Proliferative kidney disease (PKD), a condition associated with high mortality in salmonid fish, represents an abnormal immune response to the presence of an enigmatic myxozoan, which has been designated simply as PKX organism because its generic and specific status are obscure. Phylogenetic analyses of partial sequences of the 18S rDNA of PKX and of myxozoan parasites infecting the bryozoans Cristatella mucedo, Pectinatella magnifica and Plumatella rugosa, including the previously named Tetracapsula bryozoides from C. mucedo, showed that these taxa represent a distinct clade that diverged early in the evolution of the Myxozoa before the radiation of the other known myxozoan genera. A common feature of the myxozoans in this clade may be the electron-dense sporoplasmosomes with a lucent bar-like structure, which occur in T. bryozoides and PKX but not in the myxozoans belonging to the established orders Bivalvulida and Multivalvulida. Variation of 0·5–1·1% was found among the PKX 18S rDNA sequences obtained from fish from North America and Europe. The 18S rDNA sequence for T. bryozoides showed that it is a distinct taxon, not closely related to PKX but some sequences from myxozoans infecting 2 of the bryozoan species were so similar to those of PKX as to be indistinguishable. Other sequences from the new myxozoans in bryozoans at first appeared distinct from PKX in a maximum likelihood tree but, when analysed further, were also found to be phylogenetically indistinguishable from PKX. We propose that at least some variants of these new myxozoans from bryozoans are able to infect and multiply in salmonid fish, in which they stimulate the immune reaction and cause PKD but are unable to form mature spores to complete their development.

Tetracapsuloides bryosalmonae is the myxozoan that causes the commercially and ecologically important proliferative kidney disease of salmonid fish species. Immunohistochemistry and electron microscopy were used to examine the development of this parasite within the kidney of the brown trout Salmo trutta. The main replicative phase of T. bryosalmonae is a cell doublet composed of a primary cell and a single secondary cell. Engulfment of one secondary cell by another to form a secondary-tertiary doublet (S-T doublet) heralded the onset of sporogony whereupon the parasite migrated to the kidney tubule lumen. Within the tubule, the parasite transformed into a pseudoplasmodium and anchored to the tubule epithelial cells via pseudopodial extensions. Within each pseudoplasmodium developed a single spore, composed of 4 valve cells, 2 polar capsules and 1 sporoplasm. The pseudoplasmodia formed clusters suggesting that large numbers of spores develop within the fish. This examination of T. bryosalmonae suggests that the main replicative phase of freshwater myxozoans within vertebrates is via direct replication of cell doublets rather than through the rupturing of extrasporogonic stages, while tertiary cell formation relates only to sporogony. Taken in conjunction with existing phylogenetic data, 5 distinct sporogonial sequences are identified for the Myxozoa.

Proliferative kidney disease (PKD), caused by the malacosporean parasite Tetracapsuloides bryosalmonae, causes significant losses among salmonids in Western Europe and North America. The role of salmonid fish in the life-cycle of this parasite has been conjectured upon for over a quarter of a century. To examine whether fish can transmit the infection to bryozoans, the known invertebrate host, water containing parasitized brown trout Salmo trutta was pumped into tanks containing colonies of Fredericella sultana collected from the wild. The specific parasite-free status of these colonies being first assessed, by PCR and prolonged laboratory culture. After 6 weeks exposure to the brown trout aquarium effluent, portions of these colonies displayed overt infections with T. bryosalmonae. This was in contrast to control bryozoans, derived from the experimental colonies prior to exposure, which remained T. bryosalmonae negative. In addition, spores obtained from the experimentally infected colonies were exposed to naïve rainbow trout, resulting in clinical PKD, thus completing a cycle of transmission. During the experiments, the infection was noted to inhibit statoblast formation within bryozoans and appeared to be pathogenic, finally killing the bryozoan host. These findings indicate that fish can transmit the parasite to bryozoans and are an integral part of this parasite's life-cycle.