Acute mortality of Penaeus vannamei larvae in farm hatcheries associated with the presence of Vibrio sp. carrying the Vp PirAB toxin genes

High and sudden mortalities of Penaeus vannamei post-larvae stage 1+ in Latin American hatcheries are attributed to a species of Vibrio carrying Vp PirAB genes. Mortalities occasionally occurred within 2 h from presenting a normal appearance to experiencing 100% mortality. This study analyzed historical samples of diseased and healthy P. vannamei from commercial shrimp hatcheries that had experienced sudden and significant mortality rates, to investigate the matter. Post-larvae samples (PL1–PL5) of P. vannamei were collected from a total of 22 tanks located in six distinct commercial shrimp hatcheries in Latin America that had reported occurrences of mortality among their shrimp. The samples underwent microbiological, molecular-biological, and histopathological analyses. Histopathology revealed massive sloughing and detachment of hepatopancreocytes. Disease progression can be categorized into two phases: an early phase characterized by a light infiltration of hemocytes prior to the sloughing of cells, followed by the acute-terminal phase where there is massive sloughing of hepatopancreatic epithelial cells, necrosis, a loss of hepatopancreatic architecture, cell debris in the lumen, and the loss of the peritrophic membrane. The rapid onset and progression of the early phase is frequently missed and, in most cases, was difficult to observe; the subsequent pronounced hepatopancreatic infiltration of hemocytes, massive sloughing, and absence of the peritrophic membrane can be used as an indication that a similar pathology is present. Molecular studies in combination with histological evidence are needed to confirm disease etiology. This condition is tentatively termed as post-larvae acute hepatopancreatic necrosis disease (PL-AHPND) to differentiate this from other pathologies affecting post-larval shrimp.