Effect of aroA, htrA and aroA-htrA Deletion Mutation on Ability of Salmonella Abortusequi to Survive and Multiply in Macrophages

To understand the problem of host specificity of Salmonella enterica subspecies enterica serovar Abortusequi (S. Abortusequi), five isogenic strains including aroA, htrA and aroA-htrA deletion mutants, virulence plasmid cured and wild type parent strains were tested for invasion, survival and multiplication (up to 30 h) in cattle, goat, buffalo, horse and guinea pig macrophages and murine macrophage like cells (J-744). Invasion of different S. Abortusequi strains in different macrophages not varied significantly however, in goat macrophages invasion rate was comparatively lower (two to three log10) than in other macrophages. All the five strains persisted over the experiment period in equine and caprine macrophages but in other macrophages mutants got cleared but parent and plasmid cured strains persisted except in guinea pig macrophages where none of the five strains survived. Multiplication of wild type and virulence plasmid cured S. Abortusequi in horse macrophages and J-744 cells only indicated that answer to host adaptation lies not in survival but in multiplication of salmonellae in macrophages. The study revealed that aroA and htrA genes have important role in macrophages as both aroA and htrA deletion mutants failed to survive in cattle and buffalo macrophages and in macrophage like cells (J-744).