| Abstract
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A previously undescribed herpesvirus was isolated from juvenile lake trout (Salvelinus namaycush) undergoing epizootics of unknown etiology. The virus appears to be the etiological agent of the epizootics based on the following criteria: (1) it was isolated only from infected fish; (2) the disease could be induced with purified virus and 450 nm filtrates prepared from infected fish; (3) it produced clinical signs and lesions consistent with those observed during natural epizootics; (4) virus could be re-isolated from moribund fish experimentally infected with the virus and (5) the antibiotic oxytetracycline proved ineffective against it. The virus possesses all the characteristics of the family Herpesviridae. The virus is enveloped and measures 220-235 nm. The capsid has a diameter of 100-105 nm and contains 162 capsomeres, each of which has a hollow center. The virus is sensitive to chloroform, pH 3 and 11, and a temperature of 50C for 30 min. Fine structure studies of infected cells from skin of moribund fish also showed characteristics of herpesvirus. The infected cells contained numerous hexagonal virus particles, electron-dense fibrillar structures and donut shaped dense bodies in the nucleus. In the extracellular spaces, enveloped virus containing an eccentric nucleocapsid surrounded by an electron dense tegument were observed. The same type of structures have been described for other herpesviruses such as Herpes salmonis, channel catfish virus, Herpes simplex and cytomegalovirus. The herpesvirus caused mass mortality among juvenile lake trout. A study was conducted to determine the mechanism of death. Histopathogical studies of infected fish revealed extensive hypertrophy, hyperplasia, vacuolation and necrosis of the epithelium of the skin and oral mucosa. Some fish also showed hypertrophy, hyperplasia and fusion of gill epithelium with edema. Lesions of the kidney consisted of dilated capillaries of the glomeruli which filled Bowman's capsule. Measurements of the concentration of plasma sodium, potassium, chloride ions and plasma osmolality in 15 experimentally infected fish revealed a significant decrease. Plasma Na, K, and Cl concentrations, and plasma osmolality decreased 16%, 66%, 21% and 19% respectively. The total plasma protein concentration between infected and non-infected fish did not show any significant differences. It is hypothesized that the loss of integrity of the skin and oral mucosa, resulted in disruption of homeostasis which ultimately caused death.
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