The Politics of Disease Control. Mari K. Webel
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daytime sleepiness, culminating in a coma-like inability to be awakened, characterize late stages of infection and give the disease its colloquial name.8 The parasites causing human disease, T. b. gambiense and T. b. rhodesiense, cannot be differentiated by appearance during microscopic examination, but cause radically different clinical manifestations of disease.9 Clinicians distinguish them by the speed of their progress to second-stage illness and death. T. b. rhodesiense causes the acute form of disease, moving swiftly, with outward signs of advanced disease appearing as early as two months after infection, and an average duration absent treatment of around six months until death. T. b. gambiense presents, by contrast, as a chronic illness, with a slow progress and an average of around two years absent treatment before coma and death.10 The two parasites have different and distinctive geographic distribution on the African continent. Historically limited in their spread to the north by the Sahara Desert, T. b. rhodesiense has predominated across southern and eastern Africa, while T. b. gambiense has predominated in western and central Africa, with possible convergence points at Lake Victoria. Species of flies that transmit the disease prefer two common ecologies in eastern Africa—either the damp environments and thick vegetation found near many bodies of water or in forests (riverine tsetse or forest-dwelling tsetse) or the dense grasses and brush of open grasslands (savannah tsetse). Cattle and wild ruminants are important reservoirs for T. b. rhodesiense and implicated in outbreaks of human illness, but no nonhuman reservoir exists for T. b. gambiense.11 This consensus about the etiology and transmission of sleeping sickness has evolved over the course of the twentieth century. During the period discussed in this book, however, neither Africans nor Europeans understood the illness consistently on these biomedical terms.
RECONSIDERING SLEEPING SICKNESS CONTROL AND COLONIAL PUBLIC HEALTH
We now understand that epidemic sleeping sickness exploded in communities around Lake Victoria and Lake Tanganyika at the turn of the twentieth century, concomitant with apparently unprecedented mortality—an estimated 250,000 people purportedly died around Lake Victoria alone—before 1920. Parallel epidemics in the Congo River basin killed hundreds of thousands of people.12 The epidemic followed several difficult decades for the region’s populations, during which internal political conflict, drought, famine, cattle disease, sand fleas (Tunga penetrans) and other epidemics struck in succession, preceding and alongside European colonial incursion.13 The wide extent of sleeping sickness across regions of eastern and central Africa in the late 1890s connected to new, extractive colonial economies and the widespread disruption of ecological and agricultural circumstances brought by the imposition of European colonial rule. Across a wide territory, African political authorities acted to cope with this seemingly new form of misfortune and severe illness. In 1902, British scientists at work in Uganda identified the causative parasite and fly carrier. Thereafter, with rising fears of the impact of sleeping sickness on colonial economies, European colonial administrations kicked prevention and control campaigns into high gear.
Between 1902 and 1914, German, British, and Belgian colonial authorities in the Great Lakes region imposed myriad measures to try to control the disease’s spread. Anti–sleeping sickness measures were European authorities’ first attempts to focus specifically on African health as part of wider colonial health concerns, in contrast to attending primarily to European survival in the tropics in the prior decades.14 These measures ranged widely, from the forced depopulation of the lakeshores to the local eradication of crocodiles to experimental chemotherapies to the deforestation of fly habitats to the internment of the sick in isolation camps. Colonial authorities sought to alter how African communities fished, farmed, hunted, traveled, and sought healing, often under coercion and sometimes by force. Anti–sleeping sickness measures took place concurrently with increasingly strong assertions of colonial influence in royal politics, pressure to cultivate cash crops, and efforts to enumerate and locate populations to facilitate taxation and control mobility. Likewise, they occurred amid increasingly frequent efforts on the part of targeted populations to evade the brunt of such political and economic impositions. Sleeping sickness prevention and control measures differed across colonial regimes, but all involved strategies aimed at breaking the cycle of transmission by limiting contact between humans and flies.15 Prior to World War I, there was no durable pharmaceutical cure for sleeping sickness and the drugs being tested had serious and sometimes deadly side effects. Drug treatments that were later developed were often toxic and difficult for patients to endure.16 The majority of people infected with trypanosome parasites ultimately died. After the 1920s, mortality rates seemed to drop off precipitously across Africa for several decades, before the disease roared back to life among the rural African poor in the 1970s and 1980s.17
Epidemic sleeping sickness is often understood as a great rupture in turn-of-the-century Africa. Both the disease and colonial responses to it had significant and enduring impacts on African lives and livelihoods. While I, too, share an interest in understanding the nature and extent of the disruption that the epidemics in the Great Lakes region caused, diverse evidence indicates that these epidemics also had strong continuities with past experiences and illnesses. Widespread illness and death in new forms may have shaken communities deeply, but people did not meet either at a standstill. In this book, I seek to disrupt and expand our histories of sleeping sickness by orienting around affected communities and how they responded to and made sense of illness amid colonial control measures. I center key local contexts of colonial public health—place, politics, and mobility—in examining how sleeping sickness prevention measures functioned. Each requires attention to a deeper past. People living on the shorelines of the Great Lakes drew on intellectual and practical resources based on past experiences and utilized established strategies to address widespread illness. Interlacustrine societies’ ideas, practices, and strategies, in turn, shaped the horizons of possibility for a particular colonial intervention that is a core concern of this book: the sleeping sickness isolation camp. In the camps established by German authorities at Lake Victoria and Lake Tanganyika, colonial medical officers concentrated on identifying and diagnosing cases, isolating the sick, and experimentally treating people with a variety of drugs; camps also served as a base for work to destroy fly vector habitats, all within a wide catchment area.18 But these sleeping sickness camps had contingent, unpredictable stories, rife with negotiation, conflict, hope, misunderstanding, and shrewd calculation. Their history offers new insight on the continued importance of African intellectual worlds and of established systems of healing in how new colonial public health programs functioned.
This book argues that reorienting explorations of sleeping sickness around interlacustrine African concerns can generate productive new insights for an admittedly well-studied phenomenon in African history. Such a reorientation requires viewing sleeping sickness prevention and control from a different perspective, subordinating biomedical priorities and scientific detail to focus instead on the social, environmental, and political contexts of public health. To illustrate this shift and its consequences, consider two German colonial maps (figures I.1 and I.2) produced during the sleeping sickness epidemic. Figure I.1 is a 1907 map depicting Lake Victoria and its immediate environs and figure I.2 is a map of the northeastern littoral of Lake Tanganyika and its environs, circa 1913. Each map resulted from the combined efforts of colonial cartographers, medical researchers, and countless auxiliaries and assistants in the early twentieth century.19 The Lake Victoria map emphasizes three spaces, each roughly equidistant on the three sides of the lake in German colonial territory, and highlights known outbreaks of human illness around the northern arc of the lakeshore. Colonial borders are important on the Lake Victoria map, which draws the eye to where British Uganda and German East Africa meet as bright red hotspots, concentrations of human cases in German territory; important, too, are sketches of green along the lakeshore, depicting the range of the tsetse fly vector and suggesting the epidemic’s potential spread. A map-reader anticipates a problem—what would happen if the green and red zones should overlap?—and thus also considers the potential location of some checkpoint or intervention in those areas of impending overlap