The Viral Storm (14 page)

A young man with monkeypox.
(
Lynn Johnson / National Geographic / Getty Images
)

I’ve been working on monkeypox since 2005 with Anne Rimoin, an epidemiologist from UCLA, and her colleagues in the DRC, including Jean-Jacques Muyembe. Annie’s spent much of the last ten years pushing deeper into the logistical nightmare of conducting high-quality surveillance for novel diseases like monkeypox in some of the most rural regions in the world. She manages to do it with flare. I’ve seen her touch up her eyeliner in the mirror of an off-road motorbike in a rural town in central DRC.

In 2007 we reported that monkeypox does not simply appear in outbreaks. The long-term work Annie and her colleagues did showed us that the virus should probably be considered endemic among humans—it is a permanent part of our world. Rather than follow the traditional method for investigating monkeypox outbreaks, Annie and her team set up shop in regions that had known infections. Through constant monitoring, it became clear that there were monkeypox cases all year long. And the number of cases was growing.

Dr. Anne Rimoin in DRC.
(
Prime Mulembakani
)

In the final analysis it was just a matter of how hard you looked. During my visits to these sites, I’ve always seen cases of monkeypox. Some of these cases were the result of exposure to infected animals, but a number of them were the result of person-to-person transmission, the hallmark of a virus that’s beginning to fully transition to a new host species.

You might wonder how such frightening cases of monkeypox could exist without the world being aware of them. The answer is that the region where we conducted this work is among the most remote in the world. Just to get to this area requires a chartered flight on a small plane or a three-week boat trip on tributaries of the Congo River that are only navigable during the rainy season. The setting is austere and beautiful, with very few roads. Most villages are linked together by simple footpaths. The research uses rugged off-road motorbikes traveling sometimes for as long as ten hours to get to the site of a case. Just dodging the chickens and pigs represents a major challenge.

Despite the incredible dedication and skill of our Congolese colleagues, the idea that the current meager resources devoted to health in the DRC could permit full coverage of a country four times the size of France is crazy. Yet this is one of the most important places in the world for the emergence of new viruses. Without a doubt, an interconnected world that doesn’t invest in the infrastructure needed to monitor these viruses is doomed to fall victim to more epidemics.

*   *   *

Whether or not monkeypox has the potential to join the pantheon of our Category Four agents remains to be seen. Microbes that reach Category Four can live exclusively in humans while simultaneously continuing to live in animal reservoirs. Microbes in Category Four include dengue, discussed in chapter 4. Dengue maintains itself in human populations but also persists in a forest cycle spread by mosquitos among nonhuman primates.

Category Four agents represent the final step on the journey to become a human-specific microbe. They also present particular problems for public health. When scientists finally succeed at generating a vaccine for dengue, it will help countless people. But vaccination alone does not mean that we can eradicate dengue. Even if every single human were vaccinated, the fact that the virus can persist among monkeys in forests in Asia and Africa means that it will always have the potential to reenter human populations.

Monkeypox still ranks as a Category Three agent, but that could certainly change. Since our work in 2007, we’ve shown that the cases of monkeypox continue to grow in the DRC. Part of the explanation for this is that after smallpox was eradicated in 1979 the smallpox immunization program was stopped. As more and more nonimmunized, and therefore susceptible, children have been born into the population, the number of cases has steadily risen. And each additional case represents an opportunity for a unique monkeypox virus to jump or mutate. One of these may have the potential to spread and push monkeypox to the next level, which is why we keep tabs on this particular virus.

*   *   *

Only a handful of the microbes that have started on the path toward becoming exclusive human microbes have succeeded. The examples that have made it represent the mainstay of contemporary disease control. Viruses like HIV are generally considered to be present exclusively in humans, as are bacterial microbes like tuberculosis and parasites like malaria.
5
Yet it’s often difficult to make the human-exclusivity call. Unless we have comprehensive data about the diseases of wildlife, it’s hard to know if there may be a hidden reservoir of a supposedly exclusive human agent that could reenter human populations. And our understanding of the diversity of microbes in wild animals is still in its infancy. We know very little about what’s out there.

Agents like human papilloma virus and herpes simplex virus almost certainly reside exclusively in humans, but they have likely been with us for millions of years. With an agent like HIV, we get into a gray area. Could the virus that seeded HIV a hundred or so years ago continue to live on in chimpanzees? Viruses very close to HIV have been found in chimpanzees, but we haven’t sampled every chimpanzee in nature, so even closer relatives might still be out there. Similarly, given the diversity of malaria parasites we’ve seen in some of the African apes during recent studies, the possibility remains that some population of ape in some forest shares “human” malaria.

The question of reservoirs is an important one. We celebrated with great fanfare the eradication of smallpox in 1979. Eliminating that scourge from the human population was probably the greatest feat in public health history. Yet much remains unknown about how smallpox originated.

Smallpox appears to have first emerged during the domestication revolution. Evidence points to an origin in camels, which are infected with the closest known viral relative to smallpox, camelpox. Yet camels may very well have been a bridge host permitting the virus to jump from rodents, where most of the viruses like smallpox reside. If so, could there be a virus out there living in some North African, Middle Eastern, or central Asian rodent that’s too close for comfort? A virus close enough to smallpox to reemerge and spread in humans? If so it might look a lot like monkeypox, and, like monkeypox, it might be largely missed.

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For our purposes we should certainly consider smallpox to be one of our Category Five agents—a virus that made it to the point where it could live and survive exclusively in humans. And we should be proud of the herculean and successful effort to wipe it out.

Smallpox certainly had the right stuff. It probably killed more humans than any virus that has ever infected our species. Following the domestication revolution, the growing human populations and domestic animal populations (like camels) set the stage for the virus to gain a true foothold in our species.

We’ll probably never know definitively what the first real pandemic was, but smallpox is a good candidate. It spread throughout the Old World after its likely camel origins but never made it to indigenous human populations in the New World on its own. When the Old World and New World collided at the onset of global travel some five hundred years ago, smallpox had the chance to make the jump, killing millions of the completely susceptible inhabitants of the Americas. That jump across continents positions it as the most likely candidate for the first real pandemic.

By the middle of the eighteenth century, smallpox had not only spread to every part of the world but had established itself just about everywhere, save for some island nations. And it killed. During the eighteenth century, it’s estimated that smallpox killed around four hundred thousand people a year in Europe. The death rates elsewhere may have been even higher.

*   *   *

The human tendency to travel, to explore, and to conquer would accelerate dramatically over the five hundred years that would follow the discovery of the New World—and the coinciding smallpox pandemic. Global transportation networks would tie humans and animals together in a way that would accelerate the emergence of new viruses. These connections would result in a single, interconnected world—a world vulnerable to plague.

6

ONE WORLD

In 1998 scientists working independently in Australia and Central America announced that they were finding massive numbers of dead frogs in the forests where they worked. The large-scale die-off was especially dramatic. Global amphibian populations had been declining for some time, but these mounting frog deaths occurred in pristine habitats—places far less likely to have been exposed to toxic by-products of human cities or other man-made environmental threats. Field biologists and tourists alike witnessed the large numbers of dead frogs scattered about the forest floor. This was rare indeed since scavengers quickly eat dead animals. To see so many indicated that the predators already had their fill of free frogs and these were the leftovers. In fact, it was just the tip of the iceberg. A massive and unprecedented amphibian carnage was under way.

The expiring frogs all displayed similar and worrying symptoms. They became lethargic, their skin sloughed off, and they often lost their ability to right themselves if turned over. In the months that followed the first announcements, a number of possible explanations came forth—pollution, ultraviolet light, and disease among them. Yet the particular pattern of death was most consistent with an infectious agent. Animal deaths spread in wavelike patterns from one location to the next suggesting the spread of a microbe, a contagion sweeping through the Central American and Australian frog world.

Frogs killed by the amphibian chytrid fungus.
(
Joel Sartore / National Geographic / Getty Images
)

The solution to the mystery came in July 1998, when an international team of scientists reported the source of the frog disease. The team found evidence that a majority of the frog species succumbing to the die-offs were infected with a particular species of fungus. The fungus they identified was
Batrachochytrium dendrobatidis
, known more simply as the chytrid fungus (pronounced KIT-rid). They found evidence of chytrid, which had previously been seen exclusively in insects and on decaying vegetation, on a number of dead frogs. Tellingly, when they scraped the fungus from the dead and infected healthy laboratory tadpoles with it, they were able to re-create the fatal symptoms. The fungus was to blame.

Since the 1998 report, this fungus is now documented on all continents that have frog populations. It can survive at sea level but also wreaks havoc at altitudes up to twenty thousand feet. And it’s a killer. In Latin America alone, chytrid fungus has been linked to extinction in 30 of the 113 species of the strikingly beautiful harlequin toads. Thirty species forever removed from the biological diversity of our planet.

While the spread and devastation of chytrid has now been well documented, much about it remains unknown. The large-scale declines in amphibian populations predated the emergence of the fungus, so it is not the only problem that is devastating global frog populations, but it’s definitely among them. Another key factor is the steady decline in available frog habitat as the human footprint has increased over the last hundred years.

The questions of where the fungus originated and how it spreads are largely outstanding. Work done on archived specimens from South Africa shows that the fungus has infected African frogs since at least the 1930s, decades before it hit any other continent. This points to an African origin. Yet at some time, the fungus spread and did so quite effectively. How did it manage to get so cosmopolitan so quickly?

One possibility is the exportation of frogs. The researchers who discovered the early evidence of chytrid in South Africa also noted that some of the species of the frogs infected were commonly used in human pregnancy tests. When injected by lab technicians with urine from pregnant women, African clawed frogs (
Xenopus laevis
) ovulate—which made for an early, if significantly more cumbersome, version of the common pregnancy dipsticks used today! Following the discovery of this human pregnancy test in the early 1930s, thousands of these frogs were transported internationally for this purpose. Perhaps they took chytrid fungus with them.