Figure 1.

Kinetoplastid transmission cycles. The life cycles of kinetoplastid protozoan parasites show development stages in both invertebrate and vertebrate hosts. In leishmaniasis, promastigotes (flagellate and mobile forms) are inoculated into the skin along with the saliva of phlebotomine vectors (Diptera: Psychodidae). In the vertebrate hosts, they are maintained inside phagocytic cells under the proliferative form, amastigotes. When ingested by insect vectors, the amastigote forms are transformed into promastigotes which multiply in the intestinal tissue, then migrate as metacyclic promastigotes into the stomodal valve to be later injected into the skin during blood meal. In Chagas’ disease, the etiologic agent Trypanosoma cruzi is transmitted to vertebrate hosts as a metacyclic trypomastigote forms by infected triatomine bugs (Triatominae: Reduviidae) during blood feeding. Once in the vertebrate, trypomastigotes differentiate into intracellular amastigote forms. These proliferative stages multiply by binary division, and then differentiate into trypomastigotes, which are released into the bloodstream. When the triatomine bug takes a blood meal from an infected vertebrate host containing circulating parasites, the ingested trypomastigotes forms to differentiate into epimastigotes in the medium intestine of the vector, multiplying by binary division, after which they differentiate into infective metacyclic trypomastigote forms. In sleep sickness or human African trypanosomiasis, the parasite Trypanosoma brucei is transmitted by the bite of the tsetse fly (Glossinidae: Glossina). The parasite exists in the saliva of the invertebrate vector and is injected when the insect feeds on human blood. Unlike Trypanosoma cruzi, trypomastigotes of T. brucei do not invade host cells and, therefore, does not differentiate into intracellular amastigote forms. Instead, T. brucei parasites multiply as trypomastigotes in the blood of infected vertebrate host. The parasite cycle continues when a new vector feeds on a contaminated individual. In the invertebrate vector, the parasites differentiate into proliferative epimastigotes forms, invading the insect salivary glands to continue the cycle.