Establishment of Ascaridia galli in betamethasone-treated chickens

Twenty-five day-old White Leghorn chickens were each infected orally with 500 (Group I), 1000 (Group II) and 2000 (Group III) infective eggs of Ascaridia galli and were killed 30 days after the infection. A high percentage of the infecting dose (6.5%) established as adult worms in the intestine of chickens receiving the lowest level of primary infection, but as the amount of primary infection given to birds increased, there was a significant fall in the percentage establishment of adult worms in the intestine. A similar pattern of worm establishment was shown by chickens of the same age and receiving similar levels of primary infections, but which were treated with betamethasone at a dose of 2 mg/kg body weight commencing 5 days before and continuing up to 15 days after the infection. Betamethasone-treated birds, however, showed more establishment of worms in the intestine, but lower weight gains in comparison to the birds which were not treated. Different levels of primary infections given, with or without treatment with betamethasone, had no effect on the sex ratio of the resultant male/female worm populations, which became established in almost equal numbers in the intestine of chickens.     

Genetic resistance to Ascaridia galli infections in chickens.

Ascaridiosis is still a cause of economic losses in modern poultry production systems. Improving genetic resistance to this disease provides an attractive alternative for free-range organic poultry producers and will eventually reduce the extensive use of anthelmintic drugs. An experiment was conducted to compare resistance to Ascaridia galli infections in Lohman Brown (LB) and Danish Landrace (DL) chickens. A self-cure mechanism to A. galli infections was observed in both breeds. However, significantly higher worm burdens and egg excretion were seen in the DL compared to LB chickens during primary infection. This indicates that breeding for resistance to A. galli is possible in chickens.     

Effect of anthelmintics on phosphatases in Ascaridia galli.

In vitro addition of the drugs tetramisole (TMS) and levamisole (LMS) caused an inhibition of the specific activities of acid phosphatase and Mg(++)-dependent adenosine triphosphatase. The inhibition was non-competitive in nature. No significant inhibition was caused by TMS in the activity of glucose-6-phosphatase, but LMS inhibited the enzyme in a non-competitive manner. The activity of alkaline phosphatase was, however, increased in the presence of both TMS and LMS.     

Anthelmintic activity of ivermectin against experimental Ascaridia galli infection in chickens

The efficacy of ivermectin against Ascaridia galli infection was evaluated in chickens under controlled laboratory conditions in two separate experiments. In each experiment 22 White Leghorn chicks were randomly assigned to three groups of 10 (infected-treated), 9 (infected-control) and 3 (uninfected-control) birds. Each bird in the former two groups was orally infected with 1,500 embryonated A. galli eggs. The chicks in the treated group were subcutaneously injected with ivermectin at a dose of 0.3 mg kg-1 body weight on Day 10 (Experiment 1) and Day 35 post-infection (Experiment 2) for immature and adult infections, respectively. The treated birds had 0.9% (Experiment 1) and 0.4% (Experiment 2) worm recovery compared with 8.7 and 8% in the infected-untreated controls of the respective experiments. The fall in post-treatment faecal egg counts was 81 and 92% in birds treated on Days 10 and 35, respectively. The drug was found to be 90 and 95% effective against immature and adult worms, respectively. The lower lesion score and post-treatment near-normal haematobiochemical picture in treated birds confirmed these observations. The treated birds also had a better growth rate than the untreated chickens. The mature worms in the intestinal lumen of the host were more sensitive to the treatment than the immature stages of the parasite in the tissue phase.     

The effect of Plasmodium gallinaceum on a challenge infection with Ascaridia galli in chickens

The effect of a primary infection with the haemoparasite Plasmodium gallinaceum on the establishment of a challenge infection with the nematode Ascaridia galli in chickens was studied. Four groups were infected as follows. Group 1: inoculated intravenously with 10(6) P. gallinaceum-infected erythrocytes on day 0; group 2: orally infected with 500 embryonated A. galli eggs on day 10; group 3: infected with P. gallinaceum on day 0 and A. galli on day 10; and group 3: non-infected control birds. The results of this investigation demonstrates that a primary infection with P. gallinaceum in chickens alters the course of a subsequent infection with A. galli. Thus, an antagonistic effect was seen in which the malaria infection caused a significant reduction on the establishment of the nematode in concurrently infected animals.     

In vitro hatching of the infective eggs of Ascaridia galli in tissue extracts

Extracts of proventriculus (PE) and small intestine (IE) of fowl were used, for the first time, as media for the in vitro hatching of infective eggs of Ascaridia galli. Hatching was successful in a mixture of equal parts of PE and IE (MIP) under normal air and under different concentrations of CO2, but not under 100% CO2. A very highly significant retardation (P less than 0.001) in the rate of hatching appeared as the concentration of CO2 was increased, indicating that high levels of CO2 inhibit the process of hatching. 100% of the eggs hatched in PE in 40.5 min whereas they did not hatch at all in IE, suggesting that IE alone has no influence on egg hatching. The shortest time taken for 100% of the eggs to hatch in this study suggests that the present method of hatching is faster than all previous methods used by different workers.     

Humoral and cell-mediated immune responses in chickens with infectious bursal disease

Primary and secondary immune responses to Newcastle disease virus (NDV) was evaluated in chickens infected with infectious bursal disease virus (IBDV) at one and 28 days of age. The geometric mean primary hemagglutination-inhibition antibody titers (GMT) of chickens infected with IBDV at one day of age was significantly lower (P less than or equal to 0.01) than those infected at 28 days of age. Infection with IBDV had no influence on secondary immune response to NDV. The effect of IBDV infection at one day of age on the cell-mediated immunity of chickens was evaluated by skin allograft acceptance or survival time. There was no significant difference between the percentage of grafts accepted in IBDV infected and noninfected control chickens. However, the mean graft survival time in the IBDV infected chickens was significantly longer (P less than or equal to 0.05) than those in the control group. This suggested a suppression of cell-mediated immunity due to IBDV infection.     

Localization of Ascaridia galli larvae in the jejunum of chickens 3 days post infection

The normal habitat of the parasitic stages of Ascaridia galli is in the small intestine of poultry but the exact localization is poorly understood. Therefore, a histological study was conducted in order to localize the larvae during the early phase of infection. Six layer pullets seven-week old were infected orally with 20,000 embryonated A. galli eggs each, whereas four chickens were left as un-infected controls. At necropsy 3 days after infection the first half of jejunum/ileum was divided into two equally sized sections (J1 and J2). After taking samples for histology from the middle of J1 and J2 and the junction between these determined JX, the two sections were subjected to parasitological examination. A higher number of A. galli larvae were recovered from section J2 than J1 and the majority of larvae were recovered from the most profound layers. Based on histology 144 larvae were identified and their location was noted. The highest number of larvae was observed in the JX sample as compared to J1 and J2 (P<0.001). Most of them were located in the profound crypt zone of the mucosa (51%) as compared to the other zones (P<0.05). The number of larvae was higher in the lumen (63%) compared to the epithelium (32%) and lamina propria (5%) (P<0.001). A significantly higher number of eosinophils were found in lamina propria of the infected group compared to the control group (P<0.001). This experiment clearly showed that only few larvae had penetrated the epithelium and were positioned in the lamina propria at 3 days post infection. It was far more common that the larvae were localized within the epithelium or in the lumen of the crypts. It is therefore suggested that at least in this early phase "mucosal phase" is a more appropriate term to be used for the A. galli larval localization as compared to the term "histotrophic phase" currently used in many textbooks.     

Effect of dietary xylitol on growth and inflammatory responses in immune stimulated chickens

It has been argued that stimulation of the immune system depresses performance. Accordingly, an experiment was conducted to determine the effect of dietary xylitol (150 g/kg diet) on growth and selected inflammatory responses in male broiler chickens. During the final 6 d of the experimental periods, chicks were injected with antigens: Escherichia coli lipopolysaccharide (LPS) on days 1, 3 and 5 and with Sephadex-G50 superfine on days 2 and 4 to stimulate macrophage functions. The immune stimulation reduced body weight gain and food intake, but enhanced alpha 1 acid glycoprotein (AGP) concentration and interleukin (IL-1) like activity in plasma. Feeding the xylitol diet partially, but significantly, prevented the reductions in body weight gain and food intake, without affecting the early stage of inflammatory responses triggered by LPS and Sephadex injections.     

The effect of concurrent infections with Pasteurella multocida and Ascaridia galli on free range chickens

Pasteurella multocida and Ascaridia galli are observed with high prevalences in free range chickens in Denmark, but the impact is unknown. A study was carried out to examine the interaction between A. galli and P. multocida in chickens and the impact on production.Five groups, each with 20 18-week-old Lohmann Brown chickens were infected. Group 1 was orally infected with 1000+/-50 embryonated A. galli eggs. Group 2 received 10(4) cfu P. multocida intratracheally. Group 3 was infected with A. galli and subsequently with P. multocida. Group 4 was infected with P. multocida followed by A. galli. Group 5 was the control. The study ran for 11 weeks where clinical manifestations, weight gain and egg production were recorded. Excretion of P. multocida was determined on individual basis and blood smears were made for differential counts. At the end of the study pathological lesions and the number of adult worms, larvae and eggs in the faeces were recorded.The birds were more severely affected when infected with both pathogens compared to single infections with A. galli or P. multocida, respectively. A lower weight gain and egg production was observed with dual infections. A. galli infection followed by a secondary P. multocida infection resulted in more birds with pathological lesions and continued P. multocida excretion.In conclusion a negative interaction between A. galli and P. multocida was observed and it is postulated that free range chickens are at higher risk of being subjected to outbreaks of fowl cholera when they are infected with A. galli.     

Response of two breeds of chickens to Ascaridia galli infections from two geographic sources

Comparative resistance to different isolates of Ascaridia galli was investigated in a local chicken breed from Jordan (LC) and in the Lohmann LSL white chicken (LW) strain. In two trials, birds of LC and LW were inoculated orally at 1-day old with 250 embryonated A. galli eggs. In the first trial a German source of A. galli was used, whereas in the second trial, a Jordan source of A. galli was used. At week 7 of infection, infected LC birds harbored significantly (P<0.05) fewer worms and excreted less A. galli eggs than infected LW birds. A. galli isolated from Jordan were less infectious than A. galli from Germany. Results suggest that the variation in genetic background between LC and LW is involved in the resistance to A. galli infection. A. galli isolates from different geographic areas differ in their ability to infect different chicken genotypes.     

Age-related differences of Ascaridia galli egg output and worm burden in chickens following a single dose infection

Ninety white chickens (Lohmann LSL) were reared under helminth-free conditions and divided into five groups. Four groups were artificially infected with 250 embryonated Ascaridia galli eggs at the age of 6, 12, 18 or 24 weeks. Ten birds were kept as uninfected controls. Six and 10 weeks after infection (p.i.), individual faecal egg counts (FEC) were performed. The birds were slaughtered after the second sampling and their gastrointestinal tracts were examined for the presence of adult A. galli. The FEC increased from the first to the second sampling significantly in all the infected groups. The highest increase was shown in the group infected at 12 weeks of age, whereas the increase in the other groups was relatively moderate. However, the total worm burden and mean FEC at the second sampling were highest (p<0.01) in those birds infected at an age of 12 or 18 weeks. The serum protein and triiodothyronine (T3) levels did not differ significantly (p>0.05) between any of the groups. Thyroxine (T4) was significantly different between the groups infected at 6 and 18 weeks of age (p<0.05), and those at 6 and 24 weeks of age (p<0.01). The thyroid hormone levels correlated significantly with the FEC. Age does not seem to play a major role in resistance to A. galli infections in layers, whereas a bird's hormonal and immune status, related to laying activity, seems to have a significant negative impact on resistance.     

Infection dynamics of Ascaridia galli in non-caged laying hens

The infection dynamics of Ascaridia galli in laying hens was investigated in six commercial non-caged flocks. Three flocks were managed in accordance with the regulations for organic production and had outdoor access, whereas three flocks were housed indoors in aviaries or traditional floor systems. Faecal egg counts and total worm burdens were determined at specified intervals during the first 50 weeks of the production period. In two conventional flocks the efficacy of flubendazole on lumenal stages was investigated. All flocks became infected following the arrival of the birds (post placement) with residual infective eggs derived from the previous flock. In four flocks (two organic and two conventional) parasite eggs were first detected in faeces 6-7 weeks post placement, whereas parasite eggs were not detected until after 17-18 weeks in two flocks. This delay was observed in two of three flocks that were housed in barns that had been thoroughly cleaned and disinfected by chlorocresol. In three flocks (two conventional and one organic) flubendazole was administered to the birds in the drinking water for approximately one week. Both conventional flocks were dewormed twice approximately 20 weeks apart, whereas the organic flock was dewormed only once about 40 weeks post placement. Parasite eggs reappeared after deworming in all flocks, often within 2-4 weeks, followed by a rapid increase in parasite egg expulsion. Our results suggested impairment of host immunity post treatment, as the egg counts exceeded pre-treatment levels after 7-8 weeks on both conventional farms. Accordingly, the way by which anthelmintics and/or disinfectants are used in non-caged chicken flocks must be refined.     

Energy and nitrogen metabolism of diseased chickens: interaction of Ascaridia galli infestation and vitamin A status.

1. Effects of Ascaridia galli infection on the energy and nitrogen (N) metabolism were studied on groups of 5 cross-bred cockerels aged about 5 weeks and given a diet deficient or adequate in vitamin A at two levels of feeding in respiration chambers. 2. Metabolisability of dietary energy was 67% and N retention 33% in infected chickens compared with 71 and 41% respectively, in uninfected chickens. 3. Maintenance energy requirement of vitamin A-deficient birds was 882 kJ/kgW d compared with 998 kJ/kgW d for normal birds. N balance of the deficient chickens was also less when compared at the same energy balance. Infection did not affect maintenance energy requirement nor N balance. 4. Starvation heat production of infected chickens (619 kJ/kgW d) was higher than that of uninfected controls (586 kJ/kgW d). When infection treatments were combined, vitamin A-adequate chickens had a higher heat production (615 kJ/kg d) than the vitamin A-deficient (580 kJ/kgW d). Endogenous N excretion (mg/gW) was less in vitamin A-deficient than in adequate, starved birds. 5. Deficient chickens had undetectable liver reserves of vitamin A and only very low plasma concentrations. There was a difference in the length of larvae (17 d after infection) associated with vitamin A status, and with level of feeding.