6 D. Grigg, The World Food Problem (Oxford, Eng.: Basil Blackwell, 1985).
7 T. McKeown, The Origins of Human Disease (Oxford, Eng: Basil Blackwell, 1988).
8 F. Moore Lappe and J. Collins, World Hunger: Ten Myths (4th ed.; San Francisco: Institute for Food and Development Policy, 1979).
9 In the spring of 1993 the Russian government confirmed that nearly all Soviet heath statistics released during the communist era, and possibly during the prior czarist regime, were “artificially generated.†No data could be considered reliable if released before December 1992, according to the Yeltsin government.
10 World Bank, Annual Report (Washington, D.C., 1978).
11 World Bank, World Development Report (Washington, D.C., 1978).
12 “Carter en Route to Africa,†Africa, December 1977.
13 J. J. Gilligan, “America’s Stake in the Developing World,†U.S. Department of State Bulletin 77 (1977): 687–91.
14 World Bank, Health Sector Policy Paper (Washington, D.C., 1980).
15 Ibid.
16 Among the key water-related diseases are:
Disease Pathogen (vector)
Amoebic dysentery protozoa
Ascariasis helminth
Bacillary dysentery bacteria
Cholera bacteria
Clonorchiasis helminth (snail, fish)
Diarrheal disease miscellaneous
Diphyllobothriasis helminth (copepod, fish)
Dracunculiasis helminth
Enteroviruses virus
Fasciolopsiasis helminth (snail, plant)
Gastroenteritis miscellaneous
Infectious hepatitis virus
Leptospirosis spirochete
Paragonimiasis helminth (snail, crab)
Paratyphoid bacteria
Schistosomiasis helminth (snail)
Typhoid bacteria
In addition, several disease insect vectors thrive in conditions of ample fresh water, including:
Dengue (all types) virus (mosquito)
Filariasis helminth (mosquito)
Malaria protozoa (mosquito)
Onchocerciasis helminth (blackfly)
Rift Valley fever virus (mosquito)
Trypanosomiasis protozoa (tsetse fly)
Yellow fever virus (mosquito)
Adapted from R. Feachem, M. McGarry, and D. Mara, eds., Water, Wastes, and Health in Hot Climates (London: John Wiley & Sons, 1977); and A. Dievler and M. R. Reich, “The Aswan High Dam,†distributed by the Pew Curriculum for Health Policy and Management, Harvard School of Public Health, Boston, 1984.
17 World Bank, Health Sector Policy Paper (1980), op. cit., 13.
18 Dievler and Reich (1984), op. cit.; A. B. Mobarak, “The Schistosomiasis Problem in Egypt,†American Journal of Tropical Medicine and Hygiene 31: (1982): 87–91; and WHO Expert Committee, The Control of Schistosomiasis, Technical Report Series 728 (Geneva: World Health Organization, 1985).
19 Mobarak (1982), op. cit.
20 R. Daubney, J. R. Hudson, and P. C. Gamham, “Enzootic Hepatitis of Rift Valley Fever: An Undescribed Virus Disease of Sheep, Cattle and Man from East Africa,†Journal of Pathology and Bacteriology 31 (1931): 546–79.
21 F. Fenner, B. R. McAuslan, C. A. Mims, et al., The Biology of Animal Viruses (New York: Academic Press, 1974), 636.
22 Mims, C. A. “Rift Valley Fever in Mice. VI. Histological Changes in the Liver in Relation to Virus Multiplication.†Australian Journal of Experimental Biology and Medical Science 35 (1957): 595.
23 J. M. Meegan, “Rift Valley Fever in Egypt: An Overview of the Epizootic in 1977 and 1978,†Controversies in Epidemiology and Biostatistics 3 (1978): 100–13.
24 A. Jouan, I. Coulibaly, F. Adam, et al., “Analytical Study of a Rift Valley Fever Epidemic,†Research Virology 140 (1989): 175–86; J. Morvan, J. F. Saluzzo, D. Fontenille, et al., “Rift Valley Fever on the East Coast of Madagascar,†Research Virology 142 (1991): 475–82; A. Jouan, F. Adam, D. Riou, et al., “Evaluation of the Indicators of Health in the Area of Trarza During the Epidemic of Rift Valley Fever in 1987,†Bulletin de la Société de Pathologie Exotique et de ses Filiales 83 (1990): 621–27; and, R. E. Shope and A. S. Evans, “Assessing Geographic and Transport Factors, and Recognition of New Viruses,†in S. S. Morse, ed., Emerging Viruses (Oxford, Eng.: Oxford University Press, 1993), 114.
25 World Bank, Health Sector Policy Paper (1980), op. cit., 14.
26 Ibid., 35.
27 Data obtained from ibid., 68–85.
28 J. Nyerere, Arusha Declaration Ten Years After (Dar es Salaam: Oxford University Press, 1977).
29 “In Tanzania, the Road to Medicine Is Paved with Magic,†Hospital Practice, April 1974: 133–57.
30 The world has experienced eight pandemic waves of cholera since 1837. The seventh pandemic began in Indonesia in 1961 and spread slowly around most of the world’s poor nations. The eighth pandemic began in Madras, India, in December 1992.
31 “East Africa,†Africa, June 1979.
32 M. Honey, “How Amin Ran His Economy,†African Business, July 1979.
33 F. J. Bennett, “A Comparison of Community Health in Uganda with Its Two East African Neighbors in the Period 1970–1979,†in C. P. Dodge and P. D. Wiebe, eds., Crisis in Uganda (Oxford, Eng.: Pergamon Press, 1985), 43–52.
34 F. Rodhain, J. P. Gonzalez, E. Mercier, et al., “Arbovirus Infections and Viral Haemorrhagic Fevers in Uganda: A Serological Survey in Karamoja District, 1984,†Transactions of the Royal Society of Tropical Medicine and Hygiene 83 (1989): 851–54.
35 A. Enns, “The Clocks Have Stopped in Uganda,†in Dodge and Wiebe (1985), op. cit., 53–54.
36 “WHO: How It Is Making Public Health a Global Cause,†Hospital Practice, September 12, 1973: 205–18.
37 In the 1990s, it would become the capital of the nation of Kazakhstan.
38 G.A. res. 2200A (XXI), and 999 U.N.T.S. 171, March 23, 1976.
39 G.A. res. 2200A (XXI), 993 U.N.T.S. 3, entered into force January 3, 1976.
40 W. H. McNeill, Plagues and Peoples (New York: Doubleday, 1976).
41 Recently, McNeill described the microbial decimation of the Amerindians in greater detail, citing it as the key factor responsible for stimulating his initial interest in historic epidemics. Cortez, McNeill wrote, had fewer than 400 soldiers at his disposal when he laid siege to Tenochtitlán (Mexico City), yet they strolled right into the Aztec capital, taking power almost effortlessly. McNeill believes the smallpox devastation of the Aztecs, coupled with a variety of other European microbes, was so overwhelming that the Aztec people surrendered, having decided that their gods had sided with the white-skinned invaders. See W. H. McNeill, “Patterns of Disease Emergence in History,†Chapter 3 in Morse (1993) op. cit.
42 For a collection of representative views, see D. Brothwell and A. T. Sandison, eds., Diseases in Antiquity: A Survey of the Diseases, Inquiries and Surgery of Early Populations (Springfield, IL: Charles C Thomas, 1967).
43 M. Burnet and D. O. White, Natural History of Infectious Disease (4th ed.; Cambridge, Eng.: Cambridge University Press, 1972).
44 R. Dubos and J. Dubos, The White Plague: Tuberculosis, Man and Society (New Brunswick, NJ: Rutgers University Press, 1992), 207.
45 R. Dubos, Mirage of Health: Utopias, Progress, and Biological Change (Garden City, NY: Anchor Books, 1961), 138–39.
46 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 (1974): 391–422.
47 R. C. Baron, J. B. McCormick, and O. A. Zubeir, “Ebola Virus Disease in Southern Sudan: Hospital Dissemination and Intrafamilial Spread,†Bulletin of the World Health Organization 61 (1983): 997–1003.
48 Time would prove McCormick sadly correct, as conditions in southern Sudan worsened steadily year by year. Widespread famine, over a decade of civil war, and massive refugee migrations would render the area a highly vulnerable ecology for the microbes. By mid-1993 the region would be suffering massive epidemics of AIDS, visceral leishmaniasis or kala-azar, tuberculosis, bacterial meningitis, a host of diarrheal diseases, leprosy, measles, and malaria. If Ebola and Marburg diseases were also rampant at that time they were undetectable, hidden under an overlay of so much disease that nearly every southern Sudanese seemed stricken by at least one potentially life-threatening ailment.
For further details, see Leishmaniasis Epidemic in Southern Sudan, WHO/6 (Geneva: World Health Organization, January 26, 1993); R. W. Ashford and M. C. Thomson, “Visceral Leishmaniasis in Sudan: A Delayed Development Disaster?†Annals of Tropical Medicine and Parasitology 85 (1991): 571–72; W. A. Perea, T. Ancelle, A. Moren, et al., “Visceral Leishmaniasis in Southern Sudan,†Transactions of the Royal Society of Tropical Medicine and Hygiene 85 (1991): 48–53; R. Rosenblatt, “The Last Place on Earth,†Vanity Fair, July 1993: 89–91, 114–20; and J. Seaman, D. Pryce, H. E. Sandorp, et al., “Epidemic Visceral Leishmaniasis in Sudan: A Randomized Trial of Aminosidine Plus Sodium Stibogluconate Versus Sodium Stiboglutinate Alone,†Journal of Infectious Diseases 168 (1993): 715–19.
8. Revolution
1 J. D. Watson and F. H. C. Crick, “A Structure for Deoxyribonucleic Acid,†Nature 171 (1953): 737.
2 There are many excellent resources for further information about recombinant DNA techniques. They include P. Berg and M. Singer, Dealing with Genes: The Language of Heredity (Mill Valley, CA: University Science Books, 1992); M. Singer and P. Berg, Genes to Genomes (Mill Valley, CA: University Science Books, 1991); and J. D. Watson, N. H. Hopkins, J. W. Roberts, et al., Molecular Biology of the Gene (4th ed.; Menlo Park, CA: Benjamin/Cummings Publishing Co., 1987).
3 For an excellent review of McClintock’s work and its subsequent impact on molecular biology, see N. V. Federoff, “Maize Transposable Elements.†Chapter 14 in D. E. Berg and M. M. Howe, eds., Mobile DNA (Washington, D.C.: American Society for Microbiology, 1989). One of McClintock’s seminal papers is B. McClintock, “The Origin and Behavior of Mutable Loci in Maize,†Proceedings of the National Academy of Sciences 36 (1950): 344–55.
4 James Watson has written four editions of his grand guide to molecular biology, each of which, since the first in 1965, has been considerably larger than its predecessor, reflecting the explosion of scientific discovery. The most recent edition of Molecular Biology of the Gene, completed in 1987 (op. cit.), has this marvelous description of the mobile DNA phenomenon: “Moveable DNA segments called transposons occasionally jump around chromosomes, thus fundamentally altering chromosomal structure. In addition to neatly moving genes, transposons also scramble DNA, making deletions, inversions, and other rearrangements. It is becoming clear that such changes are a critical feature of chromosome evolution, particularly in eucaryotic cells. We now appreciate that recombination is not accidental, but is instead an essential cellular process catalyzed by enzymes that cells encode and regulate for the purpose.â€
5 D. Baltimore, “Retroviruses and Cancer,†Hospital Practice, January 1978: 49–57.
6 S. S. Morse, “Evolution, Viral,†Encyclopedia of Microbiology, Vol. 2 (New York: Academic Press, 1992), 141–55.
7 For an excellent list of key transposable elements in common use for genetic engineering, see C. M. Berg, D. E. Berg, and E. A. Groisman, “Transposable Elements and Genetic Engineering,†Chapter 41 in Berg and Howe, eds. (1989), op. cit.
8 J. M. Bishop, “Viruses, Genes, and Cancer,†Harvey Lecture, March 17, 1983.
9 D. H. Spector, H. E. Varmus, and J. M. Bishop, “Nucleotide Sequences Related to the Transforming Gene of Avian Sarcoma Virus Are Present in DNA of Uninfected Vertebrates,†Proceedings of the National Academy of Sciences 75 (1978): 4102–06; and D. Stehelin, H. E. Varmus, J. M. Bishop, and P. K. Vogt, “DNA Related to the Transforming Gene(s) of Avian Sarcoma Viruses Is Present in Normal Avian DNA,†Nature 260 (1976): 170–73.
10 Bishop (1983), op. cit.
11 J. M. Bishop, “Oncogenes,†Scientific American 246 (1982): 80–92; and H. E. Varmus, “Form and Function of Retroviral Proviruses,†Science 216 (1982): 812–20.
12 K. Takatsuki, T. Uchiyama, K. Sagawa, and J. Yodoi, in S. Seno, F. Takaku, and S. Irino, eds., Topics in Hematology (Amsterdam: Excerpta Medica, 1977), 73–77.
13 Though the acronym HTLV would remain, Gallo—at the urging of numerous scientific colleagues—later changed the L in HTLV from “leukemia†to “lymphotropic,†reflecting increasing evidence that the virus rarely caused leukemia but always attacked lymphoid cells.
14 B. J. Poiesz, F. W. Ruscetti, M. Reitz, et al., “Isolation of a New Type C Retrovirus (HTLV) in Primary Uncultured Cells of a Patient with Sezary T-Cell Leukemia,†Nature 294 (1981): 268–75.
15 Robert Gallo’s version of these events appears in his 1991 book, Virus Hunting—AIDS, Cancer, and the Human Retrovirus: A Story of Scientific Discovery (New York: New Republic). The Japanese perspective has not been published. Also see B. J. Poiesz, F. W. Ruscetti, A. F. Gazdar, et al., “Detection and Isolation of Type-C Retrovirus Particles from Fresh and Cultured Lymphocytes of a Patient with Cutaneous T-Cell Lymphoma,†Proceedings of the National Academy of Sciences 77 (1980): 7415–19.
16 I. Miyoshi, M. Fujishita, H. Taguchi, et al., “Natural Infection in Non-human Primates with Adult T-Cell Leukemia Virus or a Closely Related Agent,†International Journal of Cancer 32 (1983): 333–36.
17 I. Miyoshi, S. Yoshimoto, M. Fujishita, et al., “Natural Adult T-Cell Leukemia Virus Infection in Japanese Monkeys,†Lancet II (1982): 658.
18 An interesting side note to this story concerns the ultimate fate of the MO line. It has always been difficult to grow normal human cells under laboratory conditions; nearly all studies are done on human cancer cells cloned from specific tumor lines because cancer cells will grow under all sorts of conditions, including inside glass tubes. These clones are given names and the cell lines are sold to researchers all over the world. Such a line, if proven free of contamination and relatively indicative of general human cell activity, can fetch good prices. Golde thought MO might prove a fantastic experimental cell line, and filed a U.S. patent petition. If granted a patent, he would be able to reap royalties from all MO sales to researchers worldwide and profit from any products derived from the cell line. Golde’s plans backfired, however, when the patient, John Moore, a Seattle salesman, questioned Golde’s right to patent his cells, which had been removed from his spleen. The issue became more heated as the profit potentials grew. Moore’s MO cells were the source of the discovery of the immune system protein GM-CSF, as well as the HTLV-II virus, which greatly increased the value of the line. As of 1993 the dispute continued to wend its way through the American legal system, having grown extraordinarily complex. A good review of the MO controversy appeared in J. Stone, “Cells for Sale,†Discover, August 1988: 33–39.
19 J. S. Y. Chen, J. McLaughlin, J. C. Garson, et al., “Molecular Characterization of Genome of a Novel Human T-Cell Leukaemia Virus,†Nature 305 (1983): 502–5.
20 V. S. Kalyanaraman, M. G. Sarngadharan, M. Robert-Guroff, et al., “A New Subtype of Human T-cell Leukemia Virus (HTLV-II) Associated with a T-cell Variant of Hairy Cell Leukemia,†Science 218 (1982): 571–73.
21 A good example of the public perspective at the time can be found in Larry Agran’s The Cancer Connection and What We Can Do About It (Boston: Houghton Mifflin, 1977). Agran asserted that “we can change the man-m
ade environment that causes 90 percent of all human cancer.â€
22 G. Hunsmann, J. Schneider, J. Schmitt, and N. Yamamoto, “Detection of Serum Antibodies to Adult T-Cell Leukemia Virus in Non-Human Primates and in People from Africa,†International Journal of Cancer 32 (1983): 329–32.
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