Read Plagues and Peoples Online
Authors: William H. McNeill
Tags: #Non-fiction, #20th Century, #European History, #disease, #v.5, #plague, #Medieval History, #Social History, #Medical History, #Cultural History, #Biological History
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
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,
Microorganisms 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.
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.