A study of the sequential clinical and pathological changes during proliferative kidney disease in rainbow trout, Salmo gairdneri Richardson

Abstract

. A histological study of 0+ rainbow trout, exposed to proliferative kidney disease (PKD) on an infected farm, showed evidence of infection from the beginning of June, gross pathological changes from the beginning of July, and clinical signs from mid‐July. Evidence of healing was present in some samples from the second week of August. Kidney samples were divided into five grades (0–4) representing increasing severity of pathology. A sixth grade (H) was applied to kidneys showing signs of healing. The most frequent clinical signs were abdominal distension and exophthalmos. Melanosis, corneal cloudiness and ecchymoses were observed occasionally. Apart from renal enlargement, other internal gross pathological changes included ascites, gill and liver pallor, oedema, petechiation, and splenic enlargement. The majority of clinical signs and internal changes were only seen in fish with advanced renal swelling (grades 3 and 4). Histopathology was most marked in the kidney and was of three types: haemopoietic hyperplasia, vascular pathology and diffuse inflammatory change. Vascular changes, including occlusion of blood vessels in several organs and apparent haemoglobin crystallization, and destruction of renal excretory structures within areas of chronic diffuse inflammation were marked features of the histopathology in fish with clinical signs. The pathogenesis of PKD is discussed with reference to the histopathological changes.

Reno-, hepato- and splenomegaly of common carp fingerlings (Cyprinus carpio L.) diseased in swimbladder inflammation caused by Sphaerospora renicola Dyková et Lom, 1982

“…While S. renicola spores and pseudoplasmodia cause damage to the host organism primarily by occupying space within the renal tubules, the PKX pseudoplasmodia of Tetraspora bryozoides causing proliferative kidney disease grow in the renal interstitium and the proteins released by disintegrating mother cells exert a continuous antigen effect on the humoral and cellular defence mechanisms of the host (Clifton-Hadley et al, 1987;Feist et al, 2002).…”

Lectin histochemistry and ultrastructure of rainbow trout Oncorhynchus mykiss kidneys affected by proliferative kidney

“…Later in infection, the parasites are found mainly in the renal interstitium and often surrounded by macrophages and lymphocytes (Ghittin0 1984, Clifton-Hadley et al 1987, McConnell et al 1988. Although this strong immunological reaction is thought to provide immunity to fishes recovering from infection, it also contributes to the mortality associated with PKD (Klontz et al 1986).…”

Further consideration of the haematology of proliferative kidney disease (PKD) in rainbow trout, Salmo gairdneri Richardson

“…Total serum protein levels were found depressed by Hoffmann & Lommel (1984) but within normal limits by Scott (1984). Increased splenic iron deposits, indicative of haemolysis, were seen in clinicallyaffected fish by Hoffmann & Lommel (1984) but were only an occasional finding in similar fish by Clifton-Hadley, Bucke & Richards (1987).…”