The myxosporean (PKX) that causes proliferative kidney disease in salmonid fishes is found primarily in the kidney interstitium of clinically affected fish, where it invokes a severe inflammatory response. Incomplete spores are observed in the lumen of kidney tubules in recovering fish. PKX-infected rainbow trout, Salmo gairdneri, were immunosuppressed with cortisol implants to determine if a reduction in renal interstitial inflammation would enhance the development of the parasite. Immunosuppression of these fish was indicated by high plasma cortisol levels, chronic mortality due to opportunistic pathogens, and depressed leucocrits when compared to infected fish not receiving cortisol implants. Cortisol-treated PKX-infected fish had 20 times the density of interstitial PKX compared with nontreated fish, but showed less interstitial inflammation. All of the former group examined at 4 wk postimplantation exhibited intraluminal sporogonic forms of PKX, whereas no sporogonic forms were detected in the nontreated fish. Suppression of the inflammatory response clearly enhanced the parasite's ability to reach the sporogonic stage, but did not induce complete development of the spore. Possibly the kidney tubules of rainbow trout do not provide the proper physiological environment for complete sporulation of PKX and a nonsalmonid fish may be the primary host.