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Chromosomal mapping of host resistance loci to Trichinella spiralis nematode infection in rats.

The differences in host response among strains of rats to intestinal nematode parasite Trichinella spiralis infection could provide a powerful benefit for further elucidation of molecular interactions between the host and the parasite. Using several strains of rats, we previously observed that DA strain is a strong responder and F344 strain is a weak responder with respect to expulsion of the adult worm. To identify the host resistance loci, quantitative trait loci (QTLs) analysis in F2 population from crosses between DA and F344 strains was performed. One significant QTL (designated as Tspe) was mapped to the middle region of chromosome 9. In addition, the effect of DA allele at Tspe locus could act recessively and lead to the rejection of more adult worms from the gut. The results from the present study provide more insights on host-parasite interactions, which may be useful in facilitating the development of novel approaches for treatment and control of intestinal parasites in human and domestic livestock.

Animals↗

Seasonal occurrence of infective nematode larvae in California Sierra foothill pastures grazed by cattle.

Worm-free Holstein tracer calves were used to assess the seasonal variation in number and course of development of nematode parasites of cattle on an irrigated pasture located in the California Sierra foothills. The most common genera of nematodes found in the abomasum and small intestine were Ostertagia and Cooperia, respectively. The infective Ostertagia larvae on herbage were most numerous in early spring and lowest in summer months. Arrested development of Ostertagia occurred in mid-to-late spring. The percentage of the population of Ostertagia found to be arrested larvae was constant (73% to 95%) over 4 years, even though the total number of nematodes in the genus was markedly different. Levels of infection with Ostertagia and Cooperia were found to correlate with pasture contamination occurring in the preceding fall and concurrent winter months. In the cecum and large intestine, Oesophagostomum venulosum was found to be the most common nematode. It is suggested that this species may replace Os radiatum as the cattle nodular worm in regions where climate is similar to that of the southwestern coast of North America. Evidence of seasonal hypobiotic development of Oe venulosum was found. Other genera of nematodes observed in tracer calves were Trichostrongylus, Haemonchus, Bunostomum, Trichuris, and Dictyocaulus.

Animal Feed↗

Gastrointestinal nematode infection is associated with variation in innate immune responsiveness.

Ex vivo monocyte cytokine responses (IL-1beta, TNF-alpha, IL-12p70, IL-10, TGF-beta) to bacterial TLR2 and TLR4 ligands were quantified in 47 gastrointestinal (GI) nematode-exposed children in Pemba Island, Tanzania. Worminess (estimated by faecal egg counts (FEC)) had a positive relationship with pro-inflammatory TNF-alpha and IL-1beta responsiveness to the TLR ligands. In particular, there was a strong significant relationship with TNF-alpha response to TLR4 ligand (LPS). There were no significant associations between regulatory responses (IL-10, TGF-beta) and worminess. These results are consistent with the possibility that GI nematodes modulate innate responses and may indicate a potential mechanism for interactions between GI nematodiasis and important bystander pathogens.

Ancylostomatoidea↗

Constitutive expression of mouse mast cell protease-1 in normal BALB/c mice and its up-regulation during intestinal nematode infection.

Rodent intestinal mucosal mast cells (IMMC) store and secrete soluble granule serine proteases, the beta-chymases, which may promote epithelial permeability during intestinal hypersensitivity reactions. The beta-chymase mouse mast cell protease-1 (mMCP-1) is generally considered to be expressed late in the in vitro differentiation of mast cells. The purpose of this study was to determine the kinetics of mMCP-1 transcription and expression in vivo during nematode-induced IMMC hyperplasia. Concentrations of mMCP-1 in blood and jejunum of BALB/c mice were quantified by enzyme-linked immunosorbent assay before and at various stages after infection with the intestinal nematode Nippostronglyus brasilliensis. Mature mMCP-1 enzyme was detected in jejunal homogenate (194 ng/mg soluble protein) and in blood (8.3 ng/ml serum) from normal uninfected BALB/c mice. Maximal IMMC hyperplasia occurred 7-14 days post infection and was significantly correlated with increased levels of mMCP-1 in jejunum (r = 0.58, P < 0.001) and with raised concentrations of mMCP-1 in serum (r = 0.66, P < 0.001). Transcription of the mMCP-1 gene was detected by RNA blotting in normal, uninfected jejunum, but transcription was up-regulated after infection with maximal transcription occurring on days 7 and 14. In conclusion, mMCP-1 transcription, storage and secretion occur constitutively in normal BALB/c jejunum but this basal secretion is up-regulated during nematode infection, suggesting both a physiological and pathological function for this protease.

Animals↗

[Use of an albendazole bolus against gastrointestinal nematode infections in first year cattle].

Thirty first year grazing calves were allocated to two groups of 15 calves each on the basis of bodyweight and were administered albendazole boli or placebo boli, respectively, 30 days after turnout. The albendazole bolus prevented the nematode egg output almost completely for about 4 months, whereas the controls had mean egg counts of up to 206. Pepsinogen concentrations were significantly higher in the control group and reached mean values of 3055 mU tyrosine compared to less than 1000 mU tyrosine in the albendazole treated group after bolus administration. Pasture contamination with trichostrongylid larvae was markedly lower on pastures of the albendazole group than on the controls. Mean weight gains were significantly higher in the albendazole group than in the controls with a difference of 10.7 kg per animal at the end of the season.

Albendazole↗