The effect of immune inhibition on pleomorphism in Trypanosoma brucei rhodesiense

Abstract

The effect of immune inhibition on the pleomorphism of Trypanosoma brucei was studied by counting trypomastigotes and their granules on agar. A statistical analysis is presented. Busulphan 32 mg/kg, given 24 h before inoculation, caused an inhibition of the infection detectable at 72 h, but not thereafter. Immune inhibition caused by busulphan was associated with increased numbers both of agranular forms and forms containing lipid (type II) granules. After 96 h, treatment did not alter the proportion of agranular to granular forms. The remission was delayed 24 h in treated rats, the remaining trypomastigotes being more sluggish, more fragile and containing more numerous granules of increased size. We conclude that the remission is not produced by the immune reaction but by an innate process of dissolution of the ageing trypomastigotes.

Polymorphism in Trypomastigotes of Trypanosoma (Megatrypanum) minasense in the blood of experimentally infected squirrel monkey and marmosets

“…The morphological variations showed by T. minasense during the course of the experimental infections reported here may be due to polymorphism as previously described in other species as (Brener 1979, Urdaneta-Morales 1983, Penin et al 1996 as well as in several African trypanosome species (Miles 1970, Hoare 1972, Ormerod et al 1974, Nantulya et al 1978, Ormerod 1979, Barry et al 1979, Evans & Brightman 1980, Vickerman 1985. There is much controversy regarding the biological significance of polymorphism in the genus Trypanosoma and the mechanisms which control it.…”

Similarities of lipid metabolism in mammalian and protozoan cells: an evolutionary hypothesis for the prevalence of atheroma.

“…The evidence so far seems to suggest that the formation of lipid globules and the action of trypanocidal HDL are not the same phenomenon, since the dynamics of the two processes differ considerably: the formation of globules is, on the one hand, a slow process which takes 3 to 5 days to reach a maximum, after which the trypanosomes are gradually destroyed over a period of about 24 h by liberation of hydrolytic enzymes, as described above (61); trypanocidal HDL, on the other hand, acts rapidly and will produce complete lysis on incubation in vitro for 15 min.…”

“…Trypanosomes Part of the life cycle of T. brucei occurs in the blood and involves the transformation of a long, narrow, and highly active trypomastigote, which emerges from the tissues, into a stumpy, leaf-like, and rather sluggish form; during the course of this transformation, cell division occurs and the residual stumpy form, in which division has ceased, accumulates globules of lipid (61). At the same time, the stumpy form acquires an excess of cholesterol, mostly as the ester which is presumably contained in these globules (90).…”