December 13th, 2021

ID Learning Units from Inpatient ID Consults

Nerve cells in a dog’s olfactory bulb, from Camillo Golgi’s Sulla fina anatomia degli organi centrali del sistema nervoso (1885).

Need a break from all-things COVID-19? Feeling OH-verwhelmed by OH-muh-kron?

(I guess that’s how some pronounce it … or AWE-mee-kron… or oh-MIKE-ron … or who knows. Two things for sure — there’s no “n” after the “m”, and it’s a drag regardless of how it’s pronounced.)

To cheer everyone up, here’s a palate cleanser of non-COVID-19 ID Learning Units from a stretch on the inpatient ID service earlier in the fall. I’ve been storing them up just for today.

Here are the criteria for inclusion:

  1. Has to be related to a case.
  2. Has to be posted each consecutive day. (Careful readers will note I missed one so did two on one day. Mea culpa.)
  3. Has to have a reference.
  4. Has to be interesting.
  5. Has to have no patient confidentiality issues.

And for this batch, it has to be a non-COVID-19 topic. Though some may find it hard to believe, there are other infectious diseases out there — in fact the entire field of ID existed before SARS-CoV-2 ever jumped its way to humans and started this dismal pandemic.

As always when on service, I’m very grateful to have worked with a couple of highly energetic and smart ID fellows, an ID pharmacy team (faculty and resident) who taught me something daily, plus a medical resident who seems destined (I hope) to be a great future ID doc.

Hooray for that!

Off we go, each with a bit of commentary about why they were selected:

#1:

NADIA is one of the most practice-changing studies in HIV medicine in a while — which ironically will be more relevant in clinical practice for those already suppressed than those with treatment failure, even though the latter is the study population.

Key question — can essentially all people with HIV on 3-class regimens or NRTIs plus boosted PIs due to resistance switch to tenofovir/FTC plus DTG? Or even simpler, to BIC/FTC/TAF? I think so, provided they have full susceptibility to INSTIs.

#2:

The results of this study greatly expedite the tuberculosis rule-out, which in low-prevalence settings is done on many patients with an extremely low pre-test probability of TB. As always, no test is 100% perfect in the real-world setting, which means that for high pre-test probability cases, we might need to keep up precautions even with negative testing.

#3:

I find myself citing this study repeatedly, probably because there are so few clinical trials of long-term antibiotic use that so clearly demonstrate benefit. And don’t forget the compression stockings, another effective measure!

#4:

This is the only randomized trial comparing TMP/SMX to pyrimethamine plus sulfadiazine for HIV-related cerebral toxoplasmosis, and it’s woefully underpowered (a fancy way of saying, “too small”). But globally many more use TMP/SMX for this infection — it’s more readily available, less expensive, and much easer for patients to take.

Since it’s highly doubtful that there ever will be another controlled clinical trial, at what point do guidelines shift to recommend TMP/SMX over pyrimethamine-sulfa solely on the weight of clinical experience? I’d vote soon, since it’s not as if the pyrimethamine-sulfa strategy itself was ever subject to a controlled studies. (And no, I don’t know why this 1998 study was reprinted in December 2020.)

#5:

Hi Louie! A self-indulgent post about a little known dog-related fact.

#6:

Anecdotal impression:  Among hospital-based clinicians (hospitalists and medical residents), there is much greater awareness of this notable adverse effect of cefepime — especially with the decline in use of vancomycin plus piperacillin-tazobactam due to concerns about its renal toxicity.

#7:

“Steno” is such a tough bug to treat, and TMP/SMX at high dose can’t be used for everyone. Spoiler alert — another good observational study on TMP/SMX vs levofloxacin about to be published soon in a journal near you.

#8:

This is one of those inexplicable clinical trials, with an important outcome — deaths! — happening more in the experimental cefiderocol than the control arm, for reasons that still are not clear. (Reminds me of the early clinical trials of bedaquiline.) I suspect it’s because the heterogeneity of the patients with these infections is so huge that there’s the chance of death for multiple noninfectious reasons too, but I don’t know. For now, as we await more data, cefiderocol is increasingly used for treatment of highly resistant gram-negative infections in the hospital.

#9:

Reminder to emergency room, primary care, and urgent care clinicians everywhere — get blood cultures before starting antibiotics. Thank you very much, you’ve just made a lot of ID doctors very happy.

#10:

This particular question — can we use cefazolin over oxacillin or nafcillin for CNS infections due to MSSA — comes up all the time. The short answer is probably yes, with the bad reputation of cefazolin for this indication likely a carry-over from observations about another first-generation cephalosporin, cephalothin.

#11:

Back when linezolid was a branded antimicrobial and cost a ton, many didn’t believe this company-sponsored clinical trial, discounting the results on various methodologic issues.

However, a second study found the same result (linezolid better than vancomycin), and hence this is one recommendation I frequently make when consulted on a case of MRSA pneumonia — switch the vancomycin to linezolid.

#12:

Since I don’t really understand this difference in recommendations for preventive therapy, allow me to quote Dr. Patrick Hickey:  “Meningococcus is one of those infections for which every time there is a possible exposure physicians dutifully review the guidelines and then (more often than not) don’t follow them.” Agree!

#13:

More on linezolid! A reminder that impaired renal function is a risk factor for drug toxicity, which can be severe. Seems like dose reduction for this drug in some patients would be warranted, but is not now currently recommended.

#14:

Monotherapy studies with boosted PIs and dolutegravir have invariably failed despite their high resistance barrier, with more virologic rebound and development of resistance. As demonstrated in the NADIA trial (see #1, above), this can be overcome with just partial NRTI activity — which here in MOBIDIP is lamivudine despite the M184V mutation.

That’s a wrap! I’ll be on again over the holidays, will likely do the same.

Now enjoy this amazing visual (just a clip) of an extraordinarily beautiful piece — Un Sospiro (A Sigh), by Franz Liszt, played and displayed in a novel way. In dark times, it’s helpful to remember that human beings can do remarkable things.

https://twitter.com/YouTube/status/1350533338998693891?s=20

Plenty more where that come from!

4 Responses to “ID Learning Units from Inpatient ID Consults”

  1. Kat says:

    Excellent! Please post more pearls in this format!

  2. Kimon Zachary says:

    Re: cefiderocol, remember the hullabaloo about increased mortality with cefepime, back in 2010?

  3. Mimi Breed says:

    Thanks for the Lizst moment. How do you find these little gems every week? Do you have seven dwarfs out there mining the internet?

  4. Daniel Clinton says:

    Hi Dr. Sax,
    Well timed for you to reference a study about both linezolid vs vancoymcin and potential nephrotoxicity with linezolid. I think this might make an interesting blog post, what antibiotic do you prefer for MRSA coverage in the context of acute kidney injury, and when do you believe an ID consult is warranted. I currently have a relative at Beth Israel who presented with DKA and COVID pneumonia necessitating positive pressure ventilation. He was being covered with azithromycin, ceftriaxone, and vancomycin. During his first two days his creatinine rose from 1.0 to 2.1. At that time, it wasn’t known if it was pre-renal or intra-renal. I expressed concern about the vancomycin and requested ID and nephrology consults because that seemed a challenging clinical context, but the critical care service pushed back and didn’t order the consults believing his AKI was within their realm of expertise. His AKI was subsequently found to be ischemic acute tubular necrosis and he doesn’t have MRSA, but were my concerns about vanco, especially at troughs above 15, easily becoming toxic in the context of declining kidney function valid, and when should critical care specialists bring in ID for help with antibiotics in the context of AKI?

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HIV Information: Author Paul Sax, M.D.

Paul E. Sax, MD

Contributing Editor

NEJM Journal Watch
Infectious Diseases

Biography | Disclosures | Summaries

Learn more about HIV and ID Observations.