THE GREAT MICROBE BOTTLENECK

THE GREAT MICROBE BOTTLENECK 

We knew it was somewhere nearby, but the area didn’t seem quite right. Driving 

through miles of seemingly endless savanna in Uganda’s Queen Elizabeth National 

Park, we saw only a dozen or so trees, and not the right kind. These were short, 

solitary, wide-crowned trees, completely engulfed by the never-ending dry grass. 

Small groups of zebra and the unique Ugandan Kob antelope dotted the landscape. 

But this did not seem like a place for a rain forest—certainly not for chimpanzees. 

It was too open, too dry, too much of a, well, savanna. Yet as we came to the peak 

of an embankment, there it was—a massive gaping vein of green in the sea of yel- 

low grass. The Kyambura Gorge. 

The gorge, while not the only one of its kind, is unusual. Cut through the center 

by a river flowing from a rain forest some hundred or so miles away, it provides a 

unique microclimate—a well-hydrated strip in an otherwise dry landscape. Along 

that strip, rain forest trees and the animals that depend upon them slowly migrated 

downstream. This occurred over tens and hundreds of thousands of years, but 

now when you sit in the middle of the usually dry savanna habitat in Queen Eliz- 

abeth Park, you see a thriving rain forest, complete with chimpanzees. Effectively, 

you see the finger of a faraway forest snaking its way into the savanna.

This gorge provides a unique interface. For contemporary researchers, it pro- 

vides a fairly easy way to follow chimpanzees. By simply driving along the 

unobstructed sides of the gorge, we can follow the calls of chimpanzees and then 

dip down into the gorge to locate them. This is a far cry from the much more chal- 

lenging work of chasing them through the forest on foot. For the chimpanzees, the 

gorge provides something much more meaningful. Instead of the few grassland 

edges in a normal chimpanzee habitat, river gorges like Kyambura provide miles 

and miles of savanna border along a relatively typical chimpanzee habitat, allowing 

chimpanzees to explore and utilize the grassland much more than their rain forest 

contemporaries. And use it they do. Some populations enjoy spending a good deal 

of time in the savanna, even hunting savanna animals. 

Sometime after the split between the lineages that would lead to chimpanzees 

and bonobos on the one hand and humans on the other, our ancestors embarked 

upon a trajectory that would include a series of changes moving them away from 

the lifestyle of the common ancestor. Sitting on the edge of Kyambura Gorge, it is 

hard not to consider one of the most dramatic of these changes: the shift from 

being a primarily forest-based animal to an animal with the capacity to live in and

utilize grassland. While the order of the events remains somewhat opaque, at some 

point our ancestors began to make forays into the savanna. This move would ulti- 

mately alter their microbial repertoire and their future. 

As contemporary humans, we normally think of chimpanzees and bonobos, if we 

think of them at all, as a side-note species. They are interesting animals, certainly, 

with much to teach us about our history, yet they hover somewhere near the brink 

of extinction and live in marginal forest habitats, certainly not species that could 

compete with humans. Shocking as it may seem, this was not always the case. If 

we could see the world millions of years ago, say around that time that human lin- 

eages and chimpanzee/bonobo lineages diverged, it would be very different. Six 

million years ago, it was an ape’s world. 

In our modern world with over six billion humans and only an estimated one to 

two hundred thousand chimpanzees and ten thousand bonobos, humans have 

reached every point on Earth, and all of the wild chimpanzees and bonobos remain 

confined to central Africa. We have to stretch our brains to imagine a world in 

which we were the minority. Yet for some periods prior to the advent of agriculture 

around ten thousand years ago, that was exactly the world in which our ancestors 

lived. 

Chimpanzees and bonobos are not fossils. Contemporary species, whether 

chimpanzees, bonobos, or humans, have all changed since this aforementioned 

ancient time. Nevertheless, around six million years ago when our own ancestors 

took their first tentative steps toward becoming human, they would have seemed 

much closer to our chimpanzee and bonobo relatives than to ourselves. Our rela- 

tives at that time were almost certainly covered with thick hair. When on the 

ground, they primarily moved around by walking on all fours but really spent the 

majority of their time in the trees. They hunted—collective and strategic hunting as 

we’ve seen. But they didn’t cook their meat, didn’t use tools that couldn’t be simply 

modified from tree branches, and kept largely to the forest.

As our own lineage changed and began to display some of the features that we 

equate with humans, the world was a different place. The use of grasslands was 

perhaps not completely foreign, and even today some small groups of chim- 

panzees utilize mosaic environments with forest as well as grasslands, like the 

Kyambura chimpanzees, yet they did not likely make long journeys into these habi- 

tats. At that early time, the individuals that spent time in grasslands were the odd 

ones. 

Often when groups of individuals veer into new areas, they do so to escape in- 

tense competition, and as our own ancestors moved to savanna habitats, they 

probably did so less to break new ground than simply to find somewhere they 

could exist with fewer rivals. Such habitat moves often led to marked inefficiencies, 

and when our early ancestors relocated, they probably experienced profound disad- 

vantages. Being unsuited, at least at first, to function in grasslands, our early 

ancestors suffered a number of consequences that likely included smaller popu- 

lation sizes. Or near extinction. 

Determining historic population sizes, particularly prior to periods in which we 

have written records, is fraught with difficulty. But studies suggest that our ances- 

tors’ population densities were sometimes very low, with lower numbers than 

those of current gorilla and chimpanzee populations, and at least once teetered on 

the brink of extinction. Our ancestors would have been an endangered species. We 

believe this to be the case because our genes maintain some of these records, and 

by comparing the genetic information among contemporary human populations 

with that of our close ape relatives, we can tease out inklings of relevant infor- 

mation. 

The information revealed is striking. Analyses of the human mitochondrial 

genome, a region of genetic information that passes only from mother to daughter, 

as well as studies of mobile genetic elements that accumulate in regions of the 

genome in a clocklike way provide clues to our historic population size and

suggest it was much smaller than we might expect. 

Our preagricultural ancestors likely lived in small groups, which is not neces- 

sarily surprising. Most of our evolutionary history as primates was spent in forest- 

ed environments. And while exact timelines for the main events remain unknown, 

moving from forested environments to savanna habitats, shifting from largely fixed 

territories to a more nomadic lifestyle, and adapting to the various new conditions 

imposed by these changes must have been traumatic. An apt comparison might be 

the idea of contemporary humans living on Mars. The generations of our ancestral 

populations that confronted the savanna frontier probably did so at some cost. But 

our interest in small population sizes here is less about the consequences for hu- 

mans and more about the consequences for microbes. 

Low population densities, such as those exhibited by our ancestors, have a marked 

impact on the transmission of infectious agents. Infections need to spread. If 

population sizes are low, it is much harder for this to happen. The scientific term 

for substantially reduced population sizes is population bottlenecks, and when 

population bottlenecks occur, species should be expected to lose their microbial 

diversity. 

Microbes can be largely divided into two different groups, acute and chronic, 

and each group is impaired in small host populations. In the case of acute agents 

(like measles, poliovirus, and smallpox) infections are brief and lead either to 

death or immunity from future infections: they kill you or make you stronger. Acute 

microbes require relatively large populations; otherwise, they will simply burn 

through the susceptible individuals, leaving only the immune or the dead. In either 

case, they go extinct. If there’s no one left to infect, that’s the end of the line for a 

microbe. 

Chronic agents (like HIV and hepatitis C virus), unlike acute agents, do not lead 

to long-lasting immunity in their hosts. They hang on to their hosts, at times hold- 

ing on for a host’s entire lifetime. These agents have a better capacity than acute

suggest it was much smaller than we might expect. 

Our preagricultural ancestors likely lived in small groups, which is not neces- 

sarily surprising. Most of our evolutionary history as primates was spent in forest- 

ed environments. And while exact timelines for the main events remain unknown, 

moving from forested environments to savanna habitats, shifting from largely fixed 

territories to a more nomadic lifestyle, and adapting to the various new conditions 

imposed by these changes must have been traumatic. An apt comparison might be 

the idea of contemporary humans living on Mars. The generations of our ancestral 

populations that confronted the savanna frontier probably did so at some cost. But 

our interest in small population sizes here is less about the consequences for hu- 

mans and more about the consequences for microbes. 

Low population densities, such as those exhibited by our ancestors, have a marked 

impact on the transmission of infectious agents. Infections need to spread. If 

population sizes are low, it is much harder for this to happen. The scientific term 

for substantially reduced population sizes is population bottlenecks, and when 

population bottlenecks occur, species should be expected to lose their microbial 

diversity. 

Microbes can be largely divided into two different groups, acute and chronic, 

and each group is impaired in small host populations. In the case of acute agents 

(like measles, poliovirus, and smallpox) infections are brief and lead either to 

death or immunity from future infections: they kill you or make you stronger. Acute 

microbes require relatively large populations; otherwise, they will simply burn 

through the susceptible individuals, leaving only the immune or the dead. In either 

case, they go extinct. If there’s no one left to infect, that’s the end of the line for a 

microbe. 

Chronic agents (like HIV and hepatitis C virus), unlike acute agents, do not lead 

to long-lasting immunity in their hosts. They hang on to their hosts, at times hold- 

ing on for a host’s entire lifetime. These agents have a better capacity than acute  population bottleneck: a diverse population (top) is greatly diminished by a near- 

extinction event (middle), resulting in a more homogenous population (bottom). 

(Dusty Deyo) 

Sometime following the split between the chimpanzee/bonobo lineage and our 

own, another important change occurred in our ancestors that would have dra- 

matic consequences for our microbial repertoires: they learned to cook. Not 

Michelin three-star cuisine, of course, but cooking nonetheless: using heat to pre- 

pare food. Exactly when our ancestors harnessed the power of fire remains a mys- 

tery. Presumably, fire first provided warmth and security from predators and com- 

petitors. Yet it appears to have quickly become a profound way of altering food. 

Richard Wrangham, my mentor from Harvard, discusses cooking and its conse- 

quences in depth in his well-researched book Catching Fire: How Cooking Made Us 

Human. Among other things, he analyzes in detail cooking’s origins. 

When our ancestors began to cook extensively, in addition to the advantages 

that cooking offered them by making food more manageable and palatable, they also benefited from its remarkable ability to kill microbes. While some microbes 

can survive at incredible temperatures (such as the hot spring microbial hyperther- 

mophiles that grow and reproduce at temperatures above the boiling point of 

water), the vast majority of microbes that make their living off of animals cannot 

survive the temperatures associated with cooking. As microbes are heated during 

cooking, their normally solid, densely packed proteins are made to unfold and 

open, allowing digestive enzymes quick and easy access to destroy any capacity to 

function. As with the population bottlenecks that our ancestors swung through, the 

cooking that became their standard way of life served to again diminish their up- 

take of new microbes, helping limit their microbial diversity. 

The earliest solid evidence that humans controlled fire comes from archaeo- 

logical finds in northern Israel where burned stone flakes dating back almost eight 

hundred thousand years were found near fire pits. This is almost certainly an un- 

derestimate. African sites dating to over a million years ago contain burned bones 

that could be the remains of cooking, yet the lack of archaeological evidence makes 

these finds more ambiguous. In Wrangham’s analysis, the evidence of cooking 

goes back much further. By examining the remains of our ancient ancestors, pa- 

leontologists have found physiological clues indicating that they consumed cooked 

food. For example Homo erectus, a human ancestor from 1.8 million years ago, had 

exactly the larger bodies and smaller digestive tracks and jaws to imply that they 

consumed higher-energy diets that were easy to chew and easy to digest—in other 

words, foods that had been cooked. 

Whatever the exact date of our ancestors’ culinary dawn, it has certainly ex- 

ploded since then. Cooked foods make up the vast majority of contemporary diets. 

In my work with hunters around the world, I’ve had a chance to sample from a vast 

range of these foods—from roasted porcupine and python in Cameroon to fried 

wood grubs in rural DRC. On one occasion, my “friendly” Kadazan collaborator in 

Borneo even gave me dog stew as a practical joke (I didn’t really see the humor). 

I’ve had a chance to sample food far beyond the beef, lamb, and chicken staples 

that I grew up eating in America. Yet no matter what I’ve eaten, or where I’ve eaten it, one thing can be certain: if the food has been cooked sufficiently, the likelihood 

that it will make me sick is small. 

The dual factors of diminished population sizes and cooking were not the only 

things that served to decrease the microbial repertoires of our early ancestors. The 

transition from rain forest habitat to a savanna habitat meant different vegetation 

and climate but also an entirely different set of animals to interact with and hunt. 

And different animals meant different microbes. 

While we still understand very little about the ecological factors that lead to 

microbial diversity, there are some key factors that certainly play a role. We know, 

for example, that the biodiversity of animals, plants, and fungi supported by trop- 

ical rain forest systems is higher than any other ecosystem on land. When our 

ancestors left the rain forest, they entered into regions with diminished biodi- 

versity. The diversity of microbes would almost certainly have been reduced, as 

would the diversity of the host animals that they infected. So the savanna grassland 

habitats likely housed fewer animals and a lower diversity of microbes capable of 

infecting them, which in turn contributed to lower microbial repertoires for our 

ancestors. 

The kinds of animals living in the savanna also differed in critical ways from 

those in the forests, including a marked contrast in the diversity of apes and other 

primates. Simply put—primates love forests. The king of the jungle is a primate, 

not a lion. While some primates, like baboons and vervet monkeys, live very suc- 

cessfully in savanna habitats, forest regions trump savanna regions in terms of pri- 

mate diversity. When we consider the microbes that could most easily infect our 

ancestors, the diversity of primates in any given habitat plays an important role. 

They are certainly not the only species that contribute to our microbial reper- 

toires—in my own studies, I focus not only on primates but also on bats and ro- 

dents—but they do play an important role. 

Some years ago, I began considering what factors might improve or decrease the 

chances that a microbe would jump from one host to the next successfully enough 

to catch on and spread in the new host. It may seem that bats and snakes, for 

example, would provide similar sources for novel microbes. Yet there is a strong 

argument against this idea. Long evident to those doing work on microbes in lab- 

oratories is the fact that closely related animals have similar susceptibility to cer- 

tain infectious agents. So a mammal, like a bat, would have many more microbes 

that could be successfully shared with a human than a snake. If not for the logis- 

tics and ethics, chimpanzees would make the ideal models for studying just about 

every human infectious disease. As our closest living relatives, they have nearly 

identical susceptibility to the microbes that infect us. Over time, less and less labo- 

ratory research on human microbes is conducted in chimpanzees, but this is large- 

ly because of the valid ethical concerns associated with conducting research on 

them and the difficulty of controlling these large and aggressive animals in cap- 

tivity. 

Closely related animal species will share similar immune systems, physiologies, 

cell types, and behaviors, making them vulnerable to the same groups of infectious 

agents. In fact, the taxonomic barriers that we place on species are constructs of 

our own scientific systems, not nature. Viruses don’t read field guides. If two dif- 

ferent hosts share sufficiently similar bodies and immune systems, the bug will 

move between them irrespective of how a museum curator would separate them. I 

named this concept the academically accurate but unwieldy taxonomic transmission 

rule, and it holds up for chimpanzees and humans as it would for dogs and 

wolves.¹ The idea is that the more closely related any two species are, the higher 

the probability that a microbe can successfully jump between them. 

Most of the major diseases of humans originated at some point in animals, 

something I analyzed in a paper for Nature, written with colleagues in 2007. We 

found that among those for which we can easily trace an animal origin, virtually all

came from warm-blooded vertebrates, primarily from our own group, the mam- 

mals, which includes the primary subjects of my own research, the primates, bats, 

and rodents. In the case of primates, while they constitute only 0.5 percent of all 

vertebrate species, they seeded nearly 20 percent of major infectious diseases in 

humans. When we divided the number of animal species in each of the following 

groups by the number of major human diseases they contributed, we obtained a 

ratio that expresses the importance of each group for seeding human disease. The 

numbers are striking: 0.2 for apes, 0.017 for the other nonhuman primates, 0.003 

for mammals other than primates, and a number approaching 0 for animals other 

than vertebrates. So as our early ancestors left the primate-packed rain forests and 

spent more time with lower overall primate biodiversity in savanna habitats, they 

moved into regions that likely had a lower diversity of relevant microbes. 

Multiple factors likely conspired to decrease the microbial repertoires of our early 

ancestors. As they spent more time in savanna habitats, our early ancestors inter- 

acted with fewer host species, and those hosts were on average more distantly re- 

lated to them. The advent of cooking increased the safety of meat consumption 

and stopped many of the microbes that would have normally crossed over during 

the course of hunting, butchering, and ingesting raw meat. And the population bot- 

tlenecks that our ancestors went through further winnowed down the diversity of 

microbes that already infected them. All in all, the conditions associated with 

becoming human served to decrease the diversity of microbes present in our an- 

cient relatives. Though many microbes undoubtedly remained in our early ances- 

tors, there were likely far fewer than those that were retained in the separate lin- 

eages of our ape relatives. 

During the time that our own ancestors went through their microbial cleansing, 

their ape cousins continued to hunt and accumulate novel microbes. They also 

maintained microbes that would have been lost in our own lineage. From a human 

perspective, the ape lineages served as a repository for the agents we’d lose—a microbial Noah’s ark of sorts, preserving the bugs that would disappear from our 

own bloodlines. These great ape² repositories would collide with expanding human 

populations many centuries later, leading to the emergence of some of our most 

important human diseases. 

Perhaps the single most devastating infectious disease that afflicts humans today 

is malaria.³ Spread by mosquitoes, it is estimated to kill a staggering two million 

people each year. Malaria has had such a profound impact on humanity that our 

own genes maintain its legacy in the form of sickle cell disease. Sickle cell, a ge- 

netic disease, exists because its carriers are protected from malaria. Protection was 

so important that natural selection maintained it despite the debilitating disease 

that appears in approximately 25 percent of the offspring of couples that each carry 

the gene. People who are afflicted with sickle cell have their origins almost exclu- 

sively in one of the world’s most intensely malaria affected areas—west central 

Africa. 

My interest in malaria is both personal and professional. During my time work- 

ing in malaria-infested areas of Southeast Asia and central Africa, I was infected by 

it on three separate occasions. On the last of those occasions, I almost died. The 

first two times I’d had malaria were both in regions where malaria was common. 

I’d exhibited all the typical symptoms—severe neck ache (similar to how you’d feel 

if you slept in a strained position) followed by intense fever and profuse sweating. 

On each of my first two bouts, I simply went to a local doctor and received a quick 

diagnosis and treatment. While the pain and illness were miserable, they both re- 

solved reasonably quickly. 

I was in complete denial at the time I had my third round with this deadly dis- 

ease. I wasn’t in the tropics; I was in Baltimore! I had returned from Cameroon to 

do research at Johns Hopkins University, and I had very different symptoms, led by 

intense abdominal pain. I must have also had fever since I remember complaining 

to friends who were putting me up in their local bed and breakfast that my room was too cold. These new symptoms and the fact that I’d left Africa many weeks ear- 

lier fed my denial that this could possibly be malaria. I finally realized I needed ur- 

gent care while sitting half delirious in a tub of scalding water and watching the 

overflow hit the floor of my friends’ bathroom. Although I recovered after a few 

days in the hospital, the illness brought home for me the huge impact that this dis- 

ease has on the millions of people who are regularly sickened by it. 

My professional interest in malaria had started much earlier. As a doctoral stu- 

dent studying the malaria of orangutans in Borneo, I’d had the good fortune to 

spend a year working with some of the world’s foremost experts on malaria evolu- 

tion at the CDC in Atlanta. There I had the luxury of spending afternoons with Bill 

Collins, perhaps the world’s greatest expert on the malaria parasites of primates, 

discussing how malaria might have originated. Among the prominent themes of 

our chats was the importance of wild apes. 

At the time, we knew that wild apes had a number of seemingly distinct malaria 

parasites. One of them was particularly intriguing. Plasmodium reichenowi was 

named after a famous German parasitologist, Eduard Reichenow, who had first 

documented the parasites in chimpanzees and gorillas in central Africa. Reichenow 

and his contemporaries saw a number of these particular parasites, collector’s 

items for the German researcher, and correctly identified them through exami- 

nation by microscope as closely related to our own Plasmodium falciparum. In the 

1990s, during my time at the CDC, molecular techniques were paving the way to 

detailed examination of these parasites, allowing us to compare them accurately to 

our own parasites and providing much greater evolutionary resolution than a 

microscope could ever offer. Sadly, all of the parasites of Reichenow’s time had 

been lost, and all that remained was a single lone specimen. 

Initial work with this lone P. reichenowi parasite showed that in fact it was the 

closest of the many primate malarias to our own deadly human malaria, P. 

falciparum. Yet with only a single specimen, it remained impossible to say much 

about the origins of these parasites. Perhaps, long ago, the common ancestor had 

a parasite that over millions of years had gradually evolved into distinct lineages of P. reichenowi and P. falciparum, a hypothesis favored by some at the time. Or per- 

haps the ape parasite simply resulted from the transmission of the common 

human parasite to wild apes at some point in fairly recent evolutionary history. A 

third possibility, neglected by most considering the huge number of humans and 

the incredible proliferation of P. falciparum among them compared to the existence 

of only a few dozen known parasites in apes, was that perhaps P. falciparum was in 

fact an ape parasite that had moved over to human populations. 

Bill and I understood that to truly address the evolutionary history of these para- 

sites we’d need to get more samples from wild apes, ideally many. As a young doc- 

toral student, I was ambitious yet still naïve about the difficulties associated with 

getting these kinds of samples. But I promised Bill I’d do it and set about planning 

ways to sample apes in the wild. 

Unbeknownst to me at the time, I was about to be called away by my soon-to-be 

postdoctoral mentor Don Burke to conduct research in Cameroon. I was unaware 

at the time that I’d spend nearly five years establishing a long-term 

infectious-disease-monitoring site there in Cameroon. Eventually, though, I did fol- 

low through on my promise to Bill and got those ape samples. Ultimately, in col- 

laboration with sanctuaries in Cameroon that helped to provide homes to orphan 

chimpanzees, we discovered that ape malaria parasites were not as uncommon as 

people had suspected. By teaming up with Fabian Leendertz, a veterinary virologist 

who had done similar work in the Ivory Coast, molecular parasitologist Steve Rich, 

and the legendary evolutionary biologist Francisco Ayala, we took an important 

step toward cracking the origin of this disease. 

Together we were able to compare the genes in hundreds of human P. falci- 

parum samples that already existed with around eight new P. reichenowi specimens 

from chimpanzees in locations throughout west Africa. The genetic comparison 

surprised us all. Amazingly, we found that the entire diversity of P. falciparum (the 

human malaria) was dwarfed by the diversity of the handful of P. reichenowi chim- 

panzee parasites we’d managed to uncover. This discovery told us that the most 

compelling explanation for P. falciparum was that it had been an ape parasite and only jumped over to humans through a bite by some confused mosquito, some- 

time after our split with the chimpanzee lineage. Human malaria had, in fact, origi- 

nated in wild apes. In the years that followed our work, a number of researchers 

documented more and more of the parasites in wild apes. 

Subsequent work by my collaborators Beatrice Hahn and Martine Peeters (the 

same scientists who have done work on SIV evolution) has shown that the malaria 

parasites infecting wild apes are even more diverse than our study indicated. They 

have shown that the ape parasites most closely related to human P. falciparum exist 

in wild gorillas, rather than chimpanzees. How these parasites have been main- 

tained among wild apes and whether or not they’ve moved back and forth between 

chimpanzees and gorillas remain questions for future studies. Either way, there is 

no longer any doubt that human P. falciparum moved from wild apes into humans 

and not in the opposite direction. 

That malaria crossed from a wild ape into humans makes great sense when viewed 

from the perspective of the evolution of our lineage. The microbial cleansing that 

resulted from habitat change, cooking, and population bottlenecks among our own 

ancestors had cleared our microbial slate, decreasing the diversity of microbes that 

were present before. Perhaps the many years with leaner microbial repertories had 

also decreased selective pressure on the many innate mechanisms that we have to 

fight against infectious diseases, effectively robbing us of some of our protective 

disease-fighting tactics. 

In more recent times, as our population sizes began to increase, wild ape dis- 

eases, some of which we’d lost millions of years earlier, had the potential to infect 

us again. When these diseases reentered humans, they acted on us like uniquely 

suited novel agents. Malaria was not the sole microbe to make the leap from apes 

to modern humans, and the stories of others, like HIV, tell a strikingly similar tale. 

The loss of microbial diversity in our early ancestors and the resulting decrease in 

their genetic defenses would make us susceptible to the microbial repositories that our ape cousins maintained during our own microbial cleansing. While we con- 

tinued to change as a species, yet another part of the stage would be set for the 

brewing viral storm. 

THE HUNTING APE

THE HUNTING APE

I wiped the sweat out of my eyes and swatted away the prickly branches in my path 

as I tried to listen for the screeches and hollers of the wild chimpanzees my col- 

leagues and I had been trailing through Uganda’s Kibale Forest for the past five 

hours. The sudden silence of the three large male chimpanzees could only mean 

trouble. At times, such silence can foreshadow a sudden murderous rush into a 

neighboring territory to kill competing males. Or perhaps scientists. Chimpanzee 

warfare was not, thankfully, in the air that day. When our group emerged into a 

small clearing, we observed the chimpanzees seeming to quietly confer with one 

another as a crew of red colobus monkeys ate and played in the fig trees above, un- 

aware of any danger. As two of the males inched up two nearby trees, the third— 

the apparent leader—created a diversion by screaming and scrambling up the tree 

toward the monkeys. Commotion ensued as the monkeys scrambled out of the tree 

and landed in the path of the other two hunters, waiting. One of the chimpanzees 

grabbed a young monkey and made his way to the ground to share his catch with 

his teammates. 

As the chimpanzees feasted on the monkey’s raw flesh, a rush of thoughts ran 

through my brain: teamwork, strategy, flexibility. All in this close relative to hu- 

mans. Truly, this was why people studied chimpanzees. While the rigors of scien- 

tific literature would never allow us to state this in technical journal articles, the 

reality seemed clear enough—these chimpanzees had worked collectively and 

strategically to mount a coordinated attack. The leader had diminished his chances 

of landing a kill by making a noisy attack, but the knowledge that his actions would 

increase the chances of success for his partners made this a strategic approach. In 

the end, they’d share the meat no matter who made the kill, exactly the sort of 

behavior that humans display every day. As the chimpanzees tore through the ani- 

mal, it also occurred to me that the contact with the monkey’s blood and guts pro- 

vided the ideal opportunity for our carnivorous kin to contract microbes. 

Studying our closest living primate relatives affords us the opportunity to better 

understand ourselves, genetically, socially, and otherwise. However imperfect the

conclusions we draw about ourselves from studying wild primates, we’re lucky to 

have them since the fossil record only offers its gems sporadically. Humans love 

the idea that we’re the chosen species—unique among the members of the animal 

kingdom—yet such claims should meet a high standard of proof. If our ape 

cousins share our supposedly unique traits, then perhaps they’re not unique traits 

after all. If, for example, we’d like to know if humans evolved the capacity to hunt 

or share food independently, we can look to chimpanzees and bonobos and ask if 

they exhibit the same behaviors. If they do, then Occam’s razor should push us to- 

ward concluding that we all share these traits because of shared descent: evolving 

the ability to hunt collectively twice or thrice within the very same close lineage is a 

less parsimonious explanation than simply concluding that hunting emerged in 

our joint ancestors before we split with them.¹ That a human trait is interesting 

does not mean it is unique to us. Many undoubtedly have ancient origins. 

Some people have an almost instinctually negative response to the discovery 

that a treasured aspect of humanity is in fact not unique—that it’s actually some- 

thing we share with other animals. Of course, the objective of science is not to un- 

cover the things that make us comfortable but rather the things as they are. 

Another perspective on these shared traits is that they can help us feel less alone 

and more connected to the rest of life on our planet. 

The parsimony rule of thumb applies not only to our behaviors. Each organ, 

each cell type, each infectious disease presents a new point of comparison with 

our kin. Are they found in us alone, or are they found in multiple other species 

along our same branch of the evolutionary tree? Through careful studies of hu- 

mans and our closest living relatives we have the potential to at least begin to sort 

through historical mysteries and solidify which elements of humanity are unique 

and which are not. Already, earlier ideas that human traits like using tools or fight- 

ing wars were unique have been overturned by discoveries that chimpanzees en- 

gage in the same behaviors. What other supposedly unique human traits will fall 

next remains to be seen. 

Fortunately, we have close living relatives that we can observe. The apes, our 

own branch of the primate lineage, include humans, chimpanzees, bonobos, as 

well as gorillas, orangutans, and the least studied apes, the gibbons. Studies of ape 

skeletons during the past hundred years provide a rough guide to the historical 

relationships among all of us. Over the last decade, a mass of genetic data from

these animals has further refined the picture, providing a clear pattern of primate 

relationships. The information, commonly represented by the geneticists who 

study these data in phylogenetic trees such as the one below, helps to graphically 

describe how the relationships shake out. 

The research reveals that for humans, two key species, chimpanzees and bono- 

bos, lie closest to us. The other apes (gorillas, orangutans, and gibbons) differ 

substantially more and thus represent distant cousins of our human-chimpanzee- 

bonobo group. This relationship has led to the notion that humans are best seen 

as the third chimpanzee species, described in great detail in Jared Diamond’s book 

of the same title. 

Once referred to as pygmy chimpanzees, scientists now recognize bonobos as 

an entirely separate species, yet one closely related to chimpanzees. Bonobos live 

only south of the Congo River in central Africa, while chimpanzees live only north 

of it. And while they look very similar, bonobos and chimpanzees have evolved to 

exhibit significant differences in their behavior and physiology during the time 

they’ve been separated by the great river. Current estimates suggest that the chim- 

panzees and bonobo lineages diverged roughly one to two million years ago. This 

divergence occurred some time after our own lineage separated from these 

cousins, around five to seven million years ago. 

Phylogenetic tree, representing the evolution of apes. (Dusty Deyo) 

This research helps point us to a very pivotal and informative character in the 

evolution of our own species, a character referred to by anthropologists as the

Phylogenetic tree, representing the evolution of apes. (Dusty Deyo) 

This research helps point us to a very pivotal and informative character in the 

evolution of our own species, a character referred to by anthropologists as the 

most recent common ancestor, which I’ll refer to simply as the common ancestor. 

Around eight million years ago in central Africa lived an ape species whose descen- 

dants would go on to include humans as well as the chimpanzees and bonobos. 

We can use our parsimony rule of thumb and simple common sense to imagine 

the common ancestor in a bit more detail. It had extensive body hair and likely 

spent much of its time in the trees as do chimpanzees and bonobos. It lived in 

central Africa and consumed a diet dominated by fruit, tropical fruit in the fig fam- 

ily probably making up the major staple. Had we been able to study this ape, it 

would certainly have told us important things about what would come for us in the 

future, what changes were brewing. One thing that would end up affecting the fu- 

ture of our relationship with infectious diseases was a new tendency present in this 

animal: the urge and ability to hunt and eat meat. 

An artist’s conception of “Ardi,” a female Ardipithecus ramidus, 4.4 million years 

old, representative of the most recent common ancestor between humans and 

chimpanzees. (Science Magazine / Jay Matternes)

That humans share with chimpanzees the trait of hunting animals has been known 

for some time. It first emerged in the early 1960s when the British primatologist 

Jane Goodall documented wild chimpanzees hunting and eating meat at Gombe 

National Park in Tanzania during her pioneering efforts to study wild chimpanzee 

behavior. Before the Goodall studies and a related set of studies conducted by 

Japanese colleagues in the Mahale region of Tanzania, our understanding of chim- 

panzee behavior in the wild was largely nonexistent. The finding that chimpanzees 

hunted came as a shock to anthropologists, many of whom had come to believe 

that hunting had emerged after our split with chimpanzees and shaped our evolu- 

tion in a way that distinguished us from them. 

Since then, detailed studies in Gombe and Mahale as well as in some of the 

half-dozen more recently studied wild chimpanzee communities have solidified 

our understanding of the important role of meat in the chimpanzee diet. While 

chimpanzees hunt opportunistically, it is by no means sporadic. Chimpanzees can 

hunt forest antelopes and other apes (even humans), but they tend to specialize in 

a few critical species of monkey as prey. Their hunting is not only cooperative and 

strategic; it is also very effective. 

In the 1990s the primatologist Craig Stanford set out to study red colobus mon- 

keys, but because so many of them died at the hands of chimpanzees, he ended up 

switching his study to just that: how and why chimpanzees hunt these red colobus 

monkeys. He found that chimpanzees were so successful in the hunting of red 

colobus that the entire social structure of these monkeys was swayed by the annual 

patterns of chimpanzee hunting. He calculated that some of the most successful 

communities can bring down nearly a ton of monkey meat in a single year. Subse- 

quent work among some groups of chimpanzees living in west Africa has shown 

that they even employ tools for hunting, using a specially modified branch spear to 

kill prey that nest within the holes of tree trunks. 

And hunting is by no means restricted to chimpanzees. Related studies among

bonobos have been hampered by ongoing (human) wars and the lack of infra- 

structure in the Democratic Republic of Congo (DRC), the only country in the 

world with wild bonobo populations. Nevertheless, recent studies have begun to 

detail the lives of these important relations. Evidence from research conducted 

over the last ten years or so shows that bonobos, like their chimpanzee (and 

human) cousins, actively hunt. Some bonobo sites show meat consumption at lev- 

els similar to those that have been documented among chimpanzees. 

In contrast to humans, chimpanzees, and bonobos, studies of our more distant 

ape relatives—the gorillas, orangutans, and gibbons—have shown strikingly lim- 

ited evidence of meat consumption and no evidence to date of hunting. It appears 

that some of these apes may occasionally scavenge, but even that seems to be 

quite limited. Taken together the evidence shows that hunting emerged sometime 

before the split between humans and the lineage that would include chimpanzees 

and bonobos. Our early common ancestor, living around eight million years ago, 

probably hunted whatever it could get its hands on but almost certainly hunted the 

monkeys in the forest habitats in which it lived. 

The advent of hunting in these early ancestors surely had many advantages. The 

increased caloric intake from hunted animals must have played well in a primarily 

fruit- and leaf-eating species. The regular supply of monkeys must have increased 

food stability in a constantly fluctuating food environment. It would have also 

opened the door for future migration to regions with different kinds of food, a topic 

to which we will return in chapter 3. Hunting, while undoubtedly beneficial for the 

first of our ancestors who engaged in it, presents certain undeniable risks for ac- 

quiring new and potentially deadly microbes—risks that would continue to have an 

impact on their descendants for millions of years to come. 

Hunting, with all of its messy, bloody activity provides everything infectious agents 

require to move from one species to another. The minor skirmishes that our early 

ancestors likely had with other species probably resulted in minor cuts, scratches,

and bites—insignificant compared to the intense exposure of one species to an- 

other that is a direct result of hunting and butchering. 

The chimpanzees who were devouring their feast of red colobus monkey in 

Kibale forest that day were an instant, visual example of the blurring of lines be- 

tween species. The manner in which they were ingesting and spreading fresh blood 

and organs was creating the ideal environment for any infectious agents present in 

the monkeys to spread to the chimpanzees. The blood, saliva, and feces were spat- 

tering into the orifices of their bodies (eyes, noses, mouths, as well as any open 

sores or cuts on their bodies)—providing the perfect opportunity for direct entry of 

a virus into their bodies. And since they hunted a range of animals, their exposure 

to new microbes would have been broad. Those conditions emerged in our ances- 

tors around eight million years ago, forever changing the way that we would inter- 

act with the microbes in our world. 

While we still only understand the basics of how microbes move through 

ecosystems, extensive research on toxins gives us an idea of how it works. 

Microbes, like toxins, have the potential to negotiate their way up through different 

levels of a food web, a process referred to as biological magnification. 

Many pregnant woman are aware that there are risks associated with consuming 

certain kinds of fish during pregnancy. This health suggestion follows from knowl- 

edge of how certain chemicals move through food webs. In the complex food webs 

of the oceans, small crustaceans are consumed by larger fish that are in turn con- 

sumed by larger fish and so on. This goes on until we reach the top predator—a 

hunter who is never hunted—the top of the food chain. Crustaceans have some 

levels of toxins, such as mercury, that they’ve accumulated from the environment. 

The fish that prey on crustaceans accumulate many of these toxins, and the fish 

that consume these second-order predators accumulate even more. The higher in 

the food chain we go, the higher the concentrations of such chemicals. So top 

predator fish like tuna have high enough concentrations of toxins to represent a 

potential threat to the fetus. 

In the same way, animals higher in the food chain should generally be expected

 to maintain a wider diversity of microbes than those lower on the food chain. They 

have accumulated microbes like the mercury among fish, in a process we can think 

of as microbial magnification. When our ancestors some eight million years ago 

took up hunting, they changed the way they would interface with other animals in 

their environment. And this would mean not only increased interaction with their 

prey animals. It also meant increased contact with their prey’s microbes. 

In the twenty years since its discovery, HIV-1 has caused death and illness on a 

previously unimaginable scale. The AIDS pandemic has affected people in every 

country in the world. Even today with antiviral drugs that can control HIV, the virus 

that causes AIDS, it continues to spread, infecting over 33.3 million people at last 

count. The spread of HIV in contemporary society has a range of determinants, 

from poverty and access to condoms to cultural practices that dictate whether or 

not a child is circumcised. The pandemic now has economic and religious 

significance—and it invites commentary and discussion from philosophers and 

social activists. Yet it was not always that way. 

The history of HIV begins with a relatively simple ecological interaction—the 

hunting of monkeys by chimpanzees in central Africa. While people normally think 

about the origins of HIV as occurring sometime during the 1980s, the story actu- 

ally begins about eight million years ago when our ape ancestors began to hunt. 

More precisely, the story of HIV begins with two species of monkey, the red- 

capped mangabey and the greater spot-nosed guenon of central Africa. They hardly 

seem the villains at the center of the global AIDS pandemic, yet without them this 

pandemic would have never occurred. The red-capped mangabey is a small mon- 

key with white cheeks and a shocking splash of red fur on its head. It is a social 

species living in groups of around ten individuals and eating a diet primarily of 

fruit. It is listed as vulnerable, meaning its population numbers are threatened. The 

greater spot-nosed guenon is a tiny monkey, one of the most diminutive of the Old 

World monkeys. It lives in small groups consisting of one male and multiple 

females and is able to communicate alarm calls that vary depending on the kind of 

predator it encounters. One of the things these monkeys share is that they are 

naturally infected with SIV, the simian immunodeficiency virus. Each monkey has 

its own particular variant of this virus, something it and its ancestors have prob- 

ably lived with for millions of years. Another thing these monkeys have in common 

is that chimpanzees find them very tasty.

The simian immunodeficiency virus is a retrovirus. That means that unlike most 

forms of life on the planet that use DNA as their code, which translates into RNA 

and then into the protein building blocks that make up the meat of us all, SIV

works in reverse—hence the name “retro” virus. The retrovirus class of viruses be- 

gins with RNA genetic code, which is translated into DNA before it can insert itself 

into the DNA of its host. It then proceeds with its life cycle, creating its viral prog- 

eny. 

Many African monkeys are infected with SIV, and the red-capped mangabey and 

greater spot-nosed guenon are among them. While few studies have been con- 

ducted on the impact of these viruses on wild monkeys, it is suspected that they do 

the monkeys no substantial harm. Yet when the viruses move from one host 

species to the next, they can kill. This would become their destiny. 

The work that deciphered the evolutionary history of the chimpanzee SIV was 

reported in 2003 by my collaborators Beatrice Hahn and Martine Peeters and their 

colleagues. Over the past decade, Hahn and Peeters have worked tirelessly to chart 

the evolution of SIV—and they’ve succeeded. In 2003 they showed that the chim- 

panzee SIV was in fact a mosaic virus consisting of bits of the red-capped 

mangabey SIV and bits of the greater spot-nosed guenon SIV. Since SIV has the 

potential to recombine, or swap, genetic parts, the findings showed that rather than 

coming from an early chimpanzee ancestor, the virus had jumped into chim- 

panzees. 

It is tempting to imagine a single chimpanzee hunter as patient zero—an indi- 

vidual, the first of its species to harbor the novel virus—acquiring these viruses in 

short order from the monkeys it hunted, possibly on the same day. Alternatively, 

the mangabey virus may have crossed sometime earlier and gained the ability to 

spread among chimpanzees sexually, with patient zero acquiring it from another 

chimpanzee and only subsequently acquiring the guenon virus through hunting. Or 

perhaps both the guenon and mangabey viruses circulated for some time in chim- 

panzees after they were acquired through hunting, with the final moment of genetic 

mixing coming in a chimpanzee already infected by the two viruses. No matter 

what the particular order of cross-species jumps, at some moment a chimpanzee 

became infected with both the guenon virus and the mangabey virus. The two 

viruses recombined, swapping genetic material to create an entirely new mosaic

variant—neither mangabey virus nor guenon virus. 

This hybrid virus would go on to succeed in a way that neither the mangabey 

nor guenon virus alone could, spreading throughout the range of chimpanzees and 

infecting individual chimpanzees from as far west as the Ivory Coast to the sites in 

East Africa where Jane Goodall began her work in the 1960s. The virus, now known 

to harm chimpanzees,² would persist in chimpanzee populations for many years 

before it would jump from chimpanzees to humans some time in the late nine- 

teenth or early twentieth century. And it all started because chimpanzees hunt. 

For a large and growing part of humanity, the meat we consume arrives clean and 

prepackaged, and goes straight to our refrigerators. The killing and butchering of 

the animals occurs far away on a farm or in a factory that we have never seen and 

can scarcely imagine. Rarely do we witness blood or body fluids from these ani- 

mals that were living and breathing beings even a few days earlier. This is because 

the hunting and butchering of animals is a messy process. We don’t want to see it 

or even think about it; we just want the steak. 

During the years I’ve spent working with people hunting and butchering wild 

game in places like the DRC and rural Malaysia, I’ve never become completely 

accustomed to exactly what is required to prepare meat for consumption. We take 

for granted what it means to remove hair and skin from a dead animal, the effort 

needed to separate meat from the many bones distributed in an animal to support 

its movement. We forget how many parts of an animal must be negotiated to get to 

the prime cuts: the lungs, the spleen, the cartilage. Watching the process on the 

dirt floor of a hut or on leaves spread out on the ground in a hunting camp, seeing 

the blood-covered hands that separate the various parts of the animal and hearing 

the bits of discarded meat and bone hit the floor still shocks me. It also helps to re- 

mind me of the microbial significance of the event. 

We tend to think of events like sex or childbirth as intimate, and they certainly 

bring together individuals in ways that normal interactions cannot. But from the

perspective of a microbe, hunting and butchering represent the ultimate intimacy, a 

connection between one species and all of the various tissues of another, along 

with the particular microbes that inhabit each one of them. 

The butchering in our own kitchen bears little resemblance to the hunting and 

butchering that our common ancestor would have engaged in eight million years 

ago. While these first hunting events are now lost, they probably held much in 

common with the chimpanzees I saw sharing their red colobus meal in Kibale—the 

dominant male holding down the animal with one hand and using its other hand 

and teeth to pull apart the skin of the gut while seeking a preferred organ. I remem- 

ber seeing the chimpanzee holding the organ in its hand, its fur slicked down with 

blood, and thinking to myself that it would be nearly impossible to imagine a better 

situation for the movement of a new microbe from one species to the next. 

While we still hunt and butcher, the ways that we do so and the methods we use 

to prepare meat differ radically from the methods of the past. The early ancestors 

of humans and chimpanzees lacked the ability to cook, they lacked tools for 

butchering, and they certainly lacked dental hygiene! Whether through a wound 

from a broken monkey bone, an open sore in the mouth, or a cut on the arm, the 

microbes of hunted animals infected these animals in ways that had not occurred 

prior to the advent of hunting. Hunting fundamentally changed how they were ex- 

posed to the microbes in their worlds, many of which had remained relatively iso- 

lated in the animals that shared the forests with them. As much as hunting repre- 

sented a milestone for our eight-million-year-old ancestors, it had equal impor- 

tance for the world of our microbes.

There are many methods for comparing animals within an ecosystem. We can 

chart the diversity of foods they consume, the diversity of habitats they utilize, the 

range of space that they cover within an average year. We can also consider them 

based on the diversity of microbes they possess, what I call their microbial 

repertoire. Each species has a particular microbial repertoire. It includes viruses, 

bacteria, parasites—all of the various microbes that can call that species home. 

And while no single animal within a species will likely have all of the various pieces 

of the microbial repertoire at any one time, it acts as a conceptual tool for mea- 

suring that species’ microbial diversity—the range of microbes that infect it. 

Species vary considerably in terms of their microbial repertoires. And hunting 

and butchering do not provide the only avenue for microbes to jump from one 

species to the next. Species that don’t hunt or butcher still have regular exposure 

to the microbes of other species. Blood-feeding insects provide an important route 

for microbes to move around. Mosquitoes, for example, often feed on a range of 

different animals, in effect acting as physical carriers on which microbes can hitch 

a ride to move from species to species within ecosystems. Similarly, contact with 

waste from other animals, either through direct contact or indirect contact through 

water, also provides critical connections in the networks that permit microbes to 

negotiate the otherwise largely separated worlds of different host species. 

Nevertheless, mosquitoes and water provide narrow paths from one host to the 

next. Mosquitoes, for example, are not syringes. They are fully functional animals 

that have their own immune systems, and even those microbes that can manage to 

evade the mosquitoes’ defenses will be limited to those in the blood. Similarly, 

water generally passes on those microbes that live in the digestive tract. Hunting 

and butchering, in contrast, provide superhighways connecting a hunting species 

directly with the microbes in every tissue of their prey. 

When our ancestors began to hunt and butcher animals, they put themselves at 

the center of the vast web of microbes living in the full range of tissues of their

various prey animals. Whether in the form of a virus in the brain of a bat, a parasite 

in the liver of a rodent, or a bacterium living on the skin of a primate, the microbial 

worlds of these various species suddenly converged on the common ancestor, 

changing for them (and ultimately us) the range of microbes that they would carry. 

The impact that the advent of hunting had on the microbial repertoires of the 

common ancestor and its descendants would continue to play itself out over mil- 

lions of years. As the lineage of the common ancestor diverged, multiple species 

(chimpanzees, bonobos, and humans) would emerge, each with the capacity to 

hunt. These species would go on to accumulate their own sets of novel microbes 

from the animals on which they preyed. At times, these species would collide when 

their habitats overlapped, allowing them to exchange microbes, with serious 

consequences for both species. 

Because humans are focused largely on our own health, we often forget that 

cross-species transmission is not a one-way street. This was brought home for me 

in vivid detail during my time working with chimpanzees in the Kibale Forest in 

Uganda. On one afternoon, people from a local village came into our research 

camp asking for assistance. The distraught villagers explained that a chimpanzee 

had grabbed an infant child and severely bitten his brother, who had tried to pro- 

tect it. The infant had not been seen again and was presumably eaten by the chim- 

panzee. Upon a visit to the village, an eyewitness confirmed the young boy’s story. 

The nasty bite wound on his upper arm was a reminder that would stay with him 

forever. 

The events made me think more carefully about chimpanzee predation, and a 

subsequent analysis with my colleagues revealed that the event was not unique. Re- 

ports from as early as the 1960s had documented similar events. Although it was 

not a common activity, chimpanzees had hunted humans, usually infants, espe- 

cially those who were left close to the edge of the forest while their mothers worked 

on their farms. While disturbing, the idea that chimpanzees occasionally hunt 

people should not surprise us. From the perspective of a chimpanzee, a red 

colobus monkey, a forest antelope, and a human infant would all represent logical 

potential prey. In the same way, humans, while occasionally observing food 

taboos, hunt opportunistically and generally consume the full variety of local ani- 

mals in their environment. Whether a closely related ape or a more distantly related 

antelope, they all present opportunities for vital calories, and both chimpanzees 

and humans exploit every one of them. 

The fact that chimpanzees hunt humans and humans hunt chimpanzees would 

come to have significance for the two species’ microbial repertoires. In the years 

that followed the advent of hunting by the common ancestor, these two closely re- 

lated but ecologically distinct species would each accumulate substantive micro- 

bial diversity through hunting and other routes. And then, critically, from time to 

time they would exchange microbes. We’ll explore the range of implications that 

this exchange has in the coming chapters. 

As the human lineage broke off and diverged, going through a near extinction 

event, but then coming back full force with agriculture, animal domestication, and, 

later, global travel and practices such as blood transfusions, the connections with 

our ape cousins would continue to have importance for our microbial repertoires 

in sometimes surprising ways. As we’ll explore, the role of this close connection 

continues now with chimpanzees and other apes acting as the missing piece of the 

puzzle in some of our most important diseases. Two close primate relatives— 

chimpanzees that live and hunt diverse animal species in central Africa, and hu- 

mans with rapidly expanding territory and globally interconnected relationships— 

would prove to be an important combination. A recipe for pandemics.