American
Trypanosoma
PARASITOLOGY
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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