Abstract
Mycoplasma bovis causes chronic pneumonia and polyarthritis in feedlot cattle. M. bovis infects the lungs of most feedlot cattle, but the majority of calves never develop disease. Competing explanations are that some strains of M. bovis are more virulent than othersor, alternatively, that calves require some other abnormality to be present in order for M. bovis to cause disease. We hypothesize that H2O2 production is an important virulence factor of M. bovis, causing oxidative injury to lung tissue. A second hypothesis is that isolates associated with caseonecrotic bronchopneumonia have an increased capacity for H2O2 production. Immunohistochemical markers of oxidative stress (4-hydroxynonenal, HN) and nitrative stress (3-nitrotyrosine, NT) were compared in lungs of calves with caseonecrotic bronchopneumonia characteristic of M. bovis infection, with other forms of bronchopneumoniaor with non-inflamed lungs. HN and NT were identified in M. bovis pneumonia, mainly in foci of caseous necrosis. HN was not observed in inflamed non-necrotic tissue in lesions typical of pneumonic pasteurellosis. H2O2 production by M. bovis was identified, but the levels did not differ in isolates from calves with caseonecrotic bronchopneumonia compared with those with non-inflamed lungs or other forms of pneumonia. These findings provide evidence that oxidative and nitrative injury contribute to the formation of the caseonecrotic lesions that are characteristic of M. bovis pneumoniaand that production of H2O2 by M. bovis may contribute to this oxidative injury.
Published Version
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