Abstract
Trypanosoma brucei and its related species (T. congolense, T. equiperdum and T. vivax) are hemoparasitic, flagellated protozoa that are the causative pathogenic agents of African sleeping sickness in humans (T. brucei rhodesiense and T. brucei gambiense) and in domestic animals. T. brucei is transmitted by the tsetse fly (genus Glossina) thereby largely restricting these diseases to the African continent. During its life cycle in the fly and subsequently in the mammalian host, T. brucei normally appears to be pleomorphic in nature exhibiting several distinctive morphological forms (1). Slender bloodstream forms are present in the initial stages of an infection while nondividing, stumpy forms accumulate at later times. The stumpy forms are ingested by the fly and are transformed into procyclic forms (the only stage lacking a defined surface coat) in the midgut of the fly (2,3). The procyclic forms eventually migrate into the salivary glands where they differentiate into a heterogeneous population of metacyclic forms which are transmitted back to the host to complete the life cycle. Evolution has imparted intricate mechanisms to the trypanosomes for maintaining chronic infections in their mammalian hosts, thereby allowing for cyclical transmission via the tsetse fly. This unique phenomenon appears to be manifested by the ability of infectious trypanosomes to temporally alter this surface antigen structure thereby evading the host’s immune response (1,4-7). The net result is that T. brucei is a brilliant parasite.
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Marcu, K.B., Williams, R.O. (1981). Microbial Surface Elements: The Case of Variant Surface Glycoprotein (VSG) Genes of African Trypanosomes. In: Setlow, J.K., Hollaender, A. (eds) Genetic Engineering. Genetic Engineering. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-7075-2_6
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