Puswhisperer 12

The Wizard of ID

Sep 4, 2019

The patient has recurrent pelvic infections/abscesses. It’s a long story, the details of which are not important.

But every time there was a new infection, she would get a rash on her fingers, and the fingers would swell. And on antibiotics, the fingers would get better.

The fingers did not look infected, like a cellulitis, but more like a contact dermatitis. Curious.

I wonder: is this an ID reaction?

Id reactions are a type of secondary inflammatory reaction that develops from a remote localized immunological insult. To date, id reactions caused by various fungal, bacterial, viral, and parasitic infections have been reported… Id reactions exhibit multiple clinical presentations, including localized or widespread vesicular lesions, maculopapular or scarlatiniform eruptions, erythema nodosum, erythema multiforme, erythema annulare centrifugum, Sweet’s syndrome, guttate psoriasis, and autoimmune bullous disease.

Usually, id reactions are due to cutaneous fungal infections, but there are cases due to bacteria.

Reading the literature is a little frustrating as there are a hodgepodge of id reactions with a hodgepodge of infections. What they have in common is the skin lesions only go away when the primary infection is treated.

Most id reactions associated with a bacterial infection are reported to result in pustules of the palms and soles, called Andrews’ bacterid or Pustulosis palmaris et plantaris.

The more eczematoid lesions, like my patient, are reported with fungi, not bacteria.

And there are a smattering of recurrent cases.

And it does get better with treating the recurrent infection.

So maybe.

As to the origin of the term, per the Wikipedia

The suffix -id has its origins in Greek, referring to a father-son relationship. Josef Jadassohn (1863–1936), the German dermatologist that coined the term id, had observed a dermatophytosis causing a secondary allergic skin dermatitis. In 1928, Bloch recorded that the peak of the dermatophyte infection corresponded with the id reaction

and so are called dermatophytid, pediculid, bacterid, and tuberculid depending on the inciting infection.

Rationalization

Cutaneous id reactions: A comprehensive review of clinical manifestations, epidemiology, etiology, and management https://www.tandfonline.com/doi/abs/10.3109/1040841X.2011.645520

PUSTULAR BACTERIDS OF THE HANDS AND FEET December 1935 https://jamanetwork.com/journals/jamadermatology/article-abstract/515711

Arch Derm Syphilol. 1948 Aug;58(2):220-3. Acute recurrent pustular bacterid; report of a case. https://ncbi.nlm.nih.gov/pubmed/18110548

Yeah, but what do you do about it?

Sep 24, 2019

Two weeks hiking in the Canadian Rockies. If you ever get the chance, go. The Athabasca Glacier has only 30 years left, and the ice fields will be gone in 80. Sorry Greta, but it is already way too late to save the ice or anything else. It is all doomed. But while it lasts, it sure is beautiful. And while Rome burns, albeit it slowly, I can fiddle with ID.

At one level, as physicians, one of our tasks is to spend other people’s money, sometimes at prodigious rates. And that can make headlines.

Back surgery saved him from paralysis. Then the bills arrived: over $650,000.

While I could bankrupt patients with the best of them, I tend to fret the little things. For many of my patients, a $650 bill is as catastrophic as a $650,000 bill. If you don’t have the money, you don’t have the money, and for many, it takes very little to tip people into homelessness. And, as I have noted before, many people can’t even find $400 for an emergency.

So I was consulted on a patient with a long history of diabetic foot infections that finally resulted in admission and debridement. It was all a soft tissue infection. Plain films showed no osteomyelitis, and in the OR, it was superficial; it did not track to bone.

But in 4 days, the patient had 3 ESRs and 3 CRAPs. You know. C ReActive Protein. CRAP. At five days, the ESR and CRAP remained elevated, and there was worry about what it meant.

There are numerous studies to show ESR’s and CRP’s are predictive of outcomes. If the ESR or the CRP remains elevated, then failure is more likely.

Trajectories of the inflammatory markers showed an association between stagnating values of ESR and CRP and poor clinical outcomes.

and

the number of elevated markers was further associated with probability of infection both at admission and last follow-up.

But what is done with the information? Nothing. It doesn’t change patient care. It adds cost and anxiety, but it doesn’t alter the course.

One doc told me he felt better if the ESR or CRP was falling. I am of the opinion that you order tests to make the patient better, not yourself.

I prefer time. Time will tell if there is a good outcome or not with more reliability than an ESR or CRP and with less cost.

You might as well take the patients purse, toss it in the toilet, and flush.

I don’t think I have ever ordered a CRP, and the only time I get an ESR is when I am worried about PMR.

Waste of my patients money.

Rationalization

Athabasca glacier melting at ‘astonishing’ rate of more than five metres a year. https://www.theglobeandmail.com/news/national/athabasca-glacier-melting-at-astonishing-rate-of-more-than-five-metres-a-year/article18835512/

What If We Stopped Pretending? https://www.newyorker.com/culture/cultural-comment/what-if-we-stopped-pretending

Angry Greta Thunberg tells global leaders she ‘will never forgive’ them for failing on climate change. https://www.cnn.com/2019/09/23/weather/greta-thunberg-unga-climate-speech-intl/index.html

Back surgery saved him from paralysis. Then the bills arrived: over $650,000 https://www.cbsnews.com/news/back-surgery-saved-him-from-paralysis-then-the-bills-arrived-over-650000/

40% of Americans can’t cover a $400 emergency expense https://money.cnn.com/2018/05/22/pf/emergency-expenses-household-finances/index.html

Int J Low Extrem Wounds. 2017 Jun;16(2):104-107. doi: 10.1177/1534734617700539. Epub 2017 Apr 9.Does Everything That’s Counted Count? Value of Inflammatory Markers for Following Therapy and Predicting Outcome in Diabetic Foot Infection. https://www.ncbi.nlm.nih.gov/pubmed/28682724

Int Wound J. 2017 Feb;14(1):142-148. doi: 10.1111/iwj.12574. Epub 2016 Mar 8.Erythrocyte sedimentation rate and C-reactive protein to monitor treatment outcomes in diabetic foot osteomyelitis. https://www.ncbi.nlm.nih.gov/pubmed/26953894

Benign Gas

Sep 25, 2019

The patient is an elderly renal transplant patient who I put on chronic cephalexin for an infected prosthetic hip. With the onset of the antibiotics, she was plagued by mild diarrhea and bloating, but no reason, including C. difficile, was found.

So she dealt with it.

Five days prior to admission, it became acutely worse: more pain and bloating, so she went to the ER. Workup included a CT abdomen that showed impressive gas throughout the small bowel. Pneumatosis intestinalis. Usually, that amount of gas results in klaxons blaring and the robot waving his arms yelling, “Danger Will Robinson.”

But no. Pneumatosis intestinalis is a known complication of transplantation and is often benign and self-limited.

Since the early days of solid organ transplantation, PI has been described in recipients of kidney, liver, heart, and lung transplant. Despite the dangerous connotations often associated with PI, case reports dating as far back as the 1970s show that PI can be benign in solid organ transplant recipients. This is an important observation, as operative intervention in these patients carries greater risk than surgical procedures in the general population.

It occurs as well in a host of other diseases. She had a totally benign abdomen on exam. So we gave antibiotics, and she got better overnight.

But there were some issues.

She wanted to know if the antibiotics had caused this. I could find no association between pneumatosis intestinalis and antibiotics, so I thought not. My hypothesis was antibiotic-associated diarrhea with a late, superimposed pneumatosis intestinalis.

I found the small bowel involvement odd. Supposedly, the source of gas is bacteria.

A bacterial theory proposes that gas-forming bacilli enter the submucosa through mucosal rents or increased mucosal permeability and produce gas within the bowel wall. Studies have shown that gas collections in the bowel wall can have a hydrogen content of up to 50%. Hydrogen is a product of bacterial metabolism and is not produced by human cells.

Which explains why bacteria sound like Mickey Mouse. Maybe Mickey had a gut bacterial overgrowth syndrome. There are not all that much bacteria in the small bowel, relatively speaking. And

Primary Pneumatosis Intestinalis is most often seen in the descending colon. Secondary Pneumatosis Intestinalis commonly occurs in the small bowel but may be seen in any region of the bowel depending on causality.

But it is what it is.

And a C. difficile was positive. Kind of. The PCR was positive, but the toxin was negative, the proverbial indeterminate result. Was that the cause?

There are a couple of case reports with an association. And C. difficile can involve small bowel. And in my long career, I have seen a few cases of cecal C. difficile who had mild diarrhea, right lower quadrant pain, a negative assay but pseudomembranes on colonoscopy. I have wondered if the toxin degrades in the large bowel under those circumstances. That clinical scenario is not reported that I can find. So a stretch.

Given the host and the uncertainty, we, and by we I mean I, gave a course of vancomycin.

She is on an antibiotic holiday for now and is hesitant to restart the cephalexin. As am I.

Time will tell.

Rationalization

Pneumatosis intestinalis in solid organ transplant recipients http://jtd.amegroups.com/article/view/19736/15553

Pneumatosis Intestinalis in the Adult: Benign to Life-Threatening Causes https://www.ajronline.org/doi/full/10.2214/AJR.06.1309

Pneumatosis Intestinalis of the Small Bowel; Radiological and Intra-operative findings https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3649088/

Thinking beyond the colon-small bowel Involvement in clostridium difficile infection https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2664326/

Localized pseudomembranous colitis in the cecum and ascending colon mimicking acute appendicitis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3662872/

Off the Wall

Sep 30, 2019

“Tell your doctor if you have been to areas where certain fungal infections are common.”

Humera TV Advertisement

Just what does that mean? I know what it means. I’m an ID doctor, but what kind of warning would that be to the general population? And outside of Antarctica, is there a continent where certain fungal infections are not common? What a ‘warning’. Specifically non-specific.

I like to practice within the parameters of science/evidence-based medicine. When I write my notes and make a recommendation for treatment, more often than not, I cut and paste the appropriate Pubmed references to support my plan. Housestaff seems to like it.

In my decade over at Science-Based Medicine I learned just how awful some of the published science and evidence could be. But still, I do have an affinity for the occasional off-the-wall idea when I have nothing to offer the patient.

The patient is an elderly female with advanced COPD from 3 packs a day for most of her life. She has frequent exacerbations where she gets short of breath, fatigue, the sputum turns green, and, more often than not, the sputum grows H. influenza. She gets better on amoxicillin and the other usual treatments for COPD.

Anything I can offer?

After my usual aich and pea, I say no.

This is not an issue of host immunity or the organism, but a structural problem due to lung damage, and I can’t fix the structural problem. Or can I?

I keep half an eye on the microbiome literature. I find it interesting and, like stem cell clinics, way over-hyped as a mechanism for disease modification.

But still.

COPD exacerbations are more likely due to a change in the microbiome than any specific organism:

Our analysis revealed a dynamic lung microbiota where changes appeared to be associated with exacerbation events and indicative of specific exacerbation phenotypes…We depict a microbial interaction network for the lung microbiome and suggest that perturbation of a few bacterial operational taxonomic units, in particular Haemophilus spp., could greatly impact the overall microbial community structure.

and

Dysbiosis of sputum microbiome was observed with significantly increased relative abundance of Moraxella in COPD versus healthy subjects and during COPD exacerbations, and Haemophilus in COPD ex-smokers versus current smokers. Multivariate modeling on sputum microbiome, host transcriptome and proteome profiles revealed that significant associations between Moraxella and Haemophilus, host interferon and pro-inflammatory signaling pathways, and neutrophilic inflammation predominated among airway host-microbiome interactions in COPD.

And one study suggested the change in the microbiome of COPD was from aspiration.

In our small study of subjects with COPD, we found oral and nasal bacteria in the lung tissue microbiota, confirming that aspiration is a source of the COPD lung microbiota.

In the past, I have suggested urine transplants for recurrent UTIs as a way to repopulate the bladder microbiome and prevent UTIs. I’m still waiting for someone to do the studies for me.

I can’t do a sputum transplant, but probiotics? There is a study in progress, and looking at the biologic plausibility is quite a stretch, mostly focused around immune-modulation, which is almost always a non-starter.

But if her upper airway is colonized with pathogens that are leading to COPD exacerbations, then, maybe, like in C.difficile, probiotics can take up mucosal binding sites, blocking pathogens.

I have never been a fan of probiotic pills. You cannot trust what is in supplements, and you can’t even be assured that if there are organisms in the probiotics, they are viable. Besides the Quack Miranda, they should have Caveat Emptor printed on every bottle in big letters.

But yogurt doesn’t have those issues.

So I told her, this is really, really, really off the wall, but try yogurt for the reasons mentioned above. If nothing else, you will get some nutrition.

And will it work? I will never know as even if she reports benefit, this N of one experiment is useless.

But still fun to think about.

Rationalization

Lung microbiome dynamics in COPD exacerbations. https://erj.ersjournals.com/content/47/4/1082

The lung microbiome: the perfect culprit for COPD exacerbations? https://erj.ersjournals.com/content/47/4/1034

Airway host-microbiome interactions in chronic obstructive pulmonary disease https://respiratory-research.biomedcentral.com/articles/10.1186/s12931-019-1085-z

Prevention of Acute Exacerbation in Subjects With COPD by Bacterial Decolonization in Lower Respiratory Tract (PAEAN) https://clinicaltrials.gov/ct2/show/NCT03449459

Probiotics in the management of lung diseases. https://www.ncbi.nlm.nih.gov/pubmed/23737654

POLL RESULTS

I

• have the occasional off the wall idea I tell patients 35%
• only treat certain fungal infections with off the wall ideas 3%
• don’t stray from the tried and true, although most of it will be proven wrong before I retire 29%
• think a foolish consistency is the hobgoblin of little doctors 23%
• just give a prescription and move on to the next patient. It’s all off the wall to me 6% Other Answers 3%
• have switched from Vicks Vapo-Rub to Povidone Iodine and Alum for toenail fungus. Look for the peer-reviewed publication in ten years or so

  Do Nothing

  Oct 3, 2019

The longer I am in medicine, the more I go from ‘don’t just stand there, do something’ to ‘don’t just do something, stand there’.

Case in point from a while ago.

I see a patient in clinic for an FUO. She has no medical problems, is in her 20’s and no risks for any unusual infections.

Just fevers to 101.8 with accompanying headache, myalgias, and malaise, worse in the afternoon/evening.

After a few days, she went to the local doc in the box. They ordered a CBC and Comp, both normal.

Fine

And a flu screen. Despite no cough. What a surprise, it is negative.

And a CMV and EBV serology. Really. Nothing that suggests a mono syndrome, you know, like sore throat, adenopathy, and exudative pharyngitis. What a surprise, these serologies are negative.

I really think that EBV serologies should be outlawed. I often get called upon to interpret EBV serologies ordered on patients with clinical syndromes with no resemblance to EBV. My attitude is you ordered them; you explain them.

She is told she has a viral syndrome and goes home.

The fevers persist, so she returns to the doc in the box and, this time, is diagnosed as sinusitis and given a course of doxycycline. Guess what. She doesn’t get better.

So she is referred on to Ultra doc in the box, where I guess they have CTs and more because she gets a pan-scan, an US, and other labs. All negative. What. A. Surprise.

And because they can’t figure out the fever, they send her to the ER.

That’s when I get called.

I can’t give good advice about an FUO over the phone with a second-hand history, so I said do nothing, and I will see her in the clinic. Where, as mentioned above, I found nothing of note.

But more importantly, it was day 17 of illness, and she had no fevers for the previous three days, only some ongoing malaise. She had improved on her own, as the young tend to do.

Here is the take-home message. Fevers in the young, with no comorbidities, focal findings, or risks are to be left alone. The fever will go away after 10-14 days, the time it takes to mount an antibody response. At most, do a CBC and comp. But otherwise, wait. Don’t do the FUO workup until the patient has an FUO.

The old? The immunoincompetent? The focal? The odd risk? They deserve an evaluation, hopefully, focused and directed by the history and physical.

Gods forbid such a patient ends up admitted; vast numbers of unneeded tests will be ordered. Been there, seen that.

I remember the old definition of an FUO: 3 weeks of fever and a negative workup after 7 days in the hospital. Those were the days when you could keep someone in the hospital for weeks for a fever; I remember them. Yes, I am that old.

One of the criteria for outpatient FUO is one week of “intelligent and invasive” ambulatory investigation. Interesting choice of words, intelligent and invasive. So snark inviting.

However, that 21 days is still essential. Most fevers are due to trivial causes in healthy, nonfocal people and will vanish with time, usually in two weeks. So do nothing for the first 3 weeks.

I did nothing, at which I think I excel. My wife would agree.

And I wonder just how much all her unneeded health care cost.

Rationalization

For once, no references to back up what I have written, but you know I am right.

But No Diarrhea

Oct 7, 2019

The patient, an elderly male, is admitted with dry heaves, abdominal pain, constipation, and a rapidly increasing WBC, going from 16,000 to 26,000 in 12 hours.

He is not a good historian due to advanced dementia, but the medical records indicate he had recently been in another hospital for a UTI and was treated with an iv cephalosporin followed by a po quinolone.

The initial workup is negative, so they call me. I don’t know. The patient has complaints of abdominal pain, but the exam is negative.

C. difficile is a common cause of a leukemoid reaction. Which this isn’t. Yet. But I am not happy with the diagnosis given the lack of diarrhea.

So for various reasons, we do a CT, and there is cecal and ascending colon thickening.

I have mentioned this before, and I will mention it again. Over the years, I have seen a smattering (less than 4 but more than 1) of cases of C. difficile that were isolated to the cecum who did not have diarrhea, only leukocytosis, and abdominal pain. The diagnosis was made on colonoscopy with pseudomembranes. I do not remember if they had a toxin sent; with solid stool, it would be rejected in this day and age.

I always assumed that there was not enough colon involved to cause diarrhea; the colon is excellent at absorbing fluid. And, perhaps with limited disease, maybe not enough toxin.

The is a grand total of one case in the Pubmeds:

Severe CDI may present without diarrhoea when the right colon or cecum is involved or when there is paralytic ileus, but usually presents with severe abdominal pain and fever….Our case illustrates a rare clinical situation where a patient developed severe CDI without any diarrhoea, abdominal pain or fever. Physicians should have a high degree of suspicion in diagnosing CDI in patients with an increasing WBC without any plausible explanation, even in the absence of diarrhoea, abdominal pain, and fever.

There has been no stool for an assay, and there are issues that preclude a colonoscopy. But C. difficile is where I am placing my money. Not that you should bet on a patient’s diagnosis.

So we, and by we I mean I, will see if he responds to po vancomycin, even though that is bias 5 from Observations on spiraling empiricism: its causes, allure, and perils, with particular reference to antibiotic therapy

Response implies diagnosis.

Sometimes it is all you have.

And he got better.

Rationalization

BMJ Case Rep. 2012; 2012: bcr0220125938. Published online 2012 Jul 27. doi: 10.1136/bcr.02.2012.5938 PMCID: PMC3391391 PMID: 22761206 Unusual association of diseases/symptoms Constipation in Clostridium difficile infection. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3391391/

A Medical-Skeptical Classic: Observations on spiraling empiricism: its causes, allure, and perils, with particular reference to antibiotic therapy https://sciencebasedmedicine.org/a-medical-skeptical-classic/

Hard to Ignore

The patient has progressive pain and dysfunction of his dominant shoulder. He has no other medical problems. It does not get red, hot, or swollen.

Plain films show the humeral head disintegrating over time. Labs are unrevealing for any medical problems, and the inflammatory parameters are normal.

There is no history of trauma or penetrating injury, or infection elsewhere.

Over about 9 months, it reaches the point where the shoulder needs replacement.

Preop the joint was aspirated with unimpressive results.

In the OR, the surgeon noted that the bone was soft, but the intra-operative gram stain was negative, so he placed a new shoulder.

Post-op, he was much better, but four separate cultures all grew C. acnes.

Pathology of the humoral head was not osteomyelitis but degenerative disease.

The surgeon was adamant: this did not look like typical DJD but also did not look like typical pyogenic infections.

So now what?

It is hard to ignore the cultures, despite the paucity of reported cases of osteomyelitis from this organism outside of trauma and surgery. But there is no other explanation for why the humeral head melted away like water on the Wicked Witch. By the way, I did not get the pun until years later, and it remains one of my all-time movie favorites.

The infection should be cured with removal, but how would I know given the inability of this organism to incite an inflammatory response? I told the patient I did not think he was infected, but as my wife would attest, my opinions are not perfect. The conservative option was a long course of po, what with metal and plastic in a possibly infected area.

And so we did.

Rationalization

Rev Med Internet. 2000 Jun;21(6):547-9. [Infectious osteoarthritis due to Propionibacterium acnes. Two new cases https://www.ncbi.nlm.nih.gov/pubmed/10909155

J Bone Jt Infect. 2019 Jan 29;4(1):40-49. doi: 10.7150/jbji.29153. eCollection 2019. Cutibacterium (formerly Propionibacterium) acnes clavicular infection. https://www.ncbi.nlm.nih.gov/pubmed/30755847

Propionibacterium acnes Osteomyelitis: Literature. https://jcmasm.org/content/jcm/25/2/251.full.pdf

The Wizard: Can I believe my eyes? Why have you come back?

Dorothy: Please, sir, we’ve done what you told us. We brought you the broomstick of the Wicked Witch of the West. We melted her.

The Wizard: Oh, you liquidated her, eh? Very resourceful.

POLL RESULTS

I can’t ignore

• cultures 23%
• my spouse 36%
• my prostate 15%
• social media 3%
• email 15% Other Answers 8%
• The Wizard of Oz
• alarms

  Ironic?*

  Oct 21, 2019

It’s like rain on your wedding day It’s a free ride when you’ve already paid It’s the treated C. difficile* with a negative toxin Who would’ve thought, it figures\ - Alanis Morissette

C. difficile has been a pain of late. I have seen a C. difficile load of diarrheas that are PCR positive, GDH positive, and toxin negative: the dreaded indeterminant.

I usually get called after the therapy is started and sometimes escalated when the patient does not get better.

I say the same thing. It is not C. difficile disease. You can’t have a toxin-mediated disease if you ain’t got no toxin.

PCR for toxin is positive. That just says the patient has the DNA/the organism.

Patients also can be colonized with or carry C. difficile without symptoms. This colonization state complicates clinical diagnosis since the organism can be detected but isn’t necessarily causing disease. Colonizations with toxigenic (ie. toxin-producing) strains occurs in up to 15% of patients, and approximately 6% of patients are colonized with nontoxigenic strains.

And the GDH?

GDH EIAs detect the enzyme produced by both toxigenic and/or nontoxigenic strains of C. difficile. GDH is produced at much higher levels than toxins A and B.

So it confirms what you knew from the PCR. They carry the organism. That is why you look for the toxin.

No toxin, no disease. GDG positive/toxin negative is a carrier, not actice C. difficile infection.

GDH negative/toxin positive (which I have yet to see) is uncertain.

And this result is born out in clinical trials:

Overall, toxin- patients had less severe diarrhea, fewer diarrhea days, and lower mortality (P < 0.001, all comparisons) than toxin+ patients. One toxin- patient (n = 1/6121; 0.02%) was diagnosed with pseudomembranous colitis, but there were no complications such as megacolon or colectomy for fulminant CDI among toxin- patients.

and

Patients with a positive molecular test result and a negative toxin immunoassay test result had outcomes that were comparable to patients without C difficile by either method.

And treating isn’t benign as

molecular tests for C difficile diagnosis is likely to result in overdiagnosis, unnecessary treatment, and increased health care costs.

Note the one series with one patient who was toxin negative but had pseudomembranes. Finding pseudomembranes is the diagnostic gold standard, right? Well maybe.

One of my patients had continued diarrhea despite an excessive amount of C. difficile targeted antibiotics and at colonoscopy had pseudomembranes. That makes the diagnosis, right?

Well, no. I did not know this, but there are more causes of pseudomembranes in heaven and earth than dreamt of in my philosophy:

…collagenous colitis, glutaraldehyde exposure, infectious organisms (Campylobacter, cytomegalovirus, Escherichia coli 0157:H7, Salmonella, and Strongyloides), inflammatory bowel disease, ischemia, and medications (nonsteroidal anti-inflammatory drugs, vasopressin) have been implicated as potential causes. Through similar mechanisms of endothelial damage with impaired blood flow and oxygenation, these conditions can predispose to pseudomembrane formation and can appear endoscopically and histologically similar.

And the pathologist was adamant: it was histologically ischemic, not C. difficile that caused the pseudomembranes.

I know. Every test has its operational characteristics, false positive, false negative, etc. So there are false negative toxin tests.

But lots of diarrhea means lots of toxin:

Fecal Clostridium difficile toxin (CDT) level correlates with disease severity and confers an increased risk of 30-day mortality.

So mild diarrhea? Maybe a false negative toxin assay. My patients? Bad diarrhea and toxin negative? A reason not C. difficile for the diarrhea.

I said don’t treat.

Rationalization

Diagnosis of C. difficile – Why So Difficult? https://www.aacc.org/publications/cln/articles/2018/november/diagnosis-of-c,-d-,-difficile

Overdiagnosis of Clostridium difficile Infection in the Molecular Test Era https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/2434732

Outcomes in patients tested for Clostridium difficile toxins. https://www.ncbi.nlm.nih.gov/pubmed/23009731

Pseudomembranous Colitis: Not Always Caused by Clostridium difficile https://www.hindawi.com/journals/crim/2014/812704/

False Negative Results in Clostridium difficile Testing https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4992222/

Advances in the diagnosis and treatment of Clostridium difficile infections https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5837143/

Clostridium difficile fecal toxin level is associated with disease severity and prognosis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6068787/

*Yes, I know

Baader-Meinhof Yet Again

Oct 23, 2019

The Baader-Meinhof phenomenon rules my life. So what’s the Baader-Meinhof phenomenon?

otherwise known as frequency illusion or recency illusion. This phenomenon occurs when the thing you’ve just noticed, experienced or been told about suddenly crops up.

It seems that as soon as I read an article, I see a case. Yeah, I know. Definitely not cause and effect. And I am well aware of the cognitive bias it represents. But still.

A couple of weeks back, I read Splenic Infarction: An Under-recognized Complication of Infectious Mononucleosis?, and a couple of days later, I get a consult referral for a young male with hepatitis, a positive EBV serology, and splenic infarcts.

Sure, I said. It’s mononucleosis and not much for me to do.

But.

Then I saw the patient. Only a mild sore throat. Minimal lymphadenopathy. 15% atypical lymphocytes. 2-3 x elevation in transaminitis. Pretty mild disease for EBV.

And the labs?

The EBV IgM was positive. But so was the CMV PCR. CMV serologies were not done, nor the EBV PCR.

So which was it? Clinically the presentation was more like CMV, and CMV can also cause splenic infarctions.

There is a literature to show that acute EBV can cause a false positive CMV IgM. They are both Herpes viruses, after all, so some antigenic relatedness. There are also a couple of cases of acute CMV causing a false positive EBV IgM, with, as in my case, the CMV PCR being the tiebreaker.

So I called it CMV mono. Not that it matters as both are self-limited, and he is already on the mend.

And to make it even messier, there was also a positive IgM for Parvovirus but no PCR. Parvovirus has also been associated with splenic infarcts, but not the rest of the clinical syndrome. And there have been false-positive EBV serologies with acute Parvovirus, although I can’t find cases of acute CMV causing a false positive Parovirus serology. But why not? IgM’s are always dicey.

The other option is a simultaneous CMV/Parvovirus infection, but I remain an Occam, not a Hickham, kind of guy.

Numquam ponenda est pluralitas sine necessitate forever.

And always take serologies with a grain of salt substitute.

Rationalization

What’s the Baader-Meinhof phenomenon? https://science.howstuffworks.com/life/inside-the-mind/human-brain/baader-meinhof-phenomenon.htm

Cytomegalovirus-associated splenic infarcts in an adult immune-competent man: a case report and review of the literature https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3978118/

Splenic Infarction: An Under-recognized Complication of Infectious Mononucleosis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5853003/

Splenic infarcts as a rare manifestation of Parvovirus B19 infection https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4865634/

Cross-Reactivity of Epstein-Barr Virus-Specific Immunoglobulin M Antibodies with Cytomegalovirus Antigens Containing Glycine Homopolymers https://www.ncbi.nlm.nih.gov/pmc/articles/PMC96137/

Immunoglobulin M for Acute Infection: True or False? https://cvi.asm.org/content/23/7/540

Acute Parvovirus B19 infection frequently causes false-positive results in Epstein-Barr virus- and herpes simplex virus-specific immunoglobulin M determinations done on the Liaison platform. https://www.ncbi.nlm.nih.gov/pubmed/19116304

Most Quoted

Oct 28, 2019

One of the changes in my practice with the advent of the EMR is the cut and paste. I rarely cut and paste from old notes as I do not like to repeat myself. Anything worth saying is worth saying once. Not. Like anyone ever goes back and reads my prior notes.

But I end most notes/consults with a reference or three cut and pasted from PubMed to back up my recommendations. What makes a specialist is, in part, my mastery of the literature, or at least my mastery of the Googles.

Housestaff and hospitalists seem to like it, and it makes it hard for people to ignore my recommendations if there is a disagreement as to the direction of the case. Besides my white beard, the references make sure they respect my authoritah!.

The medical article that has influenced me the most, and I have mentioned it many times, is Observations on spiraling empiricism: its causes, allure, and perils, with particular reference to antibiotic therapy. It should be required reading once a year by every physician in the US. It might improve medical care. National Spiraling Empiricism Day. Better the Columbus Day, to my mind, than celebrating the exchange of syphilis for smallpox and measles.

But that is not the article I reference the most. That would be Nolan and Beaty, the American Journal Medicine, 1976. I have mentioned it so many times over the last 30 years I have told my wife I want it on my tombstone. I referenced it twice today, and I should make it a dot phrase. Unlike most other papers, I am unaware of any contradictory study. Usually, papers follow Newton’s Second Law of the Medical Literature; for every study, there is an equal and opposite study. Not this one.

The main point of the paper: Community-acquired S. aureus bacteremia without a focus is endocarditis. Here is the abstract, with the most crucial point bolded

One hundred and five cases of bacteremia due to Staphylococcus aureus were reviewed to assess the current clinical spectrum of serious staphylococcal disease. Mortality was 21 percent, lower than previously reported. Patients could be separated into two groups according to the presence of identifiable primary staphylococcal infections; 63 bacteremic patients had such lesions, the remaining 42 lacked them. The latter group contained 24 of 26 cases of endocarditis.** Illnesses in that group were marked by the presence (in 38 of 42 patients) of staphylococcal foci occurring secondary to bacteremia. Such foci were responsible for five of seven instances of relapse or treatment failure encountered in that group. Secondary staphylococcal foci occurred in only five of 63 patients with primary infections, and the response of this group to conventional therapy for bacteremia was satisfactory. This study suggests that endocarditis has become an unusual complication of identifiable primary staphylococcal infection. A clinical classification based on the presence of such lesions therefore separates bacteremic patients likely to be cured by conventional antibiotic therapy (those with primary infections but no secondary foci) from others (those with secondary foci, suggesting endocarditis) who should receive a more prolonged course of antibiotics**.

I tell house staff that when they are 95, demented, and dying in the ICU, unable to recognize their family, that if someone shakes them out of their MS-induced stupor and asks them the significance of community-acquired S. aureus bacteremia without a source, their last words on this earth should be, “it’s likely endocarditis.”

For my practice, there has probably been no study with a more significant day-to-day impact on patient care. Your mileage may vary.

Rationalization

Am J Med. 1989 Aug;87(2):201-6. Observations on spiraling empiricism: its causes, allure, and perils, with particular reference to antibiotic therapy. https://www.ncbi.nlm.nih.gov/pubmed/2667357

Am J Med. 1976 Apr;60(4):495-500. Staphylococcus aureus bacteremia. Current clinical patterns. Nolan CM, Beaty HN. https://www.ncbi.nlm.nih.gov/pubmed/?term=1274983

POLL RESULTS

The reference that most impacts my practice is

• Nolan and Beaty. AJM . 1976 12%
• Observations on spiraling empiricism 6%
• House of God 35%
• How to Win Friends and Influence People 24%
• Jonathan Livingston Seagull 18% Other Answers 6%
• the beano

  When I Was an Intern

  Oct 30, 2019

Yeah. I do a lot of that ‘when I was an intern’ stuff. That was 37 years ago, and there has been a lot of pus under the bridge. I feel like one of those awful Farmer’s commercials. It always amazes me that it is someone’s job, an adult mind you, who get paid to write those commercials. But I should talk.

When I was an intern, there was no gastric acid suppression. Cimetidine was released when I was an R2 and saved my call nights; I used to get the worst dyspepsia around 2 am.

Because there were no acid medications and H. pylori was still unknown, gastric ulcers were thought to be due to stress, and I have some vague memory about ulcers in executive monkeys… huh. I just searched and found Ulcers in “executive” monkeys from 1958.

A series of experiments designed to discover the emotional stress variables related to the development of gastrointestinal lesions. Pairs of monkeys were placed in “yoked chairs” where they could be presented brief shocks on the feet at regular intervals (e.g., every 20 secs.). By pressing a lever at least once within the period, the “executive” monkey could avoid the shock for both. Each was subjected to the same physical stress (shocks at the same time and frequency) but only one was under the psychological stress to press the lever. Various training schedules were used (e.g., alternate 6-hour periods of shock-avoidance and rest); some, such as this one, led to death with evidence of gastrointestinal abnormality for the “executive.” Investigation of gastric processes during conditioning revealed maximum acid secretion during rest periods.

I’ll be damned; there’s a blast from the past. And I guess it was a lousy study—what a surprise. And poor monkeys. I’ll have to ask the medical students if they have ever heard of the executive monkey, the POTUS excluded.

I digress.

The patient comes in with acute, severe mid-epigastric pain and GI bleed, and a CT shows a gastric perforation. Endoscopy finds an ulcerating tumor, and she is placed on broad-spectrum antibiotics.

Four days later, one of the blood cultures grows a yeast, soon to be identified as C. glabrata. So they call me.

Candidemia, by the way, is yet another infection where mortality is improved by ID consult. It is a consistent finding that involving a physician who actually knows what they are doing with infections improves care. I would never have guessed. Personally, when I get sick, I want someone who knows little about my disease, randomly flailing about with diagnostic and therapeutic interventions.

One of the consequences of rampant gastric ulcers was rampant gastric perforations. I would wager, flawed, and biased my memory might be, that we saw one a month. And with it, we saw Candida peritonitis. And this was before fluconazole, and all we had was amphotericin B to treat the fungi.

Little known to youngsters today is that ulcers and Candida go together like peanut butter and jelly, which we also had a lot of when I was an intern.

Large ulcers (> 2 cm) were, however, more often colonized by Candida (75%) than smaller ones (43%) (p < 0.05).

and

These data suggest that Candida colonization of the gastrointestinal tract is common in patients with esophageal disease.

So it is no wonder when they perforate, they spill Candida into the peritoneal space.

He was going just fine when I saw him, so the only intervention I had was to increase the fluconazole to a dose (800 mg) more appropriate for his size and yeast.

Rationalization

Ulcers in “executive” monkeys. Brady, J. V. (1958). Scientific American, 199(3), 95-104. http://dx.doi.org/10.1038/scientificamerican1058-95

The Problem With The Famously Godawful Executive Monkey Study https://io9.gizmodo.com/the-problem-with-the-famously-godawful-executive-monkey-1643699082

PLoS One. 2019; 14(4): e0215996. Published online 2019 Apr 25. doi: 10.1371/journal.pone.0215996 The impact of infectious disease consultation in candidemia in a tertiary care hospital in Japan over 12 years https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6483235/

Indian J Gastroenterol. 1994 Oct;13(4):115-7. Fungal colonization of untreated peptic ulcer. https://www.ncbi.nlm.nih.gov/pubmed/7829139

Dis Esophagus. 2003;16(2):70-2. Candida colonization in patients with esophageal disease: a prospective clinical study. https://www.ncbi.nlm.nih.gov/pubmed/12823200

J Antimicrob Chemother. 2013 Apr; 68(4): 922926. Published online 2012 Dec 4. doi: 10.1093/jac/dks482 Fluconazole versus an echinocandin for Candida glabrata fungaemia: a retrospective cohort study https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3594495/

Clin Ther. 2005 Aug;27(8):1228-37. A retrospective Evaluation of fluconazole for the treatment of Candida glabrata fungemia. https://www.ncbi.nlm.nih.gov/pubmed/16199247

POLL RESULTS

When I was an intern

• we had no acid suppression 8%
• we had no third generation cephalosporins 3%
• we tied an onion on our belts, as was the style of the day 27%
• we were on call every night and walked uphill to get to work 11%
• tattoo’s meant either a sailor or a sociopath 38% Other Answers 14%
• I wasn’t.
• All of the above!

  Neurotoxic Accumulation

  Nov 4, 2019

The patient is admitted with a fever, and the work-up was mostly negative. All cultures were negative, but a TTE showed a floppy mitral valve vegetation, confirmed on TEE.

She has diabetes on dialysis and, in the weeks prior to admission, had several short courses of vancomycin and ceftriaxone for a leg ulcer/cellulitis where no blood cultures were done.

She had no exposure history to suggest an unusual cause of endocarditis, and the usual culture-negative endocarditis evaluation was negative. I figured it was likely the usual suspects, an oral Streptococcus or a Staphylococcus that was either partially treated or cured. But she had never had a definitive antibiotic course for endocarditis, so I suggested vancomycin and ceftriaxone, the latter at 2 grams a day.

A week into therapy, she became agitated, disorientated, and had hallucinations. No metabolic or other cause was found, and the hospitalist asked me if it could be the ceftriaxone.

Beta-lactams, especially penicillin and imipenem, can be neurotoxic, but I don’t think I have ever seen a case due to ceftriaxone, and one review suggested

The most high-risk agents in this group are cefazolin, cefoselis, ceftazidime, cefoperazone, and cefepime. Cephalexin, cefotaxime, and ceftriaxone have also been associated with some neurotoxic effects, but their probability of causing side effects is lower than that in the former group. The reported clinical presentations of cephalosporin-induced neurotoxicity are lethargy, tardive seizures, encephalopathy, myoclonus, chorea-athetosis, asterixis, seizures, nonconvulsive status epilepticus, and coma.

But there are a few case reports of ceftriaxone leading to neurotoxicity, half of which are in endstage renal disease.

Being excreted by way of the bile, it doesn’t get a chance to reach toxic levels. Or does it?

As CTRX is excreted via both biliary and renal excretion, patients with renal failure require no adjustment in dosage. However, in cases of ESRD, delayed clearance of CTRX has been reported. Simon et al. recommended CTRX 2 g i.v. after each dialysis session only in maintenance hemodialysis patients. We believe that CTRX accumulation in ESRD is not well recognized, as all attending doctors in our cases were not aware of it.

As I think about it, I rarely give long-term ceftriaxone in dialysis patients since it requires a central line and has to be given on non-dialysis days. We usually default to ceftazidime, which can be given at dialysis and is simpler, it avoids a new line, and for most gram-negative infections, no worse than ceftriaxone.

So yeah. Ceftriaxone accumulation in ESRD was not well recognized by me, and I was not aware of it. I am now.

I did not check a ceftriaxone level but stopped the ceftriaxone, and her mental status changes resolved.

The official recommendation for ceftriaxone dosing in renal failure is

No adjustment for hemodialysis.

Maybe not so much. Long term, a gram a day may be enough, although it would be nice to be able to check drug levels easily.

Rationalization

NI FEATURE: THE QUEST - COMMENTARY 2018 Volume 66; Issue 6; Page 1732-1740 [Neurotoxicity of the antibiotics: A comprehensive study http://www.neurologyindia.com/article.asp

Kidney Int Rep. 2017 Sep; 2(5): 984–987. Published online 2017 Apr 7. doi: 10.1016/j.ekir.2017.03.009 PMCID: PMC5733829 PMID: 29270508 Three Cases of Hemodialysis Patients Receiving High-Dose Ceftriaxone: Serum Concentrations and Its Neurotoxicity https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5733829/

A Relationship

Nov 7, 2019

At work, we get Bing now instead of Google, and I have yet to adapt. Since I like to leave references to support my recommendations at the end of consults, I often search not for new information but for references I already know and cases I have written about.

So I use my name as part of the search criteria since I am looking for something that is likely in my app or on this blog. Google isn’t bad at returning references; Google Scholar being even better. Bing is awful. I get nothing I am looking for.

But thanks to Bing. I did discover that I have a lot of bad reviews. I know there are a few people out there that hate me, thanks to my time at Science-Based Medicine. Even though I retired from the site a couple of years ago, I still get the occasional vitriolic email, badly in need of Grammarly, letting me know what a horrible human and physician I am. They never bother to argue their position from the literature, just a general wish that I rot in hell for eternity, where I will at least be with friends and family.

I might cop to arrogant, but not well-read? No way. But if anyone reading this feels the urge to write a review of me on the interwebs, please be specific about my failings. Non-specific feedback is hard to apply.

A little thing. The patient comes in with an increase in chronic seizures, fevers, and altered mental status. He refuses an LP, and he has a pacemaker, so it’s antibiotics after a negative enhanced CT.

Eventually, they call me, and I find a patient with an encephalitis/altered mental status but no meningismus. I had no great ideas except to push for an LP; treating a CNS infection without an LP is like treating diabetes without blood sugars.

So eventually, we get the LP, and it is one of those odd, traumatic, taps. No WBC. 9000 RBC Normal glucose. Protein 600. Glucose normal. The CSF PCR panel is negative.

So probably not infectious. But that protein. Too high. But what should it be? Once you get blood in an LP, it makes interpretation difficult. But there is a relationship twixt RBC and protein, at least in children (and why not adults?):

We sought to determine the relationship between cerebrospinal fluid (CSF) protein and CSF red blood cells in children with traumatic lumbar punctures. For every 1000 cell increase in CSF red blood cells per mm(3), CSF protein increases by 1.1 mg/dL.

So the protein is way too high to be from a traumatic tap. CSF proteins that elevated make me suspect an epidural abscess/CSF blockage, but nothing to suggest either by exam or studies. And he is getting better.

For now, I am declaring him not infected and see what neurology can discover.

We never did get an explaination.

Rationalization

J Pediatr. 2011 Jul;159(1):158-9. doi: 10.1016/j.jpeds.2011.02.038. Epub 2011 Apr 14. Correction of cerebrospinal fluid protein for the presence of red blood cells in children with a traumatic lumbar puncture. https://www.ncbi.nlm.nih.gov/pubmed/21492866

POLL RESULTS

I

• do not read on-line reviews 21%
• read only positive reviews 5%
• avoid all social networks 41%
• am stabbed through the heart with every critical word 8%
• am firm in the knowledge of my personal perfection 23%

  Sure. It Should Work

  Nov 12, 2019

The patient has been on CAPD for years, a failed transplant, still on low dose immunosuppressives. His renal failure was not due to diabetes. He recently changed to hemodialysis and was doing fine until fevers and rigors. Blood cultures grew MSSA, and his catheter was removed, with a rapid fall in his fever and an increase in his sense of well-being. Repeat blood cultures were negative, as was the ECHO.

Since S. aureus bacteremia leads to an automatic ID consult in my system, I saw the patient. An uncomplicated S. aureus bacteremia in a complicated patient, he needs 4 weeks of cefazolin.

The problem with renal failure patients is that the nephrologists want to leave their veins alone for future dialysis access, so no PICC. It’s another central line.

And no. Vancomycin is a bad idea, even if it is more convenient.

Hemodialysis-dependent patients with MSSA bacteremia treated with vancomycin are at a higher risk of experiencing treatment failure than are those receiving cefazolin. In the absence of patient specific circumstances (e.g., allergy to beta-lactams), vancomycin should not be continued beyond empirical therapy for hemodialysis-dependent patients with MSSA bacteremia.

If you were going to suggest that option, it is why S. aureus bacteremia should get an automatic ID consult from you as well.

But, I was asked how about giving the antibiotics in the CAPD fluid?

Interesting idea. Intraperitoneal (IP) is often the route of antibiotics administration in rats and results in good systemic drug levels. Humans? There is not a lot of data.

The mean+/-SD amount of cefazolin dose absorbed from the dialysate after the 6-hour dwell was 69.7%+/-8.0% of the administered dose. The cefazolin absorption rate constant from dialysate to serum was 0.21+/-0.1/hr (absorption half-life 3.5+/-0.8 hr). The mean serum concentrations reached at 24 and 48 hours were 52.4+/-3.7 mg/L and 30.3+/-5.9 mg/L, respectively.

resulting in

single daily dose of cefazolin dosed at 15 mg/kg actual body weight in CAPD patients is effective in achieving serum concentration levels greater than the minimum inhibitory concentration for sensitive organisms over 48 hours.

In another series with 1 g of IP cefazolin given once daily over a 6-h dwell had a

Mean plasma and dialysate concentrations at 24 h were 42.8 +/- 14.3 and 31.8 +/- 11. 7 mcg/ml, respectively, well above the minimum inhibitory concentrations (MIC) of susceptible organisms.

That’s way above the MIC of 1.0. So, sure, it should work for S. aureus bacteremia. But has anyone tried it to treat a systemic infection? Not that I could find. As another review noted

The intraperitoneal route may have a role in the treatment of systemic infections in peritoneal dialysis patients, but specific recommendations cannot be made until clinical studies have been performed.

So I talked it over with the patient, and he was willing to give it a try. And it worked.

Or he didn’t need the antibiotics as not everyone needs a long course for SAB; the problem being we don’t know in advance who those patients are.

Rationalization

Clin Infect Dis. 2007 Jan 15;44(2):190-6. Epub 2006 Dec 8. Use of vancomycin or first-generation cephalosporins for the treatment of hemodialysis-dependent patients with methicillin-susceptible Staphylococcus aureus bacteremia. https://www.ncbi.nlm.nih.gov/pubmed/17173215

Clin Pharm. 1992 Mar;11(3):246-54. Systemic absorption of intraperitoneal antimicrobials in continuous ambulatory peritoneal dialysis. https://www.ncbi.nlm.nih.gov/pubmed/1611814

Perit Dial Int. 1999 Jan-Feb;19(1):65-70. Pharmacokinetics of intermittent intraperitoneal cefazolin in continuous ambulatory peritoneal dialysis patients. https://www.ncbi.nlm.nih.gov/pubmed/10201343

J Am Soc Nephrol. 2000 Jun;11(6):1117-21. Pharmacokinetics of once daily intraperitoneal cefazolin in continuous ambulatory peritoneal dialysis patients. https://www.ncbi.nlm.nih.gov/pubmed/10820176

Karius for Carious

Nov 13, 2019

On hemodialysis for years due to hypertension, the patient has months of malaise, low-grade fevers, night sweats that wax and wane.

Work-up during this time is negative except for mildly elevated inflammatory parameters. Also, this time, he has extensive dental work for bad teeth and receives several courses of antibiotics for dental infection. It is hard to tell with certainty that he improved on oral antibiotics, but I think so.

Eventually, he was admitted with fever and SIRS, and I am called. He gets the fever evaluation and H&P has almost nothing. No exposure history to point at an unusual infection. The exam is unimpressive. Five of six blood cultures are negative, one with a coagulase-negative Staphylococcus. CT/TEE are not helpful; the latter with no vegetation, although the valves are not pristine.

So, where to go from here? He has been sick and is acting more like endocarditis than a collagen vascular disease for his symptoms.

It is one of those cases I wish I could do a PET scan, which would be good to evaluate the valve and the graft, but they are not approved for ID issues and cost a small fortune.

So I sent off a Karius test. It is a bit cheaper than a PET and may give an answer for what I think is a partially treated endovascular infection.

And it was positive for Rothia mucilaginosa. That organism shouldn’t be in the blood. It is a mouth organism, and all the prior dental work is a good reason for it to spread elsewhere.

But here is the problem. There are no cases of this organism on native valves (a few prosthetic valves) or hemodialysis fistulas (a few on CAPD catheters). And his dental issues are fixed. And for what it is worth, Rothia is not an organism identified in the blood of those who have dental manipulation.

So now what. Maybe he needs that PET scan after all.

I treated for an endovascular infection, and he improved. Meh. There is nothing I hate more than assuming the response to therapy makes a diagnosis. But for now, it’s all I have.

Rationalization

Rothia Bacteremia: a 10-Year Experience at Mayo Clinic, Rochester, Minnesota https://jcm.asm.org/content/52/9/3184

UNCOMMON PATHOGEN WITH AN AFFINITY TO THE HEART; ROTHIA MUCILAGINOSA https://www.shmabstracts.com/abstract/uncommon-pathogen-with-an-affinity-to-the-heart-rothia-mucilaginosa/

Microbiology of Odontogenic Bacteremia: beyond Endocarditis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2620633/

Dissemination of Periodontal Pathogens in the Bloodstream after Periodontal Procedures: A Systematic Review https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0098271

Shaken

Nov 18, 2019

Well, my hands are shaky and my knees are weak I can’t seem to stand on my own two feet Who do you think of when you have such luck? I’m in love I’m all shook up

The patient follows up in the clinic on the last day of a 6-week course of vancomycin.

He has done well for the duration, normal labs, and good drug levels until the last 4 days. He now had tremors. Bad tremors in both his hands and, to a lesser extent, his feet. They were severe enough to interfere with eating due to spilling.

The exam was normal except for the shakes, which were impressive, almost Waco Kid level tremors.

He did have a benign intention tremor, which had now been magnified many times over.

He was on no neurotoxic medications and wondered if the shakes were due to the vancomycin. My first response was no. I have filled a swimming pool many times over with the vancomycin and have never seen any neurologic toxicities, 8th nerve notwithstanding. But a quick Google demonstrated that Elvis was wrong as to the etiology; it was likely the vancomycin.

We present a case of severe tremor due to vancomycin that has not been previously reported in the literature. Our patient might have been prone to this adverse effect, given an underlying essential tremor. Causality is presumed based on the temporal association, while the pathophysiological link remains elusive.

This was the only case I could find on Google or Pubmed, so I have doubled the medical literature.

Like the above case, my patient improved with the cessation of the vancomycin, suggesting causality.

I can’t find any even hypothetical mechanism, so who knows — a very rare curiosity.

Rationalization

Waco Kid https://imgur.com/gallery/HNS0lgD

Severe tremor due to vancomycin therapy: a case report and literature review https://www.sciencedirect.com/science/article/pii/S1201971212001427

Only With The Culture Did It All Become Clear

Nov 20, 2019

“Fool me once, shame on … shame on you. Fool me… You can’t get fooled again!’”

G. Bush

The patient presents with a blistering, 7/10 pain along V1 and in the ear, low-grade fevers, and some lymphadenopathy. Exam shows 3 blisters near the midline, but the ear exam is normal and no paralysis, so not a Ramsey-Hunt.

Shingles, right?

Except he had the chickenpox vaccine and never had chickenpox. So why shingles?

Two hypotheses. The first, and my favorite, is that he had had mild or unrecognized chickenpox before he had the vaccine. It happens.

The second is that this is Zoster from the vaccine strain. That seems unlikely, not having, as best I can tell, been reported in normal hosts, and the presentation didn’t fit either clinical pattern:

HZ caused by vaccine strain VZV would be associated with a history of vaccine-associated rash, whereas HZ caused by wild-type VZV would be associated with prior breakthrough varicella.

A viral culture was sent. I thought if it were positive, it would be interesting to send it to the company to see if it was the vaccine strain.

Nope. HSV-1 grew. Fooled again.

Over the years, I have seen HSV show up in various atypical locations, so I should have thought of it. I told the patient that I could not think of anything but Zoster that would present like this. Premature closure? I don’t know if I failed to consider a reasonable alternative after an initial diagnosis is made. I wanted another diagnosis, and I couldn’t think of one at the time.

So further questioning. He has never had HSV, and the severity of the illness is more consistent with acute rather than reactivation disease.

His wife? Never had HSV. But most people who have HSV are asymptomatic and constantly shed at low levels:

The most frequent site of shedding was the oral mucosa, with widespread shedding throughout the oral cavity. Lesional shedding rate was 36.4% (4 of 11 days with lesions), and the asymptomatic rate was 27.1%

And, he said, his wife always kisses him daily on the forehead, has since they were dating. And here is the odd extra. He has multiple small arterial-venous malformations on his forehead on the same side as the blisters. It appears that HSV-1 has a predilection for infecting vascular endothelium, so perhaps a risk for infection in an atypical location.

So it is primary HSV of the forehead vascular endothelium from being kissed by an asymptomatic spouse.

I did not send off antibodies to prove my hypothesis about who had HSV and gave it to whom, too high a copay.

That’s my story, and I am sticking to it.

Rationalization

BMJ Case Rep. 2011; 2011: bcr0820114594. Published online 2011 Oct 7. doi: 10.1136/bcr.08.2011.4594 Learning from errors The pitfalls of premature closure: clinical decision-making in a case of aortic dissection https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3189641/

Contemp Clin Dent. 2010 Apr-Jun; 1(2): 127–129. doi: 10.4103/0976-237X.68588 Herpes zoster oticus: A rare clinical entity https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3220085/

G323(P) A case of shingles with no history of chicken pox https://adc.bmj.com/content/103/Suppl\*1/A131.1

Cutis. 2017 Mar;99(3):207-211. Herpes zoster following varicella vaccination in children. https://www.ncbi.nlm.nih.gov/pubmed/28398421

Risk of Herpes Zoster in Adults Immunized with Varicella Vaccine https://academic.oup.com/jid/article/197/Supplement\*2/S196/846024

Sex Transm Dis. 2016 Dec; 43(12): 756–760. Herpes Simplex Virus Type 1 Shedding in Tears, and Nasal and Oral Mucosa of Healthy Adults https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5117635/

Trans Am Clin Climatol Assoc. 1992; 103: 95–104. Herpes virus infection of endothelium: new insights into atherosclerosis

No Way It’s Subacute

Nov 26, 2019

The patient, an elderly male, is admitted with a month or two of failure to thrive and mild confusion. Work up shows a mild leukocytosis, and 1 of 2 bottles grow MSSA. So they call me.

Now a few weeks before admit the patient had a TTE that showed a mass on the mitral valve, and at the time, he had negative blood cultures.

I find little on the exam except for a mildly swollen three-year-old prosthetic knee, and he says it has been hurting for a couple of weeks.

I ask for the knee to be tapped, and it, too, grows MSSA. Repeat TTE shows, yep, there is still a mass on the mitral valve.

I have never, ever, seen subacute endocarditis from S. aureus. Never. Ever. I could not find a case on the interwebs, but my old boss said he absolutely saw a case back in the day, and he has never led me astray. But.

I am an Occams kind of guy, but this is a case for Hickam. I think this is a septic prosthetic joint with bacteremia, AND he has a mitral tumor, maybe a fibroelastoma?

Valvular tumor and tumor-like lesions accounted for 0.32% of adult cardiac operations. Five (45.5%) valvular lesions were papillary fibroelastomas, one (9.1%) was myxoma, 2 (18.2%) were organized thrombi, and 3 (27.3%) were calcification lesions.

It isn’t clot. No reason for marantic or pioneer endocarditis. I suppose it could be culture-negative endocarditis, but he has zero risks and nothing on exam.

But. It did not look like the usual tumors.

Papillary fibroelastomas are usually smaller than 1cm, attached to the valve by a short stalk, thereby having greater freedom and mobility… Valvular myxomas are … gelatinous, lobulated tumors, often solitary with a short stalk.

But is a mass sitting on the tip of the valve, like a booger on the end of a finger that can’t be flicked off. Or so I hope. So I don’t know, and never will. There are, as is often the care, issues that ensure there will not be a definitive diagnosis.

Rationalization

Rare Tumors. 2009 Dec 28; 1(2): e35. Published online 2009 Dec 28. doi: 10.4081/rt.2009.e35 Tumors and tumor-like lesions of the heart valves https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2994454/

I Knew That. Really.

Dec 2, 2019

The patient is admitted with fevers and several months of progressive decline. She is also a renal transplant patient who had been treated as an outpatient for BK virus.

Work-up was not impressive, with an unrevealing bronchoscopy, so they called me.

History was unrevealing except for a relentless decline in ADLS with fatigue and decreased appetite over the last several months with a negative workup.

She did, however, have significant risks for endemic fungi, having had significant time in both Cocciomycosis and Histoplasmosis territories. The CT supported the diagnosis, having calcified granuloma in the lung, spleen, and lymph nodes.

So I wondered about a sub-acute fungal infection, so I sent off diagnostics, and the 1-3 beta d glucan came back positive in the mid-two hundreds.

Bingo, right?

Well, there are a lot of reasons for false-positive fungitels.

Numerous potential causes of false BG positivity have been reported and include hemodialysis with cellulose membranes; serosal exposure to gauze or other materials that contain glucans, such as during surgery; and administration of blood products, albumin, immunoglobulin, coagulation factors, or plasma protein fraction filtered through BG-containing filters. Additionally, high triglycerides, hemoglobin (hemolyzed samples), and bilirubin have been shown to interfere with the Fungitell assay. There are also reports that some antibiotics may cause false-positive results.

Including ampicillin/sulbactam and piperacillin/tazobactam. And

There are also reports of BG positivity in patients with bacteremia, with indications that BG levels appear higher with gram-negative than gram-positive bacteremia. Some species of Streptococcus, Escherichia coli, and Pseudomonas have been shown to produce glucan or glucan-like polymers that could potentially interfere with the BG assay.

So not a great assay. Especially when you consider that most of my patients have at least one of the issues on the list that can cause a false positive.

Still, I always look at the medication list and other reasons for a false positive. Nothing. So fungus? I wrote some note to the effect that was where we should look further.

Then I got a call from pulmonary. You know, she said, he had been getting IVIG for his BK virus as an outpatient, wouldn’t that be a cause of a false positive fungitel.

Godfrey Daniels.

I knew he had been getting IVIG as an outpatient for the BK, but it wasn’t on the med list. Out of EMR, out of mind? And I knew that IVIG led to a false positive fungitel.

BDG peak levels within 3 days after IVIG ranged from 21.47 to 660.38 (median 201.4) pg/ml. BDG serum levels at 7, 14 and 21 days (+/-1 day each) after IVIG infusion were significantly higher than BDG serum levels in the control group (p < 0.001 each). By days 7, 14, and 21 (+/-1 day each) after IVIG infusion, BDG serum levels have normalized (<80 data-preserve-html-node="true" pg/ml) in 64.0%, 76.5% and 100%, respectively.

But it didn’t click; I had to be reminded by pulmonary. How embarrassing.

I even know where I learned the factoid, as part of my last MOC review. So here is my take. Information you acquire as part of patient care goes to the part of your brain where it is accessible. Information you acquire as part of a useless waste of time and money goes to the part of the brain reserved for garbage and is ignored.

It is a theory that fits the facts. That’s my story, and I’m sticking to it.

Rationalization

Transplant Proc. 2015 Mar;47(2):394-8. doi: 10.1016/j.transproceed.2015.01.012. Efficacy of intravenous immunoglobulin in the treatment of persistent BK viremia and BK virus nephropathy in renal transplant recipients. https://www.ncbi.nlm.nih.gov/pubmed/25769580

J Infect. 2018 Feb;76(2):206-210. doi: 10.1016/j.jinf.2017.10.017. Epub 2017 Nov 23. False positive serum levels of (1-3)-ß-D-Glucan after infusion of intravenous immunoglobulins and time to normalisation. https://www.ncbi.nlm.nih.gov/pubmed/29174967

Application of the 1,3-b-D-Glucan (Fungitell) Assay in the Diagnosis of Invasive Fungal Infections https://www.archivesofpathology.org/doi/pdf/10.5858/arpa.2014-0230-RS

Poll Results

I

• only remember information associated patient care 23%
• learn from the ABIM tests 0%
• learn nothing, Google everything 33%
• think it should be called a Mock, as it makes a mockery of learning 0%
• find this blog the best source of new information 33% Other Answers 10%
• can’t remember. What was the question?
• often cannot recall the first part of a sentence as I read the last part. Somehow, this does not seem to bother me. Oldness sucks.

  How and Why

  Dec 4, 2019

The patient is an elderly male who, three months ago, started to have spontaneous drainage from his chest wall. A swab grew MSSA, and he was treated with cephalexin to no avail.

A year or so earlier, he had developed an ulcer on his right wrist that also did not resolve, but he mostly ignored that.

One thing, as things tend to do, led to another, and he had the chest wall lesion I&D’d. It went down to cartilage but not bone, and the surgeon cleaned it up and sent cultures for everything.

Thank you. I am driven nuts by some of my surgical colleagues who repeatedly do not send cultures from a debridement; then, I am asked to treat the osteomyelitis or the abdominal abscess or whatever. Arg. I guess they figure I can give Antibiotics, which, if big gun, powerful or strong enough, will take care of the issue. I doubt there is a single, or married, surgeon who reads this blog, but if there is, please culture ALL infections.

Anyway. It grows Coccidiomycosis, and he is sent to me.

He has all the ‘heart-ache and the thousand natural shocks That flesh is heir to’ seen in someone who is in their 80’s, but no worrisome immunosuppression.

He used to winter in Arizona but hasn’t been there, or left Portland, in over two years.

While in Arizona, he never had an illness or pneumonia or any penetrating trauma to his chest wall or arms. His hobby? Riding those 4 wheel ATVs in the dusty desert. As he describes the pastime, minor trauma was frequent and ignored.

He has zero CNS symptoms.

Skin manifestations can be seen in three different scenarios of coccidioidal infection: 1) they can be a part of the acute pulmonary infection and present as an “acute pulmonary exanthema”; 2) they can reflect the presence of a disseminated infection (secondary cutaneous infection); or, in rare occasions, 3) they can represent a primary infection due to direct inoculation (primary cutaneous infection).

Is this two or three? Don’t know. I sent off a complement-fixation, and it came back at the annoying 1:16. Greater than 1:16 means more likely disseminated disease and the need for an LP, although that data was from the 1950s:

in the preantifungal era, indicated that 82% of patients developed CF titers within 7 weeks of infection and 91 to 98% of patients with uncomplicated pulmonary infections developed maximal CF titers of d1:16. In comparison, only 12 to 23% of disseminated cases developed titers of d1:16. Following this initial observation, patients with titers of >1:16 were considered by some to warrant additional clinical and radiologic scrutiny for evidence of disseminated coccidioidomycosis.

A more recent review found the issue to be more complicated:

The median maximal CF titers were 1:4 for pulmonary uncomplicated coccidioidomycosis patients, 1:24 for pulmonary chronic coccidioidomycosis patients, 1:128 for disseminated coccidioidomycosis patients, and 1:32 for coccidioidal meningitis patients.

It started as a nodule that ulcerated, more like primary disease; secondary disease looks more like psoriasis. Statistically, this should be disseminated disease, as primary cutaneous infection is rare. And the literature states years can pass before disseminated disease manifests.

He is now on a course of fluconazole and getting better.

And it looks like it is raining in California this week. Time to look for coccidioidomycosis.

Previous studies have found that C immitis outcompetes other fungal organisms in drought periods and thrives in subsequent wet periods.12 Changes in the amount of rainfall accounted for changing coccidioidomycosis incidence during the tested 23-year period. Thus, we speculate that we are observing an increased number of cutaneous coccidioidomycosis cases caused by the extended drought period followed by heavy rainfall, which California experienced this year.

Rationalization

An Bras Dermatol. 2015 Sep-Oct; 90(5): 610619. doi: 10.1590/abd1806-4841.20153805 Coccidioidomycosis and the skin: a comprehensive review https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631225/

A case series of primary cutaneous coccidioidomycosis after a record-breaking rainy season https://www.jaadcasereports.org/article/S2352-5126(17)30296-5/fulltext

Coccidioidomycosis Complement Fixation Titer Trends in the Age of Antifungals https://jcm.asm.org/content/56/12/e01318-18

POLL RESULTS

I

• am a surgeon and read this. 4%
• am a surgeon, and I always culture pus 0%
• am not a surgeon, but I play one on TV 42%
• say culture, smulture. Give vanc/zosin and everything (save the kidneys) will be just fine 15%
• hate those know it all smug ID docs. 12% Other Answers 27%
• am an ID doc, and I always recommend culturing pus
• Internist trying to learn about cool things
• I am an elderly unit clerk and say if I don’t know what it is I want an ID consult.
• once knew a couple of ID docs, adult and peds, who each had a brain the size of a planet. The peds doc was a brilliant humanist. The other was a prick.
• ID Physician ;)
• read this for the grins :-)

  Two Rules. No Exceptions

  Dec 19, 2019

The patient is a middle-aged heroin user. As the world’s worst speller and proofreader, I am amazed how often I see EPIC correct heroin to heroine. Poor Wonder Woman. He is admitted with fevers, pleuritic chest pain, a large loculated pleural effusion, and MSSA in multiple blood cultures.

His pain on admission was ill-defined, back or flank?, so part of the workup included an MRI of the spine. The entire T12 body was edematous, and it was called osteomyelitis.

I had been gone for a week to sunnier climes, and when I returned, I looked at the MRI.

Nope. Not osteomyelitis.

There are two rules in medicine for which I have never seen an exception. The first is osteomyelitis of vertebral bodies always involves surrounding soft tissues. Usually, the infection starts in the disc and goes into the adjacent vertebral bodies. Less often, the infection begins in the paraspinal muscles or facet joint and moves into the vertebral body. Infection never involves just the vertebral body; the spinal equivalent of a Brodies is not a thing. Ever.

When just the vertebral body is involved, it is tumor or some other non-infectious process.

I have never seen an exception to this rule. I have seen an occasional bacteremia with a similar MRI. It was tumor.

I spent a chunk of time on the Googles and the Pubmeds, looking for an exception. I could not find one that I found compelling.

One review suggested

Infection of an isolated vertebral body is thought to represent an early manifestation of a spinal infection…

But the reference was unimpressive. One other review noted

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…

That is as close as I could get. If there is a case where an isolated vertebral body was edematous on MRI, had a biopsy that grew a bacteria, I can’t find it.

There are, as is often the case with IVDA, issues that have made making a diagnosis problematic. If he does turn out to be the first-ever exception to the rule, I will let you know.

The other rule with no exception? Anyone who uses ‘strong,’ ‘big gun,’ or ‘powerful’ as adjectives to describe an antibiotic is an idiot who knows nothing about treating infections. That rule will stand for eternity.

Rationalization

MR Imaging Assessment of the Spine: Infection or an Imitation? https://pubs.rsna.org/doi/full/10.1148/rg.292085137

Unusual Manifestations of Vertebral Osteomyelitis: Intraosseous Lesions Mimicking Metastases http://www.ajnr.org/content/29/6/1104

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

POLL RESULTS

Rules in Medicine with no exceptions - Anyone who uses ‘strong’, ‘big gun’, or ‘powerful’ as adjectives to describe an antibiotic is an idiot 46% - Infection goes to soft tissue, tumor goes to bone 3% - The later the hour, the more chatty the patient 5% - Outside records will always not have the key piece of data you need, but all the data you don’t need 18% - Never said on the death bed: “Doc, I wish I had spent more time at work.” 26%

General Principles

Dec 24, 2019

A short week for this here blog. Wednesday is the most important day of the calendar year: 12/25, my wife’s birthday. It is a day that requires some preparation. And I guess there are some other, less interesting, things going on that day as well.

There are some rules of medicine that I think don’t require a whole lot of thought. Don’t stick your hand in the fire. Simple enough to avoid on general principles.

I notice people take their damn dogs with them. Everywhere. I recently went into a patients room, and she just could not be without her dog, which was sleeping on her iv. If she gets a Pasturella bacteremia, I, at least, will not be surprised. I remember years ago walking into an ICU seeing the patients cat sleeping on their post-CABG sternotomy. Not good

I think, on general principles, that animals that lick their butts have no business in the hospital, much less in the patients bed.

Rates of acquisition of MRSA and C difficile were 4.7 and 2.4 times as high, respectively, among dogs that visited human health-care facilities, compared with rates among dogs involved in other animal-assisted interventions. Among dogs that visited human health-care facilities, those that licked patients or accepted treats during visits were more likely to be positive for MRSA and C difficile.

and

The most frequently isolated organisms were Klebsiella pneumoniae ssp pneumoniae, Escherichia coli, Staphylococcus aureus, Citrobacter freundii, Enterobacter cloacae, Acinetobacter calcoaceticus, and Pasteurella species.

Just because you can bring your dog into the hospital doesn’t mean you should. It is just a matter of time before one of these dogs inadvertently kills someone.

And let’s talk about pain. I recently saw a patient with the abrupt onset of a red, hot, exquisitely painful knee. But it wasn’t that swollen. It was so painful he lay on his bed, shouting for help for hours, as he could not stand to get help. Eventually, he made it to the ER, where the tap of the joint failed to get much fluid.

My rule of thumb: most infections are not all that painful. Pain occurs when there is pus under pressure or, in the case of cellulitis, when there is fluid in the leg that cannot return. The leg is not distensible for dependent fluid, so the pressure goes up, and it hurts. It is still pressure that causes pain. Less often, pain is due to irritation of a membrane such as the pleura or the peritoneum.

A Pubmed of the why of pain and infection yields very little, a review topic for some bored academic or fellow. Even in UTIs, the cause of pain is uncertain but

differential pain responses are not correlated with bladder colonization or inflammation, but instead are intrinsic to E. coli.

There are several articles to suggest that inflammation does not account for pain in cystitis. An interesting, and perhaps widely applicable, result. Infections do hurt, but not that much. Infections don’t usually incapacitate or require narcotics. Unless.

What severe pain and infection have in common is that it usually represents a surgical problem: pus under pressure.

On general principles, if the infection hurts that much, it needs to go to the OR.

That is what I told the orthopedist, who took the knee to the OR as a result. It was filled with pus.

To one and all, I wish you my usual generic nondenominational seasonal greeting, and I hope your holiday is infection-free.

Rationalization

Incidence of Acquisition of Methicillin-Resistant Staphylococcus Aureus, Clostridium Difficile, and Other Health-Care-Associated Pathogens by Dogs That Participate in Animal-Assisted Interventions https://avmajournals.avma.org/doi/abs/10.2460/javma.234.11.1404

Oral Bacterial Flora of Dogs With and Without Rabies: A Preliminary Study in Thailand https://pubmed.ncbi.nlm.nih.gov/14971525

Being Licked by a Dog Can Be Fatal: Capnocytophaga canimorsus Sepsis with Purpura Fulminans in an Immunocompetent Man https://ejcrim.com/index.php/EJCRIM/article/view/1268/1809

Mechanisms of Pain From Urinary Tract Infection http://www.ncbi.nlm.nih.gov/pmc/articles/pmc4552327/

Host Responses to Urinary Tract Infections and Emerging Therapeutics: Sensation and Pain Within the Urinary Tract https://doi.org/10.1128/microbiolspec.uti-0023-2016 POLL RESULTS

The worst day to be born See: https://www.thrillist.com/entertainment/nation/the-21-worst-birthdays-ranked

• December 25 42%
• April 1 21%
• 9/11 13%
• May 5 0%
• July 4 5% Other Answers 18%
• Feb 29
• Feb 29
• Any date that will outlive my generation and the mess we leave.
• Feb 29th
• On the day papa has some “really important thing he absolutely does need to attend to.” Since he’s an idiot, he’ll never let it go…
• 2/29

  It Takes A Licking

  Dec 30, 2019

The patient, an elderly diabetic female, comes in the rubor, dolor, calor, tumor of the upper thigh.

Cellulitis. We have all been there, and we have all done that.

She is given cefazolin and improves. On the second day, one of two blood cultures grows gram-positive cocci in chains.

OK fine. Group G or Group A Streptococcus most likely, but it does ratchet up the worry as she has a pacemaker.

Streptococcal device infections are very rare; I can find two Group G and zero Group A Streptococcal pacemaker infections on PubMed and the Googles. But it is fret-inducing.

But it is identified as S. canis, an alpha-hemolytic Lancefield group G and

Streptococcus canis (Sc) is a zoonotic pathogen that is transferred primarily from companion animals such as dogs and cats to humans through both animal bites and other mechanisms, and usually infects immunocompromised rather than immunocompetent hosts. This species has also been isolated from a variety of other animals, including cows, rats, mink, mice, rabbits, and foxes.

There are a smattering of cases of infections from this organism in humans, the predominant presentation being diabetics with leg ulcers and dogs.

I talked with the patient, and upon direct questioning, she said her dog often licked the downstream ulcers on her leg, and, because of neuropathy, she did not notice it. So it all tied together nicely.

There is one case report, the full text I cannot get, that suggests from the title that dog licking an ulcer is counterproductive: Dog Saliva Complicates the Healing of Ulcers.

This is not the first infection I have seen from a pet licking its owner. My favorite, early in my career and pre-dating the blog, was a Pasturella meningitis in a young girl whose cat was encouraged to lick her nose with the application of tuna.

There is an excellent Wikipedia entry on the history surrounding dogs licking wounds, and there are a variety of infections reported from licking animals. Which sounds like it is the human licking the animal. Which is also a bad idea. Being licked by animals. There. That’s better.

My rule, a parallel to ‘lips that touch wine will never mine,’ is, ‘animals that can lick their butt will never lick my wound or cut.’ Not bad, if I do say so myself.

And get this quote:

If your cut is small, you may feel comfortable with your dog licking and attending to your wound. If that is the case, it is suggested that you allow your dog to lick your wound. It is important to make sure your dog has been fully dewormed and checked by the veterinarian. It can be helpful in trusting this process, so no infection is created…Therefore, if you feel safe and your dog desires to lick your wound, then it may be something to encourage and allow.

But it is a step up from:

You should be aware of the case of an Oregon teacher who was reprimanded after licking the blood from wounds on a track team member’s knee, a football player’s arm, and a high school student’s hand.

I mentioned all this to my wife. Her response? “What is wrong with people?”

I can’t disagree.

See you in 2020, where I predict a lot of vision references in headlines and articles. You read it here first.

Rationalization

Two cases of cardiac device-related endocarditis due to Streptococcus dysgalactiae subsp. equisimilis (group C or G streptococci) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3976168/

IDCases. 2017; 7: 4852. Published online 2017 Jan 20. doi: 10.1016/j.idcr.2017.01.002Human case of bacteremia caused by Streptococcus canis sequence type 9 harboring the scm gene https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5295620/

Why Do Dogs Always Lick Your Cuts https://wagwalking.com/behavior/why-do-dogs-always-lick-your-cuts

Wound licking https://en.wikipedia.org/wiki/Wound\_licking

Can Dogs Help Humans Heal? https://www.psychologytoday.com/us/blog/canine-corner/201106/can-dogs-help-humans-heal

POLL RESULTS

I

• lick my own wounds 12%
• let my pets lick my wounds 5%
• lick my pets wounds 5%
• let my pets lick my face 15%
• lick my wounds metaphorically: They look on us at distance, and, like curs/Scaped from the lion’s paws, they bay far off/And lick their wounds, and faintly threaten war. 56% Other Answers 7%
• Scrub my wounds with old toothbrush dipped in solution of 50% isopropyl alcohol, saturated Alum, and Povidone Iodine to the opacity of strong. coffee.

  The Summation of Little Injuries

  Jan 7, 2020

The patient is admitted with neutropenic fevers. She has no pulmonary symptoms of note and is quite surprised to be told that she has bilateral interstitial infiltrates and pneumonia.

They call me when fevers persist after neutropenia resolves, and evaluation for the usual suspects is negative.

Past medical history: She has autoimmune hepatitis and has been on 10 mg of prednisone and azathioprine for years. She had been in the hospital for neutropenic fever a month ago with a clear CXR. At that time, she had been finished a course doxorubicin and cyclophosphamide, just like this time.

Nothing on exposure history, except she is from China; moved to the states as a child. She had spent a decade in Illinois, moving to Oregon three years ago.

Labs were unimpressive except for a markedly elevated LDH.

So, what is the differential?

There is histoplasmosis, which can cause an elevated LDH and has a subacute progression.

Drug lung. A quick PubMed finds cases of azathioprine, doxorubicin (aka adriamycin), and cyclophosphamide are all associated with pulmonary fibrosis, another cause of elevated LDH and pulmonary infiltrates.

And PJP. But is that enough immunosuppression? Yep.

All patients with PCP were diagnosed after receipt of either three or four cycles of AC (adriamycin/cyclophosphamide) chemotherapy on a dose-dense schedule. Patients who developed PCP were treated with median 16.4 mg prednisone equivalents/day as nausea prophylaxis for a median 64 days.

And this was cycle two. But. The bronchoscopy was negative for Pneumocystis. Hm. But the beta d glucan was high, 340. But that could be up due to Histoplasma. Or maybe some of other fungi all together.

I loath treating empirically, and there are long-term issues with therapy depending on the final diagnosis. So we sent off the Karius test, which, again, came to the rescue. There was lots of PJP DNA in the blood. PJP it was.

Three weeks later, in follow-up, she noted she was feeling much better. The disease had been so insidious that she had been unaware of how much the PJP had affected her until it was gone.

Rationalization

Breast Cancer Res Trea, 154 (2), 359-67 Nov 2015 Pneumocystis Jiroveci Pneumonia (PCP) in Patients Receiving Neoadjuvant and Adjuvant Anthracycline-Based Chemotherapy for Breast Cancer: Incidence and Risk Factors. <https: data-preserve-html-node="true"//doi.org/10.1007/s10549-015-3573-2>

Case Rep Oncol Med. 2013; 2013: 954346. Published online 2013 May 16. doi: 10.1155/2013/954346 Pneumocystis pneumonia during Postoperative Adjuvant Chemotherapy for Breast Cancer. <https: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pmc/articles/PMC3670557/>

Drugs Drugs Drugs

Jan 9, 2020

I’ll start the post today with a complaint because, well, it is my blog, and to quote Cartman, “I do what I want.” I had a patient recently with an extensive, necrotic leg infection, and the resident informed me they had called the surgeon to fillet the leg.

Fillet. They always say fillet and have been for years. While fillet is a piece of meat or fish without bones, it also means to debone meat or remove the flesh from the bone. Like fillet of fish.

The surgeon is not going to fillet the leg. Or at least I hope so. I think they mean flay, but flay is defined as to peel or beat the skin of a person or animal, and not necessarily a dead one. So not really.

When I point that out, all I get is a sheepish grin.

Whatever the surgeon is going to do to the leg, I hope it is neither going to be filleted or flayed. I know language changes and word usage drifts, but this one still annoys me.

The patient is an elderly male with a recurrent/chronic MRSA infection of his knee. He is on his third prosthetic knee, and the orthopedist says it is either a medical cure after I&D or an above the knee amputation. Unfortunately, this is getting close to being filleted.

On vancomycin, his creatine climbs. So I change to daptomycin and continue the rifampin, and about two weeks in, he gets a leukocytoclastic vasculitis rash on his legs.

One of my colleagues always started noon report discussions by mentioning the top three reasons for the patients symptoms are often drugs, drugs, and drugs.

So I thought the rash was likely due to either the rifampin or the daptomycin, and I could find no cases of daptomycin vasculitis on a search. So I stopped the rifampin.

And the rash didn’t go away; it progressed.

So I changed to ceftaroline.

And the rash didn’t go away; it progressed.

So I give him an antibiotic holiday.

And the rash didn’t go away; it progressed.

During this time, his knee, while not terrible, is not so good. It is still red and hot and mildly tender, and a tap shows pus, although the cultures are negative.

So is the vasculitis from the chronic MRSA infection? Maybe. A search of the Pubmeds suggests S. aureus is occasionally associated with immune complex vasculitis, more often manifesting as glomerulonephritis.

Leukocytoclastic vasculitis may be triggered by various factors, though approximately half of cases are idiopathic. The triggering factors include infections, certain drugs or chemicals, systemic disease, or neoplastic disease. Aside from idiopathic etiology, infections and drugs are the most common triggers. Of the infectious triggers, streptococcal upper respiratory tract infection is the most common. Other infectious triggers include, but are not limited to, Mycobacterium, hepatitis B and C, Staphylococcus aureus, Chlamydia, Neisseria, and HIV.

The association of S. aureus and vasculitis is most clearly seen (i.e., clear as mud) in Wegener’s granulomatosis, and this is not Wegener’s granulomatosis. And there is an association between S. aureus and post-Staphylococcal infection Henoch–Schönlein purpura.

There are no other drugs or diseases to account for the rash. So maybe the vasculitis is an epiphenomenon of the chronic infection; we are still searching for a satisfactory solution to that problem.

Rationalization

Pathophysiological Relationship between Infections and Systemic Vasculitis <https: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pmc/articles/PMC4508375/>

Fulminant arterial vasculitis as an unusual complication of disseminated staphylococcal disease due to the emerging CC1 methicillin-susceptible Staphylococcus aureus clone: a case report <https: data-preserve-html-node="true"//bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-019-3933-3>

Infection and vasculitis <https: data-preserve-html-node="true"//academic.oup.com/rheumatology/article/48/5/475/1786981>

Staphylococcus-Associated Glomerulonephritis Mimicking Henoch-Schönlein Purpura and Cryoglobulinemic Vasculitis in a Patient With an Epidural Abscess: A Case Report and Brief Review of the Literature <https: data-preserve-html-node="true"//www.ncbi.nlm.nih.gov/pmc/articles/PMC5985547/>

Leukocytoclastic Vasculitis (Hypersensitivity Vasculitis) <https: data-preserve-html-node="true"//europepmc.org/books/NBK482159;jsessionid=81A174A2D44AEC0D699D3BBA7CE53965>

POLL RESULTS

I am annoyed when people say

• fillet the leg 3%
• PJP pneumonia 17%
• ATM machine 20%
• no quid pro quo 26%
• literally 26% Other Answers 9%
• periodic (as in the table) when talking about periodic acid
• basically
• don’t sweat the small stuff.

  Finally. A Diagnosis.

  Jan 14, 2020

The patient is a middle-aged male who moved to Oregon from S. Africa 25 years ago. For the last year, he had back pain that had been moderate in severity, but in the week prior to admission, it became acutely worse, and his legs became weak.

In the ER, the CT and MRI showed discitis, vertebral body collapse, and an epidural abscess. He was taken to the OR emergently for decompression, and the surgeon told me later it looked like pus.

The next day they called me. No past medical history of note, ROS suggests some mild malaise for which about two months ago, he had quit drinking 4 beers a night. Stopping alcohol did not resolve the slight feeling of being unwell but other zero consumptive symptoms.

Here is where it gets…interesting.

First, all the OR cultures grew a pain-sensitive coagulase-negative Staphylococcus. No reason for this organism, but it does happen.

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.

But there was a paucity of WBCs on the gram-stain, and no organisms were seen. I had trouble thinking it was the pathogen, but hard to ignore when all the cultures are positive.

And the abdominal CT? In the bases of the lung were numerous millet-sized nodules, confirmed on CXR and lung CT.

CBC and Comp were normal, quantiferon was positive, results of any prior TB testing were lost in the mists of time.

About a year ago, he had a colonoscopy, and the biopsy of the colon showed mild colitis and one noncaseating granuloma.

My clinical diagnosis was Potts disease with miliary TB. We fretted about a larger differential diagnosis, but all the fungal and other studies came back negative.

But.

Bronchoscopy was negative for TB.

Blood cultures: negative for TB.

Even sent off a Karius test. Negative for TB.

Unfortunately, no histopathology was sent from the surgery.

So we gave cefazolin and RIPE. And stewed about the lack of a diagnosis.

I was struck by the complete lack of symptoms in the patient. I know miliary TB can be subacute, but this was the subacutest TB infection I have ever seen. I wondered if this was a spontaneous remission of miliary TB, perhaps in part due to stopping drinking. The closest I could find to confirm that hypothesis was

Without treatment, 1/3 of patients with active tuberculosis die within 1 year of the diagnosis, and more than 50% during the first 5 years. Patients who have a positive sputum smear test for M. tuberculosis have a 5-year mortality rate of 65%. Those who survive past 5 years have a 60% probability of spontaneous remission.

But it wasn’t specifically about miliary TB. We also wondered about sarcoid. It can happen.

We report a case of vertebral osseous sarcoidosis which presented with pulmonary symptoms mimicking tuberculosis.

But is very rare. The problem is you cannot disprove TB, nor can you prove sarcoid.

Then the patients weakness progressed, and the epidural was larger, so back to the OR. This time, histopathology was sent. Noncaseating granuloma, no AFB seen. But. The 16S was positive. TB, it is. Finally.

It is good to have a diagnosis. We are still waiting for the cultures from the second debridement, but so often with TB, it is like waiting for Godot. If they all turn out negative, I will still wonder if this is spontaneous remission.

Rationalization

Characteristics of Spontaneous Coagulase-Negative Staphylococcal Spondylodiscitis: A Retrospective Comparative Study Versus Staphylococcus Aureus Spondylodiscitis https://pubmed.ncbi.nlm.nih.gov/29029624-characteristics-of-spontaneous-coagulase-negative-staphylococcal-spondylodiscitis-a-retrospective-comparative-study-versus-staphylococcus-aureus-spondylodiscitis/

Tuberculosis natural history, complications, and prognosis https://www.wikidoc.org/index.php/Tuberculosis\_natural\_history,\_complications\_and\_prognosis

Natural History of Tuberculosis: Duration and Fatality of Untreated Pulmonary Tuberculosis in HIV Negative Patients: A Systematic Review https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3070694/

Osseous spinal sarcoidosis: an unusual but important entity to remember https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3030116/

Picking

Jan 15, 2020

The patient is a middle-aged female, a vigorous exerciser, had been working on her abdominals. Afterward, she had the onset of progressively severe back pain over three days and is admitted to the hospital.

MRI is read as multilevel degenerative disease.

Because she is febrile, blood cultures are done and grow S. mutans. So they call me.

The initial history and physical are unimpressive except for incapacitating lower back pain. That, combined with the blood cultures, means discitis. So I review the MRI with radiology armed with the knowledge of the blood cultures, and one area of the spine, where all the pain is, could also be called early discitis. As always, with radiology studies, they need to be interpreted through the lens of the H&P to get an accurate reading. As I have said many times, always review abnormal films with the radiologist. You will learn a lot.

I have often wondered, and have never found an answer for obvious reasons, how long it takes an MRI to become classic for discitis. Based on this case, and one other, I would venture a guess that three days is not enough for Streptococci.

The other question is why. S. mutans is an oral Streptococcus and, when found in the blood, implies endocarditis, a diagnosis for which we found no supporting evidence. And her teeth? Perfection.

But.

She does more than the usual dental hygiene, flossing, brushing, and picking at least twice a day. Perhaps a bad idea:

Cases (of oral Streptoccal endocarditis) were more likely than controls… to use toothpicks, dental water jet, interdental brush, and/or dental floss…The presence of gingival inflammation, calculus, and infectious dental diseases did not significantly differ between groups.

It is not routine care but

Among these promoting factors, orodental hygiene (overuse or lack of hygiene) is by far the most predominant one.

Now that risk is for endocarditis, but there is no reason that aggressive oral care would not be a good reason for discitis from oral Streptococci as well.

On IV beta-lactam, she had a nice resolution of her pain.

It is the little things in ID that always give me pleasure. In this case, it is the toothpicks that tie it all together.

Rationalization

Clin Infect Dis, 64 (12), 1678-1685 2017 Jun 15 Oral Streptococcal Endocarditis, Oral Hygiene Habits, and Recent Dental Procedures: A Case-Control Study https://doi.org/10.1093/cid/cix237

Endless Opportunities to Look Stupid

Jan 21, 2020

The patient has been receiving experimental chemotherapy for the last 6 weeks for lung cancer. For two days, her port had been tender, and then it started to ooze pus. No fevers or other signs of infection, except she felt more fatigued.

Blood cultures from the port and the periphery grew MSSA, and I was called.

Can we salvage the port?

She looked fine, was afebrile, and except for some bloody pus and redness over the port site, looked surprisingly well. No stigmata of endocarditis whatsoever.

Nope. Pull the port.

I changed the vancomycin and cefepime to cefazolin and repeated the blood cultures 24 hours after the line was pulled. And ECHO? I wouldn’t. I know the guidelines recommend an ECHO for all S. aureus bacteremias, but they are suboptimal when the prior probability is low, and it is too soon. It takes time to make vegetation, and she had only been ill 24-48 hours. As I have mentioned before, I was taught by a world expert in endocarditis as a fellow that it takes a week or two to form a vegetation that can be seen by TTE. As I have also mentioned before, I cannot find a reference to support that factoid, but that is my memory, and I am sticking to it.

I also think we get too many ECHOs to rule out endocarditis that are not needed. I see ECHO after ECHO done on patients with little or no clinical indications, and they are virtually always negative. I like to point to

We found that TTE results do not significantly affect the duration of antibiotic therapy. Instead, duration depended solely on clinical factors. This result is also consistent with the results reported by Lindner et al. who found that clinical parameters were predictive of antibiotic course, and were unaffected by either TTE or TEE.

Wait on the repeat blood cultures. If they are negative, it is likely an uncomplicated SAB and

...echocardiography is dispensable in cases of uncomplicated community-associated and healthcare-associated SAB.

and

patients with community-onset, prolonged bacteremia, and intracardiac prosthetic devices…Patients with none of the three criteria examined in this study have a very low rate of endocarditis and may fall below the test threshold for echocardiography.

You know where this is going.

A TTE was done anyway, and there was a 2 cm vegetation on the tricuspid valve. Or, to quote the report, a large 2 cm vegetation, to be contrasted with small 2 cm vegetations.

I, as you might guess, am a wee bit opinionated and am prone to making those opinions known. At length. With references. And that, of course, leads to endless opportunities to look stupid. I figure people are more likely to remember my spectacular calls than my spectacular failures. Everyone remembers Babe Ruth led the league in home runs, but no one remembers he also led in strikeouts.

I still wonder about the etiology of the vegetation. It is huge relative to her constitutional symptoms (none), the duration of infection (a couple of days), the number of positive blood cultures (repeat were negative), CXR (clear). Is this a marantic vegetation? Maybe, but the wrong side of the heart.

Tumors relatively most frequently associated with NBTE were carcinomas of the ovaries, biliary system, pancreas, lung, and stomach. The vegetations were located mostly on the left-sided valves (mitral 64%, aortic 24%, both 9%).

I will never know. So I guess to revert to the original hypothesis.

Rationalization

Overuse of Transthoracic Echocardiography in the Diagnosis of Native Valve Endocarditis https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/754054

Clinical Reasoning of Infectious Diseases Physicians Behind the Use or Nonuse of Transesophageal Echocardiography in Staphylococcus aureus Bacteremia https://doi.org/10.1093/ofid/ofw204

Echocardiography Is Dispensable in Uncomplicated Staphylococcus Aureus Bacteremia https://doi.org/10.1097/md.0b013e318294a710

Echocardiography Has Minimal Yield and May Not Be Warranted in Staphylococcus Aureus Bacteremia Without Clinical Risk Factors for Endocarditis https://doi.org/10.1007/s10096-015-2352-7

POLL RESULTS

I appreciate the endless opportunity medicine provides to look

• stupid 27%
• erudite 15%
• wise 4%
• omniscient 4%
• barely medically literate 46% Other Answers 4%
• truly humble

  Brian Jones

  Jan 22, 2020

The patient had a month of fevers and a non-productive cough. After a couple of weeks of symptoms, he receives a course of antibiotics that did nothing.

So a CXR was done that showed a large (fist-sized. My fist, and I have small, Trumpian, hands) lung abscess and empyema that was on the verge of rupturing out the chest wall. A drain was put into the abscess, and it grew S. anginosus and E. coli. They called me for advice about the duration of antibiotics.

That part is easy: until there is a cure. The more curious question is why does he have a lung abscess/empyema.

Seven years ago, he had a lobectomy for a malignancy. Is there a stump leak? It seems improbable after that much time, although I did find a case 7200 days or 19.2 years after pneumonectomy. That is impressive.

I wondered about an esophageal-pleural fistula as a complication of long-standing GERD. It happens. But drinking methylene blue failed to turn the drainage blue.

Aspiration? His teeth are perfect, and there is no history of either loss of consciousness or an aspiration event. Except.

He did have a complicated laparoscopic cholecystectomy a month before the onset of his symptoms. A CT around that time showed the lung was pathology-free.

I wondered. Is there any relationship between the lap chole and an empyema/lung abscess? I couldn’t see how it could occur mechanistically; there is a lot between the gallbladder and the lung. But I did a PubMed anyway. Bingo.

There are a smattering of cases of dropped biliary stones migrating into the chest to cause empyema and lung abscess.

Perforation of the gallbladder is the most common complication of laparoscopic cholecystectomy and occurs in approximately 20% of cases. Spillage of stones often occurs in as much as 50% of these cases. It is estimated that only two-thirds of the dropped stones are retrieved. The reported abdominal complication rate after spillage of stones is 1.4%. Abdominal abscess represents the most frequent complication of retained stones.

And I have blogged about a few such cases. But

Migration of stones through the diaphragm has been described in case reports, but mainly secondary to subphrenic abscesses. The underlying pathophysiologic process involves inflammatory reaction secondary to the presence of retained stones. They may then erode through the diaphragm and cause a bronchopleural fistula with cholelithopthysis, thoracic empyema, or pulmonary abscess.

So I went over all the films with radiology. There were radiolucent stones before, so nothing was seen on the CT of the gallbladder. The US demonstrated stones nicely in the prior gallbladder, but no way to image them in the chest. So the x-rays didn’t help confirm my hypothesis, although radiology did tell me there are people with occasional hernias in the diaphragm, both congenital and after pneumonectomy.

So was it a rogue stone? Probably not. Or a complication of intubation etc., after the surgery? More likely. The only way to make the diagnosis is to find a stone in the chest, and that isn’t going to happen.

The old saying is it is the journey, not the destination. I want both. I love to find a curious reason for an infection, but I will have to be content with learning about an odd complication of dropped stones.

PS

It has been suggested my titles can be a bit obscure in their ‘humor’. I think this is one of my more obtuse, and, of course, I am especially happy with it.

Rationalization

Accelerated Treatment for Early and Late Postpneumonectomy Empyema https://www.annalsthoracicsurgery.org/article/S0003-4975(01)03083-1/pdf

Perforation of Barrett’s Ulcer: A Challenge in Esophageal Surgery https://www.annalsthoracicsurgery.org/article/S0003-4975(00)01310-2/pdf

Dropped Gallstones Causing Transdiaphragmatic Migration and Thoracic Empyema https://www.annalsthoracicsurgery.org/article/S0003-4975(07)01346-X/pdf

Empyema from Lost Gallstones: A Thoracic Complication of Laparoscopic Cholecystectomy https://www.researchgate.net/deref/http%3A%2F%2Fdx.doi.org%2F10.1089%2Flps.1996.6.123

POLL RESULTS

It is

• the destination 5%
• the journey 38%
• the reimbursement 5%
• the satisfaction of… 10%
• all a farce while we wait to go back to the mud. 43%

  Another Just-So

  Jan 28, 2020

This morning I get an early page from a resident who had three consults for me. They apologized. Sometimes people apologize for allowing me to make a living, pay my bills, send my kids to college, and have enormous fun. So odd. I always ask them why they apologize, but I never get a good answer. Maybe other consultants are less pleasant when asked to see patients.

The patient presents with abdominal pain and failure to thrive after surgery. A CT shows 2 abscesses where his kidney used to be. They asked me what to do, and I said have IR do an aspiration, so we have a microbiologic diagnosis.

About a month ago, he had been in the hospital with C. difficile and a renal-colonic fistula. I thought I had blogged about this case before, but it was way back in 2014 I discussed the rarity of fistulae with C. difficile. The fistula was not due to C. difficile, or at least I didn’t think so, but due to cancer surgery/radiation/renal stent as the C. difficile occurred after we started therapy for the renal abscess, etc.

He required a nephrectomy/partial colectomy to cure his infection etc. The abscess where his kidney used to be now is growing C. albicans, but none of the prior cultures had yeast.

So how did Candida get there? Here is where I wander off the track with speculation, but regular readers know I love to come up with just-so stories,

a speculative story or explanation of doubtful or unprovable validity that is put forward to account for the origin of something (such as a biological trait) when no verifiable explanation is known.

Which really does sum up many of my explanations for why there are infections.

It is established that C. difficile is a risk for disseminated Candida.

We found that nearly 1 in 10 patients with candidemia had CDI coinfection.

But why might that be?

CDI is accompanied by over-representation of Candida albicans and decreased fungal diversity, richness, and evenness… FMT nonresponders and individuals treated with antibiotics display a dominant presence of Candida. High abundance of C. albicans in donor stool also correlates with reduced FMT efficacy.

C. difficile grows more easily when co-cultured with Candida, and while C. difficile may render Candida less virulent by inhibiting hyphae and biofilm formation, but there is an animal model that suggests microbial translocation increases with C. difficile. There are a smattering of other diseases, like HIV, where there is increased fungal translocation, as measured by (1 3)-B-D-glucan, due to altered gut integrity.

That’s my just-so story for how he developed a Candida abscess. C. difficile led to a loss of gut integrity, Candida overgrowth, and the Candida leaked across the colon and into the space around the fistula.

Of course, it could have been a much more direct leak from the colon, but that wasn’t found in the OR. And I like my explanation better.

Rationalization

No one has EVER seen this before. And maybe not me. http://boards.medscape.com/forums/?128@@.2a5c1d29!comment=1

Interspecies Interactions between Clostridium difficile and Candida albicans https://msphere.asm.org/content/1/6/e00187-16

Gut fungal dysbiosis correlates with reduced efficacy of fecal microbiota transplantation in Clostridium difficile infection https://www.nature.com/articles/s41467-018-06103-6

A Tale of Two Healthcare-associated Infections: Clostridium Difficile Coinfection Among Patients With Candidemia https://pubmed.ncbi.nlm.nih.gov/30060067-a-tale-of-two-healthcare-associated-infections-clostridium-difficile-coinfection-among-patients-with-candidemia/

Mucosal Damage and Neutropenia Are Required for Candida albicans Dissemination https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.0040035

Evaluation of gastrointestinal leakage using serum (1 3)-²-D-glucan in a Clostridium difficile murine model https://academic.oup.com/femsle/article/363/18/fnw204/2197847

Oral Candida administration in a Clostridium difficile mouse model worsens disease severity but is attenuated by Bifidobacterium https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0210798

(1 3)-²-d-Glucan: A Biomarker for Microbial Translocation in Individuals with Acute or Early HIV Infection? https://escholarship.org/uc/item/2370w0g5

POLL RESULTS

Consultations require

• an apology from the referring provider 10%
• a thank you from the consultant 24%
• genuflection and a kiss on the ring. I won’t say by whom 21%
• vague indifference as all in all its just another brick in the wall 21%
• amazement that they like you. they really really like you 21% Other Answers 3%
• Adherence to advice provided!

  Eternal Questions

  Jan 29, 2020

Coke or Pepsi? I’ll take a Diet Rite.

Mac or PC? Mac.

Beach or Mountains? Beach.

Briefs or Boxers? Depends. Yeah. I am not beyond that old joke.

And the eternal ID question, TB or not TB?

After all the tests are back, I can tell patients, yes, you have tuberculosis. But I often cannot say you do not have TB. It, along with syphilis, has to be the most aggravating diseases diagnostically, as so often, the denouement is frustratingly uncertain.

A case in point.

The patient is a young male from SE Asia, who has bloating, abdominal pain, diarrhea, and doesn’t feel well.

Work up eventually led to a panendoscopy and Crohn’s was diagnosed on the basis of non-caseating granulomas on the small bowel biopsy. But is it?

He is from a tuberculous part of the world and is quantiferon positive.

But he had the BCG as a child.

And the AFB stain and PCR on the biopsy were negative.

The current evidence suggests that PCR for MTB is a promising and highly specific diagnostic method to distinguish ITB from CD. However, physicians should also keep in mind that negative results cannot exclude ITB for its low sensitivity.

And stool cultures were negative for TB.

But, while waiting for all the studies, I started RIPE and clinically, and slowly, he felt much better with on therapy. Repeat endoscopy has yet to be done. Or performed.

And then to complicate issues, there is the whole maybe Crohn’s is due to Mycobacterium avium paratuberculosis issue.

Due to the similarities between Crohn’s disease and Johne’s disease, a chronic enteritis in ruminant animals caused by Mycobacterium avium paratuberculosis (MAP) infection, MAP has long been considered to be a potential cause of Crohn’s disease. MAP is an obligate intracellular pathogen that cannot replicate outside of animal hosts. MAP is widespread in dairy cattle and because of environmental contamination and resistance to pasteurization and chlorination, humans are frequently exposed through contamination of food and water. MAP can be cultured from the peripheral mononuclear cells from 50-100% of patients with Crohn’s disease, and less frequently from healthy individuals. Association does not prove causation.

While Mycobacterium avium paratuberculosis does not reliably respond to RIPE, could it cause a false positive IRGA? Not that I can find, and most of the information suggests not.

Part of the problem is if this is Crohn’s, GI wants to give biologics, a bad idea if this is active TB.

Although, there are certain clinical (diarrhea/hematochezia/perianal disease common in CD; fever/night sweats common in ITB), endoscopic (longitudinal/aphthous ulcers common in CD; transverse ulcers/patulous ileocaecal valve common in ITB), histologic (caseating/confluent/large granuloma common in ITB; microgranuloma common in CD), microbiologic (positive stain/culture for acid fast-bacillus in ITB), radiologic (long segment involvement/comb sign/skip lesions common in CD; necrotic lymph node/contiguous ileocaecal involvement common in ITB), and serologic differences between CD and ITB, the only exclusive features are caseation necrosis on biopsy, positive smear for acid-fast bacillus (AFB) and/or AFB culture, and necrotic lymph node on cross-sectional imaging in ITB…However, therapeutic anti-tubercular therapy (ATT) trial, and subsequent clinical and endoscopic response to ATT is still required in a significant proportion of patients to establish the diagnosis. Therapeutic ATT trial is associated with a delay in the diagnosis of CD, and there is a need for better modalities for improved differentiation and reduction in the need for ATT trial.

So. No Tb? Latent Tb? Active TB?

There are some things man’s not meant to know.

I suspect latent but will treat for active TB.

Rationalization

The Diagnostic Value of Polymerase Chain Reaction for Mycobacterium tuberculosis to Distinguish Intestinal Tuberculosis From Crohn’s Disease: A Meta-Analysis https://pubmed.ncbi.nlm.nih.gov/28139494-the-diagnostic-value-of-polymerase-chain-reaction-for-mycobacterium-tuberculosis-to-distinguish-intestinal-tuberculosis-from-crohns-disease-a-meta-analysis

Mycobacterium Paratuberculosis as a Cause of Crohn’s Disease https://doi.org/10.1586/17474124.2015.1093931

QuantiFERON-TB Gold Test Conversion Is Associated with Active Tuberculosis Development in Inflammatory Bowel Disease Patients Treated with Biological Agents: An Experience of a Medical Center in Taiwan https://www.hindawi.com/journals/grp/2019/7132875/

Differentiating Crohn’s Disease From Intestinal Tuberculosis https://doi.org/10.3748/wjg.v25.i4.418

POLL RESULTS

Eternal questions

• have eternal answers 6%
• never have an answer 12%
• are best answered by the Oracle of Delphi 15%
• are false dichotomies, all answers fall on a spectrum depending on the context. - Unless it’s 42. 50%
• depends on what the meaning of is is 18%

  Treating a Local Infection Systemically

  Feb 4, 2020

What did he say? I was discussing the clinic schedule with my nurse, and he said, “We don’t need to add any more on.” Or did he say, “We don’t need to add any, moron?”

He insisted it was the former, but I wonder…

The patient is a middle-aged female with no medical problems who comes in with perforated diverticulitis. She is repaired with a diverting colostomy and receives a course of antibiotics, ceftriaxone and metronidazole.

She developed an abscess the grew ESBL E. coli and S. constellatus that was drained and treated with cefepime and clindamycin.

A month later, she returns with another infection, an infected hematoma, that grew Enterococcus and Clostridium difficile. It was drained and treated with ciprofloxicin and 250 tid of metronidazole. And no, I was not involved with patients care.

A month later, the colostomy is repaired with an uneventful course.

Five months later, he has fevers and rigors, and blood cultures grow Bacteroides fragilis and Clostridioides (Clostridium) difficile. A CT now shows a left subdiaphragmatic abscess. It is drained and also grows Clostridioides difficile.

Interesting series of cultures.

I have not seen Clostridioides difficile grow from either an abscess or in the blood. It does happen, and there are a hodgepodge of liver, splenic, peritoneal, and other organs infected with Clostridioides difficile, many without concomitant intestinal disease.

Advanced age, gastro-intestinal disruption, severe underlying diseases, and antimicrobial exposure were the major risk factors for C. difficile bacteremia.

and

Extraintestinal CDIs occur mainly in hospitalized patients with significant comorbidities. Extraintestinal CDIs in the abdominal area may result from either intestinal perforation after infection or after intestinal surgery. Wound infections may result from colonization by feces. Clostridium difficile may reach distant sites via bacteremia.

And the best treatment? Most reports suggest vancomycin or metronidazole.

I have to wonder? Was the Clostridioides difficile resistant to metronidazole, which is why the relapse? Or was the metronidazole just underdosed?

C. difficile resistance varies by location and methodology, so it is hard to say what the resistance rate is. The best number is from

A surveillance study of the antimicrobial susceptibility of C. difficile isolates in the United States showed the rate of metronidazole resistance was 3.6% in 2011.

But what marks all Clostridioides difficile infections is resistance to most systemic antibiotics and all the treatments we have developed for C. difficile are noted for their lack of systemic concentrations. It is not like I can treat it with rifaxamin or fidaxomicin. And a stool transplant isn’t going to work IV.

I figured the cure is the drainage, and I pushed the metronidazole (there is that B. fragilis as well) and gave vancomycin. Based on CT, we have a cure, although the prior 5-month gap gives me pause.

Rationalization

Clostridium difficile Bacteremia: Report of Two Cases in French Hospitals and Comprehensive Review of the Literature https://pubmed.ncbi.nlm.nih.gov/28417069-clostridium-difficile-bacteremia-report-of-two-cases-in-french-hospitals-and-comprehensive-review-of-the-literature/

Clostridium difficile extraintestinal abscess: a rare complication https://casereports.bmj.com/content/2017/bcr-2017-219957

Extraintestinal Clostridium Difficile Infections https://pubmed.ncbi.nlm.nih.gov/23771984-extraintestinal-clostridium-difficile-infections/

Update on Antimicrobial Resistance in Clostridium difficile: Resistance Mechanisms and Antimicrobial Susceptibility Testing https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5483901/

POLL RESULTS

He likely said

• more on 14%
• moron 11%
• more on, moron 11%
• idiot, but softly, under his breath, where it could not be heard 27%
• nothing, but thought volumes 38%

  Numbers

  Feb 5, 2020

I received notice from Cigna today. All high-tech radiology services have to be reviewed to ensure medical necessity by eviCore. I had to do a double-take; I read it as if there were an ‘l’ in eviCore. I wonder why.

Numbers often have an emotional component. If you tell me I have a 7-mile hike in 82-degree weather, I know just what it means. In metric? 11.25 kilometers in 27.7 C means nothing. I have long suspected that global warming educators have made a mistake, as they always write about a 1 to 3 C change. Doesn’t seem like much. A rise of 1.8 to 5.4 F means more; I have a gut feeling as to what that temperature change means.

The same holds true with medical numbers.

The patient is admitted with sepsis and has MSSA in their blood, likely from a cellulitis. He also has moderate to severe mitral stenosis. As part of the workup, they order a troponin, and it is 10.

The last time I concerned myself with diagnosing a myocardial infarction was 1986, where we did CK and LDH with isoenzymes. I do not remember if we used MBs; I don’t think so. We certainly did not have troponins.

I see a high troponin with sepsis and infection. There is plenty of literature to show that elevated troponins in infections are a bad prognostic sign.

Troponin elevation in patients with sepsis confers poorer prognosis and is a predictor of mortality.

Since there is nothing to do about it and the troponins are usually 1 or 2, I ignore them/leave it to the hospitalist.

But 10? It seems like a lot, but I have no feel for the number. Those who would know tell me it is high.

So I wondered, could it be a marker of a myocardial abscess? Even with a negative TTE, negative repeat blood cultures, and a rapid response to antibiotics?

Maybe. Like other infections, an increase in troponins is a bad prognostic sign, suggesting

that elevated levels of cardiac biomarkers (TnI, highly sensitivity cardiac troponin T, brain natriuretic peptide, N-terminal pro-B-type natriuretic peptide), associated with mortality, either as an individual primary endpoint and/or as a component of a composite outcome. However, the lack of Tn elevation in IE might correlate better with outcomes than detection of elevated serum levels.

and is associated with an abscess

In conclusion, elevated cTnI was associated with the composite of death, abscess, and central nervous system events.

And it is even true in cows. I did not know cows got endocarditis, and it must be common, as it occurred in 15 of seventy-seven clinically diseased cattle. The most common cause is Arcanobacterium pyogenes, a small gram-negative rod. There are a smattering of human endocarditis cases as well.

I could not find endocarditis incidence estimates in cows, but it sure seems that cows have a lot of congenital heart disease:

We investigated 469 cases of congenital heart diseases in malformed bovine hearts collected mainly in Miyazaki Prefecture from 1979 to 1997. A total of 893 diseases, subdivided into 53 types, were represented. Most frequently encountered was ventricular septal defect (198 cases; 42.2%).This was followed by atrial septal defect (148 cases; 31.6%), double-outlet right ventricle (66 cases; 14.1%), aortic stenosis (53 cases; 11.3%), double cranial venae cavae (50 cases; 10.7%), patent ductus arteriosus (45 cases; 9.6%), anomalos caudal vena cava with azygous continuation (42 cases; 9.0%), the tetralogy of Fallot (32 cases; 6.8%), hypoplastic left ventricle syndrome (25 cases; 6.8%), complete transposition of the great arteries (24 cases; 5.1%), and total anomalous pulmonary venous connection (21 cases; 4.5%). Simple cardiac defects were detected in 251 cases (53.5%) and complex cardiac in 218 cases (46.5%). This study demonstrates that in cattle as well as in human beings and cats, ventricular septal defect is encountered most frequently.

And with it endocarditis.

But I digress, even if I do find this information interesting.

The patient did fine, the troponin fell over three days, and we, and by we I mean the hospitalist, blamed the sepsis.

Rationalization

The Prognostic Significance of Troponin Elevation in Patients With Sepsis: A Meta-Analysis DOI: 10.1016/j.hrtlng.2014.10.002

Cardiac Troponin T as a Predictor of Short- And Long-Term Mortality in Community-Acquired Pneumonia DOI: 10.1111/resp.13020

The Prognostic Significance of Troponin Elevation in Patients With Sepsis: A Meta-Analysis DOI: 10.1016/j.hrtlng.2014.10.002

Cardiac Troponin T as a Predictor of Short- And Long-Term Mortality in Community-Acquired Pneumonia DOI: 10.1111/resp.13020

Prognostic value of cardiac troponin levels in infective endocarditis https://doi.org/10.1177/1753944712467394

Relation of Troponin Elevation to Outcome in Patients With Infective Endocarditis DOI: 10.1016/j.amjcard.2008.01.031

Serum Cardiac Troponin I Concentrations in Cattle With Cardiac and Noncardiac Disorders DOI: 10.1111/j.1939-1676.2009.0330.x

The Diagnostic Criteria Used in Bovine Bacterial Endocarditis: A Meta-Analysis of 460 Published Cases From 1973 to 2011 DOI: 10.1016/j.tvjl.2012.02.012

Morphologies of 469 Cases of Congenital Heart Diseases in Cattle https://doi.org/10.12935/jvma1951.53.205

Cardiac diseases of cattle https://www.dvm360.com/view/cardiac-diseases-cattle-proceedings

ARCANOBACTERIUM PYOGENES ENDOCARDITIS: A CASE REPORT AND LITERATURE REVIEW https://pdfs.semanticscholar.org/ba26/b523ef6b244a38ff6916567c1e2a278528eb.pdf

POLL RESULTS

I did not know

• cows got endocarditis 11%
• cows were injection drug users 15%
• cows flossed and brushed 37%
• Arcanobacterium pyogenes is now called Trueperella pyogenes 22%
• cows had heart disease 15%

  The Nose Knows

  Feb 18, 2020

Back from vacation on the Garden Island. 35 degrees warmer than home. Sigh. As you age, there is just no replacement for thermonuclear heat for warming old bones. And the vacation reemphasized that I mentally group words and letters oddly on occasion. I mentioned in the past that I always see coworker as cow orker, whatever that might be. I am also sure I am not the only one who sees slow as an adjective rather than a command in the sign that says Slow Children Playing. But we saw the sign Emergency Room Service around the island, and it took me a day to figure out it was (Emergency Room) Service and not Emergency (Room Service).

The patient has cirrhosis with coagulopathy and bleeds on occasion from here and there and is plagued by nose bleeds.

This time he is admitted with fevers and chills and has 1 of 2 blood cultures with MSSA. He responds to antibiotics, and they call me as every S. aureus bacteremia (SAB) gets an ID consult. If that is not the case at your institution, as Ricky never said, “You have some splainin’ to do.”

Repeat blood cultures were negative, as was the tte. The patient was feeling fine and non-focal. So, why the bacteremia?

While S. aureus bacteremia occurs in cirrhotics, as it does in everyone, I can’t find where there is an increased risk for S. aureus bacteremia in cirrhotics.

Escherichia coli, Klebsiella pneumoniae, and Aeromonas hydrophilia were the three most commonly detected microorganisms. Gram‐positive bacterias were detected in 21.2% of patients with bacteremia, with predominance of the Streptococcus group and Staphylococcus aureus.

Which more or less parallels bacteremias in non-cirrhotics.

But. The day before admission, he had a prolonged and profuse nosebleed.

Osler-Weber-Rendu patients have an increased risk of SAB from nose bleeds, but how about those without preexisting arterial-venous malformations.

There is a relationship between nose bleeds and S. aureus nasal carriage

Children with epistaxis are more likely to have nasal colonization with S aureus than controls. Our data would support the hypothesis that S aureus replaces existing nasal flora and causes inflammation and new vessel formation.

And the pediatric literature debates cause and effect. I bet the bleeding and trauma lead to S. aureus rather than the other way around.

And there is

While none of the blood cultures taken preoperatively were positive for any organism, the cultures obtained postoperatively were positive in 9 (12.7%) of 71 patients who underwent septoplasty, and bacteremia was more frequent among those with a greater amount of bleeding during the surgery. The results of this study suggest that although bacteremia had no clinical consequences for patients, patients with more bleeding have an increased risk of developing bacteremia which may cause complications in higher risk individuals.

Leading to one case report that I can find:

AN UNUSUAL CASE OF EPISTAXIS AND STAPHYLOCOCCUS AUREUS BACTEREMIA IN AN OLDER CHINESE WOMAN

Sounds like the title of a Sherlock Holmes short story.

But I am going to call it: epistaxis causing S. aureus bacteremia.

And is that the equivalent of uncomplicated S. aureus bacteremia from a removable focus, since the bleeding stopped? Probably not. And given the host, I opted for 28 days of therapy.

Rationalization

Eur J Clin Microbiol Infect Dis. 2012 Dec;31(12):3309-16. doi: 10.1007/s10096-012-1697-4. Epub 2012 Jul 26. Clinical significance of Staphylococcus aureus bacteremia in patients with liver cirrhosis. https://www.ncbi.nlm.nih.gov/pubmed/22833245

Bacteremia in patients with cirrhosis of the liver https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1600-0676.1991.tb00539.x

The Comparison of Bacteremia and Amount of Bleeding During Septoplasty https://pubmed.ncbi.nlm.nih.gov/22037718-the-comparison-of-bacteremia-and-amount-of-bleeding-during-septoplasty

AN UNUSUAL CASE OF EPISTAXIS AND STAPHYLOCOCCUS AUREUS BACTEREMIA IN AN OLDER CHINESE WOMAN https://onlinelibrary.wiley.com/doi/full/10.1111/j.1532-5415.2010.03044.x

Epistaxis and Staphylococcus aureus Colonization in the Nasal Vestibule: Is It a Cause or Consequence? https://journals.lww.com/jcraniofacialsurgery/Abstract/2014/11000/Epistaxis\_and\_Staphylococcus\_aureus\_Colonization.91.aspx

Childhood epistaxis and nasal colonization with Staphylococcus aureus https://journals.sagepub.com/doi/abs/10.1016/j.otohns.2007.10.029

POLL RESULTS

I like to vacation

• on the garden island 0%
• in the garden state 0%
• on fantasy island 0%
• with a garden salad 0%
• anywhere there is no access to the EMR 60%
• where I’m 35 years younger and have a Dick Newick Val trimaran and a crew that loves sailing.
• in my garden

  How Long Does It Take?

  Feb 20, 2020

The patient, who is not the best of historians due to a long history of mind-altering drug use, presents with shoulder pain.

For how long?

He says two days to the ER doc, to the hospitalist, and to me. The pain was also associated with fevers and chills.

CT demonstrated a large effusion, myositis, and osteomyelitis. He was taken to the OR, and MRSA-filled pus was in the joint and soft tissues. A septic joint in a heroin user is not that unusual. But the CT showed

right humeral head lateral margin bone cortex destruction extending over about 2.2 cm

that eroded into the medulla of the bone.

That took time, certainly more than the two days he reported pain. But how long does it take to erode through bone or get changes on plain films?

I have it in my mind that it takes at least 6 weeks before you get erosions of bone in osteomyelitis. Where does that number come from? I learned it as a fellow from my attendings, and I have carried it with me since. If there is a good reference to support that contention, I can’t find it. So perhaps it is a factoid:

an assumption or speculation that is reported and repeated so often that it becomes accepted as fact.

The closest I can find is literature in hematogenous osteomyelitis in children, which, due to increased vascular supply, is not the same disease in adults:

In 6 (16%) of these patients, typical osseous changes (periosteal new bone formation, bone destruction, osteoporosis, sequestrum formation) developed within 10 to 14 days of diagnosis

And in hematogenous osteomyelitis in 4 heroin addicts from 1976.

X-ray changes may be initially absent, only to appear within several weeks.

Several being 1 to 6.

I went back and talked to the patient, and with repeated questioning, he said he had low-grade pain for several months before it acutely worsened. I have wondered if he was just giving me the answer I was looking for, as the questions were certainly not open-ended.

I suspect this was a Brodies of the humeral head that eroded into the joint space, but radiology could neither confirm nor deny that hypothesis based on the x-rays.

As always, I do not let a lack of a confirmatory study prevent my diagnosis.

He received a long course of MRSA therapy and did well.

Rationalization

Factoid: an assumption or speculation that is reported and repeated so often that it becomes accepted as fact.

Acute hematogenous osteomyelitis and septic arthritis in children https://pdfs.semanticscholar.org/ce07/bca6cb2c1c317570a9862c1a5757453ef26f.pdf

Osteomyelitis in Heroin Addicts https://sci-hub.tw/10.7326/0003-4819-75-5-693

POLL RESULTS

What I know is

• from the literature 11%
• from my mentors 15%
• from this blog 41% made up 4%
• an hallucination induced by staring at EMR screens 19% Other Answers 11%
• that there are known unknowns and unknown unknowns
• nobody cares what I think. Ergo, this comment is a paradoxical statement.

  Who is That Masked Man?

  Feb 20,2020

An historical curiosity.

I have had a URI for the last several days and have not had the mental wherewithal to blog or podcast. All I felt like doing was binge-watch The Preacher. I probably got a virus from a kid who was coughing the entire flight back from Kauai, and I was within the zone of contagion:

Passengers seated within one row from the index patient are subject to contact risks that are one to two orders of magnitude higher than are passengers seated further away.

So for the last few days, I have been channeling my role model, Mycroft Holmes.

He has the tidiest and most orderly brain, with the greatest capacity for storing facts, of any man living. The same great powers which I have turned to the detection of crime he has used for Infectious Diseases. The conclusions of every department are passed to him, and he is the central exchange, the clearinghouse, which makes out the balance. All other men are specialists, but his specialism is omniscience. We will suppose that a Doctor needs information as to a point which involves the Surgery, Hospitalist, Pulmonologist and the fever question; he could get his separate advices from various departments upon each, but only Mycroft can focus them all, and say offhand how each factor would affect the other. They began by using him as a short-cut, a convenience; now he has made himself an essential. In that great brain of his everything is pigeon-holed and can be handed out in an instant.

Well, kind of. I am not quite that full of myself. I do want to sit in the Diogenes Club and have everyone bring me information, and I will supply them with the needed interpretation. You know. Telemedicine.

One observation from my own illness. On the last day, I had a sharp increase in URI symptoms. Sneezing, itchy eyes, and hypogeusia; I could barely taste anything. It has happened many times over the years, once just as we went to an expensive French restaurant for our anniversary.

It is well known that URI’s lead to hypogeusia,

The major smell and taste loss etiology was upper respiratory tract infection (URI) in the flavor dysfunction group and the URI rate was significantly higher in the flavor dysfunction group than in the smell and taste dysfunction group.

and

Hypogeusia, with or without dysgeusia, and hyposmia, with or without dysosmia, followed an influenzal-like infection in 87 of 143 consecutive patients

But it is the timing I am curious about. Hypogeusia always happens just before I turn the corner. Is hypogeusia due to the immune response and a marker of the onset of the antibody, sort of a nasal crisis? No data and enquiring minds want to know.

So I spent the last few days wallowing in alcohol (topical, not po), wearing a mask and my hands in my pockets, taking the history from the doorway. Not quite Mycroft yet.

And it made me wonder about masks. I don’t think I ever looked at the science behind masks. For most infection control issues, I trust in the CDC, which, as far as I am concerned, really does contain stable geniuses.

We usually use masks to prevent the spread of infectious diseases from patient to HCW and to prevent oral flora from going from surgeon to patient. With COVID soon to spew across the county and with 30 million masks stockpiled, an estimated 1/10th of what HCWs will need, much less the general population, are there other options? Beside the Clinton Technique? I always wondered. If he didn’t inhale, then how did he know if he didn’t like it? Seems like such a quaint scandal by today’s standards.

The CDC says

CDC does not recommend that people who are well wear a facemask to protect themselves from respiratory diseases, including COVID-19. Facemasks should be used by people who show symptoms of COVID-19 to help prevent the spread of the disease to others. The use of facemasks is also crucial for health workers and people who are taking care of someone in close settings (at home or in a health care facility).

Good. They are looking out for my butt.

Coronavirus is mostly spread by droplets, not airborne/aerosols. That means it is spread in coughed up gobbets o’ pus (TM) that land on you or the environment and less on being inhaled to start the infection. So masks will likely do less to prevent spread than disinfecting your hands and the environment. If you ever want to be entertained/grossed out, focus on what other people do with their hands when in their natural environment. Ew.

But the distinction between droplet and airborne is not hard and fast

and this nicely illustrates the quandary of how to classify such emerging or re-emerging pathogens into either the large droplet (short-range) versus airborne (short and possibly long-range) transmission categories. However, this delineation is not black and white, as there is also the potential for pathogens under both classifications to be potentially transmitted by aerosols between people at close range (i.e. within 1 m).

And a subset of MERS and SARS may have been airborne at close range, so surgical masks will do less than an N95, but if a gobbet of coronavirus pus hits your eye, well, c’est la vie.

Interestingly, a search for mask and Coronavirus yields nothing, you have to rely on influenza and ILI studies where, in the community, masks do little, because people can’t keep them on.

In various sensitivity analyses, we did not identify any trend in the results suggesting effectiveness of facemasks.

and

Intent-to-treat analysis showed no significant difference in the relative risk of ILI in the mask use groups compared with the control group; however, <50% data-preserve-html-node="true" of those in the mask use groups reported wearing masks most of the time.

Of course, like all infectious diseases, there is no one intervention that will stop spread, it is the summation of many interventions to prevent the probability of contagion.

Some evidence suggests that mask use is best undertaken as part of a package of personal protection especially hand hygiene. The effectiveness of masks and respirators is likely linked to early, consistent and correct usage.

In the hospital, we have tight IC practices that make masks part of sustainable prevention. In the real world, they may do a little, but, I bet, mostly give a false sense of security. The world outside the hospital is just too messy to expect much benefit from a mask.

So there is good reason to want to keep masks available for HCWs.

Are there alternatives?

You can make your own mask.

A Hanes Heavyweight 100% preshrunk cotton T-shirt (made in Honduras) was boiled for 10 minutes and air-dried to maximize shrinkage and sterilize the material in a manner available in developing countries. A scissor, marker, and ruler were used to cut out 1 outer layer (H37 × 72 cm) and 8 inner layers (<18 data-preserve-html-node="true" cm2). The mask was assembled and fitted as shown in the Figure.

There are a lot of patterns online, but they are not as good as standard masks for preventing infections:

This study is the first RCT of cloth masks, and the results caution against the use of cloth masks. This is an important finding to inform occupational health and safety. Moisture retention, reuse of cloth masks, and poor filtration may result in an increased risk of infection.

So maybe not for COVID. But in the OR? Of note, for masks in the OR,

Three trials were included, involving a total of 2113 participants. There was no statistically significant difference in infection rates between the masked and unmasked group in any of the trials.

If push came to shove and there was a mask shortage, we would let the OR staff use the homemade masks and save the real masks for, let’s say, the ID docs. Yeah. I like that idea.

As I write this, my feeds let me know there is a case of COVID in California with no known exposure/risk. I bet this is where COVID will get us: the unexpected case. President Canute can’t stop the Coronavirus. And yes, I know, that is not a classic use of the parable.

And I may have to shave my beard. Crap. It is white and the source of many a senior discount. That is just unacceptable.

Rationalization

Modeling the Fate of Expiratory Aerosols and the Associated Infection Risk in an Aircraft Cabin Environment. https://www.tandfonline.com/doi/full/10.1080/02786820802641461

Risk assessment of airborne infectious diseases in aircraft cabins https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1600-0668.2012.00773.x

[Clinical analysis of hyposmia-associated taste dysfunction]. https://www.ncbi.nlm.nih.gov/pubmed/19364046

Hypogeusia, dysgeusia, hyposmia, and dysosmia following influenza-like infection. https://www.ncbi.nlm.nih.gov/pubmed/1190677

AMERICA HAS 30 MILLION MASKS, NEEDS 300 MILLION FOR HEALTH CARE WORKERS FIGHTING CORONAVIRUS, HHS SECRETARY SAYS https://www.newsweek.com/alex-azar-coronavirus-masks-30-million-have-need-30-million-fight-america-senate-committee-1489058

Recognition of aerosol transmission of infectious agents: a commentary https://link.springer.com/article/10.1186/s12879-019-3707-y

Surgical Mask to Prevent Influenza Transmission in Households: A Cluster Randomized Trial https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2984432/

Face Mask Use and Control of Respiratory Virus Transmission in Households https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2662657/

Simple Respiratory Mask https://wwwnc.cdc.gov/eid/article/12/6/05-1468\*article

Evaluating the Efficacy of Cloth Facemasks in Reducing Particulate Matter Exposure https://doi.org/10.1038/jes.2016.42

A Cluster Randomised Trial of Cloth Masks Compared With Medical Masks in Healthcare Workers https://doi.org/10.1136/bmjopen-2014-006577

Use of Surgical Facemasks in the Operation Theatre: Effective or Habit? https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4920922/

Is King Canute misunderstood? https://www.bbc.com/news/magazine-13524677

CDC warns men about facial hair dangers as Coronavirus spreads https://nypost.com/2020/02/26/cdc-warns-men-about-facial-hair-dangers-as-coronavirus-spreads/

POLL RESULTS

When COVID hits

• I will wear a surgical mask outside the hospital 3%
• I will wear an n95 outside the hospital 3%
• I’m staying home 59%
• https://www.youtube.com/watch?v=SJUhlRoBL8M 3%
• https://www.youtube.com/watch?v=xZbKHDPPrrc 10% Other Answers 21%
• I live in Buddha Indiana ( yes it is real, look it up). Covid19 will never make it here.
• Shrink wrap my face and adapt to anaerobic living
• I´ll do my work
• Go to work sick. we are short staffed!
• I will be selling t-=shirt masks remember, that which does not kill us makes us stronger. Of course, death never takes a holiday. We’re all headed for the worm farm, eventually.

  Odd Perf

  Mar 3, 2020

Thank goodness it is all a hoax. I try and imagine what my day would have been like if we were on the verge of a real pandemic. But it is nice to know all my work is all just medical theater, all sound, and fury, signifying nothing. Nothing to see here. And, nope, that isn’t a metaphor for anything. No, Sir

Now, there are still real diseases that require care and consideration. The patient, an elderly male, is admitted with a week of diarrhea and progressive abdominal pain.

One thing leads to another, and colonoscopy shows pancolitis, biopsies typical for ulcerative colitis.

Odd disease in the elderly, but it happens:

Approximately 10% of patients at first flare of IBD are > 60 years old, with a similar distribution between ulcerative colitis (UC) and Crohn’s disease (CD); 50% of them are diagnosed between 60-70 years of age

And no other process as found: diverticulosis, medication-related, ischemic colitis, and infectious colitis.

Over the next two weeks, his symptoms did not improve, and his medications escalated, finally to steroids and biologics. Then catastrophe: acute worsening pain and free air.

In the OR, a colonic perforation was found, and required a colectomy.

Post-op, the patient, did as well as could be expected, but the pathology of the colon now showed changes of UC and CMV, the latter was most definitely not there before.

There are a variety of cases of CMV-induced GI perforation on the Pubmeds: HIV, transplant, new immunosuppression are the usual disease and the occasional immunocompetent.

I presume that it was reactivation CMV and not a primary infection, but I was not able to check a CMV IgG. Although, as I have mentioned in the past, I wonder if primary CMV infection is the cause of the occasional gastroenteritis and is underdiagnosed as few patients with colitis go on to colonoscopy. I have seen a few in my day.

I do not know how one would expect the disease. There seems to be no hint in cases of a common suggestive presentation, and there are so many other, more common, reasons for gastroenteritis. It is one of those diseases most often made serendipitously.

With colectomy and cessation of immunosuppression, the patient transiently improved but succumbed to other co-morbidities.

Rationalization

World J Gastroenterol. 2011 Jun 14; 17(22): 2734–2739. Published online 2011 Jun 14. doi: 10.3748/wjg.v17.i22.2734 Old-age inflammatory bowel disease onset: A different problem? https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3122261/

Cytomegalovirus Enterocolitis in Immunocompetent Young Children: A Report of Two Cases and Review of the Literature. https://pubmed.ncbi.nlm.nih.gov/26862673

Not A Tumor

Mar 9, 2020

I was out on my daily constitutional, and I saw someone unload a tremendous amount of diet soda and toilet paper from the back of their pickup. It looked like a Costco run in anticipation of a COVID catastrophe. If I were so inclined, and I am not, TP is the last thing I would hoard. Beer and ice cream? Absolutely. And didn’t they ever watch the Twilight Zone? As soon as there is an issue, armed groups from the neighborhood will be banging on their door, demanding to be let in so they can wipe… Never mind.

The patient, as part of a PICC line for leg osteomyelitis, had a CXR. There was a big something in the upper lobe, so a CT was done. A very thick-walled mass with a cavity in the middle. No air-fluid level.

And lots of other no’s: fever, chills, cough, shortness of breath, aspiration, poor dentition, immunosuppression, or risks for any odd infection. Also, no tobacco or reason for a malignancy, although I bet it would be a tumor.

And I would be wrong, but the title gave it away.

Biopsy: abscess. Culture: MRSA

This is not the first S.aureus cold lung abscess. My first was as an intern, 37 years ago. I thought it would be a Pancoast. It was MSSA.

Classically, cold abscesses are a manifestation of tuberculosis, and I found this from 1904 from a surgeon who in this era would be an ID doc:

Paradoxical as it may appear, cold abscesses and sinuses with all kinds of mixed infection furnish a fascination for me that years of experience in their treatment can not satisfy. Year after year, as requests from chairmen and secretaries come to present a paper for discussion, the topic chosen today comes first into mind, and because of its inexhaustibility it pleads for further discussion.

Yeah. He would also have been an ID blogger. And I find it appalling that an article from 1904 is behind a paid firewall. One of the many reasons I am not a fan of the AMA; that’s just greed. But I found a copy.

I can only find S. aureus osteoarticular cold abscesses on the web; a search for lung involvement yields nothing.

I would have bet good money I have written about other S. aureus cold lung abscesses before. And I would have been wrong again. I have a half dozen blog entries of various bacteria presenting as a cold abscess, but not S. aureus in the lung.

So this case is the first-ever reported. And you know what that means: you have to consider S. aureus as the cause of every cavitary lung mass you see. Because that is just how medicine works.

Rationalization

TREATMENT OF COLD ABSCESSES AND SINUSES IN TUBERCULOUS BONE LESIONS. https://scihub.tw/https://jamanetwork.com/journals/jama/article-abstract/463088

POLL RESULTS

I would hoard

• TP 0%
• beer 35%
• disease free bats 19%
• newspapers to remind me of better times 3%
• hope and goodwill 32% Other Answers 10%
• Cannabinoids.
• TP,rum,kippers,cabbage,caraway rye bread,peanut butter,and 8 months unread stack of The Nation,Free Inquiry, and Skeptical Inquirer. Oh. Also my wife.

  Odd All Over

  Mar 16, 2020

The hospital seems oddly quiet. There are open beds on the floor and in the ICU, maybe 80% capacity? I look at every patient on antibiotics most days for stewardship, so I have a reasonable idea of what is going on ID-wise. And I have been getting two or three consults a day, my usual pace. But it all seems subdued. Perhaps my imagination.

As of today, we have ‘only’ 38 COVID cases in Oregon, but I keep looking at Italy as our future. The US is about two weeks behind Italy in COVID epidemiology, so the next 6 months are going to be… interesting.

I think we are in the tsunami drawdown, at least in PDX, where there are receding waters just before the big one hits. When the tide goes out quickly, run for high ground. But when there is no high ground, you can only wait for the wave. Perhaps a form of learned helplessness.

But regular ID soldiers on.

Two cases. The same and different.

One is classic: nausea, abdominal pain that is localized in the RLQ, and appendicitis.

The other, not so much. Fevers and headaches. That’s it. I saw the patient, and she had no other symptoms. She looked ill, but the exam, CBC, and comp were fine. Twenty-somethings usually have trivial causes for fever, so I voted watch and wait. On day 4, she developed abdominal pain, and an on CT was an inflamed appendix.

And both had multiple, large liver abscesses that grew S. intermedius.

I will spare you all the blind alleys I considered in the second case, as it would spoil my image as an incredible ID diagnostician. But I had some spectacularly wrong ideas while we waited on the cultures. If you like to talk, as all ID docs do, there is ample opportunity to be wrong. Very wrong. But at least harmlessly wrong.

Painless appendicitis does occur.

The diagnosis of acute appendicitis has been based on the presence of right lower quadrant pain and guarding. Occasionally, the pain disappears, even in the presence of a continuing appendicular process. This phenomenon is called “the fools’ paradise.

Fool? Perhaps. But it was no paradise. The term, by the way, dates to 1895 from The Ingleby Lectures On Appendicitis and the phrase is often repeated in the older literature.

In the old days, the 1930s, appendicitis was the number one reason for liver abscess:

Pyogenic liver abscess is primarily a complication of an intra-abdominal suppurative process with the antecedent lesions in the portal area. Of these lesions, suppurative appendicitis is the most frequent. Appendicitis was the etiologic agent in 34.2 percent of the collected cases and 10.6 percent of the authors’ cases.

Nowadays, the main reason is biliary disease; I can’t remember the last time I saw a liver abscess from a bad appendix, although that could be more a manifestation of my memory.

S. intermedius is the most common organism in liver abscesses from biliary disease. I can find only one case in the modern literature of this organism from acute appendicitis; it was probably there in the old days where

The most frequently found organisms in pyogenic hepatic abscess are B. coli, streptococci, and staphylococci.

Also odd, for as best I can tell, S. intermedius is not part of the appendix microbiome. I think.

Results showed considerable diversity and interindividual variability among the microbial composition of the appendix samples. In general, however, Firmicutes was the dominant phylum, with the majority of additional sequences being assigned at various levels to Proteobacteria, Bacteroidetes, Actinobacteria, and Fusobacteria. Despite the large diversity in the microbiota found within the appendix, however, a few major families and genera were found to comprise the majority of the sequences present. Interestingly, also, certain taxa not generally associated with the human intestine, including the oral pathogens Gemella, Parvimonas, and Fusobacterium, were identified among the appendix samples.

Some have S. milleri and S. anginosus, which may have been S. intermedius. Probably. The changing Streptococcal nomenclature always makes comparisons with the past studies problematic. But it is, for modern medicine, an odd bug from an odd source,

Rationalization

[Painless Acute Appendicitis: “The Fools’ paradise”: Report of Two Cases] https://pubmed.ncbi.nlm.nih.gov/19350173/

The Ingleby Lectures On Appendicitis https://www.jstor.org/stable/20216411

A REVIEW OF SEVEN HUNDRED CASES OE ACUTE APPENDICITIS* https://pdfs.semanticscholar.org/498f/b63eaf01849eea83dac8b0223e66c6900025.pdf

Pyogenic abscess of the liver: II. An analysis of forty-seven cases with review of the literature https://www.sciencedirect.com/science/article/abs/pii/S000296103890618X

[Appendicitis Disguised as Multiple Liver Abscess] (https://journals.lww.com/ajg/Fulltext/2016/10001/Appendicitis*Disguised*as*Multiple*Liver*Abscess*.2674.aspx)

Pyogenic Liver Abscess: Incidence, Causality, Management and Clinical Outcomes in a New Zealand Cohort https://pubmed.ncbi.nlm.nih.gov/30921309/

Microbial Composition of Human Appendices from Patients following Appendectomy https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3073909/

POLL RESULTS

We are heading into a

• tsunami 7%
• stool storm 11%
• rock and a hard place 11%
• the worst of times. 7%
• walk in the park. A park between a rock and hard place filled with the worst of stool storm tsunami 57% Other Answers 7%
• meat grinder for the old and infirm.

  To Play the Odds

  Mar 18, 2020

Tick Tick Tick Tick

Work is like one of those movie scenes where the timer ticks down to zero while the protagonist works to disarm the bomb. We don’t know which wire to cut because they are all red. And we are colorblind. With no wire cutter. What is worse, the bomb is likely to blow before the timer gets to zero.

Tick Tick Tick

In the meantime, life, or a reasonable facsimile thereof, goes on.

The patient is admitted with a gangrenous gallbladder and peritonitis. In the OR, everything is fixed/drained/removed as needed, and he is moved to the ICU, septic, on, of course, piperacillin/tazobactam and vancomycin.

But by the following day, he is better. On day two, one of the blood cultures grows C. albicans and they call me.

I will note there seems to be a new practice amongst my surgical colleagues, many of whom are new in practice. They are in the OR, up to their elbows in pus and

They. Don’t. Send. Cultures.

Then they call me for antibiotic suggestions. It’s like inviting someone to participate in the Tour de France but not allowing a bicycle. Drives me nuts.

But I always think back to the STOP-IT trial, which I always consider a paper that demonstrates the surgical attitude towards ID. Patients had “infections” and received “antibiotics.” No mention of what the infection was, what organism was involved, and how it was treated. Even the supplement doesn’t get that granular. Nope. Besides source control, just treat “infections” with “antibiotics,” and the patient will do fine. Given the outcomes, you could argue it is a functional approach.

But in this case, I had no operative cultures to know, rather than assume, the source. And the patient has a prosthetic valve.

Oddly, in 30 years, I have never had a patient with candidemia and a prosthetic valve. What is the risk of seeding the valve?

Of 44 patients, 33 never developed evidence of PVE (group 1), 7 (16%) had evidence of PVE at the time of candidemia (group 2), and 4 (9%) developed PVE a mean of 232 days after candidemia (group 3). Predisposing factors including intravascular lines, prior antibiotic therapy, and an identifiable portal of entry for fungemia were common in group 1 but not group 2. Candidemia occurred significantly later after PHV surgery in group 2 (mean 270 days) as compared to groups 1 and 3 (means 48 and 15.5 days, respectively; P = 0.02).

So it can happen, and it can manifest late.

Repeat BC are negative. The 1-3 beta D Glucan? 270. And after two weeks? Undetectable. TEE? Negative.

So how long to treat? Either two weeks or forever, I guess. Odds are it is not endocarditis. I opted for two weeks. The patient did fine.

Rationalization

Wire Dilemma https://tvtropes.org/pmwiki/pmwiki.php/Main/WireDilemma

Trial of Short-Course Antimicrobial Therapy for Intraabdominal Infection https://www.nejm.org/doi/full/10.1056/NEJMoa1411162

Incidence and Risk of Developing Fungal Prosthetic Valve Endocarditis After Nosocomial Candidemia https://pubmed.ncbi.nlm.nih.gov/9236482/

(1’3)-²-D-Glucan Assay in Monitoring Response to Anti-Fungal Therapy in Fungal Endocarditis https://pubmed.ncbi.nlm.nih.gov/28820552/

POLL RESULTS

Don’t get cultures as

• antibiotics will take care of everything 15%
• what I can’t see doesn’t exist 15%
• it is the terrain, not the bacteria 4%
• I ignore them anyway as long as the patient improves 19%
• cultures are for yogurt 38% Other Answers 8%
• all the above, seriously, from the same surgeon
• the timer is a red herring. Or a kipper.

  May You Live in Interesting Times

  Mar 24, 2020

These are interesting times. By the way:

‘May you live in interesting times’ is widely reported as being of ancient Chinese origin but is neither Chinese nor ancient, being recent and western… The phrase was introduced in the 20th century in the form ‘interesting age’ rather than ‘interesting times’ and appears that way in the opening remarks made by Frederic R. Coudert at the Proceedings of the Academy of Political Science, 1939.

I had a report today of someone turning it up to 11: while transporting a patient, an HCW wore two N95 masks. Would that be an N190?

And it would appear that hydroxychloroquine is being prescribed in outpatients without cause. The whole Plaquenil/azithromycin treatment for Trump Virus COVID-19 makes for an interesting dilemma.

What do you do when you have a ‘positive’ lousy study with a toxic drug that really proves nothing, that you doubt the results are valid, but the drug is touted by a compulsive liar as a game-changing intervention? A study that is, at best, at best, hypothesis-generating, not the biggest game-changer in the history of medicine. Which is penicillin. Duh.

And a medication that is needed by people with diseases for which it does work and for whom it is in short supply?

I remember the bad old days of HIV when all sorts of therapies with no biologic plausibility were touted as effective, and none panned out. As the French say, the more things stay the same, the more things stay the same. That’s because most published research findings are false.

ID is mostly about specific drugs targeting specific sites to interfere with bacterial or viral processes. I would bet good money, at least a dime, that any drug that has effects on

rabies virus, poliovirus, HIV, hepatitis A virus, hepatitis C virus, influenza A and B viruses, influenza A H5N1 virus, Chikungunya virus, Dengue virus, Zika virus, Lassa virus, Hendra and Nipah viruses, Crimean Congo hemorrhagic fever virus and Ebola virus, as well as various DNA viruses such as hepatitis B virus and herpes simplex virus.

Will have no relevant clinical effects of note on any virus.

What are you doing to do? If most studies are false, then all azithromycin/hydroxychloroquine should provide is toxicity and cost. But as a rule, no one, except for you, of course, considers the downsides of unproven therapies, only the potential, however unlikely, of upsides.

I always prefer eating crow to saying I told you so. “It is amazing how often I am right” is for others; my wife will let you know how often I err. But I will not be surprised if azithromycin/hydroxychloroquine is all sound and fury, signifying nothing.

Interesting times indeed.

Sometimes you get a consult that at first sight is a been there, done that.

I was asked to see a patient with a recurrent Group A Streptococcus infection. Fine. Been there, done that. S. pyogenes is the usual cause of recurrent cellulitis. The reason is usually chronic lymphedema in the obese. The solution is chronic penicillin, although the almost homeopathic dose (250 mg daily) used in the NJEM article seems designed to fail and breed resistance. I tend towards amoxicillin bid and almost never see a relapse. Perhaps because the patients quit seeing me.

This, however, was recurrent bacteremia, three episodes separated by four months each and not a hint of cellulitis.

That’s odd, an impression confirmed by a quick PubMed. One case in an adult:

I report that a 75-year-old man with severe atherosclerosis experienced two episodes of bacteremia with Streptococcus pyogenes of type emm87. Recurrent sepsis with S. pyogenes is extremely rare, and a foot ulcer was the suspected point of entry. The patient did not develop opsonizing antibodies to the isolate.

The patient has no point of entry, no occult focus, and, besides age, no immunodeficiency.

So why? It would be fun to gather up his Streptococci, which are frozen in the lab, and see if they are the same strain or not. And it would be fun to see if he did develop immunity to these strains. But currently no time for that sort of shenanigans.

And then what to do? Await the fourth bacteremia? If his pattern remains true, he will get ill right in the thick of the COVID tsunami. So I elected to treat him as the equivalent of recurrent cellulitis.

Rationalization

May You Live In Interesting Times https://www.phrases.org.uk/meanings/may-you-live-in-interesting-times.html

These go to https://www.youtube.com/watch?v=KOO5S4vxi0o

Trump has made more than 16,000 false or misleading statements since inauguration: Report https://www.washingtonexaminer.com/news/trump-has-made-more-than-16-000-false-or-misleading-statements-since-inauguration-report

New insights on the antiviral effects of chloroquine against coronavirus: what to expect for COVID-19? https://www.sciencedirect.com/science/article/pii/S0924857920300881?via%3Dihub

Guys. We need to talk about this Hydroxychloroquine + Azithromycin thing. https://twitter.com/jpogue1/status/1241138975802359813

Are hydroxychloroquine and azithromycin an effective treatment for COVID-19 https://sciencebasedmedicine.org/are-hydroxychloroquine-and-azithromycin-an-effective-treatment-for-covid-19/

Why Most Published Research Findings Are False https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0020124

Clinicians Expectations of the Benefits and Harms of Treatments, Screening, and Tests A Systematic Review https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2596010

Penicillin to Prevent Recurrent Leg Cellulitis https://www.nejm.org/doi/full/10.1056/nejmoa1206300

Recurrent Sepsis Caused by Streptococcus Pyogenes https://pubmed.ncbi.nlm.nih.gov/21346045/

POLL RESULTS

When there is no proven therapy and only one lousy intervention study I

• just say no. works for drugs and sti prevention 74%
• go with the flow and never say no 6%
• give in to social pressure and hope for the best 3%
• feel it is better to harm patients with action rather than inaction 12%
• go with the advice of those with no medical education whatsoever 0% Other Answers 6%
• forget to wake up. The dead don’t make mistakes.
• Only when my Patient is dying

  It Happens

  Mar 25, 2020

Often the explanation for many infections is bad luck. And my patients have bad luck in droves. Although I have to admit my bias: I think the norm is to be infected and to be healthy/uninfected is abnormal. I guess that comes from a life of pus.

The patient is an elderly male with the common diseases of Western civilization. Although shouldn’t it be Western uncivilization of late? Non-insulin-dependent diabetes, obesity, and hypertension.

He has the onset of progressively severe low thoracic back pain and then lower extremity weakness and urinary retention.

MRI showed the expected discitis, osteomyelitis T12/L1, and epidural abscess at T10-T11. Kind of high up the spince for the usual infection. Most cases are L spine, but close enough.

There was no reason for his disease: no trauma, bacteremia, festering wounds, etc. Still, to live is to be bacteremic.

He went to the OR for debridement and decompression, and the gram-stain had pus and gram-positive cocci.

And everything, including several blood cultures, grew Staphylococcus epidermidis.

That was not on my list of causative organisms.

He did have back surgeries several years ago, but at a different levels than the infection.

But it happens:

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.

I also found the bacteremia peculiar, and there was nothing on examination or echocardiography to suggest an endovascular infection.

It makes one wonder about those percutaneous biopsies that only grow a rare coagulase-negative Staphylococcus. Real or not? Impossible to know. But hard to ignore.

Rationalization

Characteristics of Spontaneous Coagulase-Negative Staphylococcal Spondylodiscitis: A Retrospective Comparative Study Versus Staphylococcus Aureus Spondylodiscitis https://pubmed.ncbi.nlm.nih.gov/29029624/

Polymouth

Mar 30, 2020

Have we flattened the curve in Oregon? I don’t know. But COVID is accelerating slower than I thought it would. Michigan went from 80 to 6500 cases in 12 days, in the same time frame we went from 75 to 600 cases. I know our testing is minimal; all of our approach to COVID has not even been half-assed due to a lack of preparation. Don’t get me started.

But the hospitals were cleared out in anticipation of a COVID surge, and we still have lots of open beds. I can only hope this isn’t wishful thinking, but maybe people are taking our new national anthem to heart (NSFW). Or perhaps it is due to our relatively low density of people that is slowing the spread.

Internet-connected thermometers suggest it may be the real deal:

To identify clusters of coronavirus infections, Kinsa recently adapted its software to detect spikes of “atypical fever” that do not correlate with historical flu patterns and are likely attributable to the coronavirus. As of noon Wednesday, the company’s live map showed fevers holding steady or dropping almost universally across the country, with two prominent exceptions.

Not that I am complaining, but I would love to avoid the disaster that is happening in other metro areas.

And my wife is pissed I am going to work. But how could I not? I can’t see saying no is an option. But she is preparing for shortages by making masks. They are pretty nice, with a place to hold a filter. I know the data with cloth masks, but I suspect something will be better than nothing, especially if you have several cloth masks and swap for a new, dry one every hour or so. She is trying to make sure I don’t die from the pandemic, and I appreciate the concern despite my life insurance policies.

Infections continue on, COVID or not.

The patient has slowly progressive back pain over a month’s time to the point it becomes unbearable. He goes to the ER, and an MRI shows classic discitis, osteomyelitis, and epidural phlegmon.

I do the usual history and physical, and there is no reason for a back infection— everyday, boring life outside of a few farm animals.

He has a biopsy, and surprisingly because percutaneous biopsies are usually negative, it grows a bacteria. There may be a better way to do these biopsies to increase the yield. In one study of vertebral osteomyelitis, three samples (one specimen in an anaerobic blood culture bottle, one in aerobic blood culture bottle, and one in saline followed by three post-biopsy blood cultures found the organism 74% of the time. That is a remarkable yield, much better than the 40% in the literature or the maybe 10% I get.

The biopsy grows bacteria: S. mitis AND Haemophilus aphrophilus. Mouth bugs. How did they get to the spine? Got me. Brushing and flossing, I suppose. His teeth are fine. Nothing else by history. If he stuck a bleeding finger in his mouth, he does not remember.

Both organisms have case reports in the PubMeds causing spine infections, but not together. Not two great tastes that taste good together. And hematogenous polymicrobial spine infections are also unusual.

So lots of oddness.

Unlike COVID, I have effective therapies, and he is improving on the course of ceftriaxone.

Rationalization

BMC Infect Dis. 2016; 16: 141. Published online 2016 Mar 31. doi: 10.1186/s12879-016-1471-9 Polymicrobial vertebral osteomyelitis after oesophageal biopsy: a case report

Management of vertebral osteomyelitis over an eight-year period: The UDIPROVE (Udine PROtocol on VErtebral osteomyelitis) https://www.ijidonline.com/article/S1201-9712(19)30403-5/fulltext

Restrictions Are Slowing Coronavirus Infections, New Data Suggest https://www.nytimes.com/2020/03/30/health/coronavirus-restrictions-fevers.html

Butt Abscess

Apr 1, 2020

It is still weirdly quiet in PDX. We are between a rock (Washington) and a hard place (California), but the COVID cases continue to increase around 50-100 a day in the state, much more gradually than I would have expected.

I walked through the ER waiting room today, and it was empty. In 30 years, I never saw that area of the hospital empty. Do not get me wrong. We have COVID patients, but the cases are well within the ability to handle them. For now.

At Legacy Health, total hospitalizations Tuesday in Oregon and Southwest Washington stood at 22. Thatis nearly triple the count from March 25.

Here’s hoping I am not jinxing us, not that I believe in jinxing, knock on wood. But if they continue to triple, and no reason to think they will not, the hurt will come soon enough.

But as my colleagues go to war, I feel oddly guilty that I am not helping out. They storm the beaches while I sit home because of bone spurs in my feet. Our time will come, I know. And it will not be glorious. And there are still other infections that need care.

The patient is an IVDA, admitted with fevers and severe pain in the right buttock. He is a skin popper/muscler of heroin but denies injecting into his backside. He also had no remembered trauma to the area.

CT shows rim enhancing abscess in the gluteus the size of a large grapefruit. Blood cultures were negative.

OK. Been there, seen that. Most likely MRSA, let’s get it drained. So surgery surgerizes, and there is pus and gram-positive cocci.

And it grows S. pneumoniae.

I did not see that coming. I can only remember one other Pneumococcal abscess in my career, and that was almost 30 years ago.

There are more cases in the Pubmeds than I would have expected, with one review finding

A total of 35 cases of pneumococcal pyomyositis were identified, 11 in apparently healthy hosts and 24 in at-risk hosts. Two-thirds of the patients had an antecedent respiratory illness or meningitis.

My patient was mostly normal: HIV negative, no antibody or complement deficiency. He did have severe malnutrition due to a homeless life that revolved around obtaining heroin instead of food. In children and adults, malnutrition is a risk for invasive pneumococcus. So there is a reason.

Once debrided, he did fine, leaving before we had planned on a course of po amoxicillin.

Rationalization

Clin Infect Dis. 2012 Aug;55(3):e12-7. doi: 10.1093/cid/cis424. Epub 2012 Apr 20. Pneumococcal pyomyositis: report of 2 cases and review of the literature. https://www.ncbi.nlm.nih.gov/pubmed/22523257

Coronavirus hospitalizations double in six days at Providence, nearly triple at Legacy Health

POLL RESULTS

When tragedy strikes others I

• feel guilty I can’t help 49%
• feel better by sending money 6%
• feel relief, better them than me 11%
• feel schadenfreude, they had it coming 11%
• blame China, the media, and the CDC 20% Other Answers 3%
• try not to take it personally.

  It Is Not Why I Am A Doctor

  Apr 6, 2020

The patient is admitted with MRSA bacteremia. The source is likely a dog bite, although the bite is not clinically infected.

She responds clinically to iv antibiotics, repeat blood cultures are negative and has a negative TTE. Kind of a low-risk S. aureus bacteremia, I would guess.

Except for the diabetes and CLL.

So how long to treat? I opted for 4 weeks of vancomycin because it is MRSA and the diabetes and CLL.

Ten days after finishing the vancomycin, she is back with fevers and growing MRSA in the blood again.

Expletive deleted.

It is rare for me to have a relapse for S. aureus bacteremia; I tend to err on the side of longer rather than shorter. I have less than a handful that I remember, and I tend to vividly remember my failures.

Again, she responds clinically to iv antibiotics, repeat blood cultures are negative, and has a negative TEE.

Review of systems is negative, as is the exam. She has several artificial joints, but they are asymptomatic. So, where’s the MRSA?

What is annoying about the metastatic complications of S. aureus bacteremia is at least 40% of patients will have no localizing signs and symptoms of infection

The incidence of metastatic infection was similar in patients with Streptococcus species and patients with S. aureus bacteremia. Signs and symptoms guiding the attending physician in the diagnostic workup were present in only a minority of cases (41%).

I didn’t become a doctor to order tests without a reason or at least localizing symptoms, but with this case, I need to know where the S. aureus is and is not.

There is an interesting literature on the use of PET CT in S. aureus bacteremia. As one example from a consistent literature

8F-FDG PET/CT is a valuable technique for early detection of metastatic infectious foci, often leading to treatment modification. Performing 18F-FDG PET/CT is associated with significantly reduced 3-mo mortality.

I ordered the PET, and it was negative for infection of the prosthetic joints and heart but did show a paraspinal abscess in the mid-thoracic spine.

So I had a reason for relapse. It was not drainable per IR, so will treat until it is all gone.

Should I be getting more PET scans? Probably. It does have utility for a variety of ID conundrums beyond S. aureus bacteremia, like FUO and infected cysts in polycystic disease.

I can’t see doing a PET routinely and just try. Some insurance companies flat out refuse to pay for any PET that is not being done for malignancy, no matter how many clinical studies you send them.

Rationalization

Metastatic Infectious Disease and Clinical Outcome in Staphylococcus Aureus and Streptococcus Species Bacteremia https://doi.org/10.1097/md.0b013e31824d7ed2

(18)F-FDG PET/CT Optimizes Treatment in Staphylococcus Aureus Bacteremia and Is Associated with Reduced Mortality http://jnm.snmjournals.org/content/58/9/1504

POLL RESULTS

I vividly remember

• my failures 22%
• my embarrassments 37%
• my triumphs 4%
• crushing my enemies, seeing them driven before me, and hearing the lamentation of the women 11%
• the might have beens and the never-weres 20% Other Answers 7%
• the last few weeks with my Dad
• all the women who figured out that I’m worthless, and moved on.

  A Miracle?

  Apr 8, 2020

Three months ago, the patient had a fall and injured his thumb, a mild road rash on the nail side of the digit.

A month later, the thumb develops an abscess between the joint and the nail base that grows E. coli and an anaerobe. Not that odd, it is the dominant hand, and dominant hands are often near unsanitary orifices.

He gets a course of antibiotics, and at the end of therapy, the thumb is still a bit red, so they get an x-ray:

I can’t upload the image. It shows what looks to be osteomyelitis of the tip of the thumb: osteolysis and a ratty bone. If you click here, you can see the film.

and send him to me.

The thumb looks fine—a little red, non-tender, and a good range of motion.

But there was no penetrating injury, and it is the tip of the thumb that is eroded, anatomically distant from the injury. Still, it is hard to not not treat for osteomyelitis given that x-ray and the thumb of the dominant hand of a musician.

He told me he also had films done a couple of days earlier at a radiology center, the results of which were not available in EPIC. So I told him it was odd with the location and lack of penetrating injury, and we would try a course of antibiotics in part as it was his dominant thumb. I would also have the new films pushed over so I could look at them the next day.

So a repeat x-ray a little over a month after the first showed.

I can’t upload that film either. If you click here you can see the film.

It’s all better. No way. I went over the films with the radiologist, and there were other features that confirmed these were all from the same patient. And he had an MRI of the thumb that showed no osteomyelitis from the same time. An infection is not going to spontaneously resolve with the bone growing back.

Is this a miracle? Of course not. There are no miracles outside USA Olympic Hockey.

What else causes acro-osteolysis? A whole lot of things, including guitar playing:

A case of occupational acroosteolysis in a 24-year-old classical guitar player is reported. Nail tenderness was the only manifestation of initial acroosteolysis, which was due to mechanical stress on the fingers. Radiographs showed initial resorption of the 2nd, 3rd and 4th finger of the left hand.

And. He is an electric bass player, and when I told him about acroosteolysis, he told me he really thumps hard on his bass with his thumb.

What he hadn’t been doing for the last 3 months is playing bass, which is why his thumb reverted to normal.

So I stopped the antibiotics, and he did just fine.

Rationalization

Acro-osteolysis https://radiopaedia.org/articles/acro-osteolysis-1?lang=us

Occupational Acroosteolysis in a Guitar Player https://doi.org/10.2340/00015555736465

Guitar player acro-osteolysis https://link.springer.com/article/10.1007/BF00347201

It Doesn’t Stop at the Lips

Apr 13, 2020

I have filled out my selective service form. My system has reached out to all the doctors in case the COVID hits the fan, so we can be reassigned to COIVD care if the caseloads get too large.

I do not think that is going to happen here in PDX; the curve has been very nicely flattened. But to be on the safe side, I reviewed my notes from my internship, 34 years ago.

Treat TIAs with aspirin and persantine. Check.

Treat COPD and asthma with aminophylline. Check.

Suppress all ectopy with iv lidocaine and discharge on quinidine or procainamide. Check.

Treat heart failure with digoxin. And don’t forget that Swan-Ganz Check and fours views of the heart to look for cardiomegaly. Check.

See? I still have it. Just give me a Washington Manual, and I am good to go.

And, as you can tell, I am an expert in prescribing useless drugs that only offer toxicity, so giving hydroxychloroquine is right up my alley. In the meantime, before I am called up to fight, I still have germs I can actually kill.

The patient had a laminectomy six weeks ago, and for the first month, he did fine. Then he developed a big, red, tender lump on the incision that ruptured, and he came to the hospital. MRI showed only superficial infection, confirmed in the OR. The gram stain was negative, and they called me to see the patient.

I came in the next day, and the cultures were already growing a Pasturella multicida, so no mystery as to the etiology of the infection.

In talking to the patient, he has two dogs that he does not sleep with and did not lick his wounds. I know. Ick. I have seen my share of Pasturella infections from animals licking wounds. My favorite was a young girl who put tuna on her nose so her cat would lick it; the result was Pasturella meningitis.

But he lives in a trailer with his animals, a small space, and I have also seen infections where the Pasturella was picked up from the environment, and a trailer is a small space.

Most think of Pasturella as a cat organism, but it can be found in 20% of dogs’ mouths as well as pigs, rats, buffaloes, and other animals. And Pasturella causes

fowl cholera (isn’t all cholera foul?) in poultry, atrophic rhinitis in pigs, and bovine hemorrhagic septicemia in cattle and buffalo.

And there are more than just P. multicida, including a P. dagmatis, which sounds like something an ornery Walter Brennan would say.

Expect to see more Pasturella infections as

Pets, including dogs and cats, are frequently recommended to patients with chronic illness because animal therapy might provide a potential health benefit. Elderly patients may also own companion animals to combat loneliness; however, pets may be the potential source of various infections or injuries. Our retrospective survey showed that the rate of human pasteurellosis over a 13-year study period in Hungary increased from year to year and with advanced age, and the number of Pasteurella infections was higher than it was in earlier studies.

The patient did just fine after debridement and amoxicillin.

Rationalization

Stumpy https://www.youtube.com/watch?v=wsnPpt4r7mk

Human Pasteurellosis Health Risk for Elderly Persons Living with Companion Animals https://wwwnc.cdc.gov/eid/article/25/2/18-0641\*article

Pain

Apr 15, 2020

I am by no means the first to notice this, but where has all the disease gone?

Since shelter at home has been implemented, we have nicely flattened the COVID curve in Oregon, but all the usual diseases have vanished. No S. aureus bacteremias in IVDA, no late wound infections, no complicated pneumonia, no nothing. Bread and butter ID has evaporated, and my colleagues in other specialties have also noticed a decrease in new consults.

It will be interesting when COVID has declined sometime in 2022-23 to look back and explain why this happened. I hope it is not that everyone is dying at home.

The patient is admitted with shoulder pain long before COVID. He said he had fallen and perhaps twisted his shoulder when he fell, but it wasn’t an “I really hurt myself when I fell” moment.

Over the next several days, the pain progressed, and he was admitted with a red, hot, swollen, painful shoulder that did not get better with antibiotics.

Ortho saw him and, based on MRI and exam, said the patient didn’t need debridement; it was cellulitis.

I saw the patient, and I differed.

He could move the joint, but not much, without pain. And his joint didn’t hurt when pressure was placed across it. So the joint itself was not infected. It was in the tissues around the joint, in the front.

But it was narcotic requiring.

Cellulitis can be tender to touch. And cellulitis can hurt like stink when the affected limb is placed in the dependent position. But the pain should be, at worst, a 4 out of 10.

As a rule, if ‘cellulitis’ hurts enough to require narcotics, either there is an abscess, pus under pressure, or dead/dying tissue, where the pain is often out of proportion to the physical findings.

Those infections need an I&D.

So we called a general surgeon who took the patient to the OR: necrotizing myositis of the deltoid and pectoralis due to MRSA.

With I&D and antibiotics, his pain rapidly improved.

I keep telling surgeons: the patient has too much pain. It isn’t drug-seeking. There is something evil going on. They need an I&D. It is a fine point of soft tissue infections that I suspect is not emphasized.

Rationalization

Comparison of Short-Course (5 Days) and Standard (10 Days) Treatment for Uncomplicated Cellulitis Arch Intern Med. 2004;164(15):1669-1674. doi:10.1001/archinte.164.15.1669 https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/760487

POLL RESULTS

Least likely to pay attention to my always superior opinion:

• a surgeon 30%
• my spouse 18%
• my children 15%
• everyone and anyone 30%
• a hospitalist 3% Other Answers 5%
• a nurse practitioner
• most any GOP politician or voter.

  Who Da Thunk It?

  Apr 22, 2020

This is my 34th year, including my fellowship, that I have been practicing ID, and I have never been bored at work. That’s because there has always been work to do.

The last couple of weeks? Not so much. While most of the country is inundated with COVID, Oregon is getting around 50 cases a day, and at any given time, each of my two hospitals has 2 or 3 patients. Not that there is much for an ID doc to do with COVID patients, the diagnosis and treatment are straightforward. I mostly kibitz about testing and the worthlessness of game-changing drugs.

With COVID, most regular ID has evaporated, and going over my patient list yields nothing curious to write about, which is why there was no entry on Monday. It has all been bread and butter cases with no questions or uncertainties.

Usually, ID is like Bach, interesting or curious variations of a theme. Last couple of weeks? No variations. The only case of any controversy was a patient with line-related MSSA bacteremia and a painful wrist. The MRI was read as multifocal osteomyelitis of the wrist bones with joint infection and tenosynovitis.

Nope. Or perhaps. I argued that there was zero probability that the MSSA seeded multiple bones in the wrist. Hematogenous osteomyelitis is rare in adults. It was likely a false positive MRI with the usual bone edema that often happens when bone sits next to infection/inflammation. No bone destruction, no osteomyelitis.

At least usually. If a joint festers long enough, it will erode into bone, but the literature from both the diabetic foot and decubitus (my spell checker suggested dubious) ulcers is clear: take MRIs with a grain of salt substitute when they are read as osteomyelitis.

It is safe to say that work is kind of dull. I prefer more rather than less work, and I work better when I am busy. Currently, it is like putting the car in neutral and pressing on the gas pedal. Lots of energy to expend, but nowhere to go.

So I watch what is going on with COVID, locally and around the world.

Public health has two responses to a pandemic: under-prepare/under-react or over-prepare/overreact. There is no way to hit the Goldilocks point. It looks like the US has committed to the former rather than the latter.

I would never have believed that the US would respond so badly, so incompetently, so stupidly, to a pandemic. I knew any pandemic would be ugly no matter what we did, but we have so often chosen the worst path possible. It amazes me that in real-time, as the deaths and disease increase, Branch Covidians behave so counterproductively compared to reality. Some governors are deciding to have a statewide COVID-19 party on the beach to see if they can maximize death and disease in as short a time as possible. Who would have thought Georgia’s role model would be college students flying to Mexico for spring break?

And this is likely just the beginning. When this first pass of COVID is over, I have read estimates that maybe 5%, tops, of the US will have been infected. Maybe. All numbers are in flux as data trickles in. That means COVID is going to have to burn through another, what, 80-85% of the population before there is enough herd immunity to stop transmission. Or a vaccine. If so, the next couple of years are going to be unpleasant, he says with marked understatement.

It is estimated 2020 may be the warmest year on record, and that is with a solar minimum. A more sobering way to think about it is that 2020 is likely to be the coolest the earth will ever have been from 2020 forward.

My wife likes to say you can predict a person’s future behavior by looking at their behavior in the past. If the world’s response to COVID is a dry run as to how we are going to respond to the slower, more insidious, and far more potentially devastating phenomena of climate change?

We are so doomed.

POLL RESULTS

We are

• doomed from COVID 1%
• doomed from climate change 6%
• doomed from antibiotic resistance 3%
• doomed from ignorance and stupidity 55%
• doomed, doomed, doomed. 30% Other Answers 4%
• there is a book about doom and how we never suffer the predicted, to my view because we respond though now “just in the nick of time”
• Doomed from chronic alcohol intoxication because of depression from the others.
• all of the above, he says, copping an easy out.

  Lets Add A Few A’s

  Apr 28, 2020

I have mentioned this before. When I went into practice, my Dad, a cardiologist, told me that there are five A’s to being a consultant. Or a doctor. Availability. Appearance. Ability. Accountability. And Affability. I have tried to always follow the five A’s. Well, 4 out of 5 ain’t bad. But I try to be nice to everyone all the time. Even those who task me.

There are, I suppose, some A’s to avoid. A-hole. Arrogant. Although I have been called the latter many a time.

Time to add another A. Or two.

I had a patient with a well-defined infection. We knew where it was and how best to kill it. But the patient did not respond to the antibiotics as expected. He remained unstable with a leukocytosis.

I had written my note and discussed issues with the team in the late morning, and I find out after the weekend that late afternoon they changed the antibiotics from the treatment of choice to a pair of broad-spectrum antibiotics that were an inferior treatment for the infection we knew the had. Inferior as in associated with increased morbidity and mortality.

I see this often enough to want to rant. Again.

First, is there any better way to give an ID consultant the finger than to change the antibiotics and not give the courtesy of a call?

Nope.

And I was available. Note the first A.

If they had called me and asked, Dr. Crislip, should we give a pair of half-assed broad-spectrum antibiotics for infections for which the patients have no evidence instead of continuing the treatment of choice for the infection we know he has, I may have suggested, well, no, that might not be such a good idea.

Note the third A. It is why the literature clearly shows that ID consultation for these issues leads to decreased morbidity and mortality. I know what I am doing. I would not have changed the antibiotics. And it fry’s my bacon when people do the wrong thing, and a simple page could have prevented it. Seriously. Except when I am out of town, my beeper has been on since June 1990, even when I am not on call.

Because it is almost never about the antibiotics.

When you know the bug, when you have it in your hand, and the patient is not improving as you think they should on the treatment of choice, it is not the antibiotics. It is never the antibiotics. Well. Sometimes it is. There are always exceptions.

But it is either the host, as is often the case with cellulitis, or infections of the immunocompromised.

Or it is a lack of source control.

Which is the case here. There is undrained pus, and that is why the slow response to antibiotics. Antibiotics do not drain pus and are not antipyretics.

Remember the classic Fallacies in Antibiotic Therapy:

• Broader is better.
• Failure to respond is failure to cover.
• When in doubt, change or add another.
• Sickness requires immediate treatment.
• Response implies diagnosis.
• Bigger disease, bigger drugs.
• Bigger disease, newer drugs.
• Antibiotics are non-toxic.

So let’s add some more A’s to the list today. Angry. Annoyed. Aggravated. Antagonized.

At least the patient is back on the treatment of choice for their infection.

Rationalization

Kim JH, Gallis HA. (1989). Observations on spiraling empiricism: its causes, allure, and perils, with particular reference to antibiotic therapy. Am J Med, 87(2):201-6. PMID: 2667357 https://pubmed.ncbi.nlm.nih.gov/2667357/

When I was an intern, I carried a NEJM article about the Swan-Ganz around in my white coat until I really understood the concepts. I still remember when I tossed the paper into the garbage. No recycling back in the day. Now the Swan is an item of historical interest. But everyone should carry Kim et al. around until the concepts become part of the DNA. It will never become obsolete. That, and

Why Most Published Research Findings Are False https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1182327/

A Medical-Skeptical Classic https://sciencebasedmedicine.org/a-medical-skeptical-classic/

POLL RESULTS

It fry’s my bacon when

• they change my orders and don’t call me 11%
• they consult me then ignore my recommendations 42%
• they call me the I and D doctor. That would be the surgeon, thank you very much 0%
• they wait until 3 on a Friday when I am not on call to see a persisting fever that has been hospitalized for 6 weeks 42%
• I have to listen to one of those arrogant a-hole ID docs yammer on about my mistakes. Shut the hell up Dr. Aren’t I So Perfect 6%

  Dodge One Bullet, Get Hit in Another Spot

  Apr 30, 2020

The patient has two weeks of fevers, chills, and drenching night sweats.

Minimal pulmonary symptoms, but it’s April 2020, so she gets tested for COVID. Not that I object, because everyone needs to be tested for COVID. It was negative.

But COVID would not be first on my list with those symptoms and a bioprosthetic valve. It is like flu season, where I suspect everyone with signs of infection, flu-like or otherwise, gets a flu test.

She finally gets sick enough to be admitted, and all her blood cultures grow MRSA.

They call me, and the exam shows a classic embolic event in a finger. Prosthetic valve, murmur, MRSA in blood, embolic event.

So it’s MRSA endocarditis. What else do you need? I do not need an ECHO to make the diagnosis, and I rarely get ECHOs to prove the diagnosis. With a prosthetic valve, you have to play the odds and assume it is infected. A negative TEE doesn’t help, as the absence of evidence is not evidence of absence.

But there are other reasons to get an ECHO, mainly to look for complications of PVIE, such as a ring abscess, that would warrant an earlier surgical intervention.

And wouldn’t you know, her AV is clean. The vegetation is on the mitral valve, which is kind of curious. The AV has no regurgitation, so there is no backflow to damage the MV. It is just the usual elderly valve: thickened, sclerotic, and calcified. The six-year-old bioprosthesis, by comparison, is pristine.

This is not the first time the ‘wrong’ valve was infected on ECHO, and I wonder how often it happens. Rare, I guess I have seen may 2 or 3 other cases I remember. How often it is the native valve and not the prosthetic valve that is infected, I cannot glean from the Googles.

I am still going to treat for PVIE.

There are various cardiac valves: normal, altered from a variety of reasons (age, bicuspid, MVP, ARF, etc.), mechanical, and bioprosthesis.

Which is more likely to be infected? At first glance, I would have thought that the mechanical valve was the most at risk, but a mechanical valve actually has less risk of infection compared to a bioprosthetic:

The risk of infection in the artificial valve was about 50 percent higher with a biological prosthesis than with a mechanical.

It is postulated it is because

Bioprostheses are expected to undergo structural valve deterioration during a patient’s life. It is possible that the gradual degeneration of bioprostheses makes them susceptible to bacterial implantation and infection.

Maybe. But the big difference in the two groups is likely warfarin use, and I can’t see where that was included in the analysis. I would wonder if that warfarin would be protective: not clot, nowhere for the bacteria to stick. And that is hinted at as

Bioprostheses were associated with a higher long-term risk of reoperation and endocarditis but a lower risk of stroke and hemorrhage.

It is probably a little of both. But nowhere can I find the relative risk of infection of a native but old/damaged valve compared to either a mechanical or bioprosthetic valve.

Not that it matters from a practical point, but then many of the questions raised by practice are not practical, but they are curious.

Rationalization

Fewer infections in mechanical heart valves https://www.sciencedaily.com/releases/2017/07/170718103328.htm

Prosthetic Valve Endocarditis After Surgical Aortic Valve Replacement https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.117.028783

Long-Term Safety and Effectiveness of Mechanical Versus Biologic Aortic Valve Prostheses in Older Patients https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.113.002003

125 is Too Low

May 4, 2020

At the end of March, I texted my colleagues that I thought there were going to be 100,000,000 cases of COVID in the US and a million deaths in the next 18 - 24 months before the virus infected enough people to slow down. I sadly suspect I was way too optimistic and should have doubled my numbers. Man. I so want to be wrong.

But there is more than COVID to confound and surprise me.

The patient is an elderly female with Stills on a prednisone taper. She comes in with the abrupt onset of fevers and dyspnea and an interesting chest CT: multiple large round infiltrates. Bronchoscopy is negative for organisms, and the pathology shows acute inflammation.

She does not look that sick, and his cough is nonproductive. Standard pneumonia work-up negative. The pattern suggests a large inhalation insult.

You get what you are exposed to, and her only exposure of note is she is a gardener, and just before the onset of the disease, had a load of compost delivered.

Pulmonary wondered about BOOP. I didn’t think so.

From the Stills? It happens, but not with this pattern.

Parenchimal lung involvement (PLI) is present in less than 5% of AOSD cases and ranges from aspecific reticular interstitial opacities to life threatening conditions, such as acute respiratory distress syndrome (ARDS).

I bet it was either Cryptococcus (nope) or Nocardia (nope). The former is due to a negative antigen and the latter presumptively from a negative 1-3 beta-D-Glucan.

I was still worried re Nocardia. The literature on Nocardia and 1-3 beta-D-Glucan is scant. With a severe TMP-sulfa allergy, I elected for ceftriaxone and linezolid while we awaited cultures.

Linezolid is safe and efficacious in empirical treatment for moderate to severe nocardiosis in a monitored hospital setting, with 100% drug susceptibility and no difference in adverse events or outcomes compared with non-linezolid regimens.

The other disease I worried about was inhaled Tularemia, as I had seen one similar case before. While she did not mow her lawn, it was big and cut by others, so the infiltrates could have been due to inhaled puréed rabbits, although no Faget’s sign.

And I sent off a Karius test, which came back positive for Legionella micdadei. When they called me with the result, I was both surprised and not. I think I saw a similar case back when I was a fellow; it is a Legionella that often cavitates.

It is not, however, from compost but hot water. So I asked the patient, and she had a new water heater put in a few years back and knew that it was set to 120, at least 15 degrees too cool to kill Legionella. So I had a source.

But she markedly improved on the antibiotics. Perhaps it was just the natural history of the disease as the prednisone was on a taper, but there is some efficacy of linezolid against Legionella, except

Unless there was evidence for intracellular accumulation in phagocytes, such in vitro data would not suggest that these specific oxazolidinones would be likely candidates for treatment of Legionella infections.

And I have seen the occasional Legionella treated with beta-lactams and improve, the diagnosis made when the organism finally grew around the time of discharge/end of antibiotics.

So a little of both.

And finally, the Karius test also had Lactobacillus rhamosus, the same organism in his probiotics. I don’t quite know what to make of that; the company told me they often find Lactobacillus in patients, whether or not they are on probiotics. But it is interesting.

She went home on a macrolide and did fine, planning to increase the temperature of the water heater. Perhaps something all immunoincompetent people should do, but, as one review reveals, it’s complex:

Legionella contamination was associated with a centralized heater, distance from the heater point >10 m, and a water plant >10 years old. Furthermore, zinc levels of <20 data-preserve-html-node="true" μg/L and copper levels of >50 μg/L appeared to be protective against Legionella colonization. Legionella species and serogroups were differently distributed according to heater type, water temperature, and free chlorine, suggesting that Legionella strains may have a different sensibility and resistance to environmental factors and different ecologic niches.

Quite the case.

Rationalization

Respir Med Case Rep. 2017; 22: 91–94. Published online 2017 Jul 3. doi: 10.1016/j.rmcr.2017.07.001 PMCID: PMC5503835 PMID: 28725546 Pulmonary involvement in adult Still’s disease: Case report and brief review of literature https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5503835/

Safety and Outcomes of Linezolid Use for Nocardiosis https://doi.org/10.1093/ofid/ofaa090

An ID lullaby A case of Tularemia containing a song for which I am inordinately proud http://boards.medscape.com/forums/?128@@.2a007714!comment=1

An outbreak of Legionella micdadei pneumonia in transplant patients: evaluation, molecular epidemiology, and control https://www.sciencedirect.com/science/article/abs/pii/S0002934399004593

A note on the temperature tolerance of Legionella. Journal of Applied Bacteriology 56, 349–350. https://sfamjournals.onlinelibrary.wiley.com/doi/abs/10.1111/j.1365-2672.1984.tb01359.x

Legionella Infection Risk from Domestic Hot Water https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3322798/

Delay is Common

May 11, 2020

For Whom the Bell Tolls 2020 COVID Edition John Donne

I am an island, Entire of myself. You are a piece of the continent, A part of them. A clod to be washed away by the sea, I couldn’t care less. I will not social distance. Or wear a mask outside of a manor of thine own Or fret of thine friend’s co-morbidities. Each man’s death? Doesn’t bother me, For I don’t care for mankind. Therefore, send not to know For whom the bell tolls, No concern of mine.

My goal for the next two years is not to catch and/or die of COVID while it burns its way through the population. I am not optimistic. Everywhere, in the hospital or out, people are so half-assed about keeping distance and wearing masks. Perhaps it is because Oregon, relatively, hasn’t yet, been hit that hard.

But every time I see someone without a mask in public or, worse, under the chin or next to the HCW, I think, another nail in my coffin.

There is a pattern I have seen many times in my career, a pattern likely to been seen more now that we are doing more video visits, which just do not cut it.

In January, the patient had an episode of his usual bronchitis: cough, myalgias, malaise, but no fever. He improved on antibiotics.

Then relapsed.

Then, like an out-of-control shampoo loop (rinse, lather, repeat), he had a recurrence, antibiotic, improved, relapsed 3 times.

Finally, blood cultures were done, which grew a Streptococcus sanguinis MIC .25, and while he improved on levofloxacin, they called me to comment on the cultures.

Endocarditis, of course.

I had the patient come into the clinic. You can’t evaluate a patient for endocarditis over the phone, especially using EPIC with Canto, which puts the Cant in video consults. No signs of endocarditis except for a long-standing aortic murmur.

The ECHO had an AV vegetation.

Delays in the diagnosis of endocarditis are not rare because the symptoms are often non-focal, and when there is no fever, as can be the case with viridans Streptococci, bacterial processes are not considered. Yes. Bronchitis is usually not bacterial, but that does not stop antibiotics from being prescribed. That is a whole different topic.

The median days until the diagnosis was 14 days (range 2 days to 1 year). Sixty-five percent of patients received inappropriate antibiotic before the diagnosis (53). Forty percent of causative organisms were Staphylococcus aureus (MSSA 20, MRSA 13), 32% were viridans streptococci and Streptococcus bovis, 28% were others or unknown (CNS 5, Corynebacterium 3, Cardiobacterium 1, Candida 1). Subspecialties such as General Internal Medicine (15), and Orthopedics (13) were associated with delay in diagnosis. Ten patients (12%) died during follow up, and 8 of them had been received prior inappropriate antibiotics.

Two days isn’t much of a delay; one year is impressive and was due to intermittent antibiotics:

However, the duration of the most elongated case reached 4 months, 6 months, and 1 year, which was caused by intermittent oral or intravenous antibiotics without assessment of IE.

Five months may be a record for me. The reference below also notes that in the pre-ECHO era, it took 68 ± 17 days to stumble on the diagnosis of Streptococcal endocarditis.

Rationalization

Medicine (Baltimore). 2014 Dec; 93(27): e237. Published online 2014 Dec 12. doi: 10.1097/MD.0000000000000237 PMCID: PMC4602777 PMID: 25501088 Failure of Early Diagnosis of Infective Endocarditis in Japan—A Retrospective Descriptive Analysis. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4602777

Negative Nodules

May 13, 2020

The patient gets a yearly CT screening for malignancy since he is a former long-time smoker.

In 2018 there was nothing. In 2019 there were 8 nodules. The patient was asymptomatic, and the lesions were PET negative.

Infectious diseases (mycobacterial, fungal, bacterial infection), sarcoidosis, radiation pneumonitis and post-operative surgical conditions have shown intense uptake on PET scan. On the other hand, tumors with low glycolytic activity such as adenomas, bronchioloalveolar carcinomas, carcinoid tumors, low grade lymphomas, and small sized tumors have revealed false-negative findings on PET scan.

So, perhaps more likely a cancer than an infection. But you know this isn’t going to be a cancer, given this is an ID blog.

He had a percutaneous biopsy that was not diagnostic, so a VATs wedge resection was required to make the diagnosis of Echinococcus.

Then he was sent to me.

He is from the mid-east, where Echinococcus granulosus is endemic. He visits home at least twice a year, spending his time in urban areas, and I couldn’t find any specific smoking gun exposure.

Is this cystic or alveolar Echinococcus? The WHO definitions are

Cystic echinococcosis is characterized by an asymptomatic incubation period that can last many years until the parasite cysts evolve and trigger clinical signs, depending on the location and size of the cysts and the pressure exerted on the surrounding tissues. In cystic echinococcosis, the larval stages of the parasite develop as one or more cysts mainly in the liver and lungs, and less frequently in the bones, kidneys, spleen, muscles, central nervous system, and eyes. Abdominal pain, nausea and vomiting commonly occur when cysts invade the liver. If the lung is affected, clinical signs include chronic cough, chest pain and shortness of breath.

Alveolar echinococcosis is characterized by an asymptomatic incubation period of 5–15 years and the slow development of a primary tumour-like lesion which is usually located in the liver. Lesions may also involve other organs such as the spleen, lungs, and brain following dissemination of the parasite via the blood and lymphatic system. Clinical signs include weight loss, abdominal pain, general malaise, and signs of hepatic failure. If left untreated, alveolar echinococcosis is progressive and fatal.

Note the long incubation times in the descriptions; this process is less than a year old. CT of the abdomen did show a large cyst in the liver, which was also PET negative.

There are a smattering of positive PET scans with Echinococcus involving the lung and the liver, glowing from the immune reaction:

However, the target of FDG is not clear in AE lesions. In an in vitro study, it was shown that the FDG is taken up by the immune cells rather than the E. multilocularis metacestodes. PET/CT cannot explain the viability of the parasite directly, and a negative study does not mean the death of the parasites completely.

So I am not sure what to make of the imaging, but to paraphrase Rasheed Wallace, path don’t lie.

Therapy? Albendazole for some period of time depending on whether cystic or alveolar disease. My nurse told me that the current cost, before insurance, is $500 for two tabs. Hey Zeus.

Rationalization

Korean J Radiol. 2006 Jan-Mar; 7(1): 57–69. Published online 2006 Mar 31. doi: 10.3348/jr.2006.7.1.57 False Positive and False Negative FDG-PET Scans in Various Thoracic Diseases https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2667579/

[Pulmonary Hydatid Cyst Detected on FDG PET-CT] (https://journals.lww.com/nuclearmed/Abstract/2010/04000/PulmonaryHydatid\_Cyst\_Detected\_on\_FDG\_PET\_CT.25.aspx)

World J Surg Oncol. 2008; 6: 7. Published online 2008 Jan 21. doi: 10.1186/1477-7819-6-7 Pulmonary echinococcosis mimicking multiple lung metastasis of breast cancer: The role of fluoro-deoxy-glucose positron emission tomography https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2257945/

Diagn Interv Radiol. 2016 May; 22(3): 247–256. Published online 2016 Apr 12. doi: 10.5152/dir.2015.15456 Multimodality imaging in diagnosis and management of alveolar echinococcosis: an update https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4859741/

Verneuil Returns. Perhaps.

May 18, 2020

The patient is a middle-aged homeless male with a sudden onset of right shoulder pain. He could not do the chicken at all. For those who have never attended a Minnesota wedding, check out this video.

No trauma, overuse, fever, chills, and there was no rubor, calor, or tumor— just lots of dolor.

CBC and ESR were normal. He is an IVDA.

The MRI shows minimal biceps tendons synovitis, synovial enhancement of a glenohumeral joint space, and subacromial subdeltoid bursal fluid.

Maybe a septic joint/bursitis.

Now, simultaneous with the shoulder evaluation, it is noted that he also has untreated syphilis, diagnosed 5 months ago, for which he receives a shot of benzathine penicillin in the ER. Well, actually in the gluteus.

The next day I see him, and his shoulder is markedly improved. Ortho also saw the patient, who ordered an aspiration that had 42,000 WBC, but gram-stain and cultures are negative.

So. Is this syphilitic bursitis? Or, as it was called in the early 1900s, the luetic bursopathy of Verneuil?

Verneuil, in 1868, first reported four cases of syphilitic bursopathy, which he described as “hydropisie des gaines tendineuses des extenseurs des doigts dans syphilis secondaire.”

There is very little in the modern literature:

Syphilitic bursitis and Beau’s lines are long recognized features of secondary syphilis, but few case descriptions are available on modern electronic databases. Syphilitic bursitis most often affects the olecranon bursa in men, but almost any bursa may be involved. Previous trauma may play a role. Patellar syphilitic bursitis used to be recorded in patients employed as cleaners.

And it is hard to get the original text; over 100 years old, and JAMA is still behind a paywall. So what little I can glean is

Dr. Halsted at Johns Hopkins reported one case and outlined the bursae involved in the order of frequency; namely, the prepatellar, the subpatellar, the semimembranous, that between the rectus and the crureus, the anserine bursa, that of the extensor digitorum communis, the bursae of the toes and the flexors of the fingers, and that at the radial border of the first phalanx of the forefinger.

In 1889 luetic bursopathy was treated with potassium iodide and mercury; I think I will stick to benzathine penicillin.

So is it the luetic bursopathy of Verneuil? Perhaps. That is the aggravation that is lues: it is Rich Little, or something like that. But with no cultures, you can only assume and use the ever questionable response to therapy as a diagnosis.

And it is always fun to wander the old literature.

Rationalization

SYPHILITIC BURSITIS(LUETIC BURSOPATHY OF VERNEUIL) JOHN E. LANE, M.D JAMA. 1924;82(11):852-854. doi:10.1001/jama.1924.02650370020006 https://jamanetwork.com/journals/jama/article-abstract/238919

April 22, 1933 SYPHILITIC BURSOPATHY (LUETIC BURSOPATHY OF VERNEUIL) M. J. MORRISSEY, M.D.; H. S. REYNOLDS, M.D. JAMA. 1933;100(16):1229-1230. doi:10.1001/jama.1933.02740160013005 https://jamanetwork.com/journals/jama/article-abstract/242652

Am J Trop Med Hyg. 2017 Feb 8; 96(2): 261–262. doi: 10.4269/ajtmh.16-0386 PMCID: PMC5303019 PMID: 28179551 Olecranon Bursitis, Beau’s Lines, Biett’s Collarettes, and Crown of Venus https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5303019/

Drive By

May 20, 2020

Weekends are always interesting, but the patient contact/responsibility is transient. I see the patient once, render an opinion (not unlike rendering lard) and move on. There are many ways to skin the ID cat, and my opinions are well known as I tend to somewhat forcefully repeat them over and over.

One of the hospitalists suggested that I record my standard rants and publish them as some sort of virtual jukebox on the web when I retire.

Metronidazole and acute aspiration? A6.

ECHOs and S. aureus bacteremia? D12.

The world does need more Mark Crislip (TM).

The patient is a young male with sickle cell disease who comes in with thigh pain and fevers. CT shows myositis, a small abscess, and femur osteomyelitis.

One blood cultures grow a pan-sensitive Salmonella.

Interesting. While Salmonella infections are a well-known complication in sickle cell. It has been decades since my last case, and I have never seen a pyomyositis, probably because it is rare. Only 32 cases on the PubMeds

Salmonella muscle infections, and the rate of underlying conditions, were significantly higher than those in typical pyomyositis. Psoas muscle was involved more commonly in Salmonella infections than in typical pyomyositis, and the yield of positive blood cultures and, particularly, the mortality rate, were substantially higher in Salmonella muscle infections than in typical pyomyositis.

And most of the cases were not sickle cell patients. It is a disease with a high relapse rate.

To further complicated treatment, he is on high-dose prednisone and azathioprine for refractory Crohns.

I suggested, on general principals, that treating gram-negative pyomyositis without an I&D is a waste of time.

I suggested that Salmonella, an intracellular organism, will not be killed. I also suggested that the prednisone and azathioprine made sure there would be little host immune system to aid in killing it.

I remember the old, bad days of HIV when Salmonella was forever. I can’t see how this will be any different.

Surgery disagreed. He was responding to antibiotics, so continue them.

We will see. I am not so enthusiastic.

But Vell, I am just zis weekend guy, you know?

Postscript

He went to the OR. Eventually.

Rationalization

Clin Infect Dis. 1999 Sep;29(3):673-7. doi: 10.1086/598652. Muscle Infections Caused by Salmonella Species: Case Report and Review https://pubmed.ncbi.nlm.nih.gov/10530465/

J Infect Chemother . 2001 Sep;7(3):169-74. doi: 10.1007/s101560100030. Comparison of the Clinical and Laboratory Features of Muscle Infections Caused by Salmonella and Those Caused by Other Pathogens https://pubmed.ncbi.nlm.nih.gov/11810579/

POLL RESULTS

Opinions rendered on the weekend

• are less authoritative as you are not the usual ID doc 5%
• are less authoritative as you are not the usual referring doc 3%
• are unread 3%
• are ignored as no one really knows what is going - - on until the A team returns Monday 71%
• treading water 16% Other Answers 3%
• can be used to make suet blocks for next winter’s Downy woodpeckers.

  Didn’t Fit the Pattern

  May 27, 2020

Figuring out an ID diagnosis is all about risks. Where have you been, what have you done, and with whom or what. So we ask a lot of questions. As a rule in ID, age, sex, and race are less of an issue. There are exceptions, primarily anatomical. I do not consider prostatitis in a female. Being old and white and male is usually of little importance in the differential of fever of unknown origin. Unless, of course, it is.

The patient, an old white male, has a classic FUO: fevers, sweats, weight loss, and malaise. He gets the usual FUO evaluation by his primary and is sent to me when the initial screening labs are unrevealing. A little transaminitis, a little leukopenia.

When I see him, I find nothing. Exposure history: nothing. Exam: 1/6 old mitral valve murmur.

The big 4 causes of FUO are tumor, infection, collagen vascular disease, and other. It’s not tumor, as the CT of the chest/abdomen/ and pelvis are normal, and the CBC are has nothing evil.

Nothing to suggest temporal arteritis, Still’s, or polymyalgia rheumatica, and the ESR is only middling elevated.

Other? Nothing I can find.

So it must be an infection. And I bet on endocarditis. Nope. Blood cultures negative.

And during this evaluation, which takes time in the world of COVID, he slowly gets better, over about 6-7 weeks. Fevers decline, sweats remit, malaise lifts.

Good. But what is the diagnosis? I tell the patient he is likely going to get better on his own, as is often the case, but there is one last hail Mary I can send, a Karius test, that I doubt will be positive given that he is getting better. He wants no stone unturned, so it is ordered.

When it returns a week later, the patient is back to normal except for some lingering, but resolving, fatigue.

Tne Karius? EBV.

Now, this could be EBV reactivation from whatever was causing his FUO, but through the lens of the DNA result, his labs were classic for EBV, with 45% atypical lymphocytes.

I looked, but I didn’t see EBV. Why? He is an old white male. He shouldn’t get acute EBV, so I didn’t even think of it. In this case, with a lack of adenopathy and pharyngitis, the typhoidal variant.

Initially, Epstein-Barr virus (EBV) was not considered because of her age, the absence of pharyngitis and cervical adenopathy, and the higher likelihood of another diagnosis, ie, lymphoma. Eventually, her FUO was diagnosed as EBV presenting as “typhoidal mononucleosis.” Typhoidal mononucleosis is an extremely rare presentation of EBV as a cause of FUO in an adult. All of her symptoms as well as her clinical and laboratory findings resolved spontaneously.

Rare enough that there is one hit on PubMed and the Googles searching for “typhoidal mononucleosis,” and this blog now has two cases.

I suppose I now hold the world’s record for missing typhoidal EBV.

Rationalization

Fever of Unknown Origin (FUO) in an Elderly Adult Due to Epstein-Barr Virus (EBV) Presenting as “Typhoidal Mononucleosis,” Mimicking a Lymphoma https://doi.org/10.1016/j.hrtlng.2012.06.004

Typhoidal The prior case I missed. http://boards.medscape.com/forums/?128@@.2a809c7e!comment=1

Frankensteins Unicorn

Jun 1, 2020

My goal is to not find zebras but unicorns. And not just unicorns, multicolored unicorns. Of course (spoiler alert), unicorns are not real, but I enjoy the intellectual exercise of trying to put all the pieces together to make a unicorn. Case in point.

A 60 year yo male is admitted with COVID and requires intubation. He is Hispanic speaking only, undocumented, no family. So we have no history.

On admission, he has Burkholderia cepacia in the sputum, and a CT that is extensively involved with infiltrates of some sort.

Real? Burkholderia cepacia does cause the occasional community-acquired pneumonia, less than a dozen cases on PubMed

The current cases showed that community-acquired Burkholderia pneumonia is possible in healthy patients.

He is sick, so he can’t be too academented as to whether it is a pathogen. He gets treated and, over the next several weeks, gets better-ish from COVID/maybe CAP. But his MS doesn’t clear, and his CXR only somewhat improves. And we still do not have a history.

But the Burkholderia cepacia doesn’t go away. I don’t expect a microbial resolution given he is trached, but with Burkholderia cepacia, you have to think cystic fibrosis. 60 is kind of old to diagnose CF, but it does happen, albeit rarely. The oldest is a diagnosis at age 76; it depends on the mutation how severe the disease is.

And CF is seen it non-Caucasians:

Although the incidence of CF is highest in non-Hispanic Caucasians (1:3,200), the incidence in other races and ethnicities is becoming increasingly recognized. For example, CF has an incidence of 1: 9,200 in Hispanics and 1:15,000 in African-Americans.

So I got a rare plus a rare. Not looking like a unicorn. But.

There is one unexplained finding that is bugging me in the case: he has an elevated isolated alkaline phosphatase in the upper 500’s. His LFT’s/liver check out as ok, and there is no bone disease that we can find.

So to the Googles, a curious doctor’s best friend, and I found this:

Serum bone-specific alkaline phosphatase levels were elevated in CF patients (32.0 +/- 11.3 vs 21.8 +/- 7.0 U/l, p < 0.0001), but were much more closely associated with serum total alkaline phosphatase levels (r = 0.51, p = 0.001) than with age or gender.

Which he has. And

Parathyroid hormone levels were elevated (p = 0.007) and 25-hydroxyvitamin D levels were depressed (p = 0.0002) in the CF patients in comparison with controls.

Which he also had. They had been measured as an outpatient for unknown reasons about 6 months ago. So

These results indicate that adults with CF have increased bone resorption with little change in bone formation.

Hmmm. Interesting. So maybe it is CF. We will see. But if not, interesting to consider. And I think I made me a unicorn.

Rationalization

Community-acquired Burkholderia Cepacia Pneumonia: A Report of Two Immunocompetent Patients https://doi.org/10.5578/tt.1159

Late Diagnosis Defines a Unique Population of Long-term Survivors of Cystic Fibrosis https://www.atsjournals.org/doi/full/10.1164/rccm.200403-404OC

[Woman, 76, oldest patient in Ireland diagnosed with cystic fibrosis] (https://www.irishexaminer.com/ireland/woman-76-oldest-patient-in-ireland-diagnosed-with-cystic-fibrosis-285866.html)

Cystic Fibrosis in a Hispanic Adolescent https://www.ncbi.nlm.nih.gov/pubmed/23401342

Abnormal Bone Turnover in Cystic Fibrosis Adults https://pubmed.ncbi.nlm.nih.gov/11905525/

Spontaneous?

Jun 3, 2020

The patient presents to ID post-op with a destroyed pip joint of the first finger.

It started with a repetitive use injury for which she sought a worthless intervention that only offers complications, er, I mean acupuncture, to treat the pain and swelling. See <https: data-preserve-html-node="true"//sciencebasedmedicine.org/tag/acupuncture/> and my numerous articles on the topic.

Then, at some point, the joint became increasingly red, swollen, and painful, for which, after several months, she finally saw a hand surgeon. The joint was trashed, changes on plain films consistent with a septic joint with resultant osteomyelitis.

The joint was debrided and showed chronic osteomyelitis, scar, but culture and gram-stain were negative. She was sent to me, and the only potential penetrating trauma, only discovered with direct questioning, was the acupuncture.

I sent the surgical specimen for molecular testing, and it was also negative for bacteria, fungi, and mycobacteria.

A couple of issues. First, you have to ask specific questions for some kinds of trauma. I have found over the years that people do not link the trauma (acupuncture, chiropractic) with the injury (septic joint, posterior column stroke) and will not volunteer the information about the ‘alternative’ intervention.

Second, this is not the first time I have seen a septic joint from an acupuncture needle gone awry, and there are many hits on Pubmed. If you are a connoisseur of quackery, you are aware of the tendency of acupuncture needles to go too deep or in the wrong direction and the lack of fastidious infection control by practitioners. It probably exists, but in the hundreds of acupuncture pictures and videos online, I can’t find one where gloves are worn.

But those issues are old hat. The question, given all the negative studies, is this a spontaneous cure because the infection was due to the inoculation of relatively low virulence organisms, and there is no need for antibiotics?

I do not know. Over the years, I have seen a few cases of osteomyelitis where, from drug use or a lack of insurance, osteomyelitis festered for months or years, and when finally debrided, no organisms were isolated.

I can’t find much on the natural history of osteomyelitis in the pre-antibiotic era that isn’t due to S. aureus. The best I can find from 1965 is

Spontaneous remissions are common and may be prolonged.

But remission isn’t cure. Chronic osteomyelitis does wax and wane, so maybe this was a wane?

As to spontaneous cures, from 1936

Because of the peculiar nature of the bone (petrous apex ), the pathologic process in the vast majority of cases has a tendency to spontaneous cure

And a report from 1933 suggests

It is fair to say, therefore, that she had a spontaneous cure of her osteomyelitis.

Although a book from 1919 suggests

The impossibility of spontaneous cure

for chronic osteomyelitis.

The only similar disease is septic arthritis of the pubic symphysis where

many cases of low-grade pubic osteomyelitis are misdiagnosed as osteitis pubis, with slow, spontaneous cure in some cases because of immune containment. They note that vertebral osteomyelitis occasionally resolved without specific therapy in the pre-antibiotic era.

Until the antibiotic era, osteomyelitis was a surgical disease, and if there were spontaneous cures/remission, I can’t find much else on the Googles or Pubmed. And I would doubt there would be much in a world dominated by S. aureus and sub-optimal ability to culture organisms.

I still suspect this is a spontaneous eradication of low-virulence organisms in the joint/bone.

The index finger of the dominant hand? I’m still going to treat for osteomyelitis.

Rationalization

A history of osteomyelitis from the Journal of Bone and Joint Surgery 1948 TO 2006 https://online.boneandjoint.org.uk/doi/full/10.1302/0301-620X.89B5.19170

The History of Antibiotic Treatment of Osteomyelitis https://academic.oup.com/ofid/article/6/5/ofz181/5432301

PRIMARY SUBACUTE PYOGENIC OSTEOMYELITIS https://pdfs.semanticscholar.org/8f68/0cc33d961242a2f98b7295dbe07fddf6e0bc.pdf

OSTEOMYELITIS OF THE INFERIOR SURFACE OF THE PETROUS PYRAMID https://jamanetwork.com/journals/jama/article-abstract/1156691

A BENIGN FORM OF OSTEOMYELITIS OF THE SPINE https://jamanetwork.com/journals/jama/article-abstract/244244

Septic Arthritis of the Pubic Symphysis https://journals.lww.com/md-journal/Fulltext/2003/09000/Retinocochleocerebral\_Vasculopathy.6.aspx

POLL RESULTS

I see the occasional

• spontaneous cure 4%
• spontaneous conversion 4%
• spontaneous change of mind 33%
• spontaneous generation 4%
• spontaneous combustion 50% Other Answers 4%
• spontaneous nuclear decay

  Timing

  Jun 8, 2020

I am called to see a patient with S. aureus bacteremia (SAB). It has been a while. Probably my imagination, but it seems SAB has almost vanished the last three months with COVID. I can’t see why: diabetes, dialysis, and injection drug use have no reason to decline, so why would SAB?

She has the usual reasons: IDDM and dialysis through a catheter while her fistula is maturing.

The timing of the symptoms is what is curious. She felt fine the day of and during dialysis, but five minutes after the end of the three-hour run, she developed intractable rigors then fevers.

Rigors should start 1-3 hours after a bolus of endotoxin.

Endotoxin from Escherichia coli 0113:H10:k, was injected i.v. at a dose of 4 mg/kg BW into these healthy volunteers… The patients developed chills and rigors, myalgia, and fever between 1-3 h.

But that is for endotoxin, lipopolysaccharide, a constituent of gram-negative rods. S. aureus makes no endotoxin, but what is the endotoxin equivalent for fevers and rigors? S. aureus make no end of toxins, but I was always taught it was peptidoglycan that was the endotoxin equivalent for S. aureus, but I can find no studies where some sucker, er I mean, volunteer received a bolus of peptidoglycan to see what happens.

Ewes, rabbits, and guinea pigs? Yes. They get a fever after an injection of peptidoglycan. But unless my Googles is wanting, there are no human subjects. So I do not really know how long after a human gets S. aureus in the blood, there is a rigor and fever. I assume it is the same as endotoxin.

I only mention it is as I like timing.

The cause of the rigor/fever had to be with the access of the dialysis catheter. After the one bolus of S. aureus, she had no further fevers, no further rigors, felt just fine, and repeat blood cultures were negative.

The timing is perfect and clinical source suggests a transient surge of S. aureus. I can’t prove it, of course, and there have been no other bacteremias from that unit, so it likely was a one-time bacteremia.

It made no difference in the approach to the patient, but I like to understand what happened.

Rationalization

Procalcitonin increase after endotoxin injection in normal subjects. https://europepmc.org/article/med/7989463

Staphylococcus aureus toxins https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3942668/

Somnogenic, Pyrogenic, and Hematologic Effects of Bacterial Peptidoglycan https://pubmed.ncbi.nlm.nih.gov/2105668/

Endotoxin-like Properties of the Peptidoglycan https://pubmed.ncbi.nlm.nih.gov/126556/

The biology of bacterial peptidoglycans and their impact on host immunity and physiology https://onlinelibrary.wiley.com/doi/full/10.1111/cmi.12304

But Did It Keep On Ticking?

Jun 22, 2020

Back from a week on the Southern Oregon Coast. But the pus calls me home.

Six months ago, I wrote about a S. canis cellulitis/bacteremia from the patients dog licking her leg wounds.

Well, it is back. She was admitted with cellulitis, and all her blood cultures were positive for S. canis in less than 24 hours. Last time it was only 1 of 4 bottles on day 2.

Before, I had decided not to pursue a pacemaker infection and gave a course of therapy for bacteremic cellulitis. She did well for the next 4.5 months, with no signs or symptoms of infection until the day of admission.

The dog still sneaks up on her and licks her wounds, which, because of neuropathy, she doesn’t always notice right away. And once a dog has a taste for human…

Four cases of postmortem injuries caused by indoor pets (three by dogs and one by cats) are presented. A pattern which is associated with this phenomenon is described. The important common factors appear to be the presence of free-moving pets inside the house, social isolation of the deceased, and the victim having a predisposing condition causing sudden death.

Because of the high-grade bacteremia and rapid time to positivity, this time, we went looking for an endovascular infection and found a small vegetation on the pacer wire.

A relapse or reinfection? I am betting on the latter. There is no way a Streptococcus would fester on an endovascular wire for 4.5 months with no symptoms.

I always say you can’t cure a pacer wire infection, and the guidelines say take the system out. But most infections are due to Staphylococci; only 4 % are due to Streptococci, and mine is the first due to S. canis. Is that recommendation applicable to a sensitive Streptococcus? I don’t know. I suspect not. Removing a pacer is potentially a big deal.

So we, and by we I mean I, discussed with the patient the uncertainties of treatment and are going to treat it like prosthetic valve endocarditis. We will see. And she is going to work harder at keep the dog away from the wounds.

PS It was a cure.

Rationalization

It Takes a Licking. http://boards.medscape.com/forums/?128@@.2a83e095!comment=1 All the relevant references here

Horrifying Stories Of Animals Eating Their Owners https://www.buzzfeednews.com/article/natashaumer/cats-eat-your-face-after-you-die

[APA , The American Journal of Forensic Medicine and Pathology: June 1994 - p 105-109] (https://journals.lww.com/amjforensicmedicine/Abstract/1994/06000/Postmortem*Injuries*by*Indoor*Pets\*.4.aspx)

Update on Cardiovascular Implantable Electronic Device Infections and Their Management https://www.ahajournals.org/doi/full/10.1161/circulationaha.109.192665

[‘Serial killer’ animals gain taste for humans] (http://www.nbcnews.com/id/49734403/ns/technology*and*science-science/t/some-animals-may-develop-taste-human-blood/) -

Forensic scientists caught a deer munching on a human carcass for the first time ever https://www.popsci.com/deer-eating-human-remains/

POLL RESULTS

I do not want to be eaten by my pet

• dog 16%
• cat 32%
• tiger 4%
• crocodile 16%
• deer 16% Other Answers 16%
• baby girl
• snake
• peeve.
• cockroach (madegasgar)

  Bar Rot

  Jun 24, 2020

The patient presents with a four-month infection of the index finger of his left, dominant hand.

It started with a separation of the nail, then became covered with a goopy, yellow pus that did not respond to various antibiotics. Eventually, a surgeon removed the nail (cringe), and he was sent to me.

There was nothing of note in the past medical history except he is a bartender, and his hands are often wet. No trauma or other odd exposures

To me, it looked like a healing nail bed after nail removal (cringe), and the pictures on the phone looked like a paronychia/infected nail. All the cultures only grew a coagulase-negative Staphylococcus.

My coworkers (a word I always see as cow orkers, whatever that might be), he said, said it was bar rot.

Bar rot?

Yeah, he said. The nail gets eaten away by the citrus juice from lemons and limes.

Well, I said, it looks like a cured infection. I suspect it is the same as what dishwashers get, a Candida infection. The nail removal (cringe) should be a cure. Keep your hands dry at work and continue the steroid/antifungal drops.

After he left, I looked up bar rot. It is a thing, although not on the PubMeds:

Risk factors include repeatedly washing hands and trauma to the cuticle such as may occur from repeated nail biting. In the context of bartending, it is known as bar rot.

So how could the bartending be adding to the problem besides wet hands? I doubt that citrus acid is dissolving the nail, but I remembered that Candida endophthalmitis occurs from lemon juice in heroin users. So I went looking.

Fruit juices are popular soft drinks with an important role in human nutrition. Fruit juices are often infested by yeast species that can survive different storage conditions… Yeasts were isolated in all 84 samples and ranged between 0.005 x 103 and 23 x 103 colony forming units per mL (CFU mL-1). The most common yeasts identified using the API 20C AUX yeast kit included Candida guillermondii, C. krusei, C. famata, C. spherica, C. colliculosa, C. albicans, Trichosporon mucoides, Kloeckera spp. and yeast-like fungus Cryptococcus neoformans. C. guillermondii prevailed in 55.95 % of all samples.

and

Candida sp., Curvularia, Colletotrichum, and Acetobacter were observed only in citrus juice samples. Alternaria, Aspergillus terreus, A. niger, Cladosporium, and Fusarium were also observed in tested juice samples. Some of the microorganisms detected in these juice samples can cause disease in human beings, so there is need for some guidelines that can improve the quality of fruit juices.

So maybe it was the lemons and limes.

Also, a Google search found that in the alt-med world that lemons are useful as part of an anti-Candida detox because of their anti-fungal properties.

Uh-huh.

Rationalization

The Truth About Bartending http://thetruthaboutbartending.com/2012/01/27/bar-rot/

Prevalence of Candida Species in Fresh Fruit Juices https://pubmed.ncbi.nlm.nih.gov/20061245/

Role of the Lemon in Disseminated Candidiasis of Heroin Abusers https://pubmed.ncbi.nlm.nih.gov/6374399/

Microbes Associated With Freshly Prepared Juices of Citrus and Carrots https://pubmed.ncbi.nlm.nih.gov/26904628/

POLL RESULTS

Fingernail removal

• makes me cringe 34%
• give me the willies 11%
• bothers me not as long as it is not mine 40%
• makes me ill 0%
• is a source of money and pleasure 11%

  Occams Razor, not Hickams Dictum

  Which One Is False?

  Jul 1, 2020

The patient is from a Tb endemic area. She has been in the US for a decade and has not returned to the land of her birth. At the time of immigration, she was tested for TB, was skin test positive, and took nine months of INH. Her CXR is clean.

She works in a closed environment with a diverse group of people, many of whom are also from a TB endemic part of the world. No family member or coworker has had symptoms or a diagnosis of TB.

Four years ago, she developed an adalimumab (Humera) requiring rheumatologic illness, and the therapy was life-changing.

In 2016, 18, and 19, she was quantiferon negative, and in 17 and 20, she was positive, although it was not the usual >10,000 positive for the TB antigen.

So now what?

I would think that since her TB test was positive in 2010, assuming a legit PPD reading, the quantiferon would be positive for life. So I am betting the ‘real’ quantiferons were the positives.

False negatives are common:

Of the 77 patients, 44 (57.1%) were diagnosed with active pulmonary tuberculosis, and the percentage of false negative results of the QFT-GIT was 36.4% (vs. 31.8% with TST). In the TB group with >65 years old (n=12), the proportions of the indeterminate (33.3% vs. 3.1%) and the false negative results (58.3% vs. 25.0%) of the QFT-GIT were significantly higher than in the younger TB group (n=32).

and due to

The false-negative group was more likely to have immunosuppressant diseases.

On the other hand, reading PPDs is a lost art, and perhaps she received a course of INH she didn’t need as

Serial QFT testing of HCWs in North America may result in tremendous over-diagnosis and over-treatment of LTBI, with nearly thirty false-positives for every true infection diagnosed.

And as I say, it wasn’t that positive.

In TB endemic areas, conversion rates of patients on biologics run around 10%, but this patient has no exposures. And

patients who received long-term biologic therapy experienced dynamic changes in the IFN-³ level in response to TB.

But I can’t find where biologics are a reason for a false-negative.

And treatment of latent TB may lead to a decreased IFN response as well.

After chemoprophylactic therapy, the IFN-³ level decreased in 13 (68.42%) patients, whereas 11 (57.89%) patients developed reversion in the subsequent QFT-GIT test.

Although that is by no means a universal finding.

Most reactivations of TB on TNF inhibitors do so in the first few months after starting, and she has done well for 4 years. So either the INH did its job, or she never had latent TB.

I elected to do nothing.

TB and syphilis. Often never know for sure if it is there or not.

Rationalization

Factors Associated with Indeterminate and False Negative Results of QuantiFERON-TB Gold In-Tube Test in Active Tuberculosis https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3475462/

Risk factors for false-negative results of QuantiFERON-TB Gold In-Tube assay in non-HIV-infected patients with culture-confirmed tuberculosis https://www.sciencedirect.com/science/article/abs/pii/S0732889311000940

Serial testing for latent tuberculosis using QuantiFERON-TB Gold In-Tube: A Markov model https://www.nature.com/articles/srep30781

Serial QuantiFERON-TB Gold In-Tube testing for psoriatic patients receiving antitumor necrosis factor-alpha therapy https://www.sciencedirect.com/science/article/pii/S102781171400086X

POLL RESULTS

I am uncertain if it is there:

• TB 24%
• syphilis 16%
• Oakland 8%
• a bear? where? 44%
• France circa 1918 8%

  Nausea and Vomiting and Blood Cultures

  Jul 6, 2020

Two patients with the same presentation: 24 hours of intractable nausea and vomiting. Both present to the ER and are febrile. Both have blood cultures drawn. Both are positive in 1 bottle out of four.

One has S. salivarious.

One has C. glabrata.

Neither, after work-up, had an infection to account for the positive blood cultures. I say that because I think the bacteremia and fungemia are a complication of the vomiting, not the cause of the vomiting. Both cases, by history, had a primary vomiting illness.

Maybe.

The only association of S. salivarius bacteremia with nausea and vomiting I can find is in cirrhotics, who get bacteremia and SBP, probably by way of varices. And one case of S. salivarius bacteremia after dilating an esophageal stricture:

S. salivarius is a member of the normal oral floral and almost certainly was carried from the mouth to the esophagus on the bougie. Successful bougienage often requires fracturing the stricture, thus breaking the mucosal barrier and allowing transient access to the systemic circulation. In fact, bacteremia occurs in approximately 50% of dilations. Clearly, the onset of meningismus within 36 hours of bougienage and the unusual oral flora recovered implicate the bougienage as causing a S. salivarius bacteremia with seeding of the meninges.

So why not from severe vomiting? And we looked. There were no holes in the esophagus looking inside and out.

The Candida was a bit less straightforward as there was duodenal pathology: severe scar/stricture from a duodenal ulcer. But no perforation was found on endoscopy or CT.

Gastric ulcers are often colonized with Candida:

Forty seven patients (47%) with peptic ulcer were colonized by Candida as compared to 3 patients (15%) with non ulcer dyspepsia (p < 0.05). Confluent growth of Candida on culture of gastric aspirate or biopsy from ulcer edge was a more sensitive method for diagnosis of peptic ulcer-associated candidiasis than histological examination.

And, when gastric ulcers perforate, dump yeast into the peritoneum with fungemia.

There are fewer cases of Candida from duodenal disease, but they exist, but no associated fungemias I can find.

So both with positive blood cultures from the trauma of vomiting? That’s my story, and I am sticking to it.

Both patients did fine with their blood stream infections.

Rationalization

Streptococcus salivarius Bacteremia and Spontaneous Bacterial Peritonitis in Liver Transplantation Candidates https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/lt.21277

Streptococcus Salivarius Bacteremia and Meningitis Following Upper Gastrointestinal Endoscopy and Cauterization for Gastric Bleeding https://pubmed.ncbi.nlm.nih.gov/1576292/

Fungal Colonization of Untreated Peptic Ulcer https://pubmed.ncbi.nlm.nih.gov/7829139/

[Duodenal candidiasis: a rare cause of giant duodenal perforation in immunocompetent patient] (https://www.researchgate.net/publication/311903663*Candida*Associated*Giant*Non-Healing*Gastric*Ulcer*in*an*Immunocompetent*Host)

Nonhealing Duodenal Ulceration Due to Candida https://pubmed.ncbi.nlm.nih.gov/6841949/

Candidiasis of the duodenum and jejunum https://www.gastrojournal.org/article/0016-5085(81)90149-9/pdf

Experience Important?

Jul 8, 2020

I have maintained that the three most dangerous words in medicine are “In my experience.” I am even credited on some quotation websites.

But that idea only applies to deciding on treatment; experience is important in diagnosis. After all

One of the things that will be really great – the word experience is still good, I always say talent is more important than experience, I’ve always said that – but the word experience is a very important word, a very important meaning.

Um, right? But after 30 years in ID, I often come to a diagnosis within a minute, and that is because I have likely seen the diagnosis, and more importantly, missed the diagnosis in the past.

The patient has been ill for 2 months. It started with a severe sore throat and fevers, diagnosed as strep throat on a video visit, that did not respond to antibiotics. It then continued: fevers, myalgias, sore throat, arthralgias, and direct questioning, a pink rash that comes and goes. Labs had a mild transaminitis and a leukocytosis. The CT showed mild pericarditis and pleuritis.

By the time they called me, I had the benefit of what it wasn’t thanks to an extensive negative work-up: not infection. Not tumor. Not other. That left rheumatologic, and with that presentation, it meant Still’s.

Except for the lack of lymphadenopathy, the patient had every sign and symptom. I sent a ferritin, and it came back 45,000, so to my non-rheumatological mind, that clinched the diagnosis:

Besides in adult Still’s disease, serum ferritin levels of >10,000 痢/l have only been described in severe liver damage, after multiple blood transfusions or in the haemophagocytic syndrome. So the ferritin level may be an important diagnostic tool in the diagnosis of Still’s disease and should be therefore included in the classification criteria.

It was a quick and easy diagnosis for me, but as regular readers know, my experience with Still’s has not always been smooth sailing. I completely missed the first two cases in my career and was slow to make the diagnosis in a few subsequent cases.

If you really want to get a diagnosis, send the patient to a doctor who has not only seen a lot but missed a lot. It is not just experience, but learning from that experience, I suspect that makes the difference. So take heart with all those screw-ups. It is the path to becoming a better physician. I hope.

Not that everyone buys the idea of the diagnostic accuracy that comes with that very important word. I recently had a referral for treatment of a disease that, after my review, I did not think the patient had. So I didn’t feel treatment was indicated. Neither an unusual reason nor result of a consultation, although usually, it is for Lyme or EBV. This time the referring doctor called me to let me know I was an idiot (implied) and that I would be getting no further referrals from them.

Hm. So much for experience. Maybe I should rely on talent?

Rationalization

Extremely high serum ferritin levels as diagnostic tool in adult-onset Still’s disease. http://njmonline.nl/getpdf.php?id=540

POLL RESULTS

I rely on

• experience 19%
• talent 6%
• google 39%
• misdirection 3%
• the wisdom of P. T. Barnum. 19% Other Answers 13%
• my gut
• the kindness of strangers.
• Geometric logic!

  Moldy Complication

  Jul 14, 2020

The patient has COVID. No really. COVID. It is a real virus. COVID is not a lie or part of a conspiracy. She is really, truly, one of many COVID patients I have seen for the last several months. Honest. Trust me. COVID is real and can be awful.

Like many patients who end up intubated, once intubated, she has been slow to recover, staying in that awful place of too sick to get better, too well to progress. She had received remdesiver, plasma, and dexamethasone but had completed all the courses.

And then, her oxygen requirements and WBC started to increase, about two weeks into the hospitalization and three weeks into the course of COVID.

Why? Pulmonary embolism? Kind of late and on prophylaxis. CAP? No real change in the CXR, and the sputum production was minimal. And CAP is rare in my hospitals. Aspergillus? Could be; it seems to be a common late infection with COVID.

There are a hodgepodge of case reports and small series that suggest around

33% of our COVID-19 patients with putative invasive pulmonary aspergillosis.

But, as with everything COVID, there is uncertainty.

CT of the chest showed a new 4x3 cavity with a chunk of fungus/dead lung at the base, typical of Aspergillus. At this point, she was too unstable for bronchoscopy, so I sent a serum galactomannan, not really expecting a positive result since WBCs bind galactomannan, rendering the test less sensitive in the non-neutropenic.

But to my surprise, the test was quite positive. I think this is my first positive in the blood of an invasive Aspergillus patient with neutrophilia, so it must be really elevated.

The other issue I wondered about is why. Sure, Aspergillus is ubiquitous, but is there an exposure? I have mentioned the cases of post-Influenza Aspergillus I credited to smoking marijuana—no marijuana smoking in this case. Like most of the severe COVID in my hospitals, she is an Hispanic agricultural worker. Is that the source, an occupational exposure? The literature is silent. But I wonder.

On voriconazole, she improved.

Rationalization

High prevalence of putative invasive pulmonary aspergillosis in critically ill COVID-19 patients https://www.medrxiv.org/content/10.1101/2020.04.21.20064915v1

Correlation between galactomannan antigen levels in serum and neutrophil counts in haematological patients with invasive aspergillosis https://pubmed.ncbi.nlm.nih.gov/19154482/

Odd Phenomena

Jul 15, 2020

20 years ago, the patient had a severe strep throat, complicated, he said, by erythema nodosum. I do not have records to confirm the diagnosis, but the description of red, painful bumps on the legs that went away with a course of prednisone fits. And it happens.

Beta-hemolytic streptococcal infections are the most common identifiable cause of erythema nodosum. Streptococcal infections account for up to 44 percent of cases in adults and 48 percent of cases in children. Erythema nodosum eruptions may appear two to three weeks after an episode of streptococcal pharyngitis.

Strep throat is a disease I have not seen since I was a resident, so I’ll take their word for it. In my world, the most common reason for e. nodosum has been Cocciodiomycosis, which says something about my practice.

The patient is admitted for progressive back pain and an MRI and labs that are consistent with a discitis/osteomyelitis. As is so often the case, microbiologic workup does not yield a pathogen. But he has e. nodosum again. I would doubt S. pyogenes as the organism as it is not high on the causes of discitis.

Going through the list of etiologies, it appears that the patient has no other reason for the skin lesions.

I found the recurrence with the only two serious infections in his life to be curious, but there is not a lot on recurrent erythema nodosum. Some due to drugs, occasionally as a manifestation heralding lymphoma relapse, the odd vasculitis, pregnancy, sarcoidosis, and one cause of “recurrent seasonal e. nodosum of obscure etiology.”

As to the why?

Erythema nodosum is a nonspecific cutaneous reaction pattern to a variety of antigens, with many immune-mediated mechanisms implicated.

Which is how I understand most dermatologic diseases: a bunch of stuff causes a bunch of conditions.

But I could not find cases of relapse as a manifestation of a bacterial infection and likely infection due to different organisms.

Another first, courtesy of this blog.

Rationalization

Erythema Nodosum: A Sign of Systemic Disease https://www.aafp.org/afp/2007/0301/p695.html

Recurrent Widespread Erythema Nodosum https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1897228/?page=2

POLL RESULTS

When it comes to dermatology

• I hate rash decisions 35%
• it’s all maculopapular to me 19%
• if I don’t recognize it, it’s not important 6%
• it is always syphilis 19%
• I never touch a rash 10% Other Answers 10%
• a picture is worth a thousand words
• Make clinical assessment. Seek dermatologist’s opinion when required.
• every patient is just a meatbag.

  Faulty Thinking

  Jul 20, 2020

You’ve fallen for one of the two classic blunders! The first being never get involved in a land war in Asia but only slightly lesser-known: never go in against Occam when the diagnosis is on the line!

Vizzini. The Princess Bride

My wife wants me to retire, primarily because of COVID. I am in my 60’s with comorbidities, and she worried that COVID will be the death of me. Perhaps. I have always said doctors will die of their specialty, which is why I could never go into Ob/Gyn. There is just no way I could bail at the start of a pandemic. That would be wrong. I remember the contempt I had for doctors who refused to take care of HIV back in the day. I’m not going to that guy. So here is to PPE.

That’s not the faulty thinking referred to in the title. It is the case of an elderly male with COPD who comes in with progressive thoracic spine pain. CT/MRI shows a posterior mediastinal mass. Note mass. Not abscess. And two thoracic vertebral bodies have erosion/edema, but the disc is spared.

That, I declared, is tumor. Tumor goes to bone, infection to disc, and then to bone. If the disc is spared, it ain’t infection.

Plus, he had no reason or symptoms for an infection, and the posterior mediastinum is an odd place to get a primary infection. Has to be tumor.

Of course, 1/4 blood cultures then grow MSSA.

Crap. He was less than pristine skin from his rough life, and I say he has two things. I invoke Hickam, not Occam, as much as it pains me because look. The disc is spared. Spared. So he has a mediastinal tumor and maybe SAB, maybe a contaminant. Two processes.

Of course, I say, as my wife will let you know, my opinions are not perfect. So let’s give some cefazolin (hives to penicillin) and biopsy the mass. Of course, you know where this is going.

MSSA.

If you go looking for primary/spontaneous bacterial infections of the posterior mediastinum, there is nothing on the PubMeds. So it is very odd.

My mistake? The rule of disc sparing applies to disease that occurs from hematogenous spread, not direct extension from an infection next to the vertebral bodies, where the disc can be spared, as noted here. Although one review suggests that posterior mediastinal infections are from

direct extension of infections from the spine or lung affect the posterior compartment.

He had no lung disease, so if it went from spine to mediastinum, it should have involved the disc. So I’m calling it a primary mediastinal MSSA infection with spread to spine.

He progressed to an epidural abscess that required I&D, but no satisfactory reason for the infection was ever found.

Remember: ignore Occam at your peril.

Rationalization

[Non-neoplastic Disorders of the Mediastinum: Acute Mediastinitis] (https://www.pulmonologyadvisor.com/home/decision-support-in-medicine/pulmonary-medicine/non-neoplastic-disorders-of-the-mediastinum-acute-mediastinitis/)

POLL RESULTS

Faulty thinking is

• going with Occam 0%
• going with Hickam 3%
• thinking you won’t get COVID 25%
• not listening to your spouse. 33%
• believing what you think 36% Other Answers 3%
• the default choice of lazy people. That’s the main problem with democracy.

  Live and Learn

  Jul 22, 2020

Kind of the motto for medicine. Despite all I know, thanks to Google and Pubmed, I learn something new almost every day. Maybe the real motto should be Google everything. It is amazing what you can discover.

The patient, on azathioprine and hydroxychloroquine for a rheumatologic process, comes in with 5 days of feeling poorly: fevers, malaise, a non-productive cough, and a 6th nerve palsy.

CXR/CT shows a large, racquetball-sized, round infiltrate in the lung. After 48 hours of antibiotics, he is no better, so they call me. Work up to date is unrevealing, including a negative Legionella antigen. MRI and LP were negative for any pathology to account for the 6th nerve palsy.

He looks toxic/ill but does not have a lot in the way of pulmonary symptoms.

Exposure history is only significant for being a gardener. In the days before the onset, he had been replanting flowers and roses using an organic compost mix from Home Depot. Which one is uncertain, and the spouse said it had coconut husks in it.

Because of the relative lack of symptoms from the large pneumonia, I bet on Cryptococcus > non-pneumophilia Legionella > Norcardia, all from the gardening. I couldn’t factor in the 6th nerve palsy with the negative CNS studies.

After 5 days, he was much better, the palsy improving, and the PCR from the bronchoscopy was positive for Legionella.

Huh. So I Googled it. With Legionella.

The most common manifestation is encephalopathy suggesting a generalized brain dysfunction, but focal neurological manifestations such as brainstem dysfunction, cranial nerve dysfunction, and peripheral neuropathy have also been reported as rare occurrence. Reports of isolated cranial nerve involvement were of 3rd nerve, 6th nerve, and 7th nerve dysfunction.

With one review finding cranial neuropathy in 1.5% of patients and, like my patient, noting

Cranial CT scans, cerebrospinal fluid findings, and nerve and muscle biopsies were usually unremarkable.

I doubt I have seen more than a couple of dozen cases of Legionella in 35 years, so not enough to see a case with a cranial neuropathy; the Great Pacific NW being relatively Legionella free. I suspect the source was the gardening and the compost, which I had associated only with L. longbeachae, but compost is teeming with Legionella:

MPC (multipurpose compost) consists of a mixture of coconut husk, wood fines, green waste and sometimes peat, with a variety of growth-enhancing additives depending on the manufacturer. A number of studies have investigated the diversity of Legionella species in compost and found a variety of species in high numbers, ranging from 103 to 105 c.f.u. g−1. In an international collaborative paper from 2002, involving the USA, New Zealand, Switzerland and Italy, the most commonly isolated non-pneumophila Legionella species were L. longbeachae (3.2 %), Legionella bozemanae (2.4 %), Legionella micdadei, Legionella dumoffii and Legionella feeleii (2.2 % combined). In contrast, a recent European study showed a different mix of organisms isolated from compost: L. bozemanii (26.1 %), L. pneumophila 2–15 (serogroups 3, 6 and 10) (19.6 %), L. sainthelensi (13.0 %), L. micdadei (8.7 %), L. pneumophila 1 (6.5 %) and L. longbeachae from only two samples (4.3 %). These studies demonstrate the diversity of Legionella species found in composts and potting soils. Most recently, Velonakis et al. recovered a total of 21 Legionella isolates from six out of 22 samples of potting soil. It is interesting that MPC contains a large number of potentially pathogenic L. pneumophila and Legionella species but L. longbeachae infection is the most commonly associated with compost exposure.

This is my second in the last few months that had a round Legionella pneumonia in a gardener exposed to compost.

Live and learn thanks to the Googles.

Rationalization

Case Rep Med. 2011; 2011: 916859. PMID: 21461048 Legionnaires’ Disease with Facial Nerve Palsy https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3063409/

[Neurologic and psychiatric symptoms of legionella infection. Case report and overview of the clinical spectrum] https://pubmed.ncbi.nlm.nih.gov/9273465/

Legionella longbeachae serogroup 1 infections linked to potting compost https://doi.org/10.1099/jmm.0.035857-0

Autumn

Aug 3, 2020

Summertime is hiking and golf season in the Great Pacific Northwest, so much of last week was spent in those activities at the Oregon Coast. I am fortunate that two of my favorite pastimes are safe in the time of COVID 45. I disconnect from the world when I am not working, and I am always amazed at the US approach to COVID when I return to life.

We are so doomed.

But this blog could be considered the ID equivalent of the band on the Titanic, playing while the ship went under. And a one and a two.

The patient has ESLD and is admitted with abdominal pain, fevers, and rigors.

The exam has ascites, rebound, and guarding, and parameters from a paracentesis are consistent with SBP.

The ascites cultures are negative, but the blood grows a small gram-negative rod: Pasteurella multoceda. She had both a dog and a cat but no remembered trauma from either.

It happens. From 1976

Two patients with spontaneous Pasteurella multocida peritonitis in association with cirrhosis and ascites are described. Both patients had close contact with domestic animals, but neither had been bitten. Both patients died, but only one as a result of his infection. We are aware of only one previous report of cirrhosis with spontaneous peritonitis caused by this organism.

I always love ‘only’ when attached to mortality rates, which in this case was 50%. Anti-vaxers love to minimize the deaths of children with an ‘only’ before death rates of vaccine-preventable illness. And there is many an ‘only’ to found in reports of death rates from COVID. I think there is no ‘only’ for death; any death is one too many. But unlike many in the US, I lean to the John Donne philosophy of life.

Since 1976 there have been a dozen or so cases of P. multocida SBP in chronic ascites. The other risk of P. multocida SBP is CAPD. There are three times the number of reports of CAPD P. multocida peritonitis than cirrhosis on PubMed. I had one early in my career, where the patients cat slept in her bag warmer.

What made the case even more curious was she had a leak from the peritoneum into the pleural space (hepatic hydrothorax) and had empyema as well.

That also happens and not uncommonly.

Seventeen patients had 26 episodes of SBEM (Spontaneous bacterial empyema) during the study period, 56% (14 of 26) of these SBEM episodes were associated with spontaneous bacterial peritonitis (SBP) and 31% (8 of 26) were associated with bacteremia. The incidence of SBEM was 2% (17 of 862) in cirrhotic patients and 13% (17 of 132) in cirrhotics with hydrothorax.

What to do? A chest tube would be suboptimal, as she would drain her ascites out of her chest tube, not a good hemodynamic intervention.

We did two thoracenteses several days apart, and on the second one, the WBC had fallen from 22,000 to several hundred, and the other empyema parameters had reverted to near normal.

So I did what all consultants do when confronted with a problem with no well-defined solution: 2 weeks ceftriaxone.

The patient did fine.

By the way, the last case? L. longbeachae was the final ID. So the compost it was.

Rationalization

Legends and myths regarding RMS Titanic https://en.wikipedia.org/wiki/Legends\*and\*myths\*regarding\*RMS\*Titanic#Titanic’s\*band

Pasteurella Multocida Peritonitis in Hepatic Cirrhosis with Ascites https://www.sciencedirect.com/science/article/abs/pii/S0016508576801564

Combined spontaneous bacterial empyema and peritonitis in cirrhotic patients with ascites and hepatic hydrothorax. https://pubmed.ncbi.nlm.nih.gov/28579346/

Risk factors for spontaneous bacterial empyema in cirrhotic patients with hydrothorax https://pubmed.ncbi.nlm.nih.gov/14703274/

No Man is An Island John Donne

No man is an island entire of itself; every man is a piece of the continent, a part of the main; if a clod be washed away by the sea, Europe is the less, as well as if a promontory were, as well as any manner of thy friends or of thine own were; any man’s death diminishes me, because I am involved in mankind. And therefore never send to know for whom the bell tolls; it tolls for thee.

POLL RESULTS

Beware the words

• only 45%
• love 9%
• low calorie 14%
• its in the mail 0%
• my cough is not important 23% Other Answers 9%
• Rare
• “Believe me.”

  Gas

  Aug 5, 2020

The patient had surgery three months before admission for a perforated colon secondary to radiation necrosis of the bowel for cancer. She did fine during the hospitalization, but after discharge, she had pain on the right side that was felt due to radiation-induced sacral nerve injury.

She had difficulty walking due to pain in the right hip and failure to thrive, but no noted fevers as an outpatient until the day of admission. Blood cultures were done and grew a S. salivarius.

A mouth bug. But her teeth are fine, and zero stigmata of endocarditis.

So although the abdomen exam was benign outside of the known sacral nerve issues, I ordered a CT of the abdomen, figuring the most likely source of a bacteremia was a residual abscess from the perforation. And there was a big abscess in the iliacus muscle.

So her exam wasn’t so benign after all, some of the pain and dysfunction that was attributed to the plexopathy may be due to the muscle abscess.

But here is the reason I am discussing the case:

Need to import this film.

See the air in the bone marrow? Never seen that before.

Gas in bone has two reasons. There is

Intraosseous pneumatocyst is an uncommon condition of gas accumulation within a bone that was first described in 1984 by Ramirez et al. True pneumatization is not expected in any human bone except paranasal sinuses and middle ear, and other gas collections within bone are either a variant of normal or pathologic finding. The most common involved bones are ilium and sacrum near the sacroiliac joint. The lesion is benign and usually discovered while evaluating for other injuries. Although more frequent that was initially thought, the lesion is still unknown to most physicians and might cause clinical confusions.

The gas in this condition is thought to be nitrogen, sort of localized bends?

The other cause of gas in bone is osteomyelitis, of which there are a couple of dozen cases in the PubMeds. Curiously, despite being next to an abscess, the bone is intact as best as can be told from x-rays. If there is an anatomical construct that would allow bacteria to get to the marrow of the bone, I can’t find or remember it.

And, while most organisms make gas, I have never seen this much gas with an alpha strep; there must be more robust gas producers like E. coli and anaerobes. And no, cultures were not done at the prior surgery.

Emphysematous osteomyelitis is a rare condition characterized by the presence of intraosseous gas. A prompt diagnosis is required for this disease to expedite management as it is a potentially fatal condition. Many comorbidities, such as malignancy, diabetes mellitus, alcohol abuse, Crohn’s disease, and other etiologies causing immunosuppression, predispose to this condition. The causative organisms are generally anaerobes or members of Enterobacteriaceae family; however, the infection can be mono or polymicrobial.

Usually hematogenous, there are rare cases from the extension of intraabdominal infection or intraabdominal surgery, as in this case.

As is often the case, co-morbidities and anatomical issues that make IR drainage or surgery problematic, for the short term, she has done quite well on antibiotics.

Rationalization

Gas Bubbles in the Bone: A Case Report https://dx.doi.org/10.7860%2FJCDR%2F2016%2F19482.8200

Emphysematous osteomyelitis: Report of two cases and review of literature https://pubmed.ncbi.nlm.nih.gov/29692532/

Emphysematous osteomyelitis: a case report and review of the literature https://pubmed.ncbi.nlm.nih.gov/22230028/

2101

Aug 10, 2020

I feel like Norman of late. I get screened at the hospital for symptoms of COVID 45. I have no symptoms. So I can work. But 40% of COVID patients are asymptomatic. What if I am asymptomatic for COVID. So I can’t enter the hospital. But I am asymptomatic. So I can work.

Perpetually stuck, right at the boundary between fight and flight.

The patient is a cirrhotic, admitted for fevers and abdominal pain. By parameters, it is SBP, although the gram stain is negative. But the blood cultures grow a gram-negative rod. Fine. It will be E. coli, I say, continue the ceftriaxone.

Nope.

Pseudomonas mendocina.

I once counted the number of pathogens I needed to know to do my job, and I came to 1200. That was being a splitter with, for example, each Klebsiella spp. counted separately. I have found 1400 on the interwebs. I don’t think I counted Pseudomonas mendicina, so make that 1201. Or maybe I did and forgot, as there are 191 Pseudomonad species.

How many bacterial species are there? 30,000 are named and

my guess is there are a billion species, and the more I get used to this number, the more I feel it is a gross underestimate.

And most are not pathogenic to humans. I will not need to worry overmuch that

Antarctic rocks contain bacteria that only metabolize three or four hours a year when the sun is directly on them; otherwise, they are frozen.

and could infect my patients.

Pseudomonas mendocina is in the P. aerugenosa family and

There have been 14 reported cases of P. mendocina in the world. Four cases presented with meningitis and 5 with endocarditis. Beyond typical anti-pseudomonal agents, 2 of the reported cases show susceptibility of P. mendocina antibiotics such as sulfamethoxazole/trimethoprim and ceftriaxone. All documented case reports of P. mendocina infection resulted in successful treatment with antibiotics and survival of the patient.

Does this make 15? And the first with cirrhosis.

Pseudomonas mendocina is a soil/water organism, but I could find no particular exposure to an organism that is often found in landfills.

The patient was treated with a course of a third-generation cephalosporin and, like all the other cases, did just fine.

It is doubtful I will practice/live long enough to see another case, but I might as well immortalize the case here.

Rationalization

Pseudomonas Mendocina Bacteremia: A Case Study and Review of Literature. Gani M, Rao S, Miller M, Scoular S. Am J Case Rep. 2019 Apr 5;20:453-458. doi: 10.12659/AJCR.914360. https://pubmed.ncbi.nlm.nih.gov/30948701/

A Systematic Review of Human Infections by Pseudomonas mendocina Petros Ioannou Georgios Vougiouklakis https://pubmed.ncbi.nlm.nih.gov/32375225/

Species Numbers in Bacteria https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160642/

Here Today. Gone Tomorrow