In February 1991, a flock of North Carolina multiplier breeder turkeys experienced respiratory signs, sinusitis, airsacculitis, and increased mortality. Mycoplasma gallisepticum (MG) was isolated, and appropriate control measures were initiated. Ultimately, this outbreak involved several breeder flocks of an integrated turkey production company before the last infected flock was identified in May 1991. During this time, MG was also isolated from a flock of commercial layer-type chickens raised as pullets in close proximity to the index turkey flock. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis and restriction endonuclease analysis indicated that these isolates were identical to each other and to examples of the vaccinal F strain. Additionally, MG isolates from the affected turkey breeder and layer flocks were identified as MG F strain by use of an F strain-specific DNA probe and polymerase chain reaction. A separate outbreak of MG disease in several meat-turkey flocks of a Midwest producer/processor yielded isolates identified as F strain by the polymerase chain reaction. These studies demonstrated: 1) the utility of newer technologies for disease outbreak investigations; and 2) the potential of MG F strain to cause disease in breeder and meat turkeys under field conditions.

Cryptosporidium meleagridis oocysts, originally isolated from droppings of commercial turkey poults with increased mortality due to viral (reovirus) hepatitis and enteritis, were treated with peracetic acid to kill companion bacteria and viruses and then propagated by passage in young turkeys. Thirty-eight 5-day-old large white turkey poults were inoculated by crop gavage with 500,000 cryptosporidial oocysts and compared with 40 uninoculated poults. Cryptosporidial oocysts shedding began 3 days postinoculation (PI), peaked on day 4 PI, and persisted at a low level for the duration of the 21-day trial. Low to moderate cryptosporidial infections of the ileal mucosa (days 3, 6, and 15 PI), cecal mucosa (days 3, 6, and 21 PI), and bursa of Fabricius (days 6, 12, 15 and 21 PI) were found on histopathological examination. There were no differences in mean body weights between the inoculated and uninoculated groups, and no mortality or clinical signs of disease were seen in either group.

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.

SDS-polyacrylamide gel electrophoresis (PAGE) and immunoblot profiles using antisera from M. synoviae F10-2AS-inoculated chickens detected heterogeneity among 10 M. synoviae isolates. This variation was primarily seen in immunoblots as a difference in the molecular size of immunoreactive proteins below 50 kDa and corresponded to an area of variability seen in SDS-PAGE. No two isolates had the same immunoblot profile below 50 kDa. Hyperimmune antiserum to a M. synoviae F10-2AS protein of 41 kDa (p41) reacted with protein(s) ranging from 41 to 48 kDa in nine of 10 isolates and strongly with one of 87 kDa in one isolate. The immunoreactivity of antiserum from inoculated chickens and the hyperimmune antiserum to p41 varied from intense to weak with the 10 M. synoviae isolates. All of the highly immunogenic proteins of M. synoviae F10-2AS, including p41, partitioned into the Triton X-114 detergent phase, indicating that they are amphiphilic in nature and integral membrane proteins. The data suggest that M. synoviae is capable of varying the molecular size of a highly immunogenic integral membrane protein.

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.