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Numbers of immature Trypanosoma brucei brucei within a tsetse midgut remain remarkably constant after establishment throughout the course of an infection, irrespective of whether the infection eventually matures. These results suggest a system of self regulation of the parasite population in the insect gut based on a form of programmed cell death which would carry advantages for both the parasite and the vector.

Midgut infection rates of Trypanosoma congolense in Glossina palpalis palpalis and of Trypanosoma brucei rhodesiense in Glossina pallidipes are potentiated by the addition of D+ glucosamine to the infective feed, but not to the levels of super-infection reported for G.m.morsitans, G.p.palpalis and G.pallidipes are shown to possess two trypanocidal molecules: a glucosyl lectin which can be inhibited by D+ glucosamine and a galactosyl molecule inhibited by D+ galactose. Addition of both D+ glucosamine and D+ galactose to the teneral infective feed promotes super-infection of the midguts of G.p.palpalis. The glucosyl lectin is specific for rabbit erythrocytes and is present in guts of fed G.m.morsitans and G.p.palpalis, titres of lectin activity do not increase substantially after the second bloodmeal. The galactosyl specific molecule does not show any erythrocyte specificity, although haemolytic activity is observed only in G.p.palpalis and not in G.m.morsitans. The presence of two trypanocidal molecules in some species of tsetse may account for the innate refractoriness of these flies to trypanosome infection. As D+ glucosamine also inhibits the killing of procyclic trypanosomes taken as an infective feed, it is suggested that the midgut lectin is normally responsible for the agglutination of trypanosomes in the fly midgut by binding to the procyclic surface coat, prior to establishment in the ecto-peritrophic space.

The tsetse immune system has recently been shown to be involved in trypanosome maturation; lectin secreted in the midgut, normally responsible for preventing the establishment of midgut infections, induces established midgut trypanosomes to mature. We now show that a second lectin, present in tsetse haemolymph, is essential to complete the maturation process. Interactions between tsetse lectins and parasite surface coats probably determine trypanosome transmissibility and may be partly responsible for the distribution of trypanosomiasis in Africa.

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.