Spillover: Animal Infections and the Next Human Pandemic (4 page)

Among the “sentimental Greenies,” he would have included bat carers. But even some of those softhearted activists, the carers, grew concerned as evidence piled up. They had two worries, uneasily counterbalanced: that the virus would make bats even more unpopular, leading to calls (like the trainer’s) for bat extermination, and that they themselves might become infected in the course of their well-meaning work. The second was a new sort of anxiety. It must have caused some reexamination of commitment. They were
bat
lovers, after all, not
virus
lovers. Does a virus constitute
wildlife
? Not in most people’s minds. Several such carers asked to be screened for antibodies, which opened doors for a broad survey, quickly organized and led by a young epidemiologist from the University of Queensland named Linda Selvey.

Selvey tapped into the wildlife-carer networks in southeastern Australia, eventually finding 128 bat carers willing or eager to be tested. She and her field team drew the blood and asked each participant to complete a questionnaire. The questionnaires revealed that many of these people had had prolonged and close contact with flying foxes—feeding them, handling them, not infrequently getting scratched or nipped. One carer had been bitten deeply on the hand by a Hendra-positive bat. The most unexpected finding of Selvey’s survey was the percentage of those 128 carers who tested positive for antibodies: zero. Despite months and years of nurturing, despite scratches and bites and cuddling and drool and blood, not one person showed immunological evidence of having been infected with Hendra virus.

Selvey’s report appeared in October 1996. She was a grad student at the time. Later she became head of the Communicable Diseases Branch of Queensland Health. Still later, as we sat over coffee in a noisy Brisbane café, I asked her: Who
are
these bat carers?

“I don’t know how to describe them,” Selvey answered. “People with a passion for animals, I guess.” Both women and men? “Predominantly women,” she said, speculating gently that women without kids might have more time and more desire for such surrogacy. Generally they do the caring in their own homes, equipped with a sizable, comfortable cage where the bats can roost when not being handled. It seemed mystifying to me that such intimate bat-human relations, combined with such a high level of bat seroprevalence, had yielded not a single case of human infection to be detected by Selvey’s study. Not a single antibody-positive person out of 128 carers. What did that tell you, I asked her, about the nature of this virus?

“That it needed some sort of amplifier,” she said. She was alluding to the horse.

5

L
et’s think about foot-and-mouth disease for a moment. Everybody has heard of it. Everybody has seen
Hud.
Most people aren’t aware that, at least tenuously, it’s a zoonosis. The virus that causes foot-and-mouth disease (FMD) belongs to the picornaviruses, the same group that includes poliovirus and some viruses similar to those that cause the common cold. But infection with FMD virus is a rare misfortune in humans, seldom causing worse than a rash on the hands, the feet, or the mouth lining. More frequently and consequentially, it afflicts cloven-hoofed domestic animals such as cattle, sheep, goats, and pigs. (Cloven-hoofed wildlife such as deer, elk, and antelope are also susceptible.) The main clinical signs are fever, lameness, and vesicles (little blisters) in the mouth, on the snout, on the feet. In a lactating female, the teats sometimes become blistered and then, as the blisters break, ulcerated. Bad for the mother, bad for the calf. Lethality from FMD is relatively low but the morbidity (incidence of the disease within a population) tends to be high, meaning that the disease is very contagious, making livestock ill, putting them off their feed, and causing losses of productivity that, in big-volume operations with narrow profit margins, are considered disastrous. Because of such losses, plus the swiftness of contagion, it’s often treated as a terminal condition in commercial terms: Infected herds are slaughtered to prevent the virus from getting around. Nobody wants to buy stock that might be carriers, and the export trade drops to zilch. Cows, sheep, and pigs become worthless—less than worthless, an expensive liability. “
Economically, it is the most important
disease of animals in the world,” according to one authority, who reports that “an FMD outbreak in the US could cost $27 billion in lost trade and markets.” The virus spreads through direct contact, and in feces, and in milk, and is even capable of transmission by aerosol. It can travel from one farm to another on a humid breeze.

Impacts of FMD differ from one kind of animal to another. Sheep tend to carry the infection without showing symptoms. Cattle suffer openly and pass the virus to one another by direct contact (say, muzzle to muzzle) or vertically (cow to calf) by suckling. Pigs are special: They excrete far more of the virus than other livestock, and over a longer period of time, broadcasting it prodigiously in their respiratory exhalations. They sneeze it, they chuff it, they oink it, they wheeze it and burp it and cough it into the air. One experimental study found that pig breath carried thirty times as much FMD virus as the breath of an infected cow or sheep, and that once airborne it could spread for miles. That’s why pigs are considered an amplifier host of this virus.

An amplifier host is a creature in which a virus or other pathogen replicates—and from which it spews—with extraordinary abundance. Some aspect of the host’s physiology, or its immune system, or its particular history of interaction with the bug, or who knows what, accounts for this especially hospitable role. The amplifier host becomes an intermediate link between a reservoir host and some other unfortunate animal, some other sort of victim—a victim requiring higher doses or closer contact before the infection can take hold. You can understand this in terms of thresholds. The amplifier host has a relatively low threshold for becoming infected, yet it produces a vast output of virus, vast enough to overcome the higher threshold in another animal.

Not every zoonotic pathogen requires an amplifier host for successful infection of humans, but some evidently do. Which ones, and how does the process work? The disease scientists are exploring those questions, among many others. Meanwhile, the concept is a hypothetical tool. Linda Selvey didn’t mention the FMD paradigm when she used the word “amplifier” in our conversation about Hendra virus, but I knew what she meant.

Still . . . why horses? Why not kangaroos or wombats or koalas or potoroos? If the horse fills that amplifying role, one obvious fact deserves fresh attention: Horses aren’t native to Australia. They are exotic, first brought there by European settlers barely more than two centuries ago. Hendra is probably an old virus, according to the runic evidence of its genome, as read by molecular evolutionists. Distantly diverged from its morbillivirus cousins, it may have abided unobtrusively in Australia for a very long time. Bats too are an ancient part of the native fauna; the fossil record in Queensland shows that small bats have been there for at least 55 million years, and flying foxes may have evolved in the region during the early Miocene, about 20 million years ago. Human presence is more recent, dating back only tens of millennia. More precisely, humans have inhabited Australia since the pioneering ancestors of Australian aboriginal peoples first made their way, island hopping daringly in simple wooden boats, from southeastern Asia by way of the South China Sea and the Lesser Sunda Islands to the northwestern coast of the island continent. That was at least forty thousand years ago, possibly much earlier. So three of the four principals in this complex interaction—flying foxes, Hendra virus, and people—have probably coexisted in Australia since the Pleistocene era. Horses arrived in January 1788.

It was a small change on the landscape, compared to all that would follow. Those earliest horses came aboard ships of the First Fleet, under command of Captain Arthur Phillip, who had sailed out from Britain to establish a convict colony in New South Wales. After five months of navigating the Atlantic, Phillip stopped at a Dutch settlement near the Cape of Good Hope to take on provisions and livestock before continuing eastward from Africa. He rounded Van Diemen’s Land (now Tasmania) and sailed north along mainland Australia’s east coast. Captain James Cook had already come and gone, “discovering” the place, but Phillip’s group would be the first European settlers. At a spot near what is now Sydney, within the fine natural harbor there, his penal arks put ashore 736 convicts, 74 pigs, 29 sheep, 19 goats, 5 rabbits, and 9 horses. The horses included two stallions, four mares, and three foals. Until that day there was no record, either fossil or historic, of members of the genus
Equus
in Australia. Nor were there any oral traditions (none shared with the world so far, anyway) of Hendra virus outbreaks among aboriginal Australians.

As of January 27, 1788, then, the elements were almost certainly gathered in place—the virus, the reservoir hosts, the amplifier host, plus susceptible humans. And now another riddle presents itself. From the horses of Captain Arthur Phillip to the horses of Vic Rail is a gap of 206 years. Why did the virus wait so long to emerge? Or had it indeed emerged previously, maybe often, and never been recognized for what it is? How many past cases of Hendra, over two centuries or more, have been misdiagnosed as snakebite?

Answer from the scientists: We don’t know but we’re working on it.

6

H
endra virus in 1994 was just one thump in a drumbeat of bad news. The drumbeat has been sounding ever more loudly, more insistently, more rapidly over the past fifty years. When and where did it start, this modern era of emerging zoonotic diseases?

To choose one point is a little artificial, but a good candidate would be the emergence of Machupo virus among Bolivian villagers between 1959 and 1963. Machupo wasn’t called Machupo at the start, of course, nor even recognized as a virus. Machupo is the name of a small river draining the northeastern Bolivian lowlands. The first recorded case of the disease came and went, almost unnoticed, as a bad but nonfatal fever afflicting a local farmer. This was during the wet season of 1959. More such illnesses, and worse, occurred in the same region over the following three years. Symptoms included fever and chills, nausea and vomiting, body aches, nosebleeds, and bleeding gums. It became known as El Tifu Negro (the Black Typhus, for the color of vomit and stool), and by late 1961 had struck 245 people, with a case fatality rate of 40 percent. It continued killing until the virus was isolated, its reservoir identified, and its dynamics of transmission understood well enough to be interrupted by preventive measures. Mouse trapping helped enormously. Most of the scientific work was done under difficult field conditions by a patched-together team of Americans and Bolivians, including an intense young scientist named Karl Johnson, pungently candid with his opinions, deeply enthralled by the dangerous beauty of viruses, who caught the disease himself and nearly died of it. This was before the Centers for Disease Control and Prevention (CDC) in Atlanta sent out well-equipped squads; Johnson and his colleagues invented their methods and tools as they went. Having struggled through his fever at a hospital in Panama, Karl Johnson would play a large and influential role in the longer saga of emerging pathogens.

If you assembled a short list of the highlights and high anxieties of that saga within recent decades, it could include not just Machupo but also Marburg (1967), Lassa (1969), Ebola (1976, with Karl Johnson again prominently involved), HIV-1 (inferred in 1981, first isolated in 1983), HIV-2 (1986), Sin Nombre (1993), Hendra (1994), avian flu (1997), Nipah (1998), West Nile (1999), SARS (2003), and the much feared but anticlimactic swine flu of 2009. That’s a drama series more glutted and seething with virus than even Vic Rail’s poor mare.

A person might construe this list as a sequence of dire but unrelated events—independent misfortunes that have happened to us, to humans, for one unfathomable reason and another. Seen that way, Machupo and the HIVs and SARS and the others are “acts of God” in the figurative (or literal) sense, grievous mishaps of a kind with earthquakes and volcanic eruptions and meteor impacts, which can be lamented and ameliorated but not avoided. That’s a passive, almost stoical way of viewing them. It’s also the wrong way.

Make no mistake, they are connected, these disease outbreaks coming one after another. And they are not simply
happening
to us; they represent the unintended results of things we are
doing
. They reflect the convergence of two forms of crisis on our planet. The first crisis is ecological, the second is medical. As the two intersect, their joint consequences appear as a pattern of weird and terrible new diseases, emerging from unexpected sources and raising deep concern, deep foreboding, among the scientists who study them. How do such diseases leap from nonhuman animals into people, and why do they seem to be leaping more frequently in recent years? To put the matter in its starkest form: Human-caused ecological pressures and disruptions are bringing animal pathogens ever more into contact with human populations, while human technology and behavior are spreading those pathogens ever more widely and quickly. There are three elements to the situation.

One: Mankind’s activities are causing the disintegration (a word chosen carefully) of natural ecosystems at a cataclysmic rate. We all know the rough outlines of that problem. By way of logging, road building, slash-and-burn agriculture, hunting and eating of wild animals (when Africans do that we call it “bushmeat” and impute a negative onus, though in America it’s merely “game”), clearing forest to create cattle pasture, mineral extraction, urban settlement, suburban sprawl, chemical pollution, nutrient runoff to the oceans, mining the oceans unsustainably for seafood, climate change, international marketing of the exported goods whose production requires any of the above, and other “civilizing” incursions upon natural landscape—by all such means, we are tearing ecosystems apart. This much isn’t new. Humans have been practicing most of those activities, using simple tools, for a very long time. But now, with 7 billion people alive and modern technology in their hands, the cumulative impacts are becoming critical. Tropical forests aren’t the only jeopardized ecosystems, but they’re the richest and most intricately structured. Within such ecosystems live millions of kinds of creatures, most of them unknown to science, unclassified into a species, or else barely identified and poorly understood.