ABSTRACT
CASE HISTORY: A period of escalating mortality occurred among Chinook salmon (1-5 g) held in freshwater raceways at a commercial culture facility. The mortality rate peaked at 1.5% of the population per day, water temperature was 9-10 degrees C, and water quality had recently deteriorated due to an influx of suspended solids. The affected fish did not respond to several chloramine-T bath treatments (10 ppm for 1 hour). CLINICAL FINDINGS: The dead fish did not exhibit flared opercula typical of infection with bacterial gill disease (BGD) nor did the remaining fish show obvious signs of respiratory distress. Clinical lesions were limited to the gills of the fish, and were consistent with a proliferative branchitis, including substantial hyperplasia and fusion of lamellae. DIAGNOSIS: Numerous angular amoebic organisms (approximately 10 x 8 microm), with a central, large vesicular nucleus and faintly acidophilic cytoplasm, visible on H&E-stained sections, were located on the hyperplastic epithelia of the lamellae, filaments, and remaining lining of the branchial cavity. Morphologically, the amoebae were similar to representatives of the genus Cochliopodia spp. described from North American salmonids, that presented similar lesions and clinical signs; consequently, the disease was diagnosed as nodular gill disease (NGD). CLINICAL RELEVANCE: Grossly, NGD can be mistaken for BGD; the distinction is important because chloramine-T, routinely used in the treatment of BGD, is ineffective for the treatment of NGD. Static formalin baths of 170 ppm (37% formaldehyde) for 1 hour, supplemented with oxygen, may reduce amoebic infections but should be used cautiously as treatment can precipitate mortality in fish with gill disease. Cues for the onset of NGD are not completely understood, although poor water quality and elevations in temperature are likely to exacerbate infections. Similarly, the prevalence of this disease is not accurately known, but it is possible that it may be more common among salmonids in New Zealand than is presently recognised.
Subject(s)
Amebiasis/veterinary , Fish Diseases/parasitology , Gills/pathology , Salmon , Amebiasis/parasitology , Amebiasis/pathology , Animals , Fish Diseases/pathologyABSTRACT
Chinook salmon from New Zealand were shown to have a generalized membranous glomerulonephritis that was most severe in large fish. Marked thickening of the glomerular basement membrane was the most consistent lesion, with the presence of an electron-dense deposit beneath the capillary endothelium.Severely affected glomeruli also had expansion of the mesangium and loss of capillaries,synechiae of the visceral and parietal epithelium and mild fibrosis of Bowmans capsule. Chinook salmon from British Columbia, Canada with bacterial kidney disease caused by Renibacterium salmoninarum had similar histological lesions. They also had thickened glomerular basement membranes that were recognized by rabbit antiserum to rainbow trout immunoglobulin. This was true only when frozen sections of kidney were used and not formalin-fixed tissue. An attempt to experimentally produce a glomerulopathy in rainbow trout by repeated immunization with killed R. salmoninarum was not successful. Case records from the Fish Pathology Laboratory at the University of Guelph over a 10-year period revealed that a range of species were diagnosed with glomerulopathies similar to those seen in Chinook salmon. The majority of these cases were determined to have chronic inflammatory disease. This report has identified the presence of immunoglobulin within thickened basement membranes of Chinook salmon with glomerulonephritis and supports the existence of type III hypersensitivity in fish.
