Myocardial glycogen storage disease in farmed rainbow trout, Oncorhynchus mykiss (Walbaum).

This paper is the first description of a spontaneous glycogen-storage disease in a lower vertebrate, as previous descriptions deal with humans and other mammals, or fish where the condition has been experimentally induced. Affected farmed rainbow trout experienced increased mortality from 60 days post-startfeeding and displayed clinical signs of heart failure with abnormal behaviour, exophthalmia, distended abdomen and ventral skin petechiation. Necropsy revealed alterations in cardiac shape with distended atria and rounded ventricles. Microscopically, the compact wall of the ventricle was absent, uneven or thinner than normal. The cardiac myocytes contained extensive amounts of glycogen in cytoplasmic vacuoles as demonstrated by periodic acid-Schiff staining that was abolished by saliva-diastase pretreatment on serial sections. Associated lesions included conspicuous subepicardial and myocardial vascularization, epicardial thickening and necrosis of the ventricular compactum/spongiosum interphase. The lesions in cardiac myocytes had a striking resemblance to glycogenosis type II (Pompe disease), a rare autosomal recessive lysosomal storage disease in humans. This condition was more severe and mortality was higher in a replicate/parallel fish group treated perorally with 17alpha-methyltestosterone to produce all-female progeny, indicating that the hormone treatment aggravated the condition resulting in earlier and more severe manifestation of the disease in this group.

Characterization of nodavirus and viral encephalopathy and retinopathy in farmed turbot, Scophthalmus maximus (L.).

An outbreak of nodavirus infection in turbot larvae is described with respect to histopathology, immunohistochemistry, cell culture cultivation, RT-PCR amplification and sequence analysis of the capsid protein gene RNA2. Affected turbot developed classical signs of viral encephalopathy and retinopathy (VER) with abnormal swimming behaviour and high mortality levels. In the acute stage of infection, light microscopy revealed vacuolation of the central nervous system (CNS), with positive immunohistochemical staining for nodavirus. Later in the infection, CNS lesions appeared more chronic and contained clusters of cells immunopositive for nodavirus. Bacterial overgrowth in the intestines of the fish may have provoked or influenced the course of the nodavirus infection. We were unable to propagate the virus in cell culture. While RT-PCR using primers designed to detect Atlantic halibut nodavirus gave negative results, further testing with primers complementary to a more conserved region of RNA2 resulted in amplification of a product of the expected size. The entire RNA2 segment was cloned and sequenced. Sequence alignment showed that the turbot nodavirus (TNV) was different from previously described fish nodaviruses. In addition, phylogenetic analysis based on an 823 nt region of the sequence indicated that TNV clustered outside the four established fish nodavirus genotypes, suggesting a fifth genotype within the betanodaviruses.

Subclinical herpesvirus infection in farmed turbot Scophthalmus maximus.

Subclinical infections with a herpesvirus were detected by light and electron microscopic examination of juvenile turbot collected during a national surveillance programme. Virions detected in the epidermis of skin and in the epithelium of gills had a morphology consistent with those of Herpesvirus scophthalmi described from turbot in the United Kingdom and Denmark. This is the first report of herpesvirus infection in turbot in Norway.

Platyspondyly and shortness of vertebral column in farmed Atlantic salmon Salmo salar in Norway--description and interpretation of pathologic changes.

Body malformation due to shortness of the vertebral column, in most cases of unknown cause, has been observed in fish for more than 100 yr. It periodically occurs with high prevalence in farmed Atlantic salmon Salmo salar in Norway, and this paper describes the results of macroscopic, radiographic and histologic examination of parr and seawater-transferred fish. The vertebral bodies in both age groups did not acquire the length that they normally should due to a growth disturbance leading to the condition of platyspondyly and shortness in the column. The pathologic changes became visible at different ages in both groups and the process apparently starts in intervertebral tissues. There was proliferation of connective tissue and blood vessels, and sometimes infiltration with inflammatory cells, around affected vertebrae, especially in seawater-transferred fish. This is the first description of inflammation in abnormally short-spined fish, and it may indicate an infectious etiology, at least in farmed seawater-transferred salmon.