See You in December, Or Lose You to an Autumn Love

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I wrote my first novel, Skeptics in the Pub: The Cholera (available fall of 2022 from Biting Duck Press), during National Novel Writing Month.

Since then I have been working on the second novel (Skeptics in the Pub: Electric Boogaloo, no, wait, it is Skeptics in the Pub: Alien Invasion) in an at best desultory fashion. There is little time between work, life, and my scaled back blogging and podcasting.

Getting old sucks in many ways, but the loss of mental concentration and stamina might be the worst of it. I just can't focus like I used to.

So I am going to put my residual multimedia empire on hold for a month and try to write 1600 words a day for the first draft of Electric Boogaloo. It worked last time.

See you in December.

Improbable Happens All The Time

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This month I have seen two patients with lung abscess/empyema present simultaneously with their COVID. Fevers, cough, shortness of breath for about a week who went to the ER and are had COVID and a lung abscess. After maybe a decade since I have seen a good lung abscess, here are two in as many weeks.

Causal? Doubt it.

There are cases of lung abscess in COVID, mostly late and associated with Aspergillus.

There is one early case credited to COVID, but this one was still several weeks after the initial infection and was thought to be due to COVID as no other etiology was found.

Both my patients had the usual suspects grow out of the pus: oral Streptococci and anaerobes, and I can find no cases of concomitant lung abscess and COVID.

So what did the patients have in common besides acute COVID?

Bad dentition, a classic risk factor for lung abscess

Excessive alcohol use. Another classic risk factor and a reason for the delay in presentation. Given the large size of these abscesses, I suspect they had been festering under the inebriated radar for a while.

And NSAIDs. My favorite risk for lung abscess and empyema. Two of many examples:

In multivariate analyses, two factors were independently associated with the development of pleuroparenchymal complications: NSAIDs intake [Odds Ratio (OR) = 2.57 [1.02–6.64]; _p_ = 0.049] and alcohol abuse (OR = 2.68 [1.27–5.69]; _p_ = 0.01).

and

In conclusion, we found that NSAID use was associated with an increased risk of pleuropulmonary complications in patients hospitalized with CAP.

While it is so tempting to credit the acute COVID for the lung abscesses, it is just the usual reasons and a bit of the Improbability Principle:

the paradoxical idea that extremely improbable events happen frequently.

Which explains why I never run out of infections to write about.

Rationalization

Lung cavitation due to COVID-19 pneumonia https://casereports.bmj.com/content/13/7/e237245

Non-steroidal Anti-inflammatory Drugs may Worsen the Course of Community-Acquired Pneumonia: A Cohort Study https://link.springer.com/article/10.1007/s00408-016-9973-1

Nonsteroidal Antiinflammatory Drug Use and Clinical Outcomes of Community-acquired Pneumonia https://www.atsjournals.org/doi/full/10.1164/rccm.201802-0229LE

The Improbability Principle https://thatsmaths.com/2017/04/06/the-improbability-principle/

It’s Not Actually a Miracle https://slate.com/technology/2014/02/the-improbability-principle-rare-events-and-coincidences-happen-all-the-time.html

Who Knows

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Oct 26, 2021

Two consults in one workday with empyema, one with MSSA and one with MRSA and S. pyogenes. Both IVDA with no associated pneumonia, but both with trauma to the chest. Both were drained, and I was called to weigh in on how long to treat and with what.

Who knows?

I still remain amazed at the lack of evidence-based medicine to aid in deciding how to treat an empyema.

While there are numerous trials on the best mechanism for source control, there are no clinical trials on the duration of therapy and whether or not it should be IV or oral.

The British Thoracic Society says

The duration of treatment for pleural infection has not been assessed in detailed clinical trials, however, antibiotics are often continued for at least 3 weeks, again based on clinical, biochemical (eg, CRP) and radiological response

Based on nothing. With similar data, the US

recommends a minimum of 2 weeks from the time of drainage and defervescence. The final duration should be determined by the sensitivities of the infecting organism, the adequacy of drainage, and the response to therapy on follow-up. If the patient has responded to therapy, there has been source control, the isolated organism is susceptible to orally bioavailable agents, and the patient is tolerating oral intake, then a transition to oral therapy can be made.

Retrospective series suggests

Length of antimicrobial therapy from time of source control was variable, with a median (interquartile range) duration of 27 (15-31) days. Of note, longer courses of parenteral, but not oral, therapy were associated with fewer cases of clinical failure.

In children, there are studies to suggest po and iv are equal:

The frequency of complications was similar with oral therapy and OPAT for children with PPE. Oral antibiotics may be considered safe and effective for children with PPE.

There are no good recommendations for how long to treat and when to change to po. It depends on the organism, adequacy of source control, and the clinical response, and is why you get to put MD/DO after your name.

My take?

This century has demonstrated that for every infection evaluated, if there is good source control, shorter duration is equal to longer, and oral is equal to iv. And Staphylococci need more aggressive therapy than Streptococci.

I can't see where the pleural space is any different except when the infection is evaluated with CT or CXR, it looks ugly for months.

In the 21st century, it seems wrong to give multiple weeks of antibiotics if there has been good source control. I suspect that once the pus has been drained, 14 days or less, probably 5-7 days of oral, is all that is needed.

But I/we so need some EBM to guide us.

Rationalization

Management of pleural infection in adults: British Thoracic Society pleural disease guideline 2010 https://thorax.bmj.com/content/65/Suppl_2/ii41

Empyema management: A cohort study evaluating antimicrobial therapy https://www.journalofinfection.com/article/S0163-4453(16)00059-1/fulltext

The American Association for Thoracic Surgery consensus guidelines for the management of empyema https://www.jtcvs.org/article/S0022-5223(17)30152-6/fulltext

Comparative Effectiveness of Oral Versus Outpatient Parenteral Antibiotic Therapy for Empyema https://pubmed.ncbi.nlm.nih.gov/26526596/

Strikeout

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Oct 20, 2021

The patient, elderly, is being worked up for rapidly enlarging pulmonary masses. It was thought to be due to granulomatosis polyangiitis based on a positive c-ANCA and a perhaps consistent lung biopsy. Like many a skinny needle biopsy, there were a lot of artifacts that made the read soft. But the patient improved somewhat on steroids and Rituxan until a stroke.

That led to an ECHO that slowed a vegetation flopping on the aortic valve and an ID consultation.

I did not have granulomatosis polyangiitis in my head as a cause of marantic endocarditis.

It happens. Granulomatosis polyangiitis can involve mostly the aortic, and other, valves, albeit rarely. I find a handful of cases on the Pubmeds.

Cardiac valvular involvement is a rare and potentially fatal complication of GPA and may misleadingly suggest infectious endocarditis. A review of literature revealed few cases of histologically well-documented cardiac valvular involvement in GPA. Pathologists should be aware of valvular heart diseases in GPA, which usually comprise valvular necrotic lesions without any microbial agents.

But maybe the patient has two processes, even though I am an Occams kind of guy. Endocarditis and granulomatosis polyangiitis.

Multiple blood cultures are negative off antibiotics, and history for exposures has only a childhood in urban S. America and young cats at home.

Here is where it gets curious.

Bartonella (and Coxiella) endocarditis can present like granulomatosis polyangiitis even with a positive ANCA.

Bartonella infection mimicked anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis in 83% with PR3-ANCA and presented as cryoglobulinemic vasculitis in 8%. Glomerulonephritis was present in 92%, and 88% had endocarditis. ....Five cases of Coxiella infections were added to 16 from literature review. Sixteen had small-vessel vasculitides, mainly cryoglobulinemia vasculitis in 75%. One patient had polyarteritis nodosa-like vasculitis and four large-vessel vasculitis.

Conclusion: Coxiella and Bartonella are both able to induce vasculitis but display distinct vasculitis features. Bartonella mimics PR3-ANCA-associated vasculitis in the setting of endocarditis, whereas Coxiella may induce vasculitis involving all vessel sizes.

So I got all excited that this was Bartonella, a common cause of culture-negative endocarditis. Even though it is a different ANCA and pulmonary nodules do not seem to reported in the granulomatosis polyangiitis cases, it is more at the glomerulonephritis end of the disease presentation. However, there are the rare cases of Bartonella causing pulmonary nodules.

Nope. Work-up for infections, including molecular testing, is a big, fat negative.

It's all granulomatosis polyangiitis.

But still, fun to think about, And it is the strikeouts that are more edumacational than a home run.

Rationalization

Cardiovasc Pathol . Nov-Dec 2014;23(6):363-5. doi: 10.1016/j.carpath.2014.07.007. Epub 2014 Aug 4. A case of aortic and mitral valve involvement in granulomatosis with polyangiitis https://pubmed.ncbi.nlm.nih.gov/25194969/

Bartonella and Coxiella infections presenting as systemic vasculitis: case series and review of literature https://academic.oup.com/rheumatology/advance-article-abstract/doi/10.1093/rheumatology/keab691/6368082

All Lues?

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Back from a week off. As much as I like ID, I really like not working. Work has become like ice cream. I love ice cream and never tire of eating it. Especially with homemade hot fudge made from sweetened condensed milk. Mmmmmm. So good. But I grow a tad weary of this particular flavor.

The patient, middle-aged, has the new onset of headache and unilateral tenderness over the temporal artery. The ESR was only 75, but they went for a temporal artery biopsy. The pathologist called the read "difficult" after it showed a dissection but not the classic changes of temporal arteritis. Early disease? They wondered.

Steroids were started.

Then the patient developed visual changes that the ophthalmology found suspicious and sent off studies for syphilis and Tb and the RPR came back at 1:256.

LP refused.

Going through the old records, the patient had never been tested for syphilis in the past but had been at Outside Hospital a year prior for a complicated head and neck infection that, among other things, resulted in an eight-week course of ceftriaxone. I have to confess that I cannot think of any soft tissue infection that needs more than few days of therapy, but not all the information is at my disposal. Still, there is no way any Treponema would have survived that antibiotic onslaught. The Lues would have to have been acquired within the last year.

Or the patient had syphilis a year ago with an unmeasured very high RPR, and it has, a year later, fallen to 1:256. If that was the case, the Lues should have been eradicated by the two months of ceftriaxone and what we are seeing is temporal arteritis. Kind of different treatments, so we sent of studies looking for Treponemal DNA, and it was positive. So syphilis it is. But.

Does syphilis result in dissection of the temporal artery?

Aorta? Yes, but rare with syphilitic aneurysms, and it has a curious pathophysiology:

Syphlitic Aneurysms arise during tertiary syphilis due to chronic inflammation in the tunica adventitia of large elastic arteries, particularly the aorta. The inflammatory response to the spirochetes causes an obliterative endarteritis of the vaso vasorum, leading to a loss of blood supply to the elastic tunica media. Ischemia of the tunica media, combined with further syphilitic invasion into the tunica media itself, results in medial destruction and weakening, ultimately causing dilation and aneurysm-formation. Fibrosis of the vascular wall can give involved vessels a 'tree-bark'-like appearance and probably protects against aortic dissections which are not a consequence of syphilitic aneurysms.

Smaller vessels? There are reports of carotid artery dissection. And that's it. I can't find where syphilis has ever been associated with temporal artery dissection:

Your search - "temporal artery dissection" syphilis - did not match any articles.

Temporal artery dissection is a rare process outside of temporal arteritis, with only one spontaneous case reported.

I suspect this is all secondary syphilis with vasculitis, including the temporal artery with the first reported case of an associated dissection and involvement of the retinal arteries, but once ophthalmology says the eye is involved, it's treatment for tertiary syphilis.

But I am an Occams kind of guy who is worried this is a Hickam's case, since the diagnostics are not cut and dry. Too young and the ESR not that high with a nondiagnostic pathology for TA against the first case of syphlitic temporal artery dissection.

I do find the staging of syphilis unsatisfying. It is clear the spirochete is widely disseminated from the start of the chancre, including the CSF. That has been suspected since 1919 on the basis of LPs where

2% cocaine was used to anesthetize the skin. This was a great help in reducing the immediate discomfort of the puncture,

I bet it was.

It is curious how the disease smolders for years in various organs before it manifests in the oddest ways.

Rationalization

Bilateral vertebral artery and internal carotid artery dissecting aneurysms due to syphilis https://www.neurologyindia.com/article.asp?issn=0028-3886;year=2016;volume=64;issue=7;spage=131;epage=133;aulast=

Isolated superficial temporal artery dissection masquerading as giant cell arteritis https://pubmed.ncbi.nlm.nih.gov/19769813/

THE SPINAL FLUID IN PRIMARY AND SECONDARY SYPHILIS https://jamanetwork.com/journals/jama/article-abstract/222952

No Rosetta Stone Needed

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The patient, vaccinated, is admitted with SOB, a positive COVID test and is intubated. Interesting CXR on admit: a left lower lobe consolidation somewhat obscured by the heart., Not your typical COVID presentation, but over the next several days the CXR changes to a more typical pattern for COVID, but the lll consolidation persists.

Also, on admission, one of two blood cultures grows a S. anginosis and for that gets a two-week course of ceftriaxone in addition to dexamethasone and baricitinib. Three weeks later, the patient is not getting better, so as part of the evaluation, a chest CT is performed. Performed. Like it is a one-act play. But it does show a necrotizing lll abscesses, and I am called.

This was a Hickam's dictum case. The patient presented with two processes. COVID and a lung abscess and the first diagnosis obscured the second. Ye Olde Premature Closure. You know the abscess was present on admission because of the blood culture. When the S. anginosis group (S. anginosus, S. intermedius, and S. constellatus) are in the blood, the question which should be asked, and wasn't, is where is the abscess?

Because these are the abscess causing Streptococci.

The answer was in the lll, but no one looked.

I figure that there are questions three every consult should ask: what is the infection, what is the treatment, and what is the airspeed of a... no, the third is why is there an infection at all.

As I have said many a time, the name of the bacteria will often tell you why. If you understand the significance of the organism.

Exam and history also supported the diagnosis: very poor dentition and a heavy drinker.

This is a classic aspiration pneumonia—the real deal.

I do not know about your institution, but somewhere along the line, an aspiration pneumonia - lung abscess/empyema in an alcoholic/seizure/heroin user with poor dentition - became conflated with aspiration events. People have looked. For acute aspiration events, be it community, hospital, or ventilator, there are no anaerobes as part of acute aspiration and subsequent pneumonitis. But metronidazole keeps being given for acute aspirations. As if antibiotics help in acute aspiration:

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

If you want to practice medicine unhinged from reality, be Ron DeSantis's Surgeon General.

There is a certain irony. For years, I have been grumping that an aspiration event is not an aspiration pneumonia, and metronidazole is not only not needed, but it also goes against the entire medical literature. Then a classic case is admitted, not recognized, and the needed metronidazole, in addition to the Streptococcal coverage, is not given.

Sigh.

Rationalization

Clin Infect Dis .2018 Aug 1;67(4):513-518. doi: 10.1093/cid/ciy120. Prophylactic Antimicrobial Therapy for Acute Aspiration Pneumonitis https://pubmed.ncbi.nlm.nih.gov/29438467/

Diagnostic Error in Internal Medicine https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/486642

Aesthetic

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To a physicist, beauty means symmetry and simplicity. Michio Kaku,

Physicists, more than any other science, talk about the beauty in the field. Medicine? It doesn't have a lot of beauty by that definition. Medicine is usually messy and uncertain, and few things are as far from beauty as pus.

Still.

I do have an aesthetic when it comes to ID. I like the history, physical, and diagnostics to be consistent, and the therapy makes sense. Such a case may not be beautiful in the classic sense, but there is a satisfaction when a case comes together. Makes me feel very John "Hannibal" Smith.

The history, physical, and diagnostics often diverge, as patients do not read the textbook before coming to the hospital, but I find that beautiful as well. Diseases presentations are like variations on a Bach sonata. If you understand the infection, you can always hear the underlying tune. Those variations are often at the heart of this blog.

But the real ugliness comes in the treatment. And ugliness most often manifests at 2 in the morning, when inexperienced residents make decisions that are often, to quote Wolfgang Pauli, not even wrong.

And ugly.

The most common bit of ugliness is changing the antibiotics from treating the known infection, usually S. aureus, to broad-spectrum, because the patient has fevers. I have whinged about this ugliness many times. It. Drives. Me. Nuts.

But the most recent recurring aesthetic abomination is to treat stable, indolent infections with multiple antibiotics before any diagnostics are obtained for osteomyelitis. Chronic lung abscess. SBE, with an emphasis on the S. So often antibiotics are given when there is absolutely no hurry, and they only serve to mess up the cultures. Happens all the time with discitis. Ugly

Treating for organisms with no probability of being present, such as anaerobes in the edentulous or acute aspiration. Ugly.

Giving the wrong antibiotic for a known infection. Vancomycin for MSSA as the most common example. Ugly.

Not only is it suboptimal medicine, but it is also aesthetically ugly.

I am not a fan of ugly.

I don't know the solution. Sometimes I think infections should be like heme onc, treatment limited to ID docs and only ID docs. But that's not practical. It is a shame we do not have any devices that allow people to have virtually instantaneous communication with experts anytime/anywhere or allow access to the world's medical information by entering simple search terms. It would make medicine so much less ugly, like the ability to prevent severe COVID.

I guess the ugliness will just have to continue.

Rationalization

The A-Team https://www.shmoop.com/quotes/i-love-it-when-a-plan-comes-together.html

What the Hell is an Eustachian valve?

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The patient, an IVDA, presents with TNTC septic pulmonay emboli on CT and MSSA in the blood. They often say TNTC (too numerous to count) and really, if they took the time, they could count them. Not this time. I looked at the CT. No way those could be counted.

Does the patient need an ECHO? You know its tricuspid valve endocarditis; could be pulmonic valve but that is very rare. I remember one in my long and storied carrier. Probably not.

But every once and a while the ECHO shows something you don't expect. As this time. A big clot in the IVC. That is odd. Why would that happen?

Eustachian valve endocarditis shows up in a search.

What the hell is an eustachian valve?

The Eustachian valve (EV) is an embryological remnant of the inferior vena cava that during fetal life helps divert oxygenated blood from the IVC toward the foramen ovale to escape the pulmonary circulation. This remnant usually regresses after birth and is considered a benign finding in the majority of cases

Oh yeah. If I ever learned that, I long ago forgot it.

Can it get infected? Yep.

Eustachian valve (also known as the valve of the inferior vena cava) is another valve in close proximity to the tricuspid valve, which can, in rare cases, be the focus of infection. Eustachian valve endocarditis may be an under-recognised complication of Staphylococcus bacteraemia in IVDU population..

There are maybe 37 cases all told.

The location is right, although no valve was seen on TTE.

The reported cases suggest the disease is under-recognized and

demonstrates the significance of systematically interrogating the Eustachian valve during an echocardiography in all patients suspected of having endocarditis

It doesn't make a difference in the type and duration of therapy, but is a curious manifestation of an endocarditis.

I wonder how many I have missed over the years.

Rationalization

Eustachian valve endocarditis: Case report and literature review https://onlinelibrary.wiley.com/doi/full/10.1002/ajum.12078

Eustachian valve endocarditis: a case report on an under diagnosed entity https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7425621/

It's the Water

Two weeks in a row off. Wonderful. One week a staycation, the other at Mt. Rainier. There are many differences between Portland and the national park. The most notable is masking. Very rare to see anyone without a mask indoors in Portland. Whenever I go to rural counties in Oregon or Washington, mask-wearing plummets. That's also where the cases of COVID are; the rural counties of the Great Pacific NW. Huh. Wonder if there is any relationship?

There are three questions I need to answer for every consult. What is the infection, how to treat the infection, and why is there an infection. Finding the answer to the last question often is the most interesting aspect of the case. The treatment is usually the least interesting. Anyone can look up the correct treatment once the correct diagnosis is made. I have a job in part because most people don't want to bother.

The patient is admitted septic from a necrotic, spreading soft tissue infection. Blood grows Pseudomonas.

It happens.

Nosocomial acquisition, preexisting biliary disease, and recent use of immunosuppressive agents are strong predictive factors for P. aeruginosa bacteremia in cirrhotic patients.

But she had none of the above reasons for Pseudomonas bacteremia. So, from the cellulitis/soft tissue process? Pseudomonas does cause the occasional soft tissue infection in cirrhosis:

73% of culture (16/22) showed growth of gram negative organisms. The organisms were Klebsiella pneumoniae in 6 (27%) patients, Pseudomonas aeruginosa in 6 (27%) and Escherichia coli in 4 (18%) cases. Twenty seven percent (6/22) had Staphylococcus aureus of which two were methicillin-resistant Staphylococcus aureus (MRSA). Out of 45 cellulitis patients without SBP, 10 had culture positivity of which 8 were gram negative organisms (2 Pseudomonas, 4 Klebsiella, 2 E. coli) and 2 were gram positive (Staphylococcus).

The necrotic lesion had been debrided and sent for culture.

Aeromonas.

A well-known cause of necrotic soft tissue infections, the annoying issue is I do not have a concordance of cultures.

What do the two have in common? Water.

And as is so often the cause in the regions around Portland, the patient uses untreated well water for bathing and drinking.

From a total of 20 wells, five were found to contain Aeromonas species with cell number ranging from 26 to 1 609 250 ml−1. In two wells the presence of Aeromonas spp. was not associated to the presence of faecal indicators, i.e. coliforms and faecal coliforms. and

In three families, Pseudomonas aeruginosa was isolated in the well water. In a further three families, Pseudomonas aeruginosa was isolated from bathroom and kitchen components.

It's the water. It used to mean the beer; now it means the infection source.

The Pseudomonas from drinking water and the Aeromonas from bathing.

Best I could do for the why. A course of cefepime made it all better.

I have quite the number of cases in this blog of presumptive well water associated infections.

Rationalization

BMC Infect Dis.2013; 13: 332. doi: 10.1186/1471-2334-13-332 PMCID: PMC3720192 Pseudomonas aeruginosa bacteremia in patients with liver cirrhosis: a comparison with bacteremia caused by Enterobacteriaceae https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3720192/

Ann Gastroenterol. 2014; 27(4): 374–379.PMID: 25331211 Risk factors of cellulitis in cirrhosis and antibiotic prophylaxis in preventing recurrence. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4188936/

Olympia Brewing Company https://en.wikipedia.org/wiki/Olympia_Brewing_Company

The occurrence of Aeromonas spp. in natural mineral water and well water https://www.sciencedirect.com/science/article/abs/pii/S0168160500004104

Pseudomonas aeruginosa folliculitis after shower/bath exposure https://onlinelibrary.wiley.com/doi/abs/10.1046/j.1365-4362.2000.00931.x

Don't Bury the Lede

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A lede is the introductory section in journalism and thus to bury the lede refers to hiding the most important and relevant pieces of a story within other distracting information. The spelling of lede is allegedly so as to not confuse it with lead (/led/) which referred to the strip of metal that would separate lines of type.

My job is simple, me find bug, me kill bug, me go home. People want to know three things from me: what does the patient have, why do they have it, and how best to treat it. I try to get get to the point with my consults, so my notes, at least the important parts of the note, are short and sweet.

We are not paid by the word, but what we do, and the fewer used to document what we do, the better.

But it seems others cannot get to the point anymore. All text pages need is your name and return number. And when I call, lede with what is important. Question or consult. I had one page recently, "Want to talk to you about a patient." OK, Five minutes later, the doc ended... so we want to get you involved in the case. You mean a consult? Yep. Hell. Lede with that. We could have stopped after the patient's name and room number because that is all I need. Or want.

Consult. Beelzebub. Room 666.

Not that we have a room 666. It goes from 665 straight to 667, which really is 666 and is still cursed.

Or the caller goes on for several minutes before getting to what is the lede: the syphilis serology. Or the blood culture results. Or the LP results.

Recently residents have taken to paging me and saying, we thought we would reach out to you. And that means just what exactly? A consult? A question? You need a hug? No clarity or precision anymore.

Lede with what is essential when you call me.

And get off my lawn.

A common outpatient consult is prolonged fevers and transaminitis. Usually, they have a negative A, B, C, CMV, and EBV. Usually, there is no clinical reason to suspect CMV and EBV by other labs. But people tend to forget about E. A vowel movement, I suppose.

But that is what the patient had; the hepatitis E IgM was positive.

The curious reason was why. There are 4 Hepatitis E genotypes. 1 and 2 are fecal-oral/water-borne, while 3 and 4 are food-borne.

Mostly from eating pig meat, innards, home-prepared pork products, or tasting raw pig meat. One guy got it from his pet pig. Really. In Denmark and Germany, it is primarily an asymptomatic zoonosis from eating swine and wild boars. Especially common after flooding.

It is in US pigs,

Hepatitis E virus RNA was detected in 6.3% and HEV IgG in 40% of 5,033 serum samples from market-weight pigs at 25 slaughterhouses in 10 US states.

Splitting hares is a risk. And rats in LA. And ferrets. And eating camel meat and milk. There goes my diet. I'll miss camel sashimi.

Pets and eating liver are the risks; I assume these risks are rarely combined. I bet Hannibal Lecter is seropositive.

I could find no smoking gun (a new form of BBQ?) dietary reason for Hepatitis E, but about 21% of Americans are seropositive, although other studies have put it at 6%.

The weighted national seroprevalence of HEV in the U.S. is much less than previously reported. Using data obtained with a high performance assay, the seroprevalence of HEV was estimated at 6.0% in the U.S. Based on these results, the seroprevalence of HEV is only one-third as high as previously reported.

So it is likely common and just as commonlymissed. And why I only eat deep-fried food.

And why the alphabet soup? Why A,B,C,D,E? It is the worst way to classify organisms if you want to learn/remember them.

I really can't find why. The closest is

Dr. F.O. MacCallum came to the conclusion that there are two types of hepatitis, which he classified as “infectious hepatitis” (later identified as hepatitis A-HAV infection) and “homologous serum hepatitis” (later labeled as hepatitis B virus infection). This old classification corresponds to the MS1 and MS2 stratification used at the Willowbrook Institute during the controversial, yet important human transmission and prevention studies by Krugman et al.

So I guess A and B were shortcuts, a simple way of distinguishing the two, and C (non-A non-B when I was a resident), D, and E were named from laziness and a lack of imagination. There is also an F, a G, and then they skipped to TT. Of course they did.

Rationalization

Why Do We 'Bury the Lede?' We buried 'lead' so far down that we forgot how to spell it https://www.merriam-webster.com/words-at-play/bury-the-lede-versus-lead

Time trend of the prevalence of hepatitis E antibodies among farmers and blood donors: a potential zoonosis in Denmark https://pubmed.ncbi.nlm.nih.gov/18781880/

Phylogenetic and case-control study on hepatitis E virus infection in Germany https://pubmed.ncbi.nlm.nih.gov/18983248/

Hepatitis E Virus Infection in European Brown Hares, Germany, 2007–2014 https://wwwnc.cdc.gov/eid/article/25/6/18-1618_article

Hepatitis E virus in rats, Los Angeles, California, USA https://pubmed.ncbi.nlm.nih.gov/22172320/

Chronic Infection With Camelid Hepatitis E Virus in a Liver Transplant Recipient Who Regularly Consumes Camel Meat and Milk https://pubmed.ncbi.nlm.nih.gov/26551551/

Epidemiology of hepatitis E virus in the United States: results from the Third National Health and Nutrition Examination Survey, 1988-1994 https://pubmed.ncbi.nlm.nih.gov/19473098/

Current epidemiology of hepatitis E virus infection in the United States: low seroprevalence in the National Health and Nutrition Evaluation Survey https://pubmed.ncbi.nlm.nih.gov/24824965/

The History of Hepatitis A https://aasldpubs.onlinelibrary.wiley.com/doi/full/10.1002/cld.1018

History of the Discovery of Hepatitis A Virus http://perspectivesinmedicine.cshlp.org/content/9/5/a031740.full

Hepatitis F, G, and TT Viruses https://www.ncbi.nlm.nih.gov/books/NBK13296/

The Heat is On

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My wife and I enjoy seeing cover bands. One of our favorites is Cashed Out, a Johnny Cash tribute. Still not going to any shows this year while delta rips through the world. But I saw Megadeath is coming to Portland next month. Who knew there was a COVID cover band?

People, including me, are prone to seeing patterns where none exist. One of the many cognitive errors that bedevil cognition.

This month I have had three cases of Cryptococcus. Unusual in that I rarely see that many in a year.'

Clustering illusion, right?

The clustering illusion is the tendency to erroneously consider the inevitable "streaks" or "clusters" arising in small samples from random distributions to be non-random. The illusion is caused by a human tendency to underpredict the amount of variability likely to appear in a small sample of random or pseudorandom data.

But the last several months have been hot. Hottest ever. Are the two connected? Or true-true and unrelated.

Maybe related. The range of many infections and their vectors has changed since I started practice back in the cooler 1990s. Why not Cryptococcus?

The present study showed that recent climate changes have significantly affected the distribution of the fungal pathogen C. gattii VGI in Europe and the Mediterranean area. The analysis revealed a gradual expansion of the fundamental niche of the fungus from 1980 to 2009 and an impressive increase in the last decade (2010–2019), during which the environmental surface suitable for the fungal survival was more than doubled.

and

Cryptococcus deuterogattii, previously named Cryptococcus gattii VGII, was recently elevated to a species within the Cryptococcus gattii species complex. C. gattii complex species were traditionally associated with tropical and subtropical climates; however, in recent years, C. deuterogattii has emerged in the temperate regions of western Canada and the Pacific Northwest of North America, where it caused hundreds of infections in people and animals. Interestingly, C. deuterogattii has a higher level of thermal tolerance than other C. gattii complex members, indicating that it may have a greater capacity for thermal adaptation

and

C. gattii results for tree and air samples were more likely to be positive during periods of higher solar radiation.

Higer solar radiation describes July and August. So maybe.

There is at least some good news. I was asked yet again when COVID was going away, and I said never. But maybe not.

We found that 60.0% of the confirmed cases of coronavirus disease 2019 (COVID-19) occurred in places where the air temperature ranged from 5 °C to 15 °C, with a peak in cases at 11.54 °C.

That is a peak of 53 degrees for you metric impaired.

Our results indicate that approximately 85% of the COVID-19 reported cases until 1 May 2020, making approximately 3 million reported cases (out of approximately 29 million tests performed) have occurred in regions with temperature between 3 and 17 °C and absolute humidity between 1 and 9 g/m3. Similarly, hot and humid regions outside these ranges have only reported around 15% or approximately 0.5 million cases (out of approximately 7 million tests performed). This suggests that weather might be playing a role in COVID-19 spread across the world.

So the good news? When temperatures hit 120 F, COVID is unlikely to be transmitted, and that will end the pandemic.

Yeah.

Rationalization

Global warming impact on the expansion of fundamental niche of Cryptococcus gattii VGI in Europe https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8251527/

Climate change and the emergence of fungal pathogens https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1009503Climatic

Influences on Cryptococcus gattii Populations, Vancouver Island, Canada, 2002–2004 https://wwwnc.cdc.gov/eid/article/21/11/14-1161_article

Effects of Weather on Coronavirus Pandemic https://pubmed.ncbi.nlm.nih.gov/32727067/

Really. What Else Could It Be?

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Quos Deus vult perdere, prius dementat (Those whom God wishes to destroy, he first deprives of reason) US Motto 2020-2022

This isn't going to be a COVID entry, and the quote has nothing to do with what follows. I was going to modify it to suggest being smug about one's diagnostic abilities is a sure path to disaster (Those whom God wishes to destroy, he first makes diagnostically smug). But I'm one smug sob at times, and, hey, what is the point of false modesty? Sometimes I do know what I am doing.

If you include my fellowship years, this is my 35th year in the ID biz. And I will let you in on a little secret if you promise not to tell anyone.

ID just ain't that hard anymore. Every consult has three questions that need answering: what do they have, why do they have it, and how best to treat it. I can usually figure that out in about 10 minutes. Even with the most complicated case, if you can separate the wheat from the chaff, it can generally be figured out in under 30 minutes. The rest of the consult is dotting t's and crossing i's, making sure you don't get blindsided by something unexpected. You have to be complete even when you have the answer upfront. Just in case.

You have probably noticed that ID docs do love to brag about much time they spend on a case, but it is time mostly spent reviewing information that doesn't matter. The vast majority of cases can be figured out in 10 minutes and summed up in a sentence or two if you know what is and is not relevant to the case at hand. But it took me 20 plus years, a quarter of my life, to get to that point. Until then, ID was hard.

As a fellow and resident, I remember how my ID attendings would generate an extensive differential diagnosis for cases but never commit. I always construct three lists for every patient. What they have. What I don't want to miss, even if unlikely if it could kill/harm the patient. And what is the cool diagnosis?

But I like to commit to a diagnosis. I love it when the venn diagram of the three lists has the same diagnosis at the top. Frequently in error, never in doubt, that's my motto. But as I have mentioned in the past, everyone remembers Babe Ruth pointing to right field and hitting a home run. No one remembers he led the league in strikeouts. So I commit. And it impresses the hell out of people when you are right,

Case in point, an FUO.

Four months of roughly one a week rigors, fever, sweat.

CBC/Comp/Blood cultures/CT CAP as an outpatient all normal except for a mild anemia.

So right away, any number of infections, presuming it is infection, are off the table. Few diseases go on that long, and with that pattern. Two, maybe three,

PMH: recent Bells palsy.

Now we are down to one possible disease.

Further questioning shows he visits the US NE frequently, and while he does not remember any tick bite, his Bells palsy was evaluated, and he had a positive Lyme serology, which had been treated.

So in about 8 minutes, I was down to the one disease this was likely to be. Ticks spread more than one disease with a bite. So.

Babesia?

Malaria was also on the list, but a case of suitcase malaria seemed less likely. Suitcase malaria is where an infected mosquito hitches a ride in a suitcase and infects someone in a non-endemic area. I have yet to see a case.

I did the rest of the usual H&P to be complete. Nothing. No other exposure history to put him at risk for odd infections.

So sent off a thick and thin smear and bingo was his name-o. Babesia. The first case that I have ever diagnosed.

But really, what else could it be? See? ID is simple. After spending most of your adult life at it

He got all better on Babesia therapy.

Rationalization

Origin and prevention of airport malaria in France https://onlinelibrary.wiley.com/doi/10.1046/j.1365-3156.1998.00296.x.

Coinfection by the tick-borne pathogens Babesia microti and Borrelia burgdorferi: ecological, epidemiological and clinical consequences https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4713283/

I Love Me That Modern Technology

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"My god, what is this, the Dark Ages?" Bones McCoy. The Voyage Home

For most of my long and storied career, ID has been pretty low-tech. I did an H&P, then hoped we grew something on agar plates. It has been that way forever. In the 21st century, we have finally had access to technologies that allow for the routine diagnosis of some of the oddest infections.

The patient is an elderly male, mostly healthy, who has two months of intermittent fevers, rigors, sweats, and progressive malaise.

Outpatient work has yielded nothing, and by the time he is admitted, there is quite the list of negative studies, from cultures to TEE to a CT of the chest/abdomen/pelvis.

Always a challenge to add to an extensive workup. So back to the H&P to give me a hint as to where to go.

When I see him, there is little in the way of exposures for odd infections, and his exam is negative.

But he looks ill, and his CRP and ESR are markedly elevated.

The only thing of note is several years ago, he had an extensive repair of his aortic arch and descending aorta, and he is full of endovascular graft.

So it is between a vasculitis of some sort or perhaps a graft infection. Reviewing the CT with radiology, the aorta/graft doesn't look infected, but it doesn't look not infected. Too complicated to tell.

So I order a PET CT, as one of many studies notes

FDG-PET scanning showed a better diagnostic accuracy than CT for the detection of vascular prosthetic infection.

I always think FDG stands for fudge, as in "present or deal with (something) in a vague, noncommittal, or inadequate way, especially so as to conceal the truth or mislead." Like most medical studies. Except the PET.

Bingo was his name-o. One section of the arch glowed like Chernobyl. As best could be determined, the infection was in the old clot between aortic and graft and involved the graft. But from what?

And several years out for surgery, was this a new infection, or has it been festering since the repair?

So with negative blood cultures, I sent off a Karius test. Lots of Legionella micdadei DNA. I did not see that coming.

There are a grand total of 2 cases of Legionella causing aortic graft infections, both pneumophilia

So a worlds first: Legionella micdadei aortic graft infection, diagnosis made possible by high tech. Although, I still want Dr. McCoy's tricorder.

Why? No reason I can find. No good water exposure outside of Portland city water and no similar case from the time of his surgery that would point to an infection acquired in the OR.

On a quinolone, symptoms markedly improved (macrolide intolerant), but how long to treat is problematic since

The findings of this meta-analysis confirm the positive association between fluoroquinolones and the development of aortic aneurysm or dissection. The data tend to show that this association may be majorly driven by aortic aneurysm.

Does it matter, given his aorta is mostly replaced/repaired? Got me.

Rationalization

Accuracy of FDG-PET–CT in the Diagnostic Workup of Vascular Prosthetic Graft Infection https://www.sciencedirect.com/science/article/pii/S1078588410003345

Fluoroquinolones and the Risk of Aortic Aneurysm or Aortic Dissection: A Systematic Review and Meta-Analysis https://www.ingentaconnect.com/contentone/ben/chamc/2019/00000017/00000001/art00004

Not the First Case Ever

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The patient is an almost healthy female who, three days prior to admission, had her right groin catheterized as part of examining her coronary arteries.

She came in with fevers, rigors, and a red hot swollen groin.

Cellulitis.

OK.

She was started on vancomycin, and the next day I was called when both sets of blood cultures had gram-positive cocci in chains.

By the time I saw her, the erythroderma and pain at admit had nearly resolved. Kind of quick to get better.

It's going to be a Group A Streptococcus or maybe another Streptococcus. And there are the occasional pseudoaneurysms after angiography, so beware the Enterococcus.

We looked. No pseudoaneurysm.

But the next day, the organism was identified as Abiotrophia defectiva.

That's odd. A quick Pubmed found no cases of Abiotrophia defectiva as a cause of cellulitis, and it is a mouth organism. Yeah, the mouth and rectum are connected, but it seemed a stretch.

The closest was

We report a case of infective endocarditis (IE) caused by Abiotrophia defectiva in an 8 year-old boy presented initially with left ankle cellulitis and fever.

Went back to the patient armed with the microbiology. No murmur, no emboli, no nothing except on direct questioning he had three teeth extracted several days before the catheterization.

And the TEE showed a small vegetation on the aortic valve. While not the firest case ever of primary Abiotrophia cellulitis, it is the first case in an adult of endocarditis due to Abiotrophia defectiva presenting as cellulitis. I'll take it.

Rationalization

Iatrogenic femoral artery pseudoaneurysms--a review of current methods of diagnosis and treatment https://pubmed.ncbi.nlm.nih.gov/18996260/

Infective Endocarditis due to Abiotrophia defectiva presenting as Ankle Cellulitis https://www.semanticscholar.org/paper/Infective-Endocarditis-due-to-Abiotrophia-defectiva-Subhi-Yaqubi/a6f827a53def581f9ed509ea93fd665425ad5d8d

I Could Not Stay Away

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About two months ago Medscape had a change in direction for their blogs. It was not a direction I wanted to go. Nothing personal, but I had pretty much done things my way for 12 years and, being a control freak like most ID docs, did not want to give up control.

There were no hard feelings.

Well.

It would have been nice if, after 12 years, 1400 or so entries, and maybe a million words, they would have said thanks for all the work.

Nope.

If there is one lesson I cannot seem to learn is that organizations will never, ever reward hard work and devotion. Don't let the man fool you into trust and loyalty. It will never be repaid in kind. But then I am just a snowflake.

I thought it would be a good time to retire the blog, and given there were two or three people who actually seemed to notice, it seemed like a reasonable decision.

But. But. But.

I kept seeing cases and would think, "This would be a great case to blo-oh wait, I'm not doing that any more."

And I found I missed writing the blog. ID is easy and fun to write about, different from fiction which is hard and fun. I quit writing at Sceince Based Medicine in part because I grew bored, but I have yet to get bored with ID.

I also realized that blogging was too valuable a way for me to learn. The process of writing helps imprint concepts in my mind. It is why when I have a resident on service, I usually write my own notes rather than attest them. The process of putting pen to paper, or electrons to screen, crystalizes the case for me.

How often I will put up a post remains to be seen as I am now working three-quarters time. Once or twice the weeks I work, probably. And I am half considering blogging on topics unrelated to ID. Or not. I don't know. We will see. As Cartman would say, Whatever, I do what I want.

So, like Michael Corleone, I'm back in, at least for the next 3 years, 10 months, 6 days, 23 hours, 12 minutes, and 31 seconds.