Authors: Nathan Wolfe
Combining the meat of many animals and then distributing it to many people has obvious consequences. Connecting thousands of animals with thousands of consumers means that an average meat eater today will consume bits of millions of animals during their lifetimes. What previously was a direct connection between one animal and one consumer is now a massively interconnected network of animal parts and those that eat them. And while cooking the meat certainly eliminates many of the risks, the massive number of interactions increases the potential that a rogue agent will make the jump.
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This is what appears to have happened in the case of the sheep disease scrapie and bovine spongiform encephalopathy (BSE), better known as mad cow disease. BSE is among the fascinating group of infectious agents known as prions, mentioned in chapter 1. Unlike viruses, bacteria, parasites, and any other group of life we know of on the planet, prions lack the genetic blueprints of biology (i.e., RNA and DNA). Rather than the combination of genetic material and proteins that make up all other known life, prions simply have protein. While this may seem insufficient to accomplish any organic task, prions are capable of spreading. And they can cause serious disease.
BSE was first identified as a novel cattle disease in November 1986 because of the dramatic symptoms it causes in cows. They walk and stand abnormally, and after some months they experience violent convulsions and death. While there’s still some debate about its origins in cows, it appears that it came from sheep. During the 1960s and 1970s as the development of cattle feed was industrialized, one type of cow feed involved the rendering of sheep carcasses into meat and bone meal. Sheep have long been known to have a prion disease called scrapie, and it appears that processing their carcasses as cattle feed permitted the agent to jump over and adapt.
Once it jumped to cattle, BSE then spread through more feed. Some cattle carcasses, like sheep carcasses, are also ground into feed for cattle. It appears that once the prion crossed from sheep to cattle, its primary communication was through infected cattle meat and bone meal processed for the next generation of cows.
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The spread was remarkably effective. Some have suggested that during this period more than a million infected cows may have entered into the food chain. But not all of these prions stayed in cows.
Around ten years after the first identification of BSE, physicians in the UK began to recognize a fatal neurodegenerative disease among humans who were potentially exposed to contaminated beef. The patients showed evidence of dementia, severe twitching, and an increasing deterioration of muscle coordination. Evidence from the patients’ brains revealed that they had been ravaged in exactly the same ways as those of the cows. Experimental evidence showed that the disease could also be transmitted to primates whose brains were inoculated with brain tissue from infected humans. These human patients had been infected with BSE, but when found in humans, the same disease is called variant Creutzfeldt-Jakob (vCJD) disease.
While only twenty-four human cases of vCJD have been confirmed to date, there are certainly others, as the definitive diagnosis is difficult to make. Much is still unknown about vCJD, but it’s increasingly suspected that infected humans must have both genetic susceptibility for the deadly brain disorder as well as exposure to infected cow tissue. Analysis of the tonsils and appendixes removed from healthy patients suggests that as many as one in four thousand people who were exposed during the UK BSE epidemic are carriers who show no sign of disease. This is particularly worrying since vCJD has been shown to pass through organ transplantation and may also pass through blood transfusions.
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The way that we now grow and distribute meat differs fundamentally from how we did it in the past. We also transport live animals in new ways. The relative ease of international shipping means that people can move livestock from regions that were once remote. And the situation is not unique to animals. Many of our plant food sources are now transported thousands of miles and eaten by millions before any microbial contamination related illness would be detected.
In chapter 6 we discussed how monkeypox rates are rising in DRC. But monkeypox has not been restricted to Africa. In 2003 monkeypox hit the United States. Careful investigation of the 2003 US outbreak showed that it emerged from a single pet store—Phil’s Pocket Pets of Villa Park, Illinois. On April 9 of that year, around eight hundred rodents representing nine different species were shipped from Ghana to Texas. The shipment included six different groups of African rodents, including Gambian giant rats, brush-tailed porcupines, and multiple species of mice and squirrel. Subsequent testing by the CDC showed that Gambian giant rats, dormice, and rope squirrels from the shipment were all infected with monkeypox, which likely spread among the animals during shipment. Some of the infected Gambian rats ended up in close proximity to prairie dogs at the Illinois pet store, and those prairie dogs appear to have seeded the human outbreak.
Over the following months there were a total of ninety-three human cases of monkeypox in six midwestern states and New Jersey. And while most of them probably resulted from direct contact with infected prairie dogs, some may very well have resulted from human-to-human transmission.
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The moving and mingling of animals as pets and food increases the probability that new agents will enter into the human population. It also increases the chances that distinct microbes will end up in the same host and exchange genes. As discussed earlier, there are multiple ways in which a virus can change genetically: direct changes in genetic information (mutation) or the exchange of genetic information (recombination and reassortment). The first option, genetic mutation, provides an important mechanism for slow and steady production of genetic novelty. The second options, genetic recombination and reassortment, provide viruses with the capacity to quickly gain entirely novel genetic identities. When two viruses infect the same host, they have the potential to recombine, exchanging genetic information and possibly creating a completely new “mosaic” agent.
This has already occurred to important effect. As we learned in chapter 2, HIV itself represents a mosaic virus—two monkey viruses, which at some point infected a single chimpanzee, recombined and became the ancestral form of HIV. Similarly, influenza viruses have the capacity to pick up entirely new groups of genes by forming these mosaics through reassortment, where entire genes are swapped.
Influenza viruses can reassort on the farms where humans, pigs, and birds interact. Pigs have the potential to acquire some human influenza viruses. They also can acquire viruses from birds, including wild birds that may pass through on migration routes. These wild birds can infect pigs directly or indirectly through domestic birds such as chickens and ducks. When new viruses from birds interact with human viruses in an animal such as a pig, one of the outcomes is a completely new influenza virus with some parts from the circulating human virus and some parts from the bird virus. These new viruses can spread dramatically when reintroduced into human beings since they can differ sufficiently to avoid detection by natural antibodies and vaccines from earlier circulating influenza strains.
Recombination plays a potentially vital role in a number of viruses. Genetic analyses of SARS show that it’s likely a recombinant virus between a bat coronavirus and another virus, probably a separate bat virus we have yet to discover. These two viruses formed a novel recombinant mosaic virus prior to infecting humans and civets. These viruses’ potential to recombine may very well have related to the interaction of animals that previously would never have been in contact in the wild, as they made their way along market networks.
My mentor Don Burke, who now leads the University of Pittsburgh’s School of Public Health, has played a pivotal role in pointing out how recombination between viruses can help seed new epidemics. He coined the term
emerging genes
to refer to this process. Historically, virologists thought that new epidemics result from the movement of an entire microbe from an animal to a human. As we’ve seen in HIV, influenza, and SARS, recombination and reassortment provide other more stealthy methods to seed new epidemics. Rather than transplant an entire new microbe, two microbes, one old and one new, can temporarily interact in a single host and exchange genetic material. The resulting modified agent may have the potential to spread and become a completely new, and completely unprepared for, pandemic. In these cases it’s actually newly swapped genetic infomation that causes the pandemic rather than a new microbe—hence the term
emerging genes
.
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In the coming years we’ll see more and more pandemic threats. New infectious agents will spread and cause disease. New pandemics will emerge as we go deeper into the rain forests and unleash the agents previously unconnected to international transportation networks. These agents will spread as dense population centers, local culinary practices, and wild-animal trade increasingly intersect. The impact of epidemics will be augmented by HIV-caused immunosuppression that increases the risk of new agents adapting to a damaged human species. As we move animals quickly and efficiently around the world, they will, in turn, seed new epidemics. Microbes that have never encountered each other now will, and they’ll form new mosaic agents capable of spreading in ways that neither of their parents could manage. In short, we’ll experience a wave of new epidemics, ones that will devastate us if we don’t learn to better anticipate and control them.
PART III
THE FORECAST
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VIRUS HUNTERS
On December 9, 2004, primatologists working in the Dja Biosphere Reserve in southern Cameroon collected specimens from a dead chimpanzee. The chimp was sprawled out on the forest floor, eyes closed, but seemingly unmolested by a human or other predator. The team was rightfully concerned.
Belgian scientist Isra Deblauwe and her Cameroonian colleagues had started their long, tedious work some three years earlier. In the tradition of primatologists like Jane Goodall, their goal was to study wild great apes, our closest living relatives, to learn about them and ourselves.
And a few years later, they produced some interesting results. The team reported that, like other chimpanzee populations, the chimpanzees in the Dja used tools. In particular, they modified sticks to extract honey from underground bee nests. Chimpanzees, like all apes, including ourselves, love honey, and the information from the Dja team would add to the understanding of how different chimpanzee cultures use tools in different ways.
But on that rainy December day in 2004, honey was the last thing on the scientists’ minds. Four days after taking samples from the first dead chimpanzee, they took samples from another. Then on December 19 they took samples from a dead gorilla. This was worrying. Since the primatologists only followed a fraction of the population of apes in the Dja, what they’d seen was likely to be just the beginning. Many other unidentified apes might be dead, valuable wild kin whom the team had spent years working to understand. The consequences for conservation and research could be considerable.
But the threat to wild apes, while significant, was not the only problem. The researchers knew that the Ebola virus had wiped out large numbers of apes in Gabon, only a few hundred kilometers to the south. Ebola not only kills chimpanzees but from time to time has also jumped to humans causing dramatic and potentially epidemic-inducing cases. They also knew that one of their primatologist colleagues had acquired Ebola in the Ivory Coast when investigating deaths just like these. Whatever caused these ape deaths was not to be taken lightly.
Fortunately, they had responded according to a plan. First and foremost, the primatologists knew that they should not directly touch the carcasses. Months earlier, when the first dead animals had been seen, they had sent a message to colleagues in Yaoundé, Cameroon’s capital. The message in turn was transmitted to Mat LeBreton, the dedicated and skilled biologist who leads our ecology team and has pioneered a number of new techniques in viral ecology. Based in Yaoundé, LeBreton helped support an international team, including relevant ministries and laboratories in central Africa and Germany on the outbreak investigation that would follow.
The investigating team rapidly put together and deployed a mission to the Dja, a stunningly beautiful and unique rain forest habitat located along one of the major tributaries of the massive Congo River. There they worked with the primatologists to collect the specimens. They managed to obtain specimens from the skull and shoulder of the first chimpanzee. They also collected a specimen from the leg of the second chimpanzee, the jaw of the gorilla, and some muscle from a fourth victim—a chimpanzee—who died in early January 2005.
The safely preserved specimens then made the trip to expert laboratories. They went to the high containment laboratory of Eric Leroy, the virologist whom we worked with to discover the new strain of the Ebola virus discussed in chapter 5. The specimens also went to our collaborator Fabian Leendertz, a veterinarian and microbiologist working at the Robert Koch Institute in Germany who has perfected the study of ape microbes during many years spent shuttling between field sites in Africa and his lab in Berlin.
The results were surprising. While we all had come to assume that the same wave of Ebola knocking down ape populations south of the border in Gabon had killed the animals in the Dja, the specimens all came back negative for the Ebola virus. They were, however, all positive for another deadly agent—anthrax.
In 2004 Leendertz and his colleagues had reported a similar die-off of chimpanzees in the Taï forest of the Ivory Coast due to anthrax. So while the gorilla death in the Dja was the first of its kind, anthrax was already known to be a killer of forest apes. Strange perhaps but not unprecedented. How exactly a bacteria normally found in grasslands ruminants got to the apes in the Dja and Taï forests is still a mystery. There were some theories. Anthrax spores remain viable for long periods of time, even up to a hundred years. The spores can contaminate water supplies, so the apes may have picked it up from lakes or creeks. They may also have become infected while hunting or scavenging on ruminants, such as forest antelopes, that had themselves been infected. Or perhaps, at least in the Taï forest outbreak, neighboring farms had seeded the outbreak when the apes had foraged for food in cropland contaminated by anthrax from cattle.