During my ID fellowship, Robert (Bob) Rubin was my very first attending. It was the transplant service in July, and Bob and I would round with the surgeons each morning.
Early each morning. That was part of it. We needed to be there with them, before they disappeared to the OR. If we weren’t there, he explained, we might as well be invisible — they wouldn’t trust us.
This was one of Bob’s many strengths as an ID doctor, his ability to connect with our surgical colleagues. So many of us timidly leave our consult notes in the patient chart, hoping the surgical team will listen to our recommendations.
No such passivity from Bob. He spoke right to them.
It didn’t hurt that he had extraordinary clinical instincts, and was one of the most naturally intuitive clinicians I’ve ever worked with. His assessments were lightning quick, an especially notable trait in a specialty often prone to (endless) rumination and equivocation.
And, like a good surgeon, Bob was direct about everything. He knew what he knew — and told you — and knew what he didn’t know, and acknowledged this too. No hedging.
He was also by nature an active doer rather than a passive observer. In clinical care, he frequently used war and sports metaphors. No surprise — surgeons really like an ID doctor like this!
Bob is best known for his contributions in transplant infectious diseases, a field he practically created. Many of the concepts we now take for granted as accepted standard of care either originated with him or were greatly amplified by his skillful and prolific teaching.
Here are a few of these key principles (with thanks to Jay Fishman and Francisco Marty for contributing):
- The predictable timeline after transplant for the occurrence of certain opportunistic infections.
- The “net state of immunosuppression”, which is the sum of pharmacologic, nutritional, and anatomic factors contributing to infectious risk.
- The compromised host as the “sentinel chicken” (a.k.a. “canary in the coal mine”) for environmental hazards.
- The “therapeutic prescription” — he wrote: “The close linkage of infection with the nature and intensity of the immunosuppressive program has led to the concept of the therapeutic prescription. This has two components: an immunosuppressive one to prevent or treat rejection and GVHD, and an antimicrobial one to make it safe. Implicit in this statement is the recognition that changes in the immunosuppressive strategy must trigger changes in the antimicrobial program.”
- A refusal to define a specific length of antimicrobial therapy at the outset of treatment — treat “long enough”, he would say.
- The immunomodulating effects of certain opportunistic infections, in particular cytomegalovirus.
- The use of “preemptive” treatments in patients at high risk for developing infectious complications — here’s his classic review of the concept.
- Corticosteroids are like credit cards — patients (and doctors) get immediate satisfaction, but the bill comes at the end of the month. He often called them “feel goods”.
During fellowship, I remember presenting him a case one day of a man who’d had a renal transplant several years before, and was doing great — on low dose cyclosporine and prednisone, with normal renal function. He’d been struggling for the past week or so with intermittent headaches, and his primary care doctor was concerned — could this be something infectious?
My differential diagnosis was absurdly broad, including practically every known opportunistic infection that can cause headaches — listeria, cryptococcus, nocardia, aspergillus, mucor, toxoplasmosis. Cripes, I might have even mentioned acathamoeba.
Bob sat and politely listened, then kindly said — “Very good — but I’ll bet you it’s none of these things. He just doesn’t fit the pattern.”
His point — this patient was too healthy for these infections. The kind of transplant patient who usually gets these infections has been treated for repeated bouts of rejection, or experienced CMV reactivation, or has been heavily exposed to some pathogen, or is nutritionally compromised, or worst of all, all of the above — these are the “awful-awfuls”.
“If you want to send a serum cryptococcal antigen, go ahead,” he said. “But it will be negative.”
I sent it, and of course Bob was right — test negative. Turns out the patient had stopped drinking coffee because of heartburn, and was suffering from caffeine withdrawal. No acanthamoeba.
Bob died earlier this month after a lengthy illness. We will all miss him.