Cardiomyopathy in farmed Norwegian salmon

Abstract

This paper describes the gross findings, histopathology, and ultrastructural and scanning electron microscopical (SEM) appearance of farmed Norwegian Atlantic salmon dying from a disease known locally as 'acute heart failure' Pathological findings were mainly cardiac, and some fish showed haemopericardium due to rupture of the atrial wall. Lesions were largely restricted to the spongy portion of ventricle and atrium, and comprised myocardial degeneration and necrosis, with variable degrees of endocardial-associated hypercellularity, plus macrophage and lymphocyte infiltration; epicarditis was also present in most fish. Transmission electron microscope findings confirmed the myofibrillar disruption, while the SEM showed crater-like discontinuities in the endocardial plasmalemma. The cause and pathogenesis of these remarkably severe lesions are unknown; whether they are primarily degenerative or inflammatory must await a more in-depth study. Until more is known, use of the term cardiomyopathy syndrome would seem most appropriate.

Experimental transmission of cardiomyopathy syndrome (CMS) in Atlantic salmon Salmo salar

“…The fish injected with material from diseased fish developed lesions consistent with CMS (Ferguson et al 1990). Detailed results are presented in Figs. 3 & 4, and findings according to time are shown in Fig.…”

“…Sections of cardiac tissue were classified histologically based on the presence of mononuclear endo-and myocarditis, degeneration and necrosis in the spongy layer of the ventricle and atrium (Ferguson et al 1990). The atrium, epicardium, compact and spongy layers of the ventricle and the endocardium of both cardiac compartments were examined and evaluated.…”

“…Lesions may progress to such a state that the wall of the atrium or sinus venosus weakens or ruptures, with resultant haemopericardium and death. Previous studies indicate that CMS is a chronic disease developing over a period of several months prior to the terminal clinical phase (Ferguson et al 1990, Kongtorp et al 2006a.…”

“…Most CMS cases are diagnosed during the late seawater phase; typically from 14 to 18 mo after sea transfer. Mortality may be moderately elevated over a long period, or suddenly high without prior symptoms (Ferguson et al 1990, Brun et al 2003. As CMS generally affects large fish, the economic losses may be substantial, even though the cumulative mortality may be low or moderate (Brun et al 2003, Østvik & Kjerstad 2003.…”

“…Cellular infiltrates consist mainly of mononuclear cells, most probably lymphocytes and macrophages. The compact myocardium is usually not affected, but epicardial cell infiltrates may extend into the compact layer along branches of the coronary vessel (Ferguson et al 1990). Lesions may progress to such a state that the wall of the atrium or sinus venosus weakens or ruptures, with resultant haemopericardium and death.…”