Plagues and Peoples (42 page)

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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

BOOK: Plagues and Peoples
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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,
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.

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.

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