Proliferative kidney disease: cellular aspects of the rainbow trout, Oncorhynchus mykiss (Walbaum), response to parasitic infection

• Published in: Journal of fish diseases Vol. 25; no. 4; pp. 217 - 226
• Main Authors: Chilmonczyk, S, Monge, D, De Kinkelin, P
• Format: Journal Article
• Language: English
• Published: Oxford UK Blackwell Science Ltd 01.04.2002
• Subjects: cellular response; lymphoproliferation; non-specific cytotoxicity; Oncorhynchus mykiss; oxidative burst; phagocytosis; proliferative kidney disease; rainbow trout; Tetracapsula bryosalmonae
• ISSN: 0140-7775; 1365-2761
• DOI: 10.1046/j.1365-2761.2002.00362.x

Proliferative kidney disease (PKD) is an immunopathological condition of salmonid fish, caused by the hyperplastic response of their principal lymphoid tissues to infection with the spores of Tetracapsula bryosalmonae, a myxozoan parasite formerly designated proliferative kidney organism – unknown (PKX). In order to investigate the nature of cells involved in this host response and possible alterations of their functions during parasitic infection the course of PKD was studied by flow cytometry (FCM) techniques, using blood, pronephros and spleen leucocyte populations from rainbow trout infected by intraperitoneal (i.p.) injection with parasitic cells from infected donor fish. The parameters of the cellullar response studied were: cytogram of cell population, lymphoproliferation, phagocytosis, oxidative burst, and non‐specific cytotoxicity. The modifications of cell population distribution and function in the PKD‐infected fish mainly affected the pronephros cell populations and were coincident with the clinical phase of disease. During this phase, the lymphocytes constituted the major leucocyte cell population and underwent proliferation and were thus responsible for the renal tissue hyperplasia. Meanwhile, phagocytosis and oxidative burst were depressed. These data are in agreement with the patho‐epidemiological background of PKD where the enhancement of the fish sensitivity to bacterial infections reflects the impairment of certain cellular defence mechanisms of innate immunity.