Guns, Germs, and Steel: The Fates of Human Societies

by Jared Diamond

the reason for the failure of Native Americans to domesticate North American apples by the time Europeans arrived lay neither with the people nor with the apples. As far as biological prerequisites for apple domestication were concerned, North American Indian farmers were like Eurasian farmers, and North American wild apples were like Eurasian wild apples. Indeed, some of the supermarket apple varieties now being munched by readers of this chapter have been developed recently by crossing Eurasian apples with wild North American apples. Instead, the reason Native Americans did not domesticate apples lay with the entire suite of wild plant and animal species available to Native Americans. That suite’s modest potential for domestication was responsible for the late start of food production in North America.

This principle can be extended to understanding much else about life besides marriage. We tend to seek easy, single-factor explanations of success. For most important things, though, success actually requires avoiding many separate possible causes of failure. The Anna Karenina principle explains a feature of animal domestication that had heavy consequences for human history—namely, that so many seemingly suitable big wild mammal species, such as zebras and peccaries, have never been domesticated and that the successful domesticates were almost exclusively Eurasian. Having in the preceding two chapters discussed why so many wild plant species seemingly suitable for domestication were never domesticated, we shall now tackle the corresponding question for domestic mammals. Our former question about apples or Indians becomes a question of zebras or Africans.

That is, domestication involves wild animals’ being transformed into something more useful to humans. Truly domesticated animals differ in various ways from their wild ancestors. These differences result from two processes: human selection of those individual animals more useful to humans than other individuals of the same species, and automatic evolutionary responses of animals to the altered forces of natural selection operating in human environments as compared with wild environments. We already saw in Chapter 7 that all of these statements also apply to plant domestication.

DID ALL THOSE peoples of Africa, the Americas, and Australia, despite their enormous diversity, nonetheless share some cultural obstacles to domestication not shared with Eurasian peoples? For example, did Africa’s abundance of big wild mammals, available to kill by hunting, make it superfluous for Africans to go to the trouble of tending domestic stock? The answer to that question is unequivocal: No! The interpretation is refuted by five types of evidence: rapid acceptance of Eurasian domesticates by non-Eurasian peoples, the universal human penchant for keeping pets, the rapid domestication of the Ancient Fourteen, the repeated independent domestications of some of them, and the limited successes of modern efforts at further domestications.

First, when Eurasia’s Major Five domestic mammals reached sub-Saharan Africa, they were adopted by the most diverse African peoples wherever conditions permitted. Those African herders thereby achieved a huge advantage over African hunter-gatherers and quickly displaced them. In particular, Bantu farmers who acquired cows and sheep spread out of their homeland in West Africa and within a short time overran the former hunter-gatherers in most of the rest of sub-Saharan Africa. Even without acquiring crops, Khoisan peoples who acquired cows and sheep around 2,000 years ago displaced Khoisan hunter-gatherers over much of southern Africa. The arrival of the domestic horse in West Africa transformed warfare there and turned the area into a set of kingdoms dependent on cavalry. The only factor that prevented horses from spreading beyond West Africa was trypanosome diseases borne by tsetse flies.

For example, in the New Guinea villages where I work, I often see people with pet kangaroos, possums, and birds ranging from flycatchers to ospreys. Most of these captives are eventually eaten, though some are kept just as pets. New Guineans even regularly capture chicks of wild cassowaries (an ostrich-like large, flightless bird) and raise them to eat as a delicacy—even though captive adult cassowaries are extremely dangerous and now and then disembowel village people. Some Asian peoples tame eagles for use in hunting, although those powerful pets have also been known on occasion to kill their human handlers. Ancient Egyptians and Assyrians, and modern Indians, tamed cheetahs for use in hunting. Paintings made by ancient Egyptians show that they further tamed (not surprisingly) hoofed mammals such as gazelles and hartebeests, birds such as cranes, more surprisingly giraffes (which can be dangerous), and most astonishingly hyenas. African elephants were tamed in Roman times despite the obvious danger, and Asian elephants are still being tamed today. Perhaps the most unlikely pet is the European brown bear (the same species as the American grizzly bear), which the Ainu people of Japan regularly captured as young animals, tamed, and reared to kill and eat in a ritual ceremony. Thus, many wild animal species reached the first stage in the sequence of animal-human relations leading to domestication, but only a few emerged at the other end of that sequence as domestic animals. ...

STILL A FOURTH line of evidence that some mammal species are much more suitable than others is provided by the repeated independent domestications of the same species. Genetic evidence based on the portions of our genetic material known as mitochondrial DNA recently confirmed, as had long been suspected, that humped cattle of India and humpless European cattle were derived from two separate populations of wild ancestral cattle that had diverged hundreds of thousands of years ago. That is, Indian peoples domesticated the local Indian subspecies of wild aurochs, Southwest Asians independently domesticated their own Southwest Asian subspecies of aurochs, and North Africans may have independently domesticated the North African aurochs. Similarly, wolves were independently domesticated to become dogs in the Americas and probably in several different parts of Eurasia, including China and Southwest Asia. Modern pigs are derived from independent sequences of domestication in China, western Eurasia, and possibly other areas as well. These examples reemphasize that the same few suitable wild species attracted the attention of many different human societies.

IN ALL, OF the world’s 148 big wild terrestrial herbivorous mammals—the candidates for domestication—only 14 passed the test. Why did the other 134 species fail? To which conditions was Francis Galton referring, when he spoke of those other species as “destined to perpetual wildness”?

To be domesticated, a candidate wild species must possess many different characteristics. Lack of any single required characteristic dooms efforts at domestication, just as it dooms efforts at building a happy marriage. Playing marriage counselor to the zebra / human couple and other ill-sorted pairs, we can recognize at least six groups of reasons for failed domestication.

Diet. Every time that an animal eats a plant or another animal, the conversion of food biomass into the consumer’s biomass involves an efficiency of much less than 100 percent: typically around 10 percent.

As a result of this fundamental inefficiency, no mammalian carnivore has ever been domesticated for food. (No, it’s not because its meat would be tough or tasteless: we eat carnivorous wild fish all the time, and I can personally attest to the delicious flavor of lion burger.) The nearest thing to an exception is the dog, originally domesticated as a sentinel and hunting companion, but breeds of dogs were developed and raised for food in Aztec Mexico, Polynesia, and ancient China. However, regular dog eating has been a last resort of meat-deprived human societies: the Aztecs had no other domestic mammal, and the Polynesians and ancient Chinese had only pigs and dogs. Human societies blessed with domestic herbivorous mammals have not bothered to eat dogs, except as an uncommon delicacy (as in parts of Southeast Asia today). In addition, dogs are not strict carnivores but omnivores: if you are so naive as to think that your beloved pet dog is really a meat eater, just read the list of ingredients on your bag of dog food. The dogs that the Aztecs and Polynesians reared for food were efficiently fattened on vegetables

Growth Rate. To be worth keeping, domesticates must also grow quickly. That eliminates gorillas and elephants, even though they are vegetarians with admirably nonfinicky food preferences and represent a lot of meat. What would-be gorilla or elephant rancher would wait 15 years for his herd to reach adult size?

Problems of Captive Breeding. We humans don’t like to have sex under the watchful eyes of others; some potentially valuable animal species don’t like to, either. That’s what derailed attempts to domesticate cheetahs,

The princes’ efforts to breed cheetahs in captivity failed, and not until 1960 did even biologists in modern zoos achieve their first successful cheetah birth. In the wild, several cheetah brothers chase a female for several days, and that rough courtship over large distances seems to be required to get the female to ovulate or to become sexually receptive. Cheetahs usually refuse to carry out that elaborate courtship ritual inside a cage.

for reasons that include vicuñas’ long and elaborate courtship ritual before mating, a ritual inhibited in captivity; male vicuñas fierce intolerance of each other; and their requirement for both a year-round feeding territory and a separate year-round sleeping territory.

Nasty Disposition. Naturally, almost any mammal species that is sufficiently large is capable of killing a human. People have been killed by pigs, horses, camels, and cattle. Nevertheless, some large animals have much nastier dispositions and are more incurably dangerous than are others. Tendencies to kill humans have disqualified many otherwise seemingly ideal candidates for domestication.

Tendency to Panic. Big mammalian herbivore species react to danger from predators or humans in different ways. Some species are nervous, fast, and programmed for instant flight when they perceive a threat. Other species are slower, less nervous, seek protection in herds, stand their ground when threatened, and don’t run until necessary. Most species of deer and antelope (with the conspicuous exception of reindeer) are of the former type, while sheep and goats are of the latter. Naturally, the nervous species are difficult to keep in captivity. If put into an enclosure, they are likely to panic, and either die of shock or batter themselves to death against the fence in their attempts to escape.

That social structure is ideal for domestication, because humans in effect take over the dominance hierarchy. Domestic horses of a pack line follow the human leader as they would normally follow the top-ranking female. Herds or packs of sheep, goats, cows, and ancestral dogs (wolves) have a similar hierarchy. As young animals grow up in such a herd, they imprint on the animals that they regularly see nearby. Under wild conditions those are members of their own species, but captive young herd animals also see humans nearby and imprint on humans as well. Such social animals lend themselves to herding. Since they are tolerant of each other, they can be bunched up. Since they instinctively follow a dominant leader and will imprint on humans as that leader, they can readily be driven by a shepherd or sheepdog. Herd animals do well when penned in crowded conditions, because they are accustomed to living in densely packed groups in the wild. In contrast, members of most solitary territorial animal species cannot be herded. They do not tolerate each other, they do not imprint on humans, and they are not instinctively submissive. Who ever saw a line of cats (solitary and territorial in the wild) following a human or allowing themselves to be herded by a human? Every cat lover knows that cats are not submissive to humans in the way dogs instinctively are. Cats and ferrets are the sole territorial mammal species that were domesticated, because our motive for doing so was not to herd ...

There were also great differences in the completeness with which suites of crops and livestock spread, again implying stronger or weaker barriers to their spreading. For instance, while most of Southwest Asia’s founder crops and livestock did spread west to Europe and east to the Indus Valley, neither of the Andes’ domestic mammals (the llama / alpaca and the guinea pig) ever reached Mesoamerica in pre-Columbian times. That astonishing failure cries out for explanation. After all, Mesoamerica did develop dense farming populations and complex societies, so there can be no doubt that Andean domestic animals (if they had been available) would have been valuable for food, transport, and wool. Except for dogs, Mesoamerica was utterly without indigenous mammals to fill those needs. Some South American crops nevertheless did succeed in reaching Mesoamerica, such as manioc, sweet potatoes, and peanuts. What selective barrier let those crops through but screened out llamas and guinea pigs? A subtler expression of this geographically varying ease of spread is the phenomenon termed preemptive domestication. Most of the wild plant species from which our crops were derived vary genetically from area to area, because alternative mutations had become established among the wild ancestral populations of different areas. Similarly, the changes required to transform wild plants into crops can in principle be brought about by alternative new mutations or alternative courses of selection to yi...

We thus have many different phenomena converging on the same conclusion: that food production spread more readily out of Southwest Asia than in the Americas, and possibly also than in sub-Saharan Africa. Those phenomena include food production’s complete failure to reach some ecologically suitable areas; the differences in its rate and selectivity of spread; and the differences in whether the earliest domesticated crops preempted redomestications of the same species or domestications of close relatives. What was it about the Americas and Africa that made the spread of food production more difficult there than in Eurasia?

First, many of the Fertile Crescent’s founder crops don’t even occur in the wild outside Southwest Asia. For instance, none of the eight main founder crops except barley grows wild in Egypt. Egypt’s Nile Valley provides an environment similar to the Fertile Crescent’s Tigris and Euphrates Valleys. Hence the package that worked well in the latter valleys also worked well enough in the Nile Valley to trigger the spectacular rise of indigenous Egyptian civilization. But the foods to fuel that spectacular rise were originally absent in Egypt. The sphinx and pyramids were built by people fed on crops originally native to the Fertile Crescent, not to Egypt.

WHY WAS THE spread of crops from the Fertile Crescent so rapid? The answer depends partly on that east–west axis of Eurasia with which I opened this chapter. Localities distributed east and west of each other at the same latitude share exactly the same day length and its seasonal variations. To a lesser degree, they also tend to share similar diseases, regimes of temperature and rainfall, and habitats or biomes (types of vegetation). For example, Portugal, northern Iran, and Japan, all located at about the same latitude but lying successively 4,000 miles east or west of each other, are more similar to each other in climate than each is to a location lying even a mere 1,000 miles due south.

But the germination, growth, and disease resistance of plants are adapted to precisely those features of climate. Seasonal changes of day length, temperature, and rainfall constitute signals that stimulate seeds to germinate, seedlings to grow, and mature plants to develop flowers, seeds, and fruit. Each plant population becomes genetically programmed, through natural selection, to respond appropriately to signals of the seasonal regime under which it has evolved. Those regimes vary greatly with latitude. For example, day length is constant throughout the year at the equator, but at temperate latitudes it increases as the months advance from the winter solstice to the summer solstice, and it then declines again through the next half of the year. The growing season—that is, the months with temperatures and day lengths suitable for plant growth—is shortest at high latitudes and longest toward the equator.

That’s part of the reason why Fertile Crescent domesticates spread west and east so rapidly: they were already well adapted to the climates of the regions to which they were spreading. For instance, once farming crossed from the plains of Hungary into central Europe around 5400 B.C., it spread so quickly that the sites of the first farmers in the vast area from Poland west to Holland (marked by their characteristic pottery with linear decorations) were nearly contemporaneous. By the time of Christ, cereals of Fertile Crescent origin were growing over the 8,000-mile expanse from the Atlantic coast of Ireland to the Pacific coast of Japan. That west–east expanse of Eurasia is the largest land distance on Earth.

The result was the all-too-familiar course of the last two millennia of South African history. Some of South Africa’s indigenous Khoisan peoples (otherwise known as Hottentots and Bushmen) acquired livestock but remained without agriculture. They became outnumbered and were replaced northeast of the Fish River by black African farmers, whose southward spread halted at that river. Only when European settlers arrived by sea in 1652, bringing with them their Fertile Crescent crop package, could agriculture thrive in South Africa’s Mediterranean zone. The collisions of all those peoples produced the tragedies of modern South Africa: the quick decimation of the Khoisan by European germs and guns; a century of wars between Europeans and blacks; another century of racial oppression; and now, efforts by Europeans and blacks to seek a new mode of coexistence in the former Khoisan lands.

WE HAVE NOW TRACED HOW FOOD PRODUCTION arose in a few centers, and how it spread at unequal rates from there to other areas. Those geographic differences constitute important ultimate answers to Yali’s question about why different peoples ended up with disparate degrees of power and affluence. However, food production itself is not a proximate cause. In a one-on-one fight, a naked farmer would have no advantage over a naked hunter-gatherer. Instead, one part of the explanation for farmer power lies in the much denser populations that food production could support: ten naked farmers certainly would have an advantage over one naked hunter-gatherer in a fight. The other part is that neither farmers nor hunter-gatherers are naked, at least not figuratively. Farmers tend to breathe out nastier germs, to own better weapons and armor, to own more-powerful technology in general, and to live under centralized governments with literate elites better able to wage wars of conquest. Hence the next four chapters will explore how the ultimate cause of food production led to the proximate causes of germs, literacy, technology, and centralized government.

Some of us adults, and even more of our children, pick up infectious diseases from our pets. Usually they remain no more than a nuisance, but a few have evolved into something far more serious. The major killers of humanity throughout our recent history—smallpox, flu, tuberculosis, malaria, plague, measles, and cholera—are infectious diseases that evolved from diseases of animals, even though most of the microbes responsible for our own epidemic illnesses are paradoxically now almost confined to humans. Because diseases have been the biggest killers of people, they have also been decisive shapers of history. Until World War II, more victims of war died of war-borne microbes than of battle wounds. All those military histories glorifying great generals oversimplify the ego-deflating truth: the winners of past wars were not always the armies with the best generals and weapons, but were often merely those bearing the nastiest germs to transmit to their enemies.

Why was the exchange of nasty germs between the Americas and Europe so unequal? Why didn’t Native American diseases instead decimate the Spanish invaders, spread back to Europe, and wipe out 95 percent of Europe’s population? Similar questions arise for the decimation of many other native peoples by Eurasian germs, as well as for the decimation of would-be European conquistadores in the tropics of Africa and Asia.

questions of the animal origins of human disease lie behind the broadest pattern of human history, and behind some of the most important issues in human health today. (Think of AIDS, an explosively spreading human disease that appears to have evolved from a virus resident in wild African monkeys.) This chapter will begin by considering what a “disease” is, and why some microbes have evolved so as to “make us sick,” whereas most other species of living things don’t make us sick. We’ll examine why many of our most familiar infectious diseases run in epidemics, such as our current AIDS epidemic and the Black Death (bubonic plague) epidemics of the Middle Ages. We’ll then consider how the ancestors of microbes now confined to us transferred themselves from their original animal hosts. Finally, we’ll see how insight into the animal origins of our infectious diseases helps explain the momentous, almost one-way exchange of germs between Europeans and Native Americans.

The most effortless way a germ could spread is by just waiting to be transmitted passively to the next victim. That’s the strategy practiced by microbes that wait for one host to be eaten by the next host: for instance, salmonella bacteria, which we contract by eating already infected eggs or meat; the worm responsible for trichinosis, which gets from pigs to us by waiting for us to kill the pig and eat it without proper cooking; and the worm causing anisakiasis, with which sushi-loving Japanese and Americans occasionally infect themselves by consuming raw fish. Those parasites pass to a person from an eaten animal, but the virus causing laughing sickness (kuru) in the New Guinea highlands used to pass to a person from another person who was eaten. It was transmitted by cannibalism, when highland babies made the fatal mistake of licking their fingers after playing with raw brains that their mothers had just cut out of dead kuru victims awaiting cooking.

One common response of ours to infection is to develop a fever. Again, we’re used to considering fever as a “symptom of disease,” as if it developed inevitably without serving any function. But regulation of body temperature is under our genetic control and doesn’t just happen by accident. A few microbes are more sensitive to heat than our own bodies are. By raising our body temperature, we in effect try to bake the germs to death before we get baked ourselves.

That’s the principle of vaccination: to stimulate our antibody production without our having to go through the actual experience of the disease, by inoculating us with a dead or weakened strain of microbe.

some clever microbes don’t just cave in to our immune defenses. Some have learned to trick us by changing those molecular pieces of the microbe (its so-called antigens) that our antibodies recognize. The constant evolution or recycling of new strains of flu, with differing antigens, explains why your having gotten flu two years ago didn’t protect you against the different strain that arrived this year. Malaria and sleeping sickness are even more slippery customers in their ability rapidly to change their antigens. Among the slipperiest of all is AIDS, which evolves new antigens even as it sits within an individual patient, thereby eventually overwhelming his or her immune system.

slowest defensive response is through natural selection, which changes our gene frequencies from generation to generation. For almost any disease, some people prove to be genetically more resistant than are others. In an epidemic those people with genes for resistance to that particular microbe are more likely to survive than are people lacking such genes. As a result, over the course of history, human populations repeatedly exposed to a particular pathogen have come to consist of a higher proportion of individuals with those ...

We and our pathogens are now locked in an escalating evolutionary contest, with the death of one contestant the price of defeat, and with natural selection playing the role of umpire. Now let’s consider the form of the contest: blitzkrieg or guerrilla war?

Cholera epidemics come at longer intervals, the 1991 Peruvian epidemic being the first one to reach the New World during the 20th century.

The infectious diseases that visit us as epidemics, rather than as a steady trickle of cases, share several characteristics. First, they spread quickly and efficiently from an infected person to nearby healthy people, with the result that the whole population gets exposed within a short time. Second, they’re “acute” illnesses: within a short time, you either die or recover completely. Third, the fortunate ones of us who do recover develop antibodies that leave us immune against a recurrence of the disease for a long time, possibly for the rest of our life. Finally, these diseases tend to be restricted to humans; the microbes causing them tend not to live in the soil or in other animals. All four of these traits apply to what Americans think of as the familiar acute epidemic diseases of childhood, including measles, rubella, mumps, pertussis, and smallpox.

A classic illustration of how such diseases occur as epidemics is the history of measles on the isolated Atlantic islands called the Faeroes. A severe epidemic of measles reached the Faeroes in 1781 and then died out, leaving the islands measles free until an infected carpenter arrived on a ship from Denmark in 1846. Within three months, almost the whole Faeroes population (7,782 people) had gotten measles and then either died or recovered, leaving the measles virus to disappear once again until the next epidemic. Studies show that measles is likely to die out in any human population numbering fewer than half a million people. Only in larger populations can the disease shift from one local area to another, thereby persisting until enough babies have been born in the originally infected area that measles can return there. What’s true for measles in the Faeroes is true of our other familiar acute infectious diseases throughout the world. To sustain themselves, they need a human population that is sufficiently numerous, and sufficiently densely packed, that a numerous new crop of susceptible children is available for infection by the time the disease would otherwise be waning. Hence measles and similar diseases are also known as crowd diseases.

CROWD DISEASES could not sustain themselves in small bands of hunter-gatherers and slash-and-burn farmers. As tragic modern experience with Amazonian Indians and Pacific Islanders confirms, almost an entire tribelet may be wiped out by an epidemic brought by an outside visitor—because no one in the tribelet had any antibodies against the microbe. For example, in the winter of 1902 a dysentery epidemic brought by a sailor on the whaling ship Active killed 51 out of the 56 Sadlermiut Eskimos, a very isolated band of people living on Southampton Island in the Canadian Arctic. In addition, measles and some of our other “childhood” diseases are more likely to kill infected adults than children, and all adults in the tribelet are susceptible.

carried by the transatlantic slave trade to infect New World monkeys and people. Still other infections of small human populations are chronic diseases such as leprosy and yaws. Since the disease may take a very long time to kill its victim, the victim remains alive as a reservoir of microbes to infect other members of the tribelet. For instance, the Karimui Basin of the New Guinea highlands, where I worked in the 1960s, was occupied by an isolated population of a few thousand people, suffering from the world’s highest incidence of leprosy—about 40 percent! Finally, small human populations are also susceptible to nonfatal infections against which we don’t develop immunity, with the result that the same person can become reinfected after recovering. That happens with hookworm and many other parasites.

WHY DID THE rise of agriculture launch the evolution of our crowd infectious diseases? One reason just mentioned is that agriculture sustains much higher human population densities than does the hunting-gathering lifestyle—on the average, 10 to 100 times higher. In addition, hunter-gatherers frequently shift camp and leave behind their own piles of feces with accumulated microbes and worm larvae. But farmers are sedentary and live amid their own sewage, thus providing microbes with a short path from one person’s body into another’s drinking water.

the rise of farming was thus a bonanza for our microbes, the rise of cities was a greater one, as still more densely packed human populations festered under even worse sanitation conditions. Not until the beginning of the 20th century did Europe’s urban populations finally become self-sustaining: before then, constant immigration of healthy peasants from the countryside was necessary to make up for the constant deaths of city dwellers from crowd diseases. Another bonanza was the development of world trade routes, which by Roman times effectively joined the populations of Europe, Asia, and North Africa into one giant breeding ground for microbes. That’s when smallpox finally reached Rome, as the Plague of Antoninus, which killed millions of Roman citizens between A.D. 165 and 180.

For example, measles virus is most closely related to the virus causing rinderpest. That nasty epidemic disease affects cattle and many wild cud-chewing mammals, but not humans. Measles in turn doesn’t afflict cattle. The close similarity of the measles virus to the rinderpest virus suggests that the latter transferred from cattle to humans and then evolved into the measles virus by changing its properties to adapt to us. That transfer is not at all surprising, considering that many peasant farmers live and sleep close to cows and their feces, urine, breath, sores, and blood. Our intimacy with cattle has been going on for the 9,000 years since we domesticated them—ample time for the rinderpest virus to discover us nearby.

The first stage is illustrated by dozens of diseases that we now and then pick up directly from our pets and domestic animals. They include cat-scratch fever from our cats, leptospirosis from our dogs, psittacosis from our chickens and parrots, and brucellosis from our cattle. We’re similarly liable to pick up diseases from wild animals, such as the tularemia that hunters can get from skinning wild rabbits. All those microbes are still at an early stage in their evolution into specialized human pathogens. They still don’t get transmitted directly from one person to another, and even their transfer to us from animals remains uncommon.

In the second stage a former animal pathogen evolves to the point where it does get transmitted directly between people and causes epidemics. However, the epidemic dies out for any of several reasons, such as being cured by modern medicine, or being stopped when everybody around has already been infected and either becomes immune or dies. For example, a previously unknown fever termed O’nyong-nyong fever appeared in East Africa in 1959 and proceeded to infect several million Africans. It probably arose from a virus of monkeys and was transmitted to humans by mosquitoes. The fact that patients recovered quickly and became immune to further attack helped the new disease die out quickly.

A fatal disease vanishing for another reason was New Guinea’s laughing sickness, transmitted by cannibalism and caused by a slow-acting virus from which no one has ever recovered. Kuru was on its way to exterminating New Guinea’s Foré tribe of 20,000 people, until the establishment of Australian government control around 1959 ended cannibalism and thereby the transmission of kuru. The annals of medicine are full of accounts of diseases that sound like no disease known today, but that once caused terrifying epidemics and then disappeared as mysteriously as they had come.

A third stage in the evolution of our major diseases is represented by former animal pathogens that did establish themselves in humans, that have not (not yet?) died out, and that may or may not still become major killers of humanity. The future remains very uncertain for Lassa fever, caused by a virus derived probably from rodents. Lassa fever was first observed in 1969 in Nigeria, where it causes a fatal illness so contagious that Nigerian hospitals have been closed down if even a single case appears. Better established is Lyme disease, caused by a spirochete that we get from the bite of ticks carried by mice and deer. Although the first known human cases in the United States appeared only as recently as 1962, Lyme disease is already reaching epidemic proportions in many parts of our country. The future of AIDS, derived from monkey viruses and first documented in humans around 1959, is even more secure (from the virus’s perspective).

final stage of this evolution is represented by the major, long-established epidemic diseases confined to humans. These diseases must have been the evolutionary survivors of far more pathogens that tried to make the jump to us from animals—and mostly failed.

In short, diseases represent evolution in progress, and microbes adapt by natural selection to new hosts and vectors. But compared with cows’ bodies, ours offer different immune defenses, lice, feces, and chemistries. In that new environment, a microbe must evolve new ways to live and to propagate itself.

The best-studied case involves what happened when myxomatosis hit Australian rabbits. The myxo virus, native to a wild species of Brazilian rabbit, had been observed to cause a lethal epidemic in European domestic rabbits, which are a different species. Hence the virus was intentionally introduced to Australia in 1950 in the hopes of ridding the continent of its plague of European rabbits, foolishly introduced in the nineteenth century. In the first year, myxo produced a gratifying (to Australian farmers) 99.8 percent mortality rate in infected rabbits. Unfortunately for the farmers, the death rate then dropped in the second year to 90 percent and eventually to 25 percent, frustrating hopes of eradicating rabbits completely from Australia. The problem was that the myxo virus evolved to serve its own interests, which differed from ours as well as from those of the rabbits. The virus changed so as to kill fewer rabbits and to permit lethally infected ones to live longer before dying. As a result, a less lethal myxo virus spreads baby viruses to more rabbits than did the original, highly virulent myxo.