Gonadal hormones in experimental Ascaridia galli infection in chickens

Repeated injections of α-estradiol benzoate in immature females, and of testosterone propionate in immature males at the times and doses used, seemed to enable chickens to eliminate Ascaridia galli worms at a greater rate than the untreated controls. No sex difference in number of worms harbored was observed between normal males and females within the limits of age studied. The increase in resistance in hosts that received homologous sex hormones was similar in males and in females.Measurements of worms recovered indicated that gonadal hormones or their products may possibly have an effect upon the growth of the parasites. Injections of α-estradiol benzoate seemed to cause a temporary retardation in the mean rate of growth of the worms, whereas injections of testosterone propionate seemed to cause a temporary acceleration.     

Co-expulsion of Ascaridia galli and Heterakis gallinarum by chickens

Worm expulsion is known to occur in mammalian hosts exposed to mono-species helminth infections, whilst this phenomenon is poorly described in avian hosts. Mono-species infections, however, are rather rare under natural circumstances. Therefore, we quantified the extent and duration of worm expulsion by chickens experimentally infected with both Ascaridia galli and Heterakis gallinarum, and investigated the accompanying humoral and cell-mediated host immune responses in association with population dynamics of the worms. Results demonstrated the strong co-expulsion of the two ascarid species in three phases. The expulsion patterns were characterized by non-linear alterations separated by species-specific time thresholds. Ascaridia galli burden decreased at a daily expulsion rate (e) of 4.3 worms up to a threshold of 30.5 days p.i., followed by a much lower second expulsion rate (e = 0.46), which resulted in almost, but not entirely, complete expulsion. Heterakis gallinarum was able to induce reinfection within the experimental period (9 weeks). First generation H. gallinarum worms were expelled at a daily rate of e = 0.8 worms until 36.4 days p.i., and thereafter almost no expulsion occurred. Data on both humoral and tissue-specific cellular immune responses collectively indicated that antibody production in chickens with multispecies ascarid infections is triggered by Th2 polarisation. Local Th2 immune responses and mucin-regulating genes are associated with the regulation of worm expulsion. In conclusion, the chicken host is able to eliminate the vast majority of both A. galli and H. gallinarum in three distinct phases. Worm expulsion was strongly associated with the developmental stages of the worms, where the elimination of juvenile stages was specifically targeted. A very small percentage of worms was nevertheless able to survive, reach maturity and induce reinfection if given sufficient time to complete their life cycle. Both humoral and local immune responses were associated with worm expulsion.     

Ascaridia galli: effects of immunosuppressive drugs or bursectomy in chickens

Immunosuppressive drugs significantly increasing numbers of A. galli and incidences of infection were: cortisone, cortisol, 9-α-fluorohydrocortisone, 2-methyl-9-α-fluorohydrocortisone, prednisone, prednisolone, 6-mercaptopurine, 2, 6-diaminopurine, 6-thioguanine, 5-bromodeoxyridine, 5-fluorouracil, methotrexate, chlorambucil, and actinomycin D. These drugs and/or worm burdens significantly suppressed weight gains of hosts, and neither altered the male:female ratio of worms nor their growth. The following drugs neither altered worm burdens nor increased incidences of infection: corticosterone, 2-azaadenine, 8-azaguanine, azathioprine, 6-azauridine, busulfan, thio-TEPA, triethylenemelamine, vincristine, acriflavine, reserpine, and l-phenylalanine.Worm burdens and incidences of infection were increased significantly in chickens surgically bursectomized when 3 or 14 but not 35 days old. Chicks bursectomized in ovo with testerosterone propionate on Day 5 or 14 of incubation and infected on Day 14 after hatching developed significantly increased worm burdens and incidences of infection.Applying the Kolmogorov-Smirnov test for goodness of fit to data on increased worm burdens showed that the immunosuppressive drugs or bursectomy had a normalization effect on the statistical distribution.     

Ascaridia galli (Nematoda): development and survival in gnotobiotic chickens

Infection and growth rates of the fowl nematode Ascaridia galli were compared in germ-free, conventional, and other gnotobiotic chickens. Uniform experimental infections induced in chickens at 7–12 days of age showed that significantly fewer (P < 0.01) worms established themselves in germ-free chickens than in chickens with conventional flora. Numbers of worms established in monoassociated hosts (Bacillus subtilis, B. cereus, and Penicillium sp.) were intermediate between those in grossly contaminated and germ-free hosts. Mean worm lengths were shorter from germ-free than conventional hosts but differences were not statistically significant. These experiments demonstrate that some A. galli larvae may establish themselves and grow for 14 or 21 days postinoculation in a germ-free environment.     

Increased susceptibility of lead exposed chickens to experimental infection of Ascaridia galli

Two sets of one day old, white leghorn (Victoria Strain) chickens were each orally exposed to 1.0 mg lead nitrate daily for 7 days and subsequently infected with 15 and 30 A. galli eggs. These experimental chickens exposed to lead harboured significantly greater worm burden when compared to unexposed controls leading strong support to the view that lead exposure significantly suppressed their immune response to A. galli infection. It also indicated that exposure of lead prior to infection greatly impaired weakened the immune capability of such chickens.     

Consequences of concurrent Ascaridia galli and Escherichia coli infections in chickens

   

Three experiments were carried out to examine the consequences of concurrent infections with Ascaridia galli and Escherichia coli in chickens raised for table egg production. Characteristic pathological lesions including airsacculitis, peritonitis and/or polyserositis were seen in all groups infected with E. coli. Furthermore, a trend for increased mortality rates was observed in groups infected with both organisms which, however, could not be confirmed statistically. The mean worm burden was significantly lower in combined infection groups compared to groups infected only with A. galli. It was also shown that combined infections of E. coli and A. galli had an added significant negative impact on weight gain.     

Monoamine oxidase in adult Ascaridia galli

Monoamine oxidase (MAO), catalysing oxidative deamination of biogenic monoamines, has been detected in adult Ascaridia galli. MAO was present in mitochondria and deaminated noradrenaline at the maximal rate, although serotonin, adrenaline, tyramine and dopamine were also degraded but more slowly. Of the organs studied, the body wall, female reproductive organ and intestine, the body wall (containing neuronal structures) showed highest MAO activity. Km value for chick ascarid mitochondrial MAO using tyramine as substrate was 1.66 X 10(-3) M and it was most active at 2.5 mM tyramine concentration, pH 7.5 and 40 degrees C. MAO of A. galli appeared to be thermolabile as nearly 80% of its activity was lost when the incubation temperature was increased 5 degrees above optimum.     

The effect of cobalt compounds on uninfected and Ascaridia galli-infected chickens: a kinetic model for Ascaridia galli populations and chicken growth

The effect of dietary cobalt from three different sources on uninfected and Ascaridia galli-infected Hisex chickens, has been studied. The chicken diet was supplemented with 0.06 Co2+ kg-1 food either in the form of two glycine-cobalt compounds or mixed zinc-cobalt basic salt. An excess of dietary cobalt in small doses increases the gain of body weight and decreases host mortality. A greater bioefficiency of cobalt was established in infected chickens. A mathematical model has been used to provide a quantitative interpretation of the observed results. The model solutions of the kinetics of worm numbers and body weight are in a good agreement with experimental data. The model is valid for different degrees of A. galli infections and for treatment with different trace elements. The value of the kinetic parameter, regarded as a phenomenological constant of the host immune response, depends on the degree of infection.     

A kinetic model for Ascaridia galli populations in chickens treated with mixed salts of copper and zinc.

The action of mixed salts of copper and zinc (basic and neutral) on Hisex chickens experimentally infected with Ascaridia galli has been studied. The data show that the lowest host mortality and decrease in body weight gain and the highest reduction in nematode loading occurs in infected chickens treated with basic salts (in comparison with infected chickens, untreated or treated with neutral salts). A mathematical model has been proposed to provide a quantitative interpretation of the observed results. The model solutions of the kinetics of parasite numbers and of the gain in body weight are in a good agreement with the experimental data. One of the kinetic parameters in the model is defined as a phenomenological constant of the host immune response. Its value is determined in the case of infected and untreated chickens.     

Metabolism of amino acids in Ascaridia galli: transamination

Ascaridia galli, using 2-oxoglutarate as an acceptor, transaminates alanine and aspartate at significantly high rates. Among other amino acids valine, phenylalanine, leucine, isoleucine, arginine, tyrosine and methionine are metabolised at moderate rates while lysine, serine, threonine, cysteine, glycine, histidine, tryptophan, DOPA and GABA appear to be inert in this respect. Body parts mimic the whole worm in the pattern of transamination of various amino acids with the exception of methionine. Alanine, aspartate and glutamate may transfer their amino group also to pyruvate and oxaloacetate. Alanine and aspartate: 2-oxoglutarate transaminases are located mainly in the cytosol and mitochondrial fractions.     

Characterization of mitochondrial monoamine oxidase of Ascaridia galli

Oxidative deamination of various biogenic monoamines by Ascaridia galli monoamine oxidase (MAO) was blocked by different mammalian MAO inhibitors, namely, iproniazid, trans-PcP, nialamide and pargyline and the blockade was observed to be time as well as concentration dependent. The binding of inhibitors with chick ascarid MAO was of the irreversible type and the nature of the inhibition was competitive. Pargyline showed lowest I50 (8 microM) and Ki (12 microM) values. Chlorgyline and deprenyl at 100 microM concentration inhibited MAO by about 60 and 40% respectively, indicating the presence of both type A and type B MAO in A. galli.