The Coming Plague (103 page)
Authors: Laurie Garrett
Though the population was spread unevenly over a country, density trends remained favorable to the microbes. If worst-case projections for human population size came to pass, some regions would have densities in excess of 3,000 people per square mile. At that rate the distinctions between cities, suburbs, and outlying towns would blur and few barriers for person-to-person spread of microbes would remain.
With the passage of time and the increase in travel it was becoming more and more difficult to pinpoint where, exactly, a microbe first emerged. The human immunodeficiency virus was a classic case in point, as it surfaced simultaneously on three continents and spread swiftly around the globe.
Those scientists in the 1990s whose primary focus was viruses believed that the worst scales of disease and death arose from epizootic events: the movement of viruses between species. In such instances, the hosts were usually highly susceptible, as they lacked immunity to the new microbe. Ebola, PDV-2, Marburg, Machupo, Lassa, and Swine Flu were all examples of such apparently sudden emergences into the
Homo sapiens
population.
Homo sapiens
population.
Rockefeller University's Stephen Morse, who by 1988 was devoting nearly all his professional energies to emerging disease problems, labeled these movements of viruses between host species “viral trafficking.” He considered the world's fauna a vast “zoonotic pool,” each species carrying within itself an assortment of microbes that might jump across species barriers under the proper circumstances to infect an entirely different type of host.
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At Harvard, Max Essex was similarly impressed with the ferocity of new cross-species viral infections. A case he found chilling was the
Herpesvirus saimiri
, which was carried without apparent harm by
Saimiri sciureus
squirrel monkeys living in Amazonia. When the virus was first discovered in captive
Saimiri
monkeys it was thought to be a harmless microbe.
But within months after its discovery in 1968 by scientists at the New England Primate Research Center, located outside Boston, other monkey species at the center took ill. The strange herpes virus turned out to be an extraordinary cancer-causing agent: less than two months after infection Old World monkeys would develop extensive, lethal cancers of their lymphatic systems.
Herpesvirus saimiri
, which was carried without apparent harm by
Saimiri sciureus
squirrel monkeys living in Amazonia. When the virus was first discovered in captive
Saimiri
monkeys it was thought to be a harmless microbe.
But within months after its discovery in 1968 by scientists at the New England Primate Research Center, located outside Boston, other monkey species at the center took ill. The strange herpes virus turned out to be an extraordinary cancer-causing agent: less than two months after infection Old World monkeys would develop extensive, lethal cancers of their lymphatic systems.
In the early 1970s the same researchers discovered a similar herpes virus,
H. ateles
, in spider monkeys. Like
H. saimiri
, it was harmless in its normal host and infected virtually 100 percent of the host species in the wild. And it was also a potent cancer-causing virus in other monkey species. Both viruses specifically infected cells of primate immune systems, causing lymphomas and leukemias. And both approached the 100 percent lethality mark when they infected primates other than their host species. Experimental infections of rabbits also proved extraordinarily lethal.
H. ateles
, in spider monkeys. Like
H. saimiri
, it was harmless in its normal host and infected virtually 100 percent of the host species in the wild. And it was also a potent cancer-causing virus in other monkey species. Both viruses specifically infected cells of primate immune systems, causing lymphomas and leukemias. And both approached the 100 percent lethality mark when they infected primates other than their host species. Experimental infections of rabbits also proved extraordinarily lethal.
What chilled Essex wasn't the viruses' ability to cause cancer, though the appalling certainty and speed of their carcinogenic action were certainly unprecedented and frightening. Essex's concern was the mode of transmission: both herpes viruses were airborne.
In the wild such horrendously dangerous viruses might have, over the millennia, served the squirrel and spider monkeys well, residing harmlessly inside their species but killing off all other species of competitive primates. In captive animal colonies a spider monkey could simply breathe on a howler monkey and five weeks later the victim would die of leukemia.
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The viruses appeared to be able to elude monkey immune systems by manufacturing proteins that specifically switched off or dampened cellular immune responses. And the
saimiri
virus contained fifteen genes that were remarkably similar to genes found inside the monkey's DNA.
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saimiri
virus contained fifteen genes that were remarkably similar to genes found inside the monkey's DNA.
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Lab analyses of
H. saimiri
strains grown on monkey cells revealed an astonishing rate of mutation and gene swapping. The virus's DNA, in the absence of the rest of the microbe, was capable of infecting and destroying a cell. Once whole viruses were inside cells they immediately began a mutation process so pronounced that it was impossible to recover the original strain. So, though no human being was known to have been infected with either
H. saimiri
or
H. ateles
, the viruses' ability to transform themselves at such staggering speed left open the disturbing possibility that, given ample opportunityâsuch as exposure to an immunodeficient person or implantation into a
Homo sapiens
in the form of a monkey-to-human tissue transplantâthe organisms might quickly adapt to human cells, becoming a lethal airborne cancer-causing virus.
H. saimiri
strains grown on monkey cells revealed an astonishing rate of mutation and gene swapping. The virus's DNA, in the absence of the rest of the microbe, was capable of infecting and destroying a cell. Once whole viruses were inside cells they immediately began a mutation process so pronounced that it was impossible to recover the original strain. So, though no human being was known to have been infected with either
H. saimiri
or
H. ateles
, the viruses' ability to transform themselves at such staggering speed left open the disturbing possibility that, given ample opportunityâsuch as exposure to an immunodeficient person or implantation into a
Homo sapiens
in the form of a monkey-to-human tissue transplantâthe organisms might quickly adapt to human cells, becoming a lethal airborne cancer-causing virus.
Since the establishment of research animal colonies, scientists had unwittingly uncovered many other monkey and ape viruses that proved capable of producing infection and disease in the humans who handled the simians. A herpes virus, designated B virus, infected rhesus macaques and some other Old World monkeys, attacking nerve cells to produce everything from localized pain to encephalitis and death. About 10 percent of all imported
rhesus monkeys were typically infected with the B virus; infection rates inside some captive colonies reached 100 percent. Once infected, the animals carried the virus for life, whether or not they developed disease.
rhesus monkeys were typically infected with the B virus; infection rates inside some captive colonies reached 100 percent. Once infected, the animals carried the virus for life, whether or not they developed disease.
From the time of its discovery in 1975 to 1989, twenty-eight animal handlers had contracted B virus infection, twenty-five of whom went on to develop encephalitis. Only five human beings had ever survived known B virus infection.
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Other monkey viruses that held out the potential for human infection, either in their natural form or in a mutant form, included type D simian retrovirus (SRV), the simian AIDS virus (SIV), simian sarcoma-associated viruses (SSAVs), paramyxovirus simian virus 5, gibbon ape leukemia virus, and Mason-Pfizer virus (M-PMV).
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During the early 1970s, 126 American primate research facility employees were accidentally infected with monkey microbes. The precise etiology of most of their ailments was never determined. Among the microbes known to have been transmitted were tuberculosis,
Shigella
,
Streptococcus, Staphylococcus,
and influenza.
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Every year thereafter animal colony workers all over the world were exposed to, and became infected with, a variety of monkey and ape viruses, bacteria, and parasites.
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Shigella
,
Streptococcus, Staphylococcus,
and influenza.
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Every year thereafter animal colony workers all over the world were exposed to, and became infected with, a variety of monkey and ape viruses, bacteria, and parasites.
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Despite the clear presence of pathogens dangerous to humans in the simian population, there was much interest in the U.S. medical community in using the animals as sources for organ transplants. Ever since the first successful human heart transplants were performed in 1953 the use of organ transplantation had increased steadily in the United States and Europe. Development of effective drugs to suppress a recipient's immune response greatly improved the success of human-to-human organ transplant procedures, and by 1988 the five-year-survival rate exceeded 50 percent for patients undergoing all common transplants, save those of the lung. Kidney transplants, the most common of all such procedures, enjoyed a 91 percent success rate.
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As success rates mounted, so did the demand for organs. By the mid-1980s there was a very real crisis of organ availability and American television and newspapers regularly carried heart-wrenching stories about desperate children who faced imminent death unless a suitable liver, or heart, or other organ was found posthaste. A federal waiting list system was created in order to put some order into an organ procurement system that was spinning dangerously out of control. Order and fairness didn't ensure adequate availability, however. In 1990, for example, 2,206 people on the organ waiting list died before a suitable transplant donor could be found.
In 1963 the first tentative baboon-to-human transplants were performed, with little success.
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Such experiments continued over the years in the United States and South Africa.
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Such experiments continued over the years in the United States and South Africa.
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In 1992â93 researchers at the University of Pittsburgh transplanted baboon livers into two men who suffered hepatitis B virus-induced destruction of their own organs. Though both patients succumbed, the transplants
were not the causes of their deaths, and physicians hailed the breakthrough.
were not the causes of their deaths, and physicians hailed the breakthrough.
But infectious disease experts cried foul. The donor baboons came from the Southwest Foundation, the largest research monkey facility in the United States. Officials at the San Antonio-based primate center were shocked to learn that the baboon organ had been transplanted into a human being. The baboon used in the first Pittsburgh transplant experiment was infected with SIV (the simian AIDS virus), CMV (the simian cytomegalovirus), EBV (the simian type of Epstein-Barr virus), and Simian Agent 8 (the baboon form of B virus). If the thirty-five-year-old man had survived for months after receiving the baboon liver, critics asked, what might have happened with those viruses?
“We assume as a given that these primates carry pathogens that are infectious to humans,” Southwest Foundation Biomedical Research Center scientist Jon Allan said. “You assume it's something that can kill you. But then in the next breath we turn around and ship a baboon up to Pittsburgh, they open it up, probably every human in the OR is exposed to whatever is in there, and they stick its liver into a human.
“Does that seem rational?”
Another Southwest Foundation virologist, Julia Hilliard, expressed concern that monkey viruses that seemed initially harmless to people might exchange genetic material with human DNA following a transplant, resulting in highly lethal new super-bugs.
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Transplant surgeons had long known, of course, that infection was every recipient's greatest enemy. Old, latent infections were often activated by the procedure because, to avoid transplant rejection, doctors used powerful drugs to suppress the patients' immune systems. It was also possible for the transplants themselves to be infected: thus, the recipient got not only the donor's organ but also microbes such as cytomegalovirus,
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hepatitis B,
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adenoviruses,
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Epstein-Barr virus,
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and HIV.
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hepatitis B,
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adenoviruses,
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Epstein-Barr virus,
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and HIV.
For most of the world's human population, however, such exotic things as liver transplants were hardly of concern. More likely modes of epizootic disease transmission involved insects.
Yellow fever, for example, could for decades on end afflict virtually no
Homo sapiens
in a given area because the
Aedes aegypti
mosquitoes were busy feeding on monkeys and marmosets in the jungle. But with changes in either the forest environment or the social behaviors of local
Homo sapiens
the mosquito could almost overnight change its feeding patterns and a human epidemic would commence. Such was the case with yellow fever epidemics in Nigeria and Kenya in 1987, 1988, 1990, and 1993.
Homo sapiens
in a given area because the
Aedes aegypti
mosquitoes were busy feeding on monkeys and marmosets in the jungle. But with changes in either the forest environment or the social behaviors of local
Homo sapiens
the mosquito could almost overnight change its feeding patterns and a human epidemic would commence. Such was the case with yellow fever epidemics in Nigeria and Kenya in 1987, 1988, 1990, and 1993.
Tom Monath had seen it happen several times in West Africa, where such simple actions as chopping down a stand of trees and leaving the stumps in place could spawn a yellow fever outbreak. The mosquitoes left their larvae in rainwater that collected in the tree stumps.
Microbes and insect vectors could suddenly appear in areas thousands of miles from their usual habitats. For example, for reasons never understood,
the American screwworm fly, which could transmit deadly maggots to livestock, turned up quite suddenly in the deserts of Libya in 1988 and quickly spread throughout North Africa. The insects' normal habitat was the dry Southwest of the United States and northern Mexico.
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the American screwworm fly, which could transmit deadly maggots to livestock, turned up quite suddenly in the deserts of Libya in 1988 and quickly spread throughout North Africa. The insects' normal habitat was the dry Southwest of the United States and northern Mexico.
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In temperate ecologies, keeping wild insects at bay was quite easy, provided abatement and control systems remained intact and vigilant. Even a year of slackening in such an effort could, however, permit a sudden surge in insect vector populations, with resultant disease.
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In the United States there were several outbreaks of mosquito-borne diseases between 1985 and 1992, each of which could be traced to a breakdown in mosquito control efforts or public health vigilance.
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In 1990, for example, an epidemic of St. Louis encephalitis caused widespread panic in parts of Florida and southeastern Texas, forcing cancellation of baseball games and other nighttime outdoor activities. Though public health authorities had a year earlier witnessed rises in viral infection rates in chickens and other birds used for monitoring the microbes, few steps were taken to stem the increases in local mosquito populations prior to the summer 1990 epidemics.
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In 1990, for example, an epidemic of St. Louis encephalitis caused widespread panic in parts of Florida and southeastern Texas, forcing cancellation of baseball games and other nighttime outdoor activities. Though public health authorities had a year earlier witnessed rises in viral infection rates in chickens and other birds used for monitoring the microbes, few steps were taken to stem the increases in local mosquito populations prior to the summer 1990 epidemics.
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For most insect experts it came as no surprise that even a one-year slackening in mosquito control efforts could result in a surge in the bugs and the microbes that they carried. Both insects and microbes had evolved mechanisms over the millennia that ensured their mutual survival. Studies of genetic relationships between particular microbes and their most common insect vectors suggested that the species had co-evolved, developing capabilities that were primarily advantageous to the microbes.
Blood-feeding insects had over millions of years developed traits that served to aid the transmission and the evolution of microbes. When the female insects bit into human flesh they spit into the site a fluid that contained vasodilators that opened up local capillaries, anticoagulation enzymes that would prevent clotting of the wounded capillaries, and a variety of factors that destroyed immune system cells and chemicals. This ensured the insect a steady flow of food, without toxic human immune system chemicals or cells. As these chemicals were secreted out of the insect's salivary glands, the proboscis drew blood into a separate set of lobes, and eventually into the insect's midgut.
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