Comparison of the effects of immune killing mechanisms on Trypanosoma brucei parasites of slender and stumpy morphology.

Trypanosoma brucei slender forms predominate over stumpy forms as the parasite population grows but at the peak of a parasitaemic wave and during remission of infection stumpy forms predominate. To determine whether this change in predominance might be caused by selective killing of slender forms, the fates of slender and stumpy form trypanosomes in two in vitro assays of immune-mediated killing were compared. Parasite populations in which > 90% of cells were of slender morphology were observed to be killed by antibody-dependent complement-mediated lysis approximately five times faster than populations in which < 15% of cells were slender and most were of intermediate or stumpy morphology. Quantification of the relationship between the proportion of slender forms in the population and the rate of lysis indicated that slender forms were killed approximately 7.3 times faster than other forms. In an opsonization assay, no differences were observed between slender and stumpy forms in the extent to which they attached to macrophages in an antibody-dependent manner. These results suggest that the change in proportions of slender and stumpy forms at the peak of a parasitaemic wave results from slender forms being more susceptible to complement-mediated killing as the antibody response develops.

A comparison of multiplication rates in primary and challenge infections of Trypanosoma brucei bloodstream forms.

The hypothesis that division of Trypanosoma brucei slender bloodstream forms is dependent upon the availability of a host-derived growth factor has been tested by superimposing challenge doses of slender-form trypanosomes onto preexisting infections at a time during the primary infection when stumpy forms predominated. The challenge populations grew in the doubly-infected mice indicating that depletion of a putative growth factor by the expanding population of the primary infection had not prevented division of the trypanosomes although slight reductions in multiplication rates were observed. This effect was independent of the variable antigen type (VAT) of the trypanosomes and of their stock of origin.