Infection with Trypanosoma cruzi during pregnancy in rats and a decrease in chronic myocardial lesions in their infected offspring.

To ascertain whether maternal infection with Trypanosoma cruzi may influence the course of the parasitic infection in offspring, two groups of female 1 rats were mated with syngeneic sires. One group of females was infected with 10(6) trypomastigotes of T. cruzi three times at weekly intervals. All offspring were nursed by their mothers until weaning and then separated into two groups of young, one to be infected with the same dose of T. cruzi, and the other to remain uninfected. Infection of pregnant rats caused no aggravated disease but resulted in a self-controlled infection that did not cause any deaths or affect their reproductive capacity. The number of young delivered, litter size, fertility coefficient, and offspring weights at weaning were also unaffected by maternal infection; however, the survival coefficient decreased in comparison with values recorded in the offspring of uninfected mothers. The latter finding is likely due to neonatal transmission, since bloodstream forms of T. cruzi were observed in a few offspring of infected mothers. While infected offspring whose mothers had been inoculated with T. cruzi during pregnancy were not protected from acute infection, the occurrence of chronic focal myocarditis was less prevalent when compared with that recorded in chronically infected offspring born to uninfected mothers.

[Delayed cutaneous response to different antigens in household contacts of leprosy patients and controls]. / La respuesta cutánea tardía a diferentes antígenos en convivientes de pacientes lepromatosos y testigos.

The delayed type hypersensitivity (DTH) response to PPD, candidin and histoplasmin, and Mitsuda reaction (MR) in household contacts (HC) of multibacillary (HCM) and paucibacillary (HCP) leprosy patients, and non exposed controls was studied. Intradermal tests with 0.1 ml. of each antigen were performed and read after 48 hours. Late nodular reaction to ML (MR) was evaluated at the 21st day post-challenge. As we had formerly demonstrated, MR was depressed in HCM. Interestingly, this reaction was also depressed in HCP to a lesser magnitude. HCM had a lower DTH response to histoplasmin in relation to PPD and candidin when persons were simultaneously challenged with the three antigens. According to these results we conclude that: a), HCM have a depression in late lepromin reaction; b), in HCP the depression in MR is of a lower magnitude. We hypothesize that in healthy contacts of bacilliferous patients an active mechanism of immunosuppression to mycobacterial antigens may be produced. Alterations in the skin response to histoplasmin is discussed.