The World’s Deadliest Poison

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by John S. Marr, MD, MPH, and Marcus A. Horwitz, MD

Just after midnight on December 27, 1974, the telephone rang at the home of Dr. John Marr, the New York City Health Department’s principal epidemiologist. In theory he was always on call if a disease outbreak was suddenly to be recognized, but he had never been bothered. A call was quite unusual, especially during the night, and was a bit disturbing. Six months before, as part of his initial orientation to the department, he had visited the Poison Control Center at the Bureau of Laboratories. Afterward he thanked the director and left his phone number should an emergency arise. He had been impressed by the center’s staff of largely volunteer pharmacists manning the telephones surrounded by the books and articles on poisonings they used when a call came into the phone bank about an unusual poisoning. The staff responded to calls around the clock from emergency rooms, private physicians, and a frightened public that urgently requested treatment for a noxious substance that had been ingested or inhaled. He thought he would never be called — they were experienced professionals.

That night the center’s midnight shift consisted of a single pharmacist who answered queries from the occasional caller and advised on appropriate treatment. This pharmacist’s call to Marr was to report an unusual request he had just received. A Bronx hospital doctor had asked for release of botulism antitoxin. The pharmacist said the call had come from a neurologist who wished to treat a 27-year-old woman who had signs consistent with botulism.

For years the center – the first in the country – provided a valuable resource and was one of the few sources in the country of botulism antitoxin aside from the Centers for Disease Control (CDC). Marr asked for details and upon hearing them approved the release of the antitoxin.

Botulism is quite rare in the United States, but makes up for its scarcity by its lethality. Earlier in the twentieth century case fatality rates were nearly 60% but by the 1970s with increased recognition, prompt antitoxin treatment, and the advent of intensive care units, overall mortality had dropped to under 30%. In comparison typhoid fever had a 20% mortality rate in the pre-antibiotic era but dropped to less than 1% by 1974. Botulism also shared the unique distinction (along with smallpox) that a single case was considered to be an “epidemic” by the CDC.

Marr lived in Manhattan’s upper east side. He had a vague idea where the Bronx hospital was but didn’t own a car, and a subway ride in the middle of the night was iffy. But he knew that the neurologist had to be consulted and the patient’s condition evaluated. Since he had been told the woman was now comatose and on a ventilator, her family also had to be questioned. Was this to be a single case of botulism, he thought, or the first of many? Was it due to a commercial food product or something that had been home canned? Three years prior a commercially canned vichyssoise soup had killed a man in nearby Westchester County. The entire batch of cans was recalled and six found to be contaminated. Marr knew that the food in the patient’s home had to be removed, and blood and stool specimens had to be collected for special tests.

Fortunately a bureau colleague and friend lived in the Bronx and had a car. John Welton, a lay epidemiologist with a Masters of Public Health (MPH) degree, had worked at the bureau for over a year. He sported a scruffy brown beard and mop of hair that drooped over his forehead. He commuted to work daily in an ancient Volkswagen beetle with special hand controls. In 1953, as a toddler, he and his two older brothers contracted polio several years before the vaccine was available. He required crutches and metallic leg braces in order to ambulate. His brothers were later to become a priest and cop, but Welton’s hope of becoming a doctor seemed to disappear. Marr knew Welton was an excellent epidemiologist and very good behind the beetle’s wheel. Two years before, he had driven round trip to Loma Linda, California for his training and MPH degree. Since July he frequently provided Marr with a ride home up the FDR Drive at the end of the day. Marr decided to call him.

Welton knew the hospital – the Jacobi Medical Center. He said he would interview the doctor, look at the chart, talk to the patient’s family and collect specimens. The two planned to rendezvous later in the morning at Marr’s office in the Bureau of Communicable Diseases. By 9:00 a.m. on December 27th he arrived with test tubes of blood and a container of the patient’s stool.

He reported that the young woman had been ill for a number of days, complaining of a difficulty swallowing or even talking. On the 26th of December she had difficulty in breathing and in the morning her husband took her to Bronx Lebanon Hospital Emergency Department where she was thought to be psychosomatic and was given a placebo (an injection of really nothing more than glucose water). Later that day after returning home, her husband noticed that she was turning blue from lack of oxygen. Quickly, he took her to an open window for more air. When this had no effect he called for an ambulance and began to perform CPR. By the time the paramedics arrived she was in cardiac arrest. They brought out the defibrillator and were able to revive her heart rhythm, but she remained comatose. At 5:30 p.m. on the 26th of December, she was admitted to Jacobi Medical Center. The admitting physician called in a consulting neurologist who noted signs suggesting botulism and requested the antitoxin, which was administered at 2:33 a.m. on the 27th of December. Welton added that the woman had been distraught days before becoming ill and had been treated with a mild tranquilizer by her local physician. Her complaints had been attributed to grief after her mother-in-law died two weeks before from a heart attack.

That morning Marr had already alerted the Bureau of Laboratories to be ready to test the specimens of blood, and foods that were being collected by sanitarians sent to the patient’s home. Later that morning he received a call from Dr. Eugene Gangarosa, director of the CDC’s Bacterial Disease Division, Bureau of Epidemiology. The hospital’s request for botulism antitoxin had automatically alerted the CDC. It was protocol for all states and the City to notify them whenever antitoxin was requested. Marr detected that he was on a speakerphone with Gangarosa – he wondered whether an audience of epidemiologists in training was listening in the background. The doctor asked about the status of the case and immediately offered assistance. There seemed to be subtle arm-twisting – the CDC had an undeserved reputation of riding in on a white horse at the beginning of a serious outbreak and then taking credit for its resolution. Marr thought that the investigation appeared to be under control but decided to invite the cowboys — there were too many things that needed to be investigated and his entire staff at the time consisted of Welton and 10 nurse-epidemiologists who had just begun their training. New York City did have a permanently assigned CDC Epidemic Intelligence Service (EIS) officer, but he was on vacation.

Marr arranged with Gangarosa to share specimens with CDC. Gangarosa said that an EIS officer would fly to New York to link up with him, review the data, consult with the neurologist, and interview the patient’s family. The diagnosis had not yet been confirmed but signs strongly suggested botulism.

Botulism is a deadly intoxication caused by a neurotoxin released from spore forming bacteria. It is considered one of the most lethal poisons in the world — one microgram can kill an elephant. Its toxin is much deadlier than cyanide, arsenic and strychnine and on a par with other lethal toxins found in puffer fish, jellyfish and the skin of colorful tropical tree frogs. The causative bacterium, Clostridium botulinum, is a single species within the large family of Clostridium that includes other species that cause food poisoning: (perfringens), toxic enteritis (difficile) and tetanus (tetani). Its taxonomic name was derived from a twisted bottle-shaped appearance first seen under the microscope (Greek clostridium = spindle), and Latin botulus = sausage). The first reported case of the disease was in Germany at the turn of the twentieth century. It was attributed to sausages.

There is a cruel paradox between botulism and tetanus bacteria that share the same genus. The former produces a toxin preventing release of the neurotransmitter acetylcholine across striated muscle synapses, resulting in a progressive loss of skeletal muscle function, eventually producing complete paralysis. Muscle weakness begins at the top of the body. Eye muscles, including the ciliary muscles that control iris contraction, begin to falter, resulting in dilated pupils. Loss of other eye muscle movements produce complaints of double vision and drooping eyelids. Swallowing becomes increasingly difficult; tendon reflexes are slowly lost, and eventually the diaphragm – a striated muscle — fails to rhythmically contract resulting in pulmonary arrest. Strangely, sensory functions including smell, hearing and consciousness are unaffected. Patients feel pain, are fully conscious, but cannot speak or move.

Tetanus bacteria produce a toxin with the opposite effect. The toxin blocks another inhibitory neurotransmitter allowing uncontrolled and continuous skeletal muscular stimulation – severe spasms. The term lockjaw or “trismus” is used to describe a sustained contraction of jaw muscles. Other facial muscles contort producing “risus sardonicus” – a sinister faux smile. Larger muscles in the back, arms and legs continuously contract, bending the body like a pretzel. Patients are fully conscious and in severe pain.

Marr had never seen a case of botulism but had diagnosed and treated three cases of tetanus while a resident in Metropolitan Hospital in Spanish Harlem a few years before. It was a grim disease to follow; one of the three patients survived, only to be readmitted a year later with a fatal heroin overdose. An addict that “skin popped” heroin instead of “mainlining” introduced spores into oxygen-free infected wounds. When spores germinated in the dead tissue, toxins entered the circulation. Once fixed to motor end plates, muscular contractions began. Both botulism and tetanus toxins are strongly fixed to motor neuron end plates and cases last for three to four weeks until, supported in intensive care, the toxins slowly degrade. Afterwards, botulism and tetanus patients require months of rehabilitation. Early treatment with antitoxins may neutralize circulating toxins but do not reverse toxins once fixed. If the young female patient in the Bronx had botulism it might be too late to reverse the process but the antitoxin might neutralize free-floating toxins.

New York City’s Bureau of Laboratories was ready to test the patient’s blood and stool specimens for evidence of free-floating toxin. The city’s lab dated back to 1896, founded to test for newly discovered germs like typhoid and diphtheria. In 1904 the bureau had incriminated the infamous Typhoid Mary as a chronic carrier. It now hosted the best virologists, bacteriologists and experts on fungal diseases in the country. The bureau had moved in the 1950s from the health department on Worth Street to a modern facility a few blocks from Bellevue Hospital. But a vestigial lab remained on the seventh floor of the Worth Street building. Marr was told to bring the specimens to the lab and meet Milton Lovell, a microbiologist, who would perform the tests.

When he arrived on the seventh floor, at what appeared to be an antiquated lab frozen in time, he was reminded of his high school biology lab. There were deep soapstone sinks with elbow faucets, a centrifuge, refrigerator, antiquated cabinets, and an ancient metal locker, but the room was spotless. He noticed four small cages on a counter top each containing white mice that scurried in beds of sawdust and nuzzled water bottles. Marr introduced himself to Mr. Lovell, a handsome gentleman wearing an immaculate white laboratory coat. He had neatly cropped silvery hair and a body builder’s physique. The following year, during another botulism outbreak, Lovell told Marr he had emigrated from Trinidad 30 years before. As a young man he had won a contest for the title of Mr. Trinidad. After college Lovell decided to pursue a career in microbiology in the states and was eventually employed by the Bureau of Laboratories. He still retained his muscular build and remnants of a Trinidadian accent. Aside from daily routine duties, Lovell had been selected to become the bureau’s dedicated botulism expert. It required attending a course on laboratory procedures at the CDC where he had also received the rare botulism vaccine reserved for people who had intimate contact with the organism and its toxin.

The disease was so rare throughout the country that no one ever considered the vaccine for routine public immunization, while a similar vaccine for tetanus had been successfully used for decades. Both vaccines were “toxoids” made by killing the organism and denaturing the toxin antigens into toxoids that would stimulate the immune system to produce antibodies. During World War II, all American troops received tetanus and diphtheria (TD) toxoids. Only eight cases of tetanus occurred in American troops, and most of the eight cases were attributed to those who had escaped the vaccine or were under-immunized. The Army seriously considered botulism toxoid for use prior to the Normandy invasion. Officials were concerned about Germany’s use of poisonous gas in World War I. They believed that Germany might have a large arsenal of additional poisonous gases and biological agents like botulism toxin that the enemy might release after the invasion. However a mass botulism immunization program never materialized, perhaps because another recommendation in 1942 resulted in a misadventure with a mass vaccination effort to protect troops from yellow fever. A contaminated yellow fever vaccine had led to a massive outbreak of clinical hepatitis that had infected more than 30,000 soldiers.

While the circumstantial evidence had been enough to treat the young woman in the Bronx with the botulism antitoxin, laboratory proof was needed to make a definitive diagnosis to be sure of treatment. So Lovell explained to Marr the concept behind the mouse neutralization test. He had pre-treated mice in three cages with botulism anti-A, anti-B and anti-E antitoxins. Each antitoxin would protect one set of pre-treated mice when challenged by the patient’s serum (a by product of her centrifuged blood); two sets of mice that received non-matching antitoxin would develop signs of paralysis within 24 to 36 hours – the usual incubation period between ingestion and symptom onset. A fourth cage of mice would act as a control.

Botulism A, B and E toxins are distinct from each other. The complete series of toxins had been named in alphabetical order — A through F — but only A, B and E affected humans. Types C and D caused similar signs of paralysis in animals, especially type C intoxication in ducks that foraged in murky anaerobic lake bottoms. Type F was rare — only one case had ever been reported in the country — although it was more common in Europe. The three A, B and E antitoxins were produced by repeatedly immunizing horses with micro-doses of toxins until the animals eventually developed protective antibodies that were extracted from the horses’ blood streams. A similar process was used to create the trivalent antitoxins used to treat humans.

It was around noon on December 28th when the EIS officer, Dr. Marcus Horwitz, arrived at the bureau. He told Marr that he wanted to visit Jacobi Medical Center that afternoon to review the patient’s chart, discuss the case with the consulting neurologist, and talk with family members. He knew Jacobi, a municipal teaching hospital with a large staff of residents and specialists affiliated with Albert Einstein medical school. He was also familiar with the city having gone to medical school at Columbia on the upper west side and later having done a residency in internal medicine at Albert Einstein in the Bronx. He was a tall, angular, young man who Marr immediately liked. He certainly was not a swaggering John Wayne type, more of a Gary Cooper. Horwitz had become an honorary New Yorker years before when he visited the city for the first time and was robbed after taking a wrong subway line into a dangerous part of Manhattan. He certainly knew the territory. Horwitz was curious about the recent death of the mother-in-law. She had died at Westchester Square hospital. It served the local community in the southwestern part of the borough, but Horwitz had never heard of it.

In 1974, New York City hosted more than 80 hospitals. The seven medical school hospitals were associated with an additional 12 municipal acute and chronic care hospitals like Bellevue. Federal hospitals included four large Veteran’s Administration facilities and a Public Health hospital on Staten Island that once served as a quarantine facility. The state also had a large psychiatric facility in Brooklyn. With the exception of Staten Island, there were dozens of large Catholic, Protestant and Jewish hospitals in the other four boroughs. Charitable organizations and anonymous philanthropists supported some. Over the years the smaller facilities constantly merged, split, or closed, while others changed their names. Before 1940 the Hospital for Special Surgery in Manhattan was named the Hospital for the Ruptured and Crippled.

Some mid-sized hospitals, like Westchester Square, struggled and never benefited from any philanthropist or charity. Built in 1929, like other similarly sized independent hospitals, it served the immediate neighborhood by providing routine medical, surgical and obstetric needs. But it was lingering long past its usefulness, and unlike Jacobi, it had no residents or teaching programs and only a few specialists on staff.

Earlier in the century even the smallest in-patient facilities thrived as vest- pocket sanatoria, infirmaries, dispensaries, and polyclinics with a dozen or so beds. These were vestigial remnants of a bygone era that also included private asylums referred to as loony bins by some wags. The rich committed their crazy uncles and family members that had tertiary syphilis, dementia, and dipsomania or were drug fiends. Yet, some proprietary hospitals remained as boutiques continuing to thrive by treating an affluent population wishing privacy. (One gilded hospital near Gracie Mansion posted a wine list for visitors on the wood-paneled elevator wall under a glass plaque.) The worst of all hospitals — big or small — were referred to as “pus pockets.” Many were on the list of aging hospitals that a governor’s commission planned to close over the next few years.

After Horwitz went to Jacobi, he and Marr planned to visit Westchester Square to review the chart of the mother-in-law who had died more than a week before. She had been the matriarch of a large family. Two relatives from Italy had flown in to attend her funeral but then it had been delayed after it was decided that her body would be sent to Italy for burial. Family members said the deceased had enjoyed preparing Italian delicacies and favored various home-canned (bottled) foods. After her death and waiting for mourners to arrive, she had been embalmed. A daughter said that many foods, including home-canned vegetables, had been served to more than 20 family members on Christmas day and that the left-overs were still available.

Since 1899, when botulism records were first kept, the most common source of the illness was home-canned foods. Bacteria are found in soil throughout the world but rarely cause disease. Humans ingest spores on most foods on a daily basis but the encapsulated bacteria safely pass through the gastrointestinal tract without causing illness. Stomach acids and competing micro-flora prevent spore germination. Spores remain quiescent until placed in an anaerobic, wet, and slightly alkaline environment containing an energy source such as sugar or protein, which is typical in home-jarred vegetables topped with olive oil and placed in a sealed container. Vegetables, mushrooms, fruits, beef, pork, poultry, a variety of fish, milk and milk products, and dried spices have been identified as sources of outbreaks since records have been kept.

The single U.S. outbreak of type F botulism was traced to venison jerky in California. Type E outbreaks usually occurred in the Great Lakes region and Alaska when smoked or fermented fish were hermetically sealed in foil or plastic wraps providing an environment for germination. Sixty percent of types A and B outbreaks were traced to vegetables. Unlike most fruits, vegetables and mushrooms have intimate contact with soil and most are not acidic. It has been advised that before canning vegetables they should be put into a pressure cooker to destroy the heat-resistant spores. Heating canned and jarred foods before eating denatures the fragile toxins. It is not an accident that improperly canned vichyssoise, one of the few soups (like gazpacho) that is eaten cold, can be a vehicle for the disease.

Until 1976 all botulism outbreaks were attributed to pre-formed toxins, however a newer cause of “floppy infant syndrome” was recognized that year – infant botulism. Babies and infants under the age of six months presented with signs similar to the many other causes of the syndrome but were found to be ill from toxins produced in their own guts. Until 1975 honey had been commonly used to supplement formulas. The honey contained spores able to germinate in the low acid, largely germ-free small intestines of babies. Signs of infant botulism include hypotonia, loss of suck reflex, constipation and difficulty in breathing. It was immediately recognized that the honey came from honeybees that acquired spores while clinging on flowers. The public was soon alerted and honey removed as a source of formulary supplements. Cases of infant botulism continue to occur in infants that are given other supplements like molasses, or that swallow contaminated air-borne dust that has landed on baby food.

After Horwitz visited Jacobi, examined the younger woman’s chart and discussed the findings with the neurologist, he returned to meet with Marr. He reported that the woman had received supportive care for her condition when an attending physician had consulted a neurologist that noted unusual signs and ordered a test to rule out myasthenia gravis, an autoimmune neuromuscular disease that produces signs and symptoms similar to botulism. It was negative. An electromyogram demonstrated a loss of conduction of nerve impulses to muscles and strongly pointed to botulism. The observation that the patient’s eyes did not involuntarily move after an irrigation of the ear canals with cold water also pointed to muscular paralysis. The cause of her earlier cardiac arrest could not be explained except for the possibility of a respiratory paralysis. Additional blood and stool specimens were obtained and all foodstuffs including the home-canned vegetables removed by sanitarians were sent to Lovell’s lab and shipped onto the CDC. Marr told him that the mice had not developed signs of botulism but it was too early and Lovell was monitoring their condition.

Their next plan was to visit Westchester Square hospital the following day to review the older woman’s chart and talk further with family members. They already knew that the 59-year-old woman had rheumatic heart disease, had been diagnosed as having an enlarged heart, and had complained of occasional bouts of angina. However, they noted, she had developed gastrointestinal and not cardiac symptoms a few days before she was hospitalized.

The late December temperature was unduly warm the morning of the 29th. They took the oxymoronic IRT elevated subway to a station a few blocks from the hospital and walked through the streets of the quiet neighborhood which was teetering on decay – three-story brick houses needed repairs, some apartment buildings with zigzagging fire escapes, were burned out shells, and rubbish was strewn in vacant lots. Multi-storied public housing buildings loomed like tombstones in the distance. The community, like those to the south was slowly dying except for a drugstore, bakery and grocery store.

A decade before, the six-lane Cross Bronx Expressway was finally completed extending from the George Washington Bridge east to the New England Thruway. The city’s “master builder,” Robert Moses, had performed a hemicorporectomy on a once contiguous borough and the South Bronx underwent rapid decay. It was becoming part of what later was seen on television during the 1977 World Series at Yankee Stadium and described by a commentator as “the Bronx is burning.”

Westchester Square hospital was modest and clean. Its administrators had been informed of their visit. A staff member took them to the record room. The deceased woman’s chart was not thick and chronicled the admission and subsequent events that had occurred prior to her death. It confirmed that the woman had a serious pre-existing cardiac condition. Before admission, on December 12th, she had developed nausea, vomiting, cramps and abdominal distension that were treated with an anti-emetic. The following day she complained of a sore throat and difficulty in swallowing. On December 18th after complaining of shortness of breath and chest pain she was admitted to the hospital with tentative diagnoses of pharyngitis and impending heart failure. The next day she became stuporous, was intubated and put on a ventilator three separate times, since she could not breath on her own. She died on December 22 and an autopsy found a dilated heart and evidence of bronchopneumonia. In addition to her complaints of difficulty breathing and a dry throat, the chart also revealed signs that had not been considered in the diagnosis – sluggish dilated pupils that presumably were attributed by her doctors to her cardiopulmonary arrest. Her embalmed body was being held in a local funeral home for a family viewing later in the week. Horwitz copied the chart and received permission from the family to take samples of fluid from the small and large intestines of the corpse. These samples would be sent to the CDC and the New York City Medical Examiner’s Office for evidence of botulism. There was growing suspicion she also might have had the disease. The tests would take days, but Lovell might be close to an answer from his mice.

Then a minor confrontation took place in the Westchester Square record room. A hospital surgeon saw the two men looking at the chart and asked what they were doing. They showed him their credentials and explained their mission. He was not impressed and informed them that he was the brother of Mario Procaccino, a local Bronx politician and lawyer who had once been the 1969 Democratic candidate for mayor. The annoyed surgeon allowed them to finish their review but warned that his brother would be looking into the matter. Marr never heard anything more from either Procaccino.

Marr returned to the seventh floor lab where Lovell showed him that the mice in all but one cage had difficulty using their back feet, only able to drag them while panting rapidly. It appeared that B toxin would be shown to be the causative type. Later in the day, all but the mice treated with the anti-Type B toxin died. Lovell was now preparing to test the canned mushrooms, peppers, artichokes and eggplants. The same tests would also be performed at the CDC. The results would take another few days.

On December 29th, Horwitz and Marr learned that the patient at Jacobi, the matriarch’s daughter-in-law, had just died. Still it was incumbent on the men to find the source of the poison. They recalled that according to the matriarch’s daughter, the now-deceased daughter-in-law had eaten the home-canned mushrooms at a gathering of the family. Twenty other family members had not eaten them, since the jar had been left in the kitchen and not served with the three other vegetables and main meal.

To be sure other guests were not at risk, serum was obtained from all 20. A disturbing thought occurred to Marr and Horwitz — the daughter they had been interviewing had complained of a dry throat for a few days after the family meal. She then had developed difficulty in swallowing. Upon further questioning she could not remember whether she had eaten the mushrooms but said she may have nibbled on them. A stool specimen was immediately obtained and she was empirically treated with antitoxin without waiting for results of the mouse neutralization test. Twelve other family members were admitted for observation and four had symptoms and were also given antitoxin. The daughter’s symptoms disappeared within a week, although she developed a delayed reaction to the antiserum.

A week later all canned food had been tested. Only the mushrooms contained the deadly toxin. Fragments of mushrooms were also found in the intestinal fluids taken from the mother and daughter-in-law and mushrooms taken from the daughter-in-law’s stomach at autopsy were positive for C. botulinum Type B. Intestinal contents from the mother and stool from the daughter-in-law and daughter were also positive for C. botulinum Type B. Other family members’ stool specimens were negative for toxin and C. botulinum. The investigation was unusual. Most outbreaks of botulism involved a single case, others were larger but involved people exposed at one time or over a few days. This epidemic involved three generations of a family and extended over a two-week period, exposing more than 20 people to a continuing common source.

Infectious diseases are typically characterized by the hallmarks of inflammation: rubor, dolor, tumor and calor — redness, pain, swelling and temperature. But botulism has none of these; it is an intoxication that produces no abnormal laboratory tests. Signs and symptoms are critical for a presumptive diagnosis, which favors the prepared mind.

Discussion Questions

 

  1. When the daughter-in-law came to the emergency department on December 26th, she had been ill for a number of days, complaining of difficulty in breathing, swallowing, and even talking. She was given a placebo. In hindsight, could her serious illness have been suspected earlier?
  2. Later on December 26th, the daughter-in-law was admitted to the hospital and the neurologist diagnosed botulism. The diseases most frequently confused with botulism are those that produce generalized weakness. Differentiating botulism from other diseases is essential for early initiation of therapy. How was this differential made?
  3. Many foods, including home-canned vegetables, had been served to more than 20 family members on Christmas day. In fact, the daughter (not the daughter-in-law with the fatal illness) had complained of a dry throat for a few days after the family meal. She then had developed difficulty in swallowing. Four other family members also had symptoms. All were treated with antitoxin and recovered. Comment on the epidemiological concept of “spectrum of disease” and how this applies here.

ABOUT THE AUTHORS

John S. Marr, MD, MPH, is the former State Epidemiologist for the Virginia State Department of Health. At the time of this case, he served as the Director of the Bureau of Communicable Disease for the New York City Department of Health.

Marcus A. Horwitz, MD, is a professor of Medicine and Microbiology, Immunology & Molecular Genetics at UCLA School of Medicine. At the time of this case, he served as the Epidemic Intelligence Officer (EIS) for the Centers for Disease Control and Prevention.

See also:

Read more Backstories in Epidemiology: True Medical Mysteries, coming soon:

  • “It’s All in the Bottle,” an apparent outbreak of TB in a Virginia state prison for women
  • “Bad Blood: The Gift of Giving,” a malaria outbreak in New York City
  • “Appendectomy Masquerade,” an epidemic initially attributed to appendicitis in upstate New York
  • “The Babies Are Dying,” newborn deaths in a West Virginia rural hospital nursery
  • “Clam Aches,” an outbreak at a church picnic from Maine clams
  • “Of Bites and Men: The Most Dangerous Urban Animal,” a story where the number of human bites exceeds shark bites

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