Occurrence of autoantibodies to cilia in lambs with a 'coughing syndrome'.

ABSTRACT

A respiratory disease of lambs that has been termed the 'coughing syndrome' has been observed in the mid-western region of the United States of America. Mycoplasma ovipneumoniae (M. ovipneumoniae) and Mycoplasma arginini (M. arginini) were routinely isolated from the respiratory tract of lambs with this disease. A high level of antibodies reactive with ovine cilia of the upper respiratory tract was detected in the sera from many of the lambs in affected flocks but not in sera of lambs from unaffected flocks. The reactivity of these antibodies with cilia was demonstrated by ELISA and confirmed by indirect immunofluorescent staining and western immunoblotting. These antibodies were predominantly of the IgG isotype. They were distinct from cold or warm agglutinins and could be absorbed from the sera with cilia but not with antigens of common bacterial pathogens of the sheep respiratory tract including M. ovipneumoniae, M. arginini, Pasteurella haemolytica, Pasteurella multocida or Neisseria ovis. In addition, their occurrence appeared to be independent of the specific antibodies to M. ovipneumoniae and M. arginini. Western immunoblotting indicated that the antibodies were directed primarily against an antigen with apparent molecular weight of 50 kDa. In one flock from which serial serum samples were collected from the same lambs over a 10-month period, antibodies to ovine cilia developed before the onset of the clinical disease and persisted for a period of several months until most of the lambs had apparently recovered. However, colonization of the respiratory tract of the lambs by M. ovipneumoniae preceded the production of these antibodies. Sequential serum samples taken from another flock, with no known history of this coughing, showed no such antibodies throughout the sampling period. It is suggested that an immunopathologic mechanism involving production of autoantibodies directed against a ciliary antigen of the lambs could be a contributing factor to the pathogenesis of this clinical disease.