Since 1994, an epidemic of conjunctivitis caused by Mycoplasma gallisepticum (MG) has spread throughout the eastern population of house finches (Carpodacus mexicanus). The adaptation of MG to a free-flying avian species presents potential problems for the control of mycoplasmosis in commercial poultry. To evaluate risks associated with this emerging problem, a field survey was conducted to assess prevalence of MG infection in house finches and other passerine birds associated with poultry farms. Between November 1997 and March 1999, 1058 birds were captured by mist net or trap at 17 farms and at 10 feeder stations in northeast Georgia. Birds were bled and screened by serum plate agglutination (SPA) for antibodies to MG. Birds with negative or weak positive SPA results were released at capture sites, and those with strong positive SPA reactions were kept for further evaluation. Necropsies were performed on selected house finches and individuals of 11 other passerine species, and samples were collected for MG testing by culture, polymerase chain reaction (PCR), hemagglutination inhibition, and histopathology. Testing revealed 19.1% of 671 birds caught at farms and 11.6% of 387 birds caught at feeder sites were SPA positive for MG. Three house finches captured on farms were positive for MG by culture and PCR, whereas three from feeder sites were positive only by PCR. No MG isolates were made from tufted titmice (Baeolophus bicolor), but 40% were positive by PCR. Individuals from 10 additional species were SPA positive only. Results suggest that MG persists at low levels in house finches in northeast Georgia and that tufted titmice may be nonclinical carriers of MG or a related mycoplasma. Positive SPA reactions in other species may be caused by nonspecific reactions or contact exposure. Current biosecurity recommendations should be sufficient to minimize risks of transmission between wild and domestic birds.

House sparrows were infected by aerosol with Mycoplasma gallisepticum (MG) or M. synoviae (MS). MG was reisolated from 5 to 11 sparrows 10 days postinfection, but infection appeared to be temporary. Mycoplasma-free chickens reared in the experimental house became infected with MG during the trial. MS was recovered from only one sparrow. Serological tests were unsatisfactory for diagnosing infected birds. The results suggest that house sparrows may be temporary biological carriers of MG.

Groups of 10 8-wk-old chickens that had been vaccinated 4 wk previously with the F strain, ts-11, or 6/85 strain of Mycoplasma gallisepticum (MG) were challenged by placing them in contact with 20 chickens that had been previously infected with the virulent R strain of MG. Each month, the 10 oldest chickens were removed from each pen and replaced with 10 vaccinated chickens to return the total number of chickens in each pen to 30. Chickens were bled and cultured for MG prior to contact challenge and at the time of removal from the challenge pen. The strain of all MG isolates was determined by rapid amplified polymorphic DNA. All vaccine strains were isolated from tracheas prior to contact challenge, but colonization by the 6/85 vaccine strain was inconsistent. Beginning with the group placed in contact 3 mo after the initiation of the study, F strain had begun to displace the R challenge strain. By the eight month, F strain had completely displaced the R strain in that pen. However, neither strain ts-11 nor 6/85 was able to displace the R strain under the conditions of this study.

Type-8 avian adenoviruses were isolated from chickens in a commerical flock suffering an outbreak of inclusion body hepatitis. Serum-neutralizing titer to this type, but not to 7 other types of avian adenovirus, was more than 4 times as high in convalescing chickens as in chickens from the flock bled 2 weeks previously, during the disease outbreak. A disease similar to that in the commercial flock and to inclusion body hepatitis as described in the literature was produced by intra-abdominal inoculation of a type-8 isolant, AMG 5 (2a), into 1-day-old specific-pathogen-free chicks. Pathologic features of the disease included necrotizing hepatitis, pancreatitis, and severe lymphoid depletion of the bursa of Fabricius, thymus, and spleen. It was concluded that type-8 avian adenoviruses were involved in the etiology of the naturally occurring outbreak of inclusion body hepatitis.

Mycoplasma gallisepticum strains, including a series of field strains from North Carolina, were examined by homologous and heterologous hemagglutination-inhibition (HI) tests and by restriction endonuclease DNA analysis to determine whether they were closely related. HI results indicated wide antigenic diversity. Generally, homologous HI titers were higher than heterologous titers; exceptions were probably due to relative insensitivity of individual antigen batches. Strain A5969, commonly used as an HI antigen strain in many laboratories, was insensitive for detecting antibodies against all of the strains studied. None of the antigens was efficient in detecting HI antibodies against all other strains studied. Restriction endonuclease analysis indicated that North Carolina strains K501, K1453, and K1503 were closely related or identical, as were strains K1545, K1659, and K1486. Strain K1528, isolated from a peacock originally felt to be the source of many of the outbreaks, was not closely related to any of the other strains. Most strains identical or closely related by restriction endonuclease analysis were also closely related by HI. Strains 383T and 236C were identical by restriction enzyme analysis but unrelated by HI tests.