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. 10 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.11
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 1972.12 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.13 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, fe
eling 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 world14—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.
In September, a WHO investigation reached a painful conclusion: although the Type C vaccine had been tried in only a couple of field settings and the Type A vaccine had to be considered completely experimental, nothing else could possibly stop the burgeoning epidemic.
Furthermore, WHO felt strongly that a vaccine combining immunization against Types A and C was essential, and warned that “the future of any vaccination programme will be in jeopardy†if the public loses faith in health efforts because people continue to die after receiving only the partial vaccination protection; the expected result of using only one vaccine.
The WHO decision was actually pro forma: the military government of Brazil had already decided in an August 5 meeting in Brasilia to vaccinate every citizen living in the epidemic area.15 While panic mounted, France’s Institut Mérieux agreed to manufacture the combination A/C vaccine for Brazil, and hurriedly built a new factory outside Lyons, France, for the purpose. Within four months, Mérieux would have attained the ability to manufacture and ship to Brazil 500,000 vaccine doses a week.16 The vaccine was composed of the sugary pieces—the polysaccharides—of the bacteria that gave them their A and C immunological statuses.17
Between August 1974 and mid-January 1975 while waiting for the vaccine, however, McCormick and Brazilian officials had few tools at hand. Joe decided to focus on public education, and immediately taught himself Portuguese. By October he was giving lengthy interviews and holding press conferences, calling for calm and reason.
“I’ve got to be clear about what I say,†McCormick thought, “and give the people confidence.â€
As an outsider, McCormick had a special role to play—and a delicate one. For ten years Brazil had been ruled by a military junta noted for its brutality. Countless students, labor leaders, religious activists, and representatives of the country’s underclass had “disappeared†by late 1974. “Disappearance†was a euphemism for death, preceded usually by kidnapping and torture. Rumors and fear ruled public opinion, and few of the nation’s poor trusted government pronouncements.
On the whole, however, the Brazilian Ministry of Health’s meningococcal announcements were accurate. It was part of McCormick’s diplomatic mission to publicly support the government’s statements about the epidemic while clearly maintaining a critical distance from the junta itself. Such dicey politics weren’t taught at Duke University Medical School. Or at the CDC training program.
McCormick had to wing it. Over the months he learned how to gently point out that nearly all meningitis sufferers came from communities of acute poverty, such as the massive favelas of São Paulo and Rio de Janeiro, without directly attacking the government policies responsible for that impoverishment. 18 He noted that the disease spread most rapidly in conditions of dense housing and poor hygiene, where people who lacked access to clean tap water rarely bathed or washed their clothing. The bacteria survived in such conditions, and could be passed from one family member to another via shared towels, clothing, cleaning rags, or kerchiefs.
By the time Mérieux had manufactured enough vaccine to immunize the population of São Paulo, the epidemic had claimed over 11,000 lives and caused serious illness in more than 150,000 people in at least six Brazilian states. About 30 percent of the survivors were reportedly suffering long-term neurological disorders of one kind or another.
By New Year’s the attack rate of the disease in Rio was 205 cases per 100,000 people and authorities feared the upcoming Carnival would increase its spread. The vision of millions of Brazilians and tourists dancing together for days on end in crowded streets presented the very real possibility that the epidemic would be carried all over the planet by worn-out revelers returning home.
Though they had no idea how effective the Mérieux vaccine might be, or how dangerous, Rio officials felt they had no option: on January 13 they began a twelve-day vaccination campaign with the announced goal of immunizing 80 percent of the population of greater Rio.
Within five days, over 3 million Cariocas were vaccinated and the incidence of meningitis instantly plummeted. During the dreaded Carnival week only ten people contracted the disease.
Encouraged by the Rio experience, the military government organized the largest vaccination campaign in world history. From April 21 to 24, nearly 11 million residents of São Paulo were vaccinated, representing 90 percent of the city’s population. This was accomplished by cordoning off all the commuter-intensive areas of the city and lining up as many as half a million people at a time for their shots. The entire mass media was mobilized as a huge propaganda tool for the campaign and military vehicles blasted pro-immunization announcements from roof-mounted loudspeakers.
Throughout Brazil similar militarily precise operations were soon conducted, eventually bringing the epidemic to a halt.
By early 1976, when McCormick returned to CDC headquarters in Atlanta, meningitis had ceased to be a serious problem in Brazil. But the fundamental question of where this virulent Type A strain had come from remained unsolved. At a PAHO meeting in Washington in February 1976, McCormick pushed for inclusion of the following statement in the official summary of the Brazilian episode:
It is not possible at the present time to predict when and where an epidemic of meningococcal meningitis will occur. Therefore it is not clear when and where preventive immunization should be carried out.19
Overlooked entirely in the final PAHO report was the significance—possible harbinger—of the bacteria’s ability to resist common antibiotics.
III
As was the case with malaria, polio, smallpox, and all bacterial diseases, the 1960s mood surrounding yellow fever control was one of extreme optimism. The tools were at hand: DDT and other pesticides to kill the Aedes aegypti mosquitoes that carried the yellow fever virus and an effective vaccine. Since 1937, yellow fever vaccines had been in use, and refined forms of im
munization proved so powerful that virtually every vaccinated person was protected for life by a single shot.20 Beginning with the period of the construction of the Panama Canal at the turn of the century, a variety of successful means had been used to eliminate the A. aegypti mosquitoes from the Americas.
Since the seventeenth century yellow fever had been a major and terrifying scourge in the Americas, causing endemic disease in jungle and swamp areas from Canada to Chile and claiming tens of thousands of lives in periodic urban epidemics. It would begin with a headache, fever, and a vague sense of uneasiness, within hours progressing to chills, muscle pains, and vomiting. After five days internal bleeding would commence, the liver would malfunction, and the individual would become jaundiced. If never previously exposed to the virus, the human then had a 50–50 chance of dying. A 1793 yellow fever epidemic in Philadelphia killed 15 percent of the city’s population and sent one out of three residents fleeing into the countryside.21
In West Africa, yellow fever was so ubiquitous that most surviving adults were immune to the disease. Many historians have noted that their acute vulnerability to yellow fever prevented British and French colonialists from attaining full control over West Africa.22 So obvious was this deterrence in some areas of Africa that it was celebrated in song and verse by people from the Sudan to Senegal. Well into the 1980s schoolchildren in Ibo areas of Nigeria still sang the praises of mosquitoes and the diseases they gave to French and British colonialists.23
It was generally believed the A. aegypti mosquito originated in West Africa and was brought to the New World aboard slave ships.24 The mosquito quickly adapted and thrived in the moist tropical regions of the Caribbean and the Amazon. The first epidemics occurred in Mexico’s Yucatan and Havana, Cuba, in 1648. In less than fifty years, the A. aegypti population had blanketed the Americas, and yellow fever epidemics were cropping up everywhere.
The Coming Plague Page 10
