1887

Abstract

produces a variety of virulence factors that allow it to cause a wide range of infections in humans and animals. In the latter, is a leading cause of intramammary infections. The contribution of catalase (KatA), an enzyme implicated in oxidative stress resistance, and beta-toxin (Hlb), a haemolysin, to the pathogenesis of is poorly characterized. To investigate the role of these enzymes as potential virulence factors in , we examined the intracellular survival of Δ, Δ and Δ Δ mutants in murine macrophages (J774A.1) and bovine mammary epithelial cells (MAC-T), and their virulence in different murine and ovine models. Catalase was not required for the survival of within either J774A.1 or MAC-T cells. However, it was necessary for the intracellular proliferation of the bacterium after invasion of MAC-T cells. In addition, catalase was not needed for the full virulence of in mice. Deletion of the gene had no effect on the intracellular survival of in J774A.1 cells but did cause a slight increase in survival in MAC-T cells. Furthermore, like catalase, beta-toxin was not required for complete virulence of in murine models. Unexpectedly, the Δ Δ mutant showed a notably increased persistence in both cell lines, and was significantly less virulent for mice than were the wild-type strain and single mutants. Most interestingly, it was also markedly attenuated in intramammary and subcutaneous infections in ewes and lambs.

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2009-05-01
2024-04-19
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