There is agreement today about the role that the characteristics of the pop
ulation of Trypanosoma cruzi play in the pathogenesis of the different clin
ical forms of Chagas disease. In our laboratory, we have studied the outcom
e of the infection of mice with two populations with polar biological behav
iour: RA and CA-I. We have demonstrated that the neuromuscular damage is, i
n part, mediated by different T cell subsets. We have also observed that th
e T cell phenotype responsible for the pathology and the targetted tissues
depend on the parasite population, Although we found no differences regardi
ng the reactivity of IgG to native nerve structures in sera from mice infec
ted with either strain, it is presumed that the humoral response would play
an additional role in the development of strain-dependent neuromuscular pa
thology since passive transfer of sera from mice infected with RA triggered
alterations of the nerve action potential whereas sera from CA-I-infected
mice did not. We have also detected a reduction in the fertility of female
mice infected with CA-I/K98, whereas females infected with RA showed no dif
ference in comparison with uninfected controls. However, congenital transmi
ssion was only observed in mice infected with RA. The differences observed
in fertility, in newborn survival, and in the number of fetal resorptions i
n mice infected with the myotropic strain could be attributed to the uterin
e inflammatory response, since no estrous alterations were observed between
infected and control groups.