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Cold Shock Exoribonuclease R (VacB) Is Involved in Aeromonas hydrophila Pathogenesis

Departments of Microbiology and Immunology,¹ Pathology, University of Texas Medical Branch, Galveston, Texas 77555-1070,² Departments of Medical and Research Technology and Epidemiology and Preventive Medicine, University of Maryland, Baltimore, Maryland 21201³

Received 15 January 2008/ Accepted 6 March 2008

In this study, we cloned and sequenced a virulence-associated gene (vacB) from a clinical isolate SSU of Aeromonas hydrophila. We identified this gene based on our recently annotated genome sequence of the environmental isolate ATCC 7966^T of A. hydrophila and the vacB gene of Shigella flexneri. The A. hydrophila VacB protein contained 798 amino acid residues, had a molecular mass of 90.5 kDa, and exhibited an exoribonuclease (RNase R) activity. The RNase R of A. hydrophila was a cold-shock protein and was required for bacterial growth at low temperature. The vacB isogenic mutant, which we developed by homologous recombination using marker exchange mutagenesis, was unable to grow at 4°C. In contrast, the wild-type (WT) A. hydrophila exhibited significant growth at this low temperature. Importantly, the vacB mutant was not defective in growth at 37°C. The vacB mutant also exhibited reduced motility, and these growth and motility phenotype defects were restored after complementation of the vacB mutant. The A. hydrophila RNase R-lacking strain was found to be less virulent in a mouse lethality model (70% survival) when given by the intraperitoneal route at as two 50% lethal doses (LD₅₀). On the other hand, the WT and complemented strains of A. hydrophila caused 80 to 90% of the mice to succumb to infection at the same LD₅₀ dose. Overall, this is the first report demonstrating the role of RNase R in modulating the expression of A. hydrophila virulence.

Published ahead of print on 14 March 2008.