where, when, why, and how of these skin lesions and be reading for publication. In the Grantonian.

But, as always in medicine, it is fun to think about and investigate.

Rationalization

Ann Intern Med. 1976 Oct;85(4):471-3. Pathogenesis of Osler’s nodes. https://www.ncbi.nlm.nih.gov/pubmed/788582

Osler’s Nodes and Janeway Lesions Are Not the Result of Small-Vessel Vasculitis. https://www.amjmed.com/article/S0002-9343(13)00312-4/fulltext

It Doesn’t Work

Feb 26, 2019

The patient has the abrupt onset of fevers, rigors followed by a red, hot, swollen, exquisitely painful knee. A prosthetic knee by the way.

Gram-stain showed pus but no organisms from the debridement and poly exchange.

Otherwise healthy, she had dental cleaning 48 hours before the onset of the infection, for which she had taken the usual amoxicillin.

I bet it was going to be an oral Streptococcus because prophylactic antibiotics to prevent prosthetic joint infection doesn’t work and are not recommended because

Dental procedures were not risk factors for subsequent total hip or knee infection. The use of antibiotic prophylaxis prior to dental procedures did not decrease the risk of subsequent total hip or knee infection.

And the joint culture grew S. sanguis.

See. Prophylactic antibiotics don’t work.

Well.

Maybe.

The interesting consequence of narrowing the indications for prophylactic antibiotics for endocarditis has led, perhaps, to an increase in endocarditis:

AP prescribing fell among all IE risk groups, particularly those at moderate risk. Concurrently, there was a significant increase in IE incidence among high-risk individuals, a borderline significant increase in moderate-risk individuals, and no change for those at low/unknown risk.

and

Although our data do not establish a causal association, prescriptions of antibiotic prophylaxis have fallen substantially and the incidence of infective endocarditis has increased significantly in England since introduction of the 2008 NICE guidelines.

But there is always Newtons Third Law of the Medical literature: for every study there is an equal and opposite study.

Scaling down antibiotic prophylaxis indications was not associated with an increased incidence of oral streptococcal IE.

The truth?

I bet the occasional valve or prosthetic joint infection is caused by dental work and prevented by antibiotics, probably slightly more common than making a Higgs Boson.

Theorists predict that about 90 percent of Higgs bosons are created through gluon fusion. The probability of two gluons colliding, creating a top quark-antitop pair and propitiously producing a Higgs is roughly one in 2 billion. However, because the LHC generates approximately 1 billion proton collisions every second, the odds are in scientists’ favor and the production rate for Higgs bosons is roughly one every one to two seconds.

We have all seen an endocarditis or an infected joint following closely on the heels of a dental procedure. Dental work likely slightly increases the risk. Just a smidgeon of a tiche over the baseline of infections due to the daily bacteremias of life. And antibiotics could likely prevent some of those cases.

The problem? Deciding if the risks of prophylactic antibiotics (side effects and resistance) are worth the very minimal benefits?

Probably not.

But as always, the simple concept in the title is only kinda sorta.

Rationalization

Clin Infect Dis. 2010 Jan 1;50(1):8-16. doi: 10.1086/648676. Dental procedures as risk factors for prosthetic hip or knee infection: a hospital-based prospective case-control study. https://www.ncbi.nlm.nih.gov/pubmed/19951109?dopt=Abstract

The use of prophylactic antibiotics prior to dental procedures in patients with prosthetic joints. https://jada.ada.org/article/S0002-8177(14)00019-1/fulltext?nav=rotatorJanmain#sec5

Antibiotic Prophylaxis and Incidence of Endocarditis Before and After the 2007 AHA Recommendations. https://www.sciencedirect.com/science/article/pii/S0735109718385103?via%3Dihub

Lancet. 2015 Mar 28;385(9974):1219-28. doi: 10.1016/S0140-6736(14)62007-9. Epub 2014 Nov 18. Incidence of infective endocarditis in England, 2000-13: a secular trend, interrupted time-series analysis. https://www.ncbi.nlm.nih.gov/pubmed/25467569

J Am Coll Cardiol. 2012 May 29;59(22):1968-76. doi: 10.1016/j.jacc.2012.02.029. Temporal trends in infective endocarditis in the context of prophylaxis guideline modifications: three successive population-based surveys. https://www.ncbi.nlm.nih.gov/pubmed/22624837

The patient has the abrupt onset of fevers, rigors followed by a red, hot, swollen, exquisitely painful knee. A prosthetic knee by the way.

Gram-stain showed pus but no organisms from the debridement and poly exchange.

Otherwise healthy, she had dental cleaning 48 hours before the onset of the infection, for which she had taken the usual amoxicillin.

I bet it was going to be an oral Streptococcus because prophylactic antibiotics to prevent prosthetic joint infection doesn’t work and are not recommended because

Dental procedures were not risk factors for subsequent total hip or knee infection. The use of antibiotic prophylaxis prior to dental procedures did not decrease the risk of subsequent total hip or knee infection.

And the joint culture grew S. sanguis.

See. Prophylactic antibiotics don’t work.

Well.

Maybe.

The interesting consequence of narrowing the indications for prophylactic antibiotics for endocarditis has led, perhaps, to an increase in endocarditis:

AP prescribing fell among all IE risk groups, particularly those at moderate risk. Concurrently, there was a significant increase in IE incidence among high-risk individuals, a borderline significant increase in moderate-risk individuals, and no change for those at low/unknown risk.

and

Although our data do not establish a causal association, prescriptions of antibiotic prophylaxis have fallen substantially and the incidence of infective endocarditis has increased significantly in England since introduction of the 2008 NICE guidelines.

But there is always Newtons Third Law of the Medical literature: for every study there is an equal and opposite study.

Scaling down antibiotic prophylaxis indications was not associated with an increased incidence of oral streptococcal IE.

The truth?

I bet the occasional valve or prosthetic joint infection is caused by dental work and prevented by antibiotics, probably slightly more common than making a Higgs Boson.

Theorists predict that about 90 percent of Higgs bosons are created through gluon fusion. The probability of two gluons colliding, creating a top quark-antitop pair and propitiously producing a Higgs is roughly one in 2 billion. However, because the LHC generates approximately 1 billion proton collisions every second, the odds are in scientists’ favor and the production rate for Higgs bosons is roughly one every one to two seconds.

We have all seen an endocarditis or an infected joint following closely on the heels of a dental procedure. Dental work likely slightly increases the risk. Just a smidgeon of a tiche over the baseline of infections due to the daily bacteremias of life. And antibiotics could likely prevent some of those cases.

The problem? Deciding if the risks of prophylactic antibiotics (side effects and resistance) are worth the very minimal benefits?

Probably not.

But as always, the simple concept in the title is only kinda sorta.

Rationalization

Clin Infect Dis. 2010 Jan 1;50(1):8-16. doi: 10.1086/648676. Dental procedures as risk factors for prosthetic hip or knee infection: a hospital-based prospective case-control study. https://www.ncbi.nlm.nih.gov/pubmed/19951109?dopt=Abstract

The use of prophylactic antibiotics prior to dental procedures in patients with prosthetic joints. https://jada.ada.org/article/S0002-8177(14)00019-1/fulltext?nav=rotatorJanmain#sec5

Antibiotic Prophylaxis and Incidence of Endocarditis Before and After the 2007 AHA Recommendations. https://www.sciencedirect.com/science/article/pii/S0735109718385103?via%3Dihub

Lancet. 2015 Mar 28;385(9974):1219-28. doi: 10.1016/S0140-6736(14)62007-9. Epub 2014 Nov 18. Incidence of infective endocarditis in England, 2000-13: a secular trend, interrupted time-series analysis. https://www.ncbi.nlm.nih.gov/pubmed/25467569

J Am Coll Cardiol. 2012 May 29;59(22):1968-76. doi: 10.1016/j.jacc.2012.02.029. Temporal trends in infective endocarditis in the context of prophylaxis guideline modifications: three successive population-based surveys. https://www.ncbi.nlm.nih.gov/pubmed/22624837

It Is Not Always Infection

Feb 27, 2019

The world is divided into two kinds of people: those who divide the world into two kinds of people and those who do not. That is one way to look at the world.

I tend to divide the world into those who have infections and those who do not. And while the second option is not as interesting as the first, as a consultant, you have to at least consider non-infectious etiologies as a cause of the patient’s signs or symptoms.

I am asked to see the first patient, admitted for altered mental status and found to have an MDRO E. coli in the urine. It is treated appropriately, and clinically she improves except for her leukocytosis that persists at 40,000.

So they call me.

I could not find an infection, and a CT of the abdomen had no pus collection or pyelonephritis. But.

She also is being treated for uroepithelial cancer. Bladder cancer, along with lung cancers, can make G-CSF.

Leukocytosis is often seen in patients with paraneoplastic syndromes and is related to granulocyte colony-stimulating factor (G-CSF) production. Lung cancer is the most common G-CSF-producing cancer, and, in urology, bladder cancer is reportedly the highest G-CSF producer. So we, and by we, I mean I, checked a GCSF level, and it was 60.

In 49 of 56 normal healthy persons (88%), the levels were beneath the sensitivity of the assay (less than 30 pg/mL.

And 2 months have gone by with a continued leukocytosis with no signs and symptoms of infection.

The other patient seems to be a classic FUO: 6 weeks of fevers to 102, drenching sweats, non-productive cough, weight loss starting after an aggressive dental cleaning.

The exam was negative except for some bilateral crackles. I thought it was likely endocarditis, given the lack of risks for odd infections and despite no murmur.

No. Work-up was negative for infection, but I did find a large, round, intra-pleural mass that on biopsy that on pathology was “sarcomatoid carcinoma vs biphasic mesothelioma.”

IR, based on the location and shape, told me it would be a sarcoma. And these sarcomas are a cause of fevers; there are a smattering of cases of fevers due to sarcomatoid carcinoma.

BTW:

Sarcomatoid carcinoma is an extremely rare, biphasic tumor characterized by a combination of malignant epithelial and mesenchymal cells.

And biphasic mesothelioma as a cause of fever? It appears so, but not as well reported.

And the difference between sarcomatoid carcinoma and biphasic mesothelioma? I read some references and realize I do not really want to know. I’ll leave that to oncology.

I have diagnosed a few uroepithelial cancers presenting with leukocytosis and hematuria, but this is the first, and hopefully last, FUO from sarcomatoid carcinoma.

It’s not always an infection.

Rationalization

Serum G-CSF May Be a More Valuable Biomarker than Image Evaluation in G-CSF-Producing Urothelial Carcinoma: A Case Report https://www.karger.com/Article/FullText/472250

Blood. 1989 Jan;73(1):117-22. Serum granulocyte colony-stimulating factor levels in healthy volunteers and patients with various disorders as estimated by enzyme immunoassay. https://www.ncbi.nlm.nih.gov/pubmed/2462934

High-fever as an initial manifestation of sarcomatoid carcinoma of renal pelvis: a case report and literature review. http://www.ijcem.com/files/ijcem0045092.pdf

Ann Thorac Surg. 2014 Nov;98(5):e123-5. doi: 10.1016/j.athoracsur.2014.07.046. Epub 2014 Oct 30. Esophageal sarcomatoid carcinoma presenting as a Fever with elevated serum leukocytes. https://www.ncbi.nlm.nih.gov/pubmed/25441832

Int J Surg Case Rep. 2015; 13: 48–50. Published online 2015 Jun 10. doi: 10.1016/j.ijscr. Sarcomatoid Carcinoma of the lung: A rare case of three small intestinal intussusceptions and literature review. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4529630/

Histopathology. 2003 Mar;42(3):270-9. Sarcomatoid mesothelioma and its histological mimics: a comparative immunohistochemical study. https://www.ncbi.nlm.nih.gov/pubmed/12605647

Does it mean anything?

Mar 5, 2019

The patient is elderly and has multiple medical problems; multi-organ system failure after weeks in the ICU. One of those horrible cases that are not well enough to recover from all the co-morbidities and complications.

I am asked about the patient’s fever and pneumonia.

The patient has a tracheostomy, and patchy infiltrates on CXR.

The cultures had gram-positive rods and grew C. striatum.

Treat it? I am asked.

I said yes, Corynebacterium striatum is a pathogen under these circumstances.

There are a hodgepodge of cases of Corynebacterium striatum causing pneumonia, often nosocomial.

And vancomycin is the only reliable antibiotic.

All isolates were resistant to ciprofloxacin, and all were sensitive to vancomycin (16% sensitive to vancomycin, exclusively).

So the patient was put on vancomycin and kind of improved. Many other issues intervened in the patient’s course that were more important than the pneumonia.

The other curious finding was a positive 1-3 Beta D glucan in the upper 200’s. When I was first consulted, I thought the patient had incipient Candidemia, but with treatment, the 1-3 Beta D glucan did not fall. We looked for all the other reasons for an elevated 1-3 Beta D glucan, but as best as could tell, there wasn’t one?

Or was there?

Bacterial infections can be associated with a false-positive 1-3 Beta D glucan:

The 7 Gram-negative bacteria implicated in false-positive BG test results were Escherichia coli (n = 2), Enterobacter faecalis (n = 1), Acinetobacter baumannii (n = 1), Klebsiella pneumoniae (n = 1), Providencia alcalifaciens (n = 1), and Pseudomonas aeruginosa (n = 1). The 15 Gram-positive bacteria found in cases of false-positive BG test results were Staphylococcus aureus (n = 12), Peptostreptococcus magnus (n = 1), and a Micrococcus sp. (n = 1).

Most often due to bacteremias. The patient was not bacteremic. What about the Corynebacterium striatum? I have three cases on this blog, and there are two on Pubmed of Nocardia causing an elevated 1-3 Beta D glucan. Nocardia, like Corynebacterium striatum are gram-positive rods, so….. Eh. That’s a stretch.

I can find nothing to confirm or deny that Corynebacterium makes 1-3 Beta D glucans. So who knows? But I wonder.

Rationalization

New Microbes New Infect. 2014 Jul; 2(4): 106–114. Published online 2014 Jun 27. doi: 10.1002/nmi2.48 Respiratory infection by Corynebacterium striatum: epidemiological and clinical determinants https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4184579/

Use and Limits of (1-3)-β-d-Glucan Assay (Fungitell), Compared to Galactomannan Determination (Platelia Aspergillus), for Diagnosis of Invasive Aspergillosis https://jcm.asm.org/content/52/7/2328

(1–3)-β-D-Glucan Assay: A Review of its Laboratory and Clinical Application https://academic.oup.com/labmed/article/42/11/679/2657644

We Are The Champignons

Mar 7, 2019

The patient has the sudden onset of abdominal pain followed by near syncope. He comes to the ER, meets sepsis criteria, has a Hgb of 6 and a CT that shows a huge retroperitoneal bleed. He has a right adrenal/accessory renal artery that is embolized as the likely source.

He is on anticoagulants, clopidogrel and dabigatran. Bleeding happens on anticoagulants and is reason enough for the bleed.

But this is an ID blog. So it isn’t.

Blood cultures from the ER are positive for gram-positive cocci in pairs and chains, and repeat blood cultures the next day are the same.

I sort of stick my nose in when I review the case as part of antibiotic stewardship.

He had been feeling poorly for weeks prior to the onset of his abdominal pain but no specific localizing complaints. The organism is found to be E. faecalis, but it is not found in his urine.

The way to put it together is endocarditis with a ruptured mycotic aneurysm. And the TEE shows an aortic valve vegetation.

But was it a mycotic aneurysm? Can’t say for sure, but being an Occams kind of guy, I vote yes. There was marked compression of the vessels by the bleeding, and neither the CT nor the embolism procedure saw a distinct aneurysm. Maybe just an embolus that bled.

It is rare to see mycotic aneurysms, having perhaps a smattering in my career, mostly intra-cranial.

It turns out renal artery mycotic aneurysms are unusual. I counted maybe 6 cases in non-transplant patients.

The visceral arteries are the least common sites for mycotic aneurysm formation, representing ≤1% of intra-abdominal mycotic aneurysms. Risk factors for mycotic renal artery aneurysms (MRAAs) include intravenous drug use, endocarditis [3–5], and renal transplantation. These inflammatory aneurysms grow rapidly within days to weeks and are prone to rupture.

I bet the anti-coagulation didn’t help matters.

And at the time of the embolization, we did not know the results of the blood cultures, so do I have a huge, infected clot with a foreign body to treat as well as endocarditis? Probably.

For now, it is treat the endocarditis and see how the hematoma evolves.

As you probably know, Osler has had a malign influence on the language of medicine. In 1885 he described fungal-shaped aneurysms in a patient with subacute endocarditis, hence the name mycotic. The exact quote

… the arch of the aorta presented four aneurysms, three small, not larger than cherries, and one the size of a billiard ball. The small ones were not noticeable as aneurysms from the internal surface, but presented the appearance of fresh fungal vegetations…presented a condition of mycotic endarteritis unique in my experience of aortic aneurysms.

And the name stuck.

Rationalization

Vasc Health Risk Manag. 2017; 13: 325–342. Published online 2017 Aug 23. doi: 10.2147/VHRM.S121661 Evaluation of bleeding in patients receiving direct oral anticoagulants https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5574591/

J Heart Valve Dis. 2005 May;14(3):310-6.Peripheral mycotic aneurysms in infective endocarditis. https://www.ncbi.nlm.nih.gov/pubmed/15974523

Medicine (Baltimore). 2014 Jan; 93(1): 42-52. Published online 2014 Jan 2. doi: 10.1097/MD.0000000000000014 Symptomatic Peripheral Mycotic Aneurysms Due to Infective Endocarditis A Contemporary Profile https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4616324/

Case Rep Surg. 2018; 2018: 7080813. Published online 2018 May 7. doi: 10.1155/2018/7080813 Mycotic Renal Artery Aneurysm Presenting as Critical Limb Ischemia in Culture-Negative Endocarditis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5964565/

The Gulstonian Lectures, on Malignant Endocarditis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2255866/?page=3 All autopsy findings. No cure or treatment in 1885.

PG Rating

Mar 11, 2019

The patient is admitted with bilateral cellulitis.

Yeah. I know. There is no such thing as bilateral cellulitis. But this is different. This is occurring around new bilateral chest wall expanders.

An elderly female with no prior medical problems is having reconstruction after bilateral mastectomy. A week after admission, both incision sites become red, hot, and tender with leukocytosis and fever.

It does not get better on antibiotics, so the expanders are removed, and in the OR, there is inflammation and necrosis.

On antibiotics, it progresses, and they call me.

Nothing of note in the past medical history, no odd exposures to make the infection due to an odd organism.

The gram stain has white cells, but no organisms, and the cultures are negative.

The bilateral nature of the infection makes me suspect it is something odd on the expanders.

There was the outbreak of the plastic surgeon with a hot tub who gave Mycobacterium jacuzzii, a rapidly growing Mycobacterium, to 15 women after insertion of breast implants.

It wasn’t the patient but the surgeon who was the source of contagion. But this surgeon didn’t have a hot tub.

And the infection progressed with erythema and necrosis and required another debridement.

And still, the cultures and stains were negative. Specimens were sent for 16S testing this time, but that takes a week, and the patient started to worsen with erythema and necrosis again.

Fungus? AFB? Some odd mycoplasma? What to give while waiting for the 16S.

I have no end of biases, and when I see patients, my first inclination is to suspect infection. That’s my job. Hell, that’s my raison d’etre.

But if this is not an infection, then what looks like an infection but gets worse with surgery? Pyoderma gangrenosum.

And so I looked in PubMed.

Yep. A few cases of PG after various reconstruction procedures without the usual risk factors:

Fifty to seventy percent of PG is associated with systemic inflammatory disease or hematological malignancy.3 In breast reconstruction, diagnosis can be delayed because the clinical presentation mimics an infectious process, which prompts antibiotic therapy, serial debridement, and in cases of prosthetic reconstruction, implant removal, leaving the patient with extensive scarring and need for further breast reconstruction… Postsurgical PG of the breast is not common, with 22 cases reported following breast reductions and pexies, 7 after breast reconstructions, and 2 following breast augmentations.

It is pathergy squared. There are also some cases after ports and pacemakers.

It has been a long time since I diagnosed a PG, but I called the head of the burn center, who has more experience than I, and he agreed with the clinical diagnosis.

The inflammation stopped with high-dose steroids.

PG is, unfortunately, both rare and is

a diagnosis of exclusion based on clinical factors, ulcerative characteristics, failure to respond to antibiotics, and surgical therapy.

which delays the correct therapy.

Not everything, unfortunately, is infectious.

Rationalization

An Outbreak of Mycobacterium jacuzzii Infection following Insertion of Breast Implants. https://academic.oup.com/cid/article/43/7/823/369381

Post Reconstruction Breast Pyoderma Gangrenosum: Early Recognition and Prosthesis Salvage https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4494504/

Pyoderma gangrenosum with pathergy: A potentially significant complication following breast reconstruction. https://www.ncbi.nlm.nih.gov/pubmed/28476284

It Is Not A Spider Bite

Mar 13, 2019

The patient presents with a necrotic inflammation on the thigh with surrounding erythema.

He is febrile and has a WBC of 27,000 and is admitted with a soft tissue infection.

He says it was a spider bite. He never saw the spider in question. They never do.

Why blame the poor arachnid? Got me. Somehow people have it in their minds that spiders bite and cause horrible skin reactions. In some parts on the country, perhaps.

But not in Oregon.

FYI, here is a map of the distribution of the dreaded, and rightfully so, Brown Recluse.

Not here in Oregon. We do have Hobo and Black Spiders:

The latter does cause occasional severe skin reactions. But not the Hobo.

A recent study (McKeown et al. 2014) compiled 33 verified spider bites in Oregon, including one hobo spider bite. None of the 33 bites resulted in significant medical symptoms or dermonecrosis. A fairly well known venomous spider that occasionally bites people, the brown recluse, Loxosceles reclusa, does not occur in Oregon, despite reports to the contrary. Most spiders in Oregon, even those most likely to be found inhomes, are not known to be dangerous.

and

The hobo spider bite resulted in pain, redness, twitching in the calf muscle and resolved in 12 h.

As was noted

One must wonder how and why the brown recluse spider bite became so embedded in the emergency medicine lore that it is commonly diagnosed in areas where the loxosceles spider does not exist. Outside the spider’s indigenous areas, it is probably safe to eliminate the term “spider bite” from an emergency department’s lexicon and to consider other causes of apparent dermonecrosis, especially infection.

Cultures grew Group A Streptococcus and MRSA. A nice combination for causing a necrotic soft tissue infection aka a Melany’s. And she got better on antibiotics.

Outside of the range of Loxosceles reclusa, only Peter Parker, Miguel O’Hara, and Miles Morales can blame their issues on a spider bite. For the rest:

It s Not a Spider Bite, It s Community-Acquired Methicillin-Resistant Staphylococcus aureus

Rationalization

Oregon Spiders. Fact and Fiction.

Toxicon. 2014 Jun;84:51-5. doi: 10.1016/j.toxicon.2014.03.009. Epub 2014 Apr 13. Verified spider bites in Oregon (USA) with the intent to assess hobo spider venom toxicity. https://www.ncbi.nlm.nih.gov/pubmed/24726469

Is It Really a Spider Bite? https://www.jwatch.org/em200504270000006/2005/04/27/it-really-spider-bite

It s Not a Spider Bite, It s Community-Acquired Methicillin-Resistant Staphylococcus aureus https://www.jabfm.org/content/17/3/220

Poll Results

Issues in life arise from

• spider bites 6%
• gamma radiation 18%
• yellow sun radiation 24%
• being hit by lightning while doused in chemicals 26%
• a trip down crime alley after watching Zorro 18% Other Answers 9%
• stupid people
• the human condition. Which is also a film well worth watching.
• Losing the manual to the suit given to you by aliens.

  I’m Getting Quite the Collection

  Mar 20, 2019

The patient is a youngish female, no past medical history except for distant left PID treated years ago. She presents with right-side abdominal pain, fever, chills, and vomiting.

Exam shows rebound, and she had a positive speed bump sign, one of my favorites:

Presence of pain while travelling over speed bumps was associated with an increased likelihood of acute appendicitis. As a diagnostic variable, it compared favourably with other features commonly used in clinical assessment. Asking about speed bumps may contribute to clinical assessment and could be useful in telephone assessment of patients.

I think of the speed bump sign less about appendicitis but a sign of peritonitis.

CT does not show an acute appendix but diffuse peritonitis, and this was confirmed at the e-lap. No reason for the peritonitis is found in the OR; the bowel and the GU system appear normal.

And the cultures? MRSA.

Primary peritonitis.

Primary or spontaneous bacterial peritonitis is defined as peritonitis in the absence of an evident intra-abdominal infection or pathology.

That is my fourth this century: Two from group A Streptococcus, one from M. hominis and now an MRSA. Most of the reported cases are in kids; mine have all been adults. But then, I do not take care of children.

Most cases are S. pneumoniae, Group A Streptococcus or N. meningiditis and a hodgepodge of other organisms. While one review suggests S. aureus accounts for 2-4% of cases, the few I could find had reasons for the infection: an erosion of an umbilical hernia, pregnancy, or Strongyloides. To my mind, the sine qua non of primary peritonitis is infection for no reason. If so, this would be the first with MRSA.

I put her on vancomycin, and she was very slow to get better. After a week, a repeat CT showed two large abscesses that needed draining.

I try never to use vancomycin in any infection with inadequate source control. I should have predicted that she would go on to get an abscess; there is no way they could thoroughly wash out a peritoneum filled with MRSA. Add to that; vancomycin is such a lousy drug and

Vancomycin and ciprofloxacin levels were inadequate in most abscesses.

With better source control and ceftaroline, she improved.

Rationalization

BMJ. 2012 Dec 14;345:e8012. doi: 10.1136/bmj.e8012. Pain over speed bumps in diagnosis of acute appendicitis: diagnostic accuracy study. https://www.ncbi.nlm.nih.gov/pubmed/23247977

Can J Surg. 2008 Apr; 51(2): E40E41. PMCID: PMC2386325 PMID: 18377740 Primary peritonitis in a young healthy woman: an unusual case https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2386325/

PRIMARY PERITONITIS https://publisher.medfak.ni.ac.rs/AFMN\_1/2008/3-broj/PRIMARY%20PERITONITIS.pdf

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

Poll Results

I collect

• infections 7%
• empty beer bottles 7%
• the souls of my enemies 27%
• adipose 32%
• regrets 20% Other Answers 7%
• stuff that doesn’t work, and …
• Gratitudes
• nurse’s pens

  Fourty

  Mar 25, 2019

I’m not a numerologist and find no particular significance in numbers. There are no lucky numbers or significant numbers, except, perhaps, the date of my death.

But if you search Wikipedia, there are pages devoted to numbers. Three or 13 have all sorts of information about them beyond being lucky or unlucky.

The patient, a middle-aged female, has been sick for 3 weeks: fevers, malaise, and mild weight loss. No specific localizing signs or symptoms. Her labs had a slight cytopenia and mildly elevated transaminitis.

Workup shows an IgM to CMV off the wall, a barely positive IgG, and a 9000 viral load for CMV.

I interpret this as a resolving acute CMV infection.

She, of course, wants to get well and get back to life. How long is she going to be ill?

In the old days, we called it 40-day fever:

A characteristic clinical pattern was noted: 40 days following transplantation, daily fevers recurred for periods of four to six weeks.

And four to six weeks is about 40 days.

The 40-day fever was originally in transplant patients; I saw the same pattern from transfusions in bypass patients back in the day. Or so I remember.

So I told her she would be ill for 40 days.

Treatment? Valganciclovir is pricy (no prescription benefits) and toxic, and with a viral load of only 9000 and no focal symptoms, I am not sure what good it would do.

I can’t find where anyone has treated uncomplicated CMV in normal non-focal adults.

And of all the 40 facts on Wikipedia, my favorite is

• Forty is the only integer whose English name has its letters in alphabetical order.*

But, oddly, they don’t mention 40-day fever.

Rationalization

3 https://en.wikipedia.org/wiki/3

13 https://en.wikipedia.org/wiki/13(number)

40 https://en.wikipedia.org/wiki/40(number)

West J Med. 1974 Jan;120(1):1-7. Forty-day fever. An epidemic of cytomegalovirus disease in a renal transplant population. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1129295/

Poll Results

The most important number

• 1 although it’s the loneliest number 16%
• 2 it’s as sad as one 3%
• pi like me, irrational 32%
• i the number that defines alternative medicine 13%
• 0 from which the universe erupted 19% Other Answers 16%
• e – both natural and irrational.
• 42, clearly.
• Social Security. Don’t leave home without it.
• Infinity - so much potential there

  Three Results

  Mar 27, 2019

I need to know what I am killing. Knowing the infecting organism is almost everything in deciding on treatment and being able to prognosticate.

The first patient, elderly and frail, comes in with progressively severe neck pain, and an MRI shows cervical discitis/osteomyelitis. So they give antibiotics and call me the next day.

The patient has had several months of decline but no fevers. The exam showed very poor dentition and a 3/6 murmur courtesy of the 2-year-old TAVR.

And no blood cultures were done.

Crap. People often get their discitis as a complication of endocarditis, for which he is a setup.

I order blood cultures, which, of course, are negative, and the ECHO shows a vegetation on the mitral valve, not the TAVR. I still fret about the TAVR.

I need a bug, so I resort to magic, aka the Karius test, cell-free plasma next-generation DNA sequencing. Magic.

The second is a lymphoma patient admitted with sepsis, ARDS/MOSF, and fevers. He has a couple of weeks of ICU care, but the fevers do not remit despite various antibiotics.

Studies are negative for infections, at least anything we can grow or find on CT, but all his studies are nonspecifically abnormal.

So again, I resort to magic.

The third has an FUO for months. Three months of fever to 101, sweats, severe fatigue, and weight loss. He is finally admitted for FUO workup when he can’t get out of bed, and his brother calls 911. Work-up is negative except for a vegetation on the mitral valve.

So culture-negative endocarditis. I send off the usual studies. Negative. The fevers persist. So I order magic and, in this case, a PET scan, worried about malignancy-associated marantic endocarditis. There is an interesting literature using PET’s to diagnose FUO. He is quite ill and going nowhere clinically.

The first two are positive.

The first is S. salivarious. Which fits nicely and means I do not have to give a course of empiric vancomycin. It would be nice to have an MIC to penicillin, but given the advanced age and already marginal renal and otic function, I suspect I will opt for long-term oral beta-lactam when done with the iv.

The second was more of a puzzle. It was positive for Lacobacillus rhamnosus, the same organism in his probiotics.

Hm.

I had no idea what to make of that result as he was getting better while we awaited the test, but we stopped the probiotics. True/True and unrelated or causal? Got me. I suspect the former. Whether probiotics can cause a true positive, I cannot find.

The third? Negative. As was the PET. And then? He got better. No diagnosis. We see this.

58 patients with follow-up data, who were diagnosed with FUO at admission and did not have a final diagnosis at discharge, were enrolled in this study. The median duration of follow-up was 518 (0.4–830) weeks, and the fever duration was 24.6 (6.7–763.2) weeks. Final diagnoses were established in 11 cases (19%), and the diagnostic methods included clinical diagnosis, diagnostic therapy, genetic screening, and biopsy pathology. The fever in 35 patients (60%) subsided during hospitalization or after discharge. Their condition was stable and self-limited after long-term follow-up, and they were ultimately thought to be cured

Diagnostic testing. Sometimes it helps, sometimes it confuses, and sometimes it adds nothing.

Rationalisation

Next-Generation Sequencing of Infectious Pathogens https://jamanetwork.com/journals/jama/fullarticle/2725407

Analytical and clinical validation of a microbial cell-free DNA sequencing test for infectious disease https://www.nature.com/articles/s41564-018-0349-6

Clinical features and outcomes of patients with fever of unknown origin: a retrospective study Tan et al. BMC Infectious Diseases (2019) 19:198 https://doi.org/10.1186/s12879-019-3834-5

Under Pressure

Apr 2, 2019

The patient is a paraplegic who has five months of his first decubitus ulcer, who presents with fevers and erythema along the edge of the ulcer.

An MRI is done that is consistent with osteomyelitis: bone edema. He goes to the OR, where they debrided necrotic soft tissue and biopsied the bone. Post-op the called me. The surgeon was puzzled the bone was so hard given the MRI.

I told him it was because MRIs are way too sensitive. There was a most excellent review this year, Osteomyelitis Complicating Sacral Pressure Ulcers: Whether or Not to Treat With Antibiotic Therapy, that I keep quoting (I try and include a reference or two with every consult) and should be in everyone’s files:

…many patients with chronically exposed bone do not have evidence of osteomyelitis when biopsied, and magnetic resonance imaging may not accurately distinguish osteomyelitis from bone remodeling. And the biopsy showed no osteomyelitis.

But all the soft tissue cultures grew only Corynebacterium striatum.

Hm.

I have seen a few cases of indolent pneumonia from Corynebacterium striatum but no soft tissue infections. Can Corynebacterium striatum do that? Of course. Given suitable soil, any organism can become pathogenic.

C. amycolatum was the predominant species (20%), followed by C. striatum (16%). Penicillin was least effective in vitro followed by clindamycin and ciprofloxacin. Excellent activities were shown by vancomycin, linezolid, and imipenem. Multidrug resistance was found in all the species.

And there are a smattering case reports as well.

He improved with vancomycin. Well, he improved with surgery, but I took the credit.

Rationalization

Clin Infect Dis. 2019 Jan 7;68(2):338-342. doi: 10.1093/cid/ciy559. Osteomyelitis Complicating Sacral Pressure Ulcers: Whether or Not to Treat With Antibiotic Therapy. https://www.ncbi.nlm.nih.gov/pubmed/29986022

J Clin Diagn Res. 2015 Dec; 9(12): DC19–DC21. \Non Diphtheritic Corynebacteria: An Emerging Nosocomial Pathogen in Skin and Soft Tissue Infection https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4717780/

Eur J Clin Microbiol Infect Dis. 2013 Jun;32(6):769-72. doi: 10.1007/s10096-012-1805-5. Epub 2012 Dec 28. Non-diphtheriae Corynebacterium species: an emerging respiratory pathogen. https://www.ncbi.nlm.nih.gov/pubmed/23271676

Old. Too Old?

Apr 3, 2019

It is only Wednesday. 4 times this week, a patient has commented, in one form or another, that I am an old doctor. Four times. And each patient was significantly older than my 427 in dog years. It must be the white beard, which I am keeping as I get senior discounts without asking. But with age comes the illusion of wisdom. Right? I’m not so sure.

The last month something I had worried about for years has occurred. H1N1 hit around the same time as the MRSA epidemic. It should have been a perfect storm for severe necrotizing S. aureus pneumonias, what with the propensity for MRSA to also carry the Panton-Valentine leukocidin and all. But I saw surprisingly few, at least as I remember it. It was a puzzle but not a disappointment. MRSA necrotizing pneumonia is a nasty illness.

This year? Several severe necrotizing post-influenza S. aureus pneumonias with abscesses and empyemas, with both MSSA and MRSA.

Bacterial pneumonia and Influenza go together like peanut butter and jelly,

Bacterial co/secondary infection of influenza infection appears to occur frequently. Studies have shown that up to 65% of laboratory-confirmed cases of influenza infection exhibited bacterial co/secondary infection, although Klein et al. (2016) state that in the majority of the research included in their meta-analysis, this figure ranged between 11 and 35%

Although it is Klebsiella that results in currant jelly sputum, something I have never had with peanut butter. Currant jelly. Not the sputum.

Influenza and S. aureus are synergistic in their pathogenicity and accelerate mortality in mice through a variety of mechanisms, the coolest of which is

Several strains of S. aureus produce proteases that cleave influenza HA; the more protease that is available, the more HA can be cleaved, meaning more vRNP can get into host cells meaning overall more progeny virions. This aspect contributes to the increased severity of disease caused by co-infection versus individual influenza infection.

So Influenza worsens S. aureus and S. aureus worsens Influenza. Great.

The best therapy for necrotizing S. aureus pneumonia with a thorax filled with dead lung and pus? Besides VATS? For MSSA, nafcillin. I no longer trust cefazolin when I don’t have absolute source control, especially when clindamycin resistant,

Resistances to clindamycin (OR 3.55, 95 % CI, 1.62-7.80) and erythromycin (OR 5.00, 95 % CI, 2.50-9.99) were associated with CIE positivity, presenting high specificity (92.9 %) and a negative predictive value (82.3 %). Which seems to be the case in my patients. Then the question is to add linezolid as well to mess with toxin production. I don’t know the answer to that question, although I am always attracted to inhibiting virulence factors.

For MRSA? Anything that does not rhyme with rankomicin. I look for any excuse not to give vancomycin, which most patients are on when I get consulted.

And here comes a statement that probably contains every cognitive bias known, but the patients always start to get better when I get them off the vancomycin. As I have said before, while there is no such thing as a strong, big gun, or powerful antibiotic, there are antibiotics that stink on ice, and its name is vancomycin. It has only one desirable characteristic: it is the only MRSA drug cheap enough that a SNF will accept the patient.

In severe infections, I am drawn to combination therapy, but a combination of what? Got me. The data is all over the map. As I winged about before, we really do not know the optimal antibiotic or antibiotics to treat MRSA, just lots of hints.

Age-related wisdom? Nope. I hope this flu season comes to an end soon. I really am too old for this… stuff. Yeah. Stuff.

Rationalization

Host Physiologic Changes Induced by Influenza A Virus Lead to Staphylococcus aureus Biofilm Dispersion and Transition from Asymptomatic Colonization to Invasive Disease https://mbio.asm.org/content/7/4/e01235-16

Secondary Bacterial Infections Associated with Influenza Pandemics https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5481322/

Severe Influenza and S. aureus pneumonia. For whom the bell tolls? https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3925697/

Staphylococcus aureus and Influenza A Virus: Partners in Coinfection https://mbio.asm.org/content/7/6/e02068-16

Characteristics of cefazolin inoculum effect-positive methicillin-susceptible staphylococcus aureus infection in a multicentre bacteraemia cohort. https://www.ncbi.nlm.nih.gov/pubmed/27714592

Poll Results

With age comes

• wisdom 2%
• confusion 14%
• incontinence 18%
• blithe indifference 39%
• frequently in error but never in doubt 25% Other Answers 2%
• bleu cheese.

  That Bug Does That? Of Course.

  Apr 8, 2019

In medicine, you play the odds. Common things are common. Commonly. More often than not, in my practice, uncommon things are common, because they usually do not call me for common things.

The patient has biliary cancer and an external drain in her biliary system for the last month.

She has fevers, chills, RUQ pain, and a palm-sized spreading erythema at the drain site.

His transaminases had taken a big jump, as had the WBC.

CT shows new dilation of the biliary system, and a new drain is placed, but the fluid is not sent for culture.

Bummer.

So it’s cholangitis and/or cellulitis. E. coli for the former, S. aureus or Streptococci for the latter.

But of course, that is not what grew in the blood. H. influenza, although I will likely retire by the time I get the typing back.

I rarely see H. influenza of any type (a,b,c,d,e f, and untypeable) and b has vanished thanks to the vaccine.

So does H. influenza cause cellulitis or cholangitis in adults? Of course. Any bug can cause an infection in any organ. There are easily 60 hits on the PubMeds for cellulitis in adults, not that I have ever seen a case.

Cholangitis not so much, a smattering of cases, may be less than a dozen.

The nice thing about most uncommon things is they can be killed even you don’t suspect them.

On ceftriaxone, the erythroderma subsided, and with the drain, the transaminases improved. And I saw yet another new manifestation of an old enemy.

Two Firsts in One

Apr 10, 2019

I do not keep up on vast swaths of medicine. I have enough trouble keeping up in ID; why worry about how to treat angina or how to evaluate lung cancer? I can’t remember yesterday, for crying out loud.

What I need to know about most of medicine is whether treatment/diagnosis is an infection risk or if it can mimic an infectious disease. But once I realize it does not fall in my bailiwick, I call someone else. I suppose I should say if it is not in my lane, the current meme, except I am a lousy driver, weaving all over the place as I am distracted by the scenery. Squirrel. Besides, life, the universe, and everything in my lane.

The patient is admitted to Outside Hospital after an injury that leads to back and groin pain. A T11 fracture was found, and this led to a T11 kyphoplasty. The details from both the patient and the I Don’t Care Anywhere module of EPIC are lacking. The former due to current medical issues and the latter due to the fact that the I Don’t Care Anywhere module of EPIC was coded by the Sirius Cybernetics Corporation, makers of the Nutri-Matic machine, and delivers a report that is almost, but not quite, entirely unlike useful.

Are kyphoplasty’s still a thing? I thought, along with cardiac stents and arthroscopic repairs of meniscal tears, there were no better than sham interventions. As the ever untrustworthy Cochrane review notes

We found high- to moderate-quality evidence that vertebroplasty has no important benefit in terms of pain, disability, quality of life or treatment success in the treatment of acute or subacute osteoporotic vertebral fractures in routine practice when compared with a sham procedure.

The patient leaves Outside Hospital and returns two weeks later with increasing shortness of breath and pleuritic chest pain. Oddly, she said she did not have midline back pain then or now.

CT shows an empyema and an osteomyelitis/phlegmon around T11. The literature suggests around 0.5% of kyphoplasties will get infected, usually with S. aureus, and is associated with a bad outcome:

This amounts to a mortality rate of 33.3% perioperatively. At the end of follow-up, two patients had unrestricted activities, and one patient required a walker. Of three paraparesis patients, two improved functionally and could walk unassisted and one improved but still used a wheelchair.

There is one hemothorax and one pneumothorax reported after kyphoplasty, but no empyemas. In the case of the hemothorax, the cause was when

In retrospect, it is possible to speculate on the moment of injury that caused the hemothorax. The slip of the trochanter while marching down the rib to the transverse process was the likely inciting event.

I have seen spine osteomyelitis result in empyema and vice versa, but which came first in this case I do not know and cannot tell with certainty from the history, but the pleuritic chest pain came first.

The cultures from the empyema grew a methicillin-susceptible Staphylococcus capitis, suggesting it entered with the procedure. I can find no cases of Staphylococcus capitis empyema either.

So two firsts ever, and you know the drill. Now when you see an empyema after a kyphoplasty, have S. capitis in your differential.

Not.

Rationalization

Vertebroplasty for treating spinal fractures due to osteoporosis https://www.cochrane.org/CD006349/MUSKEL\_vertebroplasty-treating-spinal-fractures-due-osteoporosis

Spine J. 2013 Dec;13(12):1809-17. doi: 10.1016/j.spinee.2013.05.053. Epub 2013 Jul 20. Infection after vertebroplasty or kyphoplasty. A series of nine cases and review of literature. https://www.ncbi.nlm.nih.gov/pubmed/23880354

BMJ Case Rep. 2017 Nov 8;2017. PII: bcr-2017-222019. doi: 10.1136/bcr-2017-222019. Spinal epidural empyema extending from a pleural empyema: case description and anatomical overview. https://www.ncbi.nlm.nih.gov/pubmed/29122901

Hemothorax after Kyphoplasty: A Case Report https://www.scitechnol.com/peer-review-pdfs/hemothorax-after-kyphoplasty-a-case-report-TzqS.pdf

Poll Results

I keep up in

• my specialty 18%
• all of medicine 5%
• NBA playoffs. Go Blazers 0%
• the Kardashian 0%
• nothing. I am behind in every aspect of life, the universe and everything. I still am trying for 41. 68% Other Answers 8%
• everybody’s field but my own.
• The Young and the Restless

  Do Not Treat?

  Apr 15, 2019

The patient, an elderly female, is admitted with shortness of breath and cough.

She has COPD/bronchiectasis for several years and has the occasional exacerbation.

Mostly the cultures have grown normal flora, but this time the sputum has a very resistant Stenotrophomonas maltophilia, and they consulted me about treatment. Inhaled aminoglycosides were being considered. That is a bit pricey for someone on a fixed income.

When I saw her two days after admission, she was already improving, with a minimal cough and a clear chest x-ray.

In talking to the patient, it turned out that, like so many of my patients, her house was supplied with untreated well water.

Stenotrophomonas maltophilia is often found in water systems and is associated with hospital outbreaks, both from drinking water.

An outbreak of S. maltophilia on ICU is described in order to highlight the risk from contaminated devices for supply of drinking water.

And from holy water.

I suspect her untreated well water was the source of the Stenotrophomonas maltophilia, and she was aerosolizing it every time she took a shower, colonizing her airway.

Treating the organisms in the sputum would likely cause cost and toxicity with no benefit as she would probably re-acquire the organism. Plus, I had the advantage of seeing her when she was well on her way to improving on antibiotics with no effect on Stenotrophomonas maltophilia.

Which is not to say that Stenotrophomonas maltophilia can’t be a pathogen in bronchiectasis but

Specific treatment for the S. maltophilia was given in 91/174 patients, however, treatment did not significantly affect resolution…It may act as a marker of disease severity.

And not the cause of disease.

Sometimes I think I am the only person who gets to ignore cultures. I did. And the patient did fine, although she was going to have her water system evaluated.

Rationalization

J Hosp Infect. 2013 Dec;85(4):303-7. doi: 10.1016/j.jhin.2013.09.007. Epub 2013 Oct 2. Outbreak of Stenotrophomonas maltophilia on an intensive care unit. https://www.ncbi.nlm.nih.gov/pubmed/24148363

Stenotrophomonas maltophilia infection in a bronchiectasis cohort https://thorax.bmj.com/content/71/Suppl\_3/A234.2

Poll Results

I ignore

• cultures 11%
• cell phone calls from the IRS 41%
• my significant other. It’s why I am - single 0%
• the voices in my head 39%
• the advice of others 4% Other Answers 4%
• anything that might conceivably make me happier or more successful.
• anything Trump says

  Blind spot

  Apr 17, 2019

If you read this blog regularly, you might come to the erroneous conclusion about my skill set as a physician. Most of the cases that I write about are diagnostic and therapeutic successes, and so create a false image of my abilities. I occasionally get a self-referral from a patient who has been impressed by my blogs and podcasts and thinks I will be the one to find the solution to their particular diagnostic or therapeutic dilemma.

Nope. Safe to say, I have always been a disappointment. If you are a potential patient reading this, remember what Gag Halfrunt said of another: Well look, Crislip’s just zis guy, ya know?

I do have my flaws and blind spots, and while I try to be aware of them, there is a reason they are called BLIND spots.

Judging from some reviews on the internet, one would be arrogance: “an attitude of superiority manifested in an overbearing manner or in presumptuous claims or assumptions.” As best I can gather, those reviews are from those who are dissatisfied that I prefer my assessment over theirs as to the validity of their Lyme or Morgellons.

I do have a consistent blind spot in my skill set, one I can think of examples going back to my internship. I do not think about starting therapy until I have a diagnosis well and truly in hand. I wonder if anyone is as averse to empiric therapy as me.

I have yet to kill anyone with that approach, but I have certainly added some unneeded morbidity to patient care over the years. The worst example was early in my practice when I saw a patient who I thought had severe adrenal insufficiency. So I ordered the cortisol and ACTH stimulation test but did not order the replacement hydrocortisone, and that night the patient crumped from adrenal crisis. She eventually did fine, but still. I should have given the cortisone.

Sometimes you need to treat before you have the diagnosis. So I have told myself for 35 years. But I do not always listen.

The patient is an elderly male, on biologics, who develops abdominal pain and distension. He was previously healthy and, prior to the start of the biologics, was Quantiferon negative.

A CT shows abdominal lymph nodes and some ascites with what looks to be peritoneal studding.

Laparoscopic biopsy? Caseating granulomas. That means TB. Right? Yep. And he had spent significant time in his youth in rural S. America doing missionary work.

But. Another Quantiferon is negative. And the special stains are negative. And the cultures are negative. And the 16 S ribosome is negative. If it is TB, I can’t find it.

I know. All these have a significant false-positive rate. But if there were TB after two years of biologics, he should be sick. He isn’t. And I have seen many a case of TB that didn’t get needed therapy. So I kept looking for another reason. As the old saying goes, All that is gold does not glitter, Not all those who wander are lost; Not all caseating granulomas are TB.

But. No fungi. No parasites. There are a lot of reasons for caseating granulomas, and I looked for them all. Nothing.

As I was waiting for the TNTC tests to return, the patient saw his rheumatologist, who sent him to another ID doc. The effrontery. And the other ID doc looked at everything I did and did the obvious: started TB meds.

And you know. That is the right thing to do. Possible TB and biologics? Treat pending test results.

My blind spot again. No harm to the patient, however, who was clinically stable.

TB or not TB? That is still the question. I am still not convinced.

But some processes deserve empiric therapy. Like Addison’s. And tuberculous peritonitis on biologics.

Rationalization

Gag Halfrunt https://alienencyclopedia.fandom.com/wiki/Gag\_Halfrunt Poll Results

My medical weakness is

• I wait for a diagnosis before treating 21%
• false modesty 9%
• none. I am a very stable genius. Anyone who says otherwise is fake news 27%
• not considering a diagnosis outside my specialty 21%
• I believe everything I read on the web 15% Other Answers 6%
• skepticism
• inertia.

  Joint Infection

  Apr 30, 2019

Been gone for a week, exploring Atlanta and Savanah. Great places to visit for a number of reasons, but I will note it is the first state I have visited where they make beer as good as here in the great Pacific Northwest. Combine that with the food, history, architecture, beaches, forests of oak with Spanish moss, and huge stinking gators, and you have everything need for a great trip.

It is nice to be home, although I will also note it is remarkable just what a filthy garbage-laden city PDX has become. It is always striking how clean other cities are compared to the City That Doesn’t Work. You can even see it from the air as you land, the city littered in both senses of the word with homeless camps.

But back to bugs.

The patient, a young female, had a baby ten days prior to admission. It was complicated by Group B Streptococcal colonization and some iv ceftriaxone.

Two days before admission, she has a progressively red, hot, swollen, and painful knee.

She is seen in the ER and admitted for a septic joint, with a WBC count of 80,000 in the joint fluid. It is washed out in the OR, and the next morning they call me.

The gram stain is negative.

She tells me that the OB doc told her the placenta was abnormal, and this is confirmed by pathology that shows inflammation/infection, but it had not been sent for culture. Her baby is doing just fine.

So how to put it all together? I figured it was a late Group B streptococcal infection of the knee. S. aureus, at least, should have been seen on the gram stain. No risks for a gram-negative, which, like streptococci, may not be seen on a gram stain.

So I kept the ceftriaxone going and waited for both the cultures to turn positive and the patient to improve. Neither of which happened.

The cultures remained negative, and the knee worsened.

Now what? What am I missing?

Because the joint is worse, I suggest the joint needs debrided again. But what is it? What can seed a joint from a delivery complicated by an infected placenta that is neither seen nor grown?

Mycoplasma and Ureaplasma?

And Google says?

One case of M. hominis in pregnancy; none with Ureaplasma. But both organisms do cause septic arthritis in those with hypogammaglobulinemia.

So immunoglobulins are ordered. I have them get me some tissue to send for 16S looking for M. hominis, change the antibiotics to doxycycline, and wait.

The immunoglobulins came back normal, but right at the lower end of normal. So close?

After a week, the 16S comes back positive for M. hominis and the joint is slowly making progress.

I just wish these molecular methods were more easily accessible and less expensive. Some day.

Rationalization

A case of Mycoplasma hominis septic arthritis postpartum. https://www.sciencedirect.com/science/article/abs/pii/S0163445307007372

Mycoplasmas and ureaplasmas in patients with hypogammaglobulinaemia and their role in arthritis: microbiological observations over twenty years. https://ard.bmj.com/content/53/3/183.short

A Question Without an Answer

May 2, 2019

I occasionally get asked to clear a patient with an infection so they can have a procedure. Of course, I can’t really do it. No one can. But I can kibbitz with the best of them.

The patient needs a pacemaker. He also has a permanent foley and a urine that has sequentially had E.coli, then Enterococcus and now Pseudomonas following various antibiotics, all this admission.

Cardiology wants a sterile urine before placing a pacemaker. I suggest while there is no specific data re: pacer placement, there is the following to consider:

1) his urine, being connected to the outside world, will never be sterile. 1) non-pathogenic/asymptomatic bacteria like the E. coli, protect against more pathogenic/symptomatic bacteria. 1) treating non-pathogenic/asymptomatic bacteria like the E. coli INCREASES the symptomatic UTI infection rate. 1) in hip surgery

We identified no case of PJI from a urinary origin in patients with asymptomatic bacteriuria whether or not they had been treated with specific antibiotics.

and in thoracic surgery

The presence of bacteriuria is not a risk factor for presenting SSI in cardiovascular surgery.

and in general surgery

The findings of this study suggest that receipt of antimicrobial therapy with activity against ASB organisms identified in preoperative urine cultures was not associated with reductions in the risk for postoperative infections, including UTI and SSI;

The organism in the urine never shows up in the wound infection. It is why we no longer get pre-op urine cultures. I hope.

5) Enterobacteriaceae are not the worry; it is Pseudomonas or Serratia,

Multivariable logistic regression analysis revealed that 3 bacterial species were associated with an increased risk for CDRI: Staphylococcus aureus, Pseudomonas aeruginosa, and Serratia marcescens.

These organisms are not generally found in the bladder, but now there are in his urine primarily due to the long-term use of likely unneeded antibiotics. But chasing the Pseudomonas and will only worsen the problem.

6) waiting to place the pacemaker to treat a UTI can lead to more harm than good:

The patients awaited acute PPM implantations for a mean of 4.5 days because of capacity problems. Overall, 83 patients (32.0%) experienced at least one adverse event during the waiting period. The present study indicates that a waiting period is dangerous as it is associated with an increased risk of adverse events.

7) ciprofloxacin is likely causing only harm without benefit, given the toxicities and side effects of C. difficile, tendinopathy, qt interval prolongation, renal failure, retinal detachment, aaa rupture, and altered mental status.

Ciprofloxacin is also a significant risk for getting MRSA, and that is the organism one should worry about the most as the new acquisition of MRSA markedly increases the risk of invasive disease:

…the risk of MRSA bacteremia is 19.89-fold higher among colonized than noncolonized patients.

Which really puts the pacermaker at risk.

That was all the relevant information I am aware of/can find. My take? Don’t test. Don’t treat. Don’t wait.

The only case I could find relating a pacemaker and a UTI was

Following pacemaker implantation, a 71-year-old female developed infection of the generator pocket. Five years after relocation posterior to the rectus muscle she suffered from cystitis. Cystoscopy revealed the pacemaker generator to be lying within the urinary bladder. Healing was achieved by removing the pacemaker and reutilizing it, after sterilization, in a new pectoral pocket.

Your interpretation of the available evidence may differ.

Rationalization

Clin 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://www.ncbi.nlm.nih.gov/pubmed/23430723

Am J Infect Control. 2018 Feb;46(2):180-185. doi: 10.1016/j.ajic.2017.08.015. Epub 2017 Sep 22. Bacteriuria is not associated with surgical site infection in patients undergoing cardiovascular surgery. https://www.ncbi.nlm.nih.gov/pubmed/28947210

JAMA Surg. 2018 Dec 12. doi: 10.1001/jamasurg.2018.4759. [Epub ahead of print] Association of Screening and Treatment for Preoperative Asymptomatic Bacteriuria With Postoperative Outcomes Among US Veterans. https://www.ncbi.nlm.nih.gov/pubmed/30540346

Open Forum Infect Dis. 2017 Jun 21;4(3):ofx132. doi: 10.1093/ofid/ofx132. eCollection 2017 Summer. The Risk of Cardiac Device-Related Infection in Bacteremic Patients Is Species Specific: Results of a 12-Year Prospective Cohort. https://www.ncbi.nlm.nih.gov/pubmed/28852678

Europace. 2012 Jul;14(7):975-80. doi: 10.1093/europace/eus016. Epub 2012 Feb 14. Waiting for a pacemaker: is it dangerous? https://www.ncbi.nlm.nih.gov/pubmed/22333242

Am J Infect Control. 2016 Apr 1;44(4):405-8. doi: 10.1016/j.ajic.2015.11.006. Risk and outcomes of methicillin-resistant Staphylococcus aureus (MRSA) bacteremia among patients admitted with and without MRSA nares colonization. https://www.ncbi.nlm.nih.gov/pubmed/27038392

Pacing Clin Electrophysiol. 1990 Jun;13(6):703-4. Unusual cause of dysuria: migration of a pacemaker generator into the urinary bladder. https://www.ncbi.nlm.nih.gov/pubmed/1695347

Is it or isn’t it? Only my microbiologist knows for sure

May 6, 2019

It still annoys me how specific memories are so vivid and other, more important pieces of information, evaporate like glaciers. Youngsters will likely have no clue what the title refers to, but commercials from the days of five television stations have lodged deep in my brain. LSMFT anyone? Yeah, we had five channels. Black and white only. No remote. But at least we had Perry Mason reruns on KPTV, every day at noon, for 48 years. Then KPTV became Fox, and Perry Mason was canceled. ’nuff said.

The patient presented with S. aureus bacteremia and an epidural abscess. It was MSSA. Then, five days later, he required another I&D of the abscess, and this one grew MRSA. I was off at the time, so the patient was changed to vancomycin. No one appeared to ask why the discordant cultures.

I got back from vacation and called the lab. Where, I asked, did that MRSA come from?

Microbiology used to be in the hospital’s basement, and when I started practice back when Perry made ground beef of Hamilton Burger, I started the day in micro, looking at cultures and talking with the techs. Then microbiology consolidated to the hospital across the river. I could still stick my head in from time to time to ask a question and learn a bit of micro. Then it moved into great digs at a new location in the city, and I will likely never smell agar again. One local hospital sends all their micro to the Eugene campus, 90 miles away. That’s just stupid.

I mention this as microbiology has become even more of a black box as the technologies change, and I am not always up to snuff. This all may be old hat to you, but a big part of what drives this blog is when I learn something new, I blog about it.

I thought MRSA was called based on the presence of the mec gene. Well, yes and no. They run the test for the mec gene on blood specimens.

But for tissue samples? Nope. They run a VITEK card, and if the S. aureus is cefoxitin resistant, a surrogate for MRSA; it is called MRSA.

What the? But it is old hat:

Using cefoxitin and NCCLS criteria for disc diffusion, the sensitivity and specificity for recognizing methicillin resistance were both 100%. Similar results were obtained when the strains were tested by the agar dilution method. The cefoxitin MICs for methicillin-susceptible strains were < or = 4 mg/L.

and

Cefoxitin will detect only MRSA with a mecA-mediated resistance mechanism…However, non-mecA-mediated methicillin resistance in S. aureus is a rare occurrence.

And is better than oxacillin disc testing.

But then nothing is ever 100%. And it all gets down to those pesky breakpoints. The VITEK errs on the side of calling MRSA when it is right around the breakpoint. And we all know how fuzzy those breakpoints can be.

It is an interesting question. Pending other studies, is it better to call a borderline test MRSA when it is MSSA? Is it better for patients to then get an antibiotic inferior to a beta-lactam? I don’t know.

Then, two days later, a different patient. MSSA/mecA negative on the blood, but the outpatient joint fluid was called MRSA, again based on the cefoxitin result on the VITEK card. And again, a borderline result right at the cutoff.

In both cases, it was MSSA, the MRSA a ‘false positive’.

Looking at the web, this is not the first time such a problem has occurred:

BioMerieux is recalling the VITEK 2 Gram-Positive Cefoxitin Screen and VITEK 2 Gram-Positive AST for Oxacillin because of false negative or false susceptible, respectively, results for some strains of MRSA.

Is it or isn’t it? Antibiotic susceptibility and resistance of bacteria are slippery characteristics, often not as clear-cut as we like. Not even the microbiologist knows for sure.

For now, the lab is testing for mecA on all S. aureus called MRSA by cefoxitin and looking into the issue deeper.

I do now wonder how many so-called MRSA from wounds weren’t, but I suspect no harm was done.

Rationalization

[Case closed: After 48 years, ’Perry Mason reruns end on Portland TV station] (https://www.oregonlive.com/movies/2014/09/case\_closed\_after\_48\_years\_per.html)

J Antimicrob Chemother. 2005 Apr;55(4):506-10. Epub 2005 Mar 2. Cefoxitin resistance as a surrogate marker for the detection of methicillin-resistant Staphylococcus aureus. https://www.ncbi.nlm.nih.gov/pubmed/15743899

Comparison of Cefoxitin and Oxacillin Disk Diffusion Methods for Detection of mecA-Mediated Resistance in Staphylococcus aureus in a Large-Scale Study https://jcm.asm.org/content/47/1/217

[BioMerieux Recalls VITEK 2 Gram-Positive Antimicrobial Susceptibility Testing (AST) Cards Due to False Results for some strains of methicillin-resistant Staphylococcus aureus (MRSA)] (https://www.fda.gov/medical-devices/medical-device-recalls/biomerieux-recalls-vitek-2-gram-positive-antimicrobial-susceptibility-testing-ast-cards-due-false)

Poll Results

I clearly remember

• all the pop song lyrics of my youth. ’Scuse me while I kiss this guy 31%
• all my failures 23%
• how much better it was back in the day, when men were real men, women were real women, and small furry creatures from alpha centuri were real small furry creatures from alpha centuri 15%
• virtually nothing but make up for - it with google. when I want not to remember I use Bing 31%
• the three case Perry Mason lost 0%

  One is all you get

  May 14, 2019

Life has been busy of late. Not my ID life; that remains much the same. Me find bug, me kill bug, me go home. My other life. Lots of fun things going on as the weather finally gets out of the Pacific NW drearies.

Go Blazers.

And that leaves little time for blogging. I came across An Ode to Being Old in my feeds that suggests wisdom compensates for declining physiologic and mental fitness. Maybe. But I have nowhere near the concentration or stamina I did back in the day and fade earlier in the day when I used to.

So one quick entry, an observation that may or may not be true, but hey, I got that old wisdom, right? Then life will keep me occupied until next week.

The patient is an elderly male who, six weeks ago, had a single rigor, then a fever, then a sweat. Then he just started to fade. Over the next month and a half, his get up and go got up and went as his usually vigorous existence dwindled to sleeping most of the day and weight loss. He never had another fever or rigor, although he did have the occasional night sweat.

He saw his doctor several times, but no diagnosis was initially made.

Then blood cultures were obtained, and they all grew S. mitis. Further evaluation confirmed the diagnosis of mitral valve endocarditis: murmur, emboli, and a vegetation on the valve.

On antibiotics, he returned to his normal self.

We all know that many patients with endocarditis do not have a fever. Euthermic endocarditis occurs from 3 to 50% of the time, depending on the study.

…first study that focuses on patients with euthermic endocarditis. Compared to febrile controls (unadjusted for other variables), euthermic patients were older and had longer symptom duration prior to IE diagnosis, and had a higher rate of valve surgery (although this result did not remain significant when controlling for group differences). Differences in survival rates at both 28-days and 365-days were not statistically significant between the two groups, either unadjusted or adjusted for baseline differences. Antipyretic use was uncommon among the euthermic patients and suggests that host-pathogen interactions are likely operative in the lack of production of fever in these patients…

But here is my observation, which may or may not be valid. But I think it is, just like Crislip’s Sign.

Patients with euthermic, viridans strep, endocarditis, if questioned carefully, often have a single rigor/fever/sweat that marks the onset of their disease. One fever, and that’s it. I have seen it many times, or so I remember.

If such a clinical observation has been noted in the literature, it is not googleable.

That’s my story, and I’m sticking to it. Now someone prove it for me.

Back to life, see you next week.

Go Blazers.

Rationalization

An Ode to Being Old https://getpocket.com/explore/item/an-ode-to-being-old

Crislip’s Sign http://boards.medscape.com/forums/?128@@.2a32c105!comment=1

Euthermic Endocarditis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3823819/

Poll Results

With age comes

• wisdom 11%
• self-delusions 21%
• incontinence 25%
• a Blazer championship 4%
• existential angst 29% Other Answers 11%
• pain
• self-delusions and incontinence
• Grandchildren. Neener, neener!

  It Appears to Be Working. But I am not happy.

  May 20, 2019

What is it about sepsis lately? Patients and their families keep asking me if the patient is septic or had sepsis, often followed by the follow-up question, just what is sepsis?

By the time I see the patient, the sepsis, if it was present, has long since resolved, but they are still worried about sepsis. I haven’t a clue where this sudden interest in sepsis comes from.

The patient presented with sepsis 8 months ago. He has a renal transplant that has been working well for the last 5 years but has an ESBL K. pneumoniae in his blood and urine and mild MOSF.

If you are going to become septic, be a transplant patient. You might have increased odds of sepsis but a decreased odds of death:

The 28-day and 90-day mortality were significantly decreased for transplant recipients compared with nontransplant patients. These findings suggest that the immunosuppression associated with transplantation may provide a survival advantage to transplant recipients with sepsis through modulation of the inflammatory response.

A good trade-off.

The K. pneumoniae is not susceptible to any oral agents, so he gets a 14-day course of cefepime.

The K. pneumoniae comes back.

CT shows no abscess.

He gets 14 days of a carbapenem.

The K. pneumoniae comes back.

He has some prostatic enlargement with mild obstruction. It is fixed.

The K. pneumoniae comes back.

I cross my fingers and try a course of fosfomycin.

The K. pneumoniae comes back after fosfomycin.

I try a 6-week course of a carbapenem.

The K. pneumoniae comes back.

And symptomatic each time: pain, frequency, fevers, hypotension, altered mental status. It is not just positive cultures. He is sick, and a couple of his relapses led to admission.

Repeat studies for a source to control are negative.

What to do? Bankrupt him with the newer CRE drugs? Stool transplant?

Fecal microbiota transplantation led to resolution of recurrent Clostridium difficile, significantly decreased recurrent UTI frequency, and improved antibiotic susceptibility profile of UTI-causing organisms.

But GI told me it could only be done for C. difficile.

One last idea: ampicillin/clavulanate plus a po cephalosporin, in this case, cefdinir.

This case series shows that the synergistic combination of ceftibuten plus amoxicillin-clavulanic acid may be an option for oral treatment of UTIs caused by ESBL producing E. coli or K. pneumoniae.

And it worked. No symptomatic infection and sterile urine for going on 2 years.

Of course, I am not happy with the idea of chronic suppression, especially with this combination, but neither he nor I are interested in seeing what happens with stopping the antibiotics. He, and I, have had enough with sepsis.

Rationalization

Clin Infect Dis. 2015 Jan 15;60(2):216-22. doi: 10.1093/cid/ciu789. Epub 2014 Oct 9. Is bacteremic sepsis associated with higher mortality in transplant recipients than in nontransplant patients? A matched case-control propensity-adjusted study. https://www.ncbi.nlm.nih.gov/pubmed/25301215

Clin Infect Dis. 2017 Oct 30;65(10):1745-1747. doi: 10.1093/cid/cix618. Fecal Microbiota Transplantation for Recurrent Clostridium difficile Infection Reduces Recurrent Urinary Tract Infection Frequency. https://www.ncbi.nlm.nih.gov/pubmed/29020210

Eur J Clin Microbiol Infect Dis. 2018 Oct;37(10):2021-2025. doi: 10.1007/s10096-018-3338-z. Epub 2018 Aug 16. Ceftibuten plus amoxicillin-clavulanic acid for oral treatment of urinary tract infections with ESBL producing E. coli and K. pneumoniae: a retrospective observational case series. https://www.ncbi.nlm.nih.gov/pubmed/30117050

POLL RESULTS

My patients have an odd interest in

• sepsis 24%
• measles 16%
• ebola 16%
• plague 28%
• influenza 8% Other Answers 8%
• not dying, and not being bankrupted by the medical care required to save their lives.
• germs

  Can’t Get It Done

  May 22, 2019

“A foolish consistency is the hobgoblin of little minds, adored by little statesmen and philosophers and referral laboratories.” ~ Ralph Waldo Emmerson

The patient now has three admissions for ESBL E. coli bacteremia. Each episode is about three months apart. For each episode, he received a course of iv antibiotics. Evaluation shows no specific reason, but the abdomen and liver are filled with cancer for which he is getting chemotherapy every three weeks. Biliary or gi translocation is a reasonable source, but there is nothing on the scans that can be called abscess to be drained. But there is so much pathology, who can say.

The organism is resistant to all oral agents. Or is it? My goal is to keep him out of the hospital and maximize his quality of life, and one of these many liver lesions could be an infection.

I am disinclined to give an extended course of antibiotics iv, but I wondered about fosfomycin. In the US, we only use fosfomycin for cystitis.

In Europe, fosfomycin is used for more prolonged periods for more serious infections, and I have given the drug for six weeks and cured a few cases of chronic prostatitis.

I remember as a fellow overhearing a drug rep tell an attending that an antibiotic was popular in Europe. His reply: So was Hitler.

I think of that every time I justify the use of an antibiotic based on European experience. But it should work:

The average concentration in pus was calculated to be 182 ± 64 mg/liter at steady state, exceeding the MIC50/90s of several bacterial species which are commonly involved in abscess formation, such as streptococci, staphylococci, and Escherichia coli. Hereby, the exceptionally long mean half-life of fosfomycin of 32 ± 39 h in abscess fluid may favor its antimicrobial effect because fosfomycin exerts time-dependent killing.

Although that was for 8 gm iv tid, fosfomycin has been used for a hodgepodge of serious infections alone and in combination with reasonable results.

But I want to know if the E. coli is sensitive. Our lab can’t do it. We don’t have the supplies; it’s a send-out.

And the reference lab, a really unhelpful place, won’t do it on any specimen except urine. Why? Because there are no interpretive standards.

Often in ID you have to be creative. You want data, however uncertain, to help guide therapy. If there is no zone of inhibition with a Kirby-Bauer disc, I doubt the antibiotic will work. If the MIC is low relative to the probable levels, maybe the antibiotic is worth a shot. I have been dealing with those uncertainties for years. Odd bugs, odd resistance patterns, no standards. As Donald Rumsfeld noted, ‘You go to war with the army you have, not the army you might want or wish to have at a later time.’

You make do.

But my reference lab will not do susceptibilities. Period. End of story. My pleas and rationale fell on deaf ears. Well, they heard me. They just preferred following the regulations.

This is a pattern in medicine that is gradually getting worse: complete inflexibility in the face of unusual circumstances. Want to attempt a diagnosis or treatment that falls outside the regulations because you have an unusual case? Forget about it. No one will help. And as we slide into the post-antibiotic era, this kind of dilemma will only become more common. Unfortunately, MRDO are not on the list of the million species expected to go extinct soon. Like so many other areas looking into the future, we are so screwed.

Sigh.

So what is the least bad option?

A long course of IV? With a bankrupting copay?

A short course of iv and see if we get E. coli bacteremia number four, with all the morbidity, not to mention spending another 5 days of limited remaining life in the hospital?

Or, knowing the odds are that the organism is susceptible

Fosfomycin resistance in Escherichia coli is rare in the United States. An extended-spectrum ²-lactamaseproducing 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.

Go with fosfomycin and see what happens? Assuming, of course, I can get it approved for a non-UTI? Probably another bureaucracy to obstruct patient care.

Double sigh.

Rationalization

Antibiotic Abscess Penetration: Fosfomycin Levels Measured in Pus and Simulated Concentration-Time Profiles https://aac.asm.org/content/49/11/4448

Antibiotic time-lag combination therapy with fosfomycin for postoperative intra-abdominal abscesses. https://www.ncbi.nlm.nih.gov/pubmed/21127935

The revival of fosfomycin https://www.ijidonline.com/article/S1201-9712(11)00166-4/fulltext

Fosfomycin Resistance in Escherichia coli, Pennsylvania, USA https://wwwnc.cdc.gov/eid/article/21/11/15-0750\_article

POLL RESULTS

The future holds

• increased inflexibility 19%
• more MRDO, fewer treatments 26%
• A Mad Max world from food insecurity and - sea level rise 32%
• more walls 3%
• faster internet. as long as I have that, who cares? 13% Other Answers 6%
• Let’s hope for a balance of forces. - After all, so much ID common sense here, like many other good things, had to derive from something positive.
• its breath, waiting for us to arrive and screw it up.

  History Always Repeats

  May 29, 2019

The patient is one of many IVDA I have seen in my years with aortic valve MRSA endocarditis.

What separates her from so many patients with endocarditis is how long she has had the disease. Months now, mostly off therapy.

She comes in, stays two or three days on vancomycin, then disappears in the middle of the night for a week or so, only to return to repeat the process.

And each time, the disease has advanced a little. The aortic valve is a little more incompetent, now a renal infarct, then a few small liver abscesses, now a painful tenosynovitis in the foot.

The MRSA spreads and destroys, slowly and surely.

She gets just enough vancomycin each time to beat down the MRSA, just enough to keep going.

I will not go into all the attempts at interventions to reverse this inexorable infection and the underlying personality/psychiatric issues on top of her heroin addiction that has made optimal care impossible. Suffice to say, she has routinely fired her caregivers, including me. Me! And it has been determined she is competent.

I have always practiced ID in the antibiotic era, and despite increasing antibiotic resistance, I have never not had an option for endocarditis therapy.

I never really thought I would get to watch as a patient succumbed to the natural history of what should be a curable illness, but the current opiate epidemic has given me opportunities I would just as soon have avoided.

I suspect the intermittent vancomycin has converted the MRSA infection from its usually acute presentation to that of a subacute bacterial endocarditis. And, sadly, the patient is another to follow in the steps of Alfred S Reinhart.

For those who are unaware,

Harvard medical student Alfred S. Reinhart had an unusual ability for self-observation combined with a gift for a vivid and picturesque turn of phrase. His observations of SBE, noted in the journal that he kept until 2 days before his death from this disease at the age of 24

from S. viridans aortic valve endocarditis.

For seven months in 1931,

SBE gradually revealed itself to Reinhart and, eventually, to his sceptical physicians. Although vascular and perivascular invasion of the left middle cerebral artery produced most of the manifestations that he experienced in the last days of his life, he actually died of aortic valve destruction, heart failure and pulmonary edema.

And he saw the bullet coming with more style and grace than I am capable of:

At any rate, at approximately one-quarter to twelve that night, I remember distinctly getting up from my chair and from the table, where my books lay, and taking off my suit coat. No sooner had I removed the left arm of my coat, than there was on the ventral aspect of my left wrist a sight which I shall never forget until I die. There greeted my eyes about fifteen or twenty bright red, slightly raised, hemorrhagic spots about 1 millimeter in diameter which did not fade on pressure and which stood defiant as if they were challenging the very gods of Olympus. … I took one glance at the pretty little collection of spots and turned to my sister-in-law, who was standing nearby, and calmly said: ‘I shall be dead within six months.

and

He all but said that it was positive for streptococcus viridans. Here was the last link in the chain. I had previously had inculcated into me the fact that I was going to die within a comparatively short period of time, but I could always find a leeway out. I could always find a loophole in the evidence here and there howsoever untenable I knew these loopholes to be, but now I was confronted with the dictum ultimatum* from which there was no escape. I do not exactly recall my reaction to this message from the Angel of Death, although as I remember it, I showed no emotional change whatsoever.*

I know what the natural course of SBE was in the past: progressive valve destruction, recurrent emboli, pain, and death.

For my patient, no loopholes; a different form of the dictum ultimatum from which there is no escape.

Plus ça change, plus c’est la même chose.

Sigh.

Rationalization

CMAJ. 2002 Dec 10; 167(12): 1379–1383. Subacute bacterial endocarditis observed: the illness of Alfred S. Reinhart. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC137358/

Oddity

May 30, 2019

HealthNet was kind enough to deny benefits/coverage to one of my patients. That is a common enough occurrence from all insurance companies. But what was impressive they wanted to make sure the patient knew, no matter what the language she spoke, that coverage was denied. 30 different languages. You a French Creole enjoying a bowl of gumbo? Rest assured, you will be denied in your native tongue. And in Punjabi, Navaho, and Tagalog. Even Cushite. I didn’t even know there was Cushite. But rest assured, you will be denied coverage in your own language. I really do admire their commitment to diversity in denial.

Next, I suppose, will be Dothraki and Klingon, so even fictional people can have their coverage denied. Klingon would probably be particularly harsh and appropriate, like the original Hamlet, and probably more in the spirit of denying benefits. If you are going to help bankrupt people, do it in Klingon: Tem bul medical coverage. LaH appeal SoH qaStaHvIS Hembogh DujDaj personal chenmoH Duy.

The patient comes in with lightheadedness and a week of progressive pain in the RLQ.

An unenhanced (age and vascular disease have left him with few nephrons) CT is read as likely hematoma/bleed. Not unreasonable. He is on apixaban, and his hemoglobin has dropped. No other cause or risk is evident from the history.

And over time, the pain spreads down and into his thigh, turning red, hot, and tender.

The patient never has a fever or a leukocytosis, but due to pain, the fluid in the thigh is sampled/decompressed. And it grows MSSA. So we drained the pelvic collection (they were connected), and it looked like blood, not abscess, and it also grew MSSA. I went over the CTs with a fine-tooth comb: no reason for this, including an infected ruptured aneurysm. Or nits.

I also could not find a reason for the infection. Nothing. So I suppose this is a spontaneous pelvic hematoma from the apixaban that immediately became secondarily infected with MSSA. There are zero cases in either the PubMeds or the Googles.

Or an MSSA infection that led to a spontaneous bleed? Seems even more of a stretch.

For now, it is drain the pus and antibiotics, and I expect an eventual cure.

But odd. And odd is unsatisfying without a good just-so.

From the comments

Cushite is the language spoken in the ancient Kingdom of Kush, modern day Sudan. The most impressive fact in this story is they found a translator capable of writing insurance content. Most speakers of Cushitic languages are illiterate and the language itself would not even have the word insurance in it.

Rationalization

The Klingon Hamlet https://en.wikipedia.org/wiki/The\_Klingon\_Hamlet

Transl Med UniSa. 2014 Sep-Dec; 10: 1317. Published online 2014 Apr 8. Spontaneous muscle haematomas: management of 10 cases https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4140424/

Oncol Rep. 1999 Jan-Feb;6(1):189-91. Spontaneous pelvic hematoma simulating neoplasm: case report and literature review. https://www.ncbi.nlm.nih.gov/pubmed/9864426

J Manag Care Spec Pharm. 2017 Sep;23(9):968-978. doi: 10.18553/jmcp.2017.23.9.968. Major Bleeding Risk During Anticoagulation with Warfarin, Dabigatran, Apixaban, or Rivaroxaban in Patients with Nonvalvular Atrial Fibrillation https://www.ncbi.nlm.nih.gov/pubmed/28854073

Just-so story https://en.wikipedia.org/wiki/Just-so\_story

POLL RESULTS

I want to be denied in

• my native language 0%
• English 5%
• Klingon 10%
• emoji’s 14% a simple middle finger will suffice 69% Other Answers 2%
• clear and distinct terms, with no grammar or spelling errors, thank you.

  Imaginary Beasts and Where Not To Find Them

  Jun 4, 2019

Call weekends make me….. grumpy. It is because I see the practice of ID that is so…….. suboptimal. A nice word, suboptimal.

It reminds me of a question I have asked before: what would happen if we practiced oncology like infectious diseases?

No oncology consult. No biopsy for diagnosis. Chemotherapy given based on fear, uncertainty, and doubt, changed on the whim of whoever was on.

A couple of consults were for abscesses that were not getting better on antibiotics. While drained, no one thought the pus needed to be sent for culture and sensitivity or even a gram stain. Think of the response if we treated tumors similarly; a mass removed but not sent for pathology, then chemo started.

But what gets me the most is not giving optimal therapy for the diagnosed infection but instead treating infections that are not there and have no reason to be there.

As examples.

The patient had MSSA endocarditis with septic pulmonary emboli. Textbook. Vegetation, positive blood cultures, not the whole 9 yards. It was the whole ten yards. So the patient is placed on nafcillin, and after three days, the fevers persist.

Well duh. Infections take time to respond to antibiotics, and, as I like to remind people, antibiotics are not antipyretics. Give acetaminophen if you want to treat a fever.

But no, the night float is called about the fever and, for reasons known only to her, decides that maybe what the patient really has is pneumonia due to gram-negative rods or MRSA.

So optimal therapy, nafcillin, is stopped, and cefepime and vancomycin are started. That covers the MSSA as well, right?

In the morning, I asked why? And why was I not called instead of making such a….suboptimal decision?

No good answers.

The other patient had K. pneumoniae in the blood and in lung abscesses. Probably a hypervirulent hyperviscous strain talking to the lab.

A virulent organism, it was resistant only to ampicillin.

Mind you, they had the bug in their hand, metaphorically speaking, yet the patient was sent home on ampicillin/clavulanate because of the worry about anaerobes in the lung abscesses. No real reason to worry about anaerobes that I could find; another imaginary beast to be killed.

I assume that levels of clavulanic acid in the periplasmic space (gram-negative bacteria put beta-lactamases into the periplasmic space between the cytoplasmic membrane and the outer membrane, where the cell wall is located) are negligible. Drug going from gut to blood to pus to periplasmic space, with a drop off of antibiotic concentration at each step.

Although of the beta-lactamase inhibitors, clavulanic acid may be best at getting to its active site.

It was shown that clavulanic acid penetrated the outer membranes of all these strains more readily than the other β‐lactamase inhibitors. For the strains of E. coli and K. pneumoniae clavulanic acid penetrated approximately 6 to 19 times more effectively than tazobactam, 2 to 9 times more effectively than sulbactam and 4 to 25 times more effectively than BRL 42715.

And after finishing the ampicillin/clavulanate, she returns with progression the K. pneumoniae abscesses.

It is as if you know the patient has lung cancer but are going to treat for lymphoma and hope the chemo also takes care of the lung cancer as well.

Who does that?

Too many. So much… suboptimal medicine due to fear, uncertainty, and doubt worrying about imaginary beasts while the grizzly walks right up and eats you.

Word to the wise from the grumpy old fart: Get cultures. And when you have the bug isolated, kill it.

Rationalization

Clin Microbiol Rev. 2010 Jan; 23(1): 160–201. doi: 10.1128/CMR.00037-09 Three Decades of β-Lactamase Inhibitors https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2806661/

Penetration of β‐lactamase inhibitors into the periplasm of Gram‐negative bacteria https://onlinelibrary.wiley.com/doi/full/10.1111/j.1574-6968.1999.tb13635.x

Gullible Rube

Jun 6, 2019

While I am proud of my skeptical bonafides, I virtually always take what they tell me at face value when it comes to what my patients tell me.

While people routinely lie about sex, drugs, and rock and roll, not to me. The vast majority of the time, people give me straight answers to my questions as they know their lives may literally depend on their answers.

Excluding the occasional Munchausen, I can remember less than a handful of patients who have looked me in the eye and acted Presidential.

The patient, young and with no medical problems, comes in with three weeks of malaise and low-grade fevers culminating in progressive shortness of breath and palpitations.

CT shows classic septic emboli, the blood cultures have MRSA, and there is a large vegetation on the tricuspid valve.

I note that echo reports often give a size and a descriptive adjective. A large 2.5 cm vegetation. As opposed to the small 2.5 cm vegetation. The adjective adds nothing.

She has been clean and sober for two years on suboxone and denies any relapse. Her lack of IVDA is supported by a lack of track marks and consistently negative drug screens.

So why the endocarditis?

MRSA loves to go to damaged valves. And IVDA, with all its inorganic and insoluble material, results in a light sandblasting of the valves that results in damage:

Eleven percent of the IDUs vs. 1% of the non-IDUs had tricuspid valve thickening

and

Thus, in IDUs without a history of IE, some extent of valvular abnormalities was seen in 20% (39 of 192, 95% CI 15% to 27%) of subjects.

So maybe this was due to distant IVDA.

Or, as is more likely, the patient has relapsed, and I am a gullible rube who just fell off the turnip truck for believing them otherwise.

Rationalization

Am J Cardiol. 2014 Jul 1;114(1):100-4. doi: 10.1016/j.amjcard.2014.04.010. Epub 2014 Apr 18. Echocardiographic findings suggestive of infective endocarditis in asymptomatic Danish injection drug users attending urban injection facilities. https://www.ncbi.nlm.nih.gov/pubmed/24819896

Acad Emerg Med. 1999 Sep;6(9):911-5. Prevalence of cardiac valve abnormalities in afebrile injection drug users. https://www.ncbi.nlm.nih.gov/pubmed/10490253

POLL RESULTS

I tend to

• take my patients at face value 5%
• trust but verify 40%
• polygraph everyone 10%
• not fret about the veracity of the story and focus on kill the bug 28%
• assume everyone lies about everything all the time. 18%

  A Classic Case Due To An Organism I Never Heard Of

  Jun 11, 2019

The patient, a middle-aged diabetic with chronic lymphedema, has the abrupt onset of rigors, fevers, and erythema spreading up the leg.

Cellulitis.

The patient is started on cefazolin, and the next day, the blood cultures are growing a gram-negative rod, so the hospitalist changes the antibiotic to a quinolone. I would have gone with cefepime. And I would have been wrong.

Gram-negative cellulitis, diffuse erythroderma with no abscess or necrosis that looks like Streptococci, is relatively rare, at least in my practice. One study found 2.8% of bacteremic cellulitis was due to gram-negative rods. Seems a bit high to me.

They called me the next day when it was identified as Myroides spp.

Never heard of that.

It turns out Myroides causes a hodgepodge of diseases in the immunocompetent, including cellulitis, of which there are a dozen. One review suggests around 50 cases reported all told. The same review says

M. odoratum are aerobic, yellow-pigmented, non-motile, non-fermenting gram-negative rods that derive their name from a characteristic fruity odor.

But which fruit? Bananas don’t smell like oranges don’t smell like pineapple. When I called the lab to ask about the organism, the tech told me: smells like grapes. Thank you.

And my strain, like reported cases, was resistant to most antibiotics except meropenem and levofloxacin.

But where did he get the infection? Myroides are found in water, soil, and gut of adult flesh flies.

In looking for reasons, I discovered that his dog does lick his diabetic foot ulcer. Ick. My mom had a dog that did that. Ick again. But Myroides are not part of dog oral or rectal, flora.

We do have flesh flies in Oregon. As I learned from the Wikipedia, flesh flies

…differ from most flies in that they are ovoviviparous, opportunistically depositing hatched or hatching maggots instead of eggs on carrion, dung, decaying material, or open wounds of mammals, hence their common name.

I wish I had known this when I saw the patient, as I have seen many a fly around diabetic feet in my day, so I never asked him.

She is semi-homeless, living in a trailer at a park, and uses the water from the park water tower for bathing and drinking. Seems a likely source.

And she improved quite rapidly on the quinolone.

Rationalization

IDCases. 2017; 8: 34–36.Published online 2017 Feb 28. doi: 10.1016/j.idcr.2017.02.012 Myroides bacteremia: A case report and concise review https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5358935/

PLoS One. 2018; 13(9): e0204036. Published online 2018 Sep 27. doi: 10.1371/journal.pone. Cellulitis in adult patients: A large, multicenter, observational, prospective study of 606 episodes and analysis of the factors related to the response to treatment https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0204036

Antibacterial activities of multi drug resistant Myroides odoratimimus bacteria isolated from adult flesh flies (Diptera: sarcophagidae) are independent of metallo beta-lactamase gene. https://www.science.gov/topicpages/m/myroides+odoratimimus+bacteria.html

Why Toxins?

Jun 12, 2019

We had a case of tetanus recently. Only the second of my career, the last one I saw was as a fellow.

By the time I was involved it was reasonably uninteresting: yep, that’s an intubated, sedated young adult with an almost normal exam, except for the scratch on the leg that was the source of his trouble.

Like my prior case, a foreign national who never had the primary vaccine series. Unlike my prior case, his tetany and vitals were well controlled.

Kind of dull really.

But I do find toxins, tetanus, and botulinum, curious. Why did toxins originally evolve and what is their ‘purpose’. For some toxins, like Cholera, it seems obvious. Others, like toxic shock toxin, not so much. And there is tetanus and botulism.

They are so close yet so different. Why, as I have asked before, do Clostridia make these toxins? What’s their real function in the wild?

Unlike the last time I looked, there is now a nice review of the topic.

Botulism toxin, at least, has primitive forbears found in Weissella oryzae SG25 although

Whether this protein is truly a neurotoxin, however, remains unknown, as do its preferred host or even cell type. Why such a toxin exists within Weissella, a lactic-acid fermenting species isolated from the grains of Japanese rice, is also unclear.

followed by the discovery of

numerous additional BoNT-like toxins have now been identified by genomic data mining methods.

in other organisms,

So it is one of many similar proteins found in other organisms, most of which act as cytotoxins, but it was Clostridia that became neurotoxic with

first neurotoxic BoNT likely originated within an ancestral Clostridium species, as suggested previously, earlier BoNT-like ancestors may have existed elsewhere (the phylum Actinobacteria has been suggested as one possible source).

But why does Clostridia paralyze? To make it easier for bugs to eat your rotting corpse. Or more scientifically

It has been hypothesized that BoNT operates as a method for the spread of the pathogen through rapid killing of vertebrate hosts, as is commonly seen in cases of avian botulism. As described by Rossetto, Pirazzini and Montecucco, botulism in the wild is propagated through a life cycle involving vertebrate decomposition and invertebrate predation. BoNT-producing clostridia are ingested or enter wounds, kill the animal, the animal carrying C. botulinum spores is decomposed by other organisms such as necrophagous fly larvae, which pick up the spores, intoxicate additional animals (e.g. birds) when they are ingested, and the cycle continues. However, there is still one unanswered question regarding the role of BoNTs in this life cyclewhat is the adaptive value of neuroparalysis? After all, there are many possible toxin modes of action that could kill an organism, so what is the ecological value of paralyzing the host with such extreme specificity? * According to forensic entomology, animal decomposition takes on a predictable succession of stages: fresh, bloat, active decay, advanced decay and dry decay, and each stage is associated with specific arthropod species that have adapted to that stage to efficiently use resources and proliferate. How might BoNT-induced paralysis influence a decomposition cycle such as this in the wild? By paralyzing the host, C. botulinum may effectively favor certain species of necrophagous invertebrates such as blowflies, effectively freezing the host before later stages of decomposition occur. A paralyzed host would provide fresh tissue before later stages of decomposition are initiated by the microbial necrobiome (anaerobic bacteria, fungi), and thus a major competitive advantage to these early-stage necrophagous insects, especially if they are also the vectors of C. botulinum spores. It is tempting to speculate that BoNTs may therefore have originally evolved due to competition between scavengers in decomposition. It is also conceivable that some BoNTs may have evolved broader host specificity to target not only the host vertebrate but also target competing necrophagous invertebrates. Members of the Calliphoridae are known to harbor C. botulinum spores, lending credence to the idea of a link to necrophagous insects. The exact nature of the relationship of BoNTs to insects and decomposition, however, remains to be seen.\

But what about tetanus?

The toxin is very similar to botulism,

Clearly, the difference between the action of botulinum and tetanus toxins is the location where the light chain is released and destroys the vesicle docking mechanism.

Yes. Clearly.

The two toxins are distantly related, about 50% similar, but unlike botulism, tetanus toxin is destroyed by the gi tract. So it seems unlikely to have the same purpose as botulinum toxin. So what is the real function of tetanus toxin? No clue.

The only reference I can find is the Wikipedia, which says

The function of tetanospasmin in bacterial physiology is unknown.

and

It has no known function for Clostridia in the soil environment where they are normally encountered.

But it has to do something in the wild, it is not just there to kill humans. It didn’t evolve to kill humans, although it sure tries.

Rationalization

Genomic insights into the evolution and ecology of botulinum neurotoxins https://academic.oup.com/femspd/article/76/4/fty040/4978416

Tetanus Toxin: A Botulinum Toxin in Disguise https://www.listlabs.com/blog/tetanus-toxin-botulinum-toxin/

Evolutionary Features in the Structure and Function of Bacterial Toxins https://www.mdpi.com/2072-6651/11/1/15/pdf

POLL RESULTS

With evolution

• everything has a purpose 3%
• everything had a purpose 12%
• everything can eventually have a purpose 18%
• some things evolve to no end 35%
• there are some things mans not meant to know 26% Other Answers 6%
• The above choices show a complete lack of understanding of evolution. Perhaps this is why antibiotic resistance and other problems are so prevalent!

  Uncertain Options

  Jun 18, 2019

The patient has extensive lung disease: COPD/bronchiectasis/lobectomy from prior smoking.

His problem is now cough with the progressive accumulation of thick sputum that he cannot clear, so he gets a bronchoscopy to clear out the secretions. He improves for a week or two, then the cycle repeats itself.

The cultures always grow the same thing: heavy Stenotrophomonas sensitive only to TMP/Sulfa.

Treat it? Pulmonary wants to, but the role of Stenotrophomonas in respiratory disease is problematic:

As there was no measurable impact of antibiotic therapy, in the absence of consolidation, a positive respiratory tract isolate of Stenotrophomonas maltophilia probably represents colonization of a severely impaired host rather than invasive disease.

and

Persistent S. maltophilia has a poor outcome in bronchiectasis. It may act as a marker of disease severity and the requirement for antibiotics, and acquisition frequently follows antibiotic use. It was also associated with the isolation of NTM. The resolution of infection is common but is not related to treatment directed against the organism. However, persistent infection is associated with increased mortality.

Part of the problem is that monthly bronchoscopy is not an option, so a trial of antibiotics is the only alternative besides letting the sputum fill him up. And 50 years ago, he had hives/SOB for some sort of sulfa; he does not remember the details but was told never to take sulfa again.

So what to do?

I tend not to believe old allergic reactions to antibiotics. Products were not as pure as today, and it may be the contaminants that caused the reaction. That is true of penicillin allergy. And who knows which sulfa he received all those years ago. But who wants to risk an allergic reaction in someone with little pulmonary reserve.

I have never needed to do it before, but there are several protocols for sulfa desensitization. So we tried one. I forget which one; it had six steps. And it went smoothly, and she left on a trial of TMP/sulfa.

But for how long? Part of the problem is that, as a rule, desensitization only counts for the antibiotic course following the process. If the antibiotic is stopped, technically would need to repeat the process for the next prescription. He does not seem a good candidate for lifetime antibiotics.

I deferred (aka weaseled out) the duration to pulmonary as they were the ones who want to treat.

And he is yet another patient on untreated well water. Stenotrophomonas is a water organism, and I suspect he could re-acquire the infection from showering. So it may all be for naught.

Rationalization

Significance of positive Stenotrophomonas maltophilia culture in acute respiratory tract infection. https://erj.ersjournals.com/content/25/5/911

P270 Stenotrophomonas maltophilia infection in a bronchiectasis cohort https://thorax.bmj.com/content/71/Suppl\_3/A234.2

Wise or Fool

Jun 19, 2019

“The whole problem with the world is that fools and fanatics are so certain of themselves and wiser people so full of doubts.” Bertrand Russell

Am I a fool? Or wise? Depends. When it comes to my practice of ID, I will bet on wise. Everything else? A fool.

As Tweedledee would recognize, for others, it is contrariwise.

I have mentioned in the past that a unique feature of ID is how others, with much less education and experience, will change my antibiotics and not tell me. They do that once, and then I emphatically voice my objections to the practice. They do not repeat it. But I am amazed that people do that. I suspect no nephrologist has ever had their dialysis orders altered.

And now and then, one of my colleagues will make a therapeutic suggestion to which I can only respond with a Scooby. The patient has an MSSA abscess that can’t be drained, bacteremia and persisting, but improving, fevers, and the surgeon suggests antifungals. Because? Got me. No reason was given. It’s like someone suggesting at the start of breast cancer therapy, hey, treat renal cell.

I don’t get why people do that. Except, I suppose, they consider me a fool rather than wise.

The patient, a male, presents to an acute care clinic with dysuria. Work up shows a UTI, and he is given a 10-day course of ciprofloxacin. After finishing the course, he relapses and becomes more ill, fevers, chills, headache, malaise. In the ER, he is hypotensive but responds to fluids and gets a repeat course of ciprofloxacin.

Both cultures are growing Salmonella enteritica.

Been a while since I have seen that as a uropathogen.

No-gi symptoms. No dietary indiscretions, not that you need it. Everything we eat has a patina of stool on it, sometimes thicker, sometimes thinner. Not immunocompromised. No reason for Schistosomiasis. Normal urinary tract.

But that is the thing with Salmonella. It is hard to get rid of, even in a cystitis.

Four patients had recurrent Salmonella UTIs (22.2%), and in 2 of them recurrence occurred after prolonged treatment during 3.5 and 5 weeks, respectively.

While one study found Salmonella cystitis to be a disease of the elderly and

Fourteen patients (73.6%) had chronic diseases; diabetes mellitus was present in 8 of them (42.1%) and 7 patients (36.8%) were undergoing immunosuppressor treatment. Eight patients (42.1%) had urologic abnormalities.

Another found Salmonella UTI

was not significantly associated with older age, male sex, diabetes, immunosuppressive states or urologic abnormalities.

As Newtons Philosophiae Naturalis Principia Medica noted in The Third Law of Medical Literature, “For every study, there is an equal and opposite study.”

But the second study did find

A significant association with urologic malignancies was demonstrated in patients with NTS UTI compared to those with GE and NTS bacteriuria or asymptomatic NTS bacteriuria.

Here I suppose the cancer predisposes to Salmonella. But there is also

Patients diagnosed with severe salmonellosis have an increased risk of developing cancer in the ascending/transverse parts of the colon. This risk concerns particularly S. Enteritidis infection, suggesting a contribution of this major foodborne pathogen to colon cancer development.

Meh. Association is not causation, but still curious. And they are even trying to weaponize S. Typhimurium to kill cancer.

Salmonella Typhimurium strains have been shown to have a remarkably high affinity for tumor cells. The use of bacterial strains to target tumors is a relatively new research method that has not yet reached the point of clinical success.

So Salmonella is associated with, causes, and cures cancer? Quite the bug.

For now, I will stick with its infection-causing capacity and see if a long course of a quinolone will cure it. It is the wise thing to do.

Rationalization

Why You Can’t Trust Yourself https://getpocket.com/explore/item/why-you-can-t-trust-yourself?utm\_source=pocket-newtab

Interaction between Salmonella and Schistosomiasis: A Review https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5131909/

Urinary tract infection due to non-typhoidal Salmonella: report of 19 cases. https://www.ncbi.nlm.nih.gov/pubmed/16824609

Urinary Tract Infections Due to Nontyphoidal Salmonella https://www.amjmedsci.com/article/S0002-9629(17)30135-0/pdf

Increased colon cancer risk after severe Salmonella infection https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5771566/

Development of Salmonella strains as cancer therapy agents and testing in tumor cell lines. https://www.ncbi.nlm.nih.gov/pubmed/18363243

POLL RESULTS

I am

• wise in medicine 6%
• wise in all things 6%
• frequently in error, never in doubt 29%
• a Peter Principle example 12%
• a devote of Dunning–Kruger 32% Other Answers 15%
• Happy. The true opposite of wise.
• dumb as a hammer
• done trying. It’s just not worth it.
• frequently in doubt

  I Beg to Differ

  Jun 25, 2019

I am asked to see a consult for a septic arthritis from chronic osteomyelitis in a patient with a Streptococcus to be identified in the blood.

Sure. Been there, done that.

The history is interesting. He has had 9 to 12 months of progressive hip pain—no other symptoms.

He also has long-standing HIV untreated due to methamphetamine use; CD4 counts around 200.

The plain film of the hip is interesting with the femoral head gone.

A tap of the joint shows no WBC but at day 4 grows the same organism as the blood: S. pneumoniae.

So I put it together differently, and, as much as I try and be an Occam’s kind of doctor, this is a case for Hickam.

I think the hip problem was avascular necrosis. No way is someone going to have S. pneumoniae osteomyelitis of the femoral head or a septic joint for a year and not have some WBC in the joint space, much less tolerate the pain for a year.

AVN is an important musculoskeletal manifestation of HIV and may be multi-focal with multi-factorial aetiology.

Plus, if there is a case of femoral head osteomyelitis from S. pneumoniae in an adult ever reported I can’t find it on the Googles or the Pubmeds.

Pneumococcal bacteremia for no good reason is a manifestation of HIV:

Patients with pneumococcal bacteremia should be evaluated for HIV infection, especially in the absence of other underlying diseases that predispose to pneumococcal bacteremia.

In the OR, there was no apparent infection, although, unfortunately, the resected femoral head was never sent to pathology.

I think we caught the bacteremia just as it was seeding the joint space. So the patient has AVN and Pneumococcal bacteremia.

We are entering the era of less is sufficient, so a short course of iv followed by po and it looks like a cure.

Rationalization

Rheumatol Int. 2013 Jan;33(1):235-8. doi: 10.1007/s00296-011-2114-5. Epub 2011 Sep 22. Avascular necrosis in HIV. https://www.ncbi.nlm.nih.gov/pubmed/23970592

South Med J. 1990 Aug;83(8):895-9. Pneumococcal bacteremia as a marker for human immunodeficiency virus infection in patients without AIDS. https://www.ncbi.nlm.nih.gov/pubmed/2382154

Short parenteral antibiotic treatment for adult septic arthritis after successful drainage https://www.sciencedirect.com/science/article/pii/S120197121201274X

Nothing is a Contaminant

Jun 26, 2019

The patient has progressive chronic back pain that requires a stimulator placement. Three days later, it has to be removed due to bleeding. He is discharged but returns to my hospital two weeks later with abdominal pain. A CT shows no abdominal pathology, but there is discitis/osteomyelitis of the spine.

The last imaging, two years ago, only had severe degenerative changes.

We did an MRI that confirmed the CT findings. Sure looks like osteomyelitis and discitis, and it was two levels away from the stimulator.

Talking with the patient, the history was consistent with an infected back but also compatible with the progression of his underlying mechanical issues.

No reason by history for an infection, nothing in the labs to confirm or deny an infectious process in the spine

I see the occasional spontaneous back infection, although usually there is some history of prior acute trauma. I think the simulator has nothing to do with the infection; the changes are too extensive to have occurred in two weeks.

So we biopsy the site.

No WBC. No organisms seen.

Hmm.

No infection? Sampling error? Self-cure?

I have seen a couple of back infections that I think were cured spontaneously, all IVDA who self-medicated the pain with heroin. A compatible history and radiography but on open biopsy only scar. If you find the literature about infected herniated discs compelling, and I do, then one way to interpret the data is that some people get better on their own, although po antibiotics are superior.

Then the cultures grow a pain-sensitive coagulase-negative Staphylococcus. Can that be ignored? Maybe. With no WBC or surgery, I would be inclined to call it contaminant except

• CoNS-spondylodiscitis involved at least 10% of spontaneous spondylodiscitis cases and was more common in elderly patients, afflicted by comorbidities, and its presentation was less virulent than that of those with SA-spondylodiscitis.*

That would be him.

So a course of therapy it is.

I keep going back to Oral versus Intravenous Antibiotics for Bone and Joint Infection and re-reading the supplementary material to see if my patients were represented in the study. He was.

So a course of cephalexin should take care of things.

Rationalization

Antibiotic treatment in patients with chronic low back pain and vertebral bone edema (Modic type 1 changes): a double-blind randomized clinical controlled trial of efficacy <https: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/23404353>

Characteristics of spontaneous coagulase-negative staphylococcal spondylodiscitis: a retrospective comparative study versus Staphylococcus aureus spondylodiscitis. <https: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pubmed/29029624>

Oral versus Intravenous Antibiotics for Bone and Joint Infection. <https: data-preserve-html-node="true"//www.nejm.org/doi/suppl/10.1056/NEJMoa1710926/suppl_file/nejmoa1710926_appendix.pdf>

What does S. aureus have in common with corn and canaries?

Jul 1, 2019

A month ago, the patient had an infection of the great toe, where she has very bad onychomycosis. It was treated with cephalexin and got better.

Now the patient has fevers to 104, rigors, weakness, and altered mental status. She goes to the ER, is admitted with sepsis, and then gets markedly better on antibiotics.

The next day the blood cultures are growing gram-positive cocci in clusters identified by PCR as S. aureus, mecA negative.

But the tech thought the colonies were too white.

It is called S. aureus as aureus means gold in some dead language or other.

Why is S. aureus gold? I never thought to ask before. The gold color is due to staphyloxanthin, a carotenoid pigment that is also a virulence factor. Staphyloxanthin is an antioxidant that allows the organism to resist hydrogen peroxide. Finally, an antioxidant that actually does something.

BTW, carotenoids per the Wikipedia, are

yellow, orange, and red organic pigments that are produced by plants and algae, as well as several bacteria and fungi. Carotenoids give the characteristic color to pumpkins, carrots, corn, tomatoes, canaries, flamingos, and daffodils.

And S. aureus.

So the tech tossed it in the MALDI-TOV. S. lugdunensis.

So can the GeneXpert MRSA/SA PCR call an S. lugdunensis an S. aureus by mistake? I think so. One article, if I read it right, suggests it:

The present study showed that 10 (13.8%) of the 72 staphylococci identified had a positive result on the Pastorex Staph Plus test, two of which were positive for spa gene on GeneXpert® PCR MRSA/SA and were considered to be false-positive results. These 10 staphylococci isolates were identified by MALDI-TOF-MS as S. lugdunensis.

That is the closest I can find.

I was also curious, given the relative virulence of Staphylococcus lugdunensis, its relatedness to S. aureus and other coagulase-negative Staphylococci, but I couldn’t find anything.

Why did she have this infection? The toe. As I have noted before, S. lugdunensis likes the toe.

Swabs from the groin and the lower extremities, especially the nail bed of the first toe, often yielded S. lugdunensis.

And S. lugdunensis in the blood raises the specter of endocarditis; there was something fuzzy on the aortic valve.

So 6 weeks of cefazolin it is.

Rationalization

Staphyloxanthin https://en.wikipedia.org/wiki/Staphyloxanthin

From Clinical Microbiology to Infection Pathogenesis: How Daring To Be Different Works for Staphylococcus lugdunensis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2223846/

PCR detection of staphylococcal enterotoxin genes and exfoliative toxin genes in methicillin-resistant and methicillin-susceptible Staphylococcus aureus strains from raw human breast milk https://www.sciencedirect.com/science/article/pii/S2352939316300562

Cellulitic Curiosities

Jul 3, 2019

The patient comes into the ICU with multi-organ system failure, MOSF, and cellulitis on the leg.

He gets the usual care, and the next day they call me when the blood cultures grow S. pyogenes. We have all been there, and we have all done that.

The curiosity was his leg. The involved leg looked like purpura fulminans, but only in the involved leg. A large patch of erythema, cool, blue toes, and scattered purpura just on the leg. The rest of this skin/extremities were spared.

There was no DIC by labs, the platelets were low normal, and he had no reason to have pre-existing vascular disease.

There are a wide variety of organisms that can cause purpura fulminans, including Group A Streptococcus. I know this wasn’t really a mono-extremity purpura fulminans, but it sure looked like it.

And the other odd thing? Hemorrhagic bullae. That is a finding that is supposed to make you think of Vibrio, especially when you take the boards. I have seen and written about, many a case of bullous cellulitis over the years, but I had never seen a case of hemorrhagic bullae due to Streptococcal cellulitis. And, in all likelihood, neither have you. There are only a smattering of cases mentioned in PubMed

Vibrio species was the most common organism from blood culture (8/16 cases) and wound culture (17/27 cases). Streptococcal species was found in only 1 patient via blood culture and 4 patients via wound culture.

and

…the most common causative disease of hemorrhagic bullae was necrotizing fasciitis. Hemorrhagic bullae are a more common clinical feature in Vibrio infection than in streptococcal infection. Hemorrhagic bullae may occur in the early stage of necrotizing fasciitis.

He went to the OR, and no necrotizing fasciitis was found. The MOSF slowly improved, but he had a prolonged, almost leukemoid reaction (35K) that took around 10 days to resolve and for which we found no other cause.

In the end he was a cure.

Rationalization

Ann Clin Microbiol Antimicrob. 2018; 17: 31. Published online 2018 Jul 9. doi: 10.1186/s12941-018-0282-9 Streptococcus pyogenes-purpura fulminans as an invasive form of group A streptococcal infection https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6036671/

Am J Emerg Med. 2008 Mar;26(3):316-9. doi: 10.1016/j.ajem.2007.07.014. Hemorrhagic bullae are not only skin deep. https://www.ncbi.nlm.nih.gov/pubmed/18358943

Another Crisis

Jul 8, 2019

The patient is a young female with acute EBV. She had the whole 9 yards: exudative pharyngitis, marked atypical lymphocytosis, splenomegaly, transaminitis, and a positive monospot.

And fever. Every day she was more febrile than the day before with myalgias that wasted her. I suppose she had the whole 10 yards.

It was the fevers that led to admission, 104 in the ER. They consulted me to bloviate on any other potential infections/complications. While mono is associated with any number of curious complications, I found none.

It’s just mono. Bad mono. But mono.

The next day she was 104.8. That is getting to dangerous levels of fever, but I postulated it might be a good thing.

Regular readers (those on stool softeners?) are aware of my affinity for the crisis.

In the old days, before antibiotics, patients with lobar pneumonia would be ill until their crisis, which marked the onset of antibody, efficiently killing of the pneumococcus and a marked worsening of the infection, after which they either died or turned the corner.

It was found that at the time of crisis or lysis the blood serum acquired constantly the property of promoting pneumococcus killing to a relatively marked degree. Other evidences of antipneumococcus reaction–mouse protection, opsonins, and agglutinins–were also demonstrable in the blood at this time. These immune changes appeared in the majority of cases at the beginning of recovery and failed to occur when the disease terminated fatally.

Of course, I practice in the antibiotic era and have never seen an actual crisis, and even in 1949, doctors were whinging about the millennials of their day:

How many of the younger generation of doctors have witnessed the “crisis” of lobar pneumonia, which this girl undoubtedly exhibited on the evening prior to my first visit ? It must be a rare clinical experience in these days of penicillin and the “sulpha” drugs.

Or with zosin and vancomycin. Crisis has never been used outside of lobar pneumonia as best I can determine, but I like to blame any exceptionally high temperature around the time antibody is kicking in (day 10-14) as the moral equivalent. I suggested she might be afebrile after this impressive spike, which was around day 14. And she was.

But when do IgM and IgG kick in for mono? Timing is all over the map, and I wonder if it because EBV infects immune cells:

VCA IgM antibodies were found as early as 8 days before symptoms were reported and persisted for as long as 420 days after onset of symptoms. All 66 subjects with primary EBV infection developed EBV VCA IgG antibody that was first detected as early as the day of onset of symptoms and as late as 91 days after onset of symptoms.

It would make predicting a crisis a bit problematic, so I was lucky in my prognosticating.

And what is the mean duration of fever for mono? Hard to find, in intervention studies, it varied from 6 to 18 days, which matches the variability of antibody response I suppose.

Rationalization

J Infect Dis. 2013 Jan 1; 207(1): 80 88. Published online 2012 Oct 24. doi: 10.1093/infdis/jis646 Behavioral, Virologic, and Immunologic Factors Associated With Acquisition and Severity of Primary Epstein Barr Virus Infection in University Students https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3523797/

Infectious Mononucleosis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4670567/

Points from Letters: The Crisis in Lobar Pneumonia - NCBI - NIH https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2049396/

MECHANISM OF RECOVERY FROM LOBAR PNEUMONIA http://jem.rupress.org/content/jem/48/4/513.full.pdf

The Crisis in lobar Pneumonia https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2049396/?page=1

My Fourth

Jul 10, 2019

The patient is an elderly female who, for the past two months, has had back pain that occurred 3 days after a fall. The pain has been gradually progressing, and she was scheduled to see a pain specialist when she had a stroke, which necessitated admission to the hospital.

She was afebrile at the time and no leukocytes, but because of abdominal pain at CT was done in the ER, which showed lumbar osteomyelitis/phlegmon and an iliopsoas abscess.

So blood cultures were drawn that grew S. gordonii.

It also turns out that the patient has an aortic bioprosthesis, so the diagnosis was simple: endocarditis that seeded her back. An echo confirmed the diagnosis with a vegetation of the aortic valve.

This is my fourth S. gordonii endocarditis and the second with an accompanying spondyloarthritis. Given the paucity of cases on the PubMeds, this may represent the largest single series in the literature. However, this blog is not peer-reviewed literature, except to note that I peer over the top of my glasses to read the entry after it is posted.

I have no great insights to add since my last case except to marvel at what I suspect was a 2 months long infection with no constitutional symptoms to suggest infection.

I have seen many a discitis with no fevers, chills, etc., but it always amazes me when an infection on a valve in the bloodstream has no signs of infection.

It should be noted that S. gordonii is found on the tooth (my patient had 4 lower teeth in fair condition), along with other Streptococci.

The mitis and sanguinis groups, including S. oralis, S. mitis, S. gordonii, and S. sanguinis, are the primary colonizers of the tooth surface and are commonly considered as commensals, although all have been implicated in cases of infective endocarditis. Oral bacteria can reach the bloodstream not only during invasive procedures such as dental extractions and oral surgery but also after simple daily activities such as mastication, brushing and flossing.

And the causes of endocarditis, as of 2018, show that

The overall distribution of streptococci was 76% viridans (n = 224), 17% pyogenic (50), 6% nutritionally variant (17), and 2% anaerobic (5). Sixty-three (21%) viridans group streptococci were not identified further. The distribution of the remaining 161 viridans group streptococci was Streptococcus mitis group 61%, S. bovis group 15%, S. mutans group 13%, S. anginosus group 9%, and S. salivarius group 1%.

I know it is flossing and brushing that are blamed for some cases of endocarditis, so I suppose dragging the gradeaux down the tooth and into the gums is the route by which tooth bacteria get in the bloodstream.

And it does give one pause that

There is weak, very unreliable evidence from 10 studies that flossing plus toothbrushing may be associated with a small reduction in plaque at 1 and 3 months. No studies reported the effectiveness of flossing plus toothbrushing for preventing dental caries.

So is the risk of endocarditis worth the lack of benefit of flossing? Got me. But consider. Endocarditis

Cases (n = 73) were more likely than controls (n = 192)…to use toothpicks, dental water jet, interdental brush, and/or dental floss…(and) they were less likely to brush teeth after meals.

The take-home: floss and brush after every meal or just brush without flossing at night if you want to avoid a Streptococcus on a valve.

The S. gordonii had a MIC to penicillin of < 0.06 and was cured with a six-week course of ceftriaxone.

Rationalization

A Strep I had not heard of. Which one? I am not telling in the title. Call it a strep tease. http://boards.medscape.com/forums/?128@@.2a008da8!comment=1

Why So Few? http://boards.medscape.com/forums/?128@@.2a802ea6!comment=1

More is not better http://boards.medscape.com/forums/?128@@.2a828e61!comment=1

Biology of Oral Streptococci https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6287261/

Distribution of streptococcal groups causing infective endocarditis: a descriptive study. https://www.ncbi.nlm.nih.gov/pubmed/29567126

Flossing for the management of periodontal diseases and dental caries in adults. https://www.ncbi.nlm.nih.gov/pubmed/22161438

Oral Streptococcal Endocarditis, Oral Hygiene Habits, and Recent Dental Procedures: A Case-Control Study. https://www.ncbi.nlm.nih.gov/pubmed/28369398

POLL RESULTS

To avoid Streptococcal endocarditis

• Never floss 24% -avoid licking needles before injecting heroin 36%
• pick my friends but not my teeth 16%
• take amoxicillin before brushing 4%
• had all my teeth removed 14% Other Answers 6%
• deny its existence, as that seems to work for the climate thingy.
• brush with Hibiclens

  Slow Decline

  Jul 24, 2019

This month starts my 30th year in practice, and today a couple of cases reminded me that the arc of an ID career, a successful ID career, is doing less every year because there is less to be done. I just need to eke it out 5 more years. Why 5 more years? I recently realized I made the mistake of marrying a younger woman, and while I am medicare eligible in three years, she is not for 5 years. So I need to work for health care insurance.

Anyway.

In 1990 the hospital was inundated with HIV related opportunistic infections. Thanks to HAART I see an OI once a year. Newer immunosuppressive therapies have made OIs in transplant patients equally rare. G-CSF, newer chemo regimens, and prophylactic antibiotics have vanquished fevers and infections in the cancer patient.

Aggressive infection control and hand hygiene have eradicated line-related bacteremias and VAP’s. I see maybe one each of those a year.

I have been fortunate in that I have never had to justify my existence to administration, but much of the success of ID is measured in what doesn’t happen; we are the dog that doesn’t bark.

Gregory (Scotland Yard detective): “Is there any other point to which you would wish to draw my attention?” Holmes: “To the curious incident of the dog in the night-time.” Gregory: “The dog did nothing in the night-time.” Holmes: “That was the curious incident.”

And now? The goal of the next couple of years is to shorten duration of iv therapy or get rid of iv therapy entirely.

This week I had a pair of consults from the surgery service enquiring as to the duration of therapy for two different abdominal abscesses that had source control.

4 days I said, and pasted the STOP-IT trial in the chart.

In patients with intraabdominal infections who had undergone an adequate source-control procedure, the outcomes after fixed-duration antibiotic therapy (approximately 4 days) were similar to those after a longer course of antibiotics (approximately 8 days) that extended until after the resolution of physiological abnormalities.

Two other consults were debrided osteomyelitis. Last year I would have set them up for a 6 week course of outpatient iv.

Nope.

I put Oral versus Intravenous Antibiotics for Bone and Joint Infection in the chart and changed the patients to oral antibiotics.

Oral antibiotic therapy was noninferior to intravenous antibiotic therapy when used during the first 6 weeks for complex orthopedic infection, as assessed by treatment failure at 1 year.

I keep going back and re-reading the supplement of that article, where are the specifics are reported.

If you have source control, really, antibiotics are needed for only a short period of time and usually oral. I am of the opinion that most of the time (S. aureus the big exception) bacteremia doesn’t matter in deciding the duration or type of therapy. The blood stream is cleared with the first slug of antibiotics. The question is the source of the bacteremia and whether it is drained.

I look forward to a compelling study that will let me treat uncomplicated S. aureus bacteremia with oral antibiotics. We are almost there, but not quite, and I don’t mess with S. aureus. Ever.

I doubt I will ever treat endocarditis with oral despite NEJM article that suggests otherwise. That is a discussion for another time perhaps.

Fewer infections. Less and less antibiotics for shorter and shorter durations. Soon I will have little if any outpatient iv antibiotic patients and no one to follow-up.

If I time it right that will happen just as I retire.

Rationalization

Trial of Short-Course Antimicrobial Therapy for Intraabdominal Infection https://www.nejm.org/doi/full/10.1056/NEJMoa1411162

Oral versus Intravenous Antibiotics for Bone and Joint Infection https://www.nejm.org/doi/10.1056/NEJMoa1710926

Small Things

Jul 29, 2019

No huge insights or jaw-dropping weirdness today. It is a small thing, something I had never seen or heard about until today. And now you have the same opportunity.

I get an email from a patient, who is on chronic suppressive antibiotics for a relapsing infected prosthesis.

My teeth, she says, have turned brown. I don’t smoke or chew. The only difference in my life the amoxicillin you put me on three months ago. Could that be the cause?

My first thought was no. How could that happen? Amoxicillin is white. It’s not like rifampin, where you have to warn the patient that their urine will turn blood red.

But what do I know? Not half enough evidently, although I am not a regular reader of Ned Tijdschr Geneeskd, Dutch and short for Nederlands Tijdschrift voor Geneeskunde.

From January 1991 until June 1995. 25 cases were reported to the Netherlands Pharmacovigilance Foundation LAREB of yellow to brown tooth discoloration following the oral use of medication; 21 cases (84%) involved antibiotics, of which 14 were amoxicillin… Discoloration was reversible in all cases, but had a protracted course in some. Presumably a pigment precipitated on (and not in) the teeth, but the nature of the pigment was uncertain.

Most of the cases are in children.

There are reports suggesting the amoxicillin is involved with fluorosis, which is why the teeth turn brown. But the studies are flawed.

The presence of several methodological issues does not allow to draw any evidence-based conclusions. No evidence of association was detected, therefore, there is a need of further well-designed studies to assess the scientific evidence of the relationship between amoxicillin and fluorosis and to restrict the prescription of this drug for recurrent upper respiratory tract infections especially acute otitis media (AOM) during the first two years of life. When it is possible can be opportune to use an alternative antibiotic treatment.

And we prefer cavities in Portland, so the water has no fluoride. After all,

Do you realize that in addition to fluoridating water, why, there are studies underway to fluoridate salt, flour, fruit juices, soup, sugar, milk, ice cream? Ice cream, Mandrake? Children’s ice cream!…You know when fluoridation began?…1946. 1946, Mandrake. How does that coincide with your post-war Commie conspiracy, huh? It’s incredibly obvious, isn’t it? A foreign substance is introduced into our precious bodily fluids without the knowledge of the individual, and certainly without any choice. That’s the way your hard-core Commie works. I first became aware of it, Mandrake, during the physical act of love… Yes, a profound sense of fatigue, a feeling of emptiness followed. Luckily I was able to interpret these feelings correctly. Loss of essence. I can assure you it has not recurred, Mandrake. Women, er, women sense my power, and they seek the life essence. I do not avoid women, Mandrake…but I do deny them my essence.

So fluorosis seems unlikely in developed, as opposed to developing, teeth, here in the land of pure precious bodily fluids. So maybe some form of mysterious precipitate? No idea.

I can find no similar reports with cephalexin, so will give that a try.

Looking up the whys of the small things often leads to interesting tidbits.

Rationalization

Ned Tijdschr Geneeskd. 1996 Jan 27;140(4):207-9. [Reversible tooth discoloration during oral use of antibiotics]. https://www.ncbi.nlm.nih.gov/pubmed/8618645

Amoxicillin Use during Early Childhood and Fluorosis of Later Developing Tooth Zones. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4556648/

Pediatr Med Chir. 2012 May-Jun;34(3):148-54. Dental enamel, fluorosis and amoxicillin. https://www.ncbi.nlm.nih.gov/pubmed/22966729

Dr. Strangelove - Precious Bodily Fluids https://www.youtube.com/watch?v=N1KvgtEnABY

POLL RESULTS

Beware

• fluoride 5%
• light beer 26%
• gluten 0%
• decaf coffee 48%
• gmo 7% Other Answers 14%
• uranium
• air
• warnings of scary stuff that may be about to upend your own life, or turn the - entire planet into a smoldering debris-ball floating through space.
• anything claiming to be organic and healthy

  What Is This, The Dark Ages?

  Jul 31, 2019

I guess.

Recently I had an article in my feeds about Lyme and the difficulties in accurately diagnosing the disease.

The biggest problem is that there is no way to test, unequivocally, for the presence of the bacteria that cause the disease.

Well, big duh.

Welcome to the practice of ID.

Unequivocally. Insert snort of derision.

The condition can be challenging to treat, in part because it is not always easy to get the diagnosis right the first time around. The biggest problem is that there is no reliable biomarker for Lyme, no way to test, unequivocally, for the presence of the bacteria, Borrelia burgdorferi, which are transmitted by tick bite and cause the disease.

Substitute syphilis or tuberculosis or ventilator-associated pneumonia or Aspergillus and on and on and on.

Unequivocally diagnose a disease? Don’t we all wish. If only I had a tricorder like Bones McCoy.

The whole article is interviews with docs who seem flabbergasted that the history, physical, and labs don’t always unequivocally follow the textbook. You want unequivocal? Get an autopsy. Otherwise, medicine is messy messy messy.

The patient, who has metastatic bowel cancer, is admitted with fevers and chills. She grows MSSA in her blood.

Can I unequivocally say it is her Groshong that is the source? Nope. But no other source is evident, so out it comes.

She deferveses, and repeat blood cultures are negative. Can I unequivocally say she does not have a metastatic complication? Nope. So a course of IV cefazolin it is.

And the ECHO has a clot in the left ventricle, a complication of a prior myocardial infarction. Was that seeded? I can find a half-dozen cases. S. aureus loves to go to clot, and while I don’t think it is infected, I can’t be unequivocal.

So maybe 4 or 6 weeks of iv instead of the usual two?

Got me. It is rare be unequivocal in either the diagnosis or the treatment.

Rationalization

The Challenge of Diagnosing Lyme Disease https://www.nytimes.com/2019/07/29/well/family/the-challenge-of-diagnosing-lyme-disease.html

What Is This, The Dark Ages? https://www.youtube.com/watch?v=UtllgbUiTt0

Infection of left ventricular thrombus in a patient with silent myocardial infarction a unique complication https://academic.oup.com/eurheartj/article-abstract/14/7/997/437472?redirectedFrom=fulltext

POLL RESULTS

• Diagnosis and treatment for me is unequivocal 2%
• a riddle, wrapped in a mystery, inside an enigma. 27%
• frequently in error but never in doubt 16%
• certainly uncertain, so I order lots of tests 8%
• the best I can do what the tools I am given 45% Other Answers 2%
• a crap shoot, given that I’m the patient now and at the mercy of the system.

  Drugs. Look to the Drugs

  Aug 5, 2019

The patient, a heroin user, is admitted with MSSA bacteremia and found to have a vegetation on her prosthetic mitral valve, a sequela of a prior episode of heroin-associated endocarditis.

She is placed on nafcillin, rifampin, and a short course of gentamicin, as per the guidelines.

The first week of therapy is uneventful, her withdrawal was kept at bay with methadone, and she responded clinically to the antibiotics.

Which is nice. Neither the patient nor the surgeons are enthusiastic about a repeat valve replacement, so maybe I will get lucky and get a medical cure.

But 5 days in, the creatinine starts to go up. The usual suspects (emboli, AIN, GN) are negative, so it was likely the aminoglycoside.

I used to think that aminoglycoside oto or nephrotoxicity was the price paid to cure some forms of endocarditis.

Now I am not so sure. Is the gentamicin really needed?

Few (if any) definitive human data demonstrate the clinical benefit of initial aminoglycoside treatment in patients with infective endocarditis due to S. aureus, and a very recent study demonstrated that initial low-dose gentamicin treatment in this setting is associated with rapid, relevant, and durable renal impairment.

and in a retrospective analysis

The addition of gentamicin to a regimen containing vancomycin or cloxacillin plus rifampicin in SPVE was not associated to better outcome.

Toxic, costly, and likely ineffective. I stopped the gentamicin. And the creatinine improved.

Two weeks in, she started to demand more pain medications and became sweaty, tremulous, tachycardic, and agitated. The house staff thought it was drug-seeking. It was, but not for the reasons they thought.

This time it was the rifampin. Few drugs are better at kicking in the p450 system, resulting in increased methadone metabolism and withdrawal. Does she need rifampin? In 34 years, I have not looked; I just followed the guidelines. I went looking and found nothing. Zip. That’s just sad.

I did not stop the rifampin, as I am still drawn to the whole kill in the biofilm issue. But the data to support the practice for S.aureus PVIE does not exist.

Instead, we increased her methadone, and she did fine. The problem was at the time for discharge to detox treatment, the effects of rifampin would hang on for a couple of weeks.

A recent report noted that 2 to 4 weeks were required for rifampin-induced midazolam clearance to return to baseline values. The authors estimated that the deinduction half-life was 7.7 days. Deinduction of hepatic enzymes is likely to depend on elimination of the inducing drug and, more importantly, the natural degradation time of the enzymes.

So how to dose her methadone? Got me.

She was discharged as a cure and, to the best of my knowledge, is alive and well.

And as I have likely mentioned before, the top three causes of the patients’ complaints are drugs, drugs, and drugs.

Rationalization

Gentamicin in Infective Endocarditis: How to Use It? https://academic.oup.com/cid/article/49/2/320/408317

J Infect Chemother. 2018 Jul;24(7):555-562. doi: 10.1016/j.jiac.2018.03.003. Epub 2018 Apr 6. Gentamicin may have no effect on mortality of staphylococcal prosthetic valve endocarditis. https://www.ncbi.nlm.nih.gov/pubmed/29628387

N Engl J Med. 1976 May 13;294(20):1104-6. Rifampin-induced methadone withdrawal. https://www.ncbi.nlm.nih.gov/pubmed/1256526

Adjunctive Use of Rifampin for the Treatment of Staphylococcus aureus Infections A Systematic Review of the Literature https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/414583

Time Course for Enzyme Induction and Deinduction https://www.pharmacytimes.com/publications/issue/2011/april2011/druginteractions-0411

If The Shoe Fits

Aug 7, 2019

I am asked to an elderly male patient for fever.

He said he started getting ill about 7 days before admission, with lightheadedness, headache, nausea, vomiting, a cough, and malaise. He did not take his temperature until 5 days in, and, much to his surprise, it was 103. He came to the ER, was admitted, and he remained febrile with a negative workup.

So they call me.

I take the usual exposure history and get little, except he is an avid indoor gardener, and he volunteers that his hands are always dirty from bags of potting soil.

Admission CXR is negative, although he is a bit hypoxic. Of note, when his temperature is 103, his pulse is 75. Hm. Fagets aka pulse-temperature disassociation. For every degree of elevated temperature, pulse goes up 10.

CBC is normal. Sodium is 129. I send an LDH; 333. Repeat CXR has slight bilateral faint infiltrates.

My diagnosis? I bet Legionella, more on the Pontiac fever end of the spectrum, and I bet L. longbeachae.

It fits the pattern.

Fever? Check. Dry Cough? Check. Na 133? Check. LDH 225? Check. All mean Legionella.

I only recently, like last month, learned that the LDH is modestly up with Legionella. But it makes sense. Legionella is an intracellular pathogen, and by destroying pulmonary cells, it would release LDH.

The potting soil and the dirty hands are a good risk:

Gardening behaviors associated with L. longbeachae disease included having unwashed hands near the face after exposure to or tipping and troweling compost or potting mix.

And Legionella causes pulse temperature disassociation.

Relative bradycardia as a characteristic feature of specific disease was found for typhoid fever (P = 0.003), Legionnaire’s disease (P = 0.005), and pneumonia caused by Chlamydia sp. (P = 0.0005), but not for mycoplasma pneumonia. It was not found for other pulmonary infections, infections caused by other Salmonella sp., other extracellular Gram-negative infections, or viral infections.

And the diagnosis is confirmed with a negative urine antigen, which does not pick up L. longbeachae. Using a negative test to confirm a diagnosis. Pretty gutsy.

I can’t find a diagnostic test for L. longbeachae that will return before he finished a course of antibiotics, so it will remain a presumptive diagnosis.

But the right one.

And he got all better on azithromycin, and maybe because of azithromycin.

Rationalization

Validation of a Prediction Rule for Legionella Pneumonia in Emergency Department Patients https://academic.oup.com/ofid/article/6/7/ofz268/5511486

Risk Factors for Legionella longbeachae Legionnaires’ Disease, New Zealand https://wwwnc.cdc.gov/eid/article/23/7/16-1429\*article

J Med Microbiol. 2016 Feb;65(2):142-6. doi: 10.1099/jmm.0.000215. Epub 2015 Dec 23. Comparison of Legionella longbeachae and Legionella pneumophila cases in Scotland; implications for diagnosis, treatment and public health response. https://www.ncbi.nlm.nih.gov/pubmed/26704297

J Infect. 1996 Nov;33(3):185-91. Relative bradycardia in infectious diseases. https://www.ncbi.nlm.nih.gov/pubmed/8945708

Why The Relapse?

Aug 20, 2019

Back after my yearly week off in Eastern Oregon hiking, biking, and golfing. Now I am beat and need a week off to recover from my week off. This year brought home the concept that I am getting old. And you youngsters reading this, don’t be fooled. 62 is old. My stamina is really on the downslope. A couple of years ago, the Canyon Creek Meadows Loop would have been nothing. This year? Man, it was hard. But an amazing hike even by Oregon standards.

The patient was admitted with fevers, chills, flank pain, and dysuria. Past medical history is significant for cirrhosis. Blood and urine grow an E. coli, resistant only to quinolones.

After rapidly responding to ceftriaxone, she is sent out to finish a 14-day course of cephalexin.

Two weeks later, she is back with the same symptoms and the same cultures. CT shows pyelonephritis. This time they call me.

So why the relapse?

It could be the host. Blood stream infections are common and complicated in cirrhosis for a variety of reasons, both anatomic and immunologic.

Liver disease leads to low complement and low mannose-binding lectin levels, but neither are all that important in E. coli infections.

How about the antibiotic? I was always told never to use cephalexin for complicated E. coli infections and the IDSA guidelines say

Other β-lactams, such as cephalexin, are less well studied but may also be appropriate in certain settings.

Less well studied is quite the understatement; I could find little on the use of cephalexin for cystitis, complicated or otherwise.

What I had never considered is the wonky pharmacokinetics of antibiotics in cirrhosis:

Patient with LC have several unique pathophysiological characteristics that can alter the PK/PD behavior and the in vivo activity of antimicrobial agents. These characteristics include: i) hypoalbuminemia and reduction binding to proteins; ii) altered distribution; iii) altered clearance of the antimicrobial.

I can’t find where anyone has ever looked at the pharmacokinetics of cephalexin in cirrhosis, but these issues are important for hydrophilic antibiotics, and generally, beta-lactams are hydrophilic. As a result

…larger loading and daily doses and are often required for hydrophilic antibiotics to achieve therapeutic blood levels.

So why the failure? Multifactorial, as is often the case.

This time I am going to suggest more and a longer course of an oral third-generation cephalosporin.

Rationalization

Association between Mannose-Binding Lectin Deficiency and Septic Shock following Acute Pyelonephritis Due to Escherichia coli https://cvi.asm.org/content/14/3/256

Oncotarget. 2018 Nov 6; 9(87): 35780–35789. Published online 2017 Dec 13. doi: 10.18632/oncotarget.23200 Bloodstream infection due to Escherichia coli in liver cirrhosis patients: clinical features and outcomes https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6254670/

Virulence. 2016 Apr; 7(3): 309–319. Published online 2016 Feb 11. doi: 10.1080/21505594.2016.1141162 Bloodstream infections in patients with liver cirrhosis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4871664/

Turtles all the way down

Aug 21, 2019

The patient was admitted with right-sided endocarditis with too numerous to count septic emboli. Well, I suppose I could count them, so let us say there are a lot.

The good news is that it is MSSA, so she is placed on nafcillin. And she doesn’t get better. Fevers persist.

Repeat blood cultures are negative, so initially we wait. You have to give antibiotics time to kick in, and with a 2 cm vegetation, that isn’t going to happen anytime soon. Antibiotics are not, contrary to popular belief, antipyretics.

But the fevers persist. At first, I presume it is a complication of the MSSA, a pocket of pus somewhere, so we go looking. No empyema or other abscesses on CT, no myocardial abscesses on TEE. Drug fever? Unlikely.

So we start getting more blood cultures.

And they grow. And grow.

Candida albicans.

And H. parainfluenza.

And Vionella spp.

And Abiotrophia

All 24 hours apart.

The sine qua non of endocarditis is a sustained bacteremia, or in this case, bacteremias.

The bacteria are mouth flora, but she denies using or licking needles or cheeking medications, or any other way for spit to gain access to the vascular system. I am a wee bit skeptical about the denials. As the Romans said, In culturis speramus.

The literature suggests around 5% of endocarditis is polymicrobial, but I see maybe one decade, and my prior record was three organisms. Candida leads the list as a co-conspirator.

Polymicrobial endocarditis may be more common than suspected. The vegetation is fertile soil for subsequent seeding by other bacteria. As I have said before, big vegetations have little vegetations upon their backs to bite them, and little vegetations have lesser vegetations, and so ad infinitum. It is endocarditis all the way down.

One curious study found in PCR of vegetations that

Biodiversity was detected in 7 of 8 resected heart valves. This comprised 13 bacterial genera and 16 species. In addition to 11 pathogens already described as being IE related, 5 bacterial species were identified as having a novel association. In contrast, valve and blood culture-based diagnosis revealed only 4 species from 3 bacterial genera and did not show any relevant antibiotic resistance. The antibiotics chosen on this basis for treatment, however, did not cover the bacterial spectra identified by our amplicon sequencing analysis in 4 of 8 cases.

After optimizing the antibiotics, the fevers persisted. Is the fever due to the bacteria? The Candida? Other non-culturable organisms? Lack of source control, and she needs her valve out? All of the above? Yep.

It will be interesting to see what they find in the OR.

Rationalization

Polymicrobial Infective Endocarditis https://academic.oup.com/ofid/article/2/suppl\*1/856/2635079

Medicine (Baltimore). 2015 Dec;94(49):e2000. doi: 10.1097/MD.0000000000002000. Polymicrobial Infective Endocarditis: Clinical Features and Prognosis. https://www.ncbi.nlm.nih.gov/pubmed/26656328

PLoS One. 2017 Apr 14;12(4):e0175569. doi: 10.1371/journal.pone.0175569. eCollection 2017. New insights into valve-related intramural and intracellular bacterial diversity in infective endocarditis. https://www.ncbi.nlm.nih.gov/pubmed/28410379

What’s My Line? Infection http://boards.medscape.com/forums/?128@@.2a022384!comment=1

Here Today. Gone Tomorrow

Aug 26, 2019

Or perhaps, there yesterday, but gone today. But that isn’t the saying.

The patient, an injection drug user, is admitted with pleuritic chest pain and diagnosed with right-sided endocarditis: the usual fevers, MSSA in the blood, septic pulmonary emboli on the CT in the ER.

Now I probably would not have ordered an ECHO. Why bother? If positive, he gets treated for endocarditis. If negative, he gets treated for endocarditis, assuming that the vegetation broke up like an asteroid hitting the atmosphere. I know there are other reasons for septic pulmonary emboli, but there was nothing to suggest infection elsewhere.

But an ECHO was ordered.

And it showed a mobile vegetation. On the right atrial wall.

Is the occasional serendipitous diagnosis a reason for ordering a test? I know that it exerts a disproportional effect on physicians. Once they found an unexpected oddity, they spent the next 30 years ordering tests because, well, you remember that time I found an oddity I wasn’t expecting?

Atrial mural wall endocarditis is rare, especially in patients with normal valves and myocardium, as most mural endocarditis occurs where the jet from the VSD or MVP hits the myocardial wall. And he had no such anomalies to predispose to mural endocarditis.

I suppose it could be an atrial myxoma, and I have seen two cases, both left-sided, of infected atrial myxoma in my day. Whatever it was, it hadn’t been there three years ago with his last bout of endocarditis.

So we got a TEE to sort things out. And it was gone with the wind, or at least the right ventricular outflow tract. So I guess it wasn’t a myxoma. And, since he had no new pulmonary symptoms, we did not repeat the CT.

And we were back to where we would have been if we had done no ECHO at all. Righted-sided MSSA endocarditis

I suppose there might be an object lesson in all this, but I don’t what it is.

Rationalization

Primary Mural Endocarditis Without Valvular Involvement https://onlinelibrary.wiley.com/doi/pdf/10.7863/ultra.16.03049

Heart Lung Circ. 2016 Oct;25(10):e119-21. doi: 10.1016/j.hlc.2015.12.095. Epub 2016 Jan 28. Two Cases of Right Atrial Mural Endocarditis Caused by Staphylococcus Aureus. https://www.ncbi.nlm.nih.gov/pubmed/27256908

Heart Lung Circ. 2014 Aug;23(8):e172-9. doi: 10.1016/j.hlc.2014.03.026. Epub 2014 Apr 13. Bacterial mural endocarditis. A case series. https://www.ncbi.nlm.nih.gov/pubmed/24816290 POLL RESULTS

The take-home is

• do the same work-up on everyone 10%
• look for the once in a lifetime zebra a second time 10%
• stuff happens. Don’t worry overmuch 55%
• more is always better with diagnostics 2%
• plus ça change, plus c’est la même chose 24%

  Be not the first by whom the new are tried, Nor yet the last to lay the old aside.

  Aug 28, 2019

Thank you, Mr. Pope. Words to live by in medicine, but timing is everything. When to try the new or abandon the old? That’s the difficulty.

Two patients in the last few weeks with a similar problem: MRSA bacteremia from a removable focus. One a leg abscess, the other a central line.

Both defervesed in 24 hours, had no murmur, negative repeat blood cultures, and ECHO.

The first had lots of psychosocial issues that made outpatient antibiotics problematic. The other had medicare and a living situation that precluded coming in for once a day antibiotics.

And neither wants to go to a SNF.

As most know, to prevent the relapse, S. aureus bacteremia is always treated with iv antibiotics. Except when it isn’t.

A few years ago, there was a study that showed an oral quinolone plus rifampin was no worse than vancomycin, which has to be the definition of damning with faint praise.

As if there are any quinolone susceptible S. aureus anymore. TMP/Sulfa is equally effective

Within the limitations of a small retrospective study, co-trimoxazole had a safety and efficacy profile similar to that of vancomycin and may offer an attractive additional therapeutic option for MRSA bacteraemia.

But even in low-risk SAB, I have been chicken to try po. I do not want to tempt fate by trying the new. I have seen too many interventions that initially looked great turn out to be, well, problematic.

And linezolid? That looks a wee bit better:

Linezolid is an option with high clinical efficacy and good safety for MRSA bacteremia patients.

and

Treatment of SAB in selected low-risk patients with an oral switch to linezolid between days 3 and 9 of treatment until completion yielded similar clinical outcomes as SPT.

So I told both patients the same thing. The standard of care is iv. That means a nursing home. Oral might work, and linezolid is perhaps the best choice. You are low risk, but S. aureus is tricky, and it could come back to bite you. I did not mention where. Do you want to take a gamble and try oral?

They both opted for linezolid, one did well, the other was lost to follow up.

But I am still uncomfortable with using oral antibiotics as the majority of people with uncomplicated SAB don’t have a metastatic focus and likely, therefore, need no antibiotics at all. So maybe my patient did fine because he required no treatment.

That’s the problem with S. aureus bacteremia and other infections. We have no way of knowing when the last pathogen is not only merely dead, but really most sincerely dead, and we can safely stop antibiotics.

There is a critical need for high-level evidence from clinical trials to allow optimally informed decisions in the treatment of MRSA bacteremia and endocarditis.

Ya think? High-level evidence from clinical trials would be nice and perhaps better than a Munchkin coroner making the diagnosis.

Rationalization

J Antimicrob Chemother. 2010 Aug;65(8):1779-83. doi: 10.1093/jac/dkq179. Epub 2010 May 27. Co-trimoxazole versus vancomycin for the treatment of methicillin-resistant Staphylococcus aureus bacteraemia: a retrospective cohort study. https://www.ncbi.nlm.nih.gov/pubmed/20507860

A Randomized Clinical Trial to Compare Fleroxacin-Rifampicin with Flucloxacillin or Vancomycin for the Treatment of Staphylococcal Infection https://academic.oup.com/cid/article/39/9/1285/403489

Zhonghua Yi Xue Za Zhi. 2017 Apr 11;97(14):1084-1088. doi: 10.3760/cma.j.issn.0376-2491.2017.14.012. [Efficacy and safety of linezolid among patients with methicillin-resistant Staphylococcus aureus bacteremia]. https://www.ncbi.nlm.nih.gov/pubmed/28395434

Early Oral Switch to Linezolid for Low-risk Patients With Staphylococcus aureus Bloodstream Infections: A Propensity-matched Cohort Study https://doi.org/10.1093/cid/ciy916

POLL RESULTS

I

• am always the first to try the new. MMMMMMM. Popeye chicken sandwich 6% am the last to try the new.
• Cholamphenicol works just fine, thank you very much 22% think if it was good enough for Galen, it - is good enough for me 6%
• think if I wait long enough, what is old will become new again. I have digoxin and aminophyline futures 33%
• pretend that the new is old hat to me when asked 25% Other Answers 8%
• Retired.
• am not about to reveal my ignorance by opining on this topic, thank you very much.