In this study, we compare the development of infection and/or disease in Beagle dogs intradermally infected with Leishmania chagasi, in the presence or absence of Lutzomyia longipalpis saliva, with those of intravenously infected animals. Spleen samples of all the animals inoculated with parasites had positive polymerase chain reaction tests for Leishmania DNA. Positive spleen cultures for Leishmania were detected earlier (P < or = 0.018) and were more frequent (five out of the five animals) in intravenously infected animals than in the intradermally infected animals, in presence (two out of the six animals) or absence (three out of the five animals) of salivary gland lysate of L. longipalpis. Significant increase in serum antibodies against Leishmania was observed only in the intravenously infected group (P = 0.004). In addition, dogs with infection confirmed by isolation of amastigotes or detection of parasite DNA were, nevertheless, negative for anti-Leishmania antibodies up to 5 months or more after infection. Only animals of the intravenously infected group developed progressive decreases in hematocrit (Pearson r = -0.8076, P = -0.0026) and hemoglobin (Pearson r = -0.8403, P = 0.0012) during the infection period. No significant difference in the course of infection was observed between groups of intradermally infected animals. The data presented herein confirms that the intradermal inoculation of dogs with Leishmania produces an asymptomatic form of infection. It also fails to show an advantage in using L. longipalpis saliva as an infection-enhancing agent in experimental canine leishmaniasis.

The sensitivity of the larval stages of Schistosoma mansoni to chemotherapy with praziquantel and oxamniquine was tested in mice during primary and secondary infections and after different intervals from cercarial exposure. Worm recovery by perfusion of the porto-mesenteric system, followed by counting and a morphometric study of the parasite, allowed the conclusion that the relative resistance of the larval stages of S. mansoni to schistosomicide drugs, demonstrated in primary infections, also persists when the host is already infected. This indicates that a therapeutic failure may result when an infected host is treated some time after being re-infected, because of the presence of migrating, drug-resistant, immature forms of the parasite. Key-words: Schistosoma mansoni. Larval stages. Praziquantel. Oxamniquine.Resumo A susceptibilidade dos estágios larvais do Schistosoma mansoni aos esquistossomicidas praziquantel e oxamniquine foi testada em camundongos durante infecção primária ou secundária, e após diferentes intervalos de tempo após a exposição cercariana. A avaliação foi feita pela contagem dos vermes após recuperação destes por perfusão do sistema porto-mesentérico e pelo estudo morfométrico dos mesmos. O estudo revelou que a relativa resistência das formas larvais aos esquistossomicidas, já demonstrada em infecção primária, persiste no caso de hospedeiros já infectados. Este fato indica que uma falha terapêutica pode resultar quando o tratamento é feito em hospedeiros re-infectados recentemente, em virtude dos mesmos apresentarem formas migrantes e imaturas do parasita, as quais são particularmente resistentes aos esquistossomicidas. Palavras-chaves: Schistosoma mansoni. Estágio Larval. Praziquantel. Oxamniquine.