THE FIRST PANDEMIC

THE FIRST PANDEMIC 

In early July 2002 in Franklin County, Tennessee, a thirteen-year-old boy named 

Jeremy Watkins picked up a sickly bat on his way home from a day of fishing. None 

of the other family members handled it, and his stepfather wisely made him release 

the animal soon after Jeremy revealed his find. 

Events like this happen all over the world with thousands of wild animals every 

day, largely without ill consequences. But Jeremy’s encounter with this particular 

bat would be quite different. 

In the CDC report that would document Jeremy’s case, the next events were de- 

scribed with clinical efficiency. On August 21 Jeremy complained of headache and 

neck pain. Then a day or so later his right arm became numb and he developed a 

slight fever. Perhaps of greater concern, he also developed diplopia, or double vi- 

sion, and a constant, queasy confusion. Three days later he was taken to the local 

hospital’s emergency room but was discharged with the incorrect diagnosis of 

“muscle strain.” The next day he was back in the emergency room, this time with a 

fever of 102°F. He had the same symptoms, but now his speech was slurred, he 

had a stiff neck, and difficulty swallowing. 

At this point, Jeremy was transferred to a local children’s hospital. By August 26 

he could no longer breathe or think normally. He was also producing copious 

amounts of saliva. Highly agitated to the point of being combative, Jeremy was se- 

dated and put on life support. His mental status deteriorated rapidly and by the 

next morning he was completely unresponsive. On August 31 Jeremy was pro- 

nounced brain-dead and, following the withdrawal of life support, he died of bat- 

borne rabies. 

Jeremy’s family did not know that bats could carry rabies, much less transmit it 

to humans. They did not remember him complaining of a bite, although that’s ex- 

actly what must have happened while he carried the bat home from his fishing 

excursion. They probably did not know that the incubation period for rabies is 

generally three to seven weeks, well within the range of the time between his expo- 

sure to the bat and the first symptoms he experienced. Detailed studies of the virus 

that killed Jeremy revealed evidence of a variety of rabies found in silver-haired and 

eastern pipistrelle bats common in Tennessee.

Rabies is a terrible way to die. It’s a disease that devastates the families of its 

victims, with patients becoming virtual zombies in the days before death. It is 

among the small number of viruses that kill virtually all of the individuals they in- 

fect. But as tragic as it is that the doctors at the local Franklin County emergency 

room sent Jeremy home with a diagnosis of muscle strain, the reality is that it was 

already too late to help the boy at that point. Without rapid postexposure prophy- 

laxis after infection, the boy was destined to die. 

If we take a different view, the virus that causes rabies is not only a deadly menace 

but also a truly amazing feat of nature. This virus, shaped like a bullet, is a meager 

180 nanometers long and 75 nanometers across. If you stacked rabies viruses one 

on top of the next, you would need more than a thousand of them to reach the 

thickness of a single human hair. Rabies has an almost trivial genome, with only 

twelve thousand bits of genetic information for a meager five proteins. It’s simple, 

tiny, and incredibly powerful. 

While diminutive, the virus accomplishes remarkably sophisticated tasks. In 

addition to the standard viral work of invading cells, releasing genes, making new 

viruses, and spreading, it has some unique tricks. From the point of entry, the virus 

travels preferentially along neural pathways, making its way into the central nervous 

system. It accumulates selectively in the saliva. The virus particles that infect the 

central nervous system modify the host’s behavior, increasing aggression, inter- 

fering with swallowing, and creating a profound fear of water. When put together, a 

rabies infection leads to an aggressive host literally foaming at the mouth with 

virus. A host that lacks the capacity to drink or swallow further increases the proba- 

bility of delivering a successful bite—a bite that gives this particular virus the abil- 

ity to advance from one individual to the next.

As frightening and deadly as rabies is, as a global community we need not fear 

it. That a virus is exceedingly and dramatically deadly does not mean it will become 

a pandemic. Rabies kills more than fifty-five thousand people a year worldwide. It is 

a cause for serious public health measures, but it does not present a global pan- 

demic threat. In all of the years that the CDC and other public health organizations 

have followed rabies, it has never once gone from person to person. Every one of 

those deaths, like the death of Jeremy Watkins, resulted from an independent ani- 

mal infection. From a pandemic perspective, it doesn’t have the right stuff. 

So, what is a pandemic? Defining them creates some trouble. The word itself 

comes from the Greek pan, meaning “all,” and demos, meaning “people.” Yet, in 

reality, it is almost impossible to imagine an infectious agent that infects the entire 

human population, a high bar to set for a virus. In humans or any hosts, different 

individuals will have different genetic susceptibility, so at least a few individuals 

will likely be incapable of sustaining an infection because of some kind of genetic 

immunity. Also, the simple logistics of spreading to every single individual in any 

population makes such a feat nearly impossible. 

Among the most common viruses infecting humans that we are aware of is the 

human papilloma virus,¹ and it doesn’t afflict 100 percent of people. HPV currently 

infects 30 percent of women between the ages of fourteen and sixty in the United 

States, a whopping high rate for a virus. Rates are likely even higher in some parts

of the world. Amazingly, the majority of sexually active humans on our planet, 

whether male or female, will get HPV at some point in their lives. The virus is made 

up of over two hundred different strains, all of which infect either skin or genital 

mucosa. Once the virus enters an individual, it generally stays active for years or 

even decades. Fortunately, the vast majority of HPV strains cause no problems for 

us. The few strains that do cause disease generally do so by causing cancer, the 

most important example being cervical cancer.² Luckily, most HPV simply spreads 

from individual to individual with little harm. 

We’re still aware of only a small percentage of all viruses that call humans their 

home. There may be viruses out there that infect even more people than HPV does; 

the work to identify all of the viruses that infect us has only just begun. Research 

over the last ten years has identified multiple previously unknown viruses circu- 

lating in humans that infect many individuals yet do not appear to cause any ill- 

ness. The TT virus was named after the first individual to be infected, a Japanese 

man with the initials T.T. Very little research has been done yet on TTV, but it may 

be quite common in some locations. A report by one of my collaborators, Peter 

Simmonds, an excellent Scottish virologist, found prevalence rates ranging from 

1.9 percent among Scottish blood donors to 83 percent among residents of The 

Gambia in Africa, a startlingly high range. Fortunately, TTV does not appear to be 

harmful. 

GB virus is another recently identified and still largely unstudied virus present in 

many people. The virus got its name from a surgeon, G. Barker; at the time, his 

hepatitis was mistakenly attributed to the virus.³ I know from my own work how 

common both TTV and GBV are. Using very sensitive approaches to viral dis- 

covery, we frequently see these two—largely to our dismay, since they interfere with 

our ability to catch the dangerous culprits we’re really looking for. 

However common TTV and GBV are, they do not infect 100 percent of humans. 

So the literal Greek-derived definition of pandemic is probably an impossibility. The 

World Health Organization (WHO) has devised a six-stage classification of pan- 

demics beginning with a class-one virus that infects just a few people and going on 

to a class-six pandemic, which occurs when infections have spread worldwide. 

The WHO faced widespread criticism for labeling H1N1 a pandemic in 2009, 

but that’s exactly what it was. H1N1 went from infecting only a few individuals in 

early 2009 to infecting people in every region of the world by the end of the same year. If that’s not a pandemic, then I don’t know what is. Whether or not we label a 

microbe that’s spreading as a pandemic is unrelated to its deadliness. It’s just a 

marker of its ability to spread. And as we discussed in chapter 1, the fact that H1N1 

doesn’t kill 50 percent of the people it infects (or even 1 percent for that matter) 

doesn’t mean it won’t kill millions of people or represent a massive threat. 

In fact, from my perspective, it’s possible that we could have a pandemic and 

not even notice it. If, for example, a symptomless virus like TTV or GBV were to 

enter into humans today and spread around the world, we probably wouldn’t be 

able to tell. Most conventional systems to detect diseases only catch things that 

cause clear symptoms. A virus that didn’t cause any immediate harm would likely 

be missed. 

Of course, “immediate” isn’t the same thing as “never.” If a virus like HIV were 

to enter into humans today and spread globally, it wouldn’t be detected for years, 

since major disease would occur sometime after initial infection. HIV causes only a 

relatively minor set of syndromes immediately, even though it starts to spread right 

away. AIDS, the major disease of HIV, doesn’t emerge until years later. Since con- 

ventional methods for detecting new pandemics rely primarily on seeing 

symptoms, a virus that spreads silently would likely miss our radar, spreading to 

devastating levels before an alarm could be triggered. 

Missing the next HIV would obviously be a catastrophic public health failure. 

Yet new viruses, even if likely to be completely harmless, like TTV and GBV, need 

to be monitored if they are moving quickly through the human population. As we 

saw in chapter 1, viruses can change. They can mutate. They can recombine with 

other viruses, mixing genetic material to create something new and deadly. If 

there’s a new virus in humans and it’s spreading globally, we need to know about 

it. The dividing line from spreading and benign to spreading and deadly is a poten- 

tially narrow one. 

  

For our purposes, we’ll define a pandemic as a new infectious agent that has 

spread to individuals on all continents (with the exception, of course, of Antarc- 

tica). One may counter that it would theoretically take only a dozen or so infected 

people to accomplish this—a few infected people per continent. That may be true, 

but it would be exceptionally rare for a microbe to spread so widely and infect so 

few individuals. And if it did manage to occur, even with twelve people, it would 

still represent a potent risk to all of us. 

Defining precisely when a new spreading agent actually becomes a pandemic is 

less important for our objective here than understanding how pandemics are born. 

What I wanted to know when I began my research on pandemics was how some- 

thing goes from being a strictly nonhuman infection to one spreading to humans 

on every continent. 

In 2007 I worked with the aforementioned polymath biologist and geographer 

Jared Diamond and the tropical medicine expert Claire Panosian to develop a five- 

step classification system for understanding how an infectious agent living exclu- 

sively in animals can become an agent that spreads globally in humans. The sys- 

tem moves stepwise from agents that infect only animals (Category One) to agents 

that exclusively infect humans (Category Five). 

Jared and I spent many afternoons pondering this process over extended writing 

sessions at his home in Los Angeles. During our lunch breaks, we’d stop writing to 

brainstorm, using thought experiments, how a virus might make this jump. We 

came up with one fairly elaborate idea centered around the Diamonds’ geriatric but 

much beloved pet rabbit, Baxter, and his invented disease—the dreaded Baxterpox. 

Even in our imaginary world, most human diseases have their start in animals.

Few of us now live on or near farms; fewer still live as hunter-gatherers sur- 

viving on wild plants and animals. We live in worlds filled with buildings and 

streets, where the dominant and notable forms of life are basically ourselves. De- 

spite living on every continent with a population of seven billion individuals, we 

still represent a very restricted segment of the biological diversity on our planet. 

As discussed in chapter 1, most of the diversity of life on our planet resides in 

the unseen world; in bacteria, archaea, and viruses. Despite our massive numbers 

and global reach, our human diversity pales in comparison. This is true even for 

our microbes. Most of the diversity in mammalian microbes resides in other ani- 

mals, not humans. Some animals house greater microbial repertoires than others. 

For example, fruit bats are a notorious reservoir species. They often live in large 

colonies and are highly mobile “travelers” connecting multiple regions with high 

levels of biodiversity. On average a species of colonial fruit bat will have a greater 

diversity of microbes than, say, a two-toed sloth living a largely solitary life. 

However you cut it, there are estimated to be over five thousand species of 

mammals on the planet and only one species of human. The diversity of microbes 

that can infect us from other mammals has and will always be substantially greater 

than the diversity of microbes that already does infect us. That’s why we concep- 

tualize the process as a pyramid, with the greatest diversity of microbes falling into 

Category One. 

We’ve seen that most of the microbes with the potential to cause new human 

pandemics live in animals. Domestic animals certainly represent a threat, but as 

discussed earlier, most of what they had to contribute to the human microbial 

repertoire has already jumped over. Right now, the threat from domestic animals 

comes more from them acting as bridges to allow the movement of wild animal 

microbes into the human population. Moreover, while the actual number of living 

domestic animals is quite high, they represent a small percentage of the diversity of 

mammals since we’ve only domesticated a small percentage of all animals. Clearly, 

when it comes to new pandemics, wild animals are where the action is. 

When I lived in Malaysia during the 1990s conducting my doctoral research, I 

spent time working with the accomplished parasitologists Janet Cox and Balbir 

Singh. Janet and Bal devised creative ways to detect malaria in blood that had been

dried on small pieces of laboratory filter paper (it looks like plain but thick white 

paper). This technique made it easier to do field screening or specimen collection 

in remote locations. Since blood could be dried easily and stored at room temper- 

ature, this method did away with the logistics of having to keep a specimen cold in 

regions without electricity. Janet and Bal taught me how to use these lab tech- 

niques, and, with their sweet kids, Jas and Serena (now both college students!), 

introduced me to the amazing Malaysian state of Kelantan. 

Kelantan is a small state on the border of Thailand that still adheres to 

Malaysian traditions that have disappeared in much of the now modern and 

economically booming country. Many of the people in Kelantan wear traditional 

Malaysian clothing, the official weekend is on Thursday and Friday, and there’s not 

a drop of alcohol to drink (at least officially) in the majority of the state. The pace 

of life in Kelantan is more relaxed than almost anywhere I’ve visited in the now 

bustling, dynamic countries of Southeast Asia. 

Among the fascinating sights to see in Kelantan was one that held particular 

scientific interest to Bal, Jan, and me—coconut-picking macaques. In a unique 

practice, some coconut farmers in northern Malaysia and southern Thailand work 

with pig-tailed macaques, a species of Southeast Asian monkey, trained to climb 

palms and harvest coconuts. A well-trained animal can pick up to fifty coconuts an 

hour—quite an efficient farmhand. 

One evening after dinner at their house, Bal told us of a report he’d heard of a 

man with a particularly devastating neurological disease, the symptoms of which 

suggested it was caused by a virus or other infectious agent. This man worked with 

the curious coconut-picking macaques. 

The close and long-term relationship between macaques and their human han- 

dlers presented an ideal chance to study the first and second stages of the classi- 

fication system I’d developed with Jared and Claire. We could study the microbes 

present in the animals and monitor them for any cross-species jumps into hu- 

mans. Among the more interesting targets of our investigation would be the deadly 

herpes B virus. 

Herpes B may not sound as if it should be particularly dreaded, but it’s among 

the deadliest viruses a human can contract. Amazingly, the virus is almost com- 

pletely benign among the macaques that sustain it. For the coconut-picking 

macaques, herpes B virus is just like herpes simplex is for a human, creating minor

lesions that spread the virus through intimate contact like a bite or sex. Incon- 

venient for these monkeys, perhaps, but certainly not deadly. Yet when the virus 

crosses into humans, it causes severe neurological symptoms and invariably re- 

sults in death. Transmission of the virus has been documented in a number of pri- 

mate handlers in the West, including a sad case of a young woman working at the 

Yerkes Regional Primate Research Center in Atlanta who became infected after a 

captive macaque spit in her eye. At the time, no one had documented the infection 

occurring among the Kelantan coconut harvesters, despite the fact that they work 

with these animals daily and with far fewer protective measures in place. 

For Bal, Janet, and me, studying the Kelantanese macaques and their handlers 

provided an interesting way to monitor the entry of these viruses into human pop- 

ulations and to witness the first step in the process of how potential pandemics are 

born. Yet, as with the case of rabies in young Jeremy Watkins, we did not expect to 

see these herpes B viruses go anywhere outside Category Two. They would remain 

as infections that had made the leap but didn’t have the potential to spread in hu- 

mans. While the victims might die from infection, the people infected by these 

monkeys would never go on to spread the virus to their families or others. Thus, 

no pandemic for herpes B. For that, we’d need a different kind of virus. 

The interface we have with the animals in our world leads to a constant flow of mi- 

crobes. Every day, millions of people are exposed to animal microbes. Some rare 

infections lead to death. Much more frequently, they are transient and benign infec- 

tions, such as a bacteria from a pet dog or cat. The vast majority of these Category 

Two viral jumps represent dead ends from the perspective of a microbe: they infect 

a single individual, and that’s that. 

Sometimes, though, something unusual happens that is potentially pivotal for 

our species: a microbe that jumps over may have the capacity to move from one 

human to another human. If a microbe accomplishes this, it moves to a Category 

Three and toward becoming a pandemic. 

In late August, 2007 information began to trickle in to health authorities on an 

unidentified illness in a remote area of the Kasai-Occidental Providence in the 

Democratic Republic of Congo. The outbreak was centered around Luebo, a town 

of some historical importance as the last point that early twentieth-century

steamers could navigate to on the Lua Lua River. The case reports listed a number 

of bad symptoms—fever, severe headache, vomiting, major abdominal pain, 

bloody diarrhea, and severe dehydration. The first recognized cases were on June 8, 

following the funerals of two village chiefs. Tellingly, the entire first group of indi- 

viduals infected had assisted with the burials. 

The symptoms and the connection to burials led the Congolese health author- 

ities to consider the possibility of Ebola, a virus that spreads through direct contact 

with blood and body fluids, and they responded accordingly. The head of the Con- 

golese team was Jean-Jacques Muyembe. Jean-Jacques is a professor and the direc- 

tor of the national biomedical research institute, the INRB. His bright laugh and 

mild-mannered demeanor belie the fact that he’s had more experience dealing with 

viral hemorrhagic fevers⁴ than perhaps any other single person in the world. I have 

fond memories of working with Jean-Jacques in a remote location in central DRC 

and watching him break into hysterics as he watched me devour a meal of pan- 

fried grub worms for dinner. 

Jean-Jacques and his team called in long-standing collaborators, including Eric 

Leroy, a crack virologist who runs the only high containment bio-safety level four 

laboratory in central Africa that is capable of studying the world’s deadliest viruses. 

Leroy, Muyembe, and colleagues at the CDC and from other groups like Médecines 

Sans Frontières (MSF) worked to contain the Luebo outbreak. They sequenced a 

small portion of the virus’s genetic information and discovered that it was, in fact, 

the Ebola virus. 

Ebola hemorrhagic fever strikes fear in the hearts of people in the DRC and 

throughout the world. The Ebola virus kills quickly and dramatically. It also 

spreads. While the exact number of cases will never be known, the Luebo outbreak 

of 2007 probably infected around four hundred people. All of them were infected 

from a single virus that jumped from an animal into the first human victim and 

then subsequently spread. Around two-thirds of them died. 

Part of the public fascination with Ebola relates to how little we know about 

something so deadly. The truth is that it largely remains a devastating and un- 

solved mystery. 

What we do know about the Ebola virus is that it appears occasionally in hu- 

mans. We know that it can enter into humans from multiple animal species. Leroy 

and his colleagues have identified the Ebola virus in a few species of bats, helping

to pinpoint them as the likely reservoir. A range of studies also documents how 

Ebola affects gorillas, chimpanzees, and some species of forest antelope. We know 

that for now it’s a Category Three microbe on the route to pandemics: it can infect 

and spread in humans, although not to the point of sustained transmission. Effec- 

tively, it’s a virus with potential for localized outbreaks. 

Together with Leroy and his colleagues, we looked in detail at the virus that 

caused the Luebo outbreak of 2007, as well as a smaller outbreak that occurred 

about a year later in December 2008 in exactly the same region of DRC. We found 

that the viruses that caused the two outbreaks were nearly identical and formed an 

entirely new type in the deadliest group of the Ebola viruses: the Zaire group. 

That the Luebo outbreaks came from a new variant virus was significant. It 

meant that the depth of the genetic pool of viruses that could jump to us from ani- 

mals was greater than we’d imagined. Now we understood that new versions of the 

Ebola virus had the potential to enter into humans, perhaps someone who hunted 

or butchered the meat of wild fruit bats. This meant that we probably haven’t seen 

everything that the Ebola virus can serve up. For now, we classify Ebola as a Cate- 

gory Three agent, but our finding suggests that there are more undiscovered 

variants of Ebola out there that can cross into us. It’s possible that a distinct and 

as yet unknown Ebola virus circulating in animals might have the potential to 

spread more broadly than any Ebola in the past. 

Does the Ebola virus have the right stuff? Could it move higher in our pyramid 

classification system? From the perspective of a pandemic, all of the Ebola hemor- 

rhagic fever outbreaks to date have been stillborn. They spread, but lucky for us, 

that spread remains limited. 

Unlike the casual contact or airborne transmission of influenza, the majority of 

cases in the Ebola hemorrhagic fever outbreaks that have been studied resulted 

from intimate contact with the blood and body fluids of a very sick person. Gener- 

ally, people become infected when preparing a previous victim for burial or when 

caring for the sick. Limited transmission makes broader, sustained spread less 

likely. 

There are other disadvantages that the Ebola virus has in the microbial race to 

become a pandemic. The incredibly nasty symptoms of Ebola are both very specific 

and also coincide with its capacity to spread. Since few other viruses cause the dra- 

matic symptoms of Ebola, it can be identified relatively quickly and the sick

individuals can be isolated. Since it’s the very sick people who spread the virus, 

isolation works to stop it. This is the approach that organizations like the CDC and 

MSF use to quell Ebola outbreaks: get in, isolate victims, stop contact with blood 

and body fluids. For the Ebola viruses that have emerged to date, it’s a strategy that 

works. This kind of strategy often fails with more nimble viruses. 

In 1996 and 1997 quite another sort of outbreak occurred in the DRC. This out- 

break lasted over a year, and while estimates vary, it likely hit over five hundred 

people. Like Ebola hemorrhagic fever, the cases began with fever, aches, and 

malaise. After a few days, rather than the bleeding characteristic of Ebola, patients 

developed a severe rash consisting of pustules all over the body, often first appear- 

ing on the face. The symptoms looked quite a bit like smallpox, perhaps the great- 

est scourge of human history. But that was impossible. Smallpox had been eradi- 

cated nearly twenty years earlier. 

The cause of this outbreak was not smallpox, but it was a virus in the same 

group of viruses (the Orthopoxvirus genus) called monkeypox. Monkeypox has 

probably affected humans for ages, but it was only first recognized in 1970 during 

the smallpox eradication effort. Prior to that, any monkeypox cases were likely 

misdiagnosed as smallpox. While the ultimate animal reservoir for monkeypox re- 

mains unknown, it’s almost certainly not a monkey, but rather a squirrel or other 

rodent. Because the virus can infect species of nonhuman primate, occasional 

human cases can result following contact with an infected monkey, hence the mis- 

nomer.

I’ve been working on monkeypox since 2005 with Anne Rimoin, an epidemi- 

ologist from UCLA, and her colleagues in the DRC, including Jean-Jacques Muyem- 

be. Annie’s spent much of the last ten years pushing deeper into the logistical 

nightmare of conducting high-quality surveillance for novel diseases like mon- 

keypox 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 out- 

breaks, 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.

In the final analysis it was just a matter of how hard you looked. During my vis- 

its 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 sim- 

ple 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 exclu- 

sively in humans while simultaneously continuing to live in animal reservoirs. Mi- 

crobes 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 per- 

sist 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 con- 

tinue 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 repre- 

sents 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 repre- 

sent 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 chim- 

panzee 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 re- 

cent 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 re- 

mains 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. 

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 exclu- 

sively 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 is- 

land nations. And it killed. During the eighteenth century, it’s estimated that small- 

pox 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 dramat- 

ically 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 emer- 

gence of new viruses. These connections would result in a single, interconnected 

world—a world vulnerable to plague.

CHURN, CHURN, CHURN

THE GREAT MICROBE BOTTLENECK 

The oysters were excellent, but the company was even more striking. As I sat in the 

small Parisian bistro with a tray of fresh shellfish, I savored the taste of the ocean. 

But the more powerful memory of that day was of another patron of the restaurant. 

At the table next to me sat an impeccably put together Frenchwoman. Her bag, 

skirt, and socks all matched—not exactly, but just enough to notice. Her dining 

companion sat to her right—a miniature poodle, sitting on the chair and drinking 

water from a bowl on the table. Pieces of his meal—chicken I think—fell over the 

side of his plate, mingling with the crumbs from his owner’s bread. 

Dogs play an important role in the lives of many people around the world. I had 

stopped only briefly in Paris on the way home from a month-long trip conducting 

research in Asia and Africa. It might have been the jet lag, but my recollection of 

the event could only be described as surreal. During my trip I’d spent time in a part 

of Borneo where people eat dog, including on at least one occasion my unsus- 

pecting self. I’d also visited Muslim areas of the Malay Peninsula, where devout 

people won’t even touch dogs because of religious beliefs. And I’d spent time in 

central Africa, where I’d seen local hunters work with their small, silent basenji 

hunting dogs—dogs that lived on their own but in exchange for scraps followed 

hunters into the forests, helping them catch their prey. In the United States, many 

people treat dogs as members of their families, paying large fees for medical ex- 

penses and mourning for them when they die. Sitting on the beach near my home 

in San Francisco, it would be hard for me to spend an hour without seeing some- 

one kiss his or her pet dog on the mouth. Watching that woman in Paris sharing a 

meal with her dog solidified just how linked we are to these animals. 

The close relationships we have with dogs, whether as companions, work animals, 

dinner guests, or a source of food, should not surprise us. Dogs play a special role

in human history. If we were to compile the “greatest hits” of human evolution, 

hunting and cooking would certainly make the cut. Language and the capacity to 

walk on two feet would also be on the list. But central among our species’ critical 

historical events is domestication—and dogs were the first in a long line of plants 

and animals that our ancestors tamed. 

The capacity to domesticate plants and animals underlies much of what we now 

think of as being human. To imagine a world without domestication, we’d have to 

spend time with one of the few dozen human populations on the planet that still 

practice hunting and gathering lifestyles, groups like the Baka and Bakoli, the so- 

called pygmies, living in central Africa that I have worked with for years, or the Aché 

that live in South America. For these groups of people, there is no bread, no rice, 

no cheese. There is no agriculture, and therefore the many rituals of our planet’s 

major traditions, including the harvest and planting pilgrimages and their asso- 

ciated festivals, are entirely absent—no holidays such as Ramadan, Easter, or 

Thanksgiving. There is no wool, no cotton, only textiles made from wild tree bark 

or grasses and the skins from hunted animals. 

These hunter-gatherer populations have complex histories, and many of them 

lived at some point with some form of agriculture before returning to a foraging 

lifestyle. Yet they provide us with interesting clues on what the lives of our ances- 

tors looked like before the advent of widespread domestication.¹ Among the traits 

hunter-gatherer populations share are small population sizes and a nomadic life- 

style. As we’ll see, these traits have an important impact on keeping the microbial 

repertoires of these populations at low levels. 

The first human foray into domestication came with modification of wolves into 

the canines we know today. Archaeological and DNA evidence suggests that pop- 

ulations in the Middle East and east Asia began domesticating gray wolves as early 

as thirty thousand years ago, turning them into guard dogs and work animals as 

well as using them for food and fur. The early history of dog domestication is still 

unclear. One hypothesis is that wolves followed humans, scavenging off of their 

kills, and over time became dependent on humans, a dependency that set the stage 

for their later domestication. But no matter how it began, by fourteen thousand 

years ago dogs played an integral role in human life and culture. In some archaeo- 

logical sites in Israel, humans and dogs were even buried together. These early 

dogs would have resembled modern-day basenjis, the silent hunting dogs pre- 

ferred by the central African hunters with whom I work. 

Occurring around twelve thousand years before we would domesticate anything 

else, the domestication of the dog was an early precursor to what would follow. 

Around ten to twelve thousand years ago, a domestication revolution occurred in 

earnest, starting with sheep and rye and then followed by a diverse group of other 

plants and animals.

The consequences and opportunities of the domestication revolution were pro- 

found. Prior to domestication, human populations were limited by the food avail- 

able in wild environments. Wild animals migrate, which forced our ancestors, who 

were dependent on the hunting of these wild animals, to do the same. The wild

fruits and other plant foods present in the local habitat were spread out, which 

again forced seasonal movement. Wild environments, with a few minor 

exceptions,² lacked the capacity to sustain large populations of people. As a conse- 

quence, human population sizes were small, probably numbering no more than 

fifty to a hundred people in a group, and mobile.

Human population through history. (Dusty Deyo) 

As domestication truly kicked in around five to ten thousand years ago, this 

would all change. With a combination of domesticated plants and animals, hu- 

mans gained the capacity to have sustained sources of calories year-round. Agri- 

culture (i.e., the domestication of plants) made it possible for human populations 

to stay in one place and avoid the constant movement that characterizes hunting- 

and-gathering populations as well as populations with only domesticated animals, 

which need to move in order to find feed for their herds. A sedentary lifestyle and 

the capacity for food surplus radically increased the potential for populations to 

grow, leading to the first real towns and cities. The particular combination of larger 

population sizes, sedentary groups of humans, and the growing populations of 

domestic animals would play a central role in transforming the relationship be- 

tween humans and microbes. But humans aren’t the only animals that tame the 

wild.

Despite conventional wisdom, the capacity for domestication is not unique to hu- 

mans. The most striking example of domestication in the animal kingdom comes 

not from primates, dolphins, or elephants—in fact, not from a vertebrate species 

of any type—but from ants. Far from simple-minded insects, ants are part of 

unique and complex colonies, each of which is perhaps better imagined not as a 

group of individual ants but rather as a collective ant “superorganism.”³ 

Leaf-cutter ant colonies exist in most tropical American habitats. Known to 

schoolchildren worldwide for their incredible strength, the workers march through 

the jungle carrying pieces of green leaves many times their own size back to the 

nest. Yet the leaf-cutter’s strength is not its most interesting feature. This amazing 

group of ants has mastered the art of domestication. Rather than eat those massive 

leaves, the workers chew them up into a fertilizer. The colony uses the fertilizer in 

order to support their gardens—for leaf-cutter ants, made up of the Atta and 

Acromyrmex groups, cultivate a fungus-based crop and have spent millions of years 

living off it. These ants are farmers. 

Domestication of fungus has helped leaf-cutter ants become one of the most 

successful species on our planet. Mature leaf-cutter colonies, measuring fifteen

meters across and five meters deep, can house upward of eight million ants. The 

massive underground colonies are sedentary, sometimes lasting for more than 

twenty years in the same location. 

These remarkable ants have attracted a number of scientists, including a Cana- 

dian researcher named Cameron Currie. Dr. Currie has used molecular tools to 

examine the genetics of the ants, their fungus, and the other members of this in- 

credible community. His research has shown the evolutionary links between the 

ants and their fungus crop. The colonies and their crop species have lived together 

for tens of millions of years, a much more mature farmer-crop relationship than 

that seen in humans. 

Like human farmers, the ants have agricultural pests, including a specialized 

fungal parasite that spoils the farms. Dr. Currie has shown that not only have the 

ants and their crops lived together for millennia; the parasitic fungus has been 

along for the ride since the beginning. Another amazing twist to this elegant sys- 

tem is that, like human farmers, the ants utilize a pesticide. They cultivate a species 

of bacteria that produces fungicidal chemicals that help the ants control their ver- 

min. Some people think of ants as pests, but these ants have their own pest prob- 

lems. 

Humans began domesticating other species merely thousands of years ago, 

rather than millions, as with the leaf-cutters. Like the ants, we’ve found that one of 

the consequences of high crop densities is parasites. The fungus species that the 

ants cultivate almost certainly had pests tens of millions of years ago, before they 

were cultivated by the leaf-cutters. But when the leaf-cutters accumulated the fun- 

gus and added fertilizer, it allowed more fungus to live closer together than re- 

sources would have permitted without active farming. Cultivation leads to concen- 

trated populations, and concentrated populations have higher burdens of para- 

sites, whether fungus or virus. 

While the leaf-cutters focus exclusively on farming fungus, humans have taken

agriculture and livestock to entirely new levels. Rather than cultivate a species or 

two over the course of a few millennia—lightning speed in evolutionary terms— 

humans domesticated a vast range of plant and animal species. 

We take it for granted, but the diversity of living things that our species culti- 

vates boggles the mind. In an average day, we might wake up in sheets (cotton) 

and wool blankets (sheep); put on leather shoes (cow) and perhaps a cashmere 

sweater (goat); eat a breakfast of eggs (chicken) and bacon (pig); bid farewell to 

our pets (dog, cat) on the way to work; for lunch we might eat a salad (lettuce, cel- 

ery, beets, cucumber, garbanzo beans, sunflower seeds) with dressing (oil from 

olives); for a snack we might eat a fruit salad (pineapple, peaches, cherries, pas- 

sionfruit) or mixed nuts (cashews, almonds, peanuts, actually a legume); for din- 

ner a caprese salad (tomato, buffalo mozzarella) and pasta (wheat) with peas and 

smoked farmed salmon with fresh basil (all domesticated). It would be an uncom- 

mon day for many of us not to interact with at least three domesticated animals 

and a dozen or so domesticated plants. We are truly masters of domestication. 

Consumption of wild foods, the source of calories for virtually all other organ- 

isms on our planet, now represents an almost quaint luxury for most humans. My 

friends Noele and Giovanni make a delicious wild asparagus pate from plants gath- 

ered in woods outside their small hillside village near Reggio, Italy. But using wild 

vegetables is now the exception rather than the rule. Wild salmon costs signif- 

icantly more than farmed salmon in the vast majority of the world. Eating wild veni- 

son, something my friends Mimi and Chris like to do each year in their Massa- 

chusetts cabin, represents a challenging “return to nature” rather than a regular 

source of calories. 

The transition from a species primarily dependent on wild sources of nutrients 

to a species that cultivates most of its food means that we don’t need to depend on 

the fluctuating food availability in uncultivated habitats. It also allows for the con- 

centration of these activities, with a few individuals focused on developing food 

while the rest of us have time to pursue other objectives, like, say, virology. We are 

freed from the daily foraging required of our ancestors before domestication. For

our purposes here, it also radically changed the way that we related to the microbes 

in our world. 

In the field sites where I work throughout the world, my collaborators and I work 

closely with hunters and monitor for new microbes that cross into them as they 

catch, prepare, and consume wild animals. Yet the hunters are not our only focus. 

Among the things we study in rural villages are the domestic animals—the dogs, 

goats, pigs, and other species that surround these people. Each animal, wild and 

domestic, has their own microbial repertoire, and when concentrated on a farm or 

in a house or herd, these microbes thrive. 

Domestic animals have contributed novel microbes to humans in different 

ways. Since these species each had their own predomestication microbial reper- 

toires, the initial close contact of farming led to an early exchange of their microbes 

to humans. My colleague Jared Diamond has provided detailed evidence for this 

exchange and its consequences for human history in his excellent book Guns, 

Germs, and Steel. Among other things, Jared showed that the preponderance of 

domestic animals in temperate regions contributed to a higher diversity of mi- 

crobes among temperate populations. For example, measles descends from rinder- 

pest, a virus of cows that entered into humans, a domestication-associated virus 

that continues to plague us. 

Humans have close interactions with domesticated animals, whether for com- 

panionship, protection, or food. These interactions reach fascinating extremes. In 

Papua New Guinea, women in some ethnic groups actually suckle their pigs, pro- 

viding human breast milk to ensure the survival of these valuable animals. This 

level of close connection has obvious implications for the movement of infectious 

agents. 

Of the microbes that originated in our domesticated animals, many entered into 

humans thousands of years ago, at or near the time that we first domesticated 

them. Acquiring the microbes that belonged to our domestic animals played an

important role in enhancing the microbial repertoire of our ancestors during the 

climax of domestication five to ten thousand years ago. Over time, this has 

changed. In the case of dogs, for example, most of the microbes that they had to 

contribute to humanity have already crossed over. In some ways, the microbial 

repertoire of our species has merged with that of dogs and the other animals we’ve 

domesticated. Even without breastfeeding our domestic animals, we often cuddle 

with them for warmth or play. We almost always have closer connections to them 

than we would to wild animals. 

The historical “predomestication” dog microbes that had the potential to cross 

into humans have largely done so, and the human microbes that could survive in 

dogs have also crossed. The ones that haven’t crossed successfully likely don’t 

have the potential to, and while they may lead to occasional infections in one or 

two individuals, they won’t have the capacity to spread—the critical trait required 

for something to have true impact. 

Over the thousands of years of interaction, we have reached a sort of microbial 

equilibrium with domestic animals. But this doesn’t mean that these animals don’t 

still contribute to our microbial repertoire; quite the contrary. Domestic animals 

continue to feed new microbes into the human species. These bugs derive not 

from the animals themselves, but from wild animal species that they are exposed 

to. Our domestic animals act as microbial bridges, permitting new agents from 

wild animals to make the jump into us. 

There are numerous examples of domestic animals bridging the microbial di- 

vide between humans and wild animals. Perhaps the best documented of these is 

the case of Nipah virus, a fascinating bug whose emergence has been studied in 

detail by my collaborators Peter Daszak and Hume Field and their colleagues. 

Through years of viral sleuthing, they have shown in exquisite detail exactly how 

the virus negotiates the complex world of humans and our farms.

Nipah virus was first detected in Malaysia, in the village that gave it its name. 

This virus kills. Of the 257 cases of infection seen during 1999 in Malaysia and 

Singapore, 100 people died, a startlingly high mortality rate. Among the survivors, 

more than 50 percent were left with serious brain damage. 

The first clues to the origin of the virus were the patterns of human cases. The 

vast majority occurred among workers in piggeries. At first, the investigators 

thought the virus causing the illness was Japanese encephalitis virus, a mosquito- 

borne virus present throughout tropical Asia. Yet menacing and distinct symptoms 

led the investigating teams to determine that it must be a new and still unidentified 

agent. 

Early symptoms of Nipah virus include those common in viral infections— 

fever, decreased appetite, vomiting, and flu-like systems. But after three to four 

days, more serious nervous system manifestations appear. The exact impact that 

the virus has differs from person to person. Some individuals experience paralysis 

and coma, while others have hallucinations. One of the first documented patients 

reported seeing pigs running around his hospital bed. 

MRI scans show serious damage to patches of the brain, and the patients who 

die usually do so within a few days of the onset of brain damage. Among the indi- 

viduals infected in Malaysia and Singapore in 1999, none appeared to seed addi- 

tional human infections, yet cases in subsequent years in Bangladesh provide evi- 

dence that the virus has the potential to spread from human to human under at 

least some circumstances. 

When scientists discover a new virus, a mad rush often ensues to identify the reser- 

voir of the virus—the animal that maintains it. While certainly useful, the concept 

of a reservoir also has limitations. Scientists often see stark divisions between 

species. We neatly divide up the world of animals into families, genera, and 

species, but we often forget that these divisions are based on our own conven- 

tions. A taxonomist can clearly sort out the difference between a colobus monkey,

a baboon, a chimpanzee, a gorilla, and a human, yet the traits that permit us to 

classify these animals as distinct are, as I’ve mentioned, often irrelevant for a mi- 

crobe. From the perspective of a virus, if cells from distinct species share the 

appropriate receptors, and ecological connections provide the appropriate op- 

portunities to make a jump, the fur of a baboon or the upright status of a human 

does not matter at all. 

Some viruses persist permanently and simultaneously in multiple hosts. 

Dengue virus, a viral infection originally called breakbone fever because of the in- 

tense pain it causes, appears largely in human cities. Yet dengue also lives in wild 

primates in tropical forests, where it is referred to as sylvatic dengue.⁴ Sylvatic 

dengue simultaneously infects multiple species of primates and does not discrim- 

inate. It has a wide host range. 

Among the numerous dry technical scientific papers that I digested as a doc- 

toral student, few are indelibly etched on my brain. One that I remember in detail 

was a report describing experiments to determine the host range of sylvatic 

dengue. 

In the study, which used outdated methods now considered unethical, scien- 

tists put various species of primate into cages and used ropes to lift the cages high 

into the canopy where dengue’s forest mosquitoes feed. There they gathered sam- 

ples of viruses to determine which species had the potential for infection. The 

study largely worked—except in one case where they brought the cage down only 

to find a massive python with a very badly distended abdomen. The large snake 

had entered the cage to consume the trapped and no doubt terrified monkey. Hav- 

ing miscalculated, the satiated snake could not squeeze through the bars to escape 

and found itself in the same trapped predicament as its monkey prey. Most likely 

the snake didn’t get infected with the virus; few viruses infect both reptiles and 

mammals. It did, however, make for a memorable photo in an otherwise dry tech- 

nical journal.

The capacity for sylvatic dengue to thrive in multiple species presumably helps 

the virus persist in regions where the population density of any single primate 

species would not be sufficient to protect the virus from extinction. And the mech- 

anism dengue uses to move from one animal to another—mosquitoes—helps 

make this movement seamless. 

For dengue, the notion of a single reservoir does not, strictly speaking, make 

sense, but when Nipah was discovered in 1999, that was still unclear. Scientists 

then asked themselves: what local animal or animals, wild or domestic, were Ni- 

pah’s reservoir? Knowing what animal or animals a virus lives in prior to infecting 

humans helps us respond to it. Depending on the reservoir, we may have the 

potential to simply change farming practices or modify human behavior to avoid 

the critical contact that leads to viral exchanges, effectively cutting off the virus’s 

ability to enter humans. 

Knowing that a microbe has the capacity to maintain itself in an animal reservoir

also changes the way that we think about public health strategies. Microbes can 

jump in both directions, so while novel human microbes like Nipah originate in 

animals, established microbes also have the potential to cross back into animals. 

Animal reservoirs for established human bugs can potentially derail control efforts. 

In effect, if we eliminate a bug in humans in a particular region, but it lives on in 

animals, the microbe may have the potential to reemerge with deadly conse- 

quences. In order to truly eradicate a human pathogen, we must know if it can also 

live outside of humans. 

When Nipah emerged in 1999, the scientists studying it moved quickly to home 

in on its reservoir. Over the years that followed, an intricate relationship among 

wild animals, domesticated animals, and plants revealed itself, a story that empha- 

sizes the complex ways that domestication can provide new avenues for bugs to 

pass into people. 

The Malaysian piggeries that Nipah entered are not small-scale affairs. They 

house thousands of pigs at very high densities, creating a ripe environment for 

viral spread. The farmers who raise the pigs work hard to maximize their income 

both from the pigs themselves, but also from the surrounding land. One of the 

practices in this area of southern Malaysia is to grow mango trees in and around 

piggeries, providing a second source of income to increase the viability of the 

farming enterprise. 

In addition to producing delicious fruit for the farmers to sell, the mango trees 

attract the flying fox, a large and appropriately named bat with the scientific name 

Pteropus. This bat was the unexpected Nipah reservoir, the virus’s link to the wild. 

Remarkably, it now appears that the Pteropus bats, while consuming their mango 

suppers, urinate and drop partially eaten mango into the pig pens. The omnivorous 

pigs consume the Nipah-infected bat saliva and urine as they eat the mango. The 

virus then spreads quickly in the dense pig populations, which, because the ani- 

mals are sometimes shipped from place to place, infect new piggeries and occa- 

sionally infect their human handlers.⁵

Emerging thousands of years after the advent of domestication, Nipah illus- 

trates the impact that domestication had on our relationship with microbes. The 

larger and more sedentary populations of humans that emerged following the do- 

mestication revolution were susceptible to outbreaks in ways that our predomestic 

ancestors never were. In the small mobile communities that dominated human life 

prior to agriculture, novel microbes that entered these communities from animals 

would often sweep through, killing certain individuals and leaving the rest of the 

small populations immune. At that point the viruses would effectively die out; a 

virus without a susceptible host is unable to survive. 

As villages and towns formed around agricultural centers, they did not do so in 

isolation. Communities were connected, at first with footpaths, then roads. While 

we might think that these towns were separate functional entities, from the per- 

spective of a microbe, they represented a single larger community. As this inter- 

connected community of towns grew, it provided the first opportunity in human 

history for an acute virus to persist permanently in the human species.

Chronic viruses that live permanently within their hosts, like hepatitis B, do not 

necessarily require large populations because they can continue to pass on their 

progeny for many years. These viruses have the potential to persist in very small 

communities, taking a long-term strategy—he who fights and hides away lives to 

fight another day. On the other hand, acute viruses, such as measles, do not re- 

main in a single individual for long and require a constant supply of susceptible 

hosts. As they burn through populations, they kill some and make the rest im- 

mune, often leaving no one to perpetuate the infection. 

Therefore, within the small, mobile hunter-gatherer lifestyle that our ancestors 

led prior to domestication, acute viruses could not survive for long unless they 

were microbes that we shared with other species. In the same way, chimpanzee 

populations, including those that were studied by the pioneering primatologist 

Jane Goodall, have sometimes been hit with polio. The virus that causes polio nor- 

mally requires large populations of contemporary humans to sustain itself. Never- 

theless, in 1966 Dr. Goodall and her colleagues saw that the wild chimpanzees they 

studied had come down with something that looked very much like human polio, 

including symptoms of flaccid paralysis. The outbreak was devastating for the 

chimpanzee community in Tanzania, killing a number of animals. 

The virus that caused chimpanzee polio was in fact the same virus that caused 

polio in humans. It had jumped over from nearby humans who were experiencing 

an outbreak at the same time. Dr. Goodall and her colleagues administered vaccine 

to the chimpanzees, which no doubt limited the harm to the community. Chim- 

panzees, like our early human ancestors prior to domestication, would not have 

had the population sizes to maintain such a virus—current estimates suggest that 

communities of over 250,000 people are necessary to sustain it. In small commu- 

nities, the virus would simply have swept through, harming some and creating 

immunity in the others, before dying out. 

But when our ancestors, with their farms and domestic animals, began to have 

interconnected towns, viruses like polio gained the ability both to infect us and to 

be maintained within our species. As more and more towns appeared and the  

connections between them improved, the number of people in contact with each 

other increased. From the perspective of a microbe, the physical separation of 

these towns didn’t matter if there were enough people moving between the towns. 

Hundreds, and later thousands, of interconnected towns effectively became a sin- 

gle megatown for microbes. Eventually, the number of interconnected people 

would become so large that viruses could maintain themselves permanently. As 

long as new people entered into the populations through birth or migration, and 

did so with enough frequency, there would always be a new person for the microbe 

to try. 

In effect, domestication provided a triple hit to our ancestors when it came to mi- 

crobes. It provided sufficiently close contact with a small set of domesticated ani- 

mals, allowing their microbes to cross over into us. At the same time, domestic 

animals provided a regular and reliable bridge to wild animals, giving their 

microbes increased opportunities to cross into us. Finally, and perhaps most cru- 

cially, it permitted us to have large and sedentary communities that could sustain 

microbes that previously would have been a flash in the pan. Together, this viral 

hat trick put us in a new microbial world—one that would lead, as we’ll see in the 

next chapter, to the first pandemic.