Plagues and Peoples (10 page)

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.
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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.
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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. Samples 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.
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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.
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By way of comparison, the nadir of the rabbit population in Australia occurred in 1953, three years after the initial outbreak of myxomatosis. Given the brevity of rabbit generations—observed as six to ten months from birth to parenthood in Australia—this three-year span was equivalent to 90 to 150 years on a human scale, if we calculate a human generation to be 25 years.
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In other words, comparable generational time may be needed for humans and for rabbits to adjust to an initially lethal new disease.

The entire process of adjustment between host and parasite may be conceived as a series of wavelike disturbances to preexisting biological equilibria. The initial disturbance is likely to be drastic, as happened among Australian rabbits in 1950. In many cases, transfer of parasitism to a new host species is too drastic to persist very long. Assuming, however, that the new infection is able to survive indefinitely, a fluctuating balance then asserts itself, with periods of unusual frequency of infection alternating with periods when the disease wanes and may almost disappear. These fluctuations tend to stabilize themselves into more or less regular cycles—that is, as long as some new major intrusion from “outside” does not alter the emerging equilibrium pattern between host and parasite. A multitude of factors enters into any such cyclic equilibrium. Seasonal changes in temperatures and moisture, for instance, tend to concentrate childhood diseases in modern cities of the temperate zone in spring months.

The number of susceptible persons in a population is also fundamental, as are the ways in which they congregate or remain apart. School and military service, for example, have
been the two most significant ways susceptible youth congregate in modern times. Any parent can attest the role of primary schools in propagating childhood diseases in contemporary western societies: in the nineteenth century, before inoculations became standard, draftees into the French army from the countryside suffered—sometimes seriously—from infectious disease to which their city-bred contemporaries were almost immune, having already been exposed. As a result, robust peasant sons had a far higher death rate in the army than did undernourished weaklings drafted from urban slums.
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The size of dose required to infect a new host, the length of time during which the infection may be transferred from one person to another, modes of such transfer, and customs affecting opportunities for exchanging infections, all play roles in determining how many get sick and when. Not infrequently a disease requires a massive, megalopolitan concentration of human hosts to survive indefinitely. In such a population the chance of encountering enough susceptible new hosts so as to keep a chain of infection going is obviously greater than when potential hosts are scattered thinly across a rural landscape. Yet when enough susceptible persons exist in rural communities, such a disease can sally forth from its urban focus and run like a terrifying brushfire from village to village, household to household. Such outbreaks, however, fade away as rapidly as they arise. As the local supply of susceptible hosts runs out, the infection dies and disappears, except in the urban center whence it had initially emerged. There, enough susceptibles will remain for the infectious organism to keep itself alive until disease-inexperienced individuals again accumulate in the rural landscape and another epidemic flare-up becomes a possibility.

All these complex factors sometimes shake down to relatively simple over-all patterns of incidence. Careful statistical study of the way measles propagates itself in modern urban communities shows a wave pattern cresting in periods of time just under two years. Moreover, it has recently been demonstrated
that to keep this pattern going, measles requires a population with at least 7,000 susceptible individuals perpetually in its ranks. Given modern birth rates, urban patterns of life and the custom of sending children to school, where measles can spread very rapidly through a class of youngsters meeting the virus for the first time, it turns out that the minimal population needed to keep measles going in a modern city is about half a million. By scattering out across a rural landscape, a smaller population suffices to sustain the chain of measles infection. The critical threshold below which the virus cannot survive falls between 300,000 and 400,000 persons. This can be demonstrated by the way the measles infection behaves among island populations ranking above and below this critical mass.
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No other disease current in our own time exhibits so precise a pattern, and none, probably, requires such large human communities for its survival. Comparably exact studies for other common childhood diseases have not been made, largely because artificial immunization procedures have altered patterns of infection in far-reaching ways in all modern countries. Yet notable changes in virulence as well as in the frequency of the most common childhood diseases have occurred as recently as the nineteenth century, when European governments first started to collect statistics on the incidence of separate infectious diseases. In other words, the adjustment between the disease-causing organisms and their human hosts was (and is) still evolving very rapidly, in response to the altering circumstances and conditions of human life.

Searching historic records for evidence of when and where the ancestors of our modern childhood diseases first invaded human populations can be quite frustrating. First of all, ancient medical terminology cannot easily be fitted to modern classifications of disease. Symptoms alter, and undoubtedly have altered, so much as to be unrecognizable. At first onset, a new disease often exhibits symptoms that later disappear when the host population in question has had time to develop resistance.

The fulminating symptoms that syphilis initially exhibited in Europe is a familiar example of this phenomenon from the past. Similar episodes can be observed today whenever a new disease invades a previously isolated community for the first time. Symptoms can, indeed, be such that they completely disguise the nature of the disease from all but expert bacteriological analysis. Thus, for example, when tuberculosis first arrived among a tribe of Canadian Indians, the infection attacked organs of their bodies which remained unaffected among whites. Symptoms—meningitis and the like—were far more dramatic, and the progress of the disease was far more rapid, than anything associated with tuberculosis infections among previously exposed populations. In its initial manifestations, only microscopic analysis allowed doctors to recognize the disease as tuberculous. By the third generation, however, the tuberculosis infection tended to concentrate in the lungs, as mutual accommodation between hosts and parasites began to approximate the familiar urban pattern.
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The process of adaptation between host and parasite is so rapid and changeable that we must assume that patterns of infection prevailing now are only the current manifestations of diseases that have in fact altered their behavior in far-reaching ways during historic times. Yet in view of the figure of half a million needed to keep measles in circulation in modern urban communities, it is noteworthy that a recent estimate of the total population of the seat of the world’s oldest civilization in ancient Sumeria comes out to exactly the same figure.
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It seems safe to assume that the Sumerian cities were in close enough contact with one another to constitute a single disease pool; and if so, massed numbers, approaching half a million, surely constituted a population capable of sustaining infectious chains like those of modern childhood diseases. In subsequent centuries, as other parts of the world also became the seats of urban civilizations, ongoing infectious chains became possible elsewhere. First here, then there, one or another disease organism presumably invaded available human
hosts and made good its lodgment in the niche increasing human density had opened for it.