Lifecycle

Human African trypanosomes are transmitted by several species of tsetse flies of the genus Glossina; although these distinctions are not absolute, it is generally accepted that T. brucei var. rhodesiense is transmitted by dry flies (G. morsitans group) and T. brucei var. gambiense by wet flies (G. palpalis group). A wide variety of vertebrate hosts may be infected and, particularly for T. brucei var. rhodesiense, serve as important zoonotic reservoirs.

The life-cycle of T. brucei is depicted in Figure 14a.2. Development in the tsetse commences when an uninfected fly bites an infected vertebrate, ingesting trypomastigote forms of T. brucei. The trypanosomes in the vertebrate's blood migrate into the vector's midgut, where the short stumpy (SS) forms complete the development of their mitochondrion and change their surface coat to differentiate into the long, slender procyclic stages. As the procyclic stages have a fully developed mitochondrion and polysomes highly loaded with mRNA, they exhibit significantly higher levels of metabolic activity and protein synthesis than do the bloodstream stages (Brecht et al., 1998). These stages have Krebs cycle enzymes and actively respire using an electron transport system. This mitochondrial development also brings about a change in the positional relationship between the nucleus and the kinetoplast-mitochondrial complex, as well as in flagellar motion and hence trypanosomal motility. The procyclic forms develop further, undergoing more morphological changes and, after numerous cycles of multiplication, migrate into the vector's salivary glands and differentiate into epimastigotes (Figure 14a.3a), which attach to the cells of the gland and continue multiplying. Eventually, some epi-mastigotes undergo a final transformation stage into non-dividing metacyclic trypomasti-gotes (Figure 14a.3b), which are short, stumpy and highly motile. They lack free flagella, and have a terminally located kinetoplast. Mature metacyclic trypomastigotes detach from the salivary gland cells, synthesise a surface coat and are then able to infect a vertebrate bitten by the vector. This completion of development of the vector stages in the salivary glands (anterior station), and subsequent inoculative transmission to the mammalian host, are characteristic of the section salivaria of the genus Trypanosoma.

After metacyclic trypomastigotes have been transmitted from the tsetse fly to the vertebrate host, they transform into long slender (LS) forms (20-40 x 0.1 The LS forms lack cytochromes and several Krebs cycle enzymes, and generate ATP solely by glycolysis. These forms multiply by binary fission until a threshold population is reached, whereupon a switch occurs, resulting in LS forms transforming first into intermediate forms and then into SS forms (15-25x3.5 This transition involves cell cycle arrest and a decrease in protein synthesis, mediated by a reduction in ribosome loading (Brecht et al., 1998). The SS forms are morphologically and functionally very different. They do not divide and have no free flagellum. Considerable changes are also seen in their kinetoplast-mitochondrion complex—the kinetoplast is posteriorly located, and the first stages of functional mitochondrial development are seen. It is likely that the SS form is the form infective for the tsetse, and the switch from a predominance of LS forms to SS forms is therefore essential for the cycle to continue (Seed, 1998).

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