Plagues and Peoples

by William H. McNeill

  Obviously human attempts to shorten the food chain within the toughest and most variegated of all natural ecosystems of the earth, the tropical rain forests and adjacent savanna regions of Africa, are still imperfectly successful, and continue to involve exceptionally high costs in the form of exposure to disease. That, more than anything else, is why Africa remained backward in the development of civilization when compared to temperate lands (or tropical zones like those of the Americas), where prevailing ecosystems were less elaborated and correspondingly less inimical to simplification by human action.

  Ecosystems in the regions of the earth where early and historically important agricultural societies first developed were all intrinsically less resistant to human alteration than in tropical Africa. In temperate zones, fewer and less formidable parasites lay in wait to take advantage of any notable increase in human numbers. But because the major breakthrough and principal alterations of natural balances took place five to ten thousand years ago, it is no longer possible to infer or observe, as one still can do in Africa, the disease costs which particular agricultural inventions and territorial expansion may have involved.

  We can, nevertheless, infer one important general alteration in disease exposure that came, sooner or later, to all civilized communities. Eventually agricultural populations became dense enough to sustain bacterial and viral infections indefinitely, even without benefit of an intermediate nonhuman host. This cannot ordinarily happen in small communities, since unlike multicelled parasites, bacterial and viral invasions provoke immunity reactions within the human body. Immunity reactions impose drastic alternatives upon the host-parasite relationship. Whenever they dominate the interaction of host and parasite, either speedy death of the infected person or full recovery and banishment of the invading organism from the host’s body tissues ensues—at least for a period of time of months or years until the immunizing antibodies fade from the bloodstream so as to permit reinfection.

  As usual in biology, things are not quite so simple as such a statement implies. Individual resistance to infection is not simply and solely a matter of the formation of antibodies. In some cases, moreover, even infections that do provoke antibodies may linger on for years or even throughout a lifetime. Individual “carriers,” like the famous “Typhoid Mary,” may harbor a disease organism indefinitely and experience no very noticeable ill effects themselves while communicating the infection to others with drastic, even fatal, results. In still other cases, an infection may become “latent,” that is, withdraw to some region of the host’s body and hide there for lengthy periods of time.

  One of the most remarkable patterns of latency allows the chicken pox virus to disappear for as much as fifty years, by retreating into the tissues of the efferent nerves, only to reappear as an affliction of the elderly known as shingles. In this way, the virus neatly solves the problem of maintaining an unbroken chain of infection within a small human community. Even if every available human host gets the chicken pox and develops immunity so that the disease disappears, still, decades later, when a new generation of susceptible human beings has had time to come into existence, the infection can recur, creeping down the efferent nerve paths to the skin of an elderly member of the community, and there manifesting itself as shingles. Transferred to a new host, however, the virus provokes the familiar childhood symptoms of chicken pox. Both the mildness of the disease for most people and the remarkable latency pattern it exhibits suggest that this is an old viral infection among humankind. In this respect chicken pox is unlike the other common childhood diseases of modern times.21

  Diseases that lack such a technique of survival and yet confront the drastic alternatives created by antibody reactions within the host’s body have to rely on numbers for their survival. Numbers, that is, of potential hosts, among whom, if the total size of the community is sufficient, there will always be someone who has not yet had the disease and therefore remains susceptible to infection. Such parasites, are, in all probability, rank newcomers in the time scale of biological evolution, even if ancient and immemorial on the time scale of human history. Only in communities of several thousand persons, where encounters with others attain sufficient frequency to allow infection to spread unceasingly from one individual to another, can such diseases persist. These communities are what we call civilized: large, complexly organized, densely populated, and without exception directed and dominated by cities. Infectious bacterial and viral diseases that pass directly from human to human with no intermediate host are therefore the diseases of civilization par excellence: the peculiar hallmark and epidemiological burden of cities and of countryside in contact with cities. They are familiar to almost all contemporary humankind as the ordinary diseases of childhood: measles, mumps, whooping cough, smallpox and the rest.22

  Contemporary global diffusion of childhood diseases required several thousand years to establish itself, and a good part of the subject matter of this book will be a consideration of critical thresholds in that diffusion process. Moreover, one must suppose that the initial establishment of these diseases (or of infections ancestral to those we know today) was itself a gradual process, involving numerous false starts and lethal encounters in which either the human hosts or the invading parasite died out locally, and thus broke off the chain of infection before it could become a normal, endemic, more or less stable element in the biological balances of civilized human life.

  Most and probably all of the distinctive infectious diseases of civilization transferred to human populations from animal herds. Contacts were closest with the domesticated species, so it is not surprising to find that many of our common infectious diseases have recognizable affinities with one or another disease afflicting domesticated animals. Measles, for example, is probably related to rinderpest and/or canine distemper; smallpox is certainly connected closely with cowpox and with a cluster of other animal infections; influenza is shared by humans and hogs.23 Indeed, according to a standard handbook, diseases human populations share today with domestic animals number as follows24 :

  Poultry 26

  Rats and mice 32

  Horse 35

  Pig 42

  Sheep and goats 46

  Cattle 50

  Dog 65

  There are many overlaps in this tabulation, since a single infection often afflicts several animal species as well as humans. Moreover, because some infections are rare while others occur commonly, a mere listing of the variety is not very significant. Nevertheless, the number of overlaps does suggest how ramified our disease relations with domesticated animals have become. It also appears obvious that the sharing of infection increases with the degree of intimacy that prevails between man and beast.

  In addition to diseases derived from or shared with domesticated animals, human populations may become diseased by intruding upon one or another disease cycle established among wild animals. Bubonic plague, at home among burrowing rodents, yellow fever at home among monkeys, and rabies at home among bats are examples of the more lethal of such infections.25

  Novel transfers of parasites from one host to another have not ceased to occur, and even in recent times such events have sometimes had abrupt and drastic consequences. Rinderpest invaded Africa in 1891, for instance, where it killed off very large numbers of domesticated cattle as well as antelope and other wild species; but its ravages were so severe and sudden—up to 90 per cent die-off occurred—that the disease did not establish itself as an endemic.26 Instead, it disappeared after a few years, presumably from lack of susceptible surviving populations of ungulates to infect. In 1959 a new human disease, called O’nyong nyong fever, appeared in Uganda, probably as a result of the transfer of a virus from monkeys. The disease spread rapidly and widely, but in this case its effects upon human beings were mild, and recovery (with the development of suitable immunity) came quickly. As a result, O’nyong nyong fever, like rinderpest among African antelopes, failed to establish itself as an endemic human infection. Instead, it disappeared
as mysteriously as it had come, presumably by retreating back into the treetops, where it was properly at home.27 A decade later, in 1969, another fever, far more lethal than the Ugandan outbreak, manifested itself in Nigeria. Termed Lassa fever from the hospital station where it was first noticed by western-trained doctors, the new disease was eventually (by 1973) traced back to rodents, the normal hosts for the parasite in question. Appropriate preventive measures were thereupon taken to check further spread of the disease.28

  As human numbers increased in particular regions of the earth with the domestication of both plants and new species of animals, we must therefore imagine a long series of episodes like these. Infections must have been transferred repeatedly to humankind from animal reservoirs, and particularly from the domesticated species with which human populations began to have extended and intimate contacts. Such infections can, of course, run multilaterally. Human beings, for example, can sometimes infect their domesticated animals. Likewise, infections can be exchanged between domesticated herds and wild populations, both within and across species lines, as chance contacts and the susceptibility of potential hosts dictate.

  In other words, disease-producing parasites were quite as successful as people in taking advantage of new opportunities for occupying novel ecological niches that opened up as a result of human actions that distorted natural patterns of plant and animal distribution. Human success meant larger numbers of fewer kinds of plants and animals: an improved feeding ground, therefore, for parasites able to flourish by invading a single species, even if, as was true for almost all viral and most bacterial infections, the invading organisms could only flourish for a few days or weeks before antibodies blocked their continuance within any one individual host’s body.

  Before proceeding further with disease history, it is worth pointing out the parallels between the microparasitism of infectious disease and the macroparasitism of military operations. Only when civilized communities had built up a certain level of wealth and skill did war and raiding become an economically viable enterprise. But seizing the harvest by force, if it led to speedy death of the agricultural work force from starvation, was an unstable form of macroparasitism. Nevertheless such events happened often enough, and deserve to be compared with parasitic invasions like the African rinderpest of 1891 that also destroyed the hosts in such numbers as to inhibit the establishment of any stable, ongoing infectious pattern.

  Very early in civilized history, successful raiders became conquerors, i.e., learned how to rob agriculturalists in such a way as to take from them some but not all of the harvest. By trial and error a balance could and did arise, whereby cultivators could survive such prédation by producing more grain and other crops than were needed for their own maintenance. Such surpluses may be viewed as the antibodies appropriate to human macroparasitism. A successful government immunizes those who pay rent and taxes against catastrophic raids and foreign invasion in the same way that a low-grade infection can immunize its host against lethally disastrous disease invasion. Disease immunity arises by stimulating the formation of antibodies and raising other physiological defenses to a heightened level of activity; governments improve immunity to foreign macroparasitism by stimulating surplus production of food and raw materials sufficient to support specialists in violence in suitably large numbers and with appropriate weaponry. Both defense reactions constitute burdens on the host populations, but a burden less onerous than periodic exposure to sudden lethal disaster.

  The result of establishing successful governments is to create a vastly more formidable society vis-à-vis other human communities. Specialists in violence can scarcely fail to prevail against men who have to spend most of their time producing or finding food. And as we shall soon see, a suitably diseased society, in which endemic forms of viral and bacterial infection continually provoke antibody formation by invading susceptible individuals unceasingly, is also vastly more formidable from an epidemiological point of view vis-à-vis simpler and healthier human societies. Macroparasitism leading to the development of powerful military and political organization therefore has its counterpart in the biological defenses human populations create when exposed to the microparasitism of bacteria and viruses. In other words, warfare and disease are connected by more than rhetoric and the pestilences that have so often marched with and in the wake of armies.29

  Initially, most transfers of bacterial and viral parasitism were probably unstable, in the same way that the recent careers of rinderpest and O’nyong nyong fever in Africa were unstable. Many times, we may imagine, human populations were sharply cut back by some new, localized epidemic. Over and over again the exhaustion of available and susceptible human hosts must have driven invading disease organisms from new grazing grounds in the tissues of early farming folk. Even so, a ready basis for reinfection remained because in all probability domesticated animals were already chronic bearers of viral and bacterial infections capable of invading and reinvading people.

  The reason for supposing that such animals as cattle, horses, and sheep may have been chronic bearers of infection can be traced to the condition of their natural existence in the wild. They were gregarious, and pastured on the grasslands of Eurasia in vast herds long before human hunters became numerous enough to make much difference in their lives. Constituting large populations of a single species, they provided exactly the condition required to allow bacterial and viral infection to become endemic, since in a sufficiently large population there is always another susceptible and available host to perpetuate the chain of infection. Indeed, the evolution of herds and parasites was presumably lengthy enough for reasonably stable biological balances to arise. Hence, a number of viral and bacterial infections probably became rife among wild herds of cattle, sheep and horses without provoking more than mild symptoms. Such infections were presumably “childhood diseases” of the herds, affecting susceptible young beasts endlessly but almost harmlessly. Transferred to human populations, however, such infectious organisms must have usually become virulent, since initially human bodies lacked any acquired immunities to the new invaders, whereas any substantial population of their accustomed host would enjoy at least partial protection from the start.30

  Eventually, however, and at different times in different places, we must assume that various viral and bacterial parasites successfully transferred to human populations, and established an ongoing relationship with their new hosts. Rapid and semicatastrophic initial adjustments were undoubtedly required in many, perhaps in all, cases. Heavy die-off of hosts and of disease organisms may have occurred repeatedly until the development of acquired immunities in the new host population and adaptations on the part of the parasite permitted the infection to become endemic. There seem to be no good examples of such a process taking place among human populations in modern times, but the fate of rabbits in Australia when exposed to an exceedingly virulent new infection may be used to illustrate the manner in which a virus infection acts when it penetrates a new population and then survives to become endemic.

  The story is indeed dramatic. English settlers introduced rabbits to Australia in 1859. In the absence of natural predators, the new species spread rapidly throughout the continent becoming very numerous and, from the human point of view, a pest that ate grass that sheep might have otherwise consumed. The Australian wool pack was thereby reduced; so were the profits of innumerable ranchers. Human efforts to reduce the number of rabbits in Australia took a new turn in 1950 when the virus of myxomatosis (a distant relative of human smallpox) was successfully transferred to the rabbit population of that continent. The initial impact was explosive: in a single season an area as great as all of western Europe was infected. The death rate among rabbits that got the disease in the first year was 99.8 per cent. In the next year, however, the death rate went down to a mere 90 per cent; seven years later mortality among infected rabbits was only 25 per cent. Obviously, very rigorous and rapid selection had occurred among rabbits and among viral strains as well. Samp
les of the virus derived from wild rabbits became measurably milder in virulence with each successive year. Despite this fact, rabbit population has not recovered its former level in Australia and may not do so for a long time—perhaps never. In 1965, only about one fifth as many rabbits lived in Australia as had been there before myxomatosis struck.31

  Before 1950 myxomatosis was a well-established disease among rabbits in Brazil. The virus provoked only mild symptoms among the wild-rabbit population of that country and exhibited a comparatively stable pattern of endemic incidence. It might be supposed, therefore, that the adaptation involved in transfer from Brazilian to Australian rabbits was less than the adaptation required for a parasite from some different host species to Homo sapiens. But this is not really the case, since despite their common name the rabbits of the Americas are of a different genus from those of Europe and Australia. Hence the shift to a new host that took place in 1950 under the eyes of experts resembled the presumed pattern whereby important human diseases once broke away from an animal host species and began to infect humankind.

  Whether or not a new disease begins as lethally as myxomatosis did, the process of mutual accommodation between host and parasite is fundamentally the same. A stable new disease pattern can arise only when both parties manage to survive their initial encounter and, by suitable biological and cultural adjustments, arrive at a mutually tolerable arrangement.32 In all such processes of adjustment, bacteria and viruses have the advantage of a much shorter time between generations. Genetic mutations that facilitate propagation of a disease organism safely from host to host are consequently able to establish themselves much more rapidly than any comparable alterations of human genetic endowment or bodily traits can occur. Indeed, as we shall see in a later chapter, historical experience of later ages suggests that something like 120 to 150 years are needed for human populations to stabilize their response to drastic new infections.33