Mycoplasma gallisepticum (MG), a respiratory pathogen of poultry, was first documented as a cause of conjunctivitis in free-living house finches (Haemorhous, formerly Carpodacus, mexicanus) in 1994. This work explores virulence and immunogenicity of several isolates of MG collected from free-living house finches, and provides evidence that individual birds can have very different courses of disease when experimentally inoculated with the same dose of MG. A quantitative PCR assay utilizing the mgc2 gene was developed to quantify MG in conjunctival swab samples. To measure house finch lachrymal antibody response, a polyclonal reagent was developed to detect house finch IgA. A region of house finch IgA heavy chain was PCR-amplified from spleen cDNA, the heavy chain fragment was produced using a bacterial expression system, and rabbit anti-sera were generated against the recombinant protein. House finches were inoculated with MG isolates Virginia (VA)1994, California (CA)2006, or North Carolina (NC)2006, which were isolated from free-living house finches with conjunctivitis in 1994, 2006, and 2006, respectively. Infection with NC2006 resulted in the most severe eye lesions, highest pathogen loads, and highest levels of MG-specific lachrymal and serum antibodies. Infection with CA2006 caused the least severe eye lesions, lowest pathogen load, and weakest antibody response. A small number of birds in each group developed protracted, severe disease in spite of robust antibody responses. Immunoblot analyses indicated     3 that isolates are antigenically similar, suggesting that there may be partial cross-protection if a house finch encounters two or more strains of MG throughout the course of its lifetime. Chronic disease was further studied with experimental inoculations of house finches using VA1994 and North Carolina (NC1995, NC1996, NC2006, NC2008) field isolates. After inoculation, birds with chronic disease had significantly higher pathogen loads and antibody responses than did birds with acute disease. Using a monoclonal antibody specific for a variant of MG VlhA immunodominant surface protein, I show that VlhA expression differs among MG isolates studied, and that in vivo VlhA changes occur in house finches infected with MG. The results provide evidence that chronic MG disease has both pathogen-mediated and immunopathologic components.     4