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Evaluating Virulence and Pathogenesis of Aeromonas Infection in a Caenorhabditis elegans Model
Published on: December 20, 2018
Distribution of 13 virulence genes among clinical and environmental Aeromonas spp. in Western Australia
M Aravena-Román1, T J J Inglis, T V Riley
1School of Pathology and Laboratory Medicine, The University of Western Australia, 35 Stirling Highway, Crawley, WA, 6909, Australia, max.aravena@health.wa.gov.au.
Abstract:
We evaluated the pathogenic potential of 98 clinical and 31 environmental Aeromonas isolates by detecting the presence of 13 virulence genes using a polymerase chain reaction (PCR)-based method. The majority (96 %) of the strains contained at least one of the virulence genes. The overall distribution was aerA/haem (77 %), alt (53 %), lafA (51 %), ast (39 %), flaA (32 %), aspA (29 %), vasH (26 %), ascV (16 %) and aexT (13 %). No amplification products were detected for the genes encoding a bundle-forming pilus (BfpA and BfpG) or a Shiga-like toxin (stx-1 and stx-2). Five or more virulence genes were detected in 42 % of environmental and 24 % of clinical isolates. Among the major species, 48 % of A. hydrophila and 42 % of A. dhakensis isolates harboured five or more virulence genes compared with 19 % in A. veronii bv. sobria and none in A. caviae isolates. Our results suggest that, in Western Australia, strains of A. dhakensis and A. hydrophila are potentially more virulent than those of A. veronii bv. sobria and A. caviae, although the pathogenic potential of Aeromonas spp. is probably strain- rather than species-dependent.
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