Summary This paper uses articles from the East African Medical Journal to trace medical authorities’ changing conceptions of East Africa’s tuberculosis problem from the 1920s through the 1970s. In the early decades of this colonial publication, contributors identified racial susceptibility as the source of East Africa’s rising tuberculosis rates. After the British Medical Research Council began collaborating on anti-tuberculosis chemotherapy experiments in the region around mid-century, contributors identified economic scarcity—specifically a lack of medical resources—as the root of East Africa’s tuberculosis problem. In reducing economic scarcity to an experimental variable, researchers construed East Africa and the developing world as naturally ‘resource poor’. At the same time, they used this identity as a backdrop for finding new chemotherapy regimens (six-month short-course chemotherapy) that worked even in low-income settings. Biomedical experiments and technologies, this paper argues, shaped and were shaped by conceptions of East African difference. tuberculosis, East Africa, chemotherapy, experiment, biomedicine In 1937 an anonymous contributor to the East African Medical Journal (EAMJ) reviewed a study of black and white tuberculosis (TB) patients conducted at the Johns Hopkins Hospital in Baltimore. ‘While it is possibly correct to assume,’ he relayed, that the African shows less resistance than the European to the tubercle bacillus because the white man has been rendered more or less immune by small infections during childhood, some evidence has recently been adduced to show that there may be inherent differences in the races.1 Circumstances and assumptions were very different 23 years later, when long-time physician and medical educator in Uganda, Arthur Williams, validated anti-TB chemotherapy trials conducted in East Africa for EAMJ readers: The need for effective, easily administered and cheap treatment for pulmonary tuberculosis in out-patient and domiciliary practice is everywhere recognized. It is of particular relevance in poor or developing countries with scattered populations. Well-tried régimes of chemotherapy may need to be modified for successful use under such circumstances. … By studying under African conditions the application and adaptation of advances made in western countries, knowledge can be gained that is relevant to both.2 For Williams, who coordinated the initial chemotherapy trials in the 1950s, resource constraints and the difficulty of drug administration lay at the root of East Africa’s TB problem. Such conditions in turn made the region a fruitful test site for therapeutics of global relevance. These two medical commentaries diverge on multiple counts. Each author identified different sources of similarity (and difference) between TB in East Africa and TB elsewhere: racialised bodies and economic conditions. Each also wrote from different positions: the former an unrecognised consumer of medical research conducted overseas, the latter a notable producer of original medical knowledge in East Africa. Finally, their explanations served particular political interests at different moments in empire. Exploring the intellectual shifts laid bare in these two statements, this article reveals how TB in East Africa went from being understood as a product of African susceptibility to a result of underdeveloped health systems. In this case, biomedical technologies and experiments played a key role in this transformation. I use articles from the EAMJ to trace medical authorities’ changing conceptions of East Africa’s TB problem from the 1920s through the 1970s, when researchers developed six-month short-course chemotherapy regimens. Founded in 1924 as a forum for colonial medical thought about Kenya, and later East Africa, the EAMJ was intended to record and circulate observations of local import for the benefit of medical practitioners working in the region.3 The journal maintained part of this provincial character even as it gained a wider international readership. Additionally, as the main journal organ for the publication of medical opinions in and about East Africa, the EAMJ served as an instrument of medical professionalisation in the colonies. Members of the East African branches of the British Medical Association (BMA) authored, edited and published the EAMJ, situating themselves into a burgeoning community of regional medical specialists.4 As such, the journal’s content reflects the shifting interests, practices and composition of a professional cohort and the expertise this cohort deemed relevant to addressing medical issues in East Africa specifically, whether that was racial biology, social medicine, clinical trials or otherwise. While the EAMJ does not capture all perspectives equally—particularly those of African practitioners who did not begin joining the East African BMA branches until the late colonial period—attending to what was published on TB and by whom reveals how the landscape and expertise of medical professionals in East Africa changed over the mid-twentieth century.5 By exposing the relations and modes of medical knowledge production in an imperial outpost, a close reading and analysis of EAMJ articles on TB also provides a new lens through which to view the relationship between disease control and colonial and post-colonial development. Medical officers, doctors and researchers in East Africa formulated their ideas about TB and its relation to local conditions by combining their own observations with knowledge produced outside the region. The ways in which EAMJ contributors did so in a given period reflects the types of experts and expertise medical professionals in East Africa valued, as well as therapeutic prospects and shifting social, political and economic circumstances in the region. As a continuous channel for intellectual exchange in East Africa, the EAMJ uniquely captures a lineage of these medical authorities’ evolving ideas. However, as the opening quotations suggest, the EAMJ was more than just a site of regional conversation about TB; it was also a critical arena in which categories of East African difference were parsed out and reconfigured over time. The ways EAMJ contributors understood and mobilised those categories had important consequences for the ways medical authorities addressed TB in East Africa and beyond. This history of changing conceptions of TB in East Africa enhances understandings of how pathologies have been constructed in colonial and post-colonial biomedicine. As anthropologists Vincanne Adams and Stacey Langwick illustrated, when constructed within medico-scientific activities, differences such as ‘modern’/ ‘traditional’, ‘science’/ ‘non science’ appear natural. One could say the same for ‘European TB’/ ‘African TB’ or ‘temperate’/ ‘tropical’ disease, distinctions which similarly emerged from attempts to explain variability through a supposed universal, Western scientific order. As Adams, Langwick and others have shown, however, the production of these binaries is inherently political and discourages particular avenues of health intervention.6 In historical terms, this article examines how and why different categories of East African difference became salient at different moments, and how these changes were linked to both medical-scientific practices and colonial and post-colonial politics. In doing so, it illustrates how categories of difference animate universalising biomedical endeavours and not simply the other way around. While changes in medical thought do not divide into neat chronologies, I divide this history into four periods to clarify my analysis: discussions of ‘African TB’ during the period between the two world wars; the post-war period and rise of social medicine; the beginning of chemotherapy experiments in the mid-1950s; and the generalisation of East Africa as a representation of the developing world during the 1960s and 1970s. Explaining ‘African TB’ between the Wars In the 1920s and 1930s contributors to the EAMJ primarily focused on describing an acute, virulent form of TB they saw among African populations in East Africa. The idea that Africans developed a different type of TB, so-called ‘African’ or ‘primitive TB’, was based on the premise that Africans had less prior contact with the bacillus than did Europeans, and thus less immunity to the disease. European assumptions of African racial inferiority reinforced this premise.7 Ideas about the connection between racial and pathological difference circulated elsewhere, including South Africa and the United States, and informed EAMJ contributors’ own discussions of ‘African TB’. These contributors offered slightly different explanations for and solutions to ‘African TB’ based on their interpretations of the similarities and differences between conditions and bodies in East Africa and those elsewhere. Nevertheless, authors effectively reduced the problem to one of African biology. To understand the ways medical authorities discussed TB in the EAMJ, it is important to understand their goals, interests and work practices. Most of the contributors during the journal’s first decades were medical officers in the Colonial Medical Service.8 Members of this professional cadre in East Africa were typically responsible for medical activities in entire districts, performing surgery, public health work and clinical medical services. These activities included surveying the district’s population on medical safaris—a political as much as medical endeavour. Although many medical officers came to the colonies with common educational backgrounds that served to homogenise their professional approach, they operated fairly independently in day-to-day activities, responding to the particular circumstances in their respective territories.9 By 1934, when the Colonial Medical Service was unified, the Colonial Office pushed to maintain a sense of policy and personnel continuity in local settings. Thus, many officers worked in the same district for nearly a decade. The nature of this colonial medical work was reflected in the articles they wrote on TB for the EAMJ. Medical officers in East Africa became aware of the growing TB problem in the 1920s due to wartime and post-war labour needs. Medical officers carried out mass inspections of Carrier Corps recruits during the First World War and found in Kenya, for example, that TB was rampant among Corps members.10 Information about South African troops who developed acute TB when deployed in France informed discussions about the rise of acute TB in East Africa as well.11 The expansion of medical services in labour ‘reserves’ and requisite medical inspections for African workers after 1920 similarly illuminated the region’s growing TB problem. Medical Officer Charles Wilcocks and Dr Charles Wilson discussed the numerous TB cases they found among European-employed Africans in Dar es Salaam and Kenya, respectively.12 Interest in uncovering the burden of TB, as with many other diseases in colonial medical campaigns, was inextricably linked to imperial needs.13 In the 1930s, medical officers devoted their EAMJ publications to describing and explaining this virulent, ‘African’ type of TB. Their explanations were based on cultural assumptions and scientific understandings of racial susceptibility.14 Many contributors drew from work done by European physicians on TB in South Africa, a place with circumstances they saw as very similar to East Africa, to explain ‘African TB’. These contributors frequently referred to S. Lyle Cummins’ work on TB in Egypt, Sudan and South Africa. Cummins popularised the idea that Africans were ‘virgin soil’ for TB.15 He also acted as an expert advisor for the 1932 South African Institute of Medical Research (SAIMR) report on TB in African mineworkers, a report which quickly made it into the Kenya Medical Department’s library.16 Senior bacteriologist R. P. Cormack advertised in the EAMJ that this report was especially valuable for understanding ‘generalised and very rapid’ TB among Africans in the region, and thought ‘a similar survey [tuberculin tests among African workers] would be of immense use in East Africa’.17 Other medical officers also invoked Cummins’ report to construe virulent TB as a racialised pathology, claiming, ‘tuberculosis is and may be expected for some time to remain an acute disease among Africans and in this the American negro population must be included’.18 As both the EAMJ and the SAIMR report circulated in East Africa’s medical departments, so too did Cummins’ ideas about race and TB. Charles Wilcocks acted as an important node in the intellectual exchange about ‘African TB’ in the EAMJ. He spearheaded a TB survey in Tanganyika in the 1930s as part of larger scientific efforts to understand diseases prevalent in Britain’s African colonies.19 Cummins—under whom Wilcocks studied at the beginning of the decade—helped design survey questions to elucidate the nature of TB among Africans in relation to TB among Europeans.20 Wilcocks published on these questions in the EAMJ, further circulating some of Cummins’ ideas about TB and African susceptibility in the journal, namely that Africans often developed virulent TB.21 Medical officers then cited Wilcocks’ work for their own articles.22 Although Wilcocks eventually diverged from Cummins’ virgin soil theory, his contributions reinforced ideas circulating in the EAMJ that Africans were more sensitive to tuberculin than Europeans and populations in East Africa were ‘midway between the completely primitive races and our relatively resistant selves’.23 This burgeoning network of medical authorities fostered a growing consensus that ‘African TB’ was an immunological phenomenon. Drawing from Cummins’ work, their own experiences and other sources of knowledge, many argued that the surrounding environment influenced one’s susceptibility to TB. Citing the SAIMR report, Tanganyika Medical Officer W. Harden Smith claimed the inability of Africans to adapt to ‘unaccustomed stress and changes in the routine of life … entailed in the change from rural to urban or industrial conditions’ was primarily responsible for increasing rates of acute TB in East Africa.24 Smith’s diagnosis fit with broader colonial antipathy to African urbanisation in East Africa, epitomised in efforts to restrict residency rights among African workers.25 Zanzibar’s Deputy Director of Sanitary Services Barugh Spearman also felt TB was an ‘environmental disease’ that proliferated in areas with overcrowded, unhygienic conditions, especially among the undernourished.26 ‘Primitive peoples’ were unsuited to ‘the stress and strain of civilization’, he wrote, and unless they were taught proper hygiene and ways of living, would ‘fall an easy prey’ to TB.27 Others assuming biological commensurability of all ‘Negro’ bodies similarly linked African American TB susceptibility to the ‘environment’, which included crowded housing, large families and low incomes.28 These conceptions of how the environment influenced Africans’ susceptibility to TB rested on assumptions of Africans’ differential immunity. The variety of solutions EAMJ contributors proposed to address conditions that exacerbated TB throughout the 1930s illustrate the different ways understandings of racial immunity intersected with colonial medical work. Those who recapitulated ideas from the SAIMR report about the stresses and strains of civilised life typically supported sending Africans back to their traditional homelands in the reserves as preventive therapy. In other words, they imported ideas and tropes borne largely out of South Africa’s urban segregation policies and mine industry labour structures.29 This served colonial interests in supporting East Africa’s plantation economy and curtailing urbanisation, even if the region’s economic activities and lack of formal segregation structures differed from that of South Africa. Medical authorities in East Africa, however, advocated for different means of repatriation based on their varying interests and circumstances. Medical missionary R. Y. Stones recommended putting African TB patients in village settlements where they could do trade or craft work. ‘Naturally,’ he believed, African village settlements would ‘look to the missionary societies and philanthropic organizations for help in the religious and sociological activities so essential for the happiness and contentment of its inhabitants.’30 De-emphasising village settlements, Smith stressed repatriation of African patients to rural areas to save money on the institutionalisation of TB cases in cash-strapped Tanganyika.31 Believing there was ‘nothing dramatic we can do about it [TB in East Africa]’, Smith also thought enforcing segregationist township and labour laws could help Africans overcome their hyper-allergic state.32 Still others thought education and propaganda about healthy habits would encourage Africans to better manage and avoid TB.33 With no effective treatment, medical authorities proposed various control strategies that implicated Africans’ maladaptation to urban conditions in the rise of ‘African TB’. Anxieties about Indian immigration also shaped proposed solutions for TB in East Africa. Some EAMJ contributors worried that Indian immigrants were spreading TB to Africans in urban areas. Their ‘mode of living facilitate[d] the spread of disease,’ one officer claimed, ‘and their penetration along the lines of commerce combined with their propensity for travelling, tend[ed] to disseminate it widely.’34 British medical authorities had blamed Asian groups for spreading infectious disease in East Africa since the turn of the century. However, the role of Indians in spreading TB seemed an especially valent issue in the 1930s, as this group gained political and economic influence in East Africa during the widespread depression.35 Changing political and economic circumstances—in this case, new pressures from an ethno-political group—informed medical ideas. Whereas in 1930 Spearman suggested helping Africans adapt to urban settings to reduce TB mortality, in 1934 he advocated limiting Indian immigration to reduce threats of TB in urban areas.36 With this emphasis on Indian contact, contributors to the EAMJ deviated from those elsewhere, including Cummins, who blamed Europeans for the spread of TB in South Africa. In East Africa, according to these authors, Indians were part of the pathological, urban environment. While contributors to the EAMJ did not always agree on how to control TB in East Africa, discourse around ‘African TB’ framed the disease as a problem of African biology: ‘methods of prevention and diminution of the disease on biological lines is a slow and tedious business. Yet it is on these lines we must work.’37 Medical officers could isolate TB cases or educate Africans on proper hygiene to reduce mortality, but ultimately Africans would continue to die from acute TB until they acquired enough immunity to make TB a chronic disease. Although medical authorities may have discussed ‘African TB’ differently elsewhere, this discourse in the EAMJ helped crystallise an exceptional African pathology that placed the burden of change on Africans rather than the colonial government.38 TB and Social Medicine In the 1940s, discussions about TB in the EAMJ began to change. Contributors’ efforts to explain the cause of ‘African TB’ in the 1920s and 1930s focused on Africans’ exposure to the disease under new colonial conditions, such as increasing industrialisation and the growing presence of Africans and Asian immigrants in towns. In turn, they advocated establishing physical and metaphorical distance between Africans and these conditions. As medical officers began to notice increasing TB rates in rural areas—areas many considered health-promoting in the 1930s—they wrote articles that focused on improving living conditions and health facilities in rural areas to prevent the further spread of disease. Wider social and economic transformations in East Africa encouraged this shift, which intellectual trends in the British metropole later reinforced. Articles in the EAMJ in the 1940s and 1950s illuminated other forms of East African difference aside from the biological. Because social and economic circumstances in East Africa became increasingly relevant to medical authorities in explaining the region’s TB problem, these men sought to address issues specific to the region in their proposed control strategies. The Second World War and subsequent influx of Africans into East Africa’s urban centres informed the conversation about TB in the EAMJ in the 1940s. Africans came to these centres during the war to take up industrial and service jobs, though many chose to travel between urban and rural areas rather than settle in the city. This urban–rural migration presented a problem, particularly when African soldiers returned to their rural homes with TB infections acquired during the war. Medical officers stationed in rural areas noticed that even people who did not travel to the city and did not work industrial jobs were infected with TB. This challenged earlier notions that the countryside was healthier than the city. As Medical Officer Henry Davies qualified, while Africans more often acquired TB infections in towns and rarely acquired infections in the open air of the country, Africans who came back to rural areas with TB could infect their entire household.39 As the war made clear, trying to keep Africans from going to cities, from encountering the stresses of civilised life that exacerbated ‘African TB’, would not work. New British colonial policy also encouraged a shift in thinking towards improving living conditions rather than limiting Africans’ participation in urban life. The combination of Britain’s strained financial resources and increasing demand for African labour during the war led African workers in ports like Mombasa and Dar es Salaam to strike and protest for higher wages. As historian Frederick Cooper documented, the British tried to contain these rising tensions and reassert political control in their African colonies through a series of economic and social development initiatives.40 The colonial administration decided to ensure control and increase economic output, by investing in social spending (building cheap housing, raising wages and improving living conditions). This policy shaped the medical discourse on environmental factors that precipitated TB in East Africa. In particular, it opened up possibilities for how EAMJ contributors could propose to address TB in the region. Although fewer in number due to the interruption of war, contributors to the EAMJ in the 1940s called for better housing and additional medical facilities to prevent the region’s TB rates from spiralling out of control. Tanganyika Senior Medical Officer Arthur Mackay believed that in a TB control scheme, one could only really control open cases and the economic condition of the community. Therefore, he advocated for a preventative public health programme in rural villages that included ‘improved housing conditions’ and ‘improved diet’.41 Davies, who believed better medical and public health care would ultimately solve the TB problem, encouraged the government to fund new units in rural areas that combined a hospital, sanatorium and chain of dispensaries. Such medical facilities, he thought, would abate a disease ‘that the war has shown’ to have spread ‘by leaps and bounds’.42 Davies interpreted the rising TB rates in rural areas as evidence that Africans would not simply acquire immunity to the disease in due time as Europeans did.43 Although these officers still invoked ‘African TB’ as a distinct pathology, their solutions were not as linked to this distinct pathology since ‘methods of prevention and diminution’ of TB ‘along biological lines’ proved untenable.44 Thus, Cummins’ work and studies on TB among African Americans played a lesser role in EAMJ discussions of the disease. Instead, contributors more often discussed the factors exacerbating rising TB rates based on their observations of the situation in East Africa. The growing popularity of social medicine in Great Britain in the 1940s had a noticeable impact on the TB literature published in the EAMJ in the 1950s. Beginning in the early 1940s, universities in Great Britain founded departments of social medicine, a discipline that considered the importance of ‘social conditions’ such as housing, nutrition and occupation in relation to disease.45 By the end of the decade, universities’ departments of social medicine offered courses on the subject for their undergraduate curriculums and initiated epidemiological research.46 Doctors who practised social medicine emphasised the need for a preventive approach to disease as a complement to clinical medicine, along with greater integration of the social sciences. Representatives of the East African medical profession embraced social medicine following the end of the war, claiming this approach could make the maintenance of the African work force more ‘efficient’.47 Contributors to the EAMJ deployed these ideas coming out of the UK to deal with TB and conditions specific to East Africa, namely the colonies’ economic limitations. In his article, ‘Social medicine in England and East Africa’, R. C. Browne extoled the virtues of preventive medicine for East Africa’s ills: The aetiology, and hence the prevention of the mass of mortality and ill-health, is clearly through a combination of education, nutrition and sanitation. … Preventive and clinical medicine must work hand in glove, but in a country with primitive sanitary standards, … it is of the utmost importance to invest the limited financial resources available in a wise preventive policy.48 Kenya medical officer A. T. G. Thomas called for preventative approaches for similar reasons. Given the government’s ‘natural limitations’, it should address bad housing, overcrowding and malnutrition rather than expand curative services.49 According to Thomas, TB ‘illustrate[d] the close relation between Preventive Medicine and Social Welfare’. As it was unlikely BCG inoculation alone could curb TB in Kenya, ‘there must also be improvement in African diet and conditions of life’.50 Such arguments dovetailed with larger, administrative conversations about implementing welfare measures to increase the economic productivity of African workers.51 For Thomas and other EAMJ contributors, preventative interventions were needed to curb this ‘social disease’, which took many African lives and a terrible economic toll. The incorporation of ideas from social medicine into the EAMJ marked the beginning of a gradual shift in the way contributors compared TB in East Africa and Europe. Previously, doctors focused on explicating differential racial immunity, looking more often to South Africa or African American populations to understand TB in East Africa. However, as British medical authorities encouraged those working in East Africa to apply social medicine in the colonies, EAMJ contributors de-emphasised racial binaries and instead focused on the need to improve social and economic conditions for proper development. Browne, for example, claimed that investment in social medicine and preventive public health policy in East Africa could bring about health improvements in the same way it did in England.52 ‘Preventive medicine,’ Thomas argued in his article, was ‘non-racial and international … disease knows no barriers of colour or race.’53 For the sake of economic sustainability, he wrote, the British National Health Service as well as administrators in Kenya had to invest in preventive health care. New colonial development policy, related fears about political and economic stability, and intellectual trends in the UK shaped the way EAMJ contributors re-conceptualised East African difference. Development discourse and ideas from social medicine circulated in the EAMJ, but rhetoric from the 1930s persisted. Although in his report on TB in Uganda, Dr W. Santon Gilmour said, ‘if the voice of preventive medicine is not listened to, there are the possibilities of catastrophic results, an uncontrollable acceleration of tuberculosis disease in the industrial workers and their families’, he perpetuated scientific understandings of ‘African TB’.54 He described the cases he saw as having ‘infantile tuberculosis—the condition now general [sic] known as “primitive tuberculosis”’ and attributed this to the fact that Africans did not have a background of ancestral infection.55 Dr William Haynes expressed similar sentiments, saying that ‘economic measures’ such as improved housing schemes and nutrition in urban centres could ‘help the tuberculosis problem’ in Kenya.56 Yet while he supported such improvements, he also asserted that, ‘racial tolerance or susceptibility to tuberculosis varies directly with the amount of exposure to infection which the race has experienced’.57 Both men drew from older ideas about virgin soil TB and racial susceptibility, articulating links between black bodies. Yet they also focused on solving a specifically East African (or Ugandan or Kenyan) problem—rising TB rates in rural and urban areas amidst financial constraints—using concepts central to social medicine. Redefining the ‘Social’ in Anti-TB Chemotherapy Experiments While ideas about primitive TB and social medicine circulated in the EAMJ, the nature of TB control and medical research in Africa were rapidly changing. Researchers had developed effective anti-TB chemotherapies by the early 1950s and, along with international health organisations, explored whether drugs could provide a universal weapon for TB control. Medical authorities in East Africa began to reorient their work around these new biomedical technologies. Doing so, they redefined both the ‘social’ and ‘economic’ factors relevant to TB control along with East African difference for readers of the EAMJ. The uptick in international TB control activities encouraged the flow of biomedical, anti-TB technologies. In the late 1940s, the World Health Organization (WHO) made TB control a main priority, collecting data from countries about their number of TB cases and available facilities. By 1951, it had also taken over the mass international BCG vaccination campaign begun by the International Tuberculosis Campaign and United Nations International Children’s Emergency Fund.58 As Sunil Amrith has discussed, the WHO wanted to tackle a now visibly pervasive disease after the war in a cost-effective way.59 This entailed integrating such promising tools as BCG vaccines or new anti-TB chemotherapies into existing national and colonial health infrastructures. For the WHO, TB cure and prevention were biomedical endeavours.60 Many doctors and medical officers working in East Africa found anti-TB chemotherapy a potentially promising solution to the region’s TB problem in the early 1950s. Upon conducting a tuberculin survey in Kenya in 1948, William Haynes estimated there were at least 55,000 cases of TB in the colony, but only 750 available beds.61 The lack of hospital facilities, a general problem throughout East Africa, meant that previously recommended therapies of bed rest, collapse therapy and surgery provided little hope of slowing the spread of disease. ‘A remedy, which is relatively cheap, easily given and which may be continued as an outpatient treatment’ therefore, ‘ha[d] a special appeal’ in a country like Kenya: ‘an undeveloped country with inadequate and over-strained hospital facilities’.62 Indeed, Uganda Medical Officer P. W. Hutton claimed, ‘the advent of powerful chemotherapeutic drugs makes it possible to extend the scope and extent of anti-tuberculosis therapy’ in East Africa.63 TB drugs, in other words, might obviate the need for developing medical facilities, which were ‘manifestly impossible to provide … for all those suffering from pulmonary tuberculosis in East Africa’.64 However, contributors to the EAMJ in the 1950s did not believe they could simply implement chemotherapies proven effective in the West in East Africa. Authors noted that the practical issues of drug cost and administration complicated the movement of these biomedical technologies into East African medical practice. In 1951 Haynes and R. R. Henderson conducted a trial of the leprosy drug diamino-diphenyl sulphone in Kenya, despite the fact that laboratory tests showed it to be considerably toxic. If this drug—which cost 14 shillings per patient per year—was effective in tuberculosis, they claimed, ‘it would bring hope of relief and perhaps cure within the means of everyone; and Government schemes would be furnished with a new weapon’.65 According to Hutton, when adopting the ‘new therapeutic approach’ one still had to consider ‘social and economic factors’ that affected the patient’s ability to access further treatment and observation: When the patient is discharged from hospital he will need to be maintained by his relatives until such time as he can work again. … In Uganda this problem occurs particularly in Buganda where there are many recent Runga immigrants with no fixed domicile. The problem will progressively increase in urban areas which attract an influx of labour dependent on wages. Such people cannot be treated satisfactorily unless the problem of out-patient maintenance and observation can be handled.66 Whether talking about the limitations of technology transfer in a general way to justify testing cheap drugs, or in specific locational terms, EAMJ contributors became occupied with getting drugs into East African bodies in the 1950s. Furthermore, ideas about the difference between European and African TB persisted among EAMJ contributors in the early 1950s. For those considering the use of chemotherapy, this meant disease in Africans might respond differently to TB drugs than did disease in Europeans. Thinking along these lines, Haynes conducted a trial among Kenyan patients to see if thiacetazone, a drug used extensively for TB treatment in Germany, had an effect on ‘African pulmonary tuberculosis’.67 The fact that thiacetazone did not appear to affect important TB indicators, such as sputum conversion rate, in Kenyan patients threatened hopes that TB drugs performed similarly in all bodies. As Dr Gilmour wrote in 1952, ‘the newer measures available’ of vaccination and chemotherapy ‘have still to prove themselves in Africa’.68 In 1953, uncertainty about whether TB drugs worked equally well in African bodies led medical personnel in Uganda to partner with the British Medical Research Council (MRC) on anti-TB chemotherapy trials. The MRC had spearheaded the famous randomised controlled trial of streptomycin in the UK in 1948. Dr Marc Daniels, who coordinated that trial and worked at the MRC’s Tuberculosis Control Unit in Hampstead, encouraged Dr Arthur Williams and colleagues to coordinate a randomised trial testing streptomycin-isoniazid against PAS-isoniazid. Doing so, they could see ‘whether in African patients and in the acute type of pulmonary tuberculosis to which they are subject, the response to antibacterial drugs would be similar to that familiar in Britain’.69 Finding sufficient similarity in drug response, this trial helped crystallise understandings of biological commensurability between African and European bodies.70 For the purposes of drug-based TB control, this biological, racial form of difference became irrelevant. It is instructive here to explore the MRC’s early history of colonial chemotherapy research in order to understand the organisation’s approach to the production of knowledge about TB drugs in East Africa. The MRC first got involved in Britain’s colonial project by developing chemotherapies for tropical diseases in UK laboratories in the mid-1930s. The British felt it important to develop these drugs in-house as one of the largest imperial consumers.71 After the war, they resumed this research, bringing it to the colonies as part of Britain’s post-war colonial development efforts. This move did not mean, however, that researchers thought the tropical environment was necessary for this basic research. As the MRC annual report for 1952–53 stated, ‘Knowledge on any medical subject obtained anywhere may, at any time, become relevant elsewhere. … Any measure which tends to segregate it according to whether it is done in the tropics or in this country is not merely artificial; it is actively harmful.’72 Pharmaceutical technologies allowed researchers to study tropical disease and therapeutics without studying the surrounding ecology. Valorising place-less therapeutic approaches and place-less medical expertise, the MRC expanded its centres of biomedical knowledge production in the ‘tropics’. In the 1950s, the MRC also expanded its anti-TB chemotherapy experiments to a number of Britain’s colonies and former colonies, including present-day Uganda, Kenya, Tanzania and Zambia—home of the East African Medical Research Council (EAMRC).73 As Arthur Williams described in 1957, East Africa seemed to be ‘an ideal place for chemotherapeutic studies in tuberculosis, just because the incidence here of acute tuberculosis [was] so extremely high’.74 Most patients in East Africa were also chemotherapy-naïve. Thus, they produced immediate, clear results about the efficacy of TB drugs without complications of drug resistance.75 Politically, it was also easier for doctors and researchers to test experimental, potentially toxic drugs in colonial East Africa, as Haynes did in the early 1950s.76 The fact that those with little money (which was most TB patients in East Africa) ‘must virtually go untreated’ encouraged such experimentation as well.77 Shifting their gaze towards the performance of drugs in bodies, and away from the underlying causes of TB in East Africa, medical personnel who partnered with the MRC began to transform East Africa into a place of biomedical knowledge production about anti-TB chemotherapy. Researchers from the MRC Tuberculosis Research Unit (TRU) and doctors working at medical centres in East Africa completed five chemotherapy trials by the end of the decade.78 These trials depended on the circulation of antibiotics, experimental protocols and experts between London and the colonies. The Tuberculosis Research Unit at Hampstead planned, designed protocols for and conducted the statistical analysis for most of these trials with input from doctors in East Africa. Sometimes it even sent technicians over to help with day-to-day work on the trials. Unsurprisingly, these experiments mirrored the MRC’s UK-based trials. They used the same inclusion criteria (acute, rapidly progressive bilateral disease). They compared two or more drug regimens, randomly allocated, that had been studied already in the UK. Researchers monitored subjects for improvements in TB indicators, as well as drug resistance.79 Transferring technologies of both anti-TB chemotherapy and the randomised controlled trial to East Africa, the MRC further ‘stabiliz[ed] some of the background noise’ that made TB in East Africa incomparable with TB in Europe.80 Certainly, EAMJ contributors recognised, the East African context did make these trials different. Going beyond showing chemotherapy worked as well in African as in European bodies, those conducting trials identified East Africa’s lack of resources as the difference that gave the experiments value. According to Williams, the MRC wanted to see if they could conduct MRC-type trials ‘under local conditions and with local [i.e. scant] resources in East Africa’.81 ‘Well-tried régimes of chemotherapy may need to be modified for successful use under such circumstances’,—those of ‘poor or developing populations’—‘because of social or economic or geographical factors, and this needs investigation’.82 Streptomycin, PAS and isoniazid were very expensive, so researchers wanted to find a combination of drugs that would be cheap, effective and limit the emergence of drug resistance. ‘The problems that emerge in these investigations,’ Williams felt, were not of ‘parochial interest only.’ This transnational research would actually be ‘of mutual advantage’ to developing as well as developed countries like Britain.83 Yes, it was necessary to consider how to make out-patient or domiciliary chemotherapy work given the dearth of hospitals in East Africa. However, such concerns—which were ‘not problems peculiar to East Africa’—were largely ‘sociological rather than therapeutic’, best addressed by ‘methods of sociological research rather than those of the therapeutic trial’.84 East African conditions of resource scarcity mattered as an experimental condition in which to investigate the efficacy of cheaper drug regimens rather than as a public health problem in and of itself. Doctors and medical officers discussing anti-TB chemotherapy focused their EAMJ articles on making drugs work in the resource-poor conditions of East Africa. ‘If the vast problem of treating tuberculosis in a poorly developed and economically backward country is to be tackled,’ Hutton argued, for example, ‘tuberculosis can no longer remain within the narrow preserve of the specialist.’85 Moreover, he told readers, ‘it is desirable to spend as little on drugs and hospital maintenance as is consistent with effective therapy if the maximum number of cases is to be treated with medical resources which are limited’.86 Kenya Medical Officer Hugh Scott highlighted the ‘special problem’ of TB in East Africa ‘not felt … in socially or economically advanced countries’: there were many cases that required multiple drugs, which ‘must be restricted in their use because of cost’.87 Scott advocated for trials with isoniazid alone, despite the danger of drug resistance, for this reason. ‘If it were not for the great difficulty of supplying free combined therapy’ to all East African TB patients—which in his estimation would cost the government £110,000 for the cheapest regimen—‘it would hardly be necessary to consider the use of isoniazid alone.’88 Just as Williams framed the MRC chemotherapy trials in terms of economic and logistical feasibility, other medical authorities in East Africa used the same frame for chemotherapy-based TB control. Biomedical solutions and technologies only worked if local ‘social and economic’ conditions allowed. Drug resistance posed one of the biggest threats, EAMJ contributors felt, to finding regimens suited to East Africa’s economic situation. Kenya’s (and the region’s) ‘unavoidable drug restriction … which has resulted from lack of finance’ complicated the search for such regimens in therapeutic trials.89 Both Hutton and A. C. E. Cole at the Infectious Disease Hospital in Dar es Salaam chastised one author for promoting a regimen of isoniazid alone, saying it put patients and the public at risk.90 Defending the drug’s use as a monotherapy, Scott argued, ‘it is not for a minute suggested that isoniazid should be given to patients in an uncontrolled manner, but until another effective and cheap drug can be produced we must seriously consider the possibility of wide scale use of this drug’.91 And, indeed, the MRC and their collaborators in East Africa conducted a trial in 1957–58 comparing isoniazid alone with isoniazid and PAS. As drug resistance became a visible problem through the MRC’s chemotherapy trials (16 per cent of patients to East African trial hospitals were found resistant to isoniazid in 1957), doctors working on the MRC’s chemotherapy trials focused on testing different, though still inexpensive, regimens that might work.92 Economic scarcity, for them, became a fixed, ‘unavoidable’ condition that limited, but could be overcome, by biomedical technologies. At the same time, it became the most salient form of East African difference. Alternative ideas about the role of the ‘social’ in TB control did circulate in the EAMJ in the 1950s despite the increasing focus on making TB drugs work. For example, Pierce Kent, Director of TB services in Kenya, compared combination therapy for TB to the combination of arsenic, bismuth and mercury as treatment for syphilis and felt that it was ‘fallacious to think of the problem as merely a simple matter of pills and patients’.93 Invoking ideas of Thomas McKeown and colleagues that improved living conditions, more so than antibiotics, led to the reduction of TB in England, he later claimed that ‘tuberculosis is not a social disease, but a socio-economic one’.94 The fact that East Africans’ inability to afford protein-rich food sources seemed to exacerbate TB illustrated this. However, this alternative, social medicine-based approach to TB in East Africa disappeared from the EAMJ in the 1960s. East Africa, the Developing World and Six-month Short-course Chemotherapy Indeed, by 1960 anti-TB chemotherapy had become the backbone of TB control in East Africa and a main subject of EAMJ articles on TB. However, as EAMJ contributors described, the region’s dearth of facilities and reliance on domiciliary treatment had encouraged the development of drug resistance. In discussing this problem, and ways of modifying therapeutic technologies to fit East Africa’s resource scarcity, these authors generalised conditions in East Africa to the developing world more broadly. At the same time, they used this image of resource scarcity as a backdrop on which to test the efficacy of shorter, six-month drug regimens. EAMJ contributors highlighted two main problems with TB in East Africa in the 1960s: an enormous number of TB cases, and an increasing proportion of cases that did not respond to first-line drug treatments. The WHO’s 1957–59 TB survey in Kenya—the largest in Africa to that point—estimated the number of adult TB cases at 110,000. This was over double what medical authorities had estimated just months before the survey results came out.95 Working in neighbouring Uganda, surgeon P. Ashman James emphasised that there was ‘no doubt whatever that it [TB] is now a major endemic disease’ in East Africa ‘as it is in so many other developing countries’.96 Additionally, the survey found many patients lived in rural areas with few hospital facilities or medical personnel. Citing WHO recommendations and experiences from India, Bolivia, Korea, Tanganyika and Kenya, Kenya Senior Medical Officer John Grounds advocated limiting case finding activities in ‘under-developed countries and backwards areas’ to high-risk groups because of this highly uneven ratio of TB patients to medical resources.97 There were not enough health workers to identify patients and, as TB specialist James Ang’awa noted, certainly not enough drugs to treat every patient in Kenya or East Africa.98 At the same time, resistance to isoniazid, PAS and, to a lesser extent, streptomycin continued to increase across the region. Although Arthur Williams described the necessity of domiciliary treatment with these cheap drugs to TB control in East Africa in 1960, EAMJ contributors began blaming this mode of distribution for increasing drug resistance.99 As Grounds reported, domiciliary schemes frequently failed to incorporate migrant workers who began chemotherapy in urban hospitals before returning to their rural homes.100 Drug shortages in rural out-patient facilities exacerbated drug resistance among this group as well. Moreover, he theorised, because of the bad taste and unpleasant side effects of PAS, patients were liable to omit the drug over their 18–24 month course of treatment.101 And because isoniazid was so cheap, it was given to those who could not afford more expensive regimens and ‘emergency’ drugs, sometimes even those patients with isoniazid-resistant TB.102 Medical resource constraints seemed to be creating a new pathology—antibiotic resistant TB—in East Africa, which authorities sought to overcome. Medical authorities looked to new or modified technologies in order to address this problem within these resource constraints. MRC-EAMRC researchers conducted trials with second-line regimens, such as combinations using thiacetazone or thiazina (combined isoniazid and thiacetazone). Their 1962–63 trial of thiazina, Ang’awa claimed, ‘proved an important milestone in the fight against tuberculosis in developing countries such as Kenya’.103 Grounds thought making the first-line regimen of isoniazid and PAS into a single powder would force patients to take the PAS. ‘All future domiciliary drug régimes,’ he added, ‘should be issued in combined form so that the patient must take the correct combination or none.’104 Together with new diagnostic methods and increased calls for surgery for ‘failed medical cases’, these constituted EAMJ contributors’ strategies for curbing drug-resistant TB.105 While authors both explicitly and implicitly compared the problems of TB in East Africa to those in other ‘developing countries’, it was in the problem of drug resistance that East Africa defied alternative representations of the developing world. Specifically, the failings of domiciliary treatment schemes challenged the India model of TB control: mass domiciliary treatment with cheap drugs. This model had emerged from the MRC’s anti-TB chemotherapy trials in Madras during the 1950s and 960s. As Sunil Amrith explored, the MRC teamed up with the WHO, Indian Council of Medical Research and Madras State Government in 1956 to investigate the impact of chemotherapy on poor patients in southern India.106 Their investigations included a controlled experiment testing whether chemotherapy worked as well in domiciliary conditions—the slums of Madras—as in sanatoria conditions. Their finding that conditions in which therapy was taken did not affect therapeutic effectiveness rendered conditions of poverty biomedically neutral. Moreover, it suggested that developing countries with few hospitals beds, like those in East Africa, could use mass domiciliary treatment to control TB. As Amrith argued, within this and subsequent trials, Madras came to represent other cities in the Third World.107 While some EAMJ contributors did cite the Madras studies, for example their criteria for assessing drug sensitivity, they saw East Africa’s short supply of medical staff, ‘scattered rural communities’, and ‘poor communications’ as dissimilarities that challenged this representation.108 The gap between India and East Africa becomes clearer when looking broadly at publications on TB research and control in developing countries. For one, the MRC and Madras-based team continued to study and publish on the suitability of mass domiciliary treatment for developing countries throughout the 1960s.109 In a 1963 lecture, for example, Wallace Fox, who directed the MRC trials in Madras, used data primarily gathered in Southeast Asia to claim that doctors in countries with scarce economic resources should, among other things, concentrate on ambulatory domiciliary chemotherapy.110 Two medical officers working in West Africa responded to Fox, saying that there was a ‘danger that they [Fox’s views] may be accepted as something of a blueprint for underdeveloped tropical Africa’.111 Out-patient chemotherapy, they claimed, was not working in either West or East Africa because these places had fewer resources than Madras to carry out this scheme.112 Defined by its lack of resources and unmitigated growth of drug-resistant TB, East Africa became a main stage for the next major, global development in anti-TB chemotherapy: six-month short-course chemotherapy. In the 1970s the MRC continued to focus on finding new technological solutions to TB in East Africa, solutions which could then be used in the entire developing world. This research was shaped by perceived complications of treating TB in East Africa but still considered conditions of poverty irrelevant to the biological functioning of chemotherapies in bodies. The MRC and EAMRC first decided to investigate six-month short-course chemotherapy after they found that the standard 18-month regimen had a treatment success rate of 95 per cent in hospitals but only 60 per cent in Kenya under ‘routine field conditions’.113 These conditions included high drug costs, insufficient drug supplies and long distances between scattered populations in rural areas and between medical facilities. It was simply not feasible for patients in a poor country to take so many drugs for so long. Moreover, Wallace Fox, who also led the MRC’s Tuberculosis Unit, wanted to see if the new, extremely potent drug rifampicin could help shorten TB treatment.114 Therefore, from April 1970 to September 1971, MRC and EAMRC researchers conducted Study R at 27 centres across East Africa. This was the first of a series of controlled clinical trials aimed at identifying short-course treatment ‘within financial capacities of all countries’.115 Researchers adjusted each subsequent trial to find even cheaper or shorter regimens that would be effective under ‘routine field conditions’ in East Africa, which came to serve as a proxy for the entire developing world. Researchers considered it important to find short-course regimens that ‘readily lend themselves to practical application by routine treatment services’, especially ‘in the developing countries where the whole organization of programmes of long-term chemotherapy has repeatedly failed and has usually proved to be beyond the capacity of the routine treatment services as currently financed, organised, equipped, and staffed’.116 Overriding local exceptionalism, these trials contributed further to the transformation of East Africans into universal representatives of underdeveloped populations. The fact that the object of research here was not a method dependent on certain geographies and resources, such as domiciliary care, but biomedical technologies presumed to work the same way everywhere, facilitated this transformation. Essentially, researchers’ particular conception of East Africa as a representation of the ‘developing world’ directed their efforts to find a universal biomedical solution that rendered irrelevant more of the variation between developing countries. Study R produced two successful regimens but neither seemed suitable for general application because of their cost. Pyrazinamide and rifampicin, first introduced into clinical practice in 1956 and 1967 respectively, were key components of successful six-month, multidrug regimens but were extremely expensive. Therefore, the MRC and EAMRC conducted more trials to see how much rifampicin, pyrazinamide and ‘difficult’ streptomycin could be reduced in an effective regimen. They even went so far as to try four-month chemotherapy to limit the amount of drugs one had to take.117 Soon after Study R, the MRC expanded short-course chemotherapy trials to their other centres in Hong Kong, Singapore, Algeria and Prague. All of these studies built on the East African trials. East Africa’s identity as an alternative representation of the developing world within these published clinical trial results seemed to exclude bad patient behaviour. While a discourse on patient non-compliance may have circulated more widely in other domains in East Africa, few contributors to the EAMJ emphasised non-compliance. Early on, in fact, investigators described patients in East Africa as very cooperative and tolerant of even the most unpleasant effects of chemotherapy.118 Although they may have written this to authorise more trials of highly toxic drugs in East Africa, medical authorities did not establish a strong discourse blaming patients in the EAMJ. One likely reason for this was that almost all the East African trials were conducted in hospitals where patient compliance was more heavily monitored.119 Rather than emphasise non-compliance, authorities often attributed high drug resistance rates to the fact that Africans had received experimental and sometimes incomplete drug regimens from doctors.120 They framed the issue as a consequence of the poor economic conditions of the region that limited access to effective drugs. East African conditions, rather than patient behaviour, were to blame. Nevertheless, the central concern of EAMJ contributors was not to improve social and economic conditions; it was how to adapt biomedical technologies to economic obstacles inevitably encountered in the ‘developing world’. Contributors to the EAMJ had acknowledged the economic and logistic limitations of TB control in East Africa to varying degrees since the 1930s, but the MRC chemotherapy trials reduced these limitations to a scientific variable. They became the laboratory conditions in which MRC and EAMRC researchers produced biomedical knowledge and assemblages of biomedical technologies for global application. This depiction of East African countries as having too few resources to control TB adequately, then, became naturalised in articles published since the 1960s. The results from the short-course chemotherapy trials, published in the EAMJ and internationally prominent medical journals, generalised the relationship between social and economic factors and TB control in developing countries. Researchers drew attention to these factors, but in doing so framed them as barriers to overcome, as conditions from which to produce biomedical technologies that rendered these conditions irrelevant. The underlying causes of TB did not disappear, but they no longer seemed to matter. Conclusion Refracting the history of TB through the EAMJ, as this article has done, illuminates a dynamic geography of biomedical knowledge production overlooked in existing studies of international health and TB control. Colonial medical professionals who contributed to the EAMJ formulated conceptions of TB in East Africa by reconciling their own observations with those produced outside the region. Their understandings of TB in East Africa shifted as the circumstances and contours of empire, medical expertise and medical technology changed. In articulating their ideas about and solutions to TB, this professional cohort also reconfigured conceptions of East African difference. In the process, they ascribed relevance to new places, experts and bodies of knowledge in controlling TB in East Africa, eventually transforming East Africa into a source of universal, biomedical knowledge. By the 1960s, after British researchers initiated anti-TB chemotherapy trials in the region, the nature of African or black bodies and the specific social and political circumstances in East Africa fell away as concerns. EAMJ contributors’ perceptions of East African difference, however, were not merely products of medical-scientific inquiry; they also informed new lines of inquiry and disease control strategies in East Africa. In setting up clinical chemotherapy trials in the region, researchers had to establish stable experimental conditions with a few select variables such as drug combination or dosage. In doing so, they construed East Africa’s lack of health and economic resources as a static and foregone problem, rather than as a result of colonial and post-colonial politics. Framing resource scarcity as a natural, stable condition of East Africa, they then designed experiments in the region to find new drug combinations that addressed the logistical and economic difficulties of providing TB drugs in East Africa and the developing world. In reducing economic scarcity to a scientific variable, researchers used this form of difference as a backdrop for testing new drug regimens. These regimens became the gold standard of TB therapy but have failed to eliminate the disease in East Africa. A history of TB control told from the vantage point of East Africa and the EAMJ, then, elucidates an important but underexplored intersection of poverty, pathologies and colonial legacies in the history of biomedicine as a global enterprise. Colonial medical authorities and their successors did not deem poverty in East Africa completely irrelevant following the introduction of generalisable biomedical tools. Rather, in identifying conditions of East African resource scarcity, and the threat these posed to therapeutic efficacy, they made poverty the perpetual crux on which biomedical investigations turned. Six-month short-course chemotherapy regimens and a reification of East Africa and the developing world as resource-poor: these were the products of experiment. Kirsten Moore-Sheeley is a doctoral candidate in the History of Medicine Department at Johns Hopkins University. She specialises in the history of public health and biomedicine in East Africa and the history of global public health. Footnotes 1 ‘Racial Differences in the Mortality of Tuberculous Children’, East African Medical Journal (EAMJ), 1937, 14, 213. 2 A. W. Williams, ‘East African Tuberculosis Therapy Trials—A Review’, EAMJ, 1960, 37, 743–64, 743. 3 This journal began in June 1923 as a news sheet circulating in Kenya’s Medical Department. In 1924 Dr Charles Wilson expanded the scope of this publication, then the Kenya Medical Journal, as editor. Largely through the support of Tanganyika’s Medical Department, the journal expanded to cover the East African colonies (Kenya, Uganda, Tanganyika, Zanzibar), becoming the Kenya and East African Medical Journal in 1927. The journal acquired its current title, the East African Medical Journal, in 1932. For more on the history of this journal, see Alan Raper, ‘Medical Writing in East Africa, The East African Medical Journal, 1924–1952’, EAMJ, 1953, 30, 315–21 and Mary Dobson et al. ‘The Voice of East Africa: the East African Medical Journal at its 75th Anniversary’, Transactions of the Royal Society of Tropical Medicine and Hygiene, 1998, 92, 685–6. 4 As Chief Editor of the journal (1930–42), James Sequiera transferred proprietorship of the EAMJ to the East African branches of the British Medical Association in the 1930s. Thereafter, the journal allocated numerous pages for Association meeting minutes, papers and demonstrations presented at Association meetings, and news from Medical Departments around East Africa. Dobson et al. ‘The voice of East Africa’. For more on the British Medical Association in the Empire, see Terence Johnson and Marjorie Caygill, ‘The British Medical Association and its Overseas Branches: A Short History’, Journal of Imperial and Commonwealth History, 1973, 1, 303–29. 5 My analysis also reflects the neglect of certain aspects of TB, such as bovine TB, in EAMJ publications and the shifting geographical representation of articles. For example, Kenya is overrepresented in later publications partly because the Kenyan Medical Department led the EAMJ (financially and legally) and because Nairobi emerged as the hub for East Africa’s anti-TB chemotherapy experiments in the 1960s. 6 Vincanne Adams, ‘Randomized Controlled Crime: Postcolonial Sciences in Alternative Medicine Research’, Social Studies of Science, 2002, 32, 659–90; Stacey Langwick, Bodies, Politics, and African Healing: The Matter of Maladies in Tanzania (Bloomington, IN: Indiana University Press, 2011); Christian McMillen, Discovering Tuberculosis: A Global History, 1900–Present (New Haven: Yale University Press, 2015); Randall Packard, ‘The “healthy reserve” and the “dressed native": Discourses on Black Health and the Language of Legitimation in South Africa’, American Ethnologist, 1989, 16, 686–703; Randall Packard, The Making of a Tropical Disease: A Short History of Malaria (Baltimore, MD: Johns Hopkins University Press, 2007). 7 Many historians have examined the medical discourse about race, biological primitiveness, and TB. See for example, Randall Packard, White Plague, Black Labor: Tuberculosis and the Political Economy of Health and Disease in South Africa (Berkeley: University of California Press, 1989); Mark Harrison and Michael Worboys, ‘A Disease of Civilization: Tuberculosis in Britain, Africa, and India, 1900–39’, in Lara Marks and Michael Worboys, eds, Migrants, Minorities, and Health (London: Routledge, 1997), 93–124; McMillen, Discovering Tuberculosis. 8 For an overview of the history of medical officers in colonial East Africa, see Anna Crozier, Practising Colonial Medicine: The Colonial Medical Service in British East Africa (London: IB Tauris & Co. Ltd, 2007). 9 Anna Greenwood (formerly Anna Crozier) and others have recently shown that the Colonial Medical Services in British Africa were more diverse than previously described, employing Indians and collaborating with mission, community and research organisations. Anna Greenwood, ed., Beyond the State: The Colonial Medical Service in British Africa (Manchester: Manchester University Press, 2016). 10 Charles Wilson, ‘Tuberculosis in the Natives of Kenya’, Kenya and East African Medical Journal, 1927, 4, 296–317, 302. 11 Charles Wilcocks, ‘Notes on Tuberculosis in Dar-es-Salaam’, Kenya and East Africa Medical Journal, 1928, 5, 200–7. 12 Ibid., 201; Wilson, ‘Tuberculosis in the Natives of Kenya’, 306. 13 John Farley, Bilharzia: A History of Imperial Tropical Medicine (Cambridge: Cambridge University Press, 1991); Myron Echenberg, Black Death, White Medicine: Bubonic Plague and the Politics of Public Health in Colonial Senegal (Portsmouth, NH: Heinemann Educational Books, 2002); Kirk Arden Hoppe, Lords of the Fly: Sleeping Sickness Control in British East Africa (Westport, CT: Praeger Publishing, 2003). 14 For more on the discourse about race and TB, see McMillen, Discovering Tuberculosis, 15–36. 15 The virgin soil theory said that because African populations historically had little exposure to the TB bacillus, when they came in contact with it they acquired a much more acute form of the disease. Europeans, by contrast, typically acquired a chronic form of TB because of their much longer historical exposure. For more on Cummins’ work, see Packard, White Plague, Black Labor; Michael Worboys, ‘Tuberculosis and Race in Britain and its Empire, 1900–50’, in Waltraud Ernst and Bernard Harris, eds, Race, Science, and Medicine, 1700–1960 (London: Routledge, 1999), 144–66; McMillen, Discovering Tuberculosis. 16 R. P. Cormack, ‘Some Subjects for Medical Research in East Africa’, EAMJ, 1934, 11, 276–85, 281. 17 R. P. Cormack, ‘Tuberculosis in Native Races’, EAMJ, 1933, 10, 119–22, 121; Cormack, ‘Some Subjects for Medical Research in East Africa’, 281. 18 W. Harden Smith, ‘Pulmonary Tuberculosis in Africans’, EAMJ, 1939, 16, 318–28, 323. 19 Helen Tilley, Africa as a Living Laboratory: Empire, Development, and the Problem of Scientific Knowledge, 1870–1950 (Chicago: University of Chicago Press, 2011), 169–216. 20 McMillen, Discovering Tuberculosis, 40. 21 Charles Wilcocks, A Tropical Doctor in Africa and London: An Autobiography (Surrey: Leatherhead, 1977), 77. For examples of the circulation of Wilcocks and Cummins ideas in the EAMJ, see Charles Wilcocks, ‘The problem of Tuberculosis in East Africa’, EAMJ, 1932, 9, 88–98 and Charles Wilcocks, ‘Tuberculosis in East Africa, with Special Reference to the Clinical Aspect’, EAMJ, 1933, 10, 20–31. 22 Smith, ‘Pulmonary Tuberculosis in Africans’. 23 McMillen, Discovering Tuberculosis, 42. Charles Wilcocks, quoted in J. H. S., ‘Dr. Wilcocks’ report on tuberculosis in Tanganyika’, EAMJ, 1938, 15, 130–40. 24 Smith, ‘Pulmonary Tuberculosis in Africans’, 321. 25 Andrew Burton, African Underclass: Urabnisation, Crime, and Colonial Order in Dar es Salaam (Oxford: James Currey, 2005). 26 B. Spearman, ‘The Prevention and Treatment of Pulmonary Tuberculosis with Special Reference to the Tropics’, EAMJ, 1930, 7, 240–55, 241. 27 Ibid., 243. 28 R. B. M., ‘Tuberculosis in the Negro as Related to Certain Conditions of Environment’, EAMJ, 1934, 11, 67–8. This was one of a few reviews of articles from US medical journals about TB among African Americans printed in the EAMJ in the 1930s. 29 Packard, ‘The “healthy reserve” and the “dressed native” ’. 30 R. Y. Stones, ‘A Scheme for Reducing Incidence of Tuberculosis in Uganda’, EAMJ, 1933, 10, 355–62, 362. 31 Smith, ‘Pulmonary Tuberculosis in Africans’. 32 Ibid., 325, 328. 33 Spearman, ‘The Prevention and Treatment of Pulmonary Tuberculosis with Special Reference to the Tropics’, 245. 34 B. Spearman, ‘The Problem of Tuberculosis in the Tropics’, EAMJ, 1934, 11, 222–32, 227. See also Smith, ‘Pulmonary Tuberculosis in Africans’, and Wilcocks, ‘The Problem of Tuberculosis in East Africa’. 35 Wealthy Indians used their position as major creditors in East Africa to exert pressure on colonial governments—increasingly low on income during the depression—for economic and political protections. Abdul Sheriff, ‘Race and Class in the Politics of Zanzibar’, Africa Spectrum, 2001, 36, 301–18. 36 Spearman, ‘The Prevention and Treatment of Pulmonary Tuberculosis with Special Reference to the Tropics’; Spearman, ‘The Problem of Tuberculosis in the Tropics’. 37 Spearman, ‘The Prevention and Treatment of Pulmonary Tuberculosis with Special Reference to the Tropics’, 245. 38 This is also described in Packard, ‘The “healthy reserve” and the “dressed native”’. 39 H. N. Davies, ‘Tuberculosis in the African: The Problem and its solution’, EAMJ, 1946, 23, 194–209, 196. 40 Frederick Cooper, Decolonization and African Society: The Labor Question in French and British Africa (Cambridge: Cambridge University Press, 1996). 41 A. G. Mackay, ‘The Control of Leprosy and Tuberculosis in Rural Areas in the Tropics’, EAMJ, 1942, 19, 150–3, 153. 42 Davies, ‘Tuberculosis in the African: The Problem and its Solution’, 209. 43 Davies challenged ideas about virgin soil earlier based on his observations running a TB clinic and dispensary in Tanganyika. However, he did not publish his work on TB in the EAMJ until the 1940s. McMillen, Discovering Tuberculosis, 39–40. 44 Spearman, ‘The Prevention and Treatment of Pulmonary Tuberculosis with Special Reference to the Tropics’, 245. 45 J. Pemberton, ‘Origins and Early History of the Society for Social Medicine in the UK and Ireland’, Journal of Epidemiology Community Health, 2002, 56, 342–6. For more on social medicine in post-colonial contexts, particularly regarding TB, see Sunil Amrith, ‘In search of a “magic bullet” for Tuberculosis: South India and Beyond, 1955–1965’, Social History of Medicine, 2004, 17, 113–30. 46 Pemberton, ‘Origins and Early History of the Society for Social Medicine in the UK and Ireland’, 343. 47 A. R. Paterson, ‘The Social Function of the British Medical Association in Kenya’, EAMJ, 1946, 23, 98–113; H. L. Gordon, ‘The Importance of Social Medicine to Kenya’, EAMJ, 1946, 23, 2–13; R. C. Browne, ‘Social Medicine in England and East Africa’, EAMJ, 1950, 27, 69–72; T. H. White, ‘Some Medical Aspects of Social Progress in an African Industrial Community’, EAMJ, 1959, 36, 585–94. 48 Browne, ‘Social Medicine in England and East Africa’, 71. 49 A. T. G. Thomas, ‘The Future of Preventative Medicine in Nairobi’, EAMJ, 1951, 28, 318–28, 320. 50 Ibid., 323. 51 Britannicus, ‘Economic Planning in the British Colonies’, Foreign Affairs, 1948, 27, 58–67; E. Grey Turner, ‘A Visit to the East African Branches’, British Medical Journal (BMJ), 1949, 1, 70–1. 52 Browne, ‘Social Medicine in England and East Africa’, 71. 53 Thomas, ‘The Future of Preventative Medicine in Nairobi’, 319. 54 W. Santon Gilmour, ‘Tuberculosis in Uganda, a Short Survey’, EAMJ, 1952, 29, 381–402, 401. 55 Ibid., 384. 56 W. S. Haynes, ‘Immunity to Tuberculosis in East Africans’, EAMJ, 1955, 32, 169–72, 169. 57 Ibid., 170. 58 World Health Organization, The First Ten Years of the World Health Organization (Geneva: WHO, 1958), 188–97. For more on the history of the BCG vaccination campaigns, see George Comstock, ‘The International Tuberculosis Campaign: A Pioneering Venture in Mass Vaccination Research’, Clinical Infectious Diseases, 1994, 19, 528–40. 59 Amrith, ‘In search of a “magic bullet” for Tuberculosis’. 60 For more on the WHO and their TB activities, see McMillen, Discovering Tuberculosis. 61 W. S. Haynes, ‘Tuberculosis in Kenya’, BMJ, 1951, 1, 67–71; W. S. Haynes, ‘Tuberculosis in Kenya’ (Nairobi: Government Printer, 1951). 62 W. S. Haynes, ‘The Treatment of Pulmonary Tuberculosis in Kenya Africans with Thiacetazone’, EAMJ, 1952, 29, 337–55, 337. 63 P. W. Hutton, ‘The Treatment of Tuberculosis in District Hospitals’, EAMJ, 1956, 33, 333–43, 333. 64 Williams, ‘East African Tuberculosis Therapy Trials’, 762. 65 W. S. Haynes, ‘The Treatment of Pulmonary Tuberculosis in Africans with Diamino-diphenyl Sulphone’, EAMJ, 1952, 29, 357–68, 357. 66 Hutton, ‘The Treatment of Tuberculosis in District Hospitals’, 333–334. 67 Haynes, ‘The Treatment of Pulmonary Tuberculosis in Kenya Africans with Thiacetazone’, 354. 68 Gilmour, ‘Tuberculosis in Uganda, a Short Survey’, 398. 69 Williams, ‘East African Tuberculosis Therapy Trials’, 744. Hutton and colleagues gave the same reasoning in the original publication of results. P. W. Hutton et al., ‘Acute Tuberculosis in East Africans: A Controlled Trial of Isoniazid in Combination with Streptomycin or PAS’, Tubercle, 1956, 37, 151–65. 70 McMillen discussed the role of this trial and small studies in Southern Rhodesia in establishing that Africans responded to chemotherapy in the same way Europeans did. McMillen, Discovering Tuberculosis, 129. 71 For more on the MRC’s early collaborations with the Colonial Office on tropical disease, see Jennifer Beinart, ‘The Inner World Of imperial Sickness: The MRC and Research in Tropical Medicine’, in Joan Austoker and Linda Bryder, eds, Historical Perspectives on the Role of the MRC: Essays in the History of the Medical Research Council of the United Kingdom and its Predecessor, the Medical Research Committee, 1913–1953 (Oxford: Oxford University Press, 1989), 109–36. 72 Quoted in, A. Landsborough Thomson, Half a Century of Medical Research, Volume Two: The Programme of the Medical Research Council (UK) (London: Her Majesty’s Stationery Office, 1975), 209. This contrasted with earlier arguments about the exceptionality of tropical diseases that had justified the building of schools of tropical medicine in the early twentieth century. 73 Wallace Fox, Gordon Ellard and Denis Mitchison, ‘Studies on the Treatment of Tuberculosis Undertaken by the British Medical Research Council Tuberculosis Units, 1946–1986, with Relevant Subsequent Publications’, International Journal of Tuberculosis and Lung Disease, 1999, 3, S231–S279. The EAMRC, originally the East African Council for Medical Research, was established under that name (EAMRC) in 1957. The development of this organisation fit with broader trends in colonial development starting in the late 1940s whereby the British established research institutions in their African colonies to study medicine, agriculture, industry and ‘social’ issues. National Academy of Sciences (US), Recommendations for Strengthening Science and Technology in Select Areas of Africa South of the Sahara (Washington, DC, 1959). For more on the history of East African research institutions in the postwar period, see Melissa Graboyes, ‘Surveying the “Pathological Museum”: A History of Medical Research and Ethics in East Africa, 1940–1965’ (PhD Thesis, Boston University, 2010). 74 A. W. Williams, ‘The Next Generation’, EAMJ, 1957, 34, 521–8, 522. 75 Hutton et al., ‘Acute Tuberculosis in East Africans’. P. W. Hutton, ‘Tuberculosis in an African Setting: The Therapeutic Problem’, Postgraduate Medical, 1962, 38, 80–5. David Jones also described how Walsh McDermott selected Navajo populations for isoniazid trials because this group had many cases of acute TB but had not received prior drug treatment. David S. Jones, Rationalizing Epidemics: Meanings and Uses of American Indian Mortality since 1600 (Cambridge, MA: Harvard University Press, 2004). 76 Haynes, ‘The Treatment of Pulmonary Tuberculosis in Africans with Diamino-diphenyl Sulphone’; Haynes, ‘The Treatment of Pulmonary Tuberculosis in Kenya Africans with Thiacetazone’. 77 H. Scott, ‘The Case for the Use of Isoniazid Alone in the Treatment of Pulmonary Tuberculosis in East Africa’, EAMJ, 1957, 34, 325–37, 325. 78 Williams, ‘East African Tuberculosis Therapy Trials’, 744. This article lists the TB drug trials conducted in East Africa from 1953 to 1960. 79 Ibid. 80 Vincanne Adams, ‘Metrics of the Global Sovereign: Numbers and Stories in Global Health’, in Vincanne Adams, ed., Metrics: What Counts in Global Health (Durham, NC: Duke University Press, 2016), 34. 81 Williams, ‘East African Tuberculosis Therapy Trials’, 744. 82 Ibid., 743. 83 Ibid., 763. 84 Ibid., 762. 85 Hutton, ‘The Treatment of Tuberculosis in District Hospitals’, 333. 86 Ibid., 334. 87 Scott, ‘The Case for the Use of Isoniazid Alone’, 325. 88 Ibid., 336. By contrast, Scott estimated a regimen of isoniazid alone for all Kenyan TB patients to be £16,000. Both estimates are based on six-month regimens—well short of the ideal 18–24 months at the time. 89 Ibid., 325. 90 P. W. Hutton, Letter to the Editor, EAMJ, 1954, 31, 34; A. C. E. Cole, Letter to the Editor, EAMJ, 1954, 31, 111–12. 91 Scott, ‘The Case for the Use of Isoniazid Alone’, 336. 92 McMillen, Discovering Tuberculosis, 119–37. 93 P. W. Kent, ‘The Control of Tuberculosis in Kenya’, EAMJ, 1957, 34, 307–14, 311–12. 94 P. W. Kent, ‘Tuberculosis—A Social Disease’, EAMJ, 1959, 35, 649–55, 653. While McKeown famously codified and popularised the thesis that improved living conditions (notably nutrition) led to the decline of TB in England and Wales during the 1970s, he began publishing on this idea in 1955. Thomas McKeown and R. G. Brown, ‘Medical Evidence Related to English Population Changes in the Eighteenth Century’, Population Studies, 1955, 9, 119–41. 95 John Grounds, ‘Initial Resistance to Isoniazid Para-aminosalicylic Acid and Streptomycin in Two Areas in Kenya’, EAMJ, 1962, 39, 682–7, 682. 96 P. Ashman James, ‘The Role of Surgery in Pulmonary Tuberculosis in East Africa, with Mention of a Modified Thoracoplasty’, EAMJ, 1964, 41, 441–7, 441. 97 John Grounds, ‘The Contacts of Cases of open Pulmonary Tuberculosis in Kisii, Kenya’, EAMJ, 1964, 41, 20–5, 23. 98 James Ang’awa, ‘Case Finding Programmes in the Control of Pulmonary Tuberculosis in Kenya’, EAMJ, 1965, 42, 666–72, 672. 99 Williams, ‘East African Tuberculosis Therapy Trials’, 743. 100 John Grounds, ‘A Sputum Survey of Cases of Pulmonary Tuberculosis Two to Three Years after Starting Treatment in a Rural Area in Kenya’, EAMJ, 1964, 41, 156–62, 161. 101 Grounds, ‘Initial Resistance to Isoniazid Para-aminosalicylic Acid and Streptomycin in Two Areas in Kenya’, 686. 102 Ibid., 685; James Ang’awa, ‘The Problem and Management of Drug-resistant Cases of Pulmonary Tuberculosis in Kenya’, EAMJ, 1964, 41, 436–40, 439. 103 Ang’awa, ‘The Problem and Management of Drug-resistant Cases of Pulmonary Tuberculosis in Kenya’, 438. 104 Grounds, ‘Initial Resistance to Isoniazid Para-aminosalicylic Acid and Streptomycin in Two Areas in Kenya’, 686. 105 John Grounds, ‘A Comparison of Tuberculin Testing by the Mantoux Method and Heaf’s Multiple Puncture Method in Kisii’, EAMJ, 1962, 39, 577–9; Anne V. C. Lloyd, ‘Bacteriological Diagnosis of TB in Children’, EAMJ, 1968, 45, 140–3; Ashman James, ‘The Role of surgery in Pulmonary Tuberculosis in East Africa’. 106 For more on the MRC’s work in India, see Amrith, ‘In search of a “magic-bullet” for Tuberculosis’. 107 Ibid., 116. 108 Grounds, ‘The Contacts of Cases of Open Pulmonary Tuberculosis in Kisii, Kenya’, 24; Ang’awa, ‘Case Finding Programmes in the Control of Pulmonary Tuberculosis in Kenya’, 667. 109 C. Evans et al., ‘A 5-year Study of Patients with Pulmonary Tuberculosis Treated at Home in a Controlled Comparison of Isoniazid plus PAS with 3 Regimens of Isoniazid Alone’, Bulletin of the World Health Organization, 1969, 41, 1–16. 110 Wallace Fox, ‘Realistic Chemotherapeutic Policies for Tuberculosis in the Developing Countries’, BMJ, 1964, 1, 135–42. 111 William Bell and P. P. Brown, ‘Tuberculosis in Developing Countries’, BMJ, 1964, 1, 501. 112 Ibid. 113 East African Tuberculosis Investigation Centre, ‘Short Course Treatment in Pulmonary Tuberculosis’, EAMJ, 1972, 49, 494–501, 494. 114 D. A. Christie and E. M. Tansey, eds, Short-Course Chemotherapy for Tuberculosis, Wellcome Witness to Twentieth Century Medicine, 24 (London: Wellcome Trust Centre for the History of Medicine, 2005), 21. 115 Amina Jindani, ‘Short-course Treatment in Pulmonary Tuberculosis’, EAMJ, 1975, 52, 472–80, 472. Jindani described how they ‘recruited’ patients for Study R in a 2005 Wellcome Trust seminar: when someone came into the hospital and was found to have TB, researchers told them they could receive a new drug treatment if they agreed to stay in the hospital for six months. 116 East African/British Medical Research Councils, ‘Controlled Clinical Trial of Short-Course (6-month) Regimens of Chemotherapy for Treatment of Pulmonary Tuberculosis’, The Lancet, 1972, 229, 1079–85, 1084; East African Tuberculosis Investigation Centre, ‘Short course Treatment in Pulmonary Tuberculosis’, 494–501. 117 These trials were dubbed ‘Study T’, ‘Study U’ and ‘Study X’. Researchers wanted to reduce ‘difficult’ streptomycin in six-month regimens because streptomycin had to be taken daily, typically through injections at hospitals. EAMRC and MRC, ‘Streptomycin plus PAS Pyrazinamide in Retreatment of Pulmonary Tuberculosis in East Africa’, EAMJ, 1972, 49, 7–15, 14; Grounds, ‘Initial Resistance to Isoniazid, Para-aminosalicylic Acid and Streptomycin in Two Areas in Kenya’, 685. 118 Haynes, ‘The Treatment of Pulmonary Tuberculosis in Kenya Africans with Thiacetazone’, 350. 119 Researchers designed hospital-based studies because they thought patients might stop taking the drugs after they felt better. 120 F. Stephen Carter, ‘Primary Tuberculosis in African Children and the Value of Isoniazid’, EAMJ, 1954, 31, 265–75, 275; Williams, ‘East African Tuberculosis Therapy Trials’, 752; H. Nsanzumuhire and P. W. Kent, ‘Short-course Treatment in Pulmonary Tuberculosis’, EAMJ, 1977, 54, 53–60, 53. Acknowledgements I would like to thank the editorial board of the Social History of Medicine and the three anonymous reviewers for their helpful comments on this paper. I would also like to thank members of the Johns Hopkins History of Medicine Department, particularly Randall Packard, Jeremy Greene and Daniel Todes, for reading and commenting on multiple drafts of this paper. Finally, I want to thank members of the African seminar at Johns Hopkins, members of the Beckman Center at the Chemical Heritage Foundation and Alexander Bay at Chapman University for their feedback. © The Author 2017. Published by Oxford University Press on behalf of the Society for the Social History of Medicine.
Social History of Medicine – Oxford University Press
Published: Jun 28, 2017
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