A physician is obligated to consider more than a diseased organ, more than even the whole man—he must view the man in his world.
—HARVEY CUSHING, MD
If the white coat is the symbol of hospital- and lab-based medical science, the bottom of a shoe with a hole in the sole is the symbol of the field epidemiologist. In fact, it is the emblem of the Epidemic Intelligence Service, whose motto is “Shoe Leather Epidemiology.” Like crime investigation, effective public health requires both the lab personnel and the detectives out at the scene.
My work with toxic shock syndrome (TSS)—which had brought me to the CDC that day in 1981—turned out to be a classic medical detective story, and one with a surprise ending. It also provided me with a number of career-defining object lessons I have never forgotten.
The term “toxic shock syndrome” was coined in 1978 by Dr. Jim Todd, chief of Pediatric Infectious Disease at Children’s Hospital in Denver. For the previous three years he had seen sporadic cases of boys and girls, ages eight to seventeen, presenting with high fever, low blood pressure, rash, fatigue, and sometimes confusion. The first case he saw, a fifteen-year-old boy, was initially diagnosed with scarlet fever, but Jim thought the symptoms seemed much more severe than he would have expected from that condition. Several more cases in the next couple of years were worked up, and although Staphylococcus aureus bacteria was detected in the patients’ mucosal linings, such as the throat and mouth, none could be isolated in their blood, cerebrospinal fluid, or urine. Based on the severe effects throughout the body, though, Jim and his team suspected a toxin, or bacterial poison, must be involved. One of his young patients had not survived. Lab analysis confirmed enterotoxin type B in blood samples. This toxin is produced by S. aureus bacteria.
They published their initial paper in the British medical journal Lancet—to more than the usual amount of skepticism from the health community. But Jim’s prescient work would serve as a critical first clue and early road map in understanding this apparent new collision between disease-causing microbes and humans.
Without warning, in the spring of 1980, cases of a TSS-like illness began showing up, primarily in Minnesota, Wisconsin, and Utah. Later we would learn that the state-by-state number of cases was largely a result of which states had health departments that were actively looking for TSS cases once the initial alarm had been set off. However, in all three states, nearly all of those afflicted were teenage girls and women in their early twenties. I had been in regular contact during this time with my close colleague and friend Dr. Jeffrey Davis, the state epidemiologist at the Wisconsin Division of Health, about the cases in our two states. Of the twelve cases in the two states, all were young women, eleven of whom had their menstrual periods at the time of their illness onset. Many of the cases were critically ill for up to several weeks; fortunately none had died at this point. Our initial findings did support that TSS was primarily occurring in young menstruating women, but we could not explain the magnitude of the risk, why it was happening, and what to do to stop new cases. We contacted the CDC and they asked other states to start looking for cases.
On May 23, the CDC published an article in MMWR describing fifty-five TSS cases in Wisconsin and Utah, forty in which a menstrual history had been obtained; thirty-eight of those—or 95 percent—had illness within five days following onset of menses. The media now started to pay attention.
On June 27, a second MMWR report summarized the results of a case-control study that included fifty-two cases—many of which were included in the May 23 report—and fifty-two age- and gender-matched controls. This is a type of epidemiologic investigation where we interview the cases—or the case’s family members if the case is too sick or has died—using a comprehensive questionnaire to systematically learn about every possible relevant factor in the case’s life that could have played a role in her illness. Then we identify “control” participants: people who are closely matched with the case individuals, for example, by age, gender, and residence, but have not been ill. We interview them using the same questionnaire. Our analysis compares the frequency of factors present among the cases and controls to determine if there are differences that can help us explain why the cases became ill.
That analysis found a statistically significant association between tampon use and TSS; in other words, the difference in tampon use between the cases and controls was very unlikely to happen by chance alone, with a much higher number of cases using tampons compared to controls.
Members of the media and some public health officials began to speculate that the recent high-visibility national rollout of Procter & Gamble’s Rely brand of tampons coincided with the increase in TSS cases, though the studies to date had not documented this finding. This media coverage would be significant over the next several months in influencing the results of subsequent epidemiologic studies.
Shortly after the June report, Jeff and I decided to collaborate on a case-control study to figure out why there was this sudden increase in TSS cases associated with menses, and the exact role that tampons and any infectious agent might be playing in this emerging public health concern. We invited the Iowa State Department of Health to participate in the study to help us more quickly identify cases. In our business, outbreaks are defined as a marked increase in cases of a disease, usually in a specific geographic area and over a limited time period.
For whatever reason, we were in the midst of an outbreak of TSS.
Our effort would become known as the Tri-State Toxic Shock Syndrome Study (TTSSS). For our study we had highly trained female investigators do the interviews in private, because they had to ask these young girls highly personal and potentially embarrassing questions. For example, we asked for detailed information about their sexual histories and the use of tampons and pads during their periods. Despite these sensitive questions, every control candidate we contacted agreed to participate. They were the real heroes in our study and helped us save many lives.
Most of the cases we studied had occurred in the previous six months, but we did find some that had occurred even several years before but that hadn’t been recognized as TSS. In all three states, we systematically searched in all our hospitals to make sure we had every likely TSS case in women included in our study, even if there was no report of menses or tampon use.
In early September, I experienced one of the lowest and most challenging moments of my career as I observed a sixteen-year-old girl lying in her hospital bed, soon to die from TSS. She was surrounded by her family as she received state-of-the-art supportive medical care. But nothing worked. I can’t even say what she had looked like before her illness; now she displayed the extensive classic TSS red rash on her face, hands, and feet. By the time I saw her, her face, arms, and legs were tremendously swollen, making her almost unrecognizable even to those who knew her. The swelling, or edema, is caused by what is known as third spacing—a condition where large volumes of fluid normally in the blood vessels and arteries leak into the patient’s soft tissue. This degree of shock, which occurs when there is inadequate fluid circulating in the arteries and veins, is very difficult to reverse. As a result, this young girl’s body had gone into multiorgan failure as it struggled futilely to maintain blood pressure. To this day, I have trouble expressing the utter helplessness that we all felt at not being able to do more for her.
As I spoke to her grief-stricken parents, all I could offer was my profound sympathy and a promise that we would get to the bottom of this; that their tragedy would help prevent this from happening to other young women. My daughter Erin—now a physician specializing in neonatology—was two at the time, and as I thought about her growing up, all of a father’s protective instinct for his children came flooding over me.
On Friday, September 19, the CDC published in the MMWR the results of what was known as the CDC-2 study. It included fifty female TSS cases and 150 female controls. The cases all had onset of their illness in July and August and were reported by a number of states to the CDC; no Minnesota or Wisconsin cases were included. The study again found that tampon use was a significant risk for developing TSS and for the first time found that cases had a 7.7 times higher risk of developing TSS using Rely brand tampons versus other brands. Overall, 71 percent of cases used Rely tampons, but only 29 percent of controls used Rely.
Rely had been developed in direct response to consumer demand. For years, women had been asking for a tampon that could absorb much more menstrual flow and prevent accidental leakage. By the early 1970s, the paper industry had created highly absorbent polymers that could retain twenty times their own weight of fluid. An obvious application was disposable diapers. Procter & Gamble borrowed from its disposable diaper technology to design a tampon that increased fluid capacity from five-to tenfold. Though other companies put out their own competing high-capacity tampons, P&G, using its marketing genius, captured more than 70 percent of the high-absorbency market.
The afternoon before the MMWR publication I received a call from an associate director of the Food and Drug Administration (FDA) regarding the pending public release of the CDC study the next day. FDA commissioner Dr. Jere Goyan and his staff had just been briefed on the study results and the Rely tampon connection. Jere was aware of our ongoing epidemiologic studies in Minnesota and Wisconsin and the concern we had expressed in conference calls with federal public health officials about the CDC study results. He requested that Jeff Davis and I fly to Washington to brief him on our ongoing case-control study, which was showing that Rely tampon use was reported in only about half of our cases, suggesting it was not the only problem product. This issue was front and center for the FDA since they regulate the safety and effectiveness of medical devices, including tampons. I agreed to fly to Washington early the next morning, in time for our afternoon meeting. This was the first time I’d ever flown anywhere on just hours’ notice, but I would do so many times in the years ahead.
The meeting at the FDA brought no consensus on the meaning of the CDC study results. I flew back to Minneapolis that night and was met with an urgent message asking me to call the senior Procter & Gamble executive overseeing the tampon business. P&G officials had been briefed by the CDC on its study findings earlier in the week. They had lots of questions and had gotten few answers. After a highly successful national launch of Rely over the past year, the officials were now pondering the possibility that their product was killing young women.
I was asked if I would attend a Scientific Advisory Group (SAG) meeting hosted by Procter & Gamble at the O’Hare Airport Hilton on Saturday afternoon and Sunday morning. SAG meetings are not uncommon in the business world, but they hardly ever happen on such an urgent basis. The members of the SAG are typically scientists from outside the company who can provide an objective assessment of what the latest science is saying about the topic at hand. This SAG represented the collective scientific think tank on TSS, although no one from the CDC was invited. I knew I had to go to Chicago despite plans for a long-planned family event on Saturday night. None of the SAG members received payment, just travel reimbursement.
The SAG was chaired by Jim Todd, the original TSS investigator, and his skills as the wise and seasoned sage were evident from the first moment. Jim would provide this same leadership in other forums for many months ahead as we worked to untangle the mystery.
We met late into Saturday evening, going over every piece of information, data, or evidence we had from the current TSS epidemiologic and microbiology studies and any other information that might give us some answers. Sunday morning we summarized our six-plus hours of deliberations. Unfortunately, we had many more questions than answers. Late Sunday morning, a P&G corporate jet from Cincinnati arrived at O’Hare carrying a number of the most senior executives, including CEO Ed Harness. They joined us in our conference room, sitting on one side of the large table. After brief introductions, Jim summed up our findings. Was Rely involved in some way with these TSS cases? The answer was a clear and compelling yes, but how and why was unknown. I continued to push our study’s conclusion that it wasn’t just Rely, so we shouldn’t consider the problem over and behind us.
I will never forget Harness looking at the SAG members and asking, “Tomorrow, can I tell the women working at Procter & Gamble it is safe to use Rely tampons, or tell the men that they are safe for their wives and daughters to use?”
I looked at Mr. Harness and said simply, “No.”
That afternoon, I remember sitting on the short flight back to Minneapolis, realizing Rely would almost assuredly be going off the market the next day. I had learned another career-defining lesson: Most companies are good corporate citizens and will do everything they can to resolve problems if they have evidence that their product is the culprit. P&G had delivered a product to market without any reason to believe they were putting anyone in harm’s way. I had no doubt that Ed Harness’s decision would be based not on some financial calculation, but on whether the women closest to him could safely use the product.
The TSS/Rely story exploded that September 19 weekend and remained in the headlines for months. The national media played on every young woman’s fears for her personal safety. By the end of 1980, LexisNexis, one of the primary companies tracking media coverage in the United States, determined that it was the third-biggest news story of the year, trailing only the presidential election and the Iranian hostage crisis. Coverage of the CDC study brought in almost 900 case reports, enough to reach national epidemic proportions. Ninety-one percent of them were associated with menstruation, and the distinct majority of them involved the use of Rely tampons. Procter & Gamble did, indeed, remove their product from the market the day after the SAG meeting, just a year after its heavily advertised national rollout.
The CDC’s public message was that Rely brand tampons were responsible for the outbreak, and with their removal from the marketplace, the threat had now been eliminated.
Rely consisted of polyester foam and a chemical called cross-linked carboxymethylcellulose, along with a coating called a surfactant. Surfactants are compounds that lower the surface tension between two liquids or between a liquid and a solid and make it possible for them to more easily blend together.
Our TTSSS investigative team never dismissed a problem with Rely for one minute. But as far as we were concerned in the Midwest, where the initial cases had presented, simply an association with a particular brand of tampons was not enough. There had to be follow-up studies to get closer to a more complete answer. This is where the TTSSS became critical. We included all cases from October 1, 1979, through September 19, 1980, in the three states. There were eighty in all, which we age- and gender-matched with 160 controls. We stopped enrolling new cases on September 19 because the CDC study reports all but guaranteed a bias toward the selective diagnosis and reporting of cases that used Rely tampons going forward.
By the time the study was fully under way, I probably knew more about tampons than 99.999 percent of the male population, more than it had ever occurred to me I’d have to wrap my brain around. I could identify all twenty-one brands and styles sold in America, both right out of the package and after use. You never know what you might face when you venture into the world of investigative epidemiology, and you have to develop a certain degree of scientific detachment. At the same time, I kept thinking about the effect this epidemic was having on millions of women and their families throughout the country. It seemed a cruel irony that this wave of illness and death had involved a product called Rely.
What we found in our study didn’t really surprise us. As we wrote in the summary of our paper that would be published in the April 1982 issue of the Journal of Infectious Diseases, “By multiple logistic regression analysis, the risk of TSS was more closely associated with tampon fluid capacity (absorbency) than with the use of all tampon brands.”
For those who used the lowest-absorbency tampon regardless of brand, there was about a 3.5-fold increase in the chance of developing TSS versus never using a tampon. For those who used the highest-absorbency tampons—of any brand—there was a 10.4-fold increase in developing TSS. However, we did find that Rely users still had a 2.9-fold increased risk compared to users of other brands. While we had evidence there was something special about the risk of using Rely tampons, the real driver in the chance of developing TSS was the fluid capacity of the tampon a woman chose to use. And the TTSSS finding virtually predicted what would happen with cases in our states in the months following the removal of Rely from the market.
The number of cases of young women with TSS did not change much; actually, it rose slightly. What happened instead was that those who came down with toxic shock syndrome were now mainly users of Tampax Super Plus brand high-absorbency tampons and a few other competing products.
Not surprisingly, young women continued to use high-absorbency tampons because no one warned them about the real risk factor. And the prime beneficiary of P&G’s decision to withdraw Rely tampons? Tampax. Suddenly it owned more than 70 percent of the high-absorbency market. It then became abundantly clear in states with active efforts to find TSS cases that the problem could not just be Rely; it had to be the use of high-absorbency tampons of any kind.
What that meant was that data from the previous CDC study had been subjected to biased, selected national case reporting due to media coverage of the role of Rely tampons in causing TSS, and was completely misinterpreted. We eventually determined that the key factor in the development of TSS and the relationship between fluid capacity was the increased release of oxygen in the vagina with high-absorbency tampons and the presence of S. aureus bacteria. As the menstrual fluid was absorbed into the highly absorbent material, oxygen was displaced into the vagina. The higher the absorbency, the more oxygen was released.
The rise in TSS cases happened to coincide with a new strain of the S. aureus bacterium that was a very effective producer of the TSS toxin. But more important, the materials of the highly absorbent tampons released a greater amount of oxygen into the vagina, which should be an anaerobic—oxygen-free—environment. With no oxygen, there is no TSS toxin produced. But this excessive oxygen transformed the bacteria into microscopic toxin-producing factories. Once produced, these toxins were absorbed through the vaginal mucosa—the membrane lining the vaginal walls—and straight into the bloodstream.
Subsequent work over the next several years by Dr. Patrick Schlievert, a microbiologist and internationally recognized expert on staph and strep toxins who had recently left the University of Minnesota for UCLA, and two other research groups demonstrated that the surfactant used for coating Rely tampons—known as pluronic L-92—also increased toxin production, and the surfactants the other companies used did not. Now the TTSSS case-control study results made perfect sense.
Ironically, shortly after the CDC announcement on September 19, the American College of Obstetricians and Gynecologists speculated publicly that it was a personal hygiene issue and recommended that menstruating women change tampons more frequently.
This turned out to be exactly the wrong advice. By telling them to change their high-absorbency tampons more frequently, the college was putting women at higher, rather than lower, risk. The more frequently a woman changed her high-absorbency tampon, the more oxygen she introduced into her vagina. Another lesson I learned from my experience investigating TSS is that if you don’t know what you’re talking about, then don’t talk, or at least say you don’t know. Yes, women wanted and needed sound and timely expert advice about the use of tampons, so it’s understandable why the American College of Obstetricians and Gynecologists felt the need to make a statement. But the only real information they had at that point supported not using tampons at all.
The prestigious National Academy of Sciences’ Institute of Medicine (IOM, now called the National Academy of Medicine) put together a blue-ribbon committee in 1981 to examine in detail the different findings from the various TSS studies and results of ongoing surveillance in states such as Minnesota. The final IOM report confirmed that our study and disease surveillance were, in their words, the “gold standard.” What really mattered was that over the ensuing months, all the tampon manufacturers, reacting to the TTSSS findings, greatly reduced the fluid capacity of their highest-absorbency styles, and cases of TSS dropped dramatically.
The TSS investigation was not only my personal launching pad into the big leagues of epidemiologic investigation and analysis; it also made me realize how easily data can be misinterpreted into flawed science and how important it is to get a number of perspectives on board. And it taught me to make sure you ask the right questions, lest you be led to the wrong answers.
In this case, I’m certain that the wrong conclusions from CDC officials regarding TSS and the continued use of high-absorbency tampons resulted in many more women becoming seriously ill and even dying. To this day, I still wonder how many of the TSS-related deaths could have been prevented had the findings of the TTSSS been supported by the CDC and promoted to the public before tampon fluid capacity was reduced by the manufacturers several years later.
Not every outbreak has to have deadly consequences to have a significant effect on a community or to provide important lessons in public health.
It was early in the afternoon of July 10, 1984, that I got a call from Dr. Ron Sorenson, an internal medicine doctor at the Brainerd Medical Center. Ron informed me that at least thirty patients had been seen at his hospital since March with unrelenting chronic diarrhea; none had yet recovered. Despite the fact that eight had been referred for further evaluation at the Mayo Clinic, the University of Minnesota Hospitals, and the Minneapolis Veterans Administration hospital, no cause could be identified.
Located about two hours’ drive north of the Twin Cities, the beautiful lake country of Brainerd, Minnesota, has been the go-to place for summer fun at one of the hundreds of crystal clear lakes. But to this day, the mental image of Brainerd takes on a double meaning for me: lakes and diarrhea, and I mean a lot of both.
No doctor or clinical laboratory director had thought to report these cases to the Minnesota Department of Health because, basically, no one knew what illness to report. To make matters more complicated, each of the eight patients seen at our state’s leading medical centers was given a different diagnosis with a generalized label like irritable bowel syndrome, nonspecific colitis, or chronic diarrhea of unknown etiology. Two of these patients were seen by the same expert physician team just two months apart, but despite identical illnesses, they came away with different diagnoses. The physicians hadn’t made the connection that both patients were from Brainerd and both had become suddenly ill at about the same time.
No one wants to talk about diarrhea; it’s almost as embarrassing as having lice. So members of the Brainerd community were unaware of the illnesses that were occurring around them. And because the Brainerd Medical Center had thirty-six physicians for a community of 14,000 people, it wasn’t until early July that the doctors made the connection that something unusual was happening.
Because I am an epidemiologist, my interest is always piqued when someone reports a regional cluster of similar illnesses that appears to be out of the ordinary. It was clear to me on that first call with Ron that the chances of seeing thirty-plus patients in the past five months with new onset of severe, chronic diarrhea in a town the size of Brainerd, and all presenting to one medical center, was like winning—or maybe losing—the lottery.
During our call, Ron provided the details of one of the patients, whom I’ll call John. John was a healthy seventy-seven-year-old man who had developed sudden onset of watery diarrhea. He had few other symptoms; no nausea, vomiting, cramps, or fever. For the next month he had ten to twenty bowel movements a day and lost more than twenty pounds. After numerous stool samples came back negative for the typical causes of infectious diarrhea, he was hospitalized as one of the eight patients noted above. The only remarkable finding was that a colonoscopy showed inflammation of his colon. He was diagnosed as having nonspecific colitis of unknown etiology. He was treated with several antibiotics but there was no change in his symptoms.
John’s social life and everyday activities suffered, as he could not be far from his bathroom. Over the course of the next year, his diarrhea continued with only a slight reduction in the number of episodes, though he realized he could eat more food without substantially changing his bathroom routine. As a result, he gained back some of the weight he’d lost. During the second year he noticed that he was having fewer and fewer diarrheal episodes. And by 550 days following his first symptoms, the frequency and volume of his stools returned to normal.
Within minutes of Ron’s call, I gathered our senior infectious disease epidemiology and laboratory team at the Minnesota Department of Health. A group of us would head to Brainerd that night to begin our investigation.
I strongly suspected an infectious disease microbe was to blame for this outbreak because of the sudden onset of illness in so many individuals. So we called our colleagues at the CDC foodborne division and shared what we’d learned so far and requested their lab support. They had two of their staff join the investigation.
The new CDC EIS officer, who was just learning the ropes of outbreak investigations and who would arrive on a plane from Atlanta the next day, would become my professional soul mate. Dr. Kristine MacDonald—now Kristine Moore—provided invaluable leadership during this investigation. When she completed her EIS stint, she took a position at the Minnesota Department of Health as the assistant state epidemiologist. We have been a synergistic team ever since, and as I tell my students frequently, epidemiology is a team sport. I couldn’t have accomplished half of what I did without Kris as my professional partner.
Kris recalls, “The biggest issue was trying to determine the etiologic agent and how people were being exposed to that agent. Then: How large was the affected cohort? How much of the community was impacted?”
The first thing we had to do when we arrived in Brainerd that night was to pore over the records of patients the clinic had seen for diarrhea in the past six months. If this was a real outbreak, we should be able to pinpoint when these cases started appearing. We also used the clinical information on the patients who’d had extensive medical workups to start to develop a case definition.
We defined a case as someone with diarrhea of unknown etiology lasting four or more weeks. As we learned more about these cases and the outbreak in general over the weeks that followed, this definition held up as being both sensitive, picking up all cases, and specific, not including any cases of diarrheal illness that were due to some other cause. Since we had not identified an infectious or chemical reason for the illness, we had to use a combination of clinical findings to define the outbreak-associated cases and distinguish them from cases with known causes like Crohn’s disease or colon cancer.
We quickly reviewed the thirty-plus cases Ron had described to us over the phone. We included the first twenty-three that met our case definition and had onset of illness between April and June 1984. We also identified forty-six gender- and age-matched controls who had not had diarrhea during this same time—sixty-nine in total. We asked about everything imaginable that might happen in a person’s life in a given month. In particular, we asked about everything they had consumed in the month before, including medications.
Kris took over as lead of the clinical and microbiologic aspects of the investigation while I concentrated on the epidemiology.
We hit pay dirt almost immediately. The first three cases, none of whom knew one another, reported that they routinely consumed raw milk sold by a local dairy located just outside the Brainerd city limits. We knew we had to be very careful while conducting our subsequent interviews so we didn’t lead interviewees into recalling a history of raw-milk consumption and biasing the results, but this lead was nonetheless a gold mine.
The critical relationship between illness and raw-milk consumption quickly became clear and compelling. The case-control study found raw-milk consumption the only one that stood out among the hundreds of factors we considered. In fact, cases were more than twenty-eight times more likely to have consumed raw milk from the local dairy than the controls.
In 1864, Louis Pasteur discovered that heating beer and wine to temperatures less than boiling for variable time periods was enough to kill most bacteria. This process prevented these beverages from spoiling while not altering their quality or taste. Today, the process of pasteurization is used widely in the dairy and food industries for microbial control, thus ensuring the safety and preservation of milk.
Raw milk, which some people still consider to be healthier and more nutritious, is not pasteurized. Before the age of routine pasteurization, many people, especially children, fell prey to a number of dangerous diseases as a result.
So we had an answer to the why in Brainerd. But there was still a lot we didn’t know. What was causing this illness? Was it an infectious disease, and if so, were the cows infected? Could others who hadn’t drunk the raw milk become infected from the ill cases? Were there any treatments that could reduce the symptoms or even cure the illness? Was this just the tip of the iceberg?
Investigative priority number one: Stop the outbreak. After confirming the local dairy’s milk as the source of the microbe or chemical causing the outbreak, our first act of business was to make sure no additional milk was sold from that farm. The farmer quickly understood the extensive body of evidence we had implicating his milk with the diarrheal illness. He agreed not to sell his raw milk to any source unless it was going straight into a plant for pasteurization. Observation and the use of epidemiologic studies allowed us to “pull the pump handle,” even though we hadn’t yet discovered the specific cause of the outbreak. After the sale of the raw milk stopped, so did new cases.
Eventually, we confirmed 122 cases of chronic diarrhea among the drinkers of raw milk from that specific dairy. The first had onset in December 1983 and the last in July 1984. Together, the Minnesota Department of Health and the CDC threw every lab resource we could into analyzing this outbreak, yet we could not identify even a suspect infectious virus, bacteria, parasite, or chemical cause in either the human cases or the cattle herd at the dairy. And it wasn’t because we didn’t have lots of fresh specimens.
After much discussion among my colleagues at the Minnesota Department of Health, the CDC, and staff at the Brainerd Medical Center, we decided this disease needed a name. We designated it “Brainerd diarrhea,” following the then current practice of using geographical names, such as Lyme (Connecticut) disease and Norwalk (Ohio) virus. Brainerd diarrhea is the officially recognized name for this condition in the medical literature.
“Despite a really extensive, elegant investigation with the most current testing methods, we never did find the etiologic agent,” says Kris. “But we really put the condition on the map.”
Through extensive efforts to uncover previously unreported outbreaks or single cases, we found a similar clinical illness among raw-milk drinkers in Minnesota (1978–79 and 1984), Oregon (1980), Wisconsin (1981–83), Idaho (1982), Massachusetts (1984), and South Carolina (1984). In addition, at least ten outbreaks have occurred since Brainerd, including large ones in Illinois and Texas. In each one, either raw milk or contaminated water was responsible.
I’m convinced that Brainerd diarrhea is caused by an infectious agent and that we will eventually find it.
As we have seen with HIV/AIDS, toxic shock syndrome, and Brainerd diarrhea, virtually nothing that happens in life is off-limits or irrelevant to the epidemiologist’s purview. It ranges from the most intimate and personal aspects of individual biology all the way up to the most public and far-reaching geopolitical clashes.
The lesson the Brainerd experience taught me was: You don’t have to have all the answers to have the critical answer. Like John Snow, we can stop or limit the occurrence and impact of infectious diseases without knowing everything about them. I often hear that we can’t act on this or that because we don’t have all the answers. That’s nonsense. We have to be prepared to go into battle with the knowledge and resources we have, beginning with basic observation.
And we can!
In the early days of the 2015–16 Zika outbreak in the Americas, I found myself repeatedly frustrated by scientists and journalists who had never been involved with an actual outbreak investigation declaring that we didn’t have proof that the Zika virus caused microcephaly and Guillain-Barré syndrome and thus that all public health recommendations were not based on conclusive evidence. From my experience, I considered the evidence abundant and conclusive, and any delay in responding was an irresponsible and indefensible position.
My colleagues and I have often been criticized by politicians and the media for “making it up as we go along,” to which I plead 100 percent guilty. When we are in the midst of pursuing a serious outbreak of unknown origin or scope, we are making it up as we go along. Being a public health official leading a serious infectious disease outbreak investigation means you often have to make quick decisions about taking action in order to prevent additional cases and even deaths. The challenge is not to be wrong, because your credibility will be forever challenged if you are.
As Bill Foege puts it, “You have to make adequate decisions based on inadequate information.” That is the very nature of epidemiological investigation. The important thing is for the public to understand this and have confidence that competent and dedicated men and women are on it: that they are telling you exactly what they know and don’t know, and what they are doing to “remove the pump handle.”