Chitotriosidase deficiency is not associated with human hookworm infection in a Papua New Guinean population.

Human chitotriosidase (CHIT1) is a chitinolytic enzyme with suggested anti-fungal properties. Previous studies have suggested that chitotriosidase may also protect individuals against filarial nematode infections and malaria. A mutant allele, which renders chitotriosidase unstable and enzymatically inactive, is found at a frequency of >20% in Caucasians and other populations. This allele is found at much lower frequency in parts of West Africa where malarial and intestinal helminth infections are endemic. Here, we investigate whether there is a significant association between chitotriosidase genotype and the intensity of hookworm infection in 693 individuals from five villages in Papua New Guinea. Individuals were genotyped for chitotriosidase using a PCR-based assay. There was no association between CHIT1 genotype and the intensity of hookworm infection as determined by faecal egg counts. The frequency of the mutant allele was 0.251, very similar to that found in non-endemic countries. The extent of geographical variation in allele frequencies across worldwide populations was not high (F(st)=0.11), and does not provide evidence for directional selection at this locus between different geographical areas. We conclude that the CHIT1 genotype does not play a crucial role in protection against hookworm infection. This does not correlate with a previous study that linked the mutant CHIT1 genotype to filariasis susceptibility. The possible reasons for this discrepancy are discussed.

Inhibition of acetylcholinesterase secretion from Nippostrongylus brasiliensis by benzimidazole anthelmintics.

Treatment of rats infected with Nippostrongylus brasiliensis with a single, oral therapeutic dose of the anthelmintic benzimidazole carbamates oxfendazole or mebendazole resulted, 24 hr later, in a marked reduction (60-90%) in the secretion of a low molecular weight acetylcholinesterase from the parasites when they were incubated in vitro. This effect coincided with the expulsion of parasites from the host as a result of the therapy. When parasites were incubated in vitro with 0.1 mM oxfendazole, mebendazole, flubendazole, parbendazole, cambendazole or thiabendazole a similar effect was observed; with oxfendazole and mebendazole the effect was apparent within 1 hr and lasted for at least 4 hr after removal to fresh, drug-free medium. Whether treated in the host or in vitro the reduction in secretion was balanced by an equivalent rise in acetylcholinesterase activity within the parasites. It is suggested that the inhibition of protein secretion may be a specific manifestation of a general effect of these compounds on microtubule function.

[Electrophoretic studies of the molecular forms of serum malate dehydrogenase in sheep and lambs after experimental infestation with Bunostomum trigonocephalum (Rudolphi, 1808)]. / Elektroforetichni prouchvaniia vurkhu molekuliarnite formi na serumnata malatdekhidrogenaza na ovtse i agneta sled eksperimentalna invaziia s Bunostomum trigonocephalum (Rudolphi, 1808).

The influence was studied of mass B. trigonocephalum infection on the isoenzyme spectrum of serum malic dehydrogenase in adult sheep and lambs. The investigations were conducted prior to infection, on day 10 post infection and following occurrence of clinical picture of bunostomiasis. It was found that on day 10 post infection, the serum of experiment sheep and lambs contained new fractions of malic dehydrogenase, NAD-specific, NADF-specific. They were observed also post occurrence of bunostomiasis clinical symptoms. The new fractions possess different electrophoretic mobility from that of malic dehydrogenase isoenzymes observed in the serum of experiment animals prior to infection. Their percentage ratio with respect to the remaining isoenzymes increases with disease development. Change in the percentage ratio of malic dehydrogenase isoenzymes normally found in sheep and lamb serum observed post infection.