Experimental infections with Piscirickettsia salmonis via intraperitoneal (IP), oral (PO) and gill (GS) routes were compared, and the importance of physical contact in the horizontal transmission of this organism was investigated. Atlantic salmon, Salmo salar L., under‐yearling parr raised in fresh water were used in this study. Samples of liver, kidney, spleen, gill and brain were collected weekly for 5 weeks after challenge, and were examined using the indirect fluorescent‐antibody technique (IFAT). The pathogen was transmitted horizontally to fish with and without physical contact. However, transmission of P. salmonis occurred significantly more rapidly among fish with physical contact. Mortalities occurred in 50% of fish experimentally challenged with P. salmonis and their cohabitants. The estimates of the relative risk of dying demonstrated that fish challenged by the IP and GS routes had a significantly higher probability of dying than fish challenged by the PO route (P < 0.005). Contact cohabitants with infected fish had a higher probability of death than non‐contact cohabitants (P < 0.005). The sequential studying using IFAT indicated that a haematogenous pattern of infection occurred among fish infected by oral and gill routes, or by cohabitation. This was different from the capsular (serosal) infection pattern observed in intraperitoneally inoculated fish. Piscirickettsia salmonis was observed within the cytoplasm of leucocytes and renal tubules, the latter indicating that elimination of this pathogen through the urine may be possible. Aeromonas salmonicida was also detected (by IFAT) in some of the fish exposed to P. salmonis, suggesting that P. salmonis may cause immunosuppression, and thus, increase the susceptibility of the host to other pathogens.

Experimental 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.

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