HIV and ID Observations

Just wrapped our our annual postgraduate course, “Infectious Diseases in Primary Care,” where each year we get together with primary care providers (doctors, nurses, PAs) and review what we hope are the most clinically relevant topics in ID.

And each year we get a great bunch of questions, some of which I’ve listed below (along with an attempt to answer them):

• I know the zoster vaccine is indicated for people who have had shingles. But how long should I wait after they’ve had it before giving it?
  Of all the questions I get about the zoster vaccine — and trust me, there are lots of them — this is currently the most common by a long shot. (Ha!) Importantly, this question gives me a chance to praise one of the most practical sources of ID information on the internet, the authoritative and incredibly useful “Ask the Experts” section of the Immunization Action Coalition’s web site. Questions like these are posted and concisely answered by, you got it, experts! And here’s what they say on this particular one: “Administering zoster vaccine to a person whose immunity was recently boosted by a case of shingles might reduce the effectiveness of the vaccine. ACIP does not have a specific recommendation on this issue. But it may be prudent to defer zoster vaccination for 6 to 12 months after the shingles has resolved so that the vaccine can produce a more effective boost to immunity.” So there’s my answer.
• What do you do when the new syphilis test [treponemal ELISA] is positive, but the RPR is negative?
  Depends. First step is to send one of the classic confirmatory tests — we use the TP-PA here, but the FTA-ABS or MHA-TP would be fine too. If that’s negative also, you’re probably dealing with a false-positive ELISA. If it’s positive, and the patient has been treated before, you’re all set — the negative RPR means he/she is cured. But if they’ve never had treatment, then it makes sense to treat for late-latent syphilis. None of this, of course, is based on firm clinical data correlating these strategies with clinical outcomes — welcome to the world of syphilis diagnostics and therapy!
• Sometimes patients request that we screen them for “every STD.” Would you include HSV serologies?
  Type-specific HSV serologies are very reasonable to send when someone makes this request, provided there is up-front education about what the results mean. Specifically, if someone tests positive for HSV-2, they are considered to have infection with this virus and could potentially transmit it even if they’ve never had symptoms. Furthermore, the positive test can’t indicate when someone acquired HSV-2, and most emphatically says nothing about from whom. And in this context (screening), forget the HSV IgM — it’s a lousy test , with tons of false positives.
• If someone can’t take doxycycline, and is allergic to penicillin, should I use azithromycin for treatment of Lyme?
  Azithromycin is less effective for Lyme than other treatments (doxycycline, amoxicillin, cefuroxime), so I’d only use azithromycin as a last resort. (Because who wants to use a less effective treatment for anything, especially Lyme. Shudder.) If we really scrutinize those antibiotic allergies, of course, we often find that it’s something very vague or isn’t an allergy at all. (“My mother told me I was allergic, so I guess I’m allergic,” says the 50-year-old man, who confesses he’s not even sure what “allergic” means.) More than 90% — some studies say way more — of those referred to allergists who have “penicillin allergy” turn out not to be allergic based on skin testing. In other words, I can’t imagine a setting where I’d have to use azithromycin for Lyme, though maybe a few doses until you sort out the allergy (or not) issue would be reasonable.
• A patient of mine had a positive PPD and a negative interferon gamma release assay (IGRA). She said she had a BCG as a child, and she has no symptoms. Which one is right?
  Can you hit the “rewind” button on your clinical encounters with her, and send only the IGRA and skip the PPD? This is one of the settings where IGRA is preferred, the patient with a BCG immunization history, as BCG will not trigger a positive IGRA and might do so for the skin test. That said, now that you have one positive and one negative, there is no way to determine whether the PPD is falsely positive due to the BCG, or the IGRA falsely negative since no test for latent TB is 100% sensitive. In other words, there’s no gold standard, so you’re sort of stuck making a clinical decision. So here’s what I do — in patients with low risk for TB exposure, go with the IGRA, and say the test is negative. If high risk, especially if contemplating something that increases the risk of TB activation (such as TNF-blockers), go with the positive PPD, and, presuming the CXR is negative, prescribe preventive therapy.
• I know that resistance to azithromycin has increased, but does this mean it actually is less effective than other antibiotics for treatment of community-acquired pneumonia?
  Way back when, before the existence of Z-paks and Zebra puppets and other brilliant azithromycin marketing, pneumococcal resistance to macrolide antibiotics was uncommon. However, the bug is now resistant to azithromycin around a third of the time in the US, with even higher rates in many other countries. While failure of treatment of otitis media with azithromycin due to resistance is well documented, the data with pneumonia are less clear — probably because the causes of pneumonia are more diverse, with a bunch caused by mycoplasma, some viral, some who-knows-what. Nonetheless, I’d be very concerned about using azithromycin as monotherapy for someone with fever, pleuritic pain, a lobar infiltrate, or other clinical features suggestive of bacterial pneumonia, and would definitely not rely on it alone for patients sick enough to be hospitalized.
• The drug-drug interaction between statins and HIV drugs is scary — which one do you recommend?
  You’re referring, of course, to the fact that metabolism of many statins is inhibited by ritonavir and cobicistat, which can lead to dangerously high statin levels. I’m a fan of using atorvastatin in this setting, and here’s why: it’s less dependent on cyp3A for metabolism than lovastatin or simvastatin, it’s more effective than pravastatin, the drug has been associated with all kinds of clinical benefits (practically every cardiologist on the planet is on it), and it’s generic. For your patients on ritonavir or cobicistat, just start with a low dose (10 mg daily) and titrate up as needed, stopping at 40 mg/day. If you want to face off with the Payor Police, pitavastatin (which has no cyp3A metabolism) is another reasonable option.
• When is next year’s course?
  Glad you asked!  October 14-16 — mark your calendars! A beautiful time of year to visit Boston.

Hey, our course this year was held between two notable fall holidays for some of you (me) — so enjoy this video. And I totally agree with the “gateway drug” analogy!