Annales de parasitologie humaine et comparee最新文献

Urografin was used in the lower cushion of discontinuous density gradient systems, for the separation of human hepatoma cells (Hep G2) infected with exoerythrocytic P. berghei forms from uninfected cells. The hepatoma cells exhibited a rather heterogeneous density distribution, masking the possible density differences between infected and uninfected cells and hindering the efficient separation of both cell types. Purely osmotic damage caused by Urografin on human erythrocytes and hepatoma cells is very limited. On the other hand, the direct toxic effects on P. falciparum blood stages and on P. berghei exoerythrocytic stages are very pronounced. The growth of the former forms is partially inhibited after a pretreatment, but remains acceptable if the contact with Urografin is relatively short. It is almost completely blocked during permanent incubation. The latter forms are killed after 1 hour of contact with Urografin.

Antileishmanial chemotherapy is hampered by the location of parasites within lysosomal vacuoles of the macrophages which restricts the bioavailability of many potential antileishmanial compounds. In this study, the effectiveness of pentamidine targeted to the infected cells by a linkage to a colloidal drug carrier, methacrylate polymer nanoparticles was explored. In the same way, polyisoalkylcyanoacrylate nanospheres which have, in vitro, trypanolytic properties were also tested. The study was performed in an in vitro model using Leishmania major amastigote stages within the U 937 human monohistiocytic cell line. The antileishmanial activities of unloaded or pentamidine-loaded nanoparticles were compared to those of the free drugs. The 50% effective concentration of targeted pentamidine was 0.10 microgram/ml, while it was up to 2.7 micrograms/ml with the free drug after a 24-hour incubation time. The pentamidine-bound nanoparticles proved to be 25 times more active than the free drug. Unloaded polyisoalkylcyanoacrylate nanoparticles destroyed intracellular amastigote stages (50% EC = 15 micrograms/ml) but at a level close to the cytotoxic concentration.

The cellular dynamic against deposited Schistosoma haematobium eggs was studied in the submucosa and muscularis of the lower ureteral segments of Saudi patients with chronic urinary schistosomiasis. This dynamic activity was greatly affected by the damaged phase of the egg embryo. Freshly deposited eggs with "healthy" embryos were entirely surrounded by long cytoplasmic extensions of fibroblasts. Eggs with partially damaged embryos were surrounded by plasma cells which were focally adhered to spines of egg-shells and releasing their granular contents over their surface. Eggs with "dead" embryos, or empty egg-shells, were surrounded by actively mobile macrophages possessing numerous lysosomes, phagocytic vacuoles, and convoluted surface projections. After "peeling" off the outer and intermediate shell layers, macrophages invaded into eggs and fused together forming multinucleate giant macrophages. This study showed that the fibroblastic extensions acted as barriers between the parasite eggs or their products, and the host tissue; the plasma cell secretion over the egg surface may be involved in the migration of macrophages towards deposited eggs; and macrophages were the only dynamic cells responsible for the egg-shell invasion possibly for elimination.

The effect of ivermectin was studied on two filaria-vector pairs, Brugia malayi-Aedes aegypti and Litomosoides sigmodontis-Bdellonyssus bacoti. The rodent hosts, respectively Mastomys coucha and Meriones unguiculatus, were treated with ivermectin doses of 0.05 mg/kg, or 0.2 mg/kg or 2 mg/kg. Batches of vectors were fed on rodents, infected or not, treated or not, from H7 to D43 post-ivermectin. Vector survival was observed and dissections were performed to study the filarial development. It appears that ivermectin has no systemic effect on vectors, or very little. The drug acts on transmission because it affects the microfilariae. Transmission of L. sigmodontis is blocked because microfilariae are eliminated from the blood. Transmission of B. malayi is blocked although microfilaremia remains present at a low level. Two particular features are observed: microfilariae are hyper-ingested, but they do not cross the stomach wall (in contrast, they cross at a high rate in the control batch of Aedes, due to the "stomach wall limitation"). These events might be explained by a muscular passivity of the microfilariae treated with ivermectin. Transmission of the two filarioid species is restored normally about D25-40 post ivermectin because a new population of microfilariae has appeared. These ivermectin experiments emphasize the diversity and complexity of two important phases of the filarial cycle in the vector: the ingestion of microfilariae and the passage through the stomach wall.