Aims and objectives

This exercise is designed to demonstrate:

1. An important humoral immune killing mechanism against Trypanosoma brucei.

2. Binding of trypanosomes to macrophages mediated by specific antibodies, the first stage in the process of opsonisation.

3. Antigenic variation by T. brucei as a mechanism of evasion of specific antibodies.

Introduction

T. brucei is one of three parasite species that collectively cause Nagana, one of the most important diseases of livestock in sub-Saharan Africa. The other two species are T. congolense and T. vivax. There are three sub-species of T. brucei, two of which, T. b. gambiense and T. b. rhodesiense, cause sleeping sickness in humans. Currently, sleeping sickness is predicted to cause 300000–500000 new cases per year. Infection is normally fatal in the absence of chemotherapy but most infected people will have no access to the relevant drugs.

Vaccination is an obvious alternative to reliance on drugs for prevention of infection and/or disease but the development of potential vaccines has been little explored in African trypanosomiasis because these parasites undergo antigenic variation. Each T. brucei parasite is enwrapped in a surface coat that is visible by electron microscopy. The coat is comprised of approximately 107 copies of a single molecular species of glycoprotein. It acts as a physical barrier preventing access to the underlying plasma membrane by components of non-specific immune responses that are lethal to uncoated parasites.