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Trypanosomiasis remains one of the most serious constraints to economic development in sub-Saharan Africa and, as a consequence, related research has been subject to strong social and political as well as scientific influences. The epidemics of sleeping sickness that occurred at the turn of the 20th Century focussed research efforts on what became known as 'the colonial disease'. This focus is thought to have produced 'vertical' health services aimed at this one disease, while neglecting other important health issues. Given the scale of these epidemics, and the fact that the disease is fatal if left untreated, it is unsurprising that sleeping sickness dominated colonial medicine. Indeed, recent evidence indicates that, if anything, the colonial authorities greatly under-estimated the mortality attributable to sleeping sickness. Differences in approach to disease control between Francophone and Anglophone Africa, which in the past have been considered ideological, on examination prove to be logical, reflecting the underlying epidemiological divergence of East and West Africa. These epidemiological differences are ancient in origin, pre-dating the colonial period, and continue to the present day. Recent research has produced control solutions, for the African trypanosomiases of humans and livestock, that are effective, affordable and sustainable by small-holder farmers. Whether these simple solutions are allowed to fulfil their promise and become fully integrated into agricultural practice remains to be seen. After more than 100 years of effort, trypanosomiasis control remains a controversial topic, subject to the tides of fashion and politics. [ABSTRACT FROM AUTHOR]

Sleeping sickness has long been a major public health problem in Uganda. From 1900 to 1920, more than 250,000 people died in an epidemic that affected the southern part of the country, particularly the Busoga region. The epidemic has traditionally been ascribed to Trypanosome brucei gambiense, a parasite now confined to central and western Africa. The Busoga region still reports sleeping sickness, although it is caused by T.b. rhodesiense, commonly believed to have spread to Uganda from Zambia in the 1940s. Our analysis of clinical data recorded in the early 1900s shows that the clinical course of sleeping sickness cases during the 1900-1920 epidemic in Uganda was markedly different from T.b. gambiense cases, but similar to T.b. rhodesiense. These findings suggest that T.b. rhodesiense was present in Uganda and contributed to the epidemic. The historic context is reassessed in the light of these data. [ABSTRACT FROM AUTHOR]

Removal of certain components from pig or cow blood greatly reduces the maturation rate of Trypanosoma congolense infections in Glossina morsitans fed on such diets. In particular, delipidation of serum has the same effect as complete removal of dietary serum with few midgut infections reaching maturity. The addition of gamma-globulin to red cells partially restores the ability of immature infections to transform suggesting that serum lipids or other serum factors are not acting directly on midgut trypanosome metabolism but indirectly through interactions between dietary constituents and the flies' metabolic processes. As susceptibility to T. congolense infection is known to be maternally inherited in G. morsitans, it is suggested that serum factors act through the flies' symbionts to induce maturation in midgut infections. [ABSTRACT FROM AUTHOR]

ABSTRACT. The process of maturation of Trypanosoma congolense Broden in tsetse has been shown to be initiated by lectin secreted in the fly midgut. In the present study the duration of lectin signal required to induce maturation was determined by the sequential addition or removal of a specific lectin inhibitor (D+glucosamine) to the diet of infected male Glossina morsitans Westwood. An established midgut infection of T.congolense was found to require, at most, 72 h exposure to midgut lectin to begin the process of maturation. Longer exposure to midgut lectin increased the frequency of maturation, suggesting clonal variation in response to lectin stimulation occurs within trypanosome stocks. It is suggested that this variation corresponds to differences in lectin binding sites on the trypanosome surface. Midgut trypanosomes retained their ability to mature throughout their life in the fly; when lectin activity in the midgut was inhibited, the trypanosomes remained as procyclic forms but when this inhibition was removed maturation was able to proceed. This indicates that the process of maturation is dependent upon a signal from the fly and is not predetermined by the trypanosomes undergoing a fixed number of division cycles. The possible role of lectins in the maturation of trypanosomes in vitro is discussed. [ABSTRACT FROM AUTHOR]

ABSTRACT. The activity of lectins in different species of tsetse was compared in vivo by the time taken to remove all trypanosomes from the midgut following an infective feed and in vitro by agglutination tests. Teneral male Glossina pallidipes Austen, G.austeni Newstead and G.p.palpalis R-D. removed 50% of all Trypanosoma brucei rhodesiense Stephens & Fantham infections within 60 h. A 'refractory' line of G.m.morsitans Westwood took 170 h to kill 50% infections while a 'susceptible' line of the same species failed to kill 50%. Agglutination tests with midgut homogenates showed differences between fly stocks which accorded with differences in rate of trypanosome killing in vivo. Flies fed before an infective feed were able to remove trypanosomes from their midguts more quickly than flies infected as tenerals. Increasing the period of starvation before infection increased the susceptibility to trypanosome infection of non-teneral flies. Teneral flies showed little agglutinating activity in vitro, suggesting that lectin is produced in response to the bloodmeal. Feeding flies before infection also abolished the differences in rate of trypanosome killing found between teneral 'susceptible' and 'refractory' G.m.morsitans, suggesting that maternally inherited susceptibility to trypanosome infection is a phenomenon limited to teneral flies. Electron micrographs of midguts of G.m.morsitans suggest that pro-cyclic trypanosomes are killed by cell lysis, presumably the result of membrane damage caused by lectin action. [ABSTRACT FROM AUTHOR]

Abstract Cyclic nucleotide signalling through cyclic adenosine monophosphate (cAMP) is thought to play an important role in the transformation of the long slender (dividing) form to the short-stumpy (arrested) form in the mammalian bloodstream but the role of cyclic nucleotides in the tsetse-based part of the trypanosome life cycle is unknown. In a series of in vivo experiments, it was found that cyclic guanosine monophosphate (cGMP) but not cAMP could induce significantly higher rates of midgut infection in tsetse. Continuous feeding of either cGMP or cAMP to tsetse had no effect on rates of maturation of established midgut infections suggesting that these two parts of the life cycle in tsetse are not linked.

The extrachromosomal DNA of Sodalis glossinidius from two tsetse fly species was sequenced and contained four circular elements: three plasmids, pSG1 (82 kb), pSG2 (27 kb), and pSG4 (11 kb), and a bacteriophage-like pSG3 (19 kb) element. The information suggests S. glossinidius is evolving towards an obligate association with tsetse flies. [ABSTRACT FROM AUTHOR]