Outbreaks of adenoviral gizzard erosion in slaughtered broiler chickens in Japan

Gizzard erosion in broiler chickens was investigated at 18 slaughterhouses in Japan. The condition was observed in 13 of them, and adenoviral gizzard erosion (AGE) was diagnosed histologically, immunohistochemically and virologically in the eroded gizzards from nine of these 13. The antigen-positive intranuclear inclusion body of group 1 fowl adenovirus was observed in the epithelial cells of the affected gizzards, and fowl adenoviruses were isolated from the lesions. In two of the slaughterhouses the total weights of the gizzards disposed of in three years were 3590 kg (0.40 per cent of the gizzards inspected) and 2880 kg (0.19 per cent). Sixteen of the 19 outbreaks of gizzard erosion on 15 farms that were confirmed in three of the slaughterhouses, including the previous two slaughterhouses, were diagnosed as AGE, and the condition was suspected in the other three outbreaks. Most of the adenoviruses isolated were identified as serotype-1 by PCR-restriction fragment length polymorphism. No apparent clinical signs were observed in any of the affected flocks.     

Epizootic outbreaks of gizzard erosion associated with adenovirus infection in chickens

Two outbreaks of gizzard erosion in slaughtered broiler chickens in Japan were examined pathologically and microbiologically. The prevalences of such lesions were 9%-11% and 4%-50% in the affected flocks. Affected chickens had no clinical signs. Group I fowl adenovirus (FAV) serotype 1 was isolated from gizzard lesions. Histologically, gizzard mucosa were necrotic. Intranuclear inclusion bodies were seen in the enlarged nuclei of degenerating epithelial cells of the gizzard. The keratinoid layer in the erosion was edematous and desquamated and contained degenerative cells. Moderate to marked inflammatory cell infiltration was observed in the lamina propria and perivascular connective tissue in the submucosa and muscle layer. Immunohistochemical staining showed evidence of FAV antigens in the intranuclear inclusion bodies within degenerating epithelial cells. Ultrastructurally, numerous viral particles were demonstrated in the inclusions.     

Pathogenicity by parenteral injection of fowl adenovirus isolated from gizzard erosion and resistance to reinfection in adenoviral gizzard erosion in chickens

The pathogenicity of a serotype-1 fowl adenovirus (FAV-99ZH), which causes adenoviral gizzard erosion by oral inoculation in chickens, was investigated in specific pathogen-free white leghorn chickens. In trial 1, 14 chickens were inoculated intravenously with the virus at 21 days of age and euthanatized for necropsy within 1-14 days of inoculation. Gizzard erosion was grossly observed from day 7 postinoculation (PI), and histologically, FAV-99ZH antigen-positive, basophilic intranuclear inclusion bodies were seen in the gizzard lesions from day 7 to 11 PI. Necrotizing pancreatitis, and cholecystitis and cholangitis associated with the inclusions were observed from day 3 to 14 PI (pancreatitis) and from day 5 to 9 PI (cholecystitis and cholangitis), respectively. The inclusions were also observed in the epithelial cells of the cecal tonsils from day 3 to 5 PI. The virus was recovered from samples of the lesions. It was revealed that FAV-99ZH causes not only gizzard erosion but also pancreatitis, cholecystitis, and cholangitis by intravenous inoculation in chickens. In trial 2, 10 chickens were inoculated orally with the virus twice, at 13 and 36 days of age, and euthanatized for necropsy within 4-17 days after reinfection. Macroscopically, focal gizzard lesions were observed; however, neither necrosis nor inclusions were observed by microscopy. Moreover, FAV was not recovered from the gizzard or rectum of any of the chickens at necropsy. This suggests that the gizzard lesions occurred as a result of the primary infection, and that the chickens were able to resist reinfection.     

Movement of broiler chickens reared in commercial conditions

1. Bird movement was studied at various ages in two flocks of 18,200 broiler chickens. 2. One-d-old chicks placed in corners of a 29 x 14 m brooding area dispersed evenly over the whole area in a period of 48 h. 3. At 15 d of age, when released from the brooding area, birds which were among the first to move to the far end of the house did not necessarily remain in that area of the house. 4. Starting at 4 and 5 weeks of age, birds marked individually were variable in their movement throughout the house during a 16- and 9-d period respectively. Even the least mobile individual covered an area of the house containing several thousand birds. 5. Closer scrutiny of movement by individual birds showed that some moved over areas of 20 m2 in an hour. Birds moved further than was necessary simply to reach food and water. No agonistic interactions were observed and there was no evidence that crowding was a physical restraint on bird movement. 6. Results indicated that birds were not generally attached to a particular site in the shed and that social factors did not restrict movement. Some implications of bird movement are discussed with regard to performance, welfare and leg abnormalities.     

Exogenous phytase and xylanase exhibit opposing effects on real-time gizzard pH in broiler chickens

ABSTRACT

1. The current study was conducted to evaluate the influence of high phytase doses and xylanase, individually and in combination, on performance, blood inositol and real-time gastric pH in broilers fed wheat-based diets.

2. In a 42-d experiment, a total of 576 male Ross 308 broiler chicks were allocated to 4 dietary treatments. Treatments consisted of a 2 × 2 factorial arrangement, with 500 or 2500 FTU/kg phytase and 0 or 16 000 BXU/kg xylanase, fed in two phases (starter 0–21; grower 21–42 d). Heidelberg pH capsules were administered to 8 birds from each treatment group, pre- and post-diet phase change, with readings captured over a 5.5-h period.

3. At 21 and 42 d, birds fed 500 FTU/kg phytase without xylanase had on average 127 and 223 g lower weight gain than all other treatments, respectively (P < 0.05). At 42 d, body weight-corrected feed conversion ratio (_bwcFCR) was reduced (P < 0.05) by supplementing 2500 FTU/kg phytase or xylanase, with the combination giving a 12 point reduction in _bwcFCR compared to birds fed 500 FTU/kg phytase without xylanase. Inositol content of plasma was twice that of the erythrocyte (P < 0.001), with 2500 FTU/kg phytase tending to increase (P = 0.07) inositol content in both blood fractions.

4. Across all treatments, capsule readings ranged from pH 0.54 to 4.84 in the gizzard of broilers. Addition of 2500 FTU/kg phytase to the grower diet reduced (P < 0.05) average gizzard pH from 2.89 to 1.69, whilst feeding xylanase increased (P < 0.001) gizzard pH from 2.04 to 2.40. In contrast, digital probe measurements showed no effect of xylanase on gizzard pH, while addition of 2500 FTU/kg phytase increased (P = 0.05) pH compared to 500 FTU/kg phytase with or without xylanase.

5. These findings suggested that xylanase and high phytase doses have opposite effects on real-time gastric pH, while similarly improving performance of broilers.     

Effects of cimetidine on broiler fattening and on stress-induced gizzard erosion in chicken.

The work describes the effects of cimetidine on stress-induced gizzard erosions (Experiment A) and the influence of the long-term application (42 days) of the same drug on weight gain and feed consumption during broiler fattening (Experiment B). For Experiment A, 60 male, three-day-old chicks were divided into two groups: C (n = 30)--control chicks treated with 0.5 ml saline; CIM (n = 30)--chicks treated with cimetidine in a dose of 5 mg/kg body weight (b. w.) intragastrically. All chicks were stressed using a modified water-immersion stress method according to which the chicks, after 24 h of feed deprivation, were immersed in tap water (17 degrees C) for a few seconds. Under chloroform anaesthesia ten chicks from each group were killed 1, 2 and 3 h after the stressing. The morphometric analysis of gizzard erosion (GE) and histopathological examinations of gizzards were performed for each chick. In Experiment B, 32 one-day-old broilers of both sexes were used. The control group was untreated (n = 16) while the CIM group (n = 16) was fed the same diet supplemented with 10 mg of cimetidine per kilogram of feed throughout the fattening period (42 days). The results of Experiment A showed decreased mean length of the GE in the cimetidine-treated birds as compared with the GE lesions of the controls. In Experiment B, the treated chicks had reduced liveweight (1835.1 g), carcass weight (1474.6 g) and increased feed consumption (2115 g of feed per kilogram of weight gain) compared to the controls in which the same parameters were 1898.5 g, 1574.2 g and 1797 g, respectively. The results show that while stress-induced GE of chicks can be medicated pharmacologically, long-term application of the same substance impairs the results of fattening.     

Serologic testing for aspergillosis in commercial broiler chickens and turkeys

Sera samples from commercial broiler chickens and turkeys diagnosed with respiratory and disseminated aspergillosis were tested for the presence of antigen and antibody to Aspergillus. Antigen detection consisted of testing for two cell-wall components, beta-glucan and galactomannan, which have been used extensively in human medicine. There were significantly higher levels of galactomannan in all broiler chicken submissions (100%) and antibody to Aspergillus in 6 out of 9 submissions (66.6%) vs. control birds. Beta-glucan analyses did not show any differences among levels in the broiler chicken groups. There were significantly higher levels of galactomannan antigen in 4 out of 7 submissions (57.1%) of aspergillosis in commercial turkeys, while only 2 out of 7 submissions (28.5%) had higher levels of antibody to Aspergillus vs. the control group. This study shows that diagnosis of respiratory and disseminated aspergillosis may be performed by detection of galactomannan antigenemia and antibodies in broiler chickens and to an extent in turkeys.     

Pathogenicity of serotype 8 fowl adenovirus isolated from gizzard erosions of slaughtered broiler chickens

The pathogenicity of serotype 8 fowl adenovirus (FAV), isolated from gizzard erosions of slaughtered broiler chickens, was investigated. In experiment 1, 29 5-day-old specific-pathogen-free (SPF) chickens were inoculated with the isolates of serotype 8 FAV, M013 (group 1) or G0054 (group 2) strain, via an oral route. There were no clinical signs in any of chickens after inoculation, and mild gizzard erosions were observed macroscopically and microscopically in three inoculated chickens of group 2. FAV was recovered from gizzards and rectums but was not recovered from pancreas and livers from chickens in both inoculated groups. In experiment 2, 27 1-day-old SPF chickens were inoculated with the G0054 strain by intramuscular route. Five, 6, and 3 inoculated chickens died on days 3, 4, and 5 postinoculation (PI), respectively. Four, 3, 1, and 1 inoculated chickens became moribund with severe clinical signs such as ruffled feathers, severe depression and closed eyes from days 3 to 6 PI, respectively. Macroscopically, the common characteristic of the gross lesions of dead chickens and euthanized moribund chickens was discoloration of liver. FAV was recovered from the gizzard, liver, pancreas and rectum. Virus titers in the liver and pancreas were high until day 6 PI. Histologically, necrotizing hepatitis and pancreatitis with intranuclear inclusion bodies were observed in the inoculated chickens. These results indicate that some strains of serotype 8 FAV are able to reproduce not only gizzard erosion by oral inoculation but inclusion body hepatitis (IBH) by intramuscular inoculation.     

Pathogenicity of serotype 1 fowl adenovirus in commercial broiler chickens.

The pathogenicity of a serotype 1 fowl adenovirus (FAV-99ZH), isolated from broiler chickens exhibiting gizzard erosion, was investigated in commercial broiler chickens. Five-, 3-, and 1-wk-old commercial broiler chickens were inoculated with FAV-99ZH by both oral and ocular routes. In the 5-wk-old chickens (trial 1), none of which had the maternal antibody to FAV-99ZH, severe gizzard erosions were observed on days 5, 7, and 10 postinoculation (PI). Among the 3-wk-old chickens (trial 2), which were separated into a control group and three treatment groups according to their maternal antibody titer levels, some chickens showed clinical signs such as depression and anorexia. Compared with the control group, all the treatment groups showed decreased weight gain. One treatment group, moreover, showed significantly decreased (P < 0.05) weight gain on day 10 PI. Severe gizzard lesions, such as erosion or ulcers, were observed from day 4 PI in all treatment groups regardless of their maternal antibody levels. The 1-wk-old chickens (trial 3) were separated into a control group and two treatment groups according to their titer levels of the inoculated virus. In spite of high maternal antibody levels, severe gizzard lesions were observed in both treatment groups, which also showed decreased weight gain. One treatment group, inoculated with the higher dose, showed significantly decreased (P < 0.05) weight gain on days 10 and 14 PI compared with the control group. Fowl adenovirus was recovered mainly from gizzard and rectal (including feces) samples from inoculated chickens but was not recovered from liver samples in any of the trials or in any of the control chickens. Although the reproduced disease was similar to that described in a previous report of experimental infection of specific-pathogen-free (SPF) white leghorn chickens with fowl adenovirus, the pathogenicity of FAV-99ZH in commercial broiler chickens was more severe than that in the SPF white leghorn chickens. The results of the present study indicate that FAV-99ZH isolated from gizzard erosion had pathogenicity and produced severe lesions in the gizzards of broiler chickens and that FAV-99ZH could infect and produce illness in broiler chickens with maternal antibodies against this virus.     

Human factors affecting the behaviour and productivity of commercial broiler chickens

1. The purpose of this study was to examine the relationship between stockperson attitude and behaviour; bird behaviour and productivity in the chicken meat industry. 2. No relationship between stockperson attitude and behaviour was observed, which is in contrast to studies in the pig and dairy industries. 3. Evidence is provided for the existence of sequential relationships between stockperson behaviour, bird fear levels and productivity in the broiler farms examined. 4. The mechanism(s) responsible for the negative relationships between fear levels and production is unclear. It is hypothesised that chronic stress or a series of acute stress responses may be the mechanism through which fear affects productivity. 5. The relationship between human behaviour, bird fear levels and productivity indicates the potential that exists to improve productivity and perhaps welfare of commercial broilers by reducing fear levels in broiler chickens.     

Genetic characterization of chicken anemia virus from commercial broiler chickens in Alabama.

Chicken anemia virus (CAV) isolates show extremely limited genetic variability worldwide. We determined the nucleotide sequence of an 823-nucleotide portion of the 2.3-kb CAV genome found in 10 liver and/or spleen specimens of Alabama 29-to-49-day-old commercial broiler chickens exhibiting lymphocyte depletion of the thymus submitted to the state diagnostic laboratory because of problems unrelated to anemia. We determined the nucleotide sequence directly from DNA isolated from tissues, without isolation of virus in culture. This procedure enabled us to characterize CAV that might not have replicated in culture and avoided the potential for changes during passage. Results confirmed the limited genetic variability of CAV. All sequences were identical in 93% of nucleotide positions. The sequences encoded only two distinct VP1 hypervariable regions, and both had been found previously in other CAV isolates. A novel amino acid, glutamine, was found at VP1 position 22 in half the sequences, replacing the histidine residue encoded by most previously characterized CAV genomes. We were able to distinguish among CAV genomes with different codons at VP1 amino acid 22 and different hypervariable regions by restriction endonuclease analysis of polymerase chain reaction products.     

Antimicrobial resistance in fecal Escherichia coli isolated from growing chickens on commercial broiler farms

To investigate the effects of rearing practices of commercial broiler chickens on the incidence of antimicrobial resistance in commensal Escherichia coli isolates, fecal E. coli isolates obtained in 4 farms were screened for anitimicrobial resistance. Ten E. coli isolates were recovered from each of the fecal samples collected from 10 birds in the farms at the ages of 2 days, 14-17 days, and 47-50 days. In 2 out of the 4 farms, no antimicrobials were used during the rearing period. In the other two farms, following collection of the fecal samples at 14 and 15 days of age, oxytetracycline (OTC), sulfadimethoxine (SDMX), and tylosin were given to birds on one farm and SDMX was used in the other. Isolates resistant to ampicillin and OTC that were obtained from an untreated flock at different sampling times were closely related to each other by pulsed-field gel electrophoresis patterns (PFGE) of XbaI-digested chromosomal DNA. PFGE analysis together with in vitro conjugation experiments suggested that diversity of resistance phenotypes within a clone may be resulted from the acquisition and loss of R-plasmids in an untreated and a treated flock. The numbers of resistance phenotypes observed among fecal isolates increased during the growth of the chickens in all the farms. The results in the present study suggest that persistence of commensal E. coli strains resistant to antimicrobials even in the absence of antimicrobial administration. It is also hypothesized that horizontal transmission of resistance determinants resulted in the emergence of different resistance phenotypes in those farms.