The trypanosome life cycle is referred to as digenetic, meaning that it undergoes two proliferative stages. The trypanosome life cycle involves a complex development of morphological distinct forms. These forms are present within the mammalian host and the insect vector. The major morphological difference involves changes in the cell structure and involves repositioning of the mitochondrial DNA that makes up the kinetoplast. During the progression of their life cycle, repositioning of the kinetoplast from the anterior to the posterior end of the trypanosome body, the flagellum begins anteriorly, passing to the posterior end and forming the end of the undulating membrane. These events were discovered to be fundamental, after transfer of the parasite from the host blood to the tsetse midgut. (Matthews, 1995)
Trypanosomes in the blood of vertebrates have been observed to have three body types; a short, broad form often without a flagellum, called the promastigote; a long and narrow form, the trypomastigote, and an intermediate between these two, the epimastigote. In arthropod hosts all developmental stages have been reported to derive from an amastigote stage, which lacks a flagellum and has a circular shape. Trypomastigote form may be active and proliferative, at this stage they are referred to as metacyclic, which is presumed to be the infective stage for vertebrates.
Trypanosome life histories state that in the blood-sucking invertebrate host the parasites multiply actively by binary fission in the lumen of the digestive tract, and commonly also by multiple division within host epithelial cells, in this particular stage the trypanosome is referred to as procyclic. The trypanosome body type is obtained from the vertebrate blood is changed first into amastigote (multiply by binary fission in T. cruzi) and then to promastigote and epimastigote stages or directly to metacyclic stages. Metacyclic stages are immature and require the environment of mammalian blood and tissues in order to become mature.
The method of infection depends upon the site of infection of the vertebrate largely depends of the accumulation of the metacyclic forms in the invertebrate. The metacyclic trypanosomes accumulate in the salivary glands or mouthparts of the invertebrate host. In most species trypanosomes multiplication is active in the vertebrate blood, also by means of binary fission or multiple division. (Noble 1955)

Studies have shown that behavior changes in the vertebrate host increases their susceptibility to be bitten by insect vectors. Experiments have shown that a change in temperature of the infected vertebrate was positively correlated to the frequency of attacks by insect vectors. The infection of the proboscis of the tsetse fly, Glossina m. moristans, by Trypanosoma brucei, and in T. congolese have been seen to have sophisticated mechanisms to induce a behavioral changes in their insect vector. They reduce the rates blood flow by a factor of almost ten. Infected individuals are unlikely to be able to detect this reduced flow as the parasites wraps around the mechanoreceptors of the labrum (mouth part) and impair their ability to monitor flow rates. Experiments have suggested that infected individuals probe for blood meals but usually fail to engorge; by moving on and attempting to feed elsewhere they raise the rates of transmission (Dobson, 1988).

References

1. Dobson, 1988, The Population of Parasite-Induced Changes in Host Behavior, Quarterly Review of Biology 63: 139-165

2. Matthews, Sherwin, Gull, 1995, Mitochodrial Genome Repositioning During the Differentiation of the African trypanosome between life cycle forms is microtubule mediated, Journal of Cell Science 108: 2231-2239

3. Noble, Elmer, 1955, The Morphology and Life Cycles of Trypanosomes, Quarterly Review of Biology 30:1-29