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Authors: Laurie Garrett

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Regrettably, these instructions would be violated repeatedly in years to come; sometimes with tragic consequences.
Nine years later, in February 1975, two young Australian students on walkabout in Southern Africa would unintentionally serve as “canaries” and prove that Marburg disease hadn't disappeared from the planet when the 1967 epidemics apparently ceased among vaccine researchers in Europe and in Uganda's monkey populations.
A twenty-year-old Australian draftsman and his nineteen-year-old girlfriend spent the Southern Hemisphere summer of 1975 hitchhiking around Rhodesia
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and South Africa. Sitting on the roadside outside the Rhodesian Gwaai River town of Wankie one morning, the young man felt a sudden sharp pain in his right leg. Looking down, he saw a red swelling and concluded he'd been bitten.
Six days later the couple was enjoying the Natal beaches near Margate, South Africa, when the young man broke out in a sudden sweat and felt a wave of fatigue that totally sapped him. After four days of escalating muscle pain, exhaustion, fever, and headaches he was admitted to Johannesburg Hospital on February 15, 1975. Four days later, he died, after suffering internal hemorrhaging so severe that the alveolar air sacs of his lungs were filled with blood.
During his four days at Johannesburg Hospital, the Australian was monitored by fifteen doctors and scientists and ten nurses, one of whom, a twenty-year-old nurse, fell ill with the disease nine days after the man died.
Two days after the Australian man's death, his girlfriend also got the disease. Dr. Margaretha Isaacson, of the South African Institute for Medical Research in Johannesburg, treated the patients with the anticoagulant heparin, saving their lives. No doubt, Isaacson concluded, the vast hemorrhaging
seen in the Australian man had been prevented in the other two Marburg victims because heparin stopped mini-clot formation throughout their vascular systems.
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Though the Johannesburg team was convinced the Marburg infection began with the bite on the young man's leg, they had no idea what sort of creature—rodent, insect, monkey—had attacked him. It was also possible the young man's mysterious bite had nothing to do with the Marburg infection. Within the ten days before he arrived at Natal, the Australian engaged in several other activities that could have put him in contact with a Marburg-carrying creature. In Rhodesia he slept outdoors on a field that was zebra grazing land; he handled raw meat in Bulawayo; he touched monkeys near the Great Zimbabwe ruins, and he hand-fed monkeys caged in a hotel lobby in Natal.
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The Johannesburg scientists were no closer than their German and Ugandan colleagues had been in 1967 to solving a key mystery: why do such deadly diseases suddenly appear, then just as suddenly disappear?
And so a mystery remained. It began with two teams of German scientists engaged in one of the most optimistic and potentially beneficial pursuits in health care: development of vaccines. It arose from monkey cells, and it ended somewhere in a geographic space so large and varied, spanning thousands of miles from Nairobi to Cape Town, that no one could begin to sift the clues.
At a time when scientists were talking about artificial hearts and advanced brain surgery it seemed almost inconceivable that twenty years later the Marburg mystery would remain utterly opaque.
But it would.
Joe McCormick walked briskly down the long emergency ward corridor of the Emilio Ribas Hospital, trying hard to ignore the terrified faces that stared at him from stretchers and chairs. Hospital staff scurried all about him, fighting against time to get acutely ill children and teenagers under treatment before they died.
“We've got to do everything we can to avoid panic,” McCormick thought, reiterating the sentence as much for his own edification as for a larger public health concern.
He stepped out into São Paulo's winter air and stood on the ambulance off-loading dock, watching as another dangerously sick child was transferred from a stretcher to a gurney. Almost in a daze, he glanced at his watch, noted the time, and started counting. In the next thirty minutes, thirteen ambulances arrived, each carrying a Brazilian child or young adult in the grip of meningitis. By day's end, over 200 patients passed through
the emergency doors, and the 1,000-bed hospital was filled well beyond capacity.
It was August 1974, and Brazil's burgeoning megacity—then boasting a greater metropolitan population of 20 million—was in the throes of an epidemic of meningococcal meningitis, a severe bacterial disease that could kill an untreated human being in less than twenty-four hours. Caused by
Neisseria meningitides
bacteria, meningococcal infection was spread directly from person to person, carried in the mucoid droplets of a sneeze. Even under the very best of circumstances, meningococcus killed 10 percent of those infected, and these were hardly the best of circumstances. Close to 15 percent of the cases admitted to Emilio Ribas Hospital were dying, and this was the premier treatment facility in São Paulo; death rates in smaller hospitals were as high as 77 percent in infants and 60 percent in adults.
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McCormick was flabbergasted by what he had already seen in his few weeks in São Paulo. He was on loan from the CDC's Special Pathogens and Bacteria Branch to the Pan American Health Organization (PAHO), with the task of assisting a team of Brazilian doctors in their efforts to stop the epidemic. Though he was relatively new to the CDC, McCormick's unique background put him in good stead for handling the unfolding Brazilian crisis.
While German public health authorities were panicking about Marburg virus in the summer of 1967, Joe McCormick had been impatiently cooling his heels in a remote northern outpost of Zaire. The former Indiana farm boy had been teaching elementary school in Zaire for two years. He had finished college in 1964, graduating with a stellar record in chemistry. The National Science Foundation offered him a full fellowship for graduate studies in physics, but he had turned it down—for Zaire, and adventure.
Shortly before the first workers fell ill in Marburg, civil war broke out in Zaire, pitting the two-year-old government of Mobutu Sese Seko against Katangan rebel forces led by white mercenaries. Mobutu, who himself came to power through military action, cracked down hard. Among the many measures taken in the summer of 1967 to quell rebellion was mandatory house arrest of all white people residing in Zaire.
This was tough luck for McCormick, who was anxiously pacing about his quarters in Wembo Nyambo. As he had surveyed his cinder-block rooms, which were under a constant state of siege by invading tropical foliage, McCormick felt that, on balance, house arrest or no house arrest, he had made the right decision in turning down the generally coveted NSF fellowship. Like hundreds of other bright members of his generation, McCormick deeply admired John F. Kennedy, was devastated by his assassination, and had planned, in the spirit of “ask what you can do for your country,” to join the Peace Corps.
There was a catch, however; the Peace Corps wouldn't let him teach in a foreign language, and McCormick desperately wanted to master at least
one language other than his native English. So, twenty-two years old and full of vinegar and wanderlust, he had signed on with a Methodist program that was sending teachers to Zaire.
Given recent events in Zaire, nobody much cared that McCormick lacked teaching credentials. Virtually all European- and American-trained professionals had fled the country over the last few years due to a chain of events that began in June 1960 with the overthrow of Belgian colonialism. That brought the country a new name (Zaire in place of the Belgian Congo) and its first independence leader, Prime Minister Patrice Lumumba. During the violent transition from colonialism to independence, an American missionary was kidnapped, taken to Stanleyville, and publicly assassinated, putting a pall over efforts to recruit foreign teachers, physicians, and other professionals.
Lumumba, an ardent African nationalist admired throughout the continent, ruled for only a few months before he was deposed by elements of the military and assassinated in what was later acknowledged by Congress to be a CIA operation. Four years of civil unrest and United Nations intervention followed, culminating in an Army takeover on November 24, 1965; General Mobutu Sese Seko proclaimed himself President of Zaire. Not all Zairians accepted Mobutu's leadership, and armed rebellion persisted throughout the country when Methodist recruiters scoured the United States and Western Europe in search of schoolteachers.
Into that tension stepped McCormick, a midwestern white kid with a head for science and a knack for repairing anything mechanical. His only knowledge of French was a cram course in Parisian dialect given to him by the missionary program just before his departure for Zaire. But McCormick discovered during his stay in Wemba Nyambo that he had a real knack for languages. He quickly began chatting with students and villagers not only in French but also in Lingala and Otetela, languages spoken by very few non-Zairians, as well as in the universal patois of African trade, Kiswahili.
It wasn't long before McCormick, in his youthful arrogance, felt he had mastered teaching, and started searching impatiently for new challenges. Impressed by the physicians at the local hospital, McCormick decided to become a doctor.
In late 1966 McCormick took the Medical College Admissions Test via correspondence examination, having boned up using whatever texts his newfound physician comrades could provide. To the surprise of no one who knew him, he aced the test and was well positioned to gain admission to a top American medical school. Just days before medical school was to begin, house arrest was lifted, and McCormick made his way to Duke University.
Over the next seven years, the always restless McCormick obtained an M.D. from Duke and a master's degree in tropical medicine, both financed by a federal training plan, activated in 1965 and designed to alleviate what
was then considered a severe shortage in the number of American doctors. Under the system, U.S. medical students were subsidized by the federal government in exchange for postgraduate duty in the Public Health Service.
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In McCormick's case, it meant putting in a few years' service at the federal Centers for Disease Control in Atlanta following completion of his medical studies. Since McCormick's plan was to devote himself to the study of tropical diseases, some time at CDC was precisely what he most desired.
In 1972 McCormick joined a two-year program under the Epidemic Intelligence Service, gaining training at CDC's Atlanta headquarters and being deployed to investigate outbreaks of diseases in the United States. His first assignment was to an American Indian reservation in Parker, Arizona, where people were falling ill from foods contaminated with
Streptococcus
bacteria.
By the time McCormick was ready to join CDC as a full employee of the agency's Special Pathogens and Bacteria Branch, he had already made a name for himself among the “cowboys” of the organization. Karl Johnson, who left Panama in 1971, was back at CDC, and he heard stories of the promising young EIS officer. He decided to keep an eye on the fellow—his Africa experience might one day come in handy.
But Africa would have to wait, for now McCormick was consumed by the crisis in Brazil.
Like most post-World War II physicians, McCormick had assumed that antibiotics would cure all bacterial infections, but it was clear this microbe could kill even children who were injected with massive doses of penicillin or ampicillin, the preferred drugs for meningococcus control.
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McCormick was worried. It looked like this epidemic involved a particularly virulent strain of the bacteria; possibly one that was resistant to the sulfa-based antibiotics. Despite drug treatment, the bacteria savagely attacked the membranes—the meninges—that enveloped victims' brains and spinal cords and caused excruciating pain and neurological damage. That apparent drug failure could force doctors to switch from treating patients with the cheap accessible penicillin-class drugs to using more expensive and less predictable antibiotics like rifampin and chloramphenicol.
When he reviewed the medical charts and laboratory findings on the epidemic cases, a few anxiety-provoking facts leapt out. First, the director of Emilio Ribas Hospital, Dr. Carlos de Oliveira Bastos, had noticed that the numbers of meningitis cases admitted to his facility had increased slowly by 21 percent between 1962 and 1971, and then more than doubled in 1972.
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During that time, the majority of the cases involved infants, and the leading pathogen was meningococcus Type C.
But between January and August of 1974 over 11,000 meningitis cases were reported to Ribas Hospital alone; the patients were older and even included a few elderly individuals, and the dominant pathogen switched from Type C to Type A.
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The typing of meningococci was based on tiny
molecules that protruded from the surface of their bacterial membranes. When people were infected, they produced disease-fighting antibodies against these typing molecules. Antibodies against Type C could not recognize and attack Type A markers. Since Type A infections were previously almost unheard of in Brazil, virtually no citizen in São Paulo was naturally immune, which would explain why some adults were coming down with what typically was a disease of immune-naïve children.
Worse yet, though there was a Type C vaccine available, research on development of a Type A vaccine was only just beginning. Furthermore, Augusto Taunay, director of the Adolfo Lutz Institute in São Paulo, was confirming that virtually all the Type C meningitis bacteria examined at his laboratory were resistant to sulfa-based antibiotics, such as penicillin.
In August, Taunay concluded that most Type C sufferers were under nine years of age, and the increase in mortality in that group was due to sulfa resistance. But Type A primarily attacked teenagers and adults under twenty-five years of age. It appeared that two simultaneous meningitis epidemics were underway.
This looked at first blush like a lose-lose situation. Brazilians generally had some natural immunity for Type C, but for those who were susceptible the bacteria had a new trick—antibiotic resistance. On the other hand, the apparently new Type A strain was vulnerable to antibiotic treatment, but few Brazilians were naturally immune; by the time they reached hospitals their meningitis cases were often too far gone to be cured with the antibacterial drugs.
Studying the patients, McCormick noticed that most had the classic acute form of the disease known as Waterhouse-Friderichsen syndrome; they went from well to severely sick in a matter of minutes, feeling sudden fevers, neck stiffness, and dizziness. Within hours their bodies were covered with tiny red dots—sites of pinpoint hemorrhages of capillaries under the skin. Within twelve to twenty hours they descended into comas, their kidneys hemorrhaged, and death soon followed.
“If you don't pick it up the first time you see it in little kids, they will be dead the next time you see them,” McCormick thought with a shudder.
Surviving the disease could result in serious lifelong disabilities. The bacteria attacked the middle of three protective meningeal layers enveloping the brain and spinal cord, and survivors were often left with a range of different types of brain damage. Or the bacteria might attack the kidneys and outer limbs, causing victims to lose their fingers, toes, even feet.
Epidemics of the disease were rare in South America, but relatively common in parts of West Africa. In Chad, for example, 1950s epidemics had attacked at rates of 11,000 cases per 100,000 people. By August 1974 São Paulo's meningitis rate was comparatively low, reaching 100 cases per 100,000 people. But McCormick had done the math, and he knew that the situation could quickly reach West African proportions. It troubled McCormick that nobody knew where the antibiotic-resistant Type C or the
Type A strain came from. Not knowing exactly when and where things started made it harder to forecast the future scope of the epidemic.
There were many possible explanations for the origin of this sudden epidemic, and at various times during his stay in São Paulo, McCormick mulled them all over. It was, for example, possible that a Brazilian had traveled to Africa, become infected, and brought the Type A bacteria to São Paulo. By 1974, over 75 million passengers were flying each year across national boundaries somewhere in the world
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—perhaps someone flew in, already infected, from West Africa. On the other hand, the bacteria could have arisen from a hospital or clinical setting locally, the result of improper antibiotic treatment. It galled McCormick that he couldn't figure out a way to track the origins of this epidemic.

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