Experience with mortalities of cultured catfish Ictalurus punctatus (Rafinesque 1818) and I. punctatus X I. Furcatus (Valenciennes 1840) caused by highly virulent strains of Aeromonas hydrophila

Epizootic outbreaks of motile aeromonad septicaemia (MAS) due to Aeromonas hydrophila infections in channel catfish Ictalurus punctatus (Rafinesque 1818) and hybrid catfish I. punctatus x I. furcatus (Valenciennes 1840) spread through West Alabama and East Mississippi, United States of America in 2009 and have been seasonally recurrent, with losses in the millions of pounds. While A. hydrophila is typically considered an opportunistic pathogen, no other primary aetiologic agent has been found. Mortalities are as high as 60 % in ponds and primarily affect larger fish, causing diseases characteristic of MAS infections that include severe skin ulceration and haemorrhage, generalized petechiation, ascites, marked splenomegaly with necrosis, and gastric haemorrhage. A multistate research group (Alabama, Arkansas, Louisiana and Mississippi) examined A. Hydrophila isolates, which were found to be highly clonal by phylogenetic analyses of gene sequences (atpD, dnaJ, dnaX, gyrA, gyrB, recA, rpoD). A representative strain of the hypervirulent A. Hydrophila pathotype (vAh), ML09-119, was found to be more virulent in channel catfish than historical A. hydrophila strains associated with traditional, opportunistic infection (tAh). Bar coded sequencing of numerous vAh and tAh isolates identified unique genomic regions associated with the epizootic isolates. A diagnostic polymerase chain reaction (PCR) targeting a unique vAh-associated genetic locus has been developed to differentiate vAh strains from tAh strains. Some of these genes were associated with myo-inositol metabolism, which corresponds with the ability of epizootic strains to utilize myo-inositol. Genes from lysogenic bacteriophage, Oantigen biosynthesis genes and transposases were also uniquely present in the epizootic strains. Collectively, these data support the conclusion that lateral gene transfer has contributed to the pathogenicity of epizootic A. hydrophila strains. Further research will need to be conducted to determine the specific contribution of the unique genetic loci to A. hydrophila virulence.