Injury Induced by Trypanosoma congolense Adhesion to Cell Membranes

Abstract

Trypanosoma congolense binds to erythrocytes and the walls of the microvasculature. Experiments were conducted to determine if the attachment of T. congolense, alone or in combination with antitrypanosome antibody, was damaging to host cells. Bovine erythrocytes were labelled with 51Cr and incubated with T. congolense to promote adhesion. Plasma from the same donor as the red blood cells was added to the erythrocyte-trypanosome aggregates and the release of 51Cr measured. There was a two- to threefold increase in 51Cr release when trypanosomes were lysed by antibody-complement interaction following adhesion to the erythrocyte. The erythrocytes were not damaged by trypanosome binding in the absence of antibody or complement. A similar mechanism may operate in vivo because experiments demonstrated an increased vascular permeability of mesenteric vessels, a site of T. congolense attachment to the microcirculation. These results suggest that the adhesion of T. congolense to host cells, followed by an immune response to the parasite, may damage the infected host by "innocent bystander" mechanisms.

Cations in body fluids ofTrypanosoma bruceiin infected rabbits

“…Most of these manifestations have also been seen in human and animal African trypanosomiases. These include convulsions (Markell and Voge, 1981); electrocar diographic changes (Murray et al, 1974); release of phar macologically active substances (Wright, 1979); and increased vascular permeability (Banks, 1980). Some of these manifestations such as splenomegaly, eosinophilia, and der matologic lesions of the eyelids, nares and testicles were observed in the present study.…”

Host-Parasite Interactions in Trypanosomiasis: on the Way to an Antidisease Strategy

“…RBC surface alterations have indeed been shown to be caused by bloodstream T. vivax, T. congolense, and T. evansi sialidases, thus leading to their subsequent phagocytosis (26,40,115,116). Although the experimental demonstration of sialidase activity in T. congolense bloodstream forms was quite recent (116), a direct interaction of this trypanosome with RBC resulting in alteration of these cells had already been shown in earlier studies (13,14). T. vivax sialidase was shown to present some host specificity, desialating camel, goat, and zebu RBC, while those from mice, dogs, and NЈDama bulls were shown to be resistant (26).…”

TNF-a mediates the development of anaemia in a murine Trypanosoma brucei rhodesiense infection, but not the anaemia associated with a murine Trypanosoma congolense infection

“…Several hypotheses have been suggested [1,4]. Increased red cell damage by haemolysins, proteases [7], phospholipases [8,9], neuraminidase [10,11] or their products have been implicated. Also immunological mechanisms have been advanced to explain increased removal of erythrocytes.…”