The Coming Plague (44 page)
Authors: Laurie Garrett
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
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 bodyâthe worst cases involving infections of the brain. But Brinkmann noted that a change in the human/parasite relationship was occurring in Mexico Cityâthen 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
of the urban center's sewage system were infected with the dangerous
Taenia solium
parasites.
49
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
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.
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
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
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.
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
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
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.
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 nameâdengue, 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 virusesâcousins of the
yellow fever microbe. The dengue viruses were carried by mosquitoes, particularly the female
Aedes aegypti.
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 virusesâcousins 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.
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 rashesâpinpoint-sized red spots, sites of breakthrough bleedingâshock, and soaring fevers. The disease seemed more lethal than any previous dengue outbreaks, and was caused by viral strain dengue-2.
56
56
Five years later dengue hemorrhagic fever, as the new disease was called, hit Bangkok, causing 2,297 illnessesâprimarily among childrenâand 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
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.
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 engulf 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 feversâas high as 107°Fâconvulsions, classic allergylike shock, and death.
58
invaders, various biochemical reactions were triggered that produced soaring feversâas high as 107°Fâconvulsions, 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 environsâeven rats.
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 environsâeven 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.
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.
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 careâa large sum for the nation of 10 million people whose per capita annual incomes were less than $1,500 that year.
Havana, with a population of 2 million and fewer than 25,000 hospital beds, was overwhelmed. More than 10,000 health care workers had to be corralled into full-time dengue treatment and control efforts, not only in Havana but eventually nationwide. Nearly 10 percent of the residents of Havana suffered symptomatic dengue-2 infection between May and September 1981.
When researchers tested the city's residents for prior exposure to dengue, they discovered that the Halstead-Yamarat theory of serial infections and immune system deception was correct: 44.5 percent of Cuba's urbanites had antibodies to dengue-1 as a result of a very mild epidemic of the virus that swept imperceptibly over the island in 1977, causing little more than mass natural immunization of the population.
But that was enough.
When dengue-2 hit Havana it found the urban population sensitized and ready to succumb to its immune system trickery.
60
60
Other books
Buy Back by Wiprud, Brian M
Pop Tarts: Omnibus Edition by Brian Lovestar
A Wolf's Desire (A BBW Paranormal Romance): The Holiday Ball by Marie Mason
Mistletoe & Michaelmas by Rose Gordon
Up West by Pip Granger
Murder at Fenway Park by Troy Soos
The Lake of Darkness by Ruth Rendell
In Dubious Battle by John Steinbeck
The Wedding Speech by Isabelle Broom
