Location: Virus and Prion ResearchTitle: Replacement of Adenylate Cyclase Toxin in a Prominent Lineage of Bordetella bronchiseptica) Author
Submitted to: Symposium Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 2/4/2008
Publication Date: 3/8/2008
Citation: Buboltz, A.M., Nicholson, T.L., Parette, M.R., Hester, S.E., Parkhill, J., Harvill, E.T. 2008. Replacement of Adenylate Cyclase Toxin in a Prominent Lineage of Bordetella bronchiseptica. Keystone Symposium Molecular Evolution as a Driving Force in Infectious Disease, April 8-13, 2008, Breckenridge, Colorado. p. 16. Interpretive Summary:
Technical Abstract: Bordetella bronchiseptica is a gram negative respiratory pathogen that infects a wide-range of hosts and causes a diverse spectrum of disease that may be due in part to the set of virulence factors utilized by different strains. In a murine model of infection, we found that virulence, as measured by mean lethal dose (LD50), of B. bronchiseptica strains varied widely. Strain 253 was less virulent than the typically studied strain, RB50. Transcriptome analysis showed that strain 253 lacked expression of adenylate cyclase toxin (ACT). Comparative genomic hybridization and genome sequencing of this strain revealed that the cya locus, which encodes ACT, was replaced non-recently by an operon predicted to encode peptide transport proteins (ptp). Other B. bronchiseptica strains from the same phylogenetic lineage as strain 253 also lacked the cya locus, contained the peptide transport genes and were less virulent than RB50. Although the loss of ACT would be expected to be counter-selected since it is conserved among the classical bordetellae and believed to be crucial to its success as a pathogen, our data indicate that a single genetic event resulted in the replacement of this toxin in an ancestral strain that expanded into a prominent lineage. This suggests that ACT may not always be critical for the success of the bordetellae and that the ptp operon replacing it may be important in overcoming the loss of this toxin.