players—such as the German scientists, British officials, Ziba royalty, Rundi or Bwari commoners, Belgian doctors, or Ssese islanders in my case studies—interacted to shape anti–sleeping sickness measures.
Following Frederick Cooper’s conceptualization of colonial power as “arterial … concentrated spatially and socially … and in need of a pump to push it from moment to moment and place to place,” I argue that sleeping sickness provided just such a “pump” for the movement of new energy and resources into rural communities in the Great Lakes region, but that unpredictable points of friction and openness within African life shaped its ultimate direction and impacts.6 The individual and communal goals and ethics of diverse stakeholders sometimes aligned to produce the programs that European policymakers envisioned, but sometimes tilted so drastically in another direction as to require a fundamental reconceptualization of colonial public health practice. In this early era of colonial civilian administration, amid processes of engagement, negotiation, contestation, and accommodation, populations living around Lake Victoria and Lake Tanganyika asserted their own moral politics and therapeutic judgements to shape sleeping sickness control. The situated, spatial dynamics of interlacustrine intellectual worlds—their place-centered politics, therapies, mobilities, and social relations—fundamentally defined the field within which colonial interventions took place.7
At the center of this study is sleeping sickness. From a biomedical standpoint, sleeping sickness, known today as human African trypanosomiasis, is an infection caused by two different trypanosome parasites (Trypanosoma brucei rhodesiense and T. b. gambiense). It is transmitted exclusively by several species of a biting fly (Glossina spp.) known widely as tsetse. Human African trypanosomiasis caused by either subspecies of parasite is generally fatal when untreated. It is, importantly, a disease of two stages; a person may not know that they have been infected for weeks, if not months, after being bitten by a fly. The first stage of illness, following transmission of the parasite by an infected fly, involves fever, malaise, local swelling of the eyelids and face, headache, and gland inflammation as the parasite becomes established in the blood, lymph, and other tissues. Inflammation of the cervical lymph glands on the back of the neck, known as Winterbottom’s sign, has been considered a telltale sign of the disease for centuries. As the parasite moves into the central nervous system and causes inflammation, “progressive neurological disturbances” appear, manifesting in changes in behavior and mood, tremors in the fingers and tongue, difficulty walking, wasting and weakness, and deeply disrupted sleep patterns. Disrupted nighttime sleep and excessive 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
