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June 30th, 2019

Antibiotic Development Is Broken, Brothers in ID Practice, and This Year’s Winner of the ID-Related Social Media Award

“I do not like thunderstorms,” said every dog, ever.

I am currently rounding on the inpatient ID service, the new ID fellows arrive shortly, and Louie needs intensive doggy psychotherapy after yesterday’s strong thunderstorms here in Boston.

Busy times!

As a result, today’s post has no unifying theme. But what it lacks in cohesiveness it more than compensates in value, as here are three highly interesting ID-related items for your perusal.

1. Antibiotic development is broken — and how to fix it. 

This fascinating perspective in the New England Journal of Medicine focuses on the problems with our current model of antibiotic drug development. Why are for-profit companies abandoning antibiotic research? If antibiotic resistance is such a problem, why isn’t this “market opportunity” giving us new and better antibiotics?

The absolute number of infections caused by each type of resistant bacterium is relatively small. Each newly approved antibiotic thus captures an ever-shrinking share of an increasingly splintered market — a problem that will only worsen over time. Short treatment durations and a coordinated program of antibiotic stewardship also contribute to low sales.

The authors’ proposed solution is to fund nonprofit organizations to develop antibiotics. Unlike private companies, they would not be beholden to shareholders to generate rapid profits. Relatively small revenues for a large private company — tens of millions of dollars annually — would, for a nonprofit, be a substantial win, and a chance to reinvest this money into further research.

Now they just have to convince some entity — government? philanthropy? — to invest the seed money to get this started.

A big hurdle, yes, but at least it’s a path forward.

2.  Two brothers chat about being in ID practice — together.

For many academic ID fellowships, the intense first year of clinical care is followed by years of research training, with relatively little clinical work occasionally sprinkled in.

Research fellows might have a once-weekly half-day in clinic, or an occasional weekend seeing consults.

That’s the pathway Dr. Steve Threlkeld followed here in Boston when I first knew him as a brilliant ID fellow. (I was just starting my first faculty job.) However, he soon came to the realization that his true love was patient care, not research.

So he did something novel — he joined his brother Mike’s private ID practice in Memphis, Tennessee.

Steve and Mike chatted with me on this OFID podcast about private practice ID, what it has in common with academic ID and what’s different, how to be a blue-leaning clinician in a red-leaning state, and the unique opportunities and challenges of being the only sibling-owned private ID practice in the universe.

OK, someone contact me if I’m wrong about that last part.

Available also on iTunes, Overcast, and soon other podcast places.

3. This Year’s Winner of ID-Related Social Media Award.

I don’t know Dr. Philip Lee, but if there’s an Academy Award for ID content on social media, he’s the unequivocal 2019 winner — and we’re only halfway through the year.

Click on this Twitter thread for the incontrovertible proof:

And fear not! One-a-Day ID Learning Units are coming soon.

June 23rd, 2019

Advice to Incoming Subspecialty Fellows — Don’t Underestimate or Belittle Your Interns and Residents

An Unsmart Bulb (Photo by Ashes Sitoula on Unsplash)

Around a million years ago, early during the first year of my ID fellowship, a medical intern consulted me about an elderly patient with a urinary tract infection.

Me:  Does she have a catheter?

Intern: I don’t know.

Me: Has she been admitted before with a UTI? Any cultures?

Intern:  I think so — wait, I’m not sure. Let me check her chart.

Me (testy):  Nevermind — we’ll come by and see her. (Slams down phone.)

It might have been a busy day for me. Or a late afternoon consult. For whatever reason, I was feeling pretty fried.

Over the next week, I channeled my frustration with this exchange by citing it several times as an example of the general cluelessness of the current interns and residents — house staff at the very fine hospital that kindly had accepted me to their fellowship.

But wait. That can’t be right.

Indeed, let the record show that I was emphatically wrong — the interns and residents during my fellowship were outstanding. This particular intern had a PhD in immunology and was just getting started as a doctor. No surprise that not all the details were immediately at her fingertips.

I bring this up today because right now, in many teaching hospitals, the interns have already begun, and the subspecialty fellows are waiting in the wings. Most start in the next week or so.

It’s therefore a perfect time to take on this commonly held (and sometimes, alas, openly voiced) opinion by some subspecialty fellows as they grow into their new roles:

These interns and residents are weak!

There are numerous triggers to this ungenerous thought. Most involve consults deemed “inappropriate” by the subspecialty fellow, for a variety of reasons:

  1. Consult called without having complete information. (My example.)
  2. Consult called without asking the right question. (How can they always know the right question if they need help on a case?)
  3. Consult called “too early” in the admission, without the house staff doing the full initial work-up.
  4. Consult called “too late” in the admission, with the house staff mismanaging the case before calling the consult. (Look how the residents can’t win here, with both #3 and #4 suggesting some magical precise correct time for calling a consult.)
  5. Consult called too late in the day.
  6. Consult called by the medical student, which is deemed insulting to the newly minted fellow. (Oh come on.)
  7. Consult called for something the fellow would have handled without a consult when they were residents. 

I bolded this last one since it’s probably the most common example. (Junior faculty sometimes succumb to this one as well. It’s an early form of, “In my day …”) What weakness!

So let me emphasize, again, by noting, emphatically, that this perception is a total illusion.

There is zero evidence that interns and residents are weaker, less thoughtful about patient care, and less thorough than we were during residency, whenever and wherever that may have been.

How do I know? Because there’s a control group — those who do their fellowships in the same hospital as their residency. These fellows sometimes cite weakness in residents who were, until very recently, their colleagues. And folks, it’s literally impossible that suddenly and unexpectedly, the entire house staff regressed, losing all their clinical skills when said fellow graduated.

So what’s behind this negative line of thought? And what can we do to correct it?

To answer these questions, a few months ago I posted the following:

Encouragingly, many responded that they feel that today’s house staff are wonderful.

But some acknowledged that the phenomenon exists, and offered various thoughts about its origins. I like this response, from ID colleague Dr. Andrej Spec (who may be better known on ID Twitter as @FungalDoc):

Nostalgia. That, and as we get better, it becomes easier to see the mistakes that we were oblivious to previously. The solution is to keep remembering the times we made mistakes. So that we put ourselves in perspective.

Or, from a rheumatologist (@Doctorkuch):

Thinking that everything you know now, you knew then (false!). #constantlylearning

These comments get right to the heart of the problem. We spend the years of residency honing our craft, becoming better at what we do through clinical experience, teaching conferences, and reading. By the time we are in our last year of residency, there’s a wonderful sense of mastery — that’s the good part.

The bad part is that we may unfairly expect similar mastery from our junior trainees.

So the next time we feel like criticizing an intern or resident for not having all the information, or not consulting at the right time, or calling a consult on a case we think we would have handled ourselves without a consult — remember what it was like to start your training.

And remember, this doctoring thing is hard — a lifelong exercise in learning, and trying to get better.

It may not be quite as difficult as getting this “smart” light bulb to work, but it’s close.

So how many ID docs does it take to change a light bulb?

June 16th, 2019

On Father’s Day, a Tribute to a Father Who Isn’t Allowed to Celebrate Father’s Day

Part 1. My Father and How I Became a Doctor

I became a doctor with encouragement from my father.

Wait, let me rephrase that to capture what happened more accurately.

I became a doctor with a fair amount of pressure from my father.

Fresh off an adventure abroad, in my early 20s, I had all kinds of pretentious ambitions for my future. 

Screenwriter. Comedy writer for a hit television series. Stand-up comedian. Fiction writer, periodically tossing off stories to The New Yorker while writing The Great American Novel. 

Mind you, I had no idea how to make these aspirations actually happen. My writing output to that point included a few comedy pieces for the Harvard Lampoon (most of them in hindsight rather unfunny), and a piece in the Boston Phoenix (may it R.I.P.) describing my experience in a yogurt taste-test. 

“Go to medical school,” said my father. “You can do anything once you have your degree.”

Absent an alternative plan — and trust me, there was no alternative plan — who was I to argue?

Spoiler alert — he was right.

Part 2. My Father, and How He Became a Doctor

My father comes from a family of doctors — and that’s understating it. His father, his uncle, his cousin, his brother — all doctors. His mother was a nurse, but probably would have been a doctor if Jewish women could go to medical school in Moscow in the early 20th century.

(His sister also married a doctor. In hindsight, what choice did she have?)

Medical pedigree notwithstanding, my father’s path to his MD was not easy. Skipped ahead twice in grade school because of his precocious reading skills, he entered college at age 15. 

Unsurprisingly, he wasn’t ready for college life, and struggled socially and academically. Lonely, homesick, and with mediocre grades, he dreaded his own father’s visit during freshman year. Apparently, my grandfather didn’t take well to academic underperformance in his children.

But that visit never came. On the way to see my father in college, my grandparents were in a bad car accident. Both were severely injured, my grandfather didn’t survive.

It’s very hard to get inside the head of anyone, but imagine yourself at a university at age 15. You’re way too young, and already not doing well. And then this happens — your father dies, your mother injured. There are a million ways this story could go, most of them not good.

But my father’s response, amazingly, was to grow up — and to grow up fast. He doubled-down on his studies; he made friends. He applied to medical school — close to home so he could support his mother — and was accepted.

After residencies in both internal medicine and psychiatry, he became a practicing psychiatrist, and an esteemed teacher, jobs he truly loves.

I’ve always wondered if his college experience drove his choice of specialty, his desire to make something positive of the lessons learned enduring that trauma.

But that’s just the psychiatrist’s son speaking.

Part 3. My Father

Having married the unsentimental, smartest person in the world, my father can’t celebrate Father’s Day.

But I can do it for him, by listing here his best character traits:

Enthusiasm. The joke in my family is that my father will eat or drink something objectively mundane — a Ritz cracker, a glass of water — and stop conversation by saying, “This is the best water.” But the great thing about this enthusiasm is that it applies up and down the spectrum of experience, from those Ritz crackers and glasses of water to Chateau Latour, German expressionist art, 19th Century American literature, and tropical fish. (That last one ended badly, at least for the fish.) And as far as I’m concerned, we can’t have too many enthusiasts in the world — these are the people who brighten up the room when they enter.

A genuine interest in others. People invited to a dinner or other social event usually stick to the people they know, the familiar faces — it’s the easy route. But my father has always viewed the newcomers or strangers at these gatherings as fascinating sources of new life stories. He is deeply interested in others, and as a result is great company. And when you think about it for two seconds, it’s the perfect character trait for a psychiatrist. No wonder he loves his work, and is so good at it.

No detail is too small. There are “big picture” people out there who can’t be bothered with the small details. Then there are those who, on finding a topic they find interesting, can’t learn enough. My father is clearly in the latter camp, a voracious reader who delves deeply into a subject until he could practically write a PhD dissertation on it. You know that tower of books everyone has by their bedside? My father must be one of the few people on the planet actually to have read his entire stack.

Supportive of the people he loves. As I wrote last month, my mother went to graduate school and back to work when I was 11, leaving us three kids at home. (Sob again, but I’ve gotten over it.) In that Mad Men era, not all men would have supported this move, but my father did just the opposite — he became my mother’s biggest fan, constantly telling us and others how successful my mother had become. Let the record show he’s had the same attitude to all our personal and professional decisions — and in hindsight I believe he would have been fine had I not attended medical school, provided I was trying to do something.

So Happy Father’s Day, Dad! And I agree, those Ritz Crackers are great.

(Back to our usual Infectious Diseases programming next week.)

 

 

June 9th, 2019

Is It Safe to Alter the CCR5 Receptor? And How Will This Influence HIV Cure Studies?

The HIV cure effort suffered a potential setback this week, as researchers reported an association between having two copies of the CCR5-∆32 mutation and shorter survival.

(Quick reminder — the CCR5 receptor is required for most HIV strains to enter target cells. People homozygous for the CCR5-∆32 mutation are almost completely protected from contracting HIV.)

By evaluating over 400,000 individuals in a British registry that included genetic information including CCR5 status, the investigators compared the prevalence of CCR5-∆32 homozygosity among people between the ages of 41 and 76. Over time, the prevalence substantially declined, consistent with a 21% increase in all-cause mortality compared to those with either no ∆32 mutation, or heterozygotes.

The authors postulate that this excess mortality may be driven by the reported worse outcomes among those with ∆32 homozygosity who develop influenza or other infectious diseases. Since most influenza deaths occur in older people, this could explain why earlier studies of populations with ∆32 reported them to be healthy.

(By contrast, it might be that historical epidemic infections of childhood and young adults — smallpox, plague, dysentery among them — could have selected for ∆32 many centuries ago, with the result that approximately 10% of people of European heritage carry at least one mutation.)

As noted in the excellent editorial accompanying the new study, the findings should give researchers pause before making permanent changes to the host genome:

The most important point raised by the current publication is that considerable risk comes with generating mutations in the genome of human beings, no matter how obvious the benefit that those mutations offer.

I’d amplify this concern by noting that individuals born with two CCR5-∆32 mutations — who grow up with it — may differ from those in whom CCR5 is altered during adulthood. We simply don’t know whether people who acquire it late in life will be better or worse off than those born with the mutation.

So why is this recent study relevant to curing HIV? Considerable research has already been done on this receptor related to HIV cure:

  • Only two people — the “Berlin” and the “London” patients — appear to have been cured of HIV. Both underwent stem cell (bone marrow) transplantation using donor cells harvested from people homozygous for the CCR5-∆32 mutation. The indications for the transplants were refractory leukemia and lymphoma for the Berlin and London patients, respectively. Both are off antiretroviral therapy with no viral rebound, and no virus detected either in blood or tissues.
  • Zinc-finger nucleases successfully excised the CCR5 receptor from some cells of people with HIV. This small study (n=12) was a first step in trying to engineer something analogous to the Berlin and London patients without the risk of stem cell transplantation.
  • A scientist reported that he used CRISPR-Cas9 genome-editing to disable the CCR5 gene of two babies. The announcement was hugely controversial, as there was zero medical justification for this experiment on these children born to an HIV-negative mother. However, the cases underscore the feasibility of altering a person’s genome using the powerful tools available today.
  • There is substantial ongoing research in coreceptor modification to prevent or cure HIV. In the linked review, it states “there are multiple clinical trials underway to evaluate how efficacious this therapy can be in human patients.”

Clinicians not actively caring for people with HIV might wonder whether the risks are worth it — isn’t HIV therapy now safe and all but 100% effective?

The reality is that there’s tremendous interest in HIV cure, especially among those with HIV, risks notwithstanding.

So great is this interest that many of us have even been asked by our patients whether they can have a bone marrow transplant:

That these questions mostly come from people doing quite well on their HIV therapy signals a powerful patient-driven motivation for HIV cure — one that sadly seems more related to ongoing HIV stigma than to the medical issues of current HIV treatment.

Which is why it’s not so clear that this latest research finding should dampen the pursuit of CCR5-driven cure strategies.

Would a lifetime 21% increase in all-cause mortality be an acceptable trade-off for a person with HIV who is deeply invested in HIV cure?

And who will get to decide?

June 2nd, 2019

A Highly Subjective Guide to Clinically Important Infections That Have Changed Names

Why do many clinically important microorganisms change names?

They haven’t married and taken their spouse’s name or gone to Hollywood and adopted a stage name.

Instead, through the tireless work of microbiologists, taxonomists, and geneticists, they have undergone sufficient reclassification so that their old name just doesn’t make sense anymore.

Or more graphically:

What we gain in accuracy, alas, is accompanied by an increase in confusion, and a heavy taxation on our memory reserves. Even we ID types can barely keep the names straight; imagine how non-ID clinicians feel?

Our colleagues in clinical microbiology recognize this problem — really they do. But spend a little time reading Name Changes for Fungi of Medical Importance, and pretty soon you get deep into the weeds with no available machete to hack your way out. How’s this for an example?

The Ajellomycetaceae contains the teleomorph species Ajellomyces dermatitidis, Ajellomyces capsulatus, and Ajellomyces duboisii, the anamorphs of which are the genera Blastomyces and Histoplasma. The Ajellomycetaceae also contains some genera that have no known teleomorphs, including Paracoccidioides and the newly described genus Emergomyces.

Well, I’m sure glad we cleared that up!

So if you’re looking for an in-depth, detailed review of some recent name changes, take a look at the references section in this editorial, kindly sent to me by ID doctor and medical microbiologist Kim Henson. Warning — they are not for the faint of heart!

But here is a more subjective list of name changes that I’ve weathered over the years, along with a few miscellaneous comments:

Clostridium difficile became Clostridioides difficile. This recent change will take a while to get used to, as it’s such a common infection that Clostridium is pretty hardwired in our neural circuits. Also, the ubiquitous abbreviation “C. diff” still works fine, so there’s not much motivation to learn how to write, or to say, Clostridioides — in fact, I just had to teach my spell checker not to flag it.

Pneumocystis carinii became Pneumocystis jirovecii. It’s now quite clear that pneumocystis is a fungus (and not a protozoan, as originally thought). It’s also widely accepted (finally) that the species encountered in corticosteroid-treated rats is different from the one infecting humans — the rat gets Pneumocystis carinii, and humans Pneumocystis jirovecii. What’s still a matter of substantial debate is how to abbreviate the pneumonia caused by Pneumocystis jirovecii, as demonstrated by this hotly-contested poll:

Haemophilus aphrophilus became Aggregatibacter aphrophilus. I attended a meeting a few years back which included several other ID geeks like myself, and we were discussing various aspects of our work. One mentioned she had just seen a case of endocarditis due to the wonderfully named Cardiobacterium hominis, which is of course the “C” in the HACEK group of organisms. I then mentioned that Haemophilus aphrophilus had been renamed Aggregatibacter aphrophilus — and suddenly there was a palpable sadness in the room. How could anyone be so heartless as to change the name of this whimsical and mellifluous-sounding microbe? Such a deep injustice, we’re still in mourning.

Streptococcus milleri became Streptococcus anginosus, intermedius, and constellatus. The name change to these abscess-forming streptococcal infections happened so long ago that many youngsters out there might not have even heard of Strep milleri. But trust me, it was tricky enough that for a while these three species were called “Strep milleri group” to help bridge the pain; now they’re called “Streptococcus anginosus group,” and milleri is no more. For the record, streptococcal taxonomy is mega-complicated and confusing — but if you think that is bad, wait until you start getting into the fungi!

Pseudallescheria boydii became Scedosporium boydii. Big improvement — Scedosporium is a wonderful word, replacing the strange and unspellable Pseudallescheria. I remember attending an ID conference during medical school that had two cases, both of which included details that caused me great confusion. The first was a streptococcal endocarditis case complicated by a “mycotic aneurysm.” Aren’t fungal infections called “mycoses”? So how did the strep cause a fungal complication — isn’t it a bacterial infection? (Turns out any infectious aneurysm is called “mycotic” — who knew?) The second was a post-traumatic fungal infection due to Pseudallescheria boydii, which I heard as “Pseudo …” which of course means “not genuine” or “sham” — you know, like “pseudo-intellectual.” So, if Pseudallescheria is the fake one, what’s the real one? I guess the real one is Scedosporium. Or not — fungal taxonomy is a total mess, right Andrej?

I am a cutie-bacterium.

Propionibacterium acnes became Cutibacterium acnes. Of all the recent name changes, this is easily my favorite! I have already thoroughly embraced this new name, and even pedantically correct people stuck on the old one — making me excellent company on rounds. Maybe Cutibacterium will give greater attention to this under-appreciated pathogen, infamous for causing prosthetic joint (especially shoulder) and neurosurgical infections. And why do I like it? First, Propionibacterium is a devil to say, good riddance. Second, Cutibacterium is adorable, especially if you pronounce it “Cutie-bacterium.”

Xanthomonas maltophilia became Stenotrophomonas maltophilia. This problematic, highly antibiotic-resistant gram-negative rod changed names long ago — so as with Streptococcus milleri, many might not even have heard of Xanthomonas. I first learned about this bug when imipenem had just been FDA-approved (yes, I’m that old), as it is one of the rare gram negatives intrinsically resistant to carbapenems. Two other points worth emphasizing:  1) Xanthomonas sounds very cool, could almost be the name of a science fiction series, “The Galactic Empires of Xanthomonas”; 2) Stenotrophomonas is real mouthful. Takes a while to learn how to say that comfortably — which is why, to many cystic fibrosis clinicians and patients, it’s just known as “steno.”

Enterobacter aerogenes became Klebsiella aerogenes. C’mon, that’s just mean, flipping one enteric gram-negative rod name to another. I suppose we’ll get used to it eventually, grumble grumble.

Rochalimaea henselae became Bartonella henselae. These agents of cat scratch disease, endocarditis, bacillary angiomatosis, and peliosis hepatis haven’t been Rochalimaea for many years. But my friend Joel Gallant used to call my other friend Rochelle Walensky “Rochalimaea” long ago when they were at Johns Hopkins together — which just goes to show that we ID doctors have a very strange sense of humor, one that may be difficult to explain to others.

Diphyllobothrium latum became Dibothriocephalus latus. This fish tapeworm of gefilte fish fame wasn’t easy to learn in medical school, so I’m going to resist this change for as long as possible. Note that even CDC hasn’t updated their page, taxonomy notwithstanding, so I appear to be on safe ground holding out at least for now. Dibothriocephalus indeed, hmmph. Try saying that three times fast.

Penicillium marneffei became Talaromyces marneffei. This dimorphic fungus, endemic to Southeast Asia, causes disseminated disease in severely immunocompromised hosts. I always liked that we had a clinically important fungus that included the name Penicillium, reminding us of the source of our first beta lactam antibiotic. Oh well. This Talaromyces name is taking a while to get used to, probably because it’s not a common infection here.

Pseudomonas cepacia became Burkholderia cepacia. It hasn’t been Pseudomonas cepacia for ages. But did you know that Burkholderia cepacia is really at least two different species, Burkholderia multivorans and Burkholderia cenocepacia? Isn’t microbiology fun?

Streptococcus bovis became Streptococcus gallolyticus — and a whole host of other things. Medical school curricula indelibly impart certain ID facts to every student — three of them are 1) daptomycin is inactivated by lung surfactant; 2) listeria and its various dietary associations; and 3) endocarditis due to Streptococcus bovis should prompt a look for colon cancer. However, they haven’t yet gotten around to updating the species name, perhaps because hardly anyone remembers it. And did I mention that streptococcal taxonomy is confusing, irrational, and complicated? Sure I did, many times — and further reviewed the whole clinical world of clinical streptococcal infections here.

And last, but not least …

Ixodes dammini became Ixodes scapularis. Hey, no fair — I have enough trouble with microorganism taxonomy, do I have to start keeping track of insects arthropods too? All I know is that Gustave Dammin was an esteemed pathologist here at the Brigham for many years, and studied both Lyme Disease and babesiosis. Which begs the question — is it an honor, or a curse, to have such a nasty little critter named after you? Let the debate begin.

Any other name changes that deserve highlighting?

May 27th, 2019

A Day in the Life of a Malaria Diagnosis “Lab” — with Apologies to Twitter’s “Thoughts of Dog”

Scene: A quiet morning, somewhere in sub-Saharan Africa. A few roosters crow in the distance. A black Labrador Retriever slowly rouses herself from sleep.

ah. nice long nighttime snoozle. my favorite thing. ending soon.

but many favorite things. partial list. i’m good with lists.

1. belly rub.
c. peanut butter.
4: stuffed toy lamb, with squeak. though missing ear now. because we played too much.
7. tennis ball left out in park. for weeks. better after warm rain. and other doggos chew.
g. last but should be first. you.

list could be longer. but hear sound of human. half open eyes. no one here yet.

back to snoozetown? not quite.

hear human sound again, coming down steps. now he’s on ground. with me. eye to eye.

nice pet behind ears. hmmm. but one ear left inside out. that’s ok. i forgive easy.

Who’s a good girl?

silly question. of course. i am. but he asks this a lot. so i tell him. i’m awesome.

stretch legs. long yawn.

Time for work! Are you ready?

not work to me. my new favorite game. there are treats. simple rules. another list.

1. take socks from small humans.
(they smell delicious. especially socks of teenage boy humans. after playing football in African heat. yum.)
d. sniff socks of small humans.
7. some smell different. sad.

Work has shown that people infected with malaria parasites produce a body odour that is detected by mosquitoes, which results in malaria mosquitoes preferentially feeding on asymptomatic, malaria-infected individuals.

g. tell human which sock is sad. sometimes i just stay. sometimes bork.
5. best part. crunchy treat.

i could do this all day. especially if it helps small human. and if there are treats.

watch.

(Inspired by a recently published paper, a brilliant Twitter feed (“only” 2.6 million followers), and h/t Rich Davis for the clever pun in the title.) 

May 19th, 2019

CDC Does Us a Huge Favor by Advising Against Annual Screening of Healthcare Workers for Latent TB

There are definitely things we do in medicine just because that’s how we’ve always done them.

Among these evidence-free actions, we can include yearly screening for latent TB infection (LTBI) in all healthcare workers

If we carefully examine the rationale behind this practice — as this thorough review nicely does — one would be hard-pressed to find any other reason for this time- and labor-intensive annual flog.

Why does annual LTBI screening make no sense?

  • Evidence from clinical studies that this strategy reduces TB incidence in US healthcare workers? Zero.
  • Incidence of TB in the US over the past several decades? Steadily down, now at historic lows.
  • Conversion of tuberculin skin tests (TSTs) or interferon gamma release assays (IGRAs) among healthcare workers without an obvious TB exposure? Vanishingly rare.
  • The testing is easy-to-do, highly accurate, and inexpensive? No to all.

Indeed, that’s why the new recommendation, from a joint effort by the National Tuberculosis Controllers Association and CDC, is so welcome:

In the absence of known exposure or evidence of ongoing TB transmission, U.S. health care personnel … without LTBI should not undergo routine serial TB screening or testing at any interval after baseline (e.g., annually).

Extra points for clarity!

Encouragingly, all the ID and TB specialists I’ve queried lend their enthusiastic support to this change in policy. And this includes that extremely careful bunch who specialize in infection control.

Now we just need to turn this policy into action — which can start by dismantling serial testing requirements in hospitals and other healthcare facilities nationally.

Think what we can do with all that freed-up time!

Maybe even correct spelling errors on fax cover sheets.

 

May 12th, 2019

On Mother’s Day, a Tribute to a Mother Who Doesn’t Celebrate Mother’s Day

My siblings and I are pretty lucky, because our mother may be the smartest person in the world.

Let me reassure you that this is not just our biased opinion. Everyone who knows her well thinks the same thing — including my wife, who told me today, on Mother’s Day, that my Mom’s remarkable brainpower should be the focus of this profile.

(Not that my mother has any time for Mother’s Day. Unsentimental in the extreme, she disparages such holidays as manipulative.)

I first had an inkling of her intellectual superpower when, after underperforming on an important test in middle school due to numerous trivial distractions (baseball, model rockets, general silliness), I received some stern comments of disapproval from my father.

When my mother rushed to my defense, he countered as follows:

Look, no one is as smart as your mother. Most people have to study to do well in school.

I assure you this was said without the slightest exaggeration.

The first person in her family to attend college, she graduated early then followed the path of many women of her generation — married at 21, done having three children by 26 (!), she could have continued down this path of domesticity without anyone even noticing. 

That’s what most women did. 

But she went back to get a graduate degree (abandoning little me at home, sob), then started a successful career as a food writer, continuing to work as a journalist (Newsday, New York Daily News, Bon Appetit) for many years. In 2000, as the internet took off, she won a James Beard award for Best Internet Writing.

As this point, I know what you’re thinking — how could a food writer be the smartest person in the world? Surely that honor must go to a neuroscientist, a mathematician, a scholar of ancient histories, some super-linguist who speaks 20 languages.

Well, here are a few examples:

  • Technology. Most people my mother’s age really don’t do well with new technology — remember the flashing clock on the VCR? But my mother was an early adopter of computers, owner of one of the first word processors — does this Wang 2200 look familiar to anyone? Although she’s not writing code or macros, she effortlessly uses computers and cell phones as tools to get things done — which is probably what most of us should do rather than obsess over the latest gadget.
  • Breadth. My mother’s expertise extends way beyond food — literature, art, music, movies, theater, current events, all seem to be in her domain. My daughter is constantly amazed at how her grandmother — my mother — gets most pop culture references. During a video interview I did with many family members at the turn of the century, I asked her what she believed to be the greatest unheralded work of art. She paused briefly and said:  “Eugene Onegin — and that’s because I just read the novel, saw the opera, and rented the movie.”
  • Math and science. Though she has degrees in art history and English literature, I can talk to her about advances in medicine and science without the slightest need to bring down the level. It’s particularly remarkable how quickly she grasps key principles of clinical research and epidemiology, concepts that many of us spend years mastering — examples include confounding, sensitivity and specificity, lead-time bias, the potential harms of excessive screening. Explain these principles once, she gets them forever.

Not included in the above Mother’s Day (sorry Mom!) tribute is that she’s been consistently supportive of my brother, sister, and me in all our life and career decisions. When I ditched a cardiology fellowship for the much less remunerative — and even stigmatized — specialty of infectious diseases, she never once even hinted at displeasure. 

So thank you, Dad, for choosing this very smart and wonderful person to be our mother.

She’s so special that I can even forgive her these two transgressions, both of which stem from this aforementioned lack of sentimentality:

  • She threw away my baseball cards when I went to college. Why should anyone save these boring pieces of cardboard?
  • She doesn’t get this whole dog thing. After all, they’re just animals.

Hey Mom, Louie forgives you, too.

May 5th, 2019

Latest Published Study on HIV Treatment as Prevention Is Déjà Vu All Over Again, But Some News Is So Good It Never Gets Old

Yogi Berra, putative author of “déjà vu all over again” and other profundities.

Even if you’re not an ID or HIV specialist, there’s an excellent chance you’ve heard of the PARTNER2 study, just published in The Lancet.

If not, the title could not be more descriptive:

Risk of HIV transmission through condomless sex in serodifferent gay couples with the HIV-positive partner taking suppressive antiretroviral therapy

And, in case you’ve just awoken from a Rumpelstiltskin Rip Van Winkle-length sleep, here are the results:

The risk is essentially zero.

This is far from the first time we’ve heard this information, either from this or other (HPTN 052, Opposites Attract) studies.

The formal publication of PARTNER2 therefore has a déjà vu quality to it, one which prompted Myles Helfand, the indefatigable and entertaining Executive Editor of the terrific HIV resource TheBody, to post the following:

“Breaking” indeed. Ha. To Myles, and to many of us, this is old news. The publication of the paper after years of comparable findings from this and other studies may seem anticlimactic, no big deal.

He’d no doubt cite that even this particular study was presented first at the AIDS 2018 conference last summer in Amsterdam. That’s over 8 months ago! Ancient history!

But here’s another take from Claire Farel, an ID doctor from the University of North Carolina (and, full disclosure, a wonderful graduate of our ID fellowship program):

(For those not in our field, that “U=U” stands for “Undetectable = untransmittable.”)

First, I am in complete agreement that telling people with HIV that their treatment prevents viral transmission is a “gift,” leading to profound and anxiety-relieving responses. It’s just as good as informing patients that if they take their HIV meds, they will not die of AIDS — and both pieces of information are equally true.

Conveying this information elicits such relief that yes, tears of happiness are often part of the mix, if you’re wondering about that Kleenex reference.

Second, the publication of a study in a peer-reviewed journal still lends far greater authenticity to scientific data than conference presentations or abstracts. This is particularly true when the journal publishing the paper is a prestigious one, such as The Lancet.

(I have cleared it with the Editorial Office that we’re allowed here at NEJM Journal Watch to write that The Lancet is prestigious. Note I didn’t say MOST prestigious.)

Don’t get me wrong — I agree that conference presentations play a critical role in rapidly getting important new data into the public domain. But there’s still room for distribution the old-fashioned way, in a journal, which is why I posted both Myles’s and Claire’s responses to this publication.

Before we leave this study, we must linger for a moment on the most unintentionally amusing sentence from PARTNER2.

It’s this:

In total, couples reported having condomless anal sex approximately 76,088 times during eligible couple-years of follow-up.

Something about the precision of that estimate — are they sure it wasn’t 76,089? — makes me smile every time.

April 28th, 2019

Even More Fun with Old Medical Images

Loyal readers of this site might note that we periodically stray from incisive, topical coverage of our exciting field of Infectious Diseases, and venture off into subjects that may or may not be ID-related.

And good news for fans of this approach, because today it’s time to release our third episode of Fun with Old Medical Images

Why today? The simple answer is that this feature appears on this site during certain holidays on the pre-Columbian Mesoamerica calendar, a calendar widely used by the Maya for centuries. I find it an excellent resource when trying to solve difficult scheduling problems.

As a reminder, here’s how Fun with Old Medical Images works:  I choose an old image from the vast National Library of Medicine collection. Then, I make up a caption and provide a brief commentary.

All this is done for you free of charge — guaranteed without hidden registration or subscription fees.

Off we go, #1:

Though he accidentally left his white hat at home, Bailey was kindly still allowed by the nurses to pose for the team photo.

What a generous group! And you go, Bailey — such a good boy, sitting so still. And those pointy, asymmetric ears are adorable.

Let’s move right on to #2, into the OR:

Even after Dr. Griswold returned from his studies in Vienna with the latest techniques in sinus surgery, his patients continued to feel some pre-op apprehension.

Not surprisingly! And I’m growing more dubious about Dr. Griswold’s Viennese studies every day. 

#3 finds us in a recreational pool for frogs:

Freddy the Frog loved the hoop dive game so much that he continued to play long after his friend had grown tired and gone home.

Say one thing for Freddy — he sure is fit! But doesn’t he know it’s time for dinner?

And in case you’re wondering, these two images are an old test for strabismus. Somehow.

Speaking of pairs, I bring you two trendy guys for #4:

The latest dance craze — don a bodysuit, shave your head, and pretend you have no neck. Fun for all!

I hear everyone’s been doing it — The Naked Bald No-Neck Strut. Kids today and their crazy dances!

Heading to #5, with a big challenge in our appearance-obsessed, digital era:

Despite generous use of Photoshop, there was only so much Connor could do to improve his Tinder profile picture.

Alas, Connor — dates will have to learn not to judge a book by its cover, your skilled Photoshop efforts notwithstanding.

Finishing with an even half-dozen, here’s #6, which brings us back to familiar ID territory:

“Head down the left mainstem bronchus and turn LEFT — you can’t miss me.”

Oh, you silly tuberculosis bacillus — we know how to find you!

So that wraps up today’s tour of Even More Old Medical Images. Please join us next time when we’ll be back with our usual erudite content.

But until then, enjoy this:

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.