Abstract

Vibriosis is one of the most prevalent fish diseases caused by bacteria belonging to the genus Vibrio. Vibriosis caused by Vibrio anguillarum has been particularly devastating in the marine culture of salmonid fish. The correlation between serotype and virulence may reflect the ability of the bacterial surface antigens to interact with the host tissues. The ferric-anguibactin receptor FatA is an 86-kDa protein that is essential for anguibactin transport. The FatA amino acid sequence is similar to other receptors involved in iron transport, e.g., FhuA and FepA of Escherichia coli, and a TonB box can be identified at its amino-terminal end. V. ordalii causes vibriosis in wild and cultured marine salmonids in the Pacific Northwest of the United States and Japan. The determination and analysis of the complete nucleotide sequence could provide information about the role of pMJ101 in the pathobiology of this fish pathogen. Juvenile salmon exposed to V. ordalii by parenteral challenge developed a systemic infection, and the bacterium was recovered from liver, kidneys, spleen, and blood immediately after the infection. However, the number of bacteria in the liver declined after 1 h and then increased 22 h after infection; bacterial numbers were high in all the organs, and 100% mortality occurred 6 days after infection. The latter observations demonstrate that artificial infection of juvenile salmon is a valid experimental model to study the mechanisms and the bacterial virulence factors involved in the pathogenesis of the infections caused by V. ordalii.

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