In 1977, for example, fifty-four passengers were grounded together for three hours while their plane underwent repairs in Alaska. None of the passengers left the aircraft, and to save fuel the air conditioning was switched off. For three hours the fifty-four passengers breathed the same air over and over again. One woman had influenza: over the following week 72 percent of her fellow passengers came down with the flu; genetically identical strains were found in everyone.51
Following the worldwide oil crisis of the 1970s, the airlines industry looked for ways to reduce fuel use. An obvious place to start was with air circulation, since it cost a great deal of fuel to draw icy air in from outside the aircraft, adjust its temperature to a comfortable 65°â€”70°F, and maintain cabin pressure. Prior to 1985 commercial aircraft performed that function every three minutes, which meant most passengers and crew breathed fresh air throughout their flight. But virtually all aircraft built after 1985 were specifically designed to circulate air less frequently; a mix of old and fresh air circulated once every seven minutes, and total flushing of the aircraft could take up to thirty minutes.52 Flight crews increasingly complained of dizziness, flu, colds, headaches, and nausea.
Studies of aircraft cabins revealed excessive levels of carbon dioxide—up to 50 percent above U.S. legal standards. Air quality for fully booked airliners failed to meet any basic standards for U.S. workplaces.53
In 1992 and 1993 the CDC investigated four instances of apparent transmission of tuberculosis aboard aircraft. In one case, a flight attendant passed TB on to twenty-three crew members over the course of several flights.
Similar concerns regarding confined spaces were raised about institutional settings, such as prisons and dormitories, where often excessive numbers of people were co-housed in energy-efficient settings.
In preparation for the June 1992 United Nations Earth Summit in Rio de Janeiro, the World Health Organization reviewed available data on expected health effects of global warming and pollution. 54 WHO concluded that evidence of increased human susceptibility to infectious diseases, due to UV-B immune system damage and pollutant impacts on the lungs and immune system, was compelling. The agency was similarly impressed with estimates of current and projected changes in the ecology of disease vectors, particularly insects.
It wasn’t necessary, of course, for the earth to undergo a 1°â€”5°C temperature shift in order for diseases to emerge. As events since 1960 had demonstrated, other, quite contemporary factors were at play. The ecological relationship between Homo sapiens and microbes had been out of balance for a long time.
The “disease cowboysâ€â€”scientists like Karl Johnson, Pierre Sureau, Joe McCormick, Peter Piot, and Pat Webb—had long ago witnessed the results of human incursion into new niches or alteration of old niches.55 Perhaps entomologist E. O. Wilson, when asked, “How many disease-carrying reservoir and vector species await discovery in the earth’s rain forests?†best summed up the predicament: “That is unknown and unknowable. The scale of the unknown is simply too vast to even permit speculation.â€
Thanks to changes in Homo sapiens activities, in the ways in which the human species lived and worked on the planet at the end of the twentieth century, microbes no longer remained confined to remote ecospheres or rare reservoir species: for them, the earth had truly become a Global Village. Between 1950 and 1990 the number of passengers aboard international commercial air flights soared from 2 million to 280 million. Domestic passengers flying within the United States reached 424 million in 1990.56 Infected human beings were moving rapidly about the planet, and the number of air passengers was expected to double by the year 2000, approaching 600 million on international flights.57
Once microbes reached new locales, increasing human population and urbanization ensured that even relatively poorly transmissible microbes faced ever-improving statistical odds of being spread from person to person. The overall density of average numbers of human beings residing on a square mile of land on the earth rose steadily every year. In the United States, even adjusting for the increased land mass of the country over time, density (according to U.S. census figures) rose as follows:
Year Total Population Persons per Square Mile
1790 3,929,214 4.5
1820 9,638,453 5.5
1850 23,191,876 7.9
1870 39,818,449 13.4
1890 62,947,714 21.2
1910 91,972,266 31.0
1930 122,775,046 41.2
1950 151,325,798 42.6
1970 203,211,926 57.5
1990 250,410,000 70.3
1992 256,561,239 70.4
In most of the world the observed increases were even more dramatic. In a comparison of 1990 and 1992 census information as collected by the United Nations, the two-year upward trend in population density was unmistakable:
Country 1990 Population 1990 Persons per Square Mile
China 1,130,065,000 288
India 850,067,000 658
Indonesia 191,266,000 255
Mexico 88,335,000 115
Rwanda 7,603,000 715
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.
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. 58
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.
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.
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.59
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.60
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 opportunity—such as exposure to an immunodeficient person or implantation into a Homo sapiens in the form of a monkey-to-human tissue transplant—the 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.
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.61
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).62
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.63 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.64
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.65
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.66 Such experiments continued over the years in the United States and South Africa.67
In 1992–93 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.
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?â€
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.68
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,69 hepatitis B,70 adenoviruses,71 Epstein-Barr virus,72 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.
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.73
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.74
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.75 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.76
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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