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THE CAMBRIDGE HISTORICAL DICTIONARY OF DISEASE

Edited by KENNETHKENNETH FF.. KKIPLEIPLE Bowling Green State University

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PUBLISHED BY THE PRESS SYNDICATE OF THE UNIVERSITY OF CAMBRIDGE The Pitt Building, Trumpington Street, Cambridge, United Kingdom

CAMBRIDGE UNIVERSITY PRESS The Edinburgh Building, Cambridge CB2 2RU, UK 40 West 20th Street, New York, NY 10011-4211, USA 477 Williamstown Road, Port Melbourne, VIC 3207, Australia Ruiz de Alarcon´ 13, 28014 Madrid, Spain Dock House, The Waterfront, Cape Town 8001, South Africa http://www.cambridge.org

C Cambridge University Press 2003

This book is in copyright. Subject to statutory exception and to the provisions of relevant collective licensing agreements, no reproduction of any part may take place without the written permission of Cambridge University Press.

First published 2003

Printed in the United States of America

Typefaces Poppl-Pontifex 8.75/12 pt. and Poppl-Laudatio System LATEX2ε [TB]

A catalog record for this book is available from the British Library.

Library of Congress Cataloging in Publication Data The Cambridge historical dictionary of disease / edited by Kenneth F. Kiple. p. cm. Includes bibliographical references and index. ISBN 0-521-80834-0 – ISBN 0-521-53026-1 (pbk.) 1. Diseases – History – Dictionaries. I. Kiple, Kenneth F., 1939– RC41 .C365 2003 616 .009 – dc21 2002031368

ISBN 0 521 80834 0 hardback ISBN 0 521 53026 1 paperback

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Contents

Preface xiii 15 Beriberi 44 Melinda S. Meade 1 Acquired Immune Deficiency Syndrome (AIDS) 1 16 49 Allan M. Brandt Katharine Park

2 African Trypanosomiasis (Sleeping 17 Black and Brown Lung Disease 52 Sickness) 7 Daniel M. Fox Maryinez Lyons 18 Bleeding Disorders 54 3 Ainhum 14 Oscar D. Ratnoff Donald B. Cooper 19 Botulism 57 4 Alzheimer’s Disease 14 William H. Barker Joseph A. Kwentus 20 Brucellosis (Malta Fever, Undulant Fever) 5 Amebic Dysentery 19 58 K. David Patterson Lise Wilkinson

6 Anemia 21 21 Bubonic Plague 60 Alfred Jay Bollet and Audrey K. Brown Ann G. Carmichael

7 Anorexia Nervosa 26 22 Cancer 63 Heather Munro Prescott Thomas G. Benedek and Kenneth F. Kiple

8 29 23 Carrion’s Disease (Oroya Fever) 67 Lise Wilkinson Oscar Urteaga-Ballon

9 Apoplexy and Stroke 31 24 Catarrh 69 Jacques Poirier and Christian Derouesne Roger K. French

10 Arboviruses 34 25 Cestode 70 Wilbur G. Downs K. David Patterson

11 Arenaviruses 38 26 Chagas’ Disease 70 Wilbur G. Downs Marvin J. Allison

12 Arthritis (Rheumatoid) 39 27 Chlorosis 71 Howard Duncan and James C. C. Leisen Robert P. Hudson

13 Ascariasis 42 28 Cholera 74 K. David Patterson Reinhard S. Speck

14 Bacillary Dysentery 43 29 Cirrhosis 79 K. David Patterson Thomas S. N. Chen and Peter S. Y. Chen

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30 Clonorchiasis 81 48 Enterobiasis 116 K. David Patterson K. David Patterson

31 Croup 81 49 Epilepsy 116 James D. Cherry Jerrold E. Levy

32 Cystic Fibrosis 83 50 120 Thomas G. Benedek John S. Haller, Jr.

33 Infection 84 51 Erysipelas 121 R. H. Kampmeier Ann G. Carmichael

34 Dengue 85 52 Fascioliasis 123 James McSherry K. David Patterson

35 Diabetes 88 53 Fasciolopsiasis 123 Leslie Sue Lieberman K. David Patterson

36 Diarrheal Diseases (Acute) 92 54 Favism 123 Herbert L. DuPont Peter J. Brown 55 Filariasis 125 37 Diphtheria 94 Todd L. Savitt Ann G. Carmichael 56 Fungus (Mycoses) 128 38 Down Syndrome 96 Geoffrey C. Ainsworth Christine E. Cronk 57 Fungus Poisoning 132 39 Dracunculiasis 98 Geoffrey C. Ainsworth Donald R. Hopkins 58 Gallstones (Cholelithiasis) 134 40 Dropsy 100 R. Ted Steinbock J. Worth Estes 59 Gangrene 136 41 Dysentery 105 Diane Quintal and Robert Jackson K. David Patterson 60 Genetic Disease 138 42 Dyspepsia 105 Eric J. Devor James Whorton 61 Giardiasis 144 43 Ebola Virus Disease 107 K. David Patterson Wilbur G. Downs 62 Glomerulonephritis (Bright’s Disease) 44 Echinococcosis (Hydatidosis) 110 144 K. David Patterson Donald M. Larson

45 Eclampsia 110 63 Goiter 146 Sally McMillen Clark T. Sawin

46 Emphysema 112 64 Gonorrhea 150 Ronald J. Knudson Richard B. Rothenberg

47 114 65 Gout 153 R. T. Ravenholt Thomas G. Benedek

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66 Heart-Related Diseases 156 83 Leprosy (Hansen’s Disease) 192 Joel D. Howell Ann G. Carmichael

67 Herpes Simplex 161 84 Leptospirosis 195 R. H. Kampmeier Otto R. Gsell

68 Herpesviruses 162 85 Leukemia 196 R. H. Kampmeier Gordon J. Piller

69 Histoplasmosis 163 86 Lupus Erythematosus 199 Scott F. Davies Thomas G. Benedek 87 Lyme Borreliosis (Lyme Disease) 201 70 Hookworm Infection 165 Robert D. Leff John Ettling 88 Malaria 203 71 Huntington’s Disease (Chorea) 168 Frederick L. Dunn Eric J. Devor 89 Marburg Virus Disease 207 72 Hypertension 169 Wilbur G. Downs Thomas W. Wilson and Clarence E. Grim 90 Mastoiditis 208 73 Infectious Hepatitis 171 John L. Kemink, John K. Niparko, and Steven A. Francis L. Black Telian

74 174 91 Measles 211 R. H. Kampmeier Robert J. Kim-Farley

75 Inflammatory Bowel Disease (Crohn’s 92 Meningitis 214 Disease, Ulcerative Colitis) 175 K. David Patterson Joseph B. Kirsner 93 Milk Sickness (Tremetol Poisoning) 218 76 Influenza 178 Thomas E. Cone, Jr. Alfred W. Crosby 94 Multiple Sclerosis 220 77 Japanese B Encephalitis 181 W. I. McDonald Edward H. Kass 95 222 78 Lactose Intolerance and Malabsorption Robert J. Kim-Farley 182 96 Muscular Dystrophy 224 Norman Kretchmer Thomas G. Benedek 79 Lassa Fever 184 97 Myasthenia Gravis 225 Wilbur G. Downs Bernard M. Patten

80 Lead Poisoning 185 98 Nematode Infection 227 Arthur C. Aufderheide K. David Patterson

81 Legionnaires’ Disease (Legionellosis, 99 Onchocerciasis 228 Pontiac Fever, Legionella Pneumonia) 189 K. David Patterson David W. Fraser 100 Ophthalmia (Trachoma, Conjunctivitis) 82 Leishmaniasis 191 230 Marvin J. Allison Mary C. Karasch

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101 Osteoarthritis 234 118 270 Charles W. Denko K. David Patterson

102 Osteoporosis 236 119 275 R. Ted Steinbock Anne Hardy

103 Paget’s Disease of Bone 238 120 Rheumatic Fever and Rheumatic Heart Roy D. Altman Disease 277 Thomas G. Benedek 104 Paragonimiasis 240 K. David Patterson 121 Rickets and Osteomalacia 280 R. Ted Steinbock 105 Parkinson’s Disease (Parkinsonism) 240 122 Rickettsial Diseases 282 Bernard M. Patten Victoria A. Harden

106 Pellagra 242 123 Rocky Mountain Spotted Fever and Elizabeth W. Etheridge Related Diseases 283 Victoria A. Harden 107 Periodontal Disease (Pyorrhea) 244 Jeffrey Levin 124 Rubella 285 Robert J. Kim-Farley 108 Pica 247 Brian T. Higgins 125 Saint Anthony’s Fire 287 Ann G. Carmichael 109 Pinta 250 Don R. Brothwell 126 Scarlet Fever 288 Anne Hardy 110 251 Ann G. Carmichael 127 Schistosomiasis 290 John Farley 111 Pneumocystis Pneumonia (Interstitial Plasma Cell Pneumonia, Pneumocystosis) 128 Scrofula 292 254 Roger K. French K. David Patterson 129 Scurvy 295 112 Pneumonia 255 Roger K. French Jacalyn Duffin 130 Sickle-Cell Anemia 298 113 Poliomyelitis 258 Georges C. Benjamin H. V. Wyatt 131 Smallpox 300 114 Protein-Energy Malnutrition 261 Alfred W. Crosby James L. Newman 132 Streptococcal Diseases 304 115 Protozoan Infection 265 Peter C. English K. David Patterson 133 Strongyloidiasis 306 116 Puerperal Fever 265 K. David Patterson K. Codell Carter 134 Sudden Infant Death Syndrome (SIDS) 117 Q Fever 267 306 S. R. Palmer Todd L. Savitt

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135 Sudden Unexplained Death Syndrome 149 Trichuriasis 336 (Asian SUDS) 309 K. David Patterson Neal R. Holtan 150 336 136 Sweating Sickness 311 William D. Johnston Ann G. Carmichael 151 Tularemia 342 137 Syphilis 312 Patrick D. Horne Jon Arrizabalaga 152 Typhoid Fever 345 138 Syphilis, Nonvenereal 317 Charles W. LeBaron and David N. Taylor Kenneth F. Kiple 153 Typhomalarial Fever 349 139 Tapeworm Infection 319 Dale Smith K. David Patterson 154 , 352 140 Tay-Sachs Disease 320 Victoria A. Harden Bradford Towne 155 Typhus, Murine 355 141 Tetanus 323 Victoria A. Harden Robert J. T. Joy 156 Typhus, Scrub (Tsutsugamushi) 355 142 Tetanus, Neonatal 326 Victoria A. Harden Sally McMillen 157 Urolithiasis 357 143 Tetany 328 R. Ted Steinbock Kenneth F. Kiple 158 144 Toxoplasmosis 330 Varicella-Zoster Virus Disease (Chickenpox) 359 K. David Patterson R. H. Kampmeier 145 Trematode Infection 331 K. David Patterson 159 Whooping Cough 360 Anne Hardy 146 Trench Fever 331 Victoria A. Harden 160 Yaws 362 Don R. Brothwell 147 The Treponematoses 331 Kenneth F. Kiple 161 Yellow Fever 365 Donald B. Cooper and Kenneth F. Kiple 148 Trichinosis 333 Donald E. Gilbertson Index 371

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1. Acquired Immune Deficiency intravenous drug users were at greatest risk. Re- Syndrome (AIDS) search focused on searching for an infectious agent transmitted sexually or through blood. In Acquired immune deficiency syndrome 1983, in French and American laboratories, an (AIDS), first identified in 1981, is an infectious unknown human retrovirus was identified and disease characterized by failure of the body’s named HIV-1 for “human immunodeficiency immunologic system. Affected individuals be- virus.” Although the biological and geographic come increasingly vulnerable to many normally origins of the organism remain obscure, the harmless microorganisms, eventually leading AIDS epidemic appears to mark the first time to severe morbidity and high mortality. The in- it has spread widely in human populations. No fection, spread sexually and through blood, has evidence exists for casual transmission of HIV. a high fatality rate, approaching 100 percent. Following identification of HIV-1, tests to de- Caused by a human retrovirus known as HIV-1, tect antibodies against it were devised in 1984. AIDS can now be found throughout the world – Although these tests do not detect the virus in both industrialized countries and developing itself, they are generally effective in identify- nations. Public-health officials throughout the ing infection because high levels of antibody world have focused attention on this are produced in most infected individuals. The and its potentially catastrophic impact on enzyme-linked immunosorbent assay (ELISA), health, resources, and social structure. Treat- followed by Western blot testing, has enabled ments for the disease have been developed, but the screening of donated blood to protect the no cure or vaccine currently exists. blood supply from HIV, as well as testing for epi- demiological and diagnostic purposes. Characteristics As HIV infection precedes the development Beginning in the late 1970s, physicians in New of AIDS, often by several years, the precise pa- York and California reported increasing in- rameters of the epidemic have been difficult cidence of a rare cancer, Kaposi’s sarcoma, to define. Although “cofactors” that may deter- and a variety of infections including pneumo- mine the onset of symptoms remain unknown, cystis pneumonia among previously healthy evidence suggests that HIV-infected individuals young homosexual men. Because of the un- will eventually develop AIDS. usual character of these diseases, which are typ- Researchers have identified three epidemi- ically associated with failure of the immune ological patterns of HIV transmission, which system, epidemiologists began seeking clues roughly follow geographic boundaries. Pattern that might link these cases. AIDS was first for- I includes North America, Western Europe, mally described in 1981, although it now ap- Australia, New Zealand, and many urban cen- pears that the virus causing the disease was ters in Latin America. In these industrial, highly silently spreading in a number of populations developed areas, transmission has been pre- during the previous decade. Early epidemiolog- dominantly among homosexual and bisexual ical studies suggested that homosexual men, men. Since the introduction of widespread blood recipients (especially hemophiliacs), and blood screening, transmission via blood in

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1. Acquired Immune Deficiency Syndrome (AIDS)

these areas now occurs principally among HIV cripples the body’s immunologic sys- intravenous drug users who share injection tem, making an infected individual vulnerable equipment. Although little evidence exists of to other disease-causing agents in the environ- widespread infection among heterosexuals in ment. The most common of these opportunistic these countries, heterosexual transmission from infections in AIDS patients has been pneumo- those infected intravenously has increased, cystis pneumonia, previously seen principally leading to a rise in pediatric cases resulting from in patients receiving immunosuppressive drugs. perinatal transmission. In addition to pneumocystis, AIDS patients are Within the United States, distribution of AIDS prone to other infectious agents such as cy- has been marked by disproportionate repre- tomegalovirus, Candida albicans (a yeastlike sentation of minorities and the poor. As the fungus), and Toxoplasma gondii (a protozoan principal mode of transmission has shifted to parasite). Moreover, a resurgence of tuberculo- intravenous drug use, AIDS has increasingly be- sis has been reported in nations with high AIDS come an affliction of the urban underclass. Sur- incidence. veys reveal that 50 percent or more of intra- Immunologic damage occurs by depletion of venous drug users in New York City are infected a specific type of white blood cell called a helper with HIV. Women are typically infected by in- T4 lymphocyte. Destruction of these cells ac- travenous drug use or by sexual contact with a counts for the vulnerability to normally harm- drug user. less infectious agents. In some cases, infection of In pattern II countries, comprised of the central nervous system with HIV may cause sub-Saharan Africa and, increasingly, Latin damage to the brain and spinal column, result- America, transmission of HIV occurs predomi- ing in severe cognitive and motor dysfunction. nantly through heterosexual contact. In some In its late manifestations, AIDS causes severe urban areas in these countries, up to 25 percent wasting. Death may occur from infection, func- of all sexually active adults are reported to tional failure of the central nervous system, or be infected, and a majority of female prosti- starvation. tutes are seropositive. Transfusion remains a HIV infection has a wide spectrum of clini- mode of transmission because universal blood cal manifestations. After infection, an individ- screening is not routine. Unsterile injections ual may remain free of symptoms for years, and medical procedures may also contribute to even a decade or longer. Some individuals ex- the spread of infection. In these areas, perinatal perience fever, rash, and malaise at the time of transmission is an important aspect of the infection when antibodies are first produced. epidemic. Patients commonly present with general lym- Pattern III countries, including North Africa, phadenopathy, weight loss, diarrhea, or an op- the Middle East, Eastern Europe, Asia, and portunistic infection. Diagnosis is confirmed by the Pacific, initially experienced less morbidity finding antibodies for HIV or by a decline in T4 and mortality from the pandemic. Apparently, cells. Most experts now agree that HIV infec- HIV-1 was not present in these areas until the tion itself be considered a disease, regardless of mid-1980s. The nature of world travel, however, symptoms. has diminished the significance of geographic Because the virus becomes encoded within isolation as a means of protecting a population the genetic material of the host cell and is highly from contact with a pathogen. mutable, the problem of finding safe and ef- In 1985, a related virus, HIV-2, was discov- fective therapies has been extremely difficult. ered in West Africa. Although early reports sug- Studies have attempted to determine the anti- gested that HIV-2 is less pathogenic, the natural HIV properties of many drugs, but the ethical history of this agent remains unclear, as does its and economic obstacles to clinical trials with prevalence. experimental drugs are formidable. Given the

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immediacy of the epidemic, it is difficult to ease and had focused its resources and attention structure appropriate randomized clinical tri- on systemic, noninfectious ailments. Thus, AIDS als, which often take considerable time, to as- appeared at a historical moment comprising lit- sess the safety and efficacy of a drug. Since tle social or political experience in confronting the beginning of the epidemic, clinical research such a public-health crisis. The epidemic frac- has refined the treatment of opportunistic tured a widely held belief in medical security. infections. Not surprisingly, early sociopolitical re- sponses were characterized by denial. Initial History theories, when few cases had been reported, In its first decade, AIDS created considerable centered on aspects of “fast-track” gay sex- suffering and generated an ongoing worldwide ual culture that might explain the outbreak health crisis. During this brief period, the epi- of immune-compromised men. Additional cases demic was identified and characterized epi- among blood recipients, however, soon led the demiologically, basic modes of transmission U.S. Centers for Disease Control and Preven- specified, a causal organism isolated, and effec- tion to the conclusion that an infectious agent tive tests for infection developed. In spite of this was the likely link. Nevertheless, in the earli- remarkable progress, which required the appli- est years of the epidemic, few wished to con- cation of sophisticated epidemiological, clini- front openly the possibility of spread beyond cal, and scientific research, the barriers to con- the specified “high-risk” groups. During this pe- trolling AIDS are imposing and relate to the riod, when government interest and funding most complex biomedical and political ques- lagged, grassroots organizations, especially in tions. AIDS has already sorely tested the capa- the homosexual community, were created to bilities of research, clinical, and public-health meet the growing need for education, counsel- institutions throughout the world. ing, patient services, and – in some instances – Because HIV is related to other recently iso- clinical research. Such groups worked to over- lated primate retroviruses, such as simian T lym- come the denial, prejudice, and bureaucratic in- photropic virus (STLV)-III in African green mon- ertia that limited governmental response. keys, many have speculated that HIV originated As the nature and extent of the epidemic in Africa. Antibodies to HIV were discovered became clearer, however, hysteria sometimes in stored blood dating back to 1959 in Zaire. replaced denial. Because the disease was pow- According to experts, it is likely that HIV has erfully associated with behaviors identified as existed for many years in isolated groups in immoral or illegal (or both), the stigma of those central Africa. Because outside contacts were infected was heightened. Victims were often di- minimal, the virus rarely spread, and vided into categories: those who acquired their could not be sustained. Once a sizable reservoir infections through transfusions or perinatally, of infection was established, however, HIV be- the “innocent victims”; and those who engaged came pandemic. As with other sexually trans- in high-risk, morally condemnable behaviors, mitted diseases, such as syphilis, no country the “guilty perpetrators” of disease. Since the wished the stigma of association with the virus’s early recognition of behavioral risks for infec- “origin.” tion, there has been a tendency to blame those The epidemic began at a moment of rela- who became infected through drug use or ho- tive complacency, especially in the developed mosexuality, behaviors viewed as “voluntary.” world, concerning epidemic infectious disease. Some religious groups in the United States and Not since the influenza of 1918–20 had an epi- elsewhere saw the epidemic as an occasion to demic appeared with such devastating poten- reiterate particular moral views about sexual tial. The developed world had experienced a behavior, drug use, sin, and disease. AIDS was health transition from infectious to chronic dis- viewed as “proof” of a certain moral order.

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AIDS victims have been subjected to a range Because biomedical technologies to prevent of discriminatory behavior, including loss of transmission appear to be some years away, employment, housing, and insurance. Since the the principal public-health approaches to con- onset of the epidemic, violence against gays trolling the pandemic rest on education and in the United States has increased. Despite behavior modification. Heightened awareness the well-documented modes of HIV transmis- of the dangers of unprotected anal intercourse sion, fears of casual transmission persist. In among gay men, for example, has led to a signif- some communities, parents protested when icant decline in new infections among this pop- HIV-infected schoolchildren were permitted to ulation. Nevertheless, as many public-health attend school. In one instance, a family with an officials have noted, encouraging the modifica- HIV-infected child was driven from a town by tion of risk behaviors, especially those relating the burning of their home. to sexuality and drug abuse, presents no simple By 1983, as potential ramifications of the task, even in the face of a dread disease. epidemic became evident, national and inter- In the developing world, AIDS threatens to national scientific and public-health institu- reverse recent advances in infant and child sur- tions began to mobilize. In the United States, vival. The epidemic is likely to have a sub- congressional appropriations for research and stantial impact on demographic patterns. Be- education began to rise significantly. The Na- cause the disease principally affects young and tional Academy of Sciences issued a con- middle-aged adults (ages 20–49), it has already sensus report on the epidemic in 1986. A had tragic social and cultural repercussions. presidential commission held public hearings Transmitted both horizontally (via sexual con- and eventually issued a report calling for tact) and vertically (from mother to infant), it protection of AIDS sufferers against discrimina- has the potential to depress the growth rate of tion and a more extensive federal commitment human populations, especially in areas of the to drug treatment. The World Health Organi- developing world. In this respect, the disease zation (WHO) established a Global Program on could destabilize the work force and depress lo- AIDS in 1986 to coordinate international efforts cal economies. in epidemiological surveillance, education, pre- AIDS has clearly demonstrated the complex vention, and research. relationship of biological and behavioral forces Despite growing recognition of the epidemic’s in determining patterns of health and disease. significance, considerable debate continued Altering the course of the epidemic by human over the most effective public-health responses. design has already proved to be no easy matter. Although some nations – such as Cuba – The lifelong infectiousness of carriers; the pri- experimented with programs mandating iso- vate, biopsychosocial nature of sexual behav- lation of HIV-infected individuals, the World ior and drug abuse; and the stigma already at- Health Organization lobbied against coercive tached to those at greatest risk – all have made measures. Given the lifelong nature of HIV in- effective public policy intervention even more fection, effective isolation would require life- difficult. Finally, the very nature of the virus time incarceration. With the available variety itself – its complex and mutagenic nature – of less restrictive measures, most nations re- makes a short-term technological breakthrough jected quarantine as both unduly coercive and unlikely. unlikely to achieve control. Traditional public- The remarkable progress in understanding health approaches to communicable disease, in- AIDS is testimony to the sophistication of con- cluding contact tracing and mandatory treat- temporary bioscience; the epidemic, however, ment, have less potential for control because is also a sobering reminder of the limits of no means exist to render an infected individual that science. Any historical assessment of the noninfectious. AIDS epidemic must be considered provisional.

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Nevertheless, it is already clear that AIDS has of schoolteachers has developed because they forced us to confront a new set of biological are dying of AIDS faster than replacements can imperatives. be trained. Allan M. Brandt In the United States – although the millions of cases of HIV infection that had been gloomily predicted by some did not materialize – 774,647 cases were reported between 1981 and 2001, Postscript and there were 448,060 deaths. By age and By way of a caveat, recent estimates of the num- sex, the breakdown of those infected was ber of HIV/AIDS infections, the competing theo- 79 percent adult males, and by ethnicity 61 per- ries of origin, conflicting interpretations of new cent were black or Hispanic. The major avenues evidence, and announcements of therapeutic of transmission have been through male ho- and preventive progress are sometimes contra- mosexual contact (48 percent) and intravenous dictory and thus constitute especially treacher- drug abuse (26 percent), although HIV infec- ous terrain. tion via heterosexual contact – generally be- Beginning with the estimates, in June of tween infected males and uninfected females – 1990 the WHO estimated that there were some is on the rise. Today the fastest growing groups 8 million HIV cases worldwide; the following of newly infected individuals are reported to year that estimate was raised to between 10 be women and their children, and gay black million and 12 million. Toward the end of the males – the latter group accounting for 42 per- decade the WHO warned that the number of cent of all new infections. The U.S. cases are cases would reach between 20 million and 30 almost all HIV-1. Despite fears of HIV-2 also million cases by the year 2000. In retrospect, spreading in North America, only 64 cases have it seems that this estimate was much too con- been documented, and these were all directly servative; by 1997 the number of cases already linked with West Africa. exceeded 30 million. By 2001, HIV had in- Among HIV/AIDS researchers a consensus fected some 56 million individuals worldwide gradually emerged that simian immunode- and killed more than 20 million of them. Left ficiency virus (SIV) had somehow managed behind were an estimated 36 million living with to jump the species barrier from African pri- HIV/AIDS and millions more expected to be- mates (for whom it seems to be a relatively be- come infected in the early years of the twenty- nign infection) to first infect humans in Cen- first century. tral and West Africa and, somewhere along the Of the 30 million cases in 1997,almost 21 mil- line, became human immunodeficiency virus or lion were in sub-Saharan Africa alone (where HIV-1 and its subtypes (the most common form in some places, such as Botswana, upwards of worldwide) and HIV-2. 36 percent of the adult population has become Another question had to do with how the infected with HIV), while South and South- species barrier was hurdled. Again a consen- east Asia and the Pacific accounted for another sus took shape; SIV had entered the blood of 6 million cases. In all, the developing world con- Africans engaged in chimpanzee butchering, af- tained 95 percent of the cases, and in 1998 it ter which it became HIV-1 (although the pos- was estimated that 70 percent of all new infec- sibility of SIV evolving into HIV in the chim- tions and 80 percent of all AIDS deaths occurred panzee was not ruled out). Moreover, lineages in sub-Saharan Africa. By 2001, average life ex- of HIV transmitted by sooty mangabeys (also pectancy south of the Sahara had declined by called the green monkey) were believed to have 10 years and infant death rates had doubled. reached humans in like fashion to become HIV- Illustrative of the impact of AIDS mortality is 2. Some, however, suspected that medicine had the example of Zambia, where a dire shortage something to do with HIV becoming a human

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infection and, therefore, that AIDS had an iatro- the drug azidothymidine (AZT) was shown genic or medical cause. to extend the period of latency for AIDS. It is Initially, the WHO smallpox vaccination cam- one of five drugs called nucleosides licensed paign in Africa from 1967 to 1980 came un- by the U.S. Food and Drug Administration, all der scrutiny for the possibility that HIV had of which are inhibitors of the viral enzyme been propelled through countless bodies with reverse transcriptase (RT), which performs the repeated use of inadequately sterilized nee- reverse transcription – the conversion of RNA dles, or even that the vaccine had been contam- into DNA that HIV must undergo to be infec- inated. These hypotheses, of course, dealt with tive. In the second half of the 1990s, protease HIV transmission and did not really confront inhibitors (which cripple a viral enzyme vital to the question of its origin. Another hypothesis, HIV reproduction) came into use and two nu- however, did – this one focusing on the cleoside inhibitors and one protease inhibitor vaccination campaign conducted in Africa (and were blended together into what was called the elsewhere) during the late 1950s. In the (then “antiviral cocktail.” The results were miraculous. Belgian) Congo, chimpanzee kidneys were used Individuals on the verge of death were going to culture the , which in turn, it was back to jobs and resuming normal lives, the argued, could have contaminated the oral polio mortality rate from AIDS in the United States vaccine used in a widespread vaccination effort fell dramatically, and it seemed that a major during 1957–58. Buttressing the case was that battle against the disease had been won. this region subsequently became the major epi- But it was an incomplete victory, because the center of the burgeoning AIDS epidemic. Also “cocktail” can produce unpleasant side effects, bolstering it was the announcement in 1999 by and just one missed dose can give the virus a group of University of Alabama researchers the opportunity to quickly mutate into a strain that they had determined that a kind of chim- that resists the drugs. In fact, drug-resistant panzee once common in West Africa was indeed strains of HIV are already complicating AIDS the source of HIV. treatment, which has led to different combina- Yet other recent evidence was not so support- tions of “cocktail” ingredients, each of which in- ive. Most recently, in 2001, it was announced terferes with certain steps in the HIV infection that a vial of the suspected polio vaccine had process. Still other drugs have been brought been found and that analysis had revealed no effectively to bear on some of the “killer” oppor- trace of HIV. Moreover, a study published in tunistic infections such as pneumocystis pneu- 2000 in Science had already cast considerable monia and tuberculosis, which are the principal doubt on the contaminated vaccine hypothe- cause of AIDS deaths worldwide. But whether sis by showing that HIV-1 may well have been the miracle will continue indefinitely remains to present in human African populations since at be seen. The therapy is new and consequently least the 1930s – almost 30 years before the the long-term success rate is unknown. More- polio vaccination campaign in the Congo. That over, a per-patient annual cost of some 10,000– date, however, is for the time that the HIV-1 12,000 U.S. dollars limits this costly drug treat- group of viruses began to diversify, and not for ment to a relatively few victims in the devel- when they were transmitted to humans. Thus, oped world. Thus far, pressure on pharmaceu- vital questions of transmission and origin re- tical manufacturers to make low- or no-cost main unresolved – that of origin because even if drugs available to the developing world’s mil- chimpanzees did pass on HIV to humans, they lions stricken with HIV/AIDS has produced little may also have been infected from yet another in the way of results. source. Work is also being done to develop a vac- Great strides have been made recently toward cine that could be both protective by preventing the goals of treatment and prevention. In 1986, infection and therapeutic for those infected,

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2. African Trypanosomiasis (Sleeping Sickness)

by prolonging survival and decreasing immune advances made and, indeed, very little research system destruction. At the turn of the twenty- done between the 1930s and the 1980s. How- first century, vaccines were being tested that ever, in the mid-1980s field trials of a promising had proven effective in protecting monkeys new drug demonstrated its efficacy in late-stage from HIV, and large-scale trials were under disease when there is central nervous system way to test them for human safety. In addi- involvement. In addition, there have been ex- tion, Merck and Company, with its enormous re- citing recent developments in the field of tsetse sources, announced in 1999 that it would begin eradication with the combined use of fly traps human trials on two vaccines. However, pro- and odor attractants. vided that a safe vaccine does become available, the problems of administering it – especially Characteristics to the millions at high risk in the developing An acute form of sleeping sickness caused by world – are daunting because it appears that one Trypanosoma brucei rhodesiense with a short primary injection will be required, followed by incubation period of 5–7 days occurs in east- three booster shots. The good news, of course, is ern and southern Africa. A chronic form (Try- that the question seems no longer to be whether panosoma brucei gambiense) of western and there will be a vaccine, but rather when a vac- central Africa can take from several weeks to cine will be available. months or even years to manifest itself. There Moreover, gene therapy holds out promise of are many species of tsetse flies, but only six act inhibiting HIV by introducing a gene into cells as vectors for the human disease. The Glossina that interferes with the viral regulatory proteins, palpalis group, or riverine tsetse, is responsi- or even one that will protect cells from HIV in- ble for the transmission of T. b. gambiense dis- fection. But all of these measures, even when ease. The Glossina morsitans group, or savanna they do bear fruit, will probably be too late tsetse, is the vector for T. b. rhodesiense, the to stop AIDS from becoming the biggest killer- cause of the rhodesiense form of sleeping sick- disease in . ness. Although tsetse flies are not easily infected Kenneth F. Kiple with trypanosomes, once infected they remain vectors of the disease for life. After being bitten by an infected fly, most victims experience local inflammation, or the 2. African Trypanosomiasis trypanosomal chancre; parasites migrate from (Sleeping Sickness) this site to multiply in blood, lymph, tissue fluids, and eventually the cerebrospinal fluid. African trypanosomiasis,or“sleeping sick- The blood trypanosome count oscillates cycli- ness,” is a fatal disease caused by a protozoan cally, with each successive wave, manifesting hemoflagellate parasite, the trypanosome. It is different surface antigens. In this manner, try- transmitted through the bite of a tsetse fly, a panosomes evade the antibodies raised against member of the genus Glossina. Sleeping sick- them by the host. Eventually, all organs are ness is endemic, sometimes epidemic, across a invaded, with central nervous system involve- wide band of sub-Saharan Africa, the so-called ment, ultimately leading to death. tsetse belt that covers some 11 million square The epidemiological pattern of sleeping sick- kilometers. Although the disease was not sci- ness varies considerably from place to place, entifically understood until the first decade of but two features are well recognized. First, the twentieth century, it had been recognized in trypanosomiasis is exceptionally focal, occur- West Africa as early as the fourteenth century. ring at or around specific geographic loca- Chemotherapy to combat trypanosomiasis tions; and second, the number of tsetse flies has remained archaic, with no significant is apparently not as important for disease

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incidence as is the nature of the human-fly voirs in the eastern African savannas. In the case contact. of T. b. rhodesiense, the usual mammalian hosts The focal nature of sleeping sickness means are wild ungulates, with humans as adventitious that the ecological settings in which it occurs hosts. Transmission of rhodesiense disease is are of vital importance for understanding its more haphazard and directly relates to occupa- epidemiology. Seemingly impossible to destroy, tions such as searching for firewood, hunting, many historical foci tend to flare up in spite fishing, honey gathering, poaching, cultivation, of concentrated eradication efforts since the cattle keeping, and being a game warden or a 1930s. Very often, villages and regions that were tourist. Whereas the gambiense form of the dis- affected decades ago remain problem areas to- ease is site related, the rhodesiense form is occu- day. The disease involves humans, parasites, pation related, which helps to explain why the tsetse flies, and wild and domesticated animals, latter characteristically affects many more men and increasing population movements have and boys than women and girls. However, when complicated the epidemiology. Tsetse species a community moves near bush infested with in- have varying food preferences, ranging from the fected flies, the entire population is at risk. blood of wild and domestic animals to that of The animal reservoir of trypanosomes is an humans, but they require a daily blood meal, important factor in the epidemiology and his- thereby making a single fly potentially highly tory of sleeping sickness. It is well established infective. that the trypanosomiases are ancient in Africa. Gambiense sleeping sickness is classically Indeed, it is conjectured that the presence of a disease of the frontier of human environ- sleeping sickness may explain why the ungulate ments, where human-created habitat meets syl- herds of the African savanna have survived van biotope. Humans are the principal reservoir human predators for so long; the wild-animal of T. b. gambiense, and they maintain the typical reservoir of trypanosomes firmly restricted the endemic cycle of the disease. It is now known, boundaries of early human settlement. Al- however, that some animals, including domestic though the wild ungulate herds became trypo- pigs, cattle, sheep, and even chickens, can act as tolerant, domestic cattle still succumb to the reservoirs. The key to understanding the gam- disease, and the vast majority of research and biense form is its chronicity and the fact that funding has been aimed at solving the problem there are usually very low numbers of parasites of animal – not human – sleeping sickness. present in the lymph and other tissue fluids. In evolutionary terms, the presence of try- Gambiense disease can be maintained by a mere panosomes in Africa may have precluded the handful of peridomestic flies – that is, those that development of some ground-dwelling faunas, have invaded bush or cultivations near human thus encouraging certain resistant primates, in- settlements. This is known as close human-fly cluding the early ancestors of humankind, to contact. fill the empty ecological niches. If so, then hu- Riverine G. palpalis are most commonly mans were exposed to trypanosomal infection found near waterways and pools; during dry at the time of their very remote origin. The par- seasons, when humans and flies are brought asites are on the whole poorly adapted to hu- together through their shared need for water, mans, which accounts for the variety of clinical the flies become particularly infective. Other symptoms and ever-changing epidemiological common foci for the disease are sacred groves, patterns. A perfectly adapted parasite does not which are often small clearings in the forest kill its host – at least in the short run. where the high humidity allows the flies to ven- An estimated 50 million people in 42 coun- ture farther from water sources. tries are at risk for trypanosomal infection, while The virulent rhodesiense sleeping sickness is it is estimated that only about 5 million to 10 a true zoonosis maintained in wild animal reser- million people have access to some form of

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protection against or treatment for the disease. derives its name. Some of the initial symp- Sleeping sickness is endemic across the wide toms of sleeping sickness are also character- band of sub-Saharan Africa known as the “tsetse istic of early malaria, which can make dif- ◦ ◦ belt” lying roughly between 20 north and 20 ferentiation between the two diseases diffi- south of the equator, where it also can attain cult in the field. A common, easily recogniz- epidemic proportions. able symptom is swelling of lymph nodes. An- The actual number of cases will never be other common symptom is called “moon face,” known, as it is a disease of remote rural ar- an edema caused by leaking of small blood eas, and even today people in such places of- vessels. A most common complication dur- ten die undiagnosed and uncounted. Most na- ing trypanosomiasis is pneumonia, which is tional statistics are grossly underreported, with a frequent cause of death. The chronic gam- the World Health Organization being notified biense form can take as long as 15 years to of about only 10 percent of new cases. The cur- develop after the victim has left an endemic rent estimate of incidence is 20,000 to 25,000 area. cases annually. Most of the victims are concen- The prospect of a vaccine for human trated in Zaire, Uganda, and southern Sudan. trypanosomiasis is bleak. The phenomenon Some villages had infection rates of up to 25 of “antigenic variation” greatly reduces the percent. In the late 1970s and 1980s, severe prospect of producing an effective vaccine, and outbreaks occurred in Cameroon, Angola, the at present very little research is under way on Central African Republic, the Ivory Coast, and vaccine development. Tanzania, as well as in Sudan, Zambia, Uganda, and Zaire. History Although trypanosomiasis has been studied The history of sleeping sickness in Africa is long for more than 80 years, much is still unknown and complex, and its complicated ecology has about the pathology of the disease. Three dramatically affected demographic patterns in phases follow the bite of an infected fly: first the sub-Saharan Africa. The parameters and den- chancre itself; then the hemolymphatic or “pri- sity of human settlement have been limited mary stage”; and finally the meningocephalitic in many regions until the present time, while or “secondary stage.” On average, people in- cattle-keeping has been prevented across vast fected with T. b. gambiense live 2–3 years before regions of the continent, thereby seriously af- succumbing, although there are recorded cases fecting the nutrition of entire populations. of infection spanning as much as 2 decades. In The “African lethargy,” or “sleepy distemper,” contrast, infection with the more virulent T. b. as trypanosomiasis has been called, was well rhodesiense, if untreated, usually leads to death known to Europeans in West Africa from as early within 6–18 weeks. as the fourteenth century, through good de- The disease manifests a bewildering array of scriptions given by Portuguese and Arab writ- clinical symptoms, which can vary from place ers. For centuries slave traders rejected Africans to place. Progressing through the two stages, with the characteristic swollen cervical glands, there is increasing parasitemia with eventual in- for it was common knowledge that those with volvement of the central nervous system. Clini- this symptom sooner or later died in the New cal symptoms can include fever, headache, and World or North Africa. As European explo- psychiatric disorders such as nervousness, iras- ration and trade along the West African coast cibility, emotionalism, melancholia, and insom- increased between 1785 and 1840, the disease nia, which reflect neuronal degeneration. Other was reported in Gambia, Sierra Leone, and west- symptoms include loss of appetite, gross emaci- ern Liberia, whereas between 1820 and 1870 it ation, sleep abnormalities, stupor, and the char- was also commonly noted along the Liberian acteristic coma from which sleeping sickness coast.

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Certainly the disease was an important factor tific research teams were dispatched to study in the history of colonial Africa. In the begin- sleeping sickness. They began with the Liver- ning, colonial administrators were concerned pool School of Tropical Medicine’s expedition to mainly with the health of Europeans and those Senegambia in 1901 and the Royal Society’s ex- few Africans in their service. But the threat of pedition to Uganda in 1902; other expeditions epidemics of sleeping sickness eventually forced followed until World War II. colonial authorities to take much more seri- Many of these were sent by new institutions ously the health of entire African populations. especially designed to investigate the exotic dis- In those colonies affected by sleeping sick- eases of warm climates. The British, for example, ness, medical services often developed in di- opened schools of tropical medicine at Liverpool rect response to this one disease, which re- and London in 1899, while other such schools sulted in the development of “vertical” health came into being in Germany, Belgium, France, service – programs aimed at controlling a Portugal, and the United States. This new field specific disease while neglecting other crucial of scientific endeavor offered the opportunity public health issues. As recently as the 1970s, for bright young men to gain international the World Health Organization urged de- acclaim and a place in the history of medicine. veloping countries to move toward “hori- It should be noted that sleeping sickness was zontal” health services that take into ac- not the only disease to receive such attention count the multifactoral nature of disease and as Europeans sought to establish themselves health. permanently in regions of the globe where Sleeping sickness, along with malaria and yel- health conditions were difficult and mortality low fever, played an important role in the de- was high. There were major discoveries by Man- velopment of the new specialties of parasitology son, who was the first to demonstrate insects and tropical medicine. In 1898, Patrick Manson, as vectors of human disease (filariasis); and by the “father of tropical medicine,” published the Ronald Ross, who found that the malaria para- first cogent discussion of the new scientific dis- site was transmitted by the Anopheles mosquito. cipline. He explained that tropical diseases were Yet, despite the fact that endemic malaria was very often insect-borne parasitical diseases, the probably the cause of far more morbidity, the chief example being trypanosomiasis. trypanosomiases attracted much attention in Trypanosomiasis at the time was very much the new field of tropical medicine for the next 2 on the minds of colonial officials. In the decade or 3 decades. between 1896 and 1906, devastating epidemics International meetings were convened to dis- killed more than 250,000 Africans in the new cuss sleeping sickness, beginning with one at British protectorate of Uganda, as well as an es- the British Foreign Office in 1907. As the num- timated 500,000 residents of the Congo basin. ber of “tryps” specialists increased, sleeping Understandably, the new colonial powers, in- sickness became a key factor in the interna- cluding Britain, France, Germany, Portugal, and tional exchange of research findings in tropi- King Leopold´ ’s Congo Free State, perceived cal medicine. The Sleeping Sickness Bureau was sleeping sickness to be a grave threat to African opened in London in 1908 to facilitate commu- laborers and taxpayers, which in turn could dra- nication of research findings on all aspects of matically reduce the utility of the new territo- the disease. Its work continues to the present ries. Moreover, the fears were not limited to the time. continent of Africa; the British also speculated After World War I and the formation of that sleeping sickness might spread to India, the the League of Nations’ Health Organization “jewel” of their empire. (the antecedent of the World Health Organiza- Thus ensued one of the most dramatic cam- tion), two major conferences in 1925 and 1928 paigns in the history of medicine, as scien- were convened to focus on African sleeping

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sickness. These conferences, following the pat- not occur to the intruders that in many cases tern of the nineteenth-century sanitation and Africans were withdrawing from areas because hygiene conferences, sought international col- of the brutal nature of colonial conquest. Half a laboration and cooperation in implementing century would pass before researchers began to public-health solutions. In Africa, special re- examine the deeper socioeconomic and political search centers on tsetse flies and sleeping causes of the dramatic changes in the African sickness appeared in many colonies includ- disease environment that had resulted in the ing Uganda, Kenya, Tanganyika (now Tanzania), spread and increased incidence of sleeping Belgian Congo (Zaire), Nigeria, Ghana, and sickness. French Equatorial Africa (Chad, Central African Medical experts at the turn of the nine- Republic, Congo-Brazzaville, and Gabon). Sleep- teenth century tended to favor the theory of ing sickness thus became an important catalyst circumstantial epidemiology, which held that for cooperation among the colonial powers in diseases were spread mainly through human Africa, which in turn aided the rapid growth agency within specific sets of circumstances. of tropical medicine as a field. In fact, sleeping Because of a lack of effective treatments, the sickness early in the twentieth century attracted principal methods of control of epidemic dis- international attention to Africa with an ur- ease consisted of segregation or isolation and gency that was repeated in the early 1980s with disinfection with acrid smoke or strong fumes AIDS. such as sulfur and vinegar. Disease was per- Response to the disease occurred within the ceived as an invader to be demolished. This private sector as well. Concerned at the possible view accounts for much of the imagery and loss of increasingly important African markets, idiom of war used in early public-health cam- the European business community encouraged paigns. A major adjunct to this theory was the and sometimes initiated research into tropical belief that once the circumstances had been diseases. For example, the principal founder of identified, most diseases in Africa could and the Liverpool School of Tropical Medicine in would be controlled, even eliminated, with tech- 1899 was the influential and powerful capital- niques and technology developed in Europe. ist Alfred Lewis Jones, chairman of a Liverpool- The European colonials assumed they would based shipping line that plied a lucrative trade succeed where Africans had failed and that along the West African coast. The businessman they would transform the continent by con- shared the imperialist’s dismay at the poten- quering the problems of tsetse and the try- tial devastation that could be caused by sleep- panosome, among others. Most colonists be- ing sickness, and together they were keen to lieved that much of the backwardness they support attempts to prevent the decimation of saw in African society was attributable, at least African populations. in part, to endemic diseases such as sleeping The politics of colonialism often reflected sickness. contemporaneous perceptions of the epidemiol- Powerful notions of the potential of West- ogy of sleeping sickness. By 1900, for example, it ern technology for solving health problems in was widely accepted that the disease had been Africa, sleeping sickness among them, have endemic in West Africa for centuries but had survived until quite recently. Rarely, if ever, only recently begun spreading into the Congo did colonial authorities consider the possibil- basin and eastward. ity that Africans not only possessed some ideas From the earliest days of colonial settlement, about the ecology of sleeping sickness but had it was not uncommon to blame sleeping sick- gained fairly effective control of their environ- ness for the abandoned villages and depopu- ment. An example of one such African strat- lated regions that Europeans encountered dur- egy was the warnings to early European travel- ing their push into the interior. It usually did ers not to travel through certain regions during

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daylight hours when tsetse flies were active and mans, tsetse flies, and trypanosomes were dis- might infect their transport animals. Moreover, rupted by European activities with the result throughout the tsetse-infested regions, there that endemic sleeping sickness flared into epi- were instances of African residence patterns demic proportions. Vivid examples of the re- that allowed coexistence with the ubiquitous sults of such ecological upheaval were the tsetse flies yet avoided population concentra- sleeping sickness epidemics in Uganda and tions conducive to epidemic outbreaks. Euro- the Congo basin that had killed hundreds of pean colonizers, by contrast, often disrupted – thousands. or destroyed – indigenous practices and sur- Epidemics continued throughout much of the vival strategies with the result that endemic colonial period, especially prior to World War sleeping sickness spread and sometimes became II, when there were serious outbreaks in both epidemic with disastrous effects. West and East Africa. Public-health regulations The colonial powers, however, held their own to control the disease affected other areas of version of the history of sleeping sickness and administration. In some colonies, sleeping sick- its evolution. Prior to their arrival, ancient, in- ness programs became so extensive and bu- tractable foci of the disease had existed in West reaucratic that they came into conflict with Africa and in the Congo basin around which, other departments, exacerbating competition from time to time, the disease would flare into for scarce staffing and financial resources within epidemic proportions. Colonials believed that colonial administrations. In addition, sleeping it really began to spread only after the Euro- sickness regulations were often responsible for pean newcomers had suppressed local wars and confrontations between the private and public slave raiding among African peoples and estab- sectors as members of the former were increas- lished law and order. This in turn allowed many ingly hindered in their attempts to exploit the Africans, for the first time ever, to move freely people and resources of Africa. and safely away from their home regions. Pro- Two major patterns emerged in the colonial tected by Pax Brittannica, Pax Belgica, and the campaigns against sleeping sickness. In one, like, the increased movements of Africans car- the focus was on tsetse eradication, whereas in ried sleeping sickness from old endemic foci to the other, the focus was on the medicalization new populations. There was some basis for this of victims. Most campaigns were a combination hypothesis, especially in West Africa such as in of features from both approaches. Within this Ghana and Rukuber of Nigeria. This widely ac- framework, national variations emerged in cepted notion of the spread of sleeping sick- the colonial campaigns. The British took a ness had an important consequence in the enor- more broadly ecological approach to control mous effect expended by the Europeans in of the disease, whereas the French and the trying to regulate African life at every level, Belgians took a more “medical” approach to and especially to limit strictly any freedom of the problem of human infection. British policy movement. was to break the chain of sleeping sickness John Ford, a British entomologist who spent transmission by separating people from flies. more than 25 years researching sleeping sick- Thus, while British administrators implemented ness, was one of the first to challenge this social policies aimed at protecting people from “classical view” of the pacification of Africa disease, the scientific community, especially and the spread of the disease. He argued the new entomologists, searched for solutions that it was not the pacific character of Eu- to the “tsetse fly problem” in Africa. The com- ropean colonization but, on the contrary, pulsory mass resettlement of Ugandans, which its brutal nature, that greatly disrupted and probably helped save lives, from lakeshore stressed African populations. In particular, the communities in Buganda and Busoga in 1908, balanced ecological relationships among hu- and the huge Anchau (northern Nigeria)

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scheme begun in 1936 are good examples the effect of removing the store of antibodies of breaking transmission chains. Likewise, from humans that had been built up through in some regions where it was ecologically long contact with the parasites. feasible, Belgians resettled groups of people Sterilization of the human reservoir was made such as those along the Semliki River in eastern possible in 1905 when the first trypanocidal Congo. drug became available in the form of an ar- Unfortunately, in the context of recently con- senical compound, atoxyl. Discovered by the quered and colonized Africans, who had rural German chemist Paul Ehrlich and adapted subsistence economies and whose culture and for use with sleeping sickness by Wolferstan tradition were intricately linked to locale, com- Thomas of the Liverpool School of Tropi- pulsory relocation sometimes had calamitous cal Medicine, atoxyl, alone or in combina- effects on those it was meant to protect. In the tion with other compounds, remained the only Belgian Congo an extraordinary amount of leg- chemotherapy for 2 decades. Atoxyl was toxic islation and effort was directed at the control of for 38 percent of patients, with dreadful side ef- populations in relation to sleeping sickness. It fects suffered by those whom it did not kill out- is not surprising that many Africans regarded right, among them the blinding of 30 percent sleeping sickness as the colonial disease be- of those injected. Later, new drugs – suramin cause of the sometimes overwhelming amount (1916-20), tryparsamide (1919–25), and pen- of administrative presence it elicited. tamidine (early 1940s) – came into use for early- French and Belgian efforts were directed stage rhodesiense and gambiense disease. An- chieflyat“sterilizing the human reservoir” of other most problematic arsenical with serious trypanosomes through mass campaigns of med- side effects, including up to 5 percent mortal- icalization, or injections. To achieve this, they ity, was and is used for second-stage disease. conducted systematic surveys of entire pop- This drug, melarsoprol (along with suramin and ulations, hoping to locate, isolate, and treat pentamidine), has remained the drug of choice all victims. Eugene` Jamot, a French parasitolo- since the 1940s. gist, developed this method in Ubangui-Chari In the early 1960s, which saw independence (French Equatorial Africa) and later introduced for many African territories, colonial rulers con- it in affected parts of Cameroon and French curred that human sleeping sickness was under West Africa. In 1916, he organized an am- control in Africa. But political upheavals, accom- bitious sleeping sickness campaign based on panied by the breakdown of medical infrastruc- mobile teams, which systematically scoured tures and large-scale population displacements, the country for victims of the disease to be once again seriously affected the epidemiology injected. of the disease. Some countries – Zaire, Uganda, A grid system was devised to ensure com- Sudan, and Ivory Coast, for instance – witnessed plete surveys, and the mobile teams worked epidemics of sleeping sickness, and it has been with true military efficiency. Between July 1917 estimated that by 1969 there were up to and August 1919, more than 90,000 individu- 1 million victims in the Congo alone. als had been examined, and 5,347 victims were Tsetse flies and the trypanosomes that cause identified and treated. Jamot’s design for a sleep- sleeping sickness will continue actively to shape ing sickness service was soon adopted by the the future of humankind in Africa. Because the Belgians in the Congo, and by 1932 there were most effective means of control is continual and five such teams operating annually in northern thorough surveillance, present-day health plan- Congo alone. Admirable as it was for its sheer ners and administrators must be aware of the scale of organization, the policy of mass medi- history of this disease and the ease with which calization did not affect the fundamental ecol- that history can repeat itself. ogy of the parasites; indeed, this approach had Maryinez Lyons

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