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Non-pathogenic trypanosomes of the subgenus Herpetosoma are normally host specific, and laboratory models include Trypanosoma lewisi in rats and Trypanosoma musculi in mice. Two isolates of Trypanosoma grosi, originating from Apodemus agrarius and Apodemus peninsulae, grew well in Mongolian jirds, Meriones unguiculatus, after intraperitoneal inoculation of 2 x 10(5) or a minimum 500 bloodstream forms. The course of T. grosi infection in jirds resembled T. musculi infection in mice, rather than T. lewisi infection in rats. At week 2 to 3 p.i. trypanosomes disappeared from the bloodstream, and neither prednisolone treatment nor splenectomy prevented parasite elimination from the bloodstream. However, these treatments induced a marked increase in peak parasite counts. Regardless of prednisolone treatment or splenectomy, all jirds after day 21 p.i. became resistant to the reinfection. Although no trypanosomes were detected in the bloodstream of recovered jirds, dividing parasites persisted in the medullary capillaries of the kidney, like T. musculi infection in mice. We propose the T. grosi infection in jirds as an additional laboratory model for the study of non-pathogenic trypanosomes.

Since skin is the only route of entry of the parasite in schistosomiasis patients, intervention at the level of skin penetration should control the infection. Several compounds were screened for their ability to protect against cercarial penetration. Hinokitiol (β-thujaplicin) was found to have a significant cercaricidal effect in vitro, although there is no information on its cercaricidal mechanisms. To study the kinetics of morphological changes in Schistosoma mansoni associated with exposure to hinokitiol in vitro, cercariae were incubated in media containing hinokitiol at different concentrations and examined by transmission electron microscopy (TEM). TEM revealed that ultrastructural changes occurred by 15 minutes post exposure, at a concentration of 25 μg/ml. Degenerative changes involving both tegument and deeper parenchymal structures were progressive with duration of exposure at the concentration of 50 μg/ml. These structural changes may account for the inability of hinokitiol-treated cercariae to infect the host.hinokitiol; Schistosoma mansoni; cercariae; transmission electron microscopy