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1 Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616, USA
2 The Centre for Environment, Fisheries, and Aquaculture Science, Weymouth Laboratory, Barrack Road, The Nothe, Weymouth, Dorset DT4 8UB, UK
3 Division of Statistics, University of California, Davis, CA 95616, USA
4 Institute of Microbiology, Department of Clinical Microbiology, The Hebrew University-Hadassah Medical School, Ein Karen, Jerusalem, Israel
Correspondence
Ronald Hedrick
rphedrick{at}ucdavis.edu
Koi herpesvirus (KHV) has been associated with devastating losses of common carp (Cyprinus carpio carpio) and koi (Cyprinus carpio koi) in North America, Europe, Israel and Asia. A comparison of virion polypeptides and genomic restriction fragments of seven geographically diverse isolates of KHV indicated that with one exception they represented a homogeneous group. A principal environmental factor influencing the onset and severity of disease is water temperature. Optimal growth of KHV in a koi fin cell line occurred at temperatures from 1525 °C. There was no growth or minimal growth at 4, 10, 30 or 37 °C. Experimental infections of koi with KHV at a water temperature of 23 °C resulted in a cumulative mortality of 95·2 %. Disease progressed rapidly but with lower mortality (89·495·2 %) at 28 °C. Mortality (85·0 %) also occurred at 18 °C but not at 13 °C. Shifting virus-exposed fish from 1323 °C resulted in the rapid onset of mortality.
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