Sudden death syndrome in turkey hens

A turkey breeder flock of 5600 31-week-old hens experienced an abrupt increase in daily mortality for a 2-day period. This higher mortality rate corresponded with the handling and moving of the hens 1 to 2 days before. No clinical illness was seen in the hens before carcasses were discovered. The four hens that were necropsied had small spleens, congested lungs, and enlarged livers. The most consistent histologic lesions were pulmonary hemorrhage and edema, and congestion of veins and capillaries in several visceral organs. One hen had subserosal hemorrhage of the oviduct and perirenal hemorrhage. The increased mortality pattern, the lack of clinical signs, and the histopathologic changes are consistent with a diagnosis of sudden death syndrome. The presence of concurrent inflammatory lesions in the lungs predisposed the hens to sudden death following the stress of handling and moving.     

Replication of infectious bursal disease virus in continuous cell lines

Three mammalian continuous cell lines--MA-104, Vero, and BGM-70--were tested for their ability to support replication of infectious bursal disease virus (IBDV). Selected tissue-culture-adapted vaccine strains and tissue-culture-adapted field isolates of IBDV replicated in the MA-104, Vero, and BGM-70 cells; cytopathic effects were most pronounced in the BGM-70 cells. The cytopathic effects of the viruses in BGM-70 cells and chicken embryo fibroblast (CEF) cultures were similar. Virus-neutralization titers of selected serum samples determined in BGM-70 cultures compared well with those obtained from CEF cultures.     

Lack of protection against Bordetella avium in turkey poults exposed to B. avium-like bacteria

Six laboratory experiments were designed to determine whether poults infected with the nonpathogenic Bordetella avium-like (BAL) bacteria would develop immunity to B. avium (BA), the causative agent of turkey coryza. The BAL bacteria were isolated from poults given that organism, but few colonies were observed by 3 weeks postexposure. No serum-agglutinating antibody to the BAL bacterium was detected in poults exposed to that organism. Poults exposed to BAL bacteria either once or twice at different ages were not protected from infection or disease following experimental challenge between 1 and 7 weeks of age with pathogenic BA.     

Modulation by colostrum-acquired maternal antibodies of systemic and mucosal antibody responses to rotavirus in calves experimentally challenged with bovine rotavirus

The effect of colostral maternal antibodies (Abs), acquired via colostrum, on passive protection and development of systemic and mucosal immune responses against rotavirus was evaluated in neonatal calves. Colostrum-deprived (CD) calves, or calves receiving one dose of pooled control colostrum (CC) or immune colostrum (IC), containing an IgG1 titer to bovine rotavirus (BRV) of 1:16,384 or 1:262,144, respectively, were orally inoculated with 105.5 FFU of IND (P[5]G6) BRV at 2 days of age. Calves were monitored daily for diarrhea, virus shedding and anti-BRV Abs in feces by ELISA. Anti-rotavirus Ab titers in serum were evaluated weekly by isotype-specific ELISA and virus neutralization (VN). At 21 days post-inoculation (dpi), all animals were euthanized and the number of anti-BRV antibody secreting cells (ASC) in intestinal and systemic lymphoid tissues were evaluated by ELISPOT. After colostrum intake, IC calves had significantly higher IgG1 serum titers (GMT=28,526) than CC (GMT=1195) or CD calves (GMT<4). After BRV inoculation, all animals became infected with a mean duration of virus shedding between 6 and 10 days. However, IC calves had significantly fewer days of diarrhea (0.8 days) compared to CD and CC calves (11 and 7 days, respectively). In both groups receiving colostrum there was a delay in the onset of diarrhea and virus shedding associated with IgG1 in feces. In serum and feces, CD and CC calves had peak anti-BRV IgM titers at 7 dpi, but IgA and IgG1 responses were significantly lower in CC calves. Antibody titers detected in serum and feces were associated with circulation of ASC of the same isotype in blood. The IC calves had only an IgM response in feces. At 21 dpi, anti-BRV ASC responses were observed in all analyzed tissues of the three groups, except bone marrow. The intestine was the main site of ASC response against BRV and highest IgA ASC numbers. There was an inverse relationship between passive IgG1 titers and magnitude of ASC responses, with fewer IgG1 ASC in CC calves and significantly lower ASC numbers of all isotypes in IC calves. Thus, passive anti-BRV IgG1 negatively affects active immune responses in a dose-dependent manner. In ileal Peyer's patches, IgM ASC predominated in calves receiving colostrum; IgG1 ASC predominated in CD calves. The presence in IC calves of IgG1 in feces in the absence of an IgG1 ASC response is consistent with the transfer of serum IgG1 back into the gut contributing to the protection of the intestinal mucosa.     

A survey of enteric viruses of turkey poults

Intestinal samples from 91 turkey flocks between 1 day and 5 weeks of age were examined for enteric viruses using electron microscopy and electropherotyping. These flocks originated from eight operations in six states. Individual flocks were sampled only once. At the time of sampling, 31 flocks were considered normal/healthy and 60 were considered to have enteric disease. The most frequently identified viruses from diseased flocks were astroviruses (78%) and rotavirus-like viruses (RVLVs) (67%). Far less frequent were rotaviruses (22%), atypical rotaviruses (12%), enteroviruses (5%), and reoviruses (2%). Only 10% of the samples from diseased flocks were negative, but 48% of the samples from normal/healthy flocks were negative. Astroviruses and RVLVs were far less frequent in normal/healthy flocks than in diseased flocks, but rotaviruses were identified slightly more often. No viruses were detected from flocks sampled within the first few days of life. Astrovirus infections seemed to occur at an earlier age than other virus infections. Seldom was only one type of virus identified. Astrovirus + RVLV was the most frequently identified combination in diseased flocks.     

Comparison of enzyme-linked immunosorbent assays and virus neutralization test for detection of antibodies to avian pneumovirus

Two different whole-virus enzyme-linked immunosorbent assays (ELISAs), developed in Ohio (OH) with APV/Minnesota/turkey/2a/97 and in Minnesota (MN) with APV/Colorado/turkey/97, and the virus neutralization (VN) test were used to test 270 turkey serum samples from 27 Minnesota turkey flocks for avian pneumovirus (APV) antibodies. In addition, 77 turkey serum samples and 128 ostrich serum samples from Ohio were tested. None of the turkey samples from Ohio had antibodies to APV by the VN test and OH ELISA. The ostrich samples were only tested with the VN test and were all negative for antibodies to APV. For the Minnesota serum samples, 107, 115, and 120 were positive by the VN test, the OH ELISA, and the MN ELISA, respectively. The Kappa values of 0.938 and 0.825 showed excellent agreement between the VN test and the OH ELISA and the MN ELISA, respectively, for detection of antibodies to the APV. The OH ELISA and MN ELISA had sensitivities of 1.0 and 0.953, specificities of 0.950 and 0.889, and accuracies of 0.970 and 0.914, respectively. Our results indicate that the 3 methods are sensitive and specific for diagnosis of the APV infection.     

Induction of vitamin A deficiency in turkeys

The objective of this study was to determine the relationship between the hepatic vitamin A (VitA) level and the pathologic changes in the oropharynx and esophagus of VitA-deficient turkeys. Study turkeys were provided with a diet sufficient (11,000 IU/kg) or deficient (2750 IU/kg) in VitA from 4 to 17 wk of age. Body weight, bacterial culture, and tissues from internal organs were collected at weekly intervals. VitA deficiency causes epithelial tissue damage in poultry. This epithelial damage was seen grossly as white plaques in the oropharynx and esophagus and histologically as squamous metaplasia of mucosal glands and keratinization of epithelium. No significant difference in body weights was seen among the groups. Moreover, no pathogenic bacteria was isolated during sampling periods. Liver VitA levels declined significantly after consumption of low VitA diet for 3 wk and were depleted after 5 wk. Squamous metaplasia due to VitA deficiency developed in the esophagus after 3 wk and in the oropharynx after 4 wk of consuming a VitA-deficient diet.