Pathobiology of Heterakis gallinarum mono-infection and co-infection with Histomonas meleagridis in layer chickens.

Little is known about the induction and modulation of gut-associated immune reactions after nematode infection in the chicken. The objective of the present study was to compare the pathogenesis, induction of immune reactions and electrophysiological changes of the gut after mono-infection with Heterakis gallinarum and after dual infection with H. gallinarum and Histomonas meleagridis in layer chickens. In two experiments 3-week-old chickens were inoculated with embryonated H. gallinarum eggs, which were positive for H. meleagridis. While birds of the first experiment were left untreated, those of the second experiment were treated with dimetridazol to prevent H. meleagridis co-infection. Mild to moderate histological lesions and local immune reactions with a significant increase in CD4(+), CD8α(+), TCRαß(+) and TCRδγ(+) cells in the lamina propria and induction of the T-helper type 2 (Th2) cytokine interleukin-13 dominated the H. gallinarum immune response at 2 weeks post infection. Co-infection with H. gallinarum and H. meleagridis induced an increase in mRNA expression of the T-helper type 1 (Th1) cytokine interferon-γ, a decrease in splenic CD4(+) cells and severe destruction of the caecal mucosa in association with strong T-cell infiltration in the caecal lamina propria. There was no obvious effect on the chloride secretion of the caecal epithelium, which was investigated once the mucosa had almost recovered from the infection, in either experiment. These results suggest that the local T-cell reactions to nematode infections in chickens may be comparable with mammals and may be shifted from a Th2-dominated to a Th1-dominated response when accompanied by a protozoan infection.

Immunopathogenesis of Ascaridia galli infection in layer chicken.

Gastro-intestinal nematode infections in mammals are associated with local T lymphocyte infiltrations, Th2 cytokine induction, and alterations in epithelial cell secretion and absorption. This study demonstrates that Ascaridia (A.) galli infection in chicken also elicits local gut-associated immune reactions and changes in the intestinal electrogenic nutrient transport. In A. galli-infected birds we observed infiltrations of different T cell populations in the intestinal lamina propria and accumulation of CD4+ lymphocytes in the epithelium. The Th2 cytokines IL-4 and IL-13 dominated the intestinal immune reactions following A. galli infection. A. galli-specific systemic IgY antibodies were detected after two weeks post infection, and did only poorly correlate with detected worm numbers. Electrogenic transport of alanin and glucose was impaired in A. galli-infected chicken. Our data provide circumstantial evidence that local immune responses and electro-physiological intestinal functions may be connected and contribute to the elimination of worm infection.

Effects of dietary non-starch polysaccharides on establishment and fecundity of Heterakis gallinarum in grower layers.

It was hypothesized that the establishment and fecundity of Histomonas meleagridis free Heterakis gallinarum may be affected by dietary non-starch polysaccharides (NSPs). One-day-old female layer chicks (N=670) were fed ad libitum for 11wk one of the following diets in a three-times repeated experiment: basal diet (CON), basal diet plus pea bran rich in insoluble NSP (I-NSP), basal diet plus chicory root meal as a source of inulin rich soluble NSP (S-NSP). At the end of wk three, each feeding group was subdivided into an uninfected and an infected group of birds each being inoculated with a placebo or with 200 H. meleagridis free eggs of H. gallinarum. The birds were slaughtered 8wk post infection and their worm burdens, the nematode egg excretion, caeca sizes and weights as well as intracaecal pH and volatile fatty acid (VFA) concentrations were determined. The NSP supplemented diets and also infection led to reduced body weights (BWs) of birds and impaired the feed conversion rate (P<0.001). The NSP supplemented diets increased average length of caecum (P<0.001) with S-NSP exerting a stronger effect than I-NSP (P<0.05). Full caeca weight was increased by S-NSP (P<0.001). Feeding S-NSP lowered intracaecal pH and molar proportion of acetate and increased that of butyrate compared to CON and I-NSP (P<0.001). Caecal pool of VFA was increased with S-NSP (P<0.001). The NSP-diets elevated incidence of infection (P<0.01), average number of larvae (P<0.009) and total worm burden (P<0.001) compared to CON. The daily amount of faeces increased in NSP-fed birds (P<0.001). Number of eggs per gram of faeces (EPG), number of eggs excreted per worm population of a bird within 24h (EPD) and female worm fecundity (EPD/female worm) were elevated after feeding S-NSP (P≤0.002), whereas I-NSP led to lower EPG/female worm (P<0.05). The EPD increased in the sequence of CON

Non-starch polysaccharides alter interactions between Heterakis gallinarum and Histomonas meleagridis.

Nutrition of the host animal may not only influence interactions between the host and its parasites, but also relations between different parasites species residing on the same host. We investigated effects of insoluble and soluble non-starch polysaccharides (NSP) on establishment and development of Heterakis gallinarum in chicken being treated or left untreated against Histomonas meleagridis. Six groups of one-day-old birds were allocated to three diets, two on each diet. The birds were fed ad libitum either a basal diet (CON), or CON+insoluble NSP (I-NSP) or CON+soluble NSP (S-NSP) until an age of 11wk. At an age of 19d, one of each diet groups was prophylactically treated for 9d with dimetridazole (0.05%, w/v) via drinking water against histomonas. The remaining three groups were left un-treated. Two days after starting dimetridazole treatment (at 3wk), each of the 6 groups was divided into two sub-groups. One dimetridazole treated and one dimetridazole un-treated groups of birds on each diet (6 groups) were infected with 200 embryonated eggs of H. gallinarum that were previously harvested from histomonas-carrying H. gallinarum infected chickens. The remaining 6 groups of uninfected birds, either treated or left un-treated against H. meleagridis, served as controls. Worm burdens of infected birds were determined 8wk p.i. Treatment against H. meleagridis significantly increased incidence of H. gallinarum infection and average worm length in all infected groups independent of the diet consumed (p<0.001). An interaction between effects of diet and dimetridazole treatment on worm burden (p<0.001) indicated that the S-NSP diet resulted in lowest worm burden in dimetridazole un-treated birds, whereas it caused the highest worm burden in the treated birds (p<0.05). Furthermore, the treatment resulted in higher worm burdens when compared to un-treated birds on the corresponding diets (p<0.05). Infection with H. gallinarum impaired body weight (BW) of the chicks (p<0.05) and H. meleagridis aggravated this effect (p<0.05). Dimetridazole treated and un-treated uninfected birds developed similar BW (p>0.05). Both NSP supplemented diets resulted in lower (p<0.05) BW when compared with the CON diet, S-NSP being inferior to I-NSP (p<0.05). It is concluded that H. meleagridis harms the definitive host as well as H. gallinarum. Both insoluble and soluble NSP supplemented diets favor H. gallinarum infection while S-NSP additionally intensifies histomonas infection, which then impairs establishment and development of H. gallinarum.