The work of epidemiology is related to unanswered questions, but also to unquestioned answers — Dr. Patricia Butler

MEDICAL EDUCATION HAS CHANGED DRAMATICALLY during the last half century. In the vanguard of these changes was Canada's " McMaster University Medical School in Hamilton. Under the leadership of cardiologist John Evans, who became its founding dean, internal medicine specialist Bill Spaulding, respirologist E.J. Moran Campbell, and medical educators Howard Barrows and Geoff Norman, McMaster — beginning in 1965 — dramatically reshaped the curriculum, de-emphasizing the traditional approach to academic lectures and formal examinations.

Instead, it created a radically new model, based on self-directed study, creative thinking and problem-based learning. The system proved so successful that universities all over the continent began to emulate it, including the prestigious Harvard Medical School, which called its own program New Pathway.

They might well have added an asterisk to that title; it was new when McMaster pioneered the concept.

An important part of the McMaster philosophy was to admit a broader range of applicants to its medical school than had previously been the norm. Thus, students with arts, philosophy or political science backgrounds — or people who had been out of school and working for some years — stood as good a chance of winning a coveted slot as recent physics and chemistry graduates. And while grades continued to be important, McMaster placed a premium on other life experience, including extracurricular activities, travel and volunteer work in the community.

My own feeling is that one's background is less important than one's character. And character is more important than curriculum. If you pick the best people and if they have the right intentions, and if they are well led by experienced physicians, you will turn out some very fine doctors. An awful lot of learning has nothing to do with textbooks or formal lectures. It's what you metaphorically absorb, osmotically, in living at the hospital and breathing the air of medicine, day after day.

When you put on the doctor's white coat, you don't leave one self behind and become a new self. You bring it all with you, your personality, your ideas, your idiosyncrasies, for better or worse. And in our increasingly globalized world, the better read, travelled and exposed to other cultures you are, the better a doctor you are likely to make.

I spent many years, both at McGill and the University of Toronto, sitting on panels of admission and interviewing prospective medical students. Of course, the applicants we accepted displayed a broad range of academic intelligence and personality traits. But only rarely did we admit someone with whom we later felt we had made a clear mistake.

I recall one particular example — a young man who consistently displayed what can only be called an egregious bedside manner. I witnessed his combination of arrogance and callousness on several occasions. The worst instance involved his treatment of an elderly heart patient.

"You have severe angina caused by atherosclerosis, by your reckless eating and drinking habits," he told him bluntly. "You could die of it!"

The stress of that exchange caused the man — who did not drink and was slim — to suffer a heart attack within minutes.

Later, I failed the student, for this and other misdemeanors. The truth is, I was failing him for lack of good character — the sine qua non of what we do. He was just not the sort of person likely to bring credit to the profession. The more I saw of his behaviour, the more certain I became that he did not belong.

He appealed the decision and used some influence to have himself reinstated. Then, he foolishly made a personal longdistance call to the United States and billed it to the hospital. When confronted, he at first denied it and then tried to blame the hospital call centre operators. In what became the last straw, he took out his anger on the operators by finding an axe and physically destroying part of their offices. That, thankfully, was the last straw — and the end of his medical career.

McMaster's first chair of medicine was Moran Campbell, a brilliant respirologist who did groundbreaking research on so-called smoker's disease — chronic obstructive pulmonary-disease (COPD). While at London's Hammersmith Hospital, Campbell observed that patients admitted to hospital with this illness often died, while those who stayed home survived. The reason: the hospital patients had been given too much oxygen, which was effectively a poison because it suppressed their respiratory drive.

McMaster's broader program in clinical epidemiology was led by another brilliant physician, David Sackett, an American who established it as a real modern science. Out of this program same a generation of A-list researchers that made major strides in a variety of topic areas and thought deeply about measurement and biostatistics in medical practice. The program promoted and elevated evidence-based medicine, which changed the fundamental ways of medical practice and, indeed, of medical education. To this day, it remains a leader in the field. Sackett wrote two enduring medical textbooks and later established the Oxford Centre for Evidence-Based Medicine in the U.K.

Another McMaster star was Jack Hirsh, an Australian-born hematologist. In one of several research breakthroughs, he assisted Henry Barnett of University Hospital in London, Ontario, in establishing once-lowly aspirin as a treatment of choice in the prevention of heart attack and stroke. Hirsh almost singlehandedly rewrote the principles of diagnosis and treatment of deep vein thrombosis and pulmonary embolism.

In the United States, the rise of evidence-based medicine was championed by epidemiologist Alvan Feinstein at Yale University. Indeed, he coined the phrase clinical epidemiology, which became one of key foundation stones of modern medical practice.

In fairness, both Sackett and Feinstein were building on the innovations of British physician Sir Austin Bradford Hill, who led the groundbreaking post-war study that, for the first time, established the indisputable link between lung cancer and cigarette smoking. Sadly, it took another 30 years — and untold millions of lung cancer deaths — before the U.S. government, under the aegis of the Surgeon-General, acknowledged the truth.

Another landmark study involved fever of unknown origin (FUO), published by physicians Robert Petersdorf and Paul Beeson in 1961. Between 1952 and 1958, the two researchers studied 100 consecutive patients with FUO in Baltimore, and concluded that they broke down into various categories: infections (36 percent); malignancies (19 percent); inflammatory or rheumatologic diseases (15 percent); miscellaneous (23 percent) and undiagnosed (including malingering, 7 percent).

Five decades later, the same rough distribution applies, although infections tend to be more common (40-60 percent) in tropical and subtropical countries. Petersdorf and Beeson denned fever of unknown origin as being anything above 38.3 degrees Celsius for more than three weeks, with the patient in hospital for at least one week. Nowadays, we substitute a week of outpatient investigation for the hospital stays, which have declined dramatically. This study had a major influence on my own generation and gave us some reliable diagnostic benchmarks for approaching FUO, a relatively common and difficult diagnostic entity, with potential for serious illness.

I was once asked to examine, Colin, a young aircraft engineer of 30 who had suddenly gone deaf in both ears. The assumption was that his long hours of environmental exposure in an aircraft assembly plant had caused the condition. But he had other serious problems, including fever of unknown origin, accompanied by chills, weight loss and anemia.

He arrived at my office with his wife and parents, who were clearly concerned.

"You've got to do something, doctor," his wife said, "or he's going to die. We have three young children."

I assured her I would do the best I could, but would need perhaps a week or 10 days to carry out some investigations. In the . meantime, I told them, "It may be necessary to have you readmitted to hospital here."

Then his mother interjected sharply. "We're not going back there. I am fighting all the time with the nurses and doctors on the ward." At that point, she removed a piece of paper from her pocket and started to recite a litany of complaints about how insensitive staff had been to her son's condition. I detected the hint of a Scottish accent as she spoke and sensed a more than common knowledge of medical issues.

 "By any chance," I said, "are you a nurse or a doctor?" "I'm a nurse," she conceded.

"And might you be from Scotland, perhaps Edinburgh?"

"How did you know that?"

"And did you work at Edinburgh Western General Hospital?"

"Yes," she said.

"Well, I was there in 1970," I said. I then rattled off the names of several doctors I had worked with, people she had known.

With that, she almost started to cry. She promptly took her paper, folded it up and put it away.   

"Doctor," she said, "just do whatever you need to do."

I was subsequently able to determine that Colin was suffering from polyarteritis nodosa, an autoimmune disorder — a form of vasculitis — that inflames the organs, joints and large blood vessels. His deafness had not, in fact, been caused by environmental exposure, but by something known as mononeuritis multiplex — damage to the nerves in both ears, caused by vasculitis of the vessels supplying blood to the auditory nerves. We started him on a course of high-dose prednisone, which led to recovery from his severe systemic illness.

Among the other cases in my own dossier, one of the most interesting involved fever of unknown origin. The patient was referred to me by a former student. Dr. Ophyr Mourad, now an accomplished internist working at another hospital and an award-winning teacher. In fact, Dr. Mourad had co-authored " a scholarly paper on FUO. He had been seeing Serge, a Quebec-born businessman in his 40s, for almost three years and, though Dr. Mourad had conducted all the right tests, had been unable to identify the cause of the fever.

Serge was seriously debilitated, losing weight and his ability to concentrate. His condition had effectively forced him to retire, since he no longer trusted himself to handle complex financial transactions. These periods of fogginess, as we subsequently learned, may have indicated the formation of protein deposits — amyloidosis — in the brain. But more of this later.

I repeated a number of the tests Dr. Mourad had performed, without new results. The cincture of time did not help. Time passed and Serge showed no improvement. Every month he was experiencing fevers of 39 and 40 degrees Celsius.

I asked him to keep a detailed record of his fevers, how long they lasted and the temperature. At the time, I wondered whether he might have Pel-Ebstein disease, a rare condition in which the fever spikes for four or five days every six weeks. But Pel-Ebstein is commonly associated with Hodgkin's lymphoma and Serge's fevers did not follow that pattern and there was no evidence of lymphoma.

I also considered familial Mediterranean fever (FMF), so-called because it typically strikes people whose genetic background is in the Middle East and North Africa — Armenians, Arabs, Turks and Jews. But there were no such links on either side of Serge's family tree — only French Catholics, for several generations — so we ruled it out clinically.

My next thought was familial Hibernian fever, otherwise known as traps (tumor necrosis factor receptor-associated periodic syndrome), which is caused by genetic mutations. These fevers, which can persist for a few days or a few months, occur every six weeks or disappear for years, only to resurface. Testing for this condition had only recently been developed. Eventually, I sent Serge to the new genetic testing facility at another hospital.

The results surprised both of us: it was familial Mediterranean fever after all. The odds of inheriting the disease are about 1 in 500. Serge was delighted to finally have a diagnosis, the more so, of course, because the condition is controllable, if not entirely curable, with colchicine, a drug that dates back at least to the time of the ancient Egyptians. An immune system modulator derived from a flower, the autumn crocus, it is also useful in treating gout and rheumatism. Although Serge still occasionally gets a fever, it does not spike as high or last for as long as it once did. More important, we almost certainly prevented the development of amyloidosis, a known complication of familial Mediterranean fever, which can lead to renal failure.

A patient's testimony — Serge W.

I was raised in Lachine, just outside Montreal. My father was a housepainter and my mother was a bookbinder. As a child — I actually had forgotten this and had to be reminded of it many years later when it became relevant — I suffered from periodic fevers. At the time, we didn't see them as anything more than childhood illnesses, though I apparently had them more often than others. People were always telling me, "Don't get your feet wet because when you do, you get a fever and a sore throat." At one point, they were going to take my tonsils out.

For years, I also suffered from severe stomach cramps, which we know now is a manifestation of familial Mediterranean fever, but at the time was diagnosed as allergies to dairy products or gluten. So I would change my diet and temporarily get better, but the pains would always return. At times, it was intense I'd be on the floor crying. I'd say, "Just kill me. Get it over with."

I earned a bachelor's degree in economics at the University of Waterloo, and in 1977 immediately went to work for Hewlett-Packard. I was there 20 years, first as a systems engineer, and then in sales development, product management and development and then in sales management. Then they sent me to Hong Kong in market development and marketing manager. I was there 11 years. I travelled about 70 percent of the year, covering Asia.

During that time, I earned an executive M.B.A. I left HP in 1994, at age 40, and started consulting in sales development, based in Hong Kong. I returned to Toronto in 1999 and became involved in various businesses — an accounting firm that I co-owned, a restaurant in which I was a silent partner and a family company in the mining business in Quebec. I still play a marginal role there, but I have largely retired.

In 2005, I became ill, emotionally and physically. I discovered that my partner was committing fraud and had to sue him, creating a lot of stress. Physically, I had abdominal pain and high fevers —103,104 degrees — and weight loss. The fevers lasted a few days to several days and every night I'd wake up in a pool of sweat. I had memory issues, sleep issues, joint pains. I was depressed and debilitated. It all impacted me.

It took seven years in total to diagnose the illness. Before then, I had every test possible: MRIS, CT scans, X-rays, lumbar punctures, upper GI scopes, lower GI scopes. Every week almost I was tested for HIV. Everything was negative. I saw rheumatologists, autoimmune specialists, endocrinologists, gastroenterologists, infectious disease doctors.

I was three years with Dr. Mourad and about four with Dr. Ho Ping Kong. We had to wait a long time, almost a year, for genetic testing, first to get provincial approval, and then do the sample and send them away to the United States for analysis; we did not have the facilities here.

They ultimately told me FMF is a rare genetic order that affects mainly Semites, about 1 in 200.1 apparently have a mutation upon the mutation, a real anomaly. My first thought was "Where the hell did that come from?" And the next was "Well, maybe we can address it now."

It was very odd, because to get FMF you have to inherit genes from both parents. On my father's side, we can trace the family back to Paris in the 17th century. On my mother's side, it's all French Roman Catholic for 100 years. My mother's father came from Manchester but, as far as we know, he was not Jewish and even then I'd need a gene from my father's side.

When I met Dr. Ho Ping Kong, we had immediate rapport, in part because he speaks French, but also because he just puts you at ease. He's a patient-oriented doctor. We could have a conversation. A lot of doctors talk to you as if you'd been to medical school. HPK speaks in words "you can understand. It never felt like a medical lecture. It was comforting. He gave me a sense of hope. I intuitively knew: this man knows a lot, though I can't tell you why. He has seen a lot. If there is going to be a solution, he will find it. And he did. I still have occasional fevers, but the drug helps modulate them. I still have stomach cramps but they are also less intense.


NOT every illness needed trials and studies in order to determine the best therapeutic response. Years of experience with penicillin had demonstrated incontrovertibly that it would cure patients with pneumonia. The same was true for mitral stenosis and atrial fibrillation, a scourge of young people for many years, because of rheumatic fever. In that population, strokes were 25 times more common than in the general population. We did not need elaborate studies to know that the best treatment to prevent strokes in mitral stenosis was anti-coagulation therapy, despite the risks of bleeding.

Until the emergence of people like Sackett and Feinstein, only 15-20 percent of our decision-making was based on hard scientific evidence. The new approach laid a much greater emphasis on the conduct of clinical trials, seeking to prove efficacy by the sheer weight of statistical probability. Today, it is estimated that as much as 40 percent is evidence-based, and that figure continues to rise.

Consider, for example, the use of statin drugs like Crestor or Lipitor for cardiac disease. We have long had evidence that if someone had already suffered a heart attack, a statin regimen could help prevent a second infarction. But what about people with high cholesterol readings or a strong genetic predisposition —yet no specific history of heart disease? In such situations, many cardiologists would prescribe statins, which would usually be effective. But each patient required a separate discussion. There was no clear research evidence to support such an approach.

In the mid-1990s, a group in West Scotland conducted a double-blind study involving almost 7,000 men, age 45-64. One group received a placebo; the second was given the drug pravastatin. The first result was perhaps no surprise. The statin lowered plasma cholesterol levels by 2 o percent, and low-density-lipoprotein cholesterol levels by 26 percent, versus no change in the placebo group. The second result was more dramatic: 248 coronary events (non-fatal myocardial infarction or death from coronary heart disease) among the placebo group, compared with 174 in the group taking pravastatin.

At Toronto Western, in the mid-1980s, we set up a curriculum for teaching evidence-based medicine. A former resident of mine who became one of the world's leading bioethicists, Dr. Peter Singer, did most of that work. (Peter appears elsewhere in this book with his own views on the art of medicine.) In turn, Singer teamed up with Allan Detsky, director of general internal medicine at Toronto General Hospital. For five years, they offered twice-a-week seminars in clinical epidemiology and evidence-based medicine that drew standing-room-only crowds of students, teaching how to evaluate patient-oriented research papers.

Several later luminaries emerged from that program, all of them making significant contributions to research. Among them was David Naylor, a former colleague who set up the Institute for Clinical Evaluative Sciences (ices) at Toronto's Sunnybrook Hospital to do independent, non-profit research on a broad range of health-related issues. Its work, in many fields, has been absolutely world class.

For almost two decades, the groundswell for evidence-based science was so strong that voices arguing for medicine as an art were largely marginalized. Today, there is more interest in what physicians do and how they ought to behave — questions that speak to the artistic side of the equation. There seems to be an understanding that perhaps we have gone too far with the scientific model, especially as we better comprehend the importance of personalized medicine — i.e., targeting disease based on an individual's unique genetic makeup.

The best physicians, in my judgment, are those who know the science backwards and forwards, but also demonstrate the distinct human touch. I don't suggest that all doctors need to have those skills. If you are about to undergo brain surgery, what matters most, surely, is the knowledge and talent of the neurosurgeon, not his or her ability to make small talk.

But most physicians, those who deal with patients on a one-to-one basis, need to have some of these qualities. You may learn some of this sensitivity by studying history and literature before entering medical school, but I think, in general, that you are who you are. You bring your genes and your attitude to the bedside with you. The onus thus falls heavily on boards of admission to choose wisely in selecting applicants.

Evidence-based medicine has been an invaluable boon to doctors. It has taught us a great deal about the diagnosis of heart disease, hypertension, various forms of cancer and other illnesses. And it has helped define the gold standards for treatment of these and many other conditions. But I still maintain that evidence-based medicine cannot provide all answers to all doctors. The profession's Grey Zone is simply too large — too many patients with clinical symptoms, clearly in need of treatment, but no reliable diagnoses. And there are too many questions that the evidence of trials and studies cannot satisfactorily answer. Thus, there will be a continuing need for the art of medicine —the importance of experience, empathy, communication, intuition, and knowing and doing the right thing.

IN 1978, while working at the Royal Victoria Hospital in Montreal, I was asked to consult on a case involving Andrei, a middle-aged Haitian man said to be suffering from pulmonary tuberculosis. He was one of the cases we discussed during our weekly ward meetings. He had all the signs of TB — fever, cough, weight loss and sweating.

What was particularly curious about his story was that he had been treated for the same disease three months earlier and ostensibly had been cured. Or so it was believed. Now the disease had returned, although its principal symptoms were less active. But in the interim, Andrei had lost his eyesight. The eyes are sometimes affected by TB, but rarely to the point of blindness. So we were all puzzled and struggled with the diagnosis. Nobody asked about sexual orientation. It wasn't remotely on our radar at the time. We treated him for TB a second time, but to no avail. He died soon afterward.

Six months later, another Montreal hospital asked me to examine a 21-year-old patient from Barbados suffering from what they said was Still's disease, an inflammatory arthritic condition. But as soon as I saw him, I knew this was the wrong diagnosis. The poor man was wasting away; he'd lost something like 50 pounds in a mere six months. We looked for evidence of tuberculosis, autoimmune disorders, rheumatoid diseases and infection. But there was nothing specific we could find, and nothing, unfortunately, that we could do. Not long afterwards, he succumbed as well.

It was only in hindsight that it became clear to me that these ,two/cases were among the first, if not the first, cases of HIV/AIDS in Canada. They had occurred several years before this terrible disease began to make its presence felt in North America. I can't definitively prove that these two Montreal patients actually were victims of aids — at the time, we did not save serum samples — but I am convinced that they were. Ten years later, the problems Andrei was having with his eyes would have been labelled cmv retinitis, a classic complication of HIV/AIDS.

In the medical literature, the first North American case was reported on June 5,1981, by the Centers for Disease Control and Prevention citing five incidences of pneumocystis carinii pneumonia (PCP) among previously healthy young gay men in Los Angeles. Two had died.

Soon enough, however, reports began to filter in of young homosexual men dying in significant numbers in major American and Canadian cities. At first, we labeled it "gay bowel syndrome." Patients would initially report severe diarrhea and weight loss. They would deteriorate from there. While the medical community recognized what was happening, many hospitals simply did not want to treat these patients. Our caseload at Toronto Western Hospital typically included young men from small or mid-sized rural communities whose own institutions had effectively turned them away. People were too scared to admit these patients.

Even at Toronto Western Hospital, where the efforts of doctors and nurses were, in my judgment, heroic, we informally capped the number of hospitalized aids patients at 20, fearing that we would otherwise compromise other aspects of the care program. We thought other hospitals needed to do their fair share. We incurred criticism for putting that ceiling in place, and we were accused of being homophobic, but it had to be done. But two of my colleagues demonstrated remarkable conviction and grace under pressure — Dr. Doug McFadden, a general internist who led the effort at Western. He had a Ph.D. in epidemiology and an open mind, and he became the first real HIV doctor in Toronto. Our second stalwart was Ann McMahon, a Scottish-born head nurse of exceptional talent, commitment and compassion, a modern incarnation of Florence Nightingale.

At one point, we faced an ethical dilemma, whether to hire a male nurse who had already been diagnosed with the disease. On the one hand, we wanted to do the right thing vis-a-vis human rights and non-discrimination. On the other, we needed to do — and be perceived as doing — the right thing for patients in the face of a growing pandemic. In the end, we decided that hiring the nurse for ward duties would inadvertently expose far more patients to what we believed was substantial risk.

The move provoked something of an uproar in the gay community, and I was cast as the villain. But it was the right decision, especially as we better came to understand the risks posed by transmission of the virus through accidental needle pricks. That happens routinely in hospitals, and it happened at Western; fortunately, no HIV/AIDS cases resulted.

On occasion, patients would turn up from all over the world showing all the symptoms of aids but not want us to perform a confirming blood test. Such cases posed a problem for us because, as matter of public health, just as we routinely do for syphilis, we should do the test. But legally, we did not have the right to compel the patient to undergo testing.

But HIV certainly changed the way we look at medicine. Before its emergence, we tended to classify disease illness as infectious, or inflammatory, or cancerous, or congenital or metabolic, HIV could be several of these things at once. It was hard to know where one category ended and the next started, and what to treat first. It was an infection that could lead to cancer and inflammation, with patients presenting with muscle and joint pain, anemia, peripheral neuropathy, blindness, brain disease, encephalitis, not only ordinary pneumonias and tuberculosis, but also more exotic forms to which a compromised immune system was vulnerable — diseases we otherwise rarely saw. It also changed hospital procedures, with barrier protection becoming commonplace.

Debate still rages in the medical community over whether a French or an American team of researchers discovered HIV — human immunodeficiency virus — first. Regardless, the cocktail of anti-viral drugs eventually assembled for treatment has made it more manageable, a chronic as opposed to a universally progressive fatal disease.

The frightening speed with which epidemics can move had already been brought home to me. In 1975, I was looking after a group of about 40 Canadian war veterans in Montreal. On a certain Friday in the dead of winter, an influenza germ found its way onto the ward. By Monday morning, 28 of my patients were dead. Their elderly immune systems were simply too compromised to fight the disease. That event had a profound influence on my thinking about epidemics.

I had seen epidemics before, of course. In 1964, during my fourth year in medical school in Jamaica, a typhoid fever epidemic struck the country — a staggering 4,000 cases. Typhoid is a tough, highly communicable disease, with a high mortality rate. It has a long duration that begins with fever and constipation and then progresses. By its third week, it infects the lymphoid tissue of the small bowel, resulting in diarrhea. By the fourth week, untreated, you will be near death from toxemia or bleeding.

Enrolled in a course called social and preventative medicine, three other students and I were dispatched to the countryside to help with the investigation. We visited one hospital near the epicentre of the epidemic. In each cot were two kids, lying foot to head, both suffering from typhoid fever. They simply did not have enough beds though, fortunately, they did have sufficient antibiotics.

We visited the origin of the outbreak — a rural river in which the mother of the first typhoid patient had washed his soiled clothes. That was the index case. Three weeks later, a mile downstream, 10 new cases were reported. Then, further downstream, a fortnight later, another 100 cases. The incubation period was 14 days and then it was from person to person. It was a classic, natural history of a waterborne epidemic.

But my formal introduction to epidemiology occurred later, during the 1968 Hong Kong flu epidemic. Only a medical intern at the time, I watched sadly as two young men experienced acute respiratory distress, then heart failure and finally died. Such experiences eventually led countries to develop programs in public health. We realized then that social and preventive medicine would become a major factor in the ongoing struggle to keep people healthy.

Three decades later, Toronto confronted another pandemic — SARS, severe acute respiratory syndrome. I recall its genesis vividly. It was Sunday, March 16, 2003. I had just returned from a winter holiday. My son, Wayne, a cardiologist at the Scarborough Hospital (Grace campus) — it would become the epicentre of the epidemic — came to visit me and said he needed his children to stay with me. He would not be going home for at least two weeks.

I was initially confused. "What are you saying to me? Are you serious ?"

"I am," he said. "There are 100 cases of an undiagnosed disease at the hospital, and people are dying."

An occasional hospital colleague announced that he was taking holidays rather than expose himself to the as-yet-unidentified virus. His cardiology partner had decided to sleep in the family basement, to avoid the risk of spreading the presumed germ to his wife and children. Wayne, and his partners, Dr. Chris Li, Dr. David Rose, and Dr. Sandy Finkelstein and their hospital colleagues, were to perform heroic work in taking care of the 100 SARS patients at Scarborough Grace.

The next day at Toronto Western Hospital, my team assessed the situation. We were just beginning to understand what was going on, but events were moving. quickly. The Centers for Disease Control in Atlanta had just conducted its first briefing, reporting 14 suspected SARS cases under investigation in the U.S. Our staff had to be prepared, both logistically and psychologically, for the possibility that we would be soon admitting SARS patients. That same night, we did — a 60-year-old Chinese gentleman, transferred from the intensive care unit at Mount Sinai Hospital and considered stable. We placed him in a special, isolated room with negative pressure. It turned out that he was the husband of one of the first victims to contract the illness in Hong Kong, not far from Guangdong, China, where the outbreak had begun the previous fall. His wife had likely given him the virus.

When we first prepared to examine him, we were fortunate enough to have a Cantonese-speaking medical student on our team; the patient himself spoke no English. We were lucky, too, to have a courageous and knowledgeable intern who ultimately supervised the case, Dr. Avijit Chatterjee. It was his suggestion — actually, his insistence — that we all be double gowned, double gloved and double masked. Today, that protective ensemble would be routine for epidemic situations, but at the time it was novel.

In fact, I was initially surprised by the recommendation and asked him why we needed to do it.

"Trust me," he said. "I have a master's degree in microbiology from McGill University. This is what we need to do."

Even then, we did not have as much physical contact with the patient as we have under ordinary circumstances, though we did make sure that he was stable and was breathing normally. He survived his ordeal.

In total, we ourselves recorded 29 SARS cases at TWH — about 15 percent of all reported or suspected Canadian cases. Four deaths occurred at Toronto Western Hospital (there were 43 in all of Canada), all in the ICU. But there were no additional infections. One reason why the death total at Western was so low was because we put our SARS patients in rooms with negative pressure, which prevents the spread of potentially fatal germs.

I witnessed several acts of heroism during that traumatic period, but few were more impressive that those of infectious disease specialist Wayne Gold. He examined every one of the SARS patients we admitted. Gold's performance, duplicated by dozens of health care professionals in Ontario — many of them from the younger generation — had an enormous impact. Dr. Gold was the sole attending physician for those patients admitted, which meant we did not have to pass patients from one physician to the next, as occurred at other institutions.

The SARS epidemic fundamentally changed the way Canadians perceived nurses and doctors, reducing complaints about the system dramatically and for several years.

Many mysteries remain from that pandemic, however. Why were some people more susceptible to the germ than others? Why did some live and others die? My son's secretary became ill. Although she survived, she must have passed it on to her father, who did not. One of his own partners in cardiology became ill with SARS and, though he recovered, he decided to take early retirement.

SARS was, of course, a new disease, caused by a new virus for which we had no immunity, no specific antibodies. Although" some deaths occurred among young people, most of those who died were elderly, with immune systems already somewhat compromised by other conditions. Among the young, the body's own immune response mechanisms can be part of the problem, kicking into such high gear that, in concert with the virus itself, they overwhelm the ability of organs to function.

It was probably because there were so many unknowns that so many of us found the crisis unnerving. We intended to manage it with fidelity to the best practices of pandemic control. But would those be sufficient to corral the virus? We just didn't know. For the first week or so, I found myself occasionally waking in the middle of the night, bathed in sweat, my heart racing and unable to get back to sleep. I was not alone; I know this anxiety was felt in many medical households. We suffered but we persevered as a profession.

We had some other close calls. One day, at the virtual height of the crisis, I was treating Samantha, a woman with Addison's, a rare disease of the adrenal glands. Her blood pressure had fallen to about 100 and she felt tired and depressed. Her skin colour had also changed, becoming more pigmented, a common feature of the disease — the result of low Cortisol levels. We sent her to Toronto General for an acth test to confirm the diagnosis.

She had been administered the test and was leaving the hospital when, in the elevator, she collapsed. Respirologist Dr. Michael Hutcheon found her and, tracing her file, called me. Her blood pressure had now fallen to 80, he reported. His question was: should he send her to Toronto General's emergency department or did I want to come and get her?

I had to make an instant decision. The easier option would have been to let her go to emergency. But I had a medical student with me and, thinking this might be a teachable moment for her, told the TGH doctor that we would take the next shuttle bus and bring Samantha back to Toronto Western. At the same time, I called a colleague of mine at Mount Sinai, Dr. Shabbir Alibhai, and asked him to cross the street to Toronto General and check on her first, to make sure she was okay. If he had said she was in bad shape, I'd have been tempted to send her to emergency and I would have met her there.

As it turned out, it was on that day that SARS appeared in TGH's emergency department. Four people there subsequently died and three staff members developed SARS. I sensed disaster looming. Had I sent Samantha there, given her already weakened condition, she would have been extremely vulnerable to the virus. So would have I, or anyone on the ward that day. At best, we would have all been quarantined.

But the key factor was my student. I wanted her to experience something about the art of medicine, specifically about empathy. You always want to act in ways that you think will be best for the patient. In this case, that meant not dispatching her to the strange impersonality of another hospital's emergency ward and; to physicians she did not know. She was my patient and therefore my responsibility, with or without the SARS crisis. The right thing to do, if I could, was to take the higher ethical road. Do what you should do and then do more. The right thing to do was to get her. We went and brought her back to my office at Toronto Western. More than a decade later, Samantha is doing very well, her disease under control. And she — and we — likely dodged a serious bullet.