The article examines the historical development of global health from its genesis in colonial-era tropical medicine, to the creation of the World Health Organization – formed to advance health rights for all. The authors call for continued reforms to the global health governance system to mitigate the enduring impact of colonialism.

This article stresses the role of colonial governments, not only national sovereign states, in Asia (and to a lesser extent, Africa) at the League of Nations in shaping global governing norms. It emphasizes the significance of lateral and horizontal cooperative actions across colonial governments, especially intercolonial networks of public health experts. It argues that the League of Nations Health Organization (LNHO) accepted these intercolonial practices in Asia in the 1920s, and that this led it to recognize colonial governments as formal and legitimate units in its intergovernmental conferences held in the mid 1930s. In the process, the LNHO provided an intercolonial channel for ‘national’ experts from colonial Asia to participate directly in regional and global governing norm-making processes. In turn, this highlights both the ambiguous nature of national experts and the intercolonial legacy in international health programmes in developing countries in the post-war period.

Dr David Livingstone died on May 1st 1873. He was 60 years old and had spent much of the previous 30 years walking across large stretches of Southern Africa, exploring the terrain he hoped could provide new environments in which Europeans and Africans could cohabit on equal terms and bring prosperity to a part of the world he saw ravaged by the slave trade. Just days before he died, he wrote in his journal about the permanent stream of blood that he was emitting related to haemorrhoids and the acute intestinal pain that had left him incapable of walking. What actually killed Livingstone is unknown, yet the years spent exploring sub-Saharan Africa undoubtedly exposed him to a gamut of parasitic and other infectious diseases. Some of these we can be certain of. He wrote prolifically and described his encounters with malaria, relapsing fevers, parasitic helminths and more. His graphic writing allows us to explore his own encounters with tropical diseases and how European visitors to Africa considered them at this time. This paper outlines Livingstone's life and his contributions to understanding parasitic diseases.

This article explores the scientific and entrepreneurial incentives for malaria research in the tea plantations of north Bengal in colonial India. In the process it highlights how the logic of ‘location’ emerged as the central trope through which medical experts, as well as colonial administrators and planters, defined malaria research in the region. The paper argues that the ‘local’ emerged as both a prerequisite of colonial governance as well as a significant component of malaria research in the field. Despite the ambiguities that such a project entailed, tropical medicine was enriched from a diverse understanding of local ecology, habitation, and structural modes of production. Nevertheless, the locality itself did not benefit from anti-malarial policy undertaken either by medical experts or the colonial state. This article suggests that there was a disjuncture between ‘tropical medicine’ and its ‘field’ that could not be accommodated within the colonial plantation system.

Intraperitoneal glucose tolerance tests were performed at 4-week intervals in groups of weanling rats before and after feeding with maize- or cassava-based diets with and without adequate protein and sublethal cyanide supplementation. Weaning weights were doubled (increase of about 50 g) after 4 weeks on control (maize-based with adequate protein) and protein-replete diets. Weight gain on the protein-deficient diets was much less (22 g or 50%), a pattern maintained by the rats on these diets until the age of 12 weeks. Plasma thiocyanate levels were identical at weaning and after 8 weeks of the control diet but increased by 200–300% after 4 weeks intake of the cassava or cyanide-supplemented feeds. Levels returned to normal in all groups after a further 4 weeks feeding with the control diet. Glucose tolerance (as assessed by the area under the 2 h glucose ν. time curve) was impaired to a varying extent in the rats after 4 weeks on the various diets: protein-replete cassava and protein-deficient maize diets by 50%, protein-deficient cassava diet by 300%, and cyanide-supplemented protein-deficient maize diet by 150%. The derangement in the rats on the protein-replete cassava diet was unaffected by a further 4 weeks intake of the control diet, unlike in the other groups where there was significant improvement in the glucose tolerance indices at the same time. It is concluded that in growing rats: (1) cassava intake and protein malnutrition may have independent and additive effects on the genesis of glucose intolerance, (2) cyanide supplementation of a cassava-free protein-replete diet has no effect on glucose tolerance.