Adenoviral gizzard erosion in commercial broiler chickens

Pathologic and immunohistochemical changes caused by group I of the fowl adenovirus (FAV) serotype-1 99ZH strain, isolated from broiler chickens exhibiting gizzard erosion, were investigated in commercial broiler chickens. One hundred twenty-two chickens were inoculated with the strain by both oral and ocular routes at 1, 3, or 5 weeks of age and euthanatized for necropsy within 4-18 days of inoculation. Focal gizzard erosions were observed in the inoculated chickens of each age group. A histologically degenerative koilin layer, necrotic mucosa, intranuclear inclusion bodies in the glandular epithelial cells, inflammatory cell infiltrations in the lamina propria, submucosa, and a muscle layer were seen in the gizzards. Immunohistochemical staining showed evidence of FAV antigens in the intranuclear inclusion bodies. These findings were recognized regardless of their maternal antibody levels for FAV serotype-1. Gizzard lesions appeared later in the lower-dose-inoculated chickens than in the higher-dose-inoculated chickens. Numerous CD3-positive cells and IgY-positive plasma cells were seen in the gizzard lesions. In 5-week-old chickens the heterophil infiltrations in the lesions were milder than in younger chickens. Intranuclear inclusion bodies also were observed in the epithelial cells of the ileum or cecal tonsils of some chickens. Thus, this study shows that FAV-99ZH causes adenoviral gizzard erosion in broiler chickens without hepatic or pancreatic lesions and that cell infiltration is more severe than in dietary gizzard erosions.     

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 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.     

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.     

Footpad dermatitis in broiler chickens in Japan

The prevalence of footpad dermatitis (FPD) in broiler chickens in Japan was investigated. In the first examination at slaughterhouses, lesions were commonly observed on the footpads of a total of 8,985 broiler chickens from 45 flocks on 36 farms. In 3 flocks, all the birds examined had lesions. In the other 42 flocks, the incidence of FPD ranged from 31.9% (81/254) to 99.5% (1/222). The footpad lesions were classified into 4 categories according to the severity of dermatitis as follows; score 0, 1,181 birds (13.1%); score 1, 2,992 birds (33.3%); score 2, 3,000 birds (33.4%); and score 3, 1,812 birds (20.2%). The mean scores of the flocks varied widely from 0.31 to 2.69. Males had higher mean scores than females. No significant differences were found between the mean scores of birds reared in windowless houses and those in open-sided houses. On 4 farms, the investigation was carried out in different seasons, and 3 of them showed higher mean scores in winter than in summer. Next, observation of 2,255 birds from 15 flocks on 5 farms during a 4-week rearing period revealed that FPD was already produced at 7 days of age and worsened with age.     

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.     

Reproduction of adenoviral gizzard erosion by the horizontal transmission of fowl adenovirus serotype 1

The horizontal transmission ability of fowl adenovirus (FAV) serotype 1 99ZH strain, isolated from chickens exhibiting gizzard erosion, was investigated. Twelve 13-day-old specific pathogen-free chickens were inoculated orally with 10(6) TCID(50)/0.05 ml of the strain. An in-pen contact group (chickens in the same pen with inoculated chickens), hedge contact group (chickens in a pen connected with pens housing inoculated chickens), non-contact group (chickens in a separate pen placed at a distance of 70 cm from the connected pens), human exposure group (chickens in the next room and attended last every day) and negative control group were examined. Each group consisted of 11 or 12 uninoculated chickens. Gizzard lesions were grossly or histologically observed from 10 days after exposure (DAE) in the in-pen contact group, and from 15 DAE in the hedge contact and non-contact groups. The FAV gene was detected by polymerase chain reaction performed on cloacal swabs taken on 5 and 13 DAE from chickens in both contact groups, and on 20 and 26 DAE from those in the non-contact group. Serum neutralizing antibodies against FAV serotype 1 were detected in chickens from 13 and 26 DAE in both contact groups and in the non-contact group, respectively. In the human exposure and negative control groups, no infection was observed. We conclude that FAV-99ZH strain spreads rapidly through direct contact with inoculated chickens, and slowly through non-contact transmission, and that adenoviral gizzard erosion is reproduced by this horizontal transmission.     

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.     

Estimation of nutrient excretion factors of broiler and layer chickens in Japan

We estimated the nitrogen (N), phosphorus (P), potassium (K) and magnesium (Mg) excretion factors of broiler and layer chickens in Japan, using two approaches and the latest data available. In the top‐down approach, we determined the nutrient amounts in the feeds and those in the products (i.e. the liveweight gain, eggs), and the national nutrient excretions were determined as the difference between these amounts. We then calculated the nutrient excretion factors by dividing the national excretions by the number of animals. In the bottom‐up approach, we calculated the amounts of nutrients in the feed and product per head using productivity parameters (feed conversion ratio, etc.). The differences between these amounts were considered the nutrient excretion factors. The average nutrient excretion factors of broilers (g/day/head) estimated using the top‐down and bottom‐up approaches were: N, 1.40 and 1.87; P, 0.36, 0.50; K, 0.54, 0.77; Mg, 0.13, 0.18, respectively. The excretion factors obtained by the top‐down approach can be used to calculate the national/regional excretions. The two approaches resulted in almost the same excretion factors for layers, and the average nutrient excretion factors of layers (g/day/head) estimated were: N, 2.20; P, 0.55; K, 0.68; Mg, 0.23. The estimated excretion factors for N (only) are smaller than the reported factors.     

肉鸡砂囊糜烂及前胃炎的致病因素

正确的诊断及鉴别这两种具有重要经济价值的疾病,将有助于通过治疗降低经济损失。许多地方的兽医经常报告肉鸡和商品蛋鸡发生砂囊糜烂。此类病变在许多乡村地区相当普遍,这是     

Characterization of a lentogenic Newcastle disease virus isolated from broiler chickens in Japan

Newcastle disease virus (NDV), named MET95, was isolated from a non-vaccinated broiler flock in Japan in 1995. The MET95 strain was determined to be a lentogenic NDV. The strain has the properties of eluting rapidly at 4 C and has low thermostability in hemagglutinating activity with chicken erythrocytes. In these studies, no difference could be found between the MET95 strain and the Hitcher B1 vaccine strain. However, the chickens inoculated with the MET95 strain, as well as chickens that they were in contact with, had a much higher hemagglutination-inhibition antibody response than those inoculated with the B1 strain. Accordingly, the MET95 strain is thought to be a promising candidate as a live ND vaccine strain. In Japan, this is the first report on the isolation of lentogenic NDV from chickens since the paper on the Ishii strain isolated in 1966.     

Myxoid leiomyosarcoma of the gizzard in a broiler chicken

A leiomyosarcoma was found in the gizzard of a 57-day-old female broiler chicken weighing 1.8 kg. Grossly, the tumor mass, 13.0 x 8.5 x 10.0 cm, enveloped the gizzard and had a gelatinous appearance due to the rich production of mucin. Miliary metastatic tumors were noted in the liver. Histopathologically, there was marked production of mucus throughout the tumor tissue, and densely or loosely arranged long spindle-shaped leiomyosarcoma cells proliferated. The tumor cells had a low rate of mitosis, showed slight cellular atypia, and, immunohistochemically, were positive for actin, alpha-smooth muscle actin, and desmin. Electron microscopically, various amounts of microfibrils with focal densities, dense patches, and basal plates were observed.     

Experimental infection of specific-pathogen-free chickens with serotype-1 fowl adenovirus isolated from a broiler chicken with gizzard erosions

Gizzard lesions were formed in specific-pathogen-free (SPF) white leghorn chickens inoculated with fowl adenovirus (FAV). The virus, serotype 1 FAV 99ZH strain (FAV-99ZH), was originally isolated from the gizzard mucosa of commercial broiler chickens exhibiting gizzard erosion with intranuclear inclusion bodies. Five-day-old and 53-day-old SPF white leghorn chickens were inoculated with FAV-99ZH by both oral and ocular routes and then examined at necropsy on days 3, 5, 7, 10, 14, and 21 postinoculation (PI). There were no clinical signs in any of the chickens after the inoculation. Focal gizzard lesions occurred macroscopically, however, in inoculated chickens at several experimental periods. FAV was recovered from tissue samples of the proventriculus, gizzard, pancreas, and rectum by day 10 or 7 PI but was not recovered from liver samples of any of the chickens. These results indicate that FAV isolated from gizzard erosion is able to reproduce gizzard lesions as necrosis and erosion in SPF white leghorn chickens and that it may have a greater degree of tissue tropism in gizzards and other digestive organs than in the liver.     

Salt poisoning in broiler chickens

The incident occurred on a small, owner-operated broiler unit that used home-mixed feed. Two flocks of broilers, one aged 6 weeks and one aged 6 days, developed signs of watery diarrhoea, thirst and weakness. Over 3 days the mortality increased considerably and many birds were noticed to show laboured breathing. The majority of dead birds had an excess of clear fluid in the pericardial sac, oedematous lungs and pale swollen kidneys. Cystic dilation of the testes was conspicuous in several birds from the younger flock killed at 12 days of age. This lesion is a specific indication of sodium toxicity in young broilers. Histological lesions were those associated with cardiovascular collapse and hypoxia. Liver levels of sodium chloride were 4 g/kg of wet weight. Broiler feed samples contained more than 7% sodium chloride whereas the nutritional specifications were for 0.4%. The rations had been correctly mixed and the problem was traced to a faulty batch of meatmeal that had been contaminated by salt used for curing hides.