Plagues and Peoples

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by William H. McNeill


  Simple cause-and-effect analysis is inadequate for such systems. Since many variables are simultaneously at work, interacting constantly and altering their magnitudes at irregular rates, it is usually misleading to concentrate attention on a single “cause” and try to attribute a particular “effect” to it. Study of simultaneity among multiple processes is presumably a better way to approach an understanding. But the conceptual and practical difficulties here are enormous. Recognition of patterns, and observation of their endurance or dissolution is, at most levels of organization, about as much as people are capable of; and at some levels, including the social, there is profound uncertainty and dispute about which patterns are worth attending to, or can, in fact, be reliably detected. Divergent terminologies direct attention to different patternings; and finding a logically convincing test, acceptable all around, that can determine whether one such system of terms is superior to its rivals, is often impossible.

  Yet the slow processes of evolution presumably apply to human societies and their symbolic systems as much as to human bodies, so that when logic cannot decide, survival eventually will. Terms that direct attention to the critically useful facets of a situation clearly do have enormous survival value for human beings. It is this aspect of our capacity to communicate with one another that has allowed Homo sapiens to become such a dominant species. Yet no system of terms is ever likely to exhaust or completely comprehend all aspects of the reality around us. We have to do the best we can with the language and concepts we inherit, and not worry about obtaining a truth that will satisfy everyone, everywhere, and for all time to come.

  Just as language is a social and historical product, so, too, within wide limits is the very concept of disease. Holy men whom Americans today would consign to hospitals for the mentally ill abound in the historic record. Conversely, nearsightedness and a dull sense of smell, which we regard as compatible with good health, would probably have been classed as crippling diseases by our hunting ancestors. But despite such variability, there remains a firm and universal nucleus to the concept of disease. A person who can no longer perform expected tasks because of bodily disorder will always seem diseased to his fellows; and many such bodily disorders arise from encounters with parasitic organisms.

  To be sure, different human beings and entire communities exhibit widely varying levels of susceptibility and/or immunity to infections. Such differences are sometimes hereditary, but more often they are the result of past exposures to invading organisms.3 Adjustment of our defenses against disease occurs constantly, not only within individual human bodies but also among entire populations. Levels of resistance and immunity rise and fall accordingly.4

  Just as human individuals and populations undergo continual alteration in response to infectious disease, so also the various infectious organisms that provoke disease undergo a process of adaptation and adjustment to their environment. Characteristically, conditions within the bodies of their hosts constitute a very important part of that environment, though not the whole of it. After all, a recurrent problem for all parasites, including disease organisms, is how to get from one host to another in a world in which such hosts are almost never contiguous entities.

  Prolonged interaction between human host and infectious organism, carried on across many generations and among suitably numerous populations on each side, creates a pattern of mutual adaptation which allows both to survive. A disease organism that kills its host quickly creates a crisis for itself, since a new host must somehow be found often enough, and soon enough, to keep its own chain of generations going. Conversely, a human body that resists infection so completely that the would-be parasite cannot find any lodgment, obviously creates another kind of crisis of survival for the infectious organism. In fact, many disease partnerships have probably failed to last into our time because of one or the other of these extremes; and if some self-confident health officers are to be believed, a number of famous and formerly important disease organisms are today in danger of extinction, thanks to widespread application of vaccination and other public health measures all round the globe.5

  Optimal conditions for host and parasite occur, often though not necessarily always, when each can continue to live in the other’s presence for an indefinite period of time with no very significant diminution of normal activity on either side. Numerous examples of this sort of biological balance exist. Human beings carry a massive population of bacteria in their lower intestines, for instance, with no noticeable ill effects. Our mouths and skins abound with organisms that normally make no substantial difference to us. Some of these creatures may assist digestion; others are believed to have a role in preventing harmful organisms from multiplying freely within our bodies. But firm data on what might be called the ecology of human infection and infestation are generally lacking.6

  Nevertheless, from an ecological point of view we may say that many of the most lethal disease-causing organisms are poorly adjusted to their role as parasites. In some cases, they are still in early stages of biological adaptation to their human hosts; though one must not assume that prolonged co-existence necessarily tends toward mutual harmlessness.7

  The malarial plasmodium, for instance, is probably among the oldest of human (and pre-human) parasites; yet it continues to inflict severe and debilitating fevers upon its human hosts.8 At least four different forms of the plasmodium infect human beings, and one of these, Plasmodium falciparum, is far more virulent than the others. Conceivably, Plasmodium falciparum entered human bloodstreams more recently, and has not had time to adjust as well to human hosts as the other forms of malarial infection. In this case, however, evolutionary adjustment between host and parasite is complicated by the diversity of hosts to which the infectious organism must accommodate itself to complete its life cycle. Accommodation that would allow the malarial plasmodium to live indefinitely within the red blood corpuscles of a human being would make no provision for successful transmission from host to host.

  The pattern that in fact prevails involves the periodic breakup and destruction of millions of red corpuscles, provoking fever in the human host and allowing the plasmodia to move through the bloodstream as free-moving organisms for a day or two until they re-establish themselves as parasites within new red corpuscles. This provokes fever and debilitating weakness in the human host; but it also permits the plasmodium to perpetuate itself by “hitching a ride” aboard mosquitoes that happen to suck in the free-living form of the plasmodium with a meal of human blood. Once arrived in a mosquito’s stomach, the plasmodia exhibit different behaviors, culminating in sexual replication. The result, after a few days, is a new generation of plasmodia which travel to the mosquito’s salivary glands, ready to penetrate a new human host in the course of the mosquito’s next meal.

  So far as can be detected, the malarial plasmodia do not trouble the mosquitoes that carry them from human host to human host in this remarkable way. The mosquitoes’ lives seem not to be shortened nor their activity diminished by the parasite that feeds on their tissues while completing its life cycle. There is an obvious reason for this. If the plasmodium is to reach a new human host, the mosquito carrying it must be vigorous enough to fly normally. A seriously sick mosquito simply could not play its part in perpetuating the malarial cycle by carrying the parasite to a new human host successfully. But a weak and feverish human being does not interfere with the cycle in the slightest. Hence it is not surprising that this very ancient form of infection should be harmless to mosquitoes and still preserve its malignancy among humans.

  Some other important human infections are like malaria inasmuch as the infectious organism must accommodate itself to more than one host. If the alternate host is somehow more important to the parasite, adaptation toward a stable biological balance will concentrate on adjustment to its nonhuman host. Such infections, when transferred to men, may therefore remain violently destructive to human life indefinitely. This is the case with bubonic plague, for example, since Pasteurella pesti
s, as the parasite in question is called, normally infects rodents and their fleas and only occasionally invades human bodies. In communities of ground-burrowing rodents, the infection can endure indefinitely. Patterns of infection and recovery, often involving more than one species of rodent host sharing the same burrows, are very complex and not fully known. Among some of the burrowing rodents that live in large underground “cities,” however, an encounter with Patsteurella pestis is a childhood disease much as smallpox or measles used to be among human city dwellers above ground. Accommodation, in other words, between rodent host and this parasitic bacillus has achieved reasonably stable patterns. It is only when the disease invades previously unexposed rodent and human populations that extraordinary consequences ensue, such as those which made visitations of bubonic plague especially awful for our ancestors.

  Schistosomiasis (transmitted via snails), sleeping sickness (transmitted via tsetse flies), typhus (transmitted via fleas and lice), and a number of other diseases remain formidable to humans because of the complexities of parasitic adjustment to two or more different hosts. Typhus is a particularly instructive case. The same or closely similar strains of the rickettsial organisms responsible for typhus inhabit certain species of ticks in a stable fashion, i.e., pass from generation to generation with no apparent ill effect upon either the tick or the parasite. Rats and their fleas, however, react to typhus infection by recovering, i.e., they reject the invading organism from their systems after a period of illness. When, however, typhus parasites transfer their activity to human lice and to human bodies, the result is always lethal to the louse and often lethal to the person. Such a pattern suggests successive transfers, from a stable co-existence with ticks to a less stable adjustment to rats and rat fleas, and to a highly unstable and presumably, therefore, recent transfer to humans and to human lice.9

  There are, however, other human diseases that pass directly from host to host with no intermediary carrier and with minimal delay. Tuberculosis, measles, smallpox, chicken pox, whooping cough, mumps, influenza fall into this class. They constitute, indeed, a roster of infectious diseases with which civilized peoples remain thoroughly familiar. For all except tuberculosis and influenza, a single infection induces prolonged, often life-long, immunity. As a result, these diseases have commonly afflicted children, and still do where vaccinations and other artificial methods have not altered the natural patterns of disease propagation.

  Such childhood diseases need not be very serious, in the sense that nursing care can usually assure recovery. Yet these same infections, when invading a human population without any previous exposure to them, are likely to kill a high proportion of those who fall sick. Young adults in the prime of life characteristically die more frequently than other age groups. In other words, when invading virgin populations, these are the infections capable of destroying or crippling entire human communities, in the way that smallpox and a succession of other diseases did to Aztec and Inca civilizations.

  Other diseases—whether chronic slow infections, mental disorders, or the debilities that come with aging—undoubtedly account for a greater sum of human suffering. They constitute a sort of “background noise” against which human life has always been lived. In recent times, such afflictions have increased in importance because we live longer than our ancestors did. But the pattern of disease with which we are familiar differs radically from the disease experience of our ancestors. Among them the sporadic outbreak of pestilence, in any of its dread forms, was a terrifying and ever-present possibility. Although statistical and clinical data allowing precise definition of which infections killed how many people, when and in what places are unattainable before the nineteenth century—and remain spotty even then—we may still observe major changes in patterns of pestilential infection. This, in fact, is the subject of this book.

  Man the Hunter

  B

  efore fully human populations evolved, we must suppose that like other animals our ancestors fitted into an elaborate, self-regulating ecological balance. The most conspicuous aspect of this balance was the food chain, whereby our forebears preyed upon some forms of life and were, in their turn, preyed upon by others. In addition to these inescapable relations among large-bodied organisms, we must also suppose that minute, often imperceptible parasites sought their food within our ancestors’ bodies, and became a significant element in balancing the entire life system of which humanity was a part. Details cannot be reconstructed; indeed the whole question of the descent of man remains obscure, since the various pre-human and proto-human skeletal remains that have been discovered (mainly in Africa) do not tell a complete story. Africa may not have constituted humanity’s only cradleland. Forms of life ancestral to man may have also existed in the tropical and subtropical parts of Asia, evolving along roughly parallel lines with the humanoid populations whose bones and tools have been discovered so abundantly at Olduvai Gorge and in other parts of sub-Saharan Africa.

  Human hairlessness, however, points unequivocally to a warm climate where temperatures seldom or never went below freezing. Accurate depth perception based on overlapping fields of vision, in conjunction with the grasping hand, and our obvious kinship with apes and monkeys who still spend much of their time in trees, point toward an arboreal habitat for human ancestors. Dentition suggests an omnivorous diet, in which nuts and fruits, grubs, and perhaps some kinds of vegetable shoots were more important than animal flesh. But what about disease and parasites?

  The sort of infections that prevail among monkeys and arboreal apes today may resemble the parasitic populations with which these remote ancestors of humankind co-existed. Though important details remain unclear, the array of parasites that infest wild primate populations is known to be formidable. In addition to various mites, fleas, ticks, flies, and worms, wild apes and monkeys apparently play host to an impressive roster of protozoa, fungi, and bacteria, not to mention more than 150 so-called arbo-viruses (i.e., arthropod-borne viruses, conveyed from one warm-blooded host to another by insects or other arthropods).1

  Among the organisms that infect monkeys and apes in the wild are fifteen to twenty species of malaria.2 Humankind normally supports only four kinds of malaria, but apes can be infected with human strains of malaria plasmodia, and people can likewise suffer from some of the kinds of malaria found among monkeys and apes. Such speciation, in addition to the specialization of habitat for different kinds of anopheles mosquitoes between the treetops, middle altitude and ground level of tropical rain forests, certainly suggests a very long evolutionary adjustment among the three parties concerned: primate, mosquito, and plasmodium.3 Moreover, given the present-day distribution of malarial organisms, and what is known about the geography of malaria in older times, sub-Saharan Africa appears to have been a principal and perhaps the exclusive center for the development of this form of parasitism.4

  Among all the diverse natural environments of the earth, tropical rain forests are the most variegated in the sense that more diverse forms of life share this kind of habitat than occupy drier, cooler regions. A corollary to this fact is that no single species of plant or animal dominates the forest—not even humankind, at least until very recently. Many tiny organisms that cannot endure freezing temperatures or low humidity thrive in tropical rain forests. In the warmth and moisture of those environments, single-celled parasites can often survive for long periods of time outside the body of any host. Some potential parasites can exist as free-living organisms indefinitely. This means that scant populations of potential hosts can still experience widespread infection and infestation. Even if contacts between the parasite and a possible host are rare occurrences because there are few hosts to be found in the forest, the parasite can wait. Applied to human populations, this means that even when our ancestors were few and scarce in the balance of nature, it was possible for an individual to pick up a full complement of parasites in the course of a normal lifetime. This remains true today; so much so that the principal obstacle to human domi
nion over the rain forests is still the rich variety of parasites lying in wait for intruders.5

  Does this mean that our pre- and proto-human ancestors were perpetually sick? Not really, for the myriad tropical forms of parasitism are characteristically slow to advance toward critical intensity, just as they are slow to recede. Another way of saying the same thing is that tropical rain forests support a highly evolved natural balance at every level: between parasites and hosts, among rival parasites, and between host and the things he eats. We may safely assume that millions of years ago, before humans began to alter the ecological context of the world’s tropical rain forests, the balance between eater and eaten was stable, or nearly so, for long periods of time.

  Hence the wide variety of foods our remote ancestors consumed was undoubtedly matched by the wide variety of para- sites that shared this food with them, in one way or another, without necessarily producing symptoms we would recognize as illness. Mild parasitic invasions may have, at times, diminished our ancestors’ strength and endurance. Low-grade infections and infestations probably flared up into fatal complications whenever serious injury or some other severe stress (famine, for instance) upset the host’s internal physiological balances. In the absence of some such serious disturbance, however, a tolerable state of health can be supposed, such as exists among wild primates of the forest today.

 

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