Comparative genetic resistance to Ascaridia galli infections of 4 different commercial layer-lines

Abstract

1. The objective of the study was to compare the establishment and effect of Ascaridia galli infections in 4 different layer-lines. 2. A total of 160 birds comprising 4 different commercial layer-lines, ISA Brown, New Hampshire, Skalborg and a cross of New Hampshire(NH) and Skalborg (Sk), were infected with A. galli eggs. The birds were examined for the presence of parasite eggs and parasites at weeks 3, 6 and 9 post infection (pi). 3. At week 6 pi the chickens of the NH line harboured more larvae compared with the three other lines. The Sk line chickens excreted more A. galli eggs throughout the study compared with the other lines. Female worms in the Sk line were more fecund than the worms in the other lines. Male and female worms recovered from the Sk line at week 9 pi were longer. Male worms recovered from the NH line 6 weeks pi were shorter than male worms from the other lines. Female worms recovered from the NH line were shorter than the female worms from the ISA line and the Sk line. No differences were seen in weight gain among the 4 lines. 4. The results suggest that genetic factors are involved in the establishment and survival of A. galli in the intestine of layers. Further studies are needed to elucidate the genetic mechanisms behind the observed parasitological findings.

Infection and excretion ofSalmonellaEnteritidis in two different chicken lines with concurrentAscaridia galliinfection

“…In addition to the impact of S. Enteritidis on the success of A. galli establishment it was shown that the probability for A. galli to establish infection was significantly higher in Hellevad chickens than Lohmann Brown chickens at the end of the experiment. This might indicate a difference in genetic resistance to A. galli , supporting earlier studies that found commercial chick-ens to be less susceptible to A. galli than more outbred chicken lines (Permin & Ranvig, 2001;Schou et al ., 2003) such as the Hellevad line. Based upon faecal shedding of Salmonella , no differences between the two lines were observed.…”

“…The mean worm burden demonstrated in all groups was relatively low, with a mean establishment rate of less than 0.3% for all groups. This is somewhat lower than observed in comparable studies (Permin et al ., 1997a(Permin et al ., ,b, 1998b(Permin et al ., , 2006Gauly et al ., 2001Gauly et al ., , 2005Permin & Ranvig, 2001;Schou et al ., 2003). It is possible that expulsion of worms had some impact on the mean worm burden as the proportion of chickens that had at least one positive faecal egg count during the study period was significantly higher than the proportion harbouring female worms at slaughtering in all groups, with the exception of Lohmann Brown chickens in group 4 where 13.3% (2/ 15) were found to harbour mature female worms at slaughtering, although all faecal samples were negative for parasite eggs.…”

An assessment of opportunities to dissect host genetic variation in resistance to infectious diseases in livestock

“…Anthelmintic treatment removes adult parasites, but it is the immature stage that causes severe damage. Breed differences have been observed in response to Ascaridia Opportunities in livestock disease genetics infection; faecal egg counts have been reported to differ between modern breeds (Permin and Ranvig, 2001;Gauly et al, 2002;Schou et al, 2003), and these differences have been shown to be both repeatable and heritable (Gauly et al, 2002).…”

Avian immunology, immunogenetics, and host immune response to Salmonella enterica serovar Enteritidis infection in chickens

“…Additional genetic disease resistance for viral pathogens in poultry has been established for Newcastle disease, infectious bursal disease, and avian leukosis (Bumstead 1998;Hassan et al, 2004). Varied resistance to intestinal parasites such as Ascaridia galli and Eimeria tenella has been shown in different commercial and outbred chicken lines, demonstrating a role of genetics in disease resistance for this class of pathogen (Pinard-Van Der Lann et al, 1998;Schou et al, 2003). Studies of response to bacteria, such as Salmonella, in the chicken show that a strong genetic component is involved (Bumstead and Barrow, 1988;Kramer et al, 2001;Kramer et al, 2003).…”