Hong Kong, a center of wealth for the Chinese-speaking world, was dumping one million tons of unprocessed human waste into the South China Sea daily. Nearby Taiwan had sewage service for only 200,000 of its 20 million people, two-thirds of whom lived in its four largest cities.
But for the poorest developing countries, the burden of making their growing urban ecologies safe for humans, rather than heavens for microbes, proved impossible. Except for a handful of East Asian states which developed strong industrial capacities (i.e., South Korea, Malaysia, Singapore), the developing world simply had no cash in 1980.
In addition to growing national debts, developing countries faced the steady capital drain of paying off development loans obtained during the 1960s and 1970s and investing in newer sources of potential revenue generation. Some countries simply couldn’t bear the burden, and shirked or attempted to renegotiate their multibillion-dollar loans.
The capital drain would turn into a hemorrhage. In 1980 the Latin American nations collectively were receiving from their external creditors—major banks, the International Monetary Fund, the World Bank—about $11 billion more than they were losing in capital transfers back to wealthy-nation interests. But by 1985 these nations would be losing $35 billion more a year in capital transfers to North America and Europe than they received in loans and investments.41
Africa was also staggering under the burden of debt servicing and capital transfer, though the impact wasn’t as profound in dollar terms as that seen in Latin America. In 1979 the recently elected Prime Minister of the U.K., Margaret Thatcher, addressed these concerns in frank terms in a speech before the Commonwealth Conference, convened that year in Lusaka, Zambia. Ministers from the poorest of England’s former colonies hoped that Thatcher would extend a pound-filled hand, but she proffered only the sorry news that the once-great Empire was itself feeling the economic pinch. In short, it was time for a global belt tightening.
The cities worsened, some coming to resemble their teeming counterparts in nineteenth-century Europe. By the mid-1980s, 100 million newly homeless adults would roam the streets of developing-world cities; at least 100 million abandoned street children would haunt the urban nights. Half the city dwellers of developing countries who were not classified as homeless would live in shantytowns and slums that, among other things, lacked safe drinking water. Forty percent would be without public sanitation or sewage facilities. A third would live in areas in which there were no garbage or solid waste collection services.
As was the case in ancient Rome, it was healthier to remain in the villages and small towns of the developing world—even in times of drought and crop failure—than to live in the filthy, unwieldy metropolises. The average child living in a typical developing-country urban slum was forty times more likely to die before his or her fifth birthday of a preventable infectious disease than was a typical rural child in the same country.42
Disasters, and the very real opportunities they afforded the microbes, were everywhere. The streets of Cairo, for example, were flooded in December 1982 with sewage water that in some places was knee-deep. The flooding persisted for day after day, while authorities struggled to identify its cause.43
Nearly every Egyptian had been, for over 4,000 years, dependent on a single water supply—the Nile. The river’s annual floods would carry away a host of human sins in the form of waste and soil overuse, and leave behind a thick layer of fresh, fertile silt.
But construction of the Aswan Dam, coupled with Egypt’s extraordinary human population explosion, had erased the Nile’s majesty. Now slow-moving and predictable, the Nile was filling up with silt, fertilizers (which the farmers now needed because they no longer got the topsoil from the annual Nile floods), sewage—both treated and untreated—and industrial waste. Scientists predicted the imminent demise of Alexandria’s freshwater delta lagoons, a rise in the level of the Mediterranean Sea, and serious public health risks due to chemical and biological pollution of the Nile. They suggested that, given Cairo’s growth rate, there was nothing that could be done to prevent future environmental and public health disasters.44
The World Bank rated 79 percent of the housing of Addis Ababa “unfit for human habitation†in 1978. A quarter of the city’s houses were without toilet facilities.
A quarter of Bangkok’s residents in 1980 had no access to health care, according to the World Bank. In the Dharavi slum of Bombay, then inhabited by over 500,000 people, conditions were so appalling that 75 percent of the women suffered chronic anemia, 60 percent of the population was malnourished, pediatric pneumonia afflicted nearly all children, and most residents contracted gastrointestinal disorders due to parasitic infections. In Jakarta in 1980, the life expectancy was only fifty years, several years less than in the countryside. By 1980, 88 percent of Manila’s population lived in squatter settlements constructed of discarded pieces of wood, cardboard, tin, or bamboo. Forty percent of Nairobi’s 827,000 people in 1979 lived in housing so poor that their neighborhoods were deliberately omitted from all official maps.45 The flood of people into the Sudanese capital, Khartoum, led to epidemics of malaria, diarrheal diseases, anemia (presumably produced by malaria), measles, whooping cough, and diphtheria in the early 1980s. In the Ivory Coast, rural tuberculosis rates by 1980 were down to 0.5 percent—a success story. But in the large capital city of Abidjan the TB rate was 3 percent and climbing.46
These and hundreds of other examples of urban squalor and its concomitant diseases were compounded by large-scale chronic malnutrition. Except in times of famine, drought, or other natural disasters—or of the man-made disaster of warfare—rural residents of even exceptionally poor countries usually had access to a variety of types of food, including protein. But when they moved to the city, people had to buy foods that were produced and marketed by others. Lacking sufficient earning power to purchase goods, the urban poor were forced to forgo adequate foods. Even in times of food plenty for the nation, most of its urban population might, as a result, be malnourished. This, of course, contributed to weakening their disease-fighting immune systems.47
III
By 1980, several traditionally rural parasitic diseases were emerging, for the first time, as urban epidemics.
Uwe Brinkmann, having left Germany following the Lassa episode and settled at the London School of Tropical Medicine and Hygiene, traveled all over West Africa surveying the incidence of onchocerciasis, or river blindness, a disease carried by blackflies. For two years Uwe, his researcher wife Agnes, and their young son went from village to village, primarily in Ghana and Togo, studying the disease and teaching villagers how to avoid it.
From there, Brinkmann moved on to study primary health care systems in Yemen and Sierra Leone, schistosomiasis in Congo and Mali, and onchocerciasis and cysticercosis in Central America.48
By 1982, when Brinkmann had joined the faculty at Harvard, he had seen disturbing evidence that the parasitic diseases that he and other scientists worldwide were so successful at limiting in the villages and farmlands of developing countries were invading the cities, often in different forms.
Cysticercosis was usually produced by tapeworms normally found in undercooked pork and some other types of animal flesh. The worms invaded numerous organs of the human body—the worst cases involving infections of the brain. But Brinkmann noted that a change in the human/parasite relationship was occurring in Mexico City—then the world’s fastest-growing megacity. People were not getting the worms from uncooked meats, which, as it turned out, they couldn’t afford to purchase. Rather, the parasite had taken advantage of the highly favorable ecology provided by the extraordinarily polluted Tula River, the city’s primary freshwater source. Tens of thousands of people living in the squalid outskirts of the megacity downstream of the urban center’s sewage system were infected with the dangerous Taenia solium parasites.49
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p; By 1980 the tapeworm had found its way to Los Angeles, carried by human immigrants from Asia and Central America. Some 500 cases of cysticercosis were treated between 1973 and 1983 at four Los Angeles hospitals. Most involved people who were infected in their home countries or while traveling in endemic areas. But at least twelve individuals acquired the disease in Los Angeles, and random stool sample assays revealed that some 0.5 percent of the tested population were infected with the tapeworms. 50
The Ascaris roundworm was another parasite that was invading cities. The Ascaris eggs lived in a dormant state in the soil, where they could survive in infectious form for over ten years. Humans and pigs became infected as a result of inhaling contaminated dust, oral contact with dirtied hands, or ingestion of unwashed foods grown in contaminated soils. Once the eggs made their way to the human gastrointestinal tract they would mature into worms that would wreak havoc upon numerous organs, including the entire gastrointestinal tract, liver, appendix, pancreas, heart, and lungs. The human would then excrete more parasite eggs, further contaminating local soils. Prior to the 1970s this cycle was considered an entirely rural, village-based problem.
During the 1970s in Dakar, however, a third of the city’s slum residents were infected with the parasite, acquired within the city limits, while less than 3 percent of their rural counterparts carried the disease.51 At the same time locally acquired ascariasis increased dramatically in the city of Cape Town, South Africa, accounting for 15 percent of all emergency room admissions for acute abdominal disorders.52
Schistosomiasis turned up in Dar es Salaam (Tanzania), Harare (Zimbabwe), Kinshasa (Zaire), and Sao Paulo and Belo Horizonte (Brazil) during the 1970s.
Chagas’ disease, caused by Trypanosoma protozoa and carried by a variety of insects, was turning up in cities all over Latin America. Capable of causing encephalitis and severe heart disease, the Trypanosoma organisms made their way into the continent’s burgeoning cities, infecting up to 60 percent of the common household bugs. Eventually the Trypanosoma found a more direct way to infect people: bypassing the insect vector, the protozoa entered the blood-bank systems. By the mid-1980s, blood-bank infection rates would be horrendous: 6 percent in Buenos Aires and up to 20 percent in other Argentine cities; 15 percent in Brazil’s capital, Brasilia; an astonishing 63 percent in Santa Cruz, Bolivia.53
For centuries sandflies had been inserting their pointed proboscises into the human epidermis, injecting anticoagulating chemicals and withdrawing enough blood to bloat the insect. In 1824 the flies of Jessore, in Bengal, added something to this process, injecting parasites along with the anticoagulants.
Tiny one-celled Leishmania donovani swam into the bloodstreams of Jessore merchants, visiting traders, women, and children. Soon kala-azar (as the disease was called) was attacking the abdominal veins of humans in cities all along the Ganges, causing deadly pneumonia and dysentery. Such illnesses may have been occurring for centuries, isolated and unnoticed. But the 1824 outbreak struck a major trading post, gaining the immediate attention of British colonial interests then controlling the subcontinent.
Another round of sandfly-carried kala-azar struck Assam, India, in 1918, killing more than 200,000 people. Still another hit the area in 1944.54
Soon leishmaniasis-producing organisms of various species were turning up in flies that infested cities in Latin America and the Indian subcontinent, producing both kala-azar and the cutaneous, or skin infection, forms of the disease. Various factors seemed to have contributed to the emergence of urban leishmaniasis, including widespread DDT spraying for malaria control. When spraying programs were stopped, either because the mosquito population was effectively controlled or due to government financial restrictions, the fly population would surge, filling the ecological niche vacated by the competitive mosquitoes.55
The surge of sandflies in the wake of the malaria eradication campaign was often dramatic. In cities and small towns all over Latin America the insects swarmed in, often hitting communities for the first time in human history. Pioneers searching for wealth in the vast Amazon rain forest often returned to Brazil’s eastern cities with little more than a whopping leish-maniasis infection. Even if the Latin American sandflies of the cities hadn’t carried the parasites before, they now picked up the microbes as they fed on recently returned Amazon fortune seekers in cities all over the continent.
The Indian kala-azar parasitic strain was able to infect dogs and domestic animals, as well as humans, providing steady reservoirs for the microbe’s continued presence in a community. By 1980 scientists in Colombia and Brazil spotted the same phenomenon developing in their cities and towns, primarily among pet dogs and chickens.
Ki denga pepo is Swahili for “it is a sudden overtaking by a spirit.†The phrase was used by East Africans to describe a mosquito-carried disease that would abruptly overwhelm human beings, producing horrible headaches, eye pain, and a swelling achiness of the joints.
When the disease swept over Philadelphia in 1780, Dr. Benjamin Rush gave it the moniker “breakbone fever,†a reference to the aching joints. By the mid-nineteenth century the disease was endemic throughout the Americas.
And it then had a permanent name—dengue, a Spanish adaptation of the Swahili denga. In most cases dengue wasn’t a life-threatening ailment, though it was certainly a miserable experience for the afflicted. The disease was caused by four different strains of dengue viruses—cousins of the yellow fever microbe. The dengue viruses were carried by mosquitoes, particularly the female Aedes aegypti.
As countries throughout the world conducted A. aegypti eradication campaigns during the early twentieth century to rid the earth of yellow fever, dengue outbreaks virtually ceased. A comfortable dengue silence set in during the 1940s.
Then, in 1953, the city of Manila was hit by an apparently new form of dengue that caused hemorrhagic petechial skin rashes—pinpoint-sized red spots, sites of breakthrough bleeding—shock, and soaring fevers. The disease seemed more lethal than any previous dengue outbreaks, and was caused by viral strain dengue-2.56
Five years later dengue hemorrhagic fever, as the new disease was called, hit Bangkok, causing 2,297 illnesses—primarily among children—and 240 deaths. Searches of human blood samples from the past revealed that various dengue viruses had infected Bangkok residents harmlessly since 1950, but the population was never infected with dengue-2 prior to World War II. After the initial urban outbreak in 1958, however, the dengue hemorrhagic fever epidemic persisted in Bangkok for five years, eventually sickening 10,367 people and killing 694.57
U.S. Army medical researcher Dr. Scott Halstead, who was based at the military’s laboratory in Bangkok at the time, teamed up with Thai microbiologist Charas Yamarat to figure out the origin of the apparently new deadly disease. They determined that, as was the case with yellow fever, the A. aegypti mosquito that carried the dengue-2 virus was a fully urbanized insect. Lacking the aggressive characteristics of wild jungle mosquitoes, A. aegypti only thrived in proximity to human beings, laying its eggs in open containers of fresh water and maturing inside human shelters.
When the men closely examined the medical records of people who suffered acute dengue hemorrhagic fever they discovered that nearly all of the victims had at some recent time been exposed to another, milder dengue strain. Though that first infection caused little or no apparent illness, it sensitized the humans’ immune systems for the later arrival of dengue-2.
Usually when people develop strong antibody immune responses against a virus they are protected against future exposure to the microbe. But dengue-2 had evolved an extraordinary ability to exploit human antibodies to its advantage. When the human antibodies attached to the outer envelope of the dengue-2 virus, the microbe played a game of stealth, allowing the antibodies to send their signals to the large immune system macrophage cells. In a process that was usually lethal to the microbes, the macrophages would then engu
lf the viruses, but instead of dying, the dengue would take control of the immune system’s primary killer cells.
Thus, dengue-2 evaded the immune system defenses and gained entry to every organ in the body, carried by macrophages that acted as Trojan horses for the virus. As the immune system struggled to overcome its sneaky invaders, various biochemical reactions were triggered that produced soaring fevers—as high as 107°F—convulsions, classic allergylike shock, and death.58
The new dengue disease paradigm spread through South and East Asia, carried by ever-expanding hordes of A. aegypti and another species, A. albopictus, otherwise known as tiger mosquitoes. Unlike A. aegypti, the A. albopictus insects were sturdy creatures adapted to coexistence not only with Homo sapiens but also with a wide range of warm-blooded creatures that thrived in urban environs—even rats.
During the 1950s and 1960s, dengue types 1, 2, and 3 all made sporadic appearances in the Americas,59 but A. aegypti control programs were strong enough to prevent epidemics. Nevertheless, the viruses were present in the region, particularly in the Caribbean, and the mosquitoes were never fully eradicated.
The stage was set, and dengue invaded the moment a slackening in mosquito abatement programs allowed the A. aegypti population to grow to critical proportions.
In May 1981, the city of Havana experienced the worst dengue hemorrhagic fever epidemic seen up to that time anywhere in the world. The epidemic raged for over six months, causing at least 344,000 illnesses, more than 116,000 hospitalizations, and 158 deaths. At its peak in July some 11,000 Havana residents sickened each day. The epidemic cost the Cuban government $103 million in control efforts and medical care—a large sum for the nation of 10 million people whose per capita annual incomes were less than $1,500 that year.
The Coming Plague Page 39