Xenoma formation during microsporidial gill disease of salmonids caused by Loma salmonae is affected by host species (Oncorhynchus tshawytscha, O. kisutch, O. mykiss) but not by salinity

Abstract

Host species and salinity often affect the development of disease in aquatic species. Eighty chinook salmon Oncorhynchus tshawytscha, 80 coho salmon O. kisutch and 80 rainbow trout O. mykiss were infected with Loma salmonae. Forty of each species were reared in seawater and 40 in freshwater. The mean number of xenomas per gill filament was 8 to 33 times greater in chinook salmon than in rainbow trout (RBT). Coho salmon had a mean xenoma intensity intermediate to that of chinook salmon and RBT. In contrast to the differences between species, salinity had no significant effect on xenoma intensity in any of these host species. The onset of xenoma formation occurred at Week 5 postexposure (PE) for chinook salmon and RBT, and at Week 6 PE for coho salmon. RBT had cleared all visible branchial xenomas by Week 9 PE, whereas xenomas persisted in coho and chinook salmon at Week 9 PE. Histologically, xenomas were visible in the filament arteries of the branchial arch in chinook and coho salmon gills but were absent from RBT gills. Fewer xenomas were seen in the central venous sinusoids of RBT than in chinook and coho salmon. The lower xenoma intensity, shorter duration of infection and pathological characteristics, common to microsporidial gill disease in RBT, suggest a degree of resistance to clinical disease that is not seen in coho and chinook salmon.KEY WORDS: Loma salmonae · Host species · Salinity · Xenoma formation · Xenoma intensity Resale or republication not permitted without written consent of the publisher

Impact of a water temperature shift on xenoma clearance and recovery time during a Loma salmonae (Microsporidia) infection in rainbow trout Oncorhynchus mykiss

“…To provide a basis for the epidemiology of MGD, the rate of sporulation (xenoma formation) and spore release (xenoma dissolution) has been the subject of intensive investigation, and it has been reported that, in large part, the rate of these processes is determined by water temperature , although the effect of species is not negligible (Ramsay et al 2002). The pathogenesis of MGD has recently been elucidated, and the key events include oral uptake of an infectious spore, intragastric spore germination, a brief residence period in the gut lamina propria, and a 2 wk merogony-like phase in the cardiac subendothelium, followed by a macrophagemediated transport of the parasite to the gill where final development (further merogony and sporogony) occurs within gill pillar cells, with sporogony leading to the formation of a distended spore-filled xenoma (Sánchez et al 2000, Rodríguez-Tovar et al 2002.…”

Comparison of Susceptibility to Kabatana takedai (Microspora) among Salmonid Fishes

“…It has been reported that chinook salmon O. tshawytscha and coho salmon O. kisutch are more susceptible to Loma salmonae than rainbow trout (Ramsay et al, 2002). Xenomas degenerated more rapidly and reduced with time in rainbow trout, as compared with the former two species.…”

“…Varied host responses among fish species or populations may be related to difference in the susceptibility to microsporidians (Ramsay et al, 2002;Lovy et al, 2007). It has been reported that chinook salmon O. tshawytscha and coho salmon O. kisutch are more susceptible to Loma salmonae than rainbow trout (Ramsay et al, 2002).…”

Low genetic variation in the salmon and trout parasite Loma salmonae (Microsporidia) supports marine transmission and clarifies species boundaries

“…Non-genetic studies have suggested there may be strains that differ in host preference (e.g. preferring coho and Chinook salmon to brook or rainbow trout) or showing different infection patterns in salmon versus trout (Bader et al 1998, Shaw et al 2000a,c, Sánchez et al 2001b, Ramsay et al 2002, Lovy et al 2004, Kent & Speare 2005.…”

“…Non-genetic studies have suggested there may be strains that differ in host preference (e.g. preferring coho and Chinook salmon to brook or rainbow trout) or showing different infection patterns in salmon versus trout (Bader et al 1998, Shaw et al 2000a,c, Sánchez et al 2001b, Ramsay et al 2002, Lovy et al 2004, Kent & Speare 2005.The present study examined genetic variation across Loma salmonae from the wild, hatcheries, sea netpen farms and laboratories in British Columbia (BC) and Prince Edward Island (PEI), Canada, in California, Colorado, and Idaho, USA, and in Chile to establish the baseline level of variation that we might expect within this species and to look for genetic variants that may correspond to different populations. Genetic data from the type host, rainbow trout Oncorhynchus mykiss in California, is essential as this parasite species is morphologically indistinguishable across its geographic and host range (Morrison & Sprague 1983, Shaw et al 1997, Brown & Kent 2002 and distinct strains or cryptic species may exist.…”