The Deadly Dinner Party: and Other Medical Detective Stories Read online

  Finally Soper got the break he needed. Just days after leaving the employ of the Warrens in Oyster Bay, Mary had taken a job on September 21, 1906, in Tuxedo, New York. Typhoid soon followed, but Mary left the household before Soper could find her. Then, in March 1907, Soper was hired to investigate a typhoid outbreak in a fashionable New York brownstone, the home of Walter Bowen at 688 Park Avenue. Soper finally found Mary Mallon and confronted her. According to his account, “I had my first talk with Mary in the kitchen of this house. . . . I was as diplomatic as possible, but I had to say I suspected her of making people sick and that I wanted specimens of her urine, feces, and blood. It did not take Mary long to react to this suggestion. She seized a carving fork and advanced in my direction. I passed rapidly down the hall, through the tall iron gate . . . and so to the sidewalk. I felt rather lucky to escape.”

  Soper then tracked Mary down to a rooming house and returned with a colleague, but, despite “as much tact and judgment as we possessed,” they could not persuade her to submit to an examination. The New York health commissioner interceded, and a group including a female physician, Dr. Josephine Baker, accompanied by the police, went to arrest Mary. Mallon greeted them once again sporting a “long kitchen fork in her hand like a rapier,” wrote Dr. Baker. “As she lunged at me with the fork, I stepped back, recoiled on the policemen, and so confused matters that by the time we had got through the door, Mary had disappeared.” She hid in a closet, but a scrap of her blue calico dress, caught in the closet door, drew their attention.

  According to Dr. Baker, a thin, bespectacled woman, “She came out fighting and swearing, both of which she could do with appalling efficiency and vigor.... She knew that she had never had typhoid fever; she was maniacal in her integrity. There was nothing to do but to take her with us. They lifted her into the ambulance and I literally sat on her all the way to the hospital; it was like being in a cage with an angry lion.”

  Mallon was placed in an isolation ward of the Willard Parker Hospital, a contagious disease unit in New York. From Mary’s perspective, the notion that she could be spreading the disease was nonsense. She had never been sick with typhoid; she must have had a very mild case that mimicked some other minor illness back when she lived in Ireland. Nevertheless, her initial cultures, as well as those taken over the ensuing eight months, all grew out typhoid bacilli. She is generally believed to be the first documented case of an asymptomatic typhoid carrier in the United States. The city health department offered her surgical removal of the gallbladder, on the theory that the typhoid bacilli settled there in carriers. Mary, not ignorant of the risks of that surgical procedure in 1907, refused the operation.

  Because health authorities were not convinced that Mary Mallon would obey their directive that she not work as a food handler or cook, she was confined in quarantine at Riverside Hospital, a small, isolated institution on North Brother Island, a thirteen-acre patch of earth in the East River (near the present site of La Guardia Airport). A very public legal battle ensued, highlighting the classic conflict between personal liberty and the public good. Lawyers tried to free her, but the courts upheld the state’s legal right to hold her involuntarily, arguing that she represented an “imminent peril.” The city officials cited two sections of the Greater New York Charter that read:

  The board of health shall use all reasonable means for ascertaining the existence and cause of disease or peril to life or health, and for averting the same, throughout the city. [Section 1169]

  Said board may remove or cause to be removed to a proper place to be by it designated, any person sick with any contagious, pestilential or infectious disease; shall have exclusive charge and control of the hospital for the treatment of such cases. [Section 1170]

  In the press coverage following the legal case, the media dubbed Mallon “Typhoid Mary.” Typhoid was a common cause of death during the early years of the twentieth century; the public had little patience with someone who knowingly spread the disease to others. It would be akin to someone nowadays knowingly exposing people to HIV or a resistant strain of tuberculosis.

  On February 19, 1910, Mary was released after promising to change jobs and be monitored by the health authorities. She did neither, and more small outbreaks were attributed to her. Again, Soper apprehended her (in 1915), and again she was held involuntarily. She remained quarantined at Riverside Hospital for the rest of her life. She died of a stroke in 1938, having spent half her life in confinement.

  Mary Mallon was personally responsible for at least 53 cases of typhoid fever and three deaths. At the time of her death, there were 349 other typhoid carriers known in New York City, but she was the only one who was confined; the others simply changed their habits and submitted to regular monitoring by the health authorities. Although other carriers, such as “Mr. N,” a cow milker from Folkestone, England, are responsible for spreading the disease more widely (to approximately two hundred people in his case), Mary Mallon is by far the most notorious.

  In the Catskill outbreak among the firefighters, both the water supply and the hotel plumbing system had been tested and exonerated as the source of the bacteria. That left the missing breakfast cook, who, as it turned out, proved even more difficult to locate than Typhoid Mary.

  Says Kondracki, “Gone are the days where college students work the Catskills. The breakfast cook who left was from Central America, where typhoid is endemic and typhoid carriers are more common. We suspect, but could never prove, that he was the source. He left Grovers before the outbreak hit the news. We tried to track him down in several ways. A Spanish-speaking public health nurse even staked out his last known New York address, but he never showed up there. We also corresponded with Social Security and the welfare folks, but we never found him.”

  Despite the failure to locate the cook, Kondracki is still pretty sure he knows precisely how the bacteria got into the orange juice. “People respond to interviews differently,” he recalls. “The first time I interviewed Watkins [the infected dishwasher], he was in the kitchen with his boss present. He was very closed mouthed. Later, I spoke with him without his boss [being present]. I took him for a stroll outside the building, and we sat at a picnic table on the side lawn and just shot the breeze a bit. When it was clear to him that I wasn’t a police-type person, he opened up. He told me that they stirred the orange juice with a two-foot-long metal whisk. I remember him saying ‘it was the one with the string on it,’ although I wasn’t sure what he meant at the time.

  “When I returned to the kitchen, there were three metal whisks hanging from the wall. One of them had a piece of string that attached the handle to the whisk. I confiscated it although I knew I’d never culture anything out since it had been though the dishwasher at 180 degrees. As I was driving out of town, I bumped into Watkins on a street corner, quite by accident. I pulled over, opened the trunk and asked him if the whisk with the string [that I had confiscated] was the one he and the missing cook had used. It was.

  “I asked him why the string was there. He told me it was to keep the whisk attached to the handle. It had kept falling off [without the string],” Kondracki says, his voice now filling with excitement. “You see the point. When it fell into the orange juice, he would have to reach his arm into the plastic bin to retrieve the thing. That established in my mind the connection. His workstation was right outside the employee’s bathroom, which was not equipped with soap and water or paper towels. I had a plausible biological explanation.”

  T o address the problem that the juice was an unusual vehicle, the state investigators performed lab experiments using the same strain of typhoid found in the epidemic, along with the orange juice, which has a very acidic pH of 3.8. They found that, although the bacteria would die in less than two hours in the orange juice concentrate, they could live for more than six hours in the reconstituted (and more diluted) juice. The report goes on to state, “Theoretical calculations of the infective dose showed that 30 – 50 gallons of orange juice could have been contami
nated with 50 mg [a miniscule amount] of fecal material, and still have achieved sufficient numbers of organisms in a glass of orange juice to cause illness.”

  Ultimately, forty-five confirmed cases were identified, making the Catskill outbreak the largest domestic typhoid epidemic in nearly a decade. Besides the confirmed cases, twenty-four others were strongly suspected to be involved but were never proved with certainty. Including both groups, the attack rate was 11 percent of hotel guests at Grovers.

  Twenty-one patients were sick enough to require hospitalization. Four developed complications: two cases of gastrointestinal bleeding and two of bowel perforation, which requires surgery. Fortunately nobody died in this epidemic.

  Roy Harvey, after four blood transfusions and a ten-day hospitalization, survived, although he remained out of work for four weeks. As for Rita, who never got sick, her husband explains, “She’s just not a juice drinker.”

  3 The Baby and the Bathwater

  It began on June 15, 1988, as one of the most routine cases in a pediatrician’s practice. After all, there are few problems more common than a toddler with diarrhea.

  At first, fourteen-month-old Katie Wolz of Cape Girardeau, Missouri, developed her diarrhea without any other symptoms, not even a fever—just diarrhea. Her mother, Kathleen Wolz, an energetic thirtyyear-old lawyer, reacted the same way most moms would. “I thought it was one of those viruses that kids are always getting,” she recalls. “She didn’t look sick, so I put her on liquids and figured it would pass.” But a few days later, it hadn’t passed. Little Katie still had diarrhea and now had begun spiking fevers to 102 degrees. “It was the middle of the summer and really hot. I was afraid she’d get dehydrated, so I took her to the pediatrician,” her mom remembers.

  So on July 20, Dr. Jesse R. Ramsey, a pediatrician in Cape Girardeau, examined Katie. He found her to be in good health and without any signs of serious dehydration. He concluded that the most likely diagnosis was a simple gastroenteritis.

  Bacteria and other microorganisms have a limited number of methods for entering the human body. One route is through the skin after it is abraded or cut, which provides an opening for the bacteria that normally lurk on the outside of the skin. The result is often a skin infection called cellulitis. Other times, a microorganism can gain access to the bloodstream through intact skin that is penetrated by the bite of a mosquito or a tick. Malaria and Lyme disease are examples of this mechanism. Another point of entrance is the respiratory system; numerous viruses and bacteria attack by this mode, hitching a ride on the very air we breathe. Tuberculosis and influenza are two bugs that attack in this manner, but there are countless others. Occasionally, microorganisms can get inside humans by penetrating mucous membranes like the eyes, throat, or genital tract. Conjunctivitis, strep tonsillitis, and syphilis are examples of attack through these routes.

  And then, of course, there is the gastrointestinal tract. Every morsel of food and every sip of a drink that we place into our mouths has the potential of carrying pathogenic hitchhikers. Most of those are inactivated by the acidity in the stomach. Others cannot withstand the assault of various digestive enzymes in the stomach and intestines. And still others are hunted down and destroyed by special immunoglobulins that are found in the gut. But in spite of this multilayered protective strategy, some pathogens overwhelm the host defense mechanisms, and when they do, they often produce the common syndrome of gastroenteritis.

  Gastroenteritis is a generic term that encompasses a host of different afflictions of the gastrointestinal tract; the condition is one of humanity’s most common ailments. It is usually heralded by nausea, vomiting, and fever, which is soon followed by abdominal cramping and diarrhea. Gastroenteritis can be caused by a wide variety of pathogens—bacteria, viruses, and parasites as well as toxins and poisons. The majority of patients improve rapidly and without antibiotics. Generally, after several days of bed rest, lots of clear liquids, and avoiding dairy products, the body successfully combats the invading microorganism or toxin and the tide of the battle tilts toward a favorable outcome for the patient.

  On the other hand, when the organism is a particularly vicious one, say cholera or typhoid, and when hydration cannot be accomplished, the resulting complications of fluid loss can be disastrous and in some cases fatal. In the third world in 1980, 4.6 million children died from dehydration that resulted from diarrhea. This mind-boggling number was reduced to 3.1 million in 1990, in large part due to the use of oral rehydration therapy that diminished the need for intravenous hydration, a prohibitively expensive and logistically difficult treatment in much of the underdeveloped world. The underlying diseases can sometimes be controlled by the body’s defense mechanisms, but if the person cannot keep up with hydration, even a “self-limiting” disease can be fatal.

  Although this progress has been impressive, diarrhea remains one of the most common causes of child mortality in the world. Even in the United States, the CDC estimates that food-borne diseases cause approximately 76 million illnesses, 325,000 hospitalizations, and 5,000 deaths each year. The deaths are usually in patients who have problems with their immune systems, are very old, or are very young.

  But Katie Wolz was not in the third world; this was Cape Girardeau, Missouri, in the heartland of America. And she had a perfectly normal immune system. Katie didn’t appear critically ill from the infection, and she was keeping down the necessary fluids, so Dr. Ramsey quite properly decided to hold off on antibiotics, and reassured Mrs. Wolz that she was already taking all the right steps. At the same time, however, he was sufficiently concerned by the persistence of fever and diarrhea; Katie had been ill for several days, enough time that Dr. Ramsey would have expected to see some improvement in many routine cases. There are approximately two hundred different diseases that can be spread through the gastrointestinal system, and knowing the specific cause can help identify the correct treatment. So Dr. Ramsey ordered a stool sample to be analyzed by the lab for the presence of various microorganisms—a perfectly routine test.

  Two days later, he received a call back from the lab with a result that was anything but routine. There was good news and bad news.

  The good news was that the specimen was negative for the usual pathogens. Rotavirus is an extremely common viral pathogen causing acute gastroenteritis in children younger than five. It gives rise to about three million cases of diarrhea each year in the United States and results in about fifty-five thousand hospitalizations. But rotavirus is usually a winter disease, and it is very contagious. This was summer, and none of Katie’s friends were ill.

  The rotavirus test was negative. The culture was also negative for the usual bacterial pathogens that the laboratory normally tests for—salmonella, campylobacter, and shigella. So much for the good news.

  The bad news, or to put the most optimistic spin on it, the surprising news, was that “an unusual” bacteria was growing. “In fact, it was one I had never heard of before,” recalls Ramsey, “Plesiomonas shigelloides. I quickly looked it up and learned that the bacterium was extremely rare in the United States, but far more common in the tropics. My initial reaction was, ‘I don’t believe it; this has got to be a mistake,’” says Dr. Ramsey. “But I couldn’t be sure, so I asked the lab to forward the sample to the state lab in Jefferson City for confirmation.” Then he telephoned Mrs. Wolz.

  “It was one of those ‘Don’t be alarmed, but’ phone calls that you really love to get from your doctor,” she remembers. “He told me that Katie’s culture was growing a rare bacteria and that he had notified the state lab. What frightened me was that nobody seemed sure what to do. But Katie, although she still was having some diarrhea, was much better and had no fever. I was reassured by that. Dr. Ramsey also said that he was going to get the health department involved.”

  Sue Tippen is a communicable diseases coordinator for the Missouri Department of Health, in the southeastern district, headquartered in Poplar Bluff. Along with all the mundane scraps of paper that find their wa
y to her desk each day was the results of Katie Wolz’s stool culture. That report stood out from all the others on that summer day because, like most health care professionals, she too had never heard of Plesiomonas shigelloides. So Tippen did a little research on the subject. Even in the library, she wasn’t able to find out very much, but one thing seemed clear: the bacteria with the long name had no business showing up in her jurisdiction.

  Tucked away on the banks of the Mississippi River, about 120 miles south of St. Louis, Cape Girardeau is a college town of about 40,000 inhabitants, many of whom are associated with Southeastern Missouri State University. Though it’s not an active port, an occasional riverboat loaded with tourists ties up at its docks. And although the town might serve as a perfect setting for a Mark Twain story, Cape Girardeau is not particularly exotic, and certainly anything but tropical.

  That’s what baffled Sue Tippen as she examined the report in front of her. As she put it, “I don’t expect subtropical diseases to be reported in southeastern Missouri.”

  Plesiomonas shigelloides, which, to preserve the reader’s sanity, I’ll simply refer to as PS, is an unusual bacterium in this country. A relative newcomer to the stage of microorganisms, at least in terms of when humans catalogued it, it was first described in 1947. It was thought to be a close cousin to the more notorious cholera bacillus. Cholera is caused by the bacterium Vibrio cholera, which was first discovered back in 1883 by the renowned bacteriologist Robert Koch. Known for its large epidemics (an outbreak in London in 1849 killed 14,137 people, and another in 1854 killed more than 5 percent of Chicago’s population), cholera is not only of historical interest. The disease is still endemic in many parts of the world. Beginning in 1991, an outbreak that lasted several years affected more than a million persons and killed nearly ten thousand. Even in the United States, sporadic cases and small clusters of cholera still occur, generally in people in the Gulf states who have been eating raw shellfish.