L.G. Goodwin

Bio: L.G. Goodwin is an academic researcher from Zoological Society of London. The author has contributed to research in topics: Endothelium & Venule. The author has an hindex of 1, co-authored 2 publications receiving 47 citations.

Pathological effects of Trypanosoma brucei on small blood vessels in rabbit ear-chambers

Abstract: The effect of Trypanosoma brucei infection on small blood vessels has been studied in regenerative ear-chambers in rabbits. Damage to the vessels was observed about 2 weeks after the animals had been inoculated with trypanosomes. Mononuclear phagocytic cells collected on the endothelium of the small venules, the blood flow was obstructed and the vessels disintegrated. Fibroblasts and collagen in the connective tissue degenerated. Few trypanosomes were present in the circulating blood but the tissue spaces contained many parasites. From time to time the trypanosomes in the tissue spaces were trapped and digested by phagocytes.

The skin is a significant but overlooked anatomical reservoir for vector-borne African trypanosomes

Abstract: The role of mammalian skin in harbouring and transmitting arthropod-borne protozoan parasites has been overlooked for decades as these pathogens have been regarded primarily as blood-dwelling organisms. Intriguingly, infections with low or undetected blood parasites are common, particularly in the case of Human African Trypanosomiasis caused by Trypanosoma brucei gambiense. We hypothesise, therefore, the skin represents an anatomic reservoir of infection. Here we definitively show that substantial quantities of trypanosomes exist within the skin following experimental infection, which can be transmitted to the tsetse vector, even in the absence of detectable parasitaemia. Importantly, we demonstrate the presence of extravascular parasites in human skin biopsies from undiagnosed individuals. The identification of this novel reservoir requires a re-evaluation of current diagnostic methods and control policies. More broadly, our results indicate that transmission is a key evolutionary force driving parasite extravasation that could further result in tissue invasion-dependent pathology.

Alternative pathway activation of complement by African trypanosomes lacking a glycoprotein coat.

Abstract: Summary An in vitro culture Trypanosoma congolense cell line was established using the mammalian cell feeder layer system. One of the principle characteristics of this parasite was its ability to multiply in culture at 35°C, as an uncoated trypanosome (lacking a glycoprotein surface coat) unlike the original blood stream form from which it was derived. This trypanosome was lysed when incubated in normal human serum in contrast to the parasite which possessed a surface coat. The lytic reaction was inhibited by EDTA but not EGTA and occurred in C2-deficient serum, demonstrating the involvement of the alternative pathway of complement activation. Similar results were obtained with procyclic forms of T. congolense and T. brucei brucei which also lacked surface coats. The results suggest that the glycoprotein surface coat protects the parasite by masking sites on the plasma membrane which are capable of promoting alternative pathway activation.

Immunosuppression in Trypanosoma brucei infections in rats and mice

Abstract: In rats in which N. brasiliensis infection was superimposed on a previously existing T. brucei infection of 3 weeks' duration, the normal process of immune expulsion of adult worms did not occur, the production of circulating protective antibody (IgG) and of reaginic antibody (IgE) was grossly impaired and there was no increase in the numbers of mast cells in the intestinal villi. In contrast to this failure of humoral and immediate-type responses, cell-mediated immunity, as measured by oxazolone sensitization of mice with a T. brucei infection, still occurred to a significant extent although not so markedly as in uninfected mice. These results, which provide further evidence that infection with T. brucei may induce a significant degree of immunosuppression of the host, are discussed with particular regard to the aetiology of the phenomenon.