My First Days at SFGH

Paul Volberding, MD

SFMMS is proud to have this exclusive preview excerpt from the work-in-progress autobiography of Dr. Volberding, a pioneer in the response to what became the AIDS pandemic and one of San Francisco’s—many would say the nation's— most renowned medical figures. This first excerpt details the start of his career and first encounters with a new, as yet unidentified pathogen.

July 1, 1981, was my first day as a University of California

San Francisco faculty member, hired to begin a new division of medical oncology non-surgical cancer care in adults at San Francisco General Hospital. Although I’d spent as much time at the General as I was allowed by my fellowship program, I was then still in training, fully 10 years after finishing my college days in Chicago. Now, I would be charged with organizing and directing the care of cancer patients and educating the fellows, residents and students who would report to me. This all was, of course, a serious responsibility and an unheard-of career acceleration! Most “division chiefs” had been faculty members for at least a decade before being given this position. I assume many of the chiefs I was joining looked quite askance at this new kid on the block and wondered how my boss, Merle Sande, had pulled this off without conducting a search! I don’t recall the weather that first day, but July in San Francisco is typically cool and foggy in the morning—always a shocker to summer tourists in tee shirts and shorts. But I do remember being thrilled at the chance to launch a new career at a hospital I’d fallen in love with during my training and to provide cancer care to the typically very ill patients of a safety net hospital. Just as I’d transitioned from the last day of my fellowship to my new position, I knew I’d meet a newly minted first day oncology fellow that day immediately following residency training in internal medicine. Soon after checking out my new office (a windowless room about 8 feet square equipped with a used Steelcase desk that occupied most of the space) I met with my fellow, Ray Stricker, also excited to be launching an important new stage in his career. Ray had recently moved from New York where he’d finished his internal medicine residency at St. Luke’s-Roosevelt Hospital after medical school at Columbia.

As we did “rounds” that day, walking around the hospital wards to introduce ourselves to the house staff and the hospitalized patients we had been asked to help care for, we met a remarkable patient I’ll call Richard. As a doctor, one cares for so many patients; relatively few are so striking to be remembered years later. But I do vividly remember Richard even after 40 years as do Ray and Sue Carlisle, Richard’s intern at that time. Sue would later have a long career at the General, eventually as the Associate UCSF Dean for the hospital. I remember Richard, his face and his disease with striking clarity and the immediate challenge his social situation represented for us as we cared for him. Richard was a 22-year-old man with an unbelievably rare cancer, Kaposi’s sarcoma, or KS. He was the case I’d heard rumors of the day before from my colleague John Klock.

On some very quick reading (a textbook as this was years before the internet and Google) I found that KS was known to occur in elderly Jewish men from the Mediterranean basin, and was a very slow growing cancer, often confined to the skin of the lower legs. As it was so slowly growing, KS in that population typically didn’t require treatment as the patients, often in their 80’s, would likely die sooner of a more serious disease. I had just been studying for my oncology qualifying exams that would certify me (for life!) as a medical oncologist and I’d completely skipped studying about KS. I was certain it wouldn’t be included in any questions. It wasn’t. But Richard’s disease was wildly different from those textbook descriptions, and he would clearly have been one of those morning report cases Molly and Chip had been encountering with Merle. My patient was originally from the deep South and had made it to San Francisco after realizing he was gay and not likely to fit in with his deeply religious family given “lifestyle”. He had no real friends and exchanged sex to survive, meeting many of his innumerable partners in bath houses and in the course of things experiencing numerous sexually transmitted infections, all treated at the City Clinic. By the time he was admitted to SFGH, Richard had lost an extreme amount of weight, had a haunted, gaunt expression and looked far too much like the concentration camp survivors I’d seen in my father’s World War II scrapbook I’d poured over for many hours as a child. Richard had smooth, purple, bruised-appearing KS tumors scattered over his entire body and face and totally encasing his thighs in a thick woody plaque. He was so weak he could barely sit unassisted. And none of this made any sense from what I’d read!

In addition to the “classical KS” in the elderly, there was a more aggressive type seen in sub-Saharan Africa, even affecting some children. Richard was not old, not Jewish, and definitely not an African child! In medical training, we are taught to expect incremental expansion of our knowledge regarding diseases we already knew. We expected to gradually learn more about hypertension, diabetes and the like and to gradually develop better treatments for them. Nothing was taught about the possibility of encountering absolutely new conditions and with no doubt this is why in retrospect so many of us missed those first cases of AIDS. Molly and Merle had seen those cases in morning report as continued on page 32

a strange coincidence and I’d seen my lymphoma patient at the university as just a case of really bad luck. On July 1st 1981, my mental impression of Richard was that he was suffering from a rare and unfortunately hideously advanced cancer, nothing more except that his disease fit nothing that had been previously seen in medicine. I could not answer Richard’s questions about what he had or what to expect but even at first glance, I did not expect a good outcome. From this first patient though—and repeated in countless times in the following years—we confronted the need to care for desperately ill persons with little in the way of support from what I called “traditional” families. My patient’s families were almost always at a distance and not uncommonly unaware that their son—my first patients were almost exclusively young men—were gay or that they had become ill. But my brand new, first-day oncology fellow Ray said that “maybe we’d seen something like this in New York.” Remember, this is before any public discussion of KS as a new condition in gay men; the very first, very brief story in the New York Times would not come out for three more days. Ray offered to call colleagues where he’d trained and they confirmed his recollection. In this case the telephone was our best social media and linked some of the very few of us as we began to deal with something absolutely new. Not yet frightening given the blinders we wore that kept us focused on what we’d learned rather than the reality in our faces. But the fear would soon follow. I’m leaving that last memory in place as a warning and reminder. It was fixed in my recollection, and I would have sworn it was true., but in recent conversations, Ray corrects me pointing out that he’d seen a case of KS as a medical student at Columbia and it was the “classical” variant in an elderly Jewish man! Memory is remarkably slippery and often biased so we remember events that best fit our own selfperception.

Things happened very quickly in mid-1981 as the medical response to this new world began. In early June, the Centers for Disease Control had published a short paper that proved of monumental significance. A young, Stanford-trained clinical immunologist at UCLA, Mike Gottlieb, had been informed by a community physician, Joel Weisman, of five cases he was seeing of gay men with a previously incredibly rare pneumonia caused by an organism called at the time, pneumocystis carinii. These cases were therefore called PCP, for pneumocystis carinii pneumonia. I’d actually seen one PCP case during my Utah days but in a desperately ill young woman who’d had a kidney transplantation and was on massive doses of immune inhibitors to prevent organ rejection. But the cases Mike investigated were young and previously in good health, and each case was a man who had sex with other men. Unlike many of the rest of us, Mike was willing to think outside the box and had a powerful new tool to help him. Monoclonal antibodies, engineered pure proteins that recognize other specific proteins and link to them physically, had only been developed six years earlier, in 1975. These antibodies were then used with another new tool called flow cytometry that had been developed in 1972. Together, this technology allowed immunologists like Mike Gottlieb to “tag” different cells in the immune system and count them separately in a rapid automated process instead of earlier primitive methods requiring counting individual cells through a microscope. He could count these cells in the blood enumerating the different populations of key components of the immune system that protect us from the incredible spectrum of microbes that they are prepared to kill.

In 1981, this technology was extremely rare even in the most advanced research universities. In all of UCSF there was only one flow cytometer—there are now many hundreds. When Mike examined the blood of the five cases of PCP at UCLA, he discovered that the expected proportions of the different types of cells that constitute a normal, healthy immune system were completely deranged. Normally cells called “helper cells” are more common than ones called “suppressor cells” but in these first-reported AIDS patients, helpers were greatly reduced. The immune system is extremely complex but it’s work requires delicate balances of the many different types of cells of which it is composed. Mike’s fundamental recognition of an underlying disturbance in the numbers of cells of the immune system leading to a serious disease was at the heart of AIDS and would drive our work for decades to come. What was causing this imbalance of cells would eventually lead us to HIV.

(To be continued….)