Trypanosomiasis in raccoons from Georgia.

Trypanosoma cruzi frequently infects wild mammals in the southern United States but little is known about the effect of the parasite on reservoir hosts such as the raccoon (Procyon lotor). To investigate this issue, 30 raccoons trapped on St. Catherine's Island (Georgia, USA) during September, 1994 were tested for T. cruzi infection by examination of wet mounts of fresh blood and by culturing blood in liver infusion tryptose medium. Thirteen animals (43%) were found to be infected with T. cruzi. Heart tissues from 10 of the infected raccoons and 4 uninfected raccoons were fixed, sectioned, stained and examined for the presence of parasites and evidence of tissue damage. One T. cruzi pseudocyst was found in cardiac tissue from the left ventricle of a female raccoon. In addition, Sarcocystis sp. sarcocysts and schizonts of Hepatozoon sp. were observed in heart tissue from seven of the T. cruzi-infected raccoons. Mild, multifocal and interstitial inflammation was observed in the heart tissues of all 10 of the infected animals. No evidence of T. cruzi pseudocysts or tissue damage was observed in heart tissue from C3H/HeJ mice infected with culture forms of the parasites isolated from raccoons. Our findings suggest that the T. cruzi parasites isolated from raccoons in Georgia are not pathogenic to this host or C3H/HeJ mice and may be of low virulence.

Succinate decarboxylation to propionate and the associated phosphorylation in Fasciola hepatica and Spirometra mansonoides.

The trematode, Fasciola hepatica, and the cestode, Spirometra mansonoides have been shown to be similar to the nematode Ascaris lumbricoides in that all three decarboxylate succinate to propionate plus CO2. Associated with this decarboxylation is an incorporation of 32Pi into organic phosphate. Both the decarboxylation and phosphorylation are markedly stimulated by the addition of propionyl-CoA, are dependent on coenzyme B12 and are inhibited by avidin. The trematode and cestode exhibit propionyl-CoA carboxylase, methylmalonyl-CoA mutase and acyl-CoA transferase activities in sonicated mitochondrial preparations. Data are consistent with the occurrence of a mitochondrial substrate level site for ATP generation which is coupled with the decarboxylation of succinate. In Fasciola preparations, acetyl-CoA stimulates the decarboxylation and phosphorylation to a considerably larger extent than propionyl-CoA, indicating the possibility that acetyl-CoA may serve physiologically in these reactions by donating the CoA moiety to succinate.