Abstract

Koi herpesvirus (KHV) appears to preferentially attack epithelial tissues of koi, especially the cells of the gills. Losses due to this virus have been reported throughout the United States in 2002-2003. However, suspected cases, based on clinical signs and history, have been reported in koi populations in the United States since 1998, causing a large economic as well as emotional impact to the koi hobby. The virus was presumably introduced to koi in the United States through importation of infected, asymptomatic koi, but it is unknown if the virus originated from fish produced in Europe, Israel, or Japan. KHV-associated disease can cause clinical changes that include gill necrosis, sloughing of the skin, excessive mucus sloughing, decreased mucus production, abnormal swimming patterns, and variable anorexia. Mortality rates as high as 100 percent have been reported in some facilities. Survivors are believed to be latently infected because naïve fish exposed to clinically normal outbreak survivors can develop disease. The temperature at which exposure will cause infection is not known, but clinical signs of the disease appear when the water is 70-80° F (± 5°). Infection and/or subsequent disease might be delayed or prevented when fish are exposed to the virus at higher or lower temperatures, but clinical evidence suggests that the virus remains viable at lower temperatures. Fish demonstrating suggestive clinical changes have been reported to recover when the water is heated to greater than 85° F, but these findings have not been scientifically proven. PCR-based assays for KHV are proving to be an invaluable diagnostic tool for the identification of KHV infected, symptomatic koi based on recent clinical cases submitted to the University of Georgia Avian and Exotic Diagnostic Laboratory. Clinical case histories including PCR-based assay tests for KHV may be useful in formulating guidelines for quarantine of koi as one method of reducing the spread of KHV in private koi populations.