Proliferative gill disease (PGD) was first reported in channel catfish Ictalurus punctatus at commercial farms in 1981 and is caused by the myxozoan parasite Henneguya ictaluri. The disease affects the gills and is characterized by severe branchial inflammation, epithelial hyperplasia, lamellar fusion, and lysis of chondrocytes. Presumptive diagnosis is based on the presence of lytic areas in the cartilage of the primary lamellae on microscopic examination and is confirmed histologically by the presence of the organism. In these trials, PGD was induced by exposing channel catfish fingerlings to fresh or aged infectious water collected from a pond containing fish diagnosed with severe PGD. The severity of disease was graded by histological scoring and microscopic examination of wet mounts to determine the percentage of gill filaments containing chondrolytic lesions. Exposure of fish to infectious pond water was shown to produce pathological lesions consistent with PGD, and the percentage of gill filaments containing chondrolytic lesions was positively correlated with histological scoring of gill pathology. The number of trophozoite stages in the gills was shown to increase with the severity of the disease. In most cases, however, parasitic cells were not observed in tissue samples with chondrolytic lesions during the early stages of infection. These observations indicate that pathology and lysis of chondrocytes can occur prior to detection of the organism by histopathology. Exposing fish to infectious pond water that was aged for 1 d produced negligible gill pathology and implies that the infectivity of the H. ictaluri actinospore stage is short lived. Removing fish from the source of infection promoted repair of damaged gill tissue; within 14 d of fish transfer to clean water, gill pathology associated with the acute infection was negligible.