The Coming Plague

The Coming Plague Page 102

by Laurie Garrett

  23 K. Yamaguchi, “Human T-Lymphotropic Virus Type I in Japan,” Lancet 343 (1994): 213–16.

  24 By 1994 Brooklyn, New York, would be an HTLV-I epicenter, due to its sizable Caribbean immigrant population. See N. S. Larsen, “Study Confirms High Rates of Adult T-Cell Leukemia in N. Y. C.,” Jonrnal of the National Cancer Institute 86 (1994): 85–86.

  25 F. A. Vyth-Dreese, P. Rumke, M. Robert-Guroff, et al., “Antibodies Against Human T-Cell Leukemia/Lymphoma Virus in Relatives of a T-Cell Leukemia Patient Originating from Surinam,” International Journal of Cancer 32 (1983): 337–42.

  26 V. Manzari, A. Gradilone, G. Barillari, et al., “HTLV-I Is Endemic in Southern Italy: Detection of the First Infectious Cluster in a White Population,” International Journal of Cancer 36 (1985): 557–59.

  27 Gallo (1991), op. cit.; “Call It Ishmael,” Hospital Practice, September 15, 1985: 29; and Z. Ben-Ishai, “Human T-Cell Lymphotropic Virus Type-1 Antibodies in Falashas and Other Ethnic Groups in Israel,” Nature 315 (1985): 665.

  28 A. F. Fleming, “HTLV from Africa to Japan,” Lancet I (1984): 279.

  29 W. F. H. Jarrett, E. M. Crawford, W. B. Martin, and F. Davie, “Leukemia in the Cat: A Virus-like Particle Associated with Leukaemia (Lymphosarcoma),” Nature 202 (1964): 567. W. D. Hardy, Jr., L. J. Old, P. W. Hess, et al., “Horizontal Transmission of Feline Leukaemia Virus,” Nature 244 (1973): 266–69; and D. P. Francis, M. Essex, and W. D. Hardy, Jr., “Excretion of Feline Leukemia Virus by Naturally Infected Pet Cats,” Nature 269 (1977): 252–54. M. Essex, G. Klein, S. P. Snyder, and J. B. Harrold, “Correlation Between Humoral Antibody and Regression of Tumours Induced by Feline Sarcoma Virus,” Nature 233 (1971): 195–96. M. Essex, W. D. Hardy, Jr., S. M. Cotter, et al., “Naturally Occurring Persistent Feline Oncornavirus Infections in the Absence of Disease,” Infection and Immunology 11 (1975): 470–75; and M. Essex, A. Sliski, S. M. Cotter, et al., “Immuno-surveillance of Naturally Occurring Feline Leukemia,” Science 190 (1975): 790–92.

  30 The lab’s interest in hepatitis B reflected Don Francis’s stay, which was briefly interrupted in 1976 by his work on Ebola in Sudan. The hepatitis B virus was discovered in 1965, and shown to cause liver cancer in 1978. See W. Szmuness, “Hepatocellular Carcinoma and the Hepatitis B Virus: Evidence for a Causal Association,” Progress in Medical Virology 24 (1978): 40–69. Francis planned to set up hepatitis B surveillance around the United States when he returned to the CDC in an effort to determine just how many Americans suffered from tumors caused by the virus. His scientific thinking about hepatitis B was described in D. P. Francis, M. Essex, and J. E. Mynard, “Feline Leukemia Virus and Hepatitis B Virus: A Comparison of Late Manifestations,” Progress in Medical Virology 27 (1981): 127–32.

  31 M. Essex, “Adult T-Cell Leukemia-Lymphoma: Role of a Human Retrovirus,” Journal of the National Cancer lnstitute 69 (1982): 981–85.

  32 J. Summers, J. M. Smolec, and R. Snyder, “A Virus Similar to Human Hepatitis B Virus Associated with Hepatitis and Hepatoma in Woodchucks,” Proceedings of the National Academy of Sciences 75 (1978): 4533–37.

  33 Forty-fifth World Assembly, “Implementation of the Global Strategy for Health for All by the Year 2000, Second Evaluation; and Eighth Report on the World Health Situation” (Geneva: World Health Organization, 1992), 10.

  34 D. Burkitt, “A Lymphoma Syndrome in Tropical Africa,” International Review of Experimental Pathology 2 (1963): 67.

  35 M. A. Epstein, B. G. Achong, and Y. M. Barr, “Virus Particles in Cultured Lymphoblasts from Burkitt’s Lymphoma,” Lancet II (1964): 702.

  36 G. Orth, F. Breitburd, M. Faure, and O. Croissant, “Papilloma-virus: A Possible Role in Human Cancer,” in H. H. Hiatt, J. D. Watson, and J. A. Winsten, eds., Origins of Human Cancer (New York: Cold Spring Harbor Laboratory, 1977).

  9. Microbe Magnets

  1 Hippocrates, “On Airs, Waters, and Places,” The Genuine Works of Hippocrates, Francis Adams, trans. (London: Leslie P. Adams, Jr., 1849).

  2 An ecological description of cities can be found in John Reader, Man on Earth (Austin: University of Texas Press, 1988), Chapter 12.

  3 J. Cairns, The History of Mortality, unpublished, 1993.

  4 W. R. MacDonell, “On the Expectation of Life in Ancient Rome, and in the Provinces of Hispania and Lusitania, and Africa,” Biometrika 9 (1913): 366–80.

  5 A. T. Sandison, “Parasitic Diseases,” in D. Brothwell and A. T. Sandison, eds., Diseases in Antiquity (Springfield, IL: Charles C Thomas, 1967).

  6 W. H. McNeill, Plagues and People (New York: Doubleday, 1976), Appendix, “Epidemics in China”; and D. Twitchett, “Population and Pestilence in T‘ang China,” in W. Baver, ed., Studia Sino-Mongolia (Wiesbaden: Franz Steiner Verlag, 1979), 35–68.

  7 A. Patrick, “Disease in Antiquity: Ancient Greece and Rome,” in Brothwell and Sandison, eds. (1967), op. cit.

  8 Jonathan Mann and his colleagues observed cases in the American Southwest during the early 1980s, David Scott studied outbreaks in Ghana in 1908 and 1924, and the World Health Organization reported further outbreaks between 1975 and 1985 in Madagascar, Uganda, Tanzania, Bolivia, Brazil, Peru, Burma, and Vietnam. See World Health Organization. “Human Plague in 1986,” Weekly Epidemiological Record 62 (1987): 299–300.

  9 Among the most accessible and fascinating accounts of the 1346 Black Death and the later 1665 plague are D. Defoe, A Journal of the Plague Year (1722), available in many published forms; McNeill, op. cit., 134–54; B. W. Tuchman, A Distant Mirror: The Calamitous l4th Century (New York: Alfred A. Knopf, 1978); and Philip Ziegler, The Black Death (London: Collins, 1969).

  10 The trend of blaming the Jews for the Black Death began in what is today called Switzerland and spread quickly throughout Europe. In most cities, the persecutions were started by lower-class tradesmen and peasants who were whipped into frenzies by overzealous monks and priests. In some cities these activities were officially sanctioned by local authorities. In Basel, for example, the town leadership voted to kill all Jews, destroy their homes, and ban Jews from entering the city for another two centuries. On the other hand, there were those in power who opposed such actions and sought to protect Europe’s Jewish population. Pope Clement VI gave Jews safe haven inside his papal residence in Avignon. Emperor Charles IV of France tried to stop persecutions in his country, but was overridden by nobles who hoped to avoid paying off debts by letting the mobs kill their Jewish creditors. Duke Albert of Austria was labeled a “Jew-master” because he protected hundreds of Jewish families, allowing them sanctuary inside his fortress. For further details, see J. F. C. Hecker, The Epidemics of the Middle Ages, B. G. Babington, trans. (London: Sydenham Society, 1844).

  11 Such a level of microbe-induced mass destruction would not be achieved again until the influenza epidemic of 1918–19. It would be surpassed by AIDS, which over a twenty-year period between 1980 and 2000 is projected to claim an estimated 24 million people, 20 million of whom will have died of the disease by the year 2000. See J. Mann, D. J. M. Tarantola, and T. W. Netter, AIDS in the World (Cambridge, MA: Harvard University Press, 1992), 127–32.

  12 Earlier circumstantial evidence led Joseph Needham to conclude that China had leprosy prior to A.D. 500, but skeletal studies found no clear leprotic remains in Asia until well after the medieval leprosy epidemic of Europe. See V. Moller-Christensen. “Evidence of Leprosy in Earlier Peoples,” in Brothwell and Sandison, eds. (1967), op. cit. Indeed, the greatest leprosy epidemics of Asia followed European colonialism of the region during the eighteenth century.

  13 For these and many other cogent details on the history of tuberculosis, see F. Ryan, The Forgotten Plague: How the Battle Against Tube
rculosis Was Won—and Lost (Boston: Little, Brown, 1993; and R. Dubos, “Tuberculosis,” Scientific American 181 (1949): 31–40.

  14 J. B. Bass, Jr., L. S. Farer, P. C. Hopewell, et al., “Diagnostic Standards and Classification of Tuberculosis: Official Statement of the American Thoracic Society,” American Review of Respiratory Diseases 142 (1990): 725–35.

  15 R. Riley, “Airborne Infection,” American Journal of Medicine 57 (1974): 466–75.

  In one particularly ingenious mid-twentieth-century study researchers placed caged guinea pigs in the sealed rooms of human tuberculosis patients. The scientists calculated that, provided the patient’s room wasn’t aired out, the tiny guinea pig lungs inhaled thirty infectious TB particles a day. The far larger human lung would presumably absorb ten to twenty times as many particles daily under the same circumstances. See R. L. Riley, C. C. Mills, F. O’Grady, et al., “Infectiousness of Air from a Tuberculosis Ward: Ultraviolet Irradiation of Infected Air: Comparative Infectiousness of Different Patients,” American Review of Respiratory Diseases 84 (1962): 511–25.

  16 Riley (1974), op. cit.

  17 W. L. Salo, A. C. Aufderheide, J. Buikstra, and T. A. Holcomb, “Identification of Mycobacterium tuberculosis DNA in a Pre-Columbian Peruvian Mummy,” Proceedings of the National Academy of Sciences 91 (1994): 2091–94.

  18 Consumption was a particular concern. The numbers of cases rose steadily. In Massachusetts, for example, death certificate reports listed consumption (tuberculosis) as the cause of death for 1,634 individuals in 1844; by 1846 that figure was 2,567. And the consumption death reports jumped to 4,593 in 1853. The state’s total population in the 1850 census was 994,665. Between 1849 and 1853, a total of 20,000 people—most of them residents of Boston—died of consumption. That was about 2 percent of the population. Far more people were sick with the disease, which, like AIDS 120 years later, killed so slowly that statistics never actually reflected at a given moment the full toll of the disease on society.

  19 There are several excellent sources for the history of the nineteenth-century cholera pandemics, including D. Barua and W. B. Greenough III, Current Topics in Infectious Disease: Cholera (New York: Plenum, 1992); J. Duffy, “Social Impact of Disease in the Late 19th Century,” in J. W. Leavitt and R. L. Numbers, eds., Sickness and Health in America (2nd ed.; Madison: University of Wisconsin, 1985), Chapter 29; and R. J. Evans, Death in Hamburg: Society and Politics in the Cholera Years 1830–1910 (Oxford, Eng.: Clarendon Press, 1987).

  20 T. McKeown, R. G. Record, and R. D. Turner, “An Interpretation of the Decline of Mortality in England and Wales During the Twentieth Century,” Population Studies 29 (1969): 391–422; and T. McKeown and R. G. Record, “Reasons for the Decline of Mortality in England and Wales During the Nineteenth Century,” Population Studies 16 (1962): 94–122.

  21 Select Committee on Population, “Domestic Consequences of United States Population Change,” report prepared for the U.S. House of Representatives, 1978.

  22 Noteworthy for the future would be a largely ignored fact in 1970: namely, that tuberculosis skin tests showed that the highest rates of infection in the United States that year were among poor African-American residents of seven Deep South states, and 85 percent of New York City residents who tested positive in TB skin tests that year were blacks who had recently moved to the city from the Deep South.

  23 S. O. Freedman, “Tuberculin Testing and Screening: A Critical Evaluation,” Hospital Practice, May 1972: 63–70.

  24 T. McKeown, The Origins of Haman Disease (Oxford, Eng.: Basil Blackwell, 1988).

  25 R. Dubos and J. Dubos, The White Plague: Taberculosis, Man and Society (Boston: Little, Brown, 1952).

  26 B. Bates, Bargaining for Life: A Social History of Tuberculosis, 1876–1938 (Philadelphia: University of Pennsylvania Press, 1992).

  27 B. Bates, “Tuberculosis in Pennsylvania,” in C. E. Rosenberg and J. Golden, eds., Framing Disease: Studies in Cultural History (New Brunswick, NJ: Rutgers University Press, 1992), 229–47.

  28 For example, between 1937 and 1947 the numbers of South African families on waiting lists for housing in Johannesburg’s black- and colored-designated communities rose from 11 to 16,195. During the subsequent decade the apartheid government decreased its commitment to subsidized housing construction for poor and working-class families from a 1949 high of 7,407 houses to 1957’s low of 155. During the same time construction of so-called economic housing, built at government expense for white working- and middle-class families, rose from 348 houses in 1947 to 15,364 in 1957.

  29 R. M. Packard, White Plague, Black Labor: Tuberculosis and the Political Economy of Health and Disease in South Africa (Berkeley: University of California Press, 1989).

  30 E. H. Hudson, “Treponematosis and Anthropology,” Annals of Internal Medicine 58 (1963): 1037.

  31 Ziegler (1991), op. cit.

  32 When the spirochete enters sores on the skin’s surface it remains in the vicinity of its initial site of infection. Over time the organism may invade local bone, cartilage, and skin, but infection is rarely systemic. In contrast, sexual transmission of the syphilis spirochete provides immediate access to the blood system, allowing for disease in every organ in the body. The localized yaws infections often resolved without treatment in a matter of weeks, but once syphilis gained entry to the bloodstream most people were fated to suffer systemic illness and, in many cases, slow death.

  33 “France: Pitchforked,” The Economist, November 28, 1992: 56–57.

  34 “Pollution in Asia,” The Economist, October 6, 1990: 19–21.

  35 United Nations, “The Prospect of World Urbanization,” Population Studies, No. 101, ST/ESA/ SER/101 (New York, 1987).

  36 A. Pryer and N. Crook, Cities of Hunger: Urban Malnutrition in Developing Countries (London: Oxfam, 1988).

  37 I. Tabibzadeh, A. Rossi-Espagnet and R. Maxwell, Spotlight on the Cities: Improving Urban Health in Developing Countries (Geneva: World Health Organization, 1989).

  38 T. Harpham, T. Lusty, and P. Vaughan, In the Shadow of the City: Community Health and the Urban Poor (Oxford, Eng.: Oxford University Press, 1988); and Tabibzadeh, Rossi-Espagnet, and Maxwell, op. cit.

  The cities projected to have attained megacity status by 2000 are:

  London is expected to drop off the list, as its population is forecast to decline to 9.2 million due to lowering birth rates and middle-class suburban outward migration.

  39 Tabibzadeh, Rossi-Espagnet, and Maxwell (1989), op. cit.

  40 “Pollution in Asia,” op. cit.

  41 Aspen Institute, U.S.A., 1989.

  42 United Nations, “The Prospect of World Urbanization,” op. cit.

  43 D. B. Ottaway, “Cairo Is Plagued with Environmental Disasters,” San Francisco Chronicle, January 12, 1983: Fl.

  44 D. J. Stanley, and A. G. Warne, “Nile Delta: Recent Geological Evolution and Human Impact,” Science 260 (1993): 628–34.

  45 A rich litany of such details of human urban existence in developing countries can be found in Harpham, Lusty, and Vaughan (1988), op. cit.

  46 N. Coulibaly, “Place et Approches des Problèmes de la Tuberculose à Abijan,” Médecine d‘Afrique Noire 28 (1981): 447–49.

  47 A. Rossi-Espagnet, “Health and the Urban Poor,” World Health, July 1983; and P. Khanjanasthiti and J. D. Wray, “Early Protein-Calorie Malnutrition in Slum Areas of Bangkok Municipality, 1970–1971,” Journal of the Medical Association of Thailand 57 (1974): 357–66.

  48 A vivid account of those years appears in Agnes Brinkmann’s Unter Afrikanischem Zauber (Hanover: Landbuch Verlag, 1992).

  49 For a description of the disease and its treatment, see T. E. Nash and F. A. Neva, “Recent Advances in
the Diagnosis and Treatment of Cerebral Cysticercosis,” New England Journal of Medicine 311 (1984): 1492–96.

  50 F. O. Richards, P. M. Schantz, E. Ruiz-Tuben, and F. J. Sorvillo, “Cysticercosis in Los Angeles County,” Journal of the American Medical Association 254 (1985): 3444–48.

  51 A. Benyoussef, “Sante, Migration et Urbanization: Une Etude Collective au Sénégal,” Bulletin of the World Health Organization 49 (1973): 517–37.

  52 M. E. Wilson, A World Guide to Infectious Diseases, Distribution, Diagnosis (Oxford, Eng.: Oxford University Press, 1991).

  53 K. E. Mott, P. Desjeux, A. Moncayo, et al., “Parasitic Diseases and Urban Development,” Bulletin of the World Health Organization 68 (1990): 691–98.

  54 R. S. Desowitz, The Malaria Capers: More Tales of Parasites and People, Research and Reality (New York: W. W. Norton, 1991).

 

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