Loma salmonae‐associated growth rate suppression in rainbow trout, Oncorhynchus mykiss (Walbaum), occurs during early onset xenoma dissolution as determined by in situ hybridization and immunohistochemistry

Abstract

AbstractExperimental infection of rainbow trout, Oncorhynchus mykiss (Walbaum), juveniles with Loma salmonae at a water temperature of 15 °C yielded detectable parasite DNA within the gills by week 2 post‐exposure (PE) and detectable spore‐wall antigen within developing xenomas by week 3 PE, as determined by in situ hybridization and monoclonal antibody (Mab) based immunohistochemistry, respectively. The microsporidian was most commonly located within endothelial cells of lamellar basal channels. Whereas the onset of xenoma formation appeared to be relatively synchronous, as expected from previous studies, xenoma dissolution followed an unexpected biphasic pattern with peaks at weeks 4 and 9 PE. The onset of significant growth rate suppression, at week 4 PE in exposed fish, was temporally associated with the appearance of gill lesions which, in turn, were centred about sites of premature xenoma dissolution. The latter was determined by the detection of spore‐wall antigen within lesions. Co‐habitant control fish began developing xenomas by week 10, indicating the infective potential of those spores released from the principal fish during early xenoma dissolution. Although infection with L. salmonae significantly affects fish growth rates, the time‐course of this suppression is limited, and as an unexpected finding, growth rate recovery commences prior to the infection’s resolution.