ND-strain of V. parahaemoliticus but was absent in non-pathogenic strains. These two genes are similar to Pir toxins produced by other species of bacteria. These type PirAB proteins secreted in bacterial cultures, are capable of producing necrosis without the presence of bacteria, suggesting that they are the causative agent of AHPND. This is the first report of protein type pirAB in bacteria of the genus Vibrio. The mode of action for pirABlike proteins has yet to be determined. However, they apparently differ from pirAB toxins that affect insects. The insecticidal PirAB toxins primarily affect the midgut, whereas the shrimp APHND toxins affect the hepatopancreas. The injection of pathogenic bacteria in hemolymph of shrimp does not cause AHPND. Oral exposure or immersion is required to develop the disease. Another difference is that the genes encoding the toxins for insects are found in the bacterial genome, whereas the pathogenic bacteria of shrimp were found in plasmids. Within the plasmid, these genes are flanked by transposases-coding sequence, that can induce horizontal gene transfer; this can result in the need for frequent screening of pathogenic strains in shrimp culture systems. This is because the genes that produce these toxins can be propagated to strains of nonpathogenic bacteria. The potential for such transfers increases when bacteria are densely colonized, either in the shrimp stomach or in pond biofilms.
Acknowledgements This work was supported by CP Foods, Bangkok Thailand.
School of Animal and Comparative Biomedical Sciences, University of Arizona, Tucson, AZ 85721, USA 2Department of Aquaculture Pathology, College of Fisheries, Nong Lam University, Ho Chi Minh City, Vietnam
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