Rituximab kills your circulating B cells; vax timing is problematic. You still have a T cell response. Can you ask Daniel what he advises for the number of months after infusion to get a vax?
Dumbfounded and Dry in Dallas writes:
Dear Dr. Griffin,
This week at my Rheumatology appointment, I asked my doctor about a Plan and recommendations in case I am exposed to Covid and test positive.
The doctor first emphasized the importance of vaccination.
[I recently had my 4th dose of the Pfizer vaccine in mid-August 2022 along w/ Fluzone HD; primary Pfizer series was in February 2021, 3rd dose in October 2021.]
I have Not had Covid and Always take extra precautions (well fitted KN95 or N95), since I am at High Risk for complications of Covid, due to age (over 65yo) and long history of autoimmune rheumatic disease [Mixed Connective Tissue Disease (MCTD) with Severe Sicca Sd (secondary Sjogren’s)]. Currently, I don’t require treatment with any DMARDs or systemic corticosteroids. Cardiac, renal, and hepatic function are all good.
I then asked the doctor specifically about treatment with Paxlovid, in particular with regard to interactions with 2 of my medications: Pravastatin 80mg (moderate; decreases levels) and Evoxac (cevimeline) 30mg tid->qid (moderate; increases levels).
My doctor told me in no uncertain terms that: “Paxlovid ‘Rebound’ is worse than no treatment (symptom directed care only w/Tylenol, fluids, etc.)”; “all my patients, every single one, 100%, that were treated with Paxlovid had a Rebound”; “I’ve consulted with our ID docs here and they have advised against use of Paxlovid”; “I’ve never seen these Rebounds with (other better/longer studied antivirals like) Tamiflu”…
[Me: “but Dr., Rebound occurs in natural infections also.”]
…”Well, we’ll see if you’re hospitalized”… (?!!!).
Not One Word was said about the strong scientific evidence supporting the use of Paxlovid to prevent severe disease/hospitalization/death in High Risk patients (nor any suggested alternatives from the treatment summary list, if Paxlovid is contraindicated)!
Thank you so much for your time and all you do!
“Dumbfounded and Dry in Dallas”
_ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _ _
Warm regards to all of the TWIV team.
P.S. I’m a retired Pathologist (AP/CP, Hematopathology) and especially enjoy your Clinical Updates, Parasitology, and PusCasts. In my former life, I used to present a lecture titled “Bugs in Blood”. We saw lots of imported Malaria at Parkland and I had the opportunity to visit the CDC’s malaria branch. My first course in Virology was in 1976 as an undergraduate at Trinity University.
First, I’d like to thank you for your commitment to the weekly clinical updates. In the early days of the pandemic I relied on a similar weekly broadcast by an ID physician on a well known physician Facebook page. When she needed to step away from that role I was lost. How else was I going to get a concise, data driven, expertly curated update? Someone recommended TWIV and I have been listening loyally ever since.
I am a pediatrician and my struggle right now is monkey pox. Monkey pox in the middle of hand, foot, and mouth season. Monkey pox in the middle of impetigo season. Monkey pox in a population that likes to get the umbilicated lesions of molluscum. It feels like the universe playing a cruel joke on the pediatricians of the world. I have listened carefully to your updates and I hear you say clinicians need to be more suspicious and test more people with rashes because we are surely missing a large number of cases. I hear you saying that lesions do NOT need to all be in the same stage. That lesions may be papular or vesicular, or pustular. That we should not fail to test because our patient is not of the “right” demographic.
But here is my problem: I am 100% telemedicine. I work for an awesome telemedicine company that is all board certified pediatricians. We strive to provide the highest quality medical care in patients’ homes but we don’t hesitate to send them for in person care when medically indicated. I see a plethora of weird rashes on my screen everyday. My question is this: how do you suggest we determine which of those children need to seek in person care for testing? It does not seem feasible (or even necessary?) to send every kid with a rash in for an exam and testing. Several times I have even asked family to take their child in to be tested and the provider that sees them declines to test! They clearly aren’t TWIV listeners! I would love your input on how we can be sure the appropriate children get seen for testing without the undue burden of every child being sent for in person care.
Again, thank you for all you do.
Dear Drs Griffin and Racaniello,
I really enjoyed TWiV 973 with Emma Thomson regarding the pediatric hepatitis investigation. I always listen when I’m out running and just hope I can remember my questions long enough to write to you later!
I have a couple questions prompted by the discussion. Since Dr. Racaniello has spent a lifetime working on polio, perhaps he can handle the second one to lighten your load, Dr. Griffin? Here goes:
HLA and myocarditis following covid or vaccination – possible connection? Dr. Thomson mentioned the potential for an auto-immune response driving the unexplained ped hepatitis. The current theory is AAV2 plus a unique class II HLA (DRB1*04:01) plus HAdv caused the hepatitis. Given the potential role of HLA here, is it possible that a specific HLA type could also drive the risk for the rare hyperinflammatory myocarditis following either covid or vaccination in young males (and some females)? Dr. Thomson mentioned that some adeno gene therapy results in fulminant hepatitis (rarely but it happens). She suggested that researchers could look for a specific HLA signature for those cases as well to see if here is a connection. Is anyone looking at myocarditis and HLA?
Polio booster for those who received OPV as kids – I was born in 1971 and as far as I can tell, I got three doses of OPV. This created mucosal immunity, and potentially long-lived immune memory, but given that OPV is a mucosal vaccine, do we know this for sure? Did it create temporary mucosal immunity? Does the attenuated virus need to cross the intestinal mucosa to create systemic immunity? Do we know that it does this? I am wondering if it makes sense for anyone born before 2000 when we switched to IPV to get one dose of IPV at this juncture? I’m sure we’ve been living with vaccine-derived polio in the environment for years, so I’ve probably gotten naturally boosted, but the scientist in me wants to know what we know 😊
Thank you very much for your investment in your listeners and providing such an incredible forum for learning. I share the pod often!
Alli Krug, MPH