Failure of irradiated Echinostoma audyi and Hypoderaeum dingeri to sensitize Lymnaea rubiginosa snails.

Attempts to induce acquired resistance in Lymnaea rubiginosa snails against the echinostomes Echinostoma audyi and Hypoderaeum dingeri by means of irradiated miracidia were unsuccessful, although Lie and coworkers using similar methods had recently sensitized Biomphalaria glabrata against Echinostoma lindoense (1975a). In contrast to the B. glabrata-E. lindoense system, in Lymnaea rubiginosa the amebocytic response to irradiated parasites was slow: irradiated E. audyi sporocysts were encapsulated 15 to 28 days and H. dingeri sporocysts 20 to 27 days postexposure. No obvious enlargement of the amebocyte-producing organ was seen. No resistance was demonstrable to subsequent homologous challenge. Development of acquired resistance to a trematode infection in snails may be related to the speed with which the snails destroy the irradiated sporocysts.

The freshwater snail lymnaea rubiginosa as an experimental host of Angiostrongylus malaysiensis: a preliminary report.

Preliminary studies have shown that Lymnaea rubiginosa, a common fresh-water snail in Peninsular Malaysia, which is easily colonized and reared in the laboratory, is a capable experimental intermediate host for Angiostrongylus malaysiensis. Overall 73% of the snails tested became infected following 6 hours exposure to infective rat faeces. Higher infection rates, up to 100%, and heavier worm loads, occurred among the larger sized snails. Snail attrition was low except when very heavy worm loads were acquired.

Increased frequency of chloroquine resistant P. falciparum on a rubber estate in Peninsular Malaysia during two years of systematic chloroquine treatment.

Chloroquine pressure was applied over a 22 month period on a somewhat isolated, malarious rubber estate by examination of residents at 4-week intervals and treatment of parasitaemias with chloroquine. During this time the monthly attack rate for P. falciparum rose four-fold to an average of nearly 18% per month, while that of P. vivax remained relatively constant at about 8%. Eight in vivo chloroquine resistance studies, which allowed both detection of late recrudescing R-I resistance and estimation of the risk of reinfection, showed an apparent rise in the drug resistance rate, from 12% to 20% prior to the study to the range of 40-50%. Virtually all resistance encountered was R-I in nature. There was no convincing evidence of chloroquine resistance among 148 tested P. vivax infections.