Bug Stories

Tsetse flies carry the protozoa, called trypanosomes, that cause sleeping sickness (trypanosomiasis) in humans and domestic livestock. There are two kinds of trypanosome and two kinds of sleeping sickness, the origins and nature of which are by no means agreed upon: some think these are different environmental responses, others that the structure of the trypanosomes differs. Thus, the two kinds are either called by the names of the protozoa—Trypanosoma gambiense and Trypanosoma rhodesiense—or by the environments in which they occur, riverain and savannah. The terminologies of both types of sleeping sickness involve hosts (sometimes called the reservoir), vectors, and ecologies. The vector is the only method of disease transmission, as the trypanosome transforms in the fly’s body over several days to become infectious. In T. gambiense, infected flies live in the shade on riverbanks and feed off humans, or occasionally reptiles, and infect them; because the disease can be transmitted from human to human, it can be spread by relatively small numbers of flies. Humans are the hosts, flies the vector. In T. rhodesiense, tsetses live in wooded areas—the bush—and feed off wild animals, which do not become infected, but they can also feed off humans or domestic ungulates when they are available: wild animals are the hosts, and the flies are the vector. Entomologists—amateur and professional—have tended to ignore the protozoon for the fly and studied the behavior of various species of tsetse in order to show how different varieties of trypanosomiasis are spread and how different ecosystems encourage that spread. Sleeping-sickness control organizations in British Africa invariably included entomologists.^[11] Protozoologists, who seem to have been more influential in francophone Africa, regarded the differences between the trypanosomes as crucial and saw T. gambiense as an entirely different disease from T. rhodesiense.^[12]

The “discovery” of sleeping sickness was truly a colonial phenomenon. While the disease had been known in West Africa for centuries, its spread in the havoc of colonial conquest to previously uninfected regions—the Congo River basin and Busoga in Uganda are perhaps the most dramatic examples—created epidemics of apocalyptic proportions. The other discovery, of the cause and etiology of the disease, is one of the great stories of tropical medicine, combining all that was exotic about epidemics in Africa with all that was memorable about scientists’ and explorers’ egos.^[13] It was a discovery that would not have been possible without the scientific advances of the late nineteenth century, particularly germ theory. Germ theory made the debilitating diseases of the tropics avoidable; they were not caused by the gaseous matter of climate and decaying organisms (miasma), as had been previously thought, but by protozoa and bacteria, which could be conquered as they had been conquered in Europe.^[14] But as Maryinez Lyons has argued, germ theory had its drawbacks. If the miasma theory had related tropical diseases to their geographical location, the bacteriology and protozoology of tropical medicine alienated disease from the landscape.^[15]

But the sleeping sickness of this grand tradition was T. gambiense; the discovery—or invention, depending on whether one stands with the protozoologists or the entomologists—of T. rhodesiense was pursued with far less excitement and even some trepidation, as researchers concerned themselves with identifying an etiology and relating its cause to the trypanosomiasis of domestic stock, called nagana. T. rhodesiense was difficult to identify in part because local doctors expected humans to develop T. gambiense and in part because victims sickened and died so rapidly that Africans only identified the last stages of the disease, and then only for adults; presumably children succumbed so rapidly that sleeping sickness was confused with other afflictions. It was only in 1912 that the Luangwa Sleeping Sickness Commission, headed by investigators from the Liverpool School of Hygiene, demonstrated that the trypanosome carried by Glossina morsitans could feed off wild animals and humans alike.^[16] Research in Nyasaland and South Africa in 1913 showed that T. rhodesiense was identical to T. brucei, discovered by David Bruce in Natal in 1894, the cause of nagana.^[17] Not everyone accepted the idea that T. rhodesiense was caused by the trypanosome of wild animals and domestic livestock, but the fact shaped sleeping-sickness and tsetse-control policies in the 1930s.

In areas where T. gambiense was prevalent, attempts to control sleeping sickness became attempts to control populations—either by restricting their movements, by isolating the sick, or by removing whole villages.^[18] But areas where T. rhodesiense was prevalent were, according to the thinking of the times, areas where cattle keeping was impossible, so that attempts to control sleeping sickness became attempts to control land use and relations between humans and wild animals. There were never as many cases of T. rhodesiense in East Africa as there were of T. gambiense on the riverbanks and lake shores of East and Central Africa. T. rhodesiense was more virulent, but since it was carried from animal to human, rather than from human to human, it was far less contagious. For that and for economic reasons, there was far more concern about nagana in East and Central Africa than there was about human sleeping sickness. Studies of T. rhodesiense tended to be centered on cattle rather than people. As late as the 1950s, when livestock losses from trypanosomiasis were less than those from rinderpest, tsetse flies and the fear thereof prevented profitable land use.^[19]

In the case of sleeping sickness, the politics of land use was mediated through the new discipline of tropical medicine. In his history of yellow fever, François Delaporte charts the origins of the field. It mapped the interactions of living things to arrive at pathologies and in doing so, imbued insect vectors not only with the power of life and death, but the power of science: they could be controlled by knowledge about them. Tropical medicine drained one ancient symbol of its meaning and replaced it with another: “[D]eath came not now in the form of a man with a scythe but of a biting insect.” ^[20] But if germ theory simply swept the miasma-ists away, along with their intimate sense of peopled locations, parasitologists swept the bacteriologists out of British tropical medicine. “Non-tropical” bacteriological diseases were ignored, and tropical medicine concentrated on worms, insects, and protozoa. The link between parasitology and tropical health convinced experts that these diseases could be prevented without studying how local populations became ill. Much colonial health policy focused on protozoa and vectors. Insect vectors and animal hosts were where protozoa spent part of their lifecycles, and killing the insect or animal could kill the protozoa.^[21]

In the case of T. rhodesiense and G. morsitans, this pitted tsetse control against a vocal hunting lobby and one faction of imperial science. When in 1913, for example, David Bruce was convinced that T. rhodesiense and the trypanosome that caused nagana were identical, he became an even stronger advocate of the extermination of wild animals than he had been previously. His reasoning had to do with ideas about what formed an infectious reservoir and how best to control it. Questioned before a 1913 Colonial Office Sleeping Sickness Committee that had many hunters on it, Bruce was asked why wild animals were the host for infectious T. rhodesiense, rather than birds, immune herds of cattle, or even people. The birds in G. morsitans country were too small and too mobile to be a good source of food for tsetse flies, there were no herds of cattle in G. morsitans country, and humans made poor hosts for T. rhodesiense, because only a few were infected and those were too sick to travel about and spread the disease, he responded.^[22] He strenuously opposed the preservation of big game in “fly country”: “It would be as reasonable to allow mad dogs to live and be protected by law in our English towns and villages.” ^[23]

Although some suggested localized experiments in game eradication,^[24] few of Bruce’s contemporaries agreed with him about the relationship of T. rhodesiense to wild animals. German scholars disputed his findings; Alward May, Northern Rhodesia’s medical officer, disregarded the findings of the Luangwa Sleeping Sickness Commission and claimed that man was the principle reservoir for T. rhodesiense; E. E. Austen of London’s Natural History Museum argued that tsetse were specific to certain habitats: these could be emptied of people and left to game, inasmuch as tsetse flies did not follow game.^[25]

Such debates about vectors and hosts, about flies and buffalo, were debates about how to classify and categorize animals. Such classifications were and are as much a part of scientific research about animals as they are artifacts of “traditional” society.^[26] In the 1920s and 1930s, what was known about T. rhodesiense was the supposedly contagious relationship between reservoir, vector, and victim. Attempts to study the specific relationships—human to landscape, human to animal—that might cause or limit the disease gave way to the study of a vector abstracted into “the fly.” While it is tempting to suspect that this was the result of pressure by the hunting lobby, it seems more likely that it was part of the intense focus on vectors and pathogens that characterized early research in tropical medicine.^[27] Thus, the very people studying fly-human or fly-animal interactions anthropomorphized tsetses—saying, “The Tsetse fly loathes the presence of man,” ^[28] for example—and the fly became as important in research as was the disease. By 1935, there was a Parliamentary Tsetse Fly Committee.

C. F. M. Swynnerton, the most important tsetse researcher in this story, understood that fly behavior was based on human observations. A naturalist of extraordinary capability, Swynnerton had come to Africa as a nineteen-year-old farm manager and first attracted attention with his study of a mixed fly belt in North Mossurise, on the Southern Rhodesia–Mozambique border, in 1921, in which he noted, among other things, that male flies sometimes traveled on humans, causing some observers to think they were attacking.^[29]

Swynnerton’s studies of the tsetse fly’s ecological niches, including his 580-page monograph The Tsetse Flies of East Africa (1936), which catalogued the various species’ eating, breeding, and resting habits, put the fly in the foreground. Swynnerton read the landscape to show how tsetse could be limited without the wholesale slaughtering of game. Knowledge of the fly, Swynnerton argued, would allow science to combat the vector without significantly disrupting the reservoir or destroying the hosts—a method of disease control that David Bruce had characterized twenty years before as “a nice pious wish.” ^[30]

Land, Flies, and Science

Different varieties of tsetse fly live in different places. In East and Central Africa, the colonial concern was about G. morsitans, the fly that carried the trypanosome fatal to domestic livestock, and, to a lesser extent, humans. While the riverbank-dwelling T. gambiense could be transmitted from human to human, the trypanosome carried by T. morsitans required an animal host, so that methods of describing and of preventing one kind of sleeping sickness came to be about the relations between humans and animals. If sleeping sickness of the savannah was carried by wild animals, then the goal of biomedical policies was to separate humans and wild animals, big and small.

From these policies came studies of “the fly.” By the 1930s, most scientific knowledge of G. morsitans was based largely on Swynnerton’s research, which demonstrated the viability of African methods of tsetse control. Nevertheless, the major impact of Swynnerton’s work both on his own career and on the shape of tsetse research was to suggest an either/or paradigm in which centralized settlements and tsetse flies were inexorably opposed.

Swynnerton showed how knowledge of various tsetse flies’ behavior could be used to control their numbers and habitats. G. morsitans, for example, breeds on barren ground toward the end of the rainy season; G. brevipalis lives in wooded undergrowth that remains in leaf throughout the year; all tsetse flies need shade. Well-timed grass burning could therefore limit the habitats of two species of Glossina. Ngoni in North Mossurise had burned grass late in the dry season, when leaves had fallen and the grass was at its driest, so that the fires would be intense enough to draw a wind. Such a fire would not only destroy the grass but much of the young growth and some high shade; with sufficient rain, however, the grass would rapidly grow back. Swynnerton became a proponent of late burning, a method of tsetse control that he believed white settlement had greatly disrupted: “Under the white man everyone burns as he pleases.” White farmers’ uncoordinated grass burning failed to check tsetse populations, and different species of fly flourished.^[31]

The behavior of wild animals, according to Swynnerton, was shaped by human intervention as well. Under Ngoni domination, large parts of the Central African countryside had centralized states with concentrated populations. Densely populated areas and mile after mile of cultivated fields surrounded by deforested areas allowed Africans to live and keep cattle in health.^[32] When the population decreased, or when an area was raided and the population scattered, the land reverted to bush and game, and tsetse became widespread—a medicalized version of tribal warfare. Swynnerton had been very impressed by Ngoni accounts of methods of tsetse control. When Umzila conquered North Mossurise in the 1860s, the somewhat scattered population lived near belts infested by G. morsitans; cattle had to be sent to highlands or they died. But Umzila ordered his population to draw near the king, moving villages and settlements to the lower altitudes of the territory. “Every one of my informants has described most graphically the result of this concentration,” wrote Swynnerton. “The bush simply disappeared and the country became bare, except for the numberless native villages…and gardens.” All that was left of the woodlands was an uncleared and uninhabited “Oblong,” virtually a game reserve for Ngoni hunting parties. Outside the Oblong, hunters tracked wild pigs and buffalo herds whenever they appeared.^[33]

It was on the strength of this research that Swynnerton was appointed the game warden of Tanganyika Territory in 1921; his goal was to control tsetse flies without the wholesale slaughter of game, the policy already in sporadic operation in Southern Rhodesia. In 1923, he chose Shinyanga for the site of his research, where he was to experiment with ideas about competing ecosystems, bush and wild animals, and cattle and cultivation—mainly through bush clearing and centralized settlements.^[34] Shinyanga had been the site of a major epidemic in 1923, but Swynnerton had selected it because of its particular cycle of retreat and advance of tsetse flies: cleared land was free of tsetse, but when the population declined or moved on, the tree roots sent up shoots on which tsetse flies from adjacent infested bush alighted and then traveled to human settlements on passersby.^[35] In practice, however, Swynnerton’s subtle analysis of the local landscape was overwhelmed by the sheer scope of widespread bush clearing, which by the mid 1920s required a levy of almost 8,000 men.^[36] Swynnerton has been contested academic terrain in recent years. Although John Ford praises his attention to seasonal details, John Iliffe sees him as a harbinger of soil erosion, and John MacKenzie as an agent of the hunting lobby.^[37] A close reading of Swynnerton’s work reveals the complexities of daily life in sleeping-sickness areas, however, rather than an ignorance of rainfall patterns or apologies for bushpig and buffalo. During the Mwanza epidemic of 1922, for example, he suggested that T. rhodesiense could be transmitted by man-to-man contact, based on his observations of the division of labor between sick and well Sukuma in their households. The absence of animal vectors, however specific, was taken up by the hunting lobby, but not because Swynnerton was their mouthpiece. He was a keen hunter and very close to the hunting lobby, but, as we shall see, from 1923 until his death in 1938, he proposed a variety of methods of tsetse control, including the seasonal and the agricultural. Time after time, however, the proposals that were implemented were those that conformed most closely to official agricultural policies.

The importance of the landscape to the location of tsetse flies made epidemiology and land use overlap. A new dimension, population density per square mile, one of the most important markers of scientific discourse in this story, became the cause and cure of sleeping sickness. There might be tsetse flies in areas with population densities as low as one person per square mile, but that was not sufficient to sustain an epidemic of sleeping sickness. Areas with population densities of five per square mile would not have enough cleared land to prevent tsetse flies, and they would have epidemics. Where there were twenty-five people per square mile, there would be enough cultivation and tillage to prevent tsetse advance. Best of all would be a hundred people per square mile, a population density that could crop and clear a fly-free area in which Africans and cattle could live in health.^[38] In 1930—a year after Swynnerton had resigned to start the Department of Tsetse Research—Tanganyika Territory attempted to establish large, compact settlements, as if population density, in and of itself, could combat tsetse flies and sleeping sickness.^[39] Concentrated villages, like tracts of cleared bush, encouraged soil erosion, however; Swynnerton’s biomedical theories of the 1920s became the environmental terrors of the 1930s and 1940s.^[40]

In tsetse research, the science enshrined in population ratios was translated to tsetse populations, which were measured according to the numbers Swynnerton’s African assistants could catch. In the early 1920s, the “fly boys” of Tanganyika Territory stood still in the bush and recorded the number of flies each caught per hour. The resulting figure—flies per boy/hour—was later rejected by two of Swynnerton’s entomologists, W. H. Potts and T. A. M. Nash, as unscientific.^[41] To time discipline, they added the discipline of distance. Potts divided the Shinyanga bush into sections according to vegetation; each fly boy was assigned a section and would then walk along a path, stopping to collect flies every twenty or hundred yards, to establish the density of flies per boy 100 yards or, where flies were densest, flies per boy/yard. These fly rounds became increasingly complex, precisely laid out in grids or octagonal spirals to compensate for seasonal variations in flies’ whereabouts or the number of flies scared away by these activities. Even so, in 1930 a zoologist, C. H. N. Jackson, published a critique of the flies per boy/mile measurements, writing that they did not systematically accommodate flies’ eating habits.^[42] By the early 1930s, if not before, the very extent of fly rounds—in some areas there were thirty miles of paths—was thought to have disturbed mammalian hosts, so that tsetse and animal populations moved elsewhere.^[43] In Northern Rhodesia, which had no official tsetse-control organization comparable to that of Tanganyika Territory, fly rounds were considered a viable research method by district officers well into the 1930s: “In order to survey the density of the fly an African (immunized by injection, of course) walked along the bush path with a white cloth pinned to the back of his shirt. A man with a notebook walked behind him and counted the flies which settled on the cloth. The result was later recorded in a graph as ‘Density of fly per boy mile.’” ^[44]

Also in Northern Rhodesia, human population densities had more than a biomedical meaning. They offered ways both to understand and to problematize citemene, the very productive and reliable system of shifting cultivation taken up by hoe cultivators when they entered the area. The Bemba, who engaged in widespread raiding until the end of the nineteenth century, had lived in large, stockaded villages. Once they too took up citemene, a very specific pattern of settlement and land use developed. Citemene cultivators scattered to mitanda, the garden huts families lived in during the growing season: by 1904, for example, no villages could be seen in Mpika.^[45] In large-circle citemene, the system of the Mambwe and the Bemba, trees are lopped, not felled, and pollarded trunks are left at chest height. Branches are carried for miles to form a large circle, often of about an acre, in a clearing and left to dry in the sun. Burning takes place late in the dry season: too early and the ash would scatter in the wind; too late and the wood stacks would be wet and the burn incomplete. After the branches are burned, the large ash circle is planted with a sequence of crops, starting with finger millet the first year. Burned-over land is sometimes cultivated for as long as five years.^[46] Citemene depleted the woodland—burned areas made up from 4 to 10 percent of deforested areas—and the intense heat of the late burning destroyed the forest canopy and retarded the growth of new trees.^[47] Nevertheless, it was burning that transformed cut branches into a garden. Burning was the only occasion Richards observed in which the Bemba acted as “one economic unit.” ^[48] Citemene was also a system of great productivity: experiments at the research station in Lunzuwa compared yields from Mambwe citemene fields and Mambwe hoed mounds: from 1935 to 1940, citemene gardens produced at least three times more finger millet per acre than hoed gardens.^[49] The official construction of citimene in the 1930s, of primitive cultivation, performed with an ax, gradually gave way to an official and scientific understanding that citimene was combined with permanent gardens and was both adaptable and productive.^[50]

However productive it might have been, citemene was considered an administrative and agricultural nightmare. Whatever it did to forests and ecosystems, it made ordinary Bemba hard to rule and harder to tax. In large-circle citemene, gardens were scattered and temporary, and for much of the year families lived in mitanda. From the early years of colonial rule, mitanda dwellers guarded their independence fiercely: they were “malcontents who renounced the authority of the chiefs and the Boma.” ^[51] Mitanda became sites of new community and social relations for Bemba.^[52] In 1906, the British South Africa Company, which then governed Northeastern Rhodesia, banned citemene. Widespread hunger followed. By 1908, the Chitimukulu, the Bemba paramount, complained of his people’s starvation and poverty. Administrators complained of a new, menacing attitude of opposition among the Bemba, and expressed some anxieties about the newfound unity of chiefs and commoners—against the boma. Citemene was restored in 1909, and in 1910 administrative units were made smaller to accommodate mitanda.^[53]

Objections to citemene did not cease, but they ceased to be described in administrative terms. The problems with citemene became agricultural, not political: environmental degradation replaced social disintegration. By the late 1930s, a new official line had emerged, claiming that while fly-infested areas had long existed, they had also been uninhabited, but as the security of Pax Britannica went on, villages broke up and smaller villagers formed, and Africans “drifted” into fly areas, just as the bigger villages ceased to function as fly barriers.^[54]

The scientific study of African land use and population densities gave expression to colonial anxieties about deforestation, late burning, and Africans’ relationship to authority. But colonial anxieties, even those sanctioned by science, were not uniform. The biomedical view was that the greater the population density, the fewer renewable resources, whereas entomologists believed that the greater the population density, the fewer the tsetse flies. Population density statistics were used in Northern Rhodesia in the 1930s to show the damage done by citemene and, sometimes, land alienation. Officials bandied grim figures for population per square mile to proclaim ecological doom, to be sure, but also to participate in scientific discourse. None of the figures so pronounced took male migrancy or environmental variations in the landscape of the plateau into account.^[55]

Animals, Flies, and Officials

Throughout the 1920s and 1930s, many officials thought that the low population densities of citemene encouraged garden raiding by elephants, which was said to cause “serious starvation” in Lundazi, for example, starting in 1919, when elephants had first come into the area. In 1922, villages in Luwingu, Lundazi, and Abercorn were said to have no food.^[56] Africans were too poorly armed to fight off garden raiders themselves, and after much debate, the district commissioner in Abercorn adopted the policy already in place in southwestern Tanganyika and gave a white hunter free license to shoot elephants in inhabited areas.^[57] Soon after, many white hunters wrote to the boma requesting employment on Tanganyika Territory terms. Throughout the 1920s, the basic structure of authorized elephant hunting remained the same. A hunter was appointed elephant control officer and was allowed to kill any elephant tracked from garden raiding. To avoid the authorization of ivory harvesting, it was specified that elephants had to be caught in the act or shortly thereafter, but according to Norman Carr’s description of elephant control in Nyasaland in the 1920s, this rarely happened. A hunter “went out, as I did, and shot the first elephant he saw with reasonable tusks and called it a garden raider.” ^[58]

The hunter’s fee for shooting an elephant was, with variations according to weight, to keep one tusk. The other tusk went to the boma and the meat went to the villagers, distributed in theory according to local hierarchies, but in practice at the discretion of the hunter.^[59] The importance of this meat is clear. Audrey Richards provides a compelling description of the meaning of meat to Bemba villagers in 1931. They claimed the meat from an antelope she had shot gave them energy, “not only before the food was digested, but before it was cooked!…The next day they went to work early, declaring that their arms were strong.” ^[60] Indeed, 1920s elephant control almost at once became a local source of meat, the sale of which proved almost as profitable for hunters as the sale of ivory. One hunter worked out complex equations by which he might profit most: he would not shoot young elephants; he would keep all tusks under thirty pounds or 35 percent of tusks under fifty pounds, or he would be allowed to sell the meat without a butcher’s license.^[61] Indeed, false reports of raiding, designed to bring a well-armed hunter into an area, were common, and attempts to withdraw hunters or verify complaints were unpopular: chiefs tended to encourage false complaints whenever continual hunger eroded their authority.^[62] By the late 1930s, for example, hunters readily acknowledged the pressures on African game rangers: they were subject to “a good deal of temptation” if posted to their own areas and were frequently used by their chiefs as suppliers of meat.^[63] Even elephant culling became a food issue, which then seeped into issues of race and propriety. Once a rudimentary Game Department was established, it was loathe to hire African game scouts, because “the villagers with whom they stay are often naturally keener on getting meat than on genuine crop protection,” and lobbied for an increase in white rather than African personnel.^[64] African game scouts may have seen the situation somewhat differently. According to Norman Carr, “A ‘fundi’…with tons of meat at his disposal became the most popular man in his community.” ^[65] For these reasons, most conservationists were uneasy about elephant control.

The official emphasis on population densities and deforestation meant that citemene was thought of solely as a system of shifting cultivation. It did not take into account the ways in which citemene engendered relationships with government hunters that could provide valuable sources of meat and prestige for chiefs. Nor did it take into account the late burning that citemene required, and the decrease in G. morsitans populations that late burning caused year after year. Not only did late burning destroy the shade tsetses needed, but grass became dense in the burned areas during the rains, destroying G. morsitans’s breeding grounds. Moreover, the barren areas produced by citemene created barriers to tsetse flies.^[66] Despite some hints in tour reports, citemene was on the whole not considered a tsetse-control measure. In all probability, this was because sleeping sickness, particularly the variety caused by T. rhodesiense, was seen as a cattle disease, the absence of which was best demonstrated when people kept cattle. As a cattle disease, T. rhodesiense implied a specific landscape, free of bush and big game, occupied by cultivators and their herds, a paradigm so powerful that scholars and scientists were disinclined to see T. rhodesiense in the same terms in which non-cattle-keeping Africans might have seen it.

Game preservation had been under attack for years for causing the spread of sleeping sickness. As early as 1911, a game park bordering Nyasaland and Northeastern Rhodesia—named, appropriately enough, Elephant Marsh—was closed because of missionary complaints about the increase in tsetse flies and sleeping sickness.^[67] By the 1930s, game parks created another layer in the either/or paradigms of tsetse control, adding the issue of people versus animals and tsetse to a landscape already mapped by official thinking of cultivation versus tsetse. The landscape that emerged from debates about game preservation and game parks was mandated to house animals for European sensibilities and hunting, rather than those of Africans. Animals in game parks, as in some tsetse-control schemes, became an undifferentiated category of prey in which hunting was racially and technologically specific, although assisted by Africans.^[68]

Where did these biomedical ideas that proposed either the destruction of fauna or the destruction of flora come from? The line between African ideas and imperial science was never a sharp divide. Swynnerton’s bush-clearing campaigns had originated in Ngoni practices of land use, relations between domestic and wild animals, and authority: in Shinyanga, he tried to make them scientific and experimentally sound.^[69] The game preservation of tsetse research and reclamation of the 1930s had European as well as African antecedents, however, and these blurred the lines between hunters, conservationists, and scientists. The creation of game parks and game preserves, for example, came out of two contradictory turn-of-the-century motivations: to safeguard the natural world, in manageable proportions, so that the modern world would not lose touch with it, and a desire to subdue that same natural world, regardless of whether or not such actions had any social context. White hunting in Africa had a very different meaning in 1885, for example, than it did in 1935. Early game parks were created to be “unpoliced spots on a map,” to be protected from African exploitation. Early colonial game parks were places where African hunting was illegal. They preserved hunting land for foreign hunters—many of whom were museum collectors and scientists as well.^[70] In the early years of game preservation, wild animals were not romanticized, white hunting was.^[71] Within the next thirty years, game parks became sites in which decreasingly important imperial interests could assert their power against growing biomedical and social lobbies.^[72]