A turkey coronavirus (TCV [NC95]) was characterized by antigenic comparison with other avian and mammalian coronaviruses using immunofluorescence (FA) and immunoperoxidase (IP) procedures. Based on FA and IP procedures, TCV (NC95) was determined to be antigenically indistinguishable from turkey enteric (bluecomb) coronavirus (TECV). In addition, TCV (NC95) and TECV were found to be closely related to infectious bronchitis virus (IBV); a one-way antigenic relationship was demonstrated. Polyclonal antibodies specific for TECV and IBV reacted strongly against TCV (NC95), as determined by FA procedures. Monoclonal antibodies (MAbs) specific for IBV matrix protein (MAb 919) reacted strongly against TCV (NC95) and TECV as determined by FA and IP procedures; an IBV peplomer protein-specific MAb (MAb 94) did not recognize the two viruses. These studies suggest an identification of TCV (NC95) as a strain of TECV, and provide evidence of a close antigenic relationship between these viruses and IBV.
Inclusion-body hepatitis was diagnosed in 1-day-old turkeys experiencing above-average mortality. At necropsy, turkeys appeared anemic and had pale yellow livers. Histopathologic examination of affected livers revealed diffuse hepatic degeneration and multifocal necrosis, with approximately 70% of the hepatocytes containing large, basophilic, intranuclear inclusion bodies. An adenovirus was isolated from affected livers and identified as a group I avian adenovirus by indirect immunofluorescence.
Fecal smears from 112 avian necropsy accessions representing 431 birds were stained with auramine O and examined for Cryptosporidium oocysts by fluorescence microscopy. Stained Cryptosporidium oocysts fluoresced bright yellow-green and were easily differentiated from extraneous material by their uniform small size (approx. 5 micron) and morphology. The rates of cryptosporidia-positive accessions were 27.3% (9/33) of broilers, 10% (3/30) of broiler breeders, and 5.9% (1/17) of layers. Further analyses of available data for various risk factors that may have influenced rates of cryptosporidia-positive samples in broilers, broiler breeders, and layers failed to show significant relationships. However, it was apparent that positive samples were clustered within accessions and not scattered throughout the population sampled. This survey also resulted in the first reported identification of Cryptosporidium oocysts from a budgerigar, macaw, and tundra swan.
Specific-pathogen-free chickens orally inoculated at 4 days of age with a moderately pathogenic vaccine strain of infectious bursal disease virus (IBDV) and/or at 5 days of age with Cryptosporidium baileyi oocysts remained free of overt clinical signs throughout a 16-day period postinoculation (PI). The prepatency period for C. baileyi oocyst shedding was shorter in chickens receiving higher numbers of oocysts, but once shedding was detected, there were no obvious differences in shedding patterns among groups receiving 10(3) through 10(6) oocysts. On days 8 and 16 PI, cryptosporidia were located primarily in the bursae of Fabricius. IBDV exposure was associated with bursal follicle atrophy, whereas C. baileyi infection resulted in bursal epithelial hypertrophy and hyperplasia, mild follicle atrophy, and heterophil infiltration of the bursal mucosa. Examination of experimental groups of 30 birds each indicated that concurrent infection with both agents resulted in more severe bursal lesions, more infected birds, and greater numbers of cryptosporidia in infected tissues. At the termination of the trial, 16 days PI, Cryptosporidium infection was associated with a 6% decrease in mean body weight compared with controls.
Depression, somnolence, and increased mortality were observed in 2-week-old turkeys inoculated intramuscularly with either eastern equine encephalitis (EEE) virus or Highlands J (HJ) virus. Mortality rates in EEE virus- and HJ virus-inoculated turkeys were 7/30 (23%) and 9/30 (27%), respectively; no sham-inoculated controls died. Both EEE virus- and HJ virus-inoculated turkeys developed viremia that lasted 2 days; peak mean titers were 5.5 and 3.2 log10 plaque-forming units per ml of blood, respectively. Pathologic changes in both EEE virus- and HJ virus-inoculated turkeys consisted primarily of multifocal necrosis in the heart, kidney, and pancreas, and lymphoid necrosis and depletion in the thymus, spleen, and bursa of Fabricius. The findings indicate that EEE virus and HJ virus are pathogenic for young turkeys.
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