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The trypomastigotes of Trypanosoma cruzi closely resemble those of T. brucei, and like them, disseminate from the site of inoculation to circulate in the peripheral blood of their mammalian hosts. Their developmental cycle, however, differs in several respects. Most significant, T. cruzi does not multiply extracellularly. The circulating trypomasti-gotes must invade tissue cells, lose their flagella, and assume the amastigote form before binary fission can occur. Continued multiplication leads to distention and eventual rup-ture of the tissue cell. Released parasites revert to trypomastigotes and regain the bloodstream. This new generation of trypomastigotes may invade other host cells, thus continuing the mammalian cycle. Alternatively, they may be ingested by a feeding reduviid and develop into epimastigotes within its midgut. On completion of the inver-tebrate cycle, the parasites migrate to the hindgut and are discharged as infectious try-pomastigotes when the reduviid defecates in the process of taking another blood meal. This process can recur at each feeding for as long as 2 years. Infection in the new host is initiated when the trypomastigotes contaminate either the feeding site or the mucous membranes.
T. cruzi comprises a number of strains, each with its own distinct geographic distribu-tion, tissue preference, and virulence. They may be distinguished from one another with specific antisera and by differences in their isoenzyme and DNA restriction patterns. All are morphologically identical. In blood specimens, the trypomastigotes can be distin-guished from those of T. brucei by their characteristic C or U shape, narrow undulating membrane, and large kinetoplast.
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