Submitted to: Current Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: October 6, 2007
Publication Date: January 23, 2008
Citation: Halling, S.M., Jensen, A.E., Olsen, S.C. 2008. Defensin Susceptibility and Colonization in the Mouse Model of AJ100, a Polymyxin B Resistant, Brucella abortus RB51 Isolate. Current Microbiology. 56(2008):274-278. Interpretive Summary: Wildlife serves as a reservoir for potential re-emergence of bovine brucellosis. The current bovine brucellosis vaccine strain affords wildlife some protection but can persist for long periods of time in vaccinated animals. A derivative of the current bovine vaccine was eliminated more quickly than the parental strain from mice in the mouse vaccine protection model, yet it afforded protection of the mice from challenge. This strain may be useful as a carrier vector to enhance protection of wildlife.
Technical Abstract: Bacterial facultative intracellular pathogens selected for sensitivity to polymyxin B have been shown to be attenuated. However, the effect on pathogenicity of increased resistance to polymyxin B has not been studied. A polymyxin resistant mutant, Brucella abortus AJ100, was characterized by comparing its minimum inhibitory concentration (MIC) value for the polycationic antibiotic polymyxin B, sensitivity to defensins, and both pathogenicity and protection from infection in the mouse model to the parental strain RB51. The MIC values of AJ100 and RB51 were 2.0 and 0.3 µg/ml, respectively, as determined by the Etest. Though AJ100 is more resistant to polymyxin B than RB51, it was more sensitive than the parental strain to the cationic defensin cecropin P1. In the mouse model, AJ100 cleared faster from the spleen than RB51. Both strains cleared from the liver similarly. Both reduced colonization of B. abortus 2308 in spleens and livers from challenged mice. Likewise, AJ100 may not persist in wildlife as long as RB51 and be a useful vector constructing efficacious wildlife vaccines expressing homologous immunogens.