1653 Epidemic in Inner Mongolia
1656 Epidemic in Kansu
1665 Epidemic in Shantung
1667 Epidemic in Kansu
1668 Epidemic in Hopei
A.D. 1670 Epidemic in Inner Mongolia
1673 Epidemic in Manchuria
1677 Epidemic in Kiangsu and Shensi
1680 Epidemic in Kiangsu
1681 Epidemic in Yunnan
1683 Epidemic in Hupeh
1692 Epidemic in Shensi
1693 Epidemic in Shantung
1694 Epidemic in Chekiang and on the island of Hainan
1697 Epidemic in Kiangsu, Shansi, Kiangsi
1698 Epidemic in Shantung and Shansi
1702 Epidemic in Kwangtung
1703 Epidemic in Inner Mongolia, Shantung, and the island of Hainan
1704 Epidemic in Hopei, Shantung, Chekiang, and Shensi
1706 Epidemic in Hupeh
1707 Epidemic in Kwangsi, Kwangtung, Hopei, and Hupeh
1708 Epidemic in Hupeh, Inner Mongolia, Kiangsi, Kansu, and Shantung
1709 Epidemic in Chekiang, Kiangsu, Anhui, Shantung, Shensi, Kwangtung, Fukien, Kiangsi
1713 Epidemic in Kwangtung
1714 Epidemic in Kwangtung
1717 Epidemic in Chekiang
1717 Epidemic in Shensi
1721 Epidemic in Chekiang
1722 Epidemic in Hopei
1723 Epidemic in Shantung
1724 Epidemic in Kiangsu, Shansi, Kwangtung, and Hopei
1727 Epidemic in Kwangtung, Hupeh
1728 Epidemic in Kiangsu, Chekiang, Shansi, Shensi, Hopei, Hupeh, Anhui, and at the eastern end of the Great Wall
1733 Epidemic in Kiangsu
1742 Epidemic in Anhui
1746 Epidemic in Hupeh
1747 Epidemic in Hopei
1748 Epidemic in Shantung
1749 Epidemic in Kiangsu, Kiangsi
1756 Epidemic in Fukien, Kiangsu, Anhui
A.D. 1757 Epidemic in Chekiang and Shansi; in Sinkiang, on the western border, everyone afflicted with the disease died without exception.
1760 Epidemic in Shansi, Chekiang, and Kansu
1767 Epidemic in Chekiang
1770 Epidemic in Kansu
1775 Epidemic in Hopei
1783 Epidemic in Chekiang
1785 Epidemic in Kiangsu
1786 Epidemic in Kiangsu, Anhui, Shantung, and Hopei
1790 Epidemic in Kansu and Yunnan
1792 Epidemic in Hopei
1793 Epidemic in Chekiang
1795 Epidemic in Chekiang
1797 Epidemic in Chekiang
1798 Epidemic in Shantung
1800 Epidemic in Chekiang
1806 Epidemic in Hopei and Shensi
1811 Epidemic in Kansu
1814 Epidemic in Hupeh
1815 Epidemic in Kiangsu, Anhui, and Shantung
1816 Epidemic in Hopei
1818 Epidemic in Shantung
1820 Epidemic in Chekiang, Shansi, Kiangsu
1821 Epidemic in Hopei, Shantung, Yunnan
1822 Epidemic in Hopei and Shensi
1823 Epidemic in Kiangsu and Hopei
1824 Epidemic in Hopei
1826 Epidemic in Shantung
1827 Epidemic in Shantung
1831 Epidemic in Chekiang
1832 Epidemic in Hupeh, Shensi, Shantung
1833 Epidemic in Shantung, Hopei, Chekiang
1834 Epidemic in Chekiang and Kiangsu
1835 Epidemic in Shantung
1836 Epidemic in Kansu, Kwantung, and Shantung
1839 Epidemic in Hopeh
1842 Epidemic in Kiangsu, Hupeh
1843 Epidemic in Hupeh, Kiangsi, and Chekiang
1847 Epidemic in Shensi
1848 Epidemic in Shensi
1849 Epidemic in Chekiang
1853 Epidemic in Honan; more than 10,000 died.
A.D. 1855 Epidemic in Kansu
1856 Epidemic in Shensi
1861 Epidemic in Shantung
1862 Epidemic in Hopei, Kiangsu, Chekiang, Hupeh, Shantung
1863 Epidemic in Kansu, Chekiang, and Shensi
1864 Epidemic in Hupeh, Chekiang, and Kiangsi
1866 Epidemic in Kansu
1867 Epidemic in Shantung and Hopei
1869 Epidemic in Hunan, Kansu, and Hupeh
1870 Epidemic in Hupeh and Hopei
1871 Epidemic in Shensi and Hupeh
1872 Epidemic in Chekiang and Hupeh
1895 Epidemic in Hopei
1911 Epidemic in Manchuria
Notes
Introduction
1. Cf. Thomas W. M. Cameron, Parasites and Parasitism (London, 1956), p. 225; Theobald Smith, Parasitism and Disease (Princeton, 1934), p. 70. When white blood corpuscles break down the cell structure of an invading organism, no usable energy or building material for human cells results. The process therefore corresponds only to the first phase of digestion.
2. Cf. the remarks of Wladimir A. Engelhardt, “Hierarchies and Integration in Biological Systems,” The American Academy of Arts and Sciences, Bulletin, 27 (1974), No. 4, 11–23. Engelhardt attributes the capacity of proteins and similarly complex molecules to reconstitute themselves to the action of weak intermolecular forces, as yet little examined; he suggests, further, that increasing organization always consumes free energy.
From such a viewpoint, it appears that humanity’s most recent caper, whereby free energy extracted from fossil fuels was employed to congregate millions of men into industrial cities, is but the most recent and complex example of the processes whereby millions of atoms are regularly assembled into the larger organic molecules. Indeed, as one would expect, human cities, being far newer and much fewer than proteins, are less precisely organized than are the larger organic molecules, not to mention cells and organisms generally. But it is at least arguable that similar rules apply up and down all the hierarchies of organization within which we appear to live and move and have our being.
3. Hereditary differences that set one human group off from another with respect to disease resistance presumably are a long-term, statistical result of ancestral exposure to particular disease organisms. Disproportionate survival of individuals whose genes somehow facilitated recovery or prevented initial infection from occurring will in time create a genetic resistance to the disease in question. Such evolutionary selection can sometimes be very rapid; indeed, the more lethal an infection, the more rapid selection for tolerance and/or resistance to the infection must be. Equally rigorous selection processes work on the side of the parasite too, of course, tending toward a more nearly stable adaptation to the host, as a result of genetic and behavioral modifications. Cf. Arno G. Motulsky, “Polymorphisms and Infectious Diseases in Human Evolution,” Human Biology, 32 (1960), 28–62; J. B. S. Haldane, “Natural Selection in Man,” Acta Gentica et Statistica Medica, 6 (1957), 321–32. Because genes raising resistance to a particular disease may also create various disadvantages for human beings, the optimal state for a population is “balanced polymorphism.” This means that some individuals will have the disease-inhibiting gene and others lack it. The exact mix and proportion of persons carrying disease-inhibiting genes will vary, depending on how severe selection for resistance to the disease in question may be, and what other selection pressures may be exerted upon the population.
4. Modern techniques even allow experts to decipher the record of individual and group encounters with a number of infectious diseases. This is done by analyzing blood samples for the presence of “antibodies” specific to particular agents. The disease history of small, isolated communities can be quite accurately determined by these techniques. Cf. Francis L. Black et al., “Evidence for Persistence of Infectious Agents in Isolated Human Populations,” American Journal of Epidemiology, 100 (1974), 230–50.
5. Cf. T. Aidan Cockburn, The Evolution and Eradication of Infectious Diseases (Baltimore and London, 1963), p. 150 and passim.
6. Cf. Theodor Rosebury, Microo
rganisms Indigenous to Man (New York, 1962).
7. Cf. Theobald Smith, Parasitism and Disease, pp. 44–65; Bichard Fiennes, Man, Nature and Disease (London, 1964), pp. 84–102.
8. L. J. Bruce-Chwatt, “Paleogenesis and Paleoepidemiology of Primate Malaria,” World Health Organization, Bulletin, 32 (1965), 363–87. The term plasmodium, applied to the organism causing malaria at a time when its biological character was imperfectly known, has become standard. The organism is in fact a protozoon, but its forms differ markedly in the different phases of its life cycle.
9. Hans Zinsser, Rats, Lice and History (New York, Bantam edition, 1965; original publication, 1935), pp. 164–71.
Chapter I
1. Richard Fiennes, Zoonoses of Primates: the Epidemiology and Ecology of Simian Diseases in Relation to Man (Ithaca, New York, 1967), pp. 121–22 and passim. Arbo is an abbreviation for arthropod-borne.
2. Authorities differ as to the exact count. Fiennes, op. cit., p. 73, tabulates five malarial species for apes and ten for monkeys; L. J. Bruce-Chwatt, “Paleogenesis and Paleoepidemiology of Primate Malaria,” World Health Organization, Bulletin, 32 (1965), 368–69, mentions twenty kinds of malarial infection among apes and monkeys, and says that as many as twenty-five species of anopheles mosquitoes may serve as vectors for malaria among men and primates.
3. Fiennes, op. cit., p. 42.
4. Bruce-Chwatt, op. cit., pp. 370–82.
5. Cf. F. L. Dunn, “Epidemiological Factors: Health and Disease in Hunter-Gatherers,” in Richard B. Lee and Irven DeVore, eds., Man the Hunter (Chicago, 1968), pp. 226–28; N. A. Croll, Ecology of Parasites (Cambridge, Massachusetts, 1966), p. 98.
6. F. Boulière, “Observations on the Ecology of Some Large African Mammals,” in F. Clark Howell and François Boulière, eds., African Ecology and Human Evolution (New York, 1963). [Viking Fund Publication in Anthropology No. 36], pp. 43–54, calculates that the biomass (i.e. kilograms /hectare) of African ungulates and other prey available to early man is far greater on the African savanna today than in any other kind of natural environment. Moreover, under modern conditions, competition among carnivores for this enormous reservoir of food is not very severe. Lions, for instance, are far less numerous than their potential food supply is capable of sustaining. If modern conditions match those of the distant age when mankind’s ancestors first began to venture onto the grasslands in search of larger game than they had been accustomed to encounter in the safety of tree branches, it seems clear that our predecessors moved into what might be called a partial vacuum, ecologically speaking, and profited accordingly.
7. A standard example is the elongation of the giraffe’s neck, which allowed grazing upon otherwise inaccessible vegetation. Cf. C. D. Darlington, The Evolution of Man and Society (London, 1969), pp. 22–27.
8. Cf. the excellent essay by Frank L. Lambrecht, “Trypanosomiasis in Prehistoric and Later Human Populations: A Tentative Reconstruction,” in Don Brothwell and A. T. Sandison, Diseases in Antiquity (Springfield, Illinois, 1967), pp. 132–51. Lambrecht argues that one form of sleeping sickness resulting from infection by Trypanosoma gambiense has evolved toward accommodation to human hosts, thus producing a milder, more chronic form of disease; but in the savanna, where ungulate hosts are abundant, evolutionary pressure to accommodate to antelopes rather than to anthropos perpetuated a death-dealing form of the disease for humankind. Accommodation to human hosts in such a circumstance would in fact have diminished (or even destroyed) the hospitable herds and therefore damaged the trypanosome’s over-all biological success.
9. Mary Douglas, “Population Control in Primitive Peoples,” British Journal of Sociology, 17 (1966), 263–73; Joseph B. Birdsell, “On Population Structure in Generalized Hunting and Collecting Populations,” Evolution, 12 (1958), 189–205.
10. Cf. lists of species extinctions in Darlington, op. cit., p. 33. These (and later North American extinctions) may or may not have been due to human agency. Cf. the debate as presented in Paul S. Martin and H. E. Wright, eds., Pleistocene Extinctions, the Search for a Cause (New Haven, 1967). Among the species that suffered extinction Darlington does not list the diverse humanoid forms of life that once existed in Africa; but it is clear that less formidable variants within the humanoid family were among the most vulnerable, with the result that by 20,000 B.C., if not earlier, only one species, Homo sapiens, survived.
11. On the peculiar concentration of protozoal and helminthic infestations in sub-Saharan Africa, see table in Darlington, op. cit., p. 662.
12. I have consulted David Pilbeam, The Ascent of Man: An Introduction to Human Evolution (New York, 1972); Frank E. Poirier, Fossil Man: An Evolutionary Journey (St. Louis, Missouri, 1973); and B. J. Williams, Human Origins, an Introduction to Physical Anthropology (New York, 1973) in connection with these remarks.
13. Joseph B. Birdsell, “Some Population Problems Involving Pleistocene Man,” Cold Spring Harbor Symposium on Quantitative Biology, 20 (1957), 47–69, estimates that a mere 2, 200 years sufficed to populate Australia. Cf. also Joseph B. Birdsell, “On Population Structure in Generalized Hunting and Collecting Populations,” Evolution, 12 (1958), 189–205;, “Some Predictions for the Pleistocene Based on Equilibrium Systems Among Recent Hunters-Gatherers,” in Richard B. Lee and Irven DeVore, eds., Man the Hunter, pp. 229–40.
14. For Australian rabbits, cf. the very instructive book, Frank Fenner and F. N. Ratcliffe, Myxomatosis (Cambridge, 1965). For the American scene, cf. Alfred W. Crosby, The Columbian Exchange: Biological and Cultural Consequences of 1492 (Westport, 1972). More generally, Charles S. Elton, The Ecology of Invasions by Animals and Plants (New York, 1958).
15. Paul S. Martin, “The Discovery of America,” Science, 179 (1973), 969–74.
16. N. A. Croll, Ecology of Parasites (Cambridge, Massachusetts, 1966), pp. 98–104 and passim. Croll is concerned mainly with multicellular parasites, but his observations are applicable to all parasitic forms of life, though, as we will see, the distribution of the viral and bacterial organisms that cause the most important forms of infectious disease among civilized populations is governed mainly by the density of potential hosts, and thus diverges widely from climatically regulated patterns. F. L. Dunn, “Epidemiological Factors: Health and Disease in Hunter-Gatherers,” in Richard B. Lee and Irven DeVore, eds., Man the Hunter, pp. 226–28, also has some interesting things to say about biological diversity and human infections in different climates. Cf. also René Dubos, Man Adapting (New Haven, 1965), p. 61.
17. Study of Cro-Magnon and Neanderthal skeletons allows tentative assignment of ages at time of death. According to the data assembled on this basis in Paul A. Janssens, Paleopathology: Diseases and Injuries of Prehistoric Man (London, 1970), pp. 60–63, 88.2 per cent of Cro-Magnon remains were less than forty years of age at the time of death, and 61.7 per cent were less than thirty. Corresponding figures for Neanderthal remains were 95 per cent and 80 per cent. Such calculations are, however, based on statistically unsatisfactory samples, and criteria for the assignment of age at death are often ambiguous.
18. Cf. Saul Jarcho, “Some Observations on Diseases in Prehistoric America,” Bulletin of the History of Medicine, 38 (1964), 1–19; T. D. Stewart, “A Physical Anthropologist’s View of the Peopling of the New World,” Southwestern Journal of Anthropology, 16 (1960), 265–66, and Lucille E. St. Hoyme, “On the Origins of New World Paleopathology,” American Journal of Physical Anthropology, 21 (1969), 295–302. J. V. Neel et al., “Studies of the Xavante Indians of the Brazilian Mato Grosso,” American Journal of Human Genetics, 16 (1964), 110, speaks of the “exuberant health” of the men of the tribe he studied, although he found the women not so vigorous or free from infestation. Travelers’ reports emphasizing the health of primitive peoples on first contact with the outside world abound, though their accuracy is suspect. Cf. Robert Fortuine, “The Health of the Eskimos as Portrayed in the Earliest Written Accounts,” Bulletin of the History of Medicine, 45 (1971), 97–114. On the other hand, in and
near the presumed original tropic home of earliest mankind, diseases of many kinds flourish among remote and isolated communities as well as in larger ones. Cf. Ivan V. Polunin, “Health and Disease in Contemporary Primitive Societies,” in Don Brothwell and A. T. Sandison, Diseases in Antiquity, pp. 69–97. On the presumed good health of Australian aborigines before European con- tact, cf. B. P. Billington, “The Health and Nutritional Status of the Aborigines,” in Charles P. Mountford, ed., Records of the American-Australian Expedition to Arnhem Land (Melbourne, 1960), I, 27–59.
Chapter II
1. The list is long (two hundred genera of herbivores and dependent carnivores), and includes such potentially useful animals as horses and camels in North America. Cf. Paul Schultz Martin and H. E. Wright, Pleistocene Extinctions, pp. 82–95 and passim. Recent calculations of biomass in Africa, where extinctions of large-bodied animals were far less catastrophic than elsewhere, show how very great a food loss the disappearance of large-bodied prey could be. Elephants and hippopotamuses alone, for instance, constitute about 70 per cent of the entire animal biomass of African savanna lands. Even in places where zebra and wildebeest are the two largest herbivores, those two species constitute at least 50 per cent of the total estimated animal biomass. Cf. F. Clark Howell and François Boulière, African Ecology and Human Evolution, pp. 44–8.
For an interesting effort to bring economic analysis to bear on the phenomenon of extinction through overkill, see Vernon L. Smith, “The Primitive Hunter Culture, Pleistocene Extinctions, and the Rise of Agriculture,” Journal of Political Economy, 83 (1975), 727–56. If Pleistocene extinctions were the work of human hunters, that catastrophic ancient overkill closely parallels our modern industrial squandering of fossil fuels. There is a difference: moderns will probably require fewer centuries to destroy the principal energy base of their existence than our prehistoric forebears needed to kill off theirs.
2. Cf. Sherwood Washburn and C. Lancaster, “The Evolution of Hunting,” in Richard C. Lee and Irven DeVore, Man the Hunter, pp. 293–303; Kent V. Flannery, “Origins and Ecological Effects of Early Domestication in Iran and the Near East,” in Peter Ucko and G. W. Dimbleby, eds., The Domestication and Exploitation of Plants and Animals (Chicago, 1969), pp. 77–87.
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