CNIDARIA bryosalmonae (PKD)

I. Causative Agent and Disease cospores, are released with the urine to Proliferative kidney disease (PKD) is infect more . Vertical transmis- caused by the PKX cnidarian myxozoan sion allows T. bryosalmonae to persist (Malacosporea), Tetracapsuloides bryo- in the bryozoan host. Brown trout are salmonae, that is a parasite of freshwater known to be subclinical carriers for at bryozoans ( sp., least 5 yrs. sp.) and salmonid fish. Waterborne spores of T. bryosalmonae are released V. Diagnosis from the bryozoan host where they in- Microscopic diagnosis is made by: fect the fish host, primarily through the Giemsa-stained imprints showing amoe- gills. The parasite travels via the blood boid PKX cells (10-20 um) with foamy to the kidney and other vascular organs cytoplasm, distinctive cell membrane where it proliferates, causing chronic and 1 mother cell (primary) nucleus with inflammation often accompanied by 1-7 daughter cells; histological exam secondary pathogen infections. indicating proliferative and granulo- matous nephritis, vascular necrosis and II. Host Species thrombi with eosinophilic PKX cells PKD has been reported in both wild among the kidney interstitial cells, often and captive salmonids and several other surrounded by attached host macro- species including whitefish and northern phages. Parasite DNA can be detected in pike in the Pacific Northwest and New- all organs by PCR and PKX cells can be foundland; trout, Atlantic and observed in kidney, spleen and liver of grayling in Europe, including Finland infected fish by immunohistochemistry. and Sweden; in Iceland. In Alaska, the parasite has been reported in VI. Prognosis for Host lake-reared juvenile and Temperature increase induces transi- two adult returning . tion from covert into overt infection where infectious stages of T. bryosalmo- III. Clinical Signs nae develop and are released into the The gross clinical signs of PKD water. Variable mortality (5-90%) occurs include pale gills, a uniformly swollen at elevated water temperatures (12-15°C) kidney (may be gray/mottled) and spleen while fish that show less severe clini- with exophthalmia, ascites and anemia. cal signs of disease largely survive the infection when water temperature is IV. Transmission lower (< 12°C). Surviving fish develop Spores, released from freshwater immunity and may clear the infection bryozoans, infect salmonids through with regeneration of damaged tissues. the skin and gills releasing ameboid The decline of wild salmonid popula- sporoplasms. A single spore is sufficient tions in several rivers has been attributed to infect a fish and cause clinical PKD. to PKD which will become an emerging These travel to the kidney and undergo fish pathogen as global warming contin- extra-sporogonic multiplication in the ues. interstitium and differentiate through sporogenesis in the kidney tubules. Resulting spores, designated fish mala-

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VII. Human Health Signifcance This parasite is a pathogen for fish. There are no human health concerns as- sociated with PKD.

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Histology of eosinophilic PKX cells (arrows) in the kidney interstitium of steelhead trout containing large primary cell nuclei (dense red) next to translucent daughter cell nuclei. PKX cells are surrounded by basophilic (blue) host infammatory cells (arrowheads); H&E, X 1000.

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PKD in exhibiting bloody ascites (A) and swollen nodular posterior kidney (arrow) due to infammation and proliferation of PKX cells (photo: M. L. Kent and R. P. Hedrick, Univ. of Calif., Davis).

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