The Coming Plague

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by Laurie Garrett


  23 In addition to interviews, details for the section were drawn from the following sources: W. N. Bonner, The Natural History of Seals (New York: Facts on File, 1990); R. Dietz, C. T. Ansen, P. Have, and M. P. Heide-Jørgensen, “Clue to Seal Epizootic?” Nature 338 (1989): 627; M. Domingo, L. Ferrer, M. Pumarola, et al., “Morbillivirus in Dolphins,” Nature 348 (1990): 21; M. A. Gracher, V. P. Kumarev, L. V. Mamaev, et al., “Distemper Virus in Baikal Seals,” Nature 338 (1989): 209; C. B. Goodhart, “Did Virus Transfer from Harp Seals to Common Seals?” Nature 336 (1988): 21; J. Harwood, “Lessons from the Seal Epidemic,” New Scientist, February 18, 1989: 38–42; S. Kennedy, J. A. Smyth, P. F. Cush, et al., “Viral Distemper Found in Porpoises,” Nature 336 (1988): 21; S. Kennedy, J. A. Smyth, S. J. McCullough, et al., “Confirmation of Cause of Recent Seal Deaths,” Nature 325 (1988): 404; B. W. J. Mahy, “Seal Plague Virus,” Chapter 17 in Morse, ed. (1993), op. cit.; C. Orvell, M. Blixenkrone-Möller, V. Svansson, and P. Have, “Immunological Relationships Between Phocid and Canine Distemper Virus Studied with Monoclonal Antibodies,” Journal of General Virology 71 (1990): 2085–92; A. D. M. E. Osterhaus, J. Gröen, P. DeVries, et al., “Canine Distemper Virus in Seals,” Nature 335 (1988): 403–4; S. Pain, “Dolphin Virus Threatens Last Remaining Monk Seals,” New Scientist, November 3, 1990: 22; I. K. G. Visser, Morbillivirus Infections in Seals, Dolphins and Porpoises, Doctoral Thesis, University of Utrecht, Seal Rehabilitation and Research Centre, Zeehondencreche Pieterburen, Netherlands, 1993; and J. Webb, “Dolphin Epidemic Spreads to Greece,” New Scientist, September 7, 1991: 18.

  24 In the Baltic salmon faced extinction in 1993–94 because of just such a mixture of events. The Baltic is heavily polluted, having been a major Soviet dumping ground for more than four decades. Salmon caught in the Baltic or nearby rivers, streams, and lakes are heavily contaminated with chlorinated hydrocarbons.

  Since 1993 Baltic salmon mothers have been behaving strangely, swimming improperly when pregnant and laying eggs that hatch fish which can’t swim. More than 90 percent of fish hatched since the fall of 1993 have died.

  The Baltic salmon species, it turns out, are newly infected with a parasite, Gyrodactylus, that may have succeeded in emerging into the Baltic salmon population because of the fish’s pollution-induced immunodeficiencies.

  25 The estimated death tolls were as follows:

  26 For a sampling of Colwell’s findings, see R. R. Colwell, J. Kaper, and S. W. Joseph, “Vibrio cholerae, Vibrio parahaemolyticus and Other Vibrios: Occurrence and Distribution in Chesapeake Bay,” Science 198 (1977): 394–96; R. R. Colwell, M. L. Tamplin, P. R. Brayton, et al., “Environmental Aspects of V. cholerae in Transmission of Cholera,” in R. B. Sack and Y. Zinnaka, eds., Advances in Research on Cholera and Related Diarrhoeas (7th ed.; Tokyo: K.T.K. Scientific Publishers, 1990), 327–43; R. R. Colwell, J. A. K. Hasan, A. Hug, et al., “Development and Evaluation of a Rapid, Simple Sensitive Monoclonal Antibody-Based Coagglutination Test for Direct Detection of V. cholerae 01,” FEMS Microbiology Letters 97 (1992): 215–20; and A. Hug, S. Parveen, F. Qadri, and R. R. Colwell, “Comparison of V. cholerae Serotype 01 Isolated from Patient and Aquatic Environment,” Journal of Tropical Medicine and Hygiene 96 (1993): 86–92.

  27 S. Pain, “Water Hides a Host of Viruses,” New Scientist, August 19, 1989: 28.

  28 Hundreds of examples could be cited. For just one illustrative case, see Centers for Disease Control, “Multistate Outbreak of Viral Gastroenteritis Related to Consumption of Oysters—Louisiana, Maryland, Mississippi, and North Carolina, 1993,” Morbidity and Mortality Weekly Report 42 (1993): 945–47.

  29 J. L. Melnick and T. G. Metcalf, “Distribution of Viruses in the Water Environment,” in B. Fields, M. A. Martin, and D. Kamely, eds., Genetically Altered Viruses and the Environment (New York: Cold Spring Harbor Laboratory, 1985), 95–102.

  30 World Bank, World Development Report 1993: Investing in Health (New York: Oxford University Press, 1993).

  31 The horrendous condition of the earth’s seas has been described in great detail elsewhere. See, for example, Proceedings, Dahlem Conference on Ocean Margin Processes in Global Change, Berlin, March 18–22, 1990 (New York: John Wiley & Sons, 1990); K. Schneider, “Ozone Depletion Harming Sea Life,” New York Times, November 16, 1991: 19; K. Sherman and L. M. Alexander, Biomass Yields and Geography of Large Marine Ecosystems (Boulder, CO: Westview Press, 1989); Groups of Experts on the Scientific Aspects of Marine Pollution (GESAMP), The State of the Marine Environment, United Nations Environment Programme Regional Seas Reports and Studies, No. 115, Nairobi, 1990; and J. Pineda, “Predictable Upwelling and the Shoreward Transport of Planktonic Larvae by Internal Tidal Bores,” Science 253 (1991): 548–49.

  32 Center for Marine Conservation, Global Marine Biological Diversity, a Strategy for Building Conservation into Decision Making, report to the World Bank, Washington, D.C., 1993.

  33 See, for example, C. W. Sullivan, K. R. Arrigo, C. R. McClain, et al., “Distributions of Phytoplankton Blooms in the Southern Ocean,” Science 262 (1993): 1832–37.

  34 A rough estimate of the planet’s species distributions, as estimated by Marjorie Readka-Kudla, in a presentation to the annual meeting of the American Association for the Advancement of Science, San Francisco, February 1994, would be as follows:

  Species Category Number of Known Species % of Total Number of Planetary Species

  Terrestrial chordates 2,000 0.1

  Insects 750,000 54.0

  Fungi 47,000 3.0

  Marine chordates 3,000 0.2

  Freshwater chordates 1,000 0.08

  Viruses and prokaryotes 6,000 4.00

  Algae 27,000 2.0

  Terrestrial plants 250,000 18.0

  Distributed over the planet as follows:

  Ecosystem Km2 (in millions) % of Earth’s Surface

  Total global surface area 511 100

  Global landmass 170.3 33.3

  [Rain forests (1990)] 11.9 2.3

  Oceans 340.1 66.7

  [Coral reefs] 0.6 0.1

  [Coastal zones] 40.9 8.0

  35 R. I. Glass, M. Claeson, P. A. Blake, et al., “Cholera in Africa: Lessons on Transmission and Control for Latin America,” Lancet 338 (1991): 791–95.

  36 A. K. Siddique, A. H. Baqui, A. Eusof, et al., “Survival of Classic Cholera in Bangladesh,” Lancet 337 (1991): 1125–27.

  37 M. S. Islam, B. S. Drasar, and D. J. Bradley, “Long-Term Persistence of Toxigenic Vibrio cholerae 01 in the Mucilaginous Sheath of a Blue-Green Alga, Anabaena variabilis,” Journal of Tropical Medicine and Hygiene 93 (1990): 133–39; and A. Hug, P. A. West, E. B. Small, et al., “Influence of Water Temperature, Salinity and pH on Survival and Growth of Toxigenic Vibrio cholerae Copepods in Laboratory Microcosms,” Applied Environmental Microbiology 48 (1984): 420–24.

  Further work demonstrated that the V. cholerae could thrive on or inside of a range of freshwater and saltwater algae. See M. J. Islam, “Increased Toxin Production by Vibrio cholerae 01 During Survival with a Green Alga, Rhizoclonium fontanum, in an Artificial Aquatic Environment,” Microbiology and Immunology 34 (1990): 557–563; M. S. Islam, B. S. Drasar, and D. J. Bradley, “Attachment of Toxigenic Vibrio cholerae 01 to Various Freshwater Plants and Survival with a Filamentous Green Alga, Rhizoclonium fontanum,” Journal of Tropical Medicine and Hygiene 92 (1989): 396–401; and M. S. Islam, B. S. Drasar, and D. J. Bradley, “Survival of Toxigenic Vibrio cholerae 01 with a Common Duckweed, Lemma minor, in Artificial Aquatic Ecosystems,” Transactions of the Royal Society of Tropical Medicine and Hygiene 84 (1990): 422–24.

  38 For an excellent summary, see R. R. Colwell and W. M. Spira, “The Ecology
of Vibrio cholerae,” Chapter 6 in D. Barua and W. B. Greenough III, eds., Cholera (New York: Plenum, 1992).

  39 These events are described in the following: P. R. Epstein, T. E. Ford, and R. R. Colwell, “Marine Ecosystems,” Lancet 342 (1993): 1216–19; A. P. M. Lockwood, “Aliens and Interlopers at Sea,” Lancet 342 (1993): 942–43; C. Anderson, “Cholera Epidemic Traced to Risk Miscalculation,” Nature 354 (1991): 255; Colwell and Spira (1992), op. cit.; World Health Organization, “Cholera Alert in Latin America,” Press Release, WHO/8/12 February 1991; “Cholera in the Americas,” Bulletin of the Pan American Health Organization 25 (1991): 267–77; Centers for Disease Control, “Cholera Outbreak—Peru, Ecuador, and Colombia,” Morbidity and Mortality Weekly Report 40 (1991): 225–27; E. W. Rice and C. H. Johnson, “Cholera in Peru,” Lancet 338 (1991): 455; V. M. Witt and F. M. Reiff, “Environmental Health Conditions and Cholera Vulnerability in Latin America and the Caribbean,” Journal of Public Health Policy (Winter 1991): 450–63; M. L. Tamplin and C. C. Parodi, “Environmental Spread of Vibrio cholerae in Peru,” Lancet 338 (1991): 1216–17; J. Sepulveda, H. Gómez-Dantes, and M. Bronfman, “Cholera in the Americas: An Overview,” Infection 20 (1992): 243–48; and R. V. Tauxe and P. A. Blake, “Cholera Epidemic in Latin America,” Journal of the American Medical Association 267 (1992): 1388–90.

  40 El Tor made its way into Brazil through the Amazon and thence to Rio.

  41 Centers for Disease Control, “Cholera—New York, 1991,” Morbidity and Mortality Weekly Report 40 (1991): 516–18; and Centers for Disease Control, “Cholera Associated with an International Airline Flight,” Morbidity and Mortality Weekly Report 41 (1992): 134–35.

  In September 1991 health authorities in Alabama discovered V. cholerae 01 in local seafood. An investigation of the bilge and ballast waters of ships from South America harbored in the Gulf of Mexico revealed that cholera-infested algae were present. See S. A. McCarthy, R. M. McPhearson, A. M. Guarino, and J. L. Gaines, “Toxigenic Vibrio cholerae 01 and Cargo Ships Entering Gulf of Mexico,” Lancet 339 (1992): 624–25.

  Polymerase chain reaction analysis of the DNA in various Latin American and Gulf of Mexico isolates of V. cholerae didn’t match up, however. The cholera found in the Gulf was never matched exactly to cholera strains anywhere else in the world, and its origin remained subject for debate in 1994. See I. K. Wachsmuth, G. M. Evins, P. I. Fields, et al., “The Molecular Epidemiology of Cholera in Latin America,” Journal of Infectious Diseases 167 (1993): 621–26.

  42 The eight drugs were ampicillin, chloramphenicol, colistin, neomycin, kanamycin, gentamicin, tetracycline, and Fansidar. See R. Tabtieng, S. Wattanasri, P. Echeverría, et al., “An Epidemic of Vibrio cholerae El Tor Inaba Resistant to Several Antibiotics with a Conjugative Group C Plasmid Coding for Type II Dihydrofolate Reductase in Thailand,” American Journal of Tropical Medicine and Hygiene 41 (1989): 680–86.

  43 A. A. Ries, D. J. Vugia, L. Beingolea, et al., “Cholera in Piura, Peru: A Modern Urban Epidemic,” Journal of Infectious Diseases 166 (1992): 1429–33; and Editorial, “Of Cabbages and Chlorine: Cholera in Peru,” Lancet 340 (1992): 20–21.

  44 See numerous bulletin reports from officials and scientists working throughout the region, all appearing in Lancet 342 (1993): 382–83, 387–90, 430–31, 925–27.

  45 P. R. Epstein, T. E. Ford, and R. R. Colwell, “Marine Ecosystems,” Lancet 342 (1993): 1216–19; and P. R. Epstein, “Cholera and the Environment,” Lancet 339 (1992): 1167–68.

  46 R. Shope, “Global Climate Change and Infectious Diseases,” Environmental Health Perspectives 96 (1991): 171–74.

  47 J. de Zulueta, “Changes in the Geographical Distribution of Malaria Throughout History,” Parasitologia 29 (1987): 193–205.

  48 D. J. Rogers and M. J. Packer, “Vector-Borne Diseases, Models, and Global Change,” Lancet 342 (1993): 1282–85.

  49 The WHO Task Group graded the sensitivities of diseases (or their vectors and transmissibility) in relation to global temperature changes on a scale of 0 to 3, with 0-graded unlikely to be affected at all and 3-graded highly susceptible to temperature variations.

  Disease 1990 Prevalence Grade

  Malaria 270 million 3

  Lymphatic filariasis 90.2 million 1

  Onchocerciasis 17.8 million 1

  Schistosomiasis 200 milion 2

  Sleeping sickness 25,000/year 1

  Leishmaniasis 12 million 1

  Dracunculiasis 1 million 0

  Dengue NS 2

  Yellow fever NS 1

  Japanese encephalitis NS 1

  St. Louis encephalitis NS 1

  All other insect-borne viral diseases NS 1

  See WHO Task Group, “Potential Health Effects of Climatic Change,” report to the World Health Organization, WHO/PEP/90/10, 1990.

  50 A. Leaf, “Potential Health Efforts of Global Climatic and Environmental Changes,” New England Journal of Medicine 321 (1989): 1577–83; A. Jeevan and M. L. Kripke, “Ozone Depletion and the Immune System,” Lancet 342 (1993): 1159–60; World Health Organization, “Ultraviolet Radiation Can Seriously Damage Your Health,” Press Release, WHO/102/17 December 1993; W. Goettsch, J. Garssen, A. Deijins, et al., “UV-B Exposure Impairs Resistance to Infection by Trichinella spiralis,” Environmental Health Perspectives 102 (1994): 298–304; C. Hassett, M. G. Mustafa, W. F. Coulson, and R. M. Elashoff, “Murine Lung Carcinogenesis Following Exposure to Ambient Ozone Concentrations,” Journal of the National Cancer Institute 75, 4 (1985): 1211–19; L. Calderón-Garcidueñas and G. Roy-Ocotla, “Nasal Cytology in Southwest Metropolitan Mexico City Inhabitants: A Pilot Intervention Study,” Environmental Health Perspectives 101 (1993): 138–44; and National Research Council, Biological Markers in Immunotoxicology (Washington, D.C.: National Academy of Sciences, 1992).

  51 M. R. Moser, T. R. Bender, H. S. Margolis, et al., “Aircraft Transmission of Influenza A,” American Journal of Epidemiology 110 (1979): 1.

  52 D. Maki, “Airline Cabin Air Quality,” testimony before the Subcommittee on Technology, Environment and Aviation, House Committee on Science, Space and Technology, July 29, 1993; and A. R. Hinman (1993), “Statement,” ibid.

  53 This was also revealed during the congressional hearings, by Niren Nagda, of ICF Kaiser International, an independent toxicology firm. Office standards for the United States were for twenty cubic feet per minute of fresh air in a standard room. In contrast, sold-out flights had an air intake rate of only nine to fourteen feet per minute.

  54 World Health Organization, Our Planet, Our Health, WHO Report to the United Nations Earth Summit, Rio de Janeiro, June 1992.

  55 In 1990 another new disease—Venezuelan hemorrhagic fever—emerged. Like Machupo and Junín, it was caused by a virus (dubbed Guanarito virus) that was carried by rodents (Sigmodan hispidus rats). The rats came in contact with Homo sapiens when large numbers of settlers moved into a previously pristine rain forest area. Guanarito killed 30 percent of the people it infected. See R. Salas, N. D. Manzione, R. B. Tesh, et al., “Venezuelan Hemorrhagic Fever,” Lancet 338 (1991): 1033–36.

  Still another hemorrhagic fever virus killed a twenty-five-year-old office worker in So Paulo, Brazil, in 1992. The origin of the Sabia virus, the cause of Brazilian hemorrhagic fever, has yet to be determined. See T. L. M. Coimbra, E. S. Nassar, M. N. Burattini, et al., “New Arenavirus Isolated in Brazil,” Lancet 343 (1994): 391–92.

  56

  COMMERCIAL AIR TRAFFIC

  Source: International Air Transportation Association, 1993.

  Year Millions of Passengers

  Interna
tional 1950 2

  1960 42

  1970 74

  1980 163

  1990 280

  Domestic, U.S.A. 1950 17

  1960 38

  1970 153

  1980 273

  1990 424

  57 In addition to human beings, hundreds of millions of animals were shipped from continent to continent annually by 1990. House pets, research animals, Thoroughbred horses, breeding livestock, illegally smuggled endangered species, aquarium fish, and a host of other broad categories of animals were routinely shipped overseas aboard airplanes or ocean liners.

  58 S. S. Morse, “Emerging Viruses: Defining the Rules for Viral Traffic,” Perspectives in Biology and Medicine 34 (1991): 387–409; and S. S. Morse, “Origins of Emerging Viruses,” Chapter 2 in Morse, ed. (1993), op. cit.

  59 B. Fleckenstein and R. C. Desrosiers, “Herpesvirus saimiri and Herpesvirus ateles,” Chapter 6 in B. Roizman, ed., The Herpesviruses, Vols. 1 and 2 (New York: Plenum, 1982); J. C. Albrecht and B. Fleckenstein, “Primary Structure of the Herpesvirus saimiri Genome,” Journal of Virology 66 (1992): 5047–58; and B. Biesinger, “Stable Growth Transformation of Human T Lymphocytes by Herpesvirus saimiri,” Proceedings of the National Academy of Sciences 89 (1992): 3116–19.

  60 The virus, wrote researchers from the Institut für Klinische und Molekulare Virologie in Erlangen, Germany, “seems to be particularly prone to sequestering cellular genes. The genome appears to function as a spontaneous vector for cellular genes that may have been acquired by a mechanism involving reverse transcription, since most of the viral counterparts have no introns. The uptake of such genes may provide functions necessary for the progression of biological properties and secure a selection advantage in the natural host.” See Albrecht and Fleckenstein (1992), op. cit.

 

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