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Experimental and natural host specificity of Loma salmonae (Microsporidia)
(2000) Shaw, Ross W.; Kent, Michael L.; Brown, A. M.; Whipps, C. M.; Adamson, Martin L.
The microsporidian Loma salmonae (Putz, Hoffman & Dunbar, 1965) Morrison & Sprague, 1981 has caused significant gill disease in Pacific salmon Oncorhynchus spp. Host specificity of the parasite was examined experimentally by per os challenge of selected salmonids and non-salmonids with infective chinook salmon O. tshawytscha gill material. Pink Oncorhynchus gorbuscha and chum salmon O. keta, brown Salmo trutta and brook trout Salvelinus fontinalis, and chinook salmon (controls) were positive, whereas Atlantic salmon Salmo salar and Arctic char Salvelinus alpinus were negative. In addition, no non-salmonids were susceptible to experimental exposure. Wild Pacific salmon species in British Columbia, Canada, were examined for L. salmonae during their freshwater life history stages (smolts, prespawning, spawning). All stages were infected, although infections in smolts were only detectable using a L. salmonae-specific PCR test. Many previous Loma spp. described from Oncorhychus spp. are likely L. salmonae based on host, parasite morphology, and site of infection.
Infection of Aulorhynchus flavidus (Gill) (Osteichthyes: Gasterosteiformes) by Kudoa thyrsites (Gilchrist) (Myxosporea: Multivalvulida)
(1997) Shaw, Ross W.; Hervio, Dominique M. L. ; Devlin, Robert H.; Adamson, Martin L.
The myxosporean parasite Kudoa thyrsites is reported from a new host, Aulorhynchus flavidus, the tube-snout, collected near Vancouver, British Columbia, Canada. Prevalence reached 100% and intensity 1,535 pseudocysts per 2 cm length of fish. Polymerase chain reaction primers specific for K. thyrsites amplified a fragment of the small subunit rDNA and confirmed identification. These primers also allowed detection of K. thyrsites in young (<4-mo-old) fish with no other apparent sign of infection. No inflammatory response or liquefaction of host tissue was associated with the infection. The number of pseudocysts per infected fish was not correlated with fish size or condition, although larger fish (total length) had larger pseudocysts (rs = 0.437, P < 0.001). This finding brings to 28 the number of potential hosts for the species. Kudoa thyrsites is a well recognized cause of soft flesh in netpen-reared Atlantic salmon in coastal waters of British Columbia. Tube-snouts are common in and around these netpens, and thus may be a significant host reservoir for K. thyrsites.
Innate susceptibility differences in Chinook salmon Oncorhynchus tshawytscha to Loma salmonae (Microsporidia)
(2000) Shaw, Ross W.; Kent, Michael L.; Adamson, Martin L.
Loma salmonae (Putz, Hoffman and Dunbar, 1965) Morrison & Sprague, 1981 (Microsporidia) is an important gill pathogen of Pacific salmon Oncorhynchus spp. in the Pacific Northwest. Three strains of chinook salmon O. tshawytscha were infected in 2 trials with L. salmonae by feeding of macerated infected gill tissue or per os as a gill tissue slurry. Intensity of infection was significantly higher in the Northern stream (NS) strain as compared to the Southern coastal (SC) and a hybrid (H) strain derived from these 2 strains. Both wet mount and histological enumeration of intensity of infection demonstrated strain differences. Survival in the NS strain was significantly lower than the other strains. The NS strain may represent a naive strain and be less able to mount an effective immune response against the parasite.
Iodophor treatment is not completely efficacious in preventing Loma salmonae (Microsporidia) transmission in experimentally challenged Chinook salmon, Oncorhynchus tshawytscha (Walbaum)
(1999) Shaw, Ross W.; Kent, Michael L.; Adamson, Martin L.
Loma salmonae is a microsporidian parasite pre-dominately infecting the endothelial cells of Pacificsalmon, Oncorhynchus spp. Loma salmonae formshypertrophied cells (xenomas) which are oftenvisible as white cysts in the gills. The parasite hasbeen associated with significant mortalities inspawning wild stocks (M. Higgins, personal com-munication), hatcheries (Hauck 1984) and inmarine netpen farms in the Pacific North-west(Kent, Elliott, Groff & Hedrick 1989; Speare,Brackett & Ferguson 1989; Shaw & Kent 1999).
Modes of transmission of Loma salmonae (Microsporidia)
(1998) Shaw, Ross W.; Kent, Michael L.; Adamson, Martin L.
Loma salmonae (Putz, Hoffman and Dunbar, 1965) Morrison and Sprague, 1981 (Microsporidia) causes prominent gill disease in pen-reared chinook salmon Oncorhynchus tshawytscha in the Pacific Northwest. Transmission of the parasite was examined by exposing Pacific salmon Oncorhynchus spp. to infectious spores by various routes: per os, intraperitoneal, intramuscular, and intravascular injection, by cohabitation with infected fish, and by placement of spores directly on the gill. All exposure methods led to infections except placement of spores on the gill. Putative sporoplasms were visible in epithelial cells of the alimentary canal within 24 h of per os exposure. L. salmonae may initially infect alimentary epithelial cells and then migrate into the lamina propia to access the blood stream. Positive results obtained by intravascular injection suggest that autoinfection from spores of ruptured xenomas in the endothelium may also occur. The cohabitation experiment demonstrates that fish may become infected by spores released from live fish.
A new species of Loma (Microsporea) in Shiner perch (Cymatogaster aggregata)
(1997) Shaw, Ross W.; Kent, Michael L.; Docker, Margaret F.; Brown, A. M.; Devlin, Robert H.; Adamson, Martin L.
Loma embiotocia n. sp. is described from the gills of shiner perch (Cymatogaster aggregata) from waters off Vancouver Island, British Columbia, Canada. Highest prevalence at a site was 15% and greatest intensity was 583 xenomas per fish. Xenomas averaged 0.13 mm in diameter (0.06-0.16 mm) and contained ovoid spores 4.8 x 2.6 (4.0-5.0 x 2.0-3.0) µm. Sporogonic stages were dispersed throughout the xenomas. The xenoma wall was smooth lacking invaginations into the cytoplasm; sporoblasts were not highly vacuolated, and the sporophorous vesicle formed before sporogony. In addition to differences in host and geographic location the new species is distinguished from Loma salmonae, the only other species in the genus known from British Columbia, by its internal transcribed spacer (ITS) ribosomal DNA sequence.
Phagocytosis of Loma salmonae (Microsporidia) spores in Atlantic salmon (Salmo salar), a resistant host, and chinook salmon (Oncorhynchus tshawytscha), a susceptible host
(2001) Shaw, Ross W.; Kent, Michael L.; Adamson, Martin L.
The in vitro phagocytosis of Loma salmonae spores by macrophages of Atlantic salmon and two strains of chinook salmon were investigated. Opsonisation of L. salmonae with plasma factors increased uptake by head kidney macrophages. Macrophages of Atlantic salmon, which are resistant to the parasite, had a significantly higher phagocytic index (PI) than those of chinook salmon, a susceptible species. This may indicate a possible mechanism contributing to resistance in Atlantic salmon or that L. salmonae is able to evade or suppress initial binding by macrophages of chinook. Non-specific binding or lectinophagocytosis was also suggested by significantly higher PI of spores from EDTA treated plasma when compared with no plasma or heat treated plasma. In comparison, uptake of Baker's yeast Saccharomyces cerevisiae by phagocytes was not significantly different between fish species and strains for all treatments.
Viability of Loma salmonae (Microsporidia) under laboratory conditions
(2000) Shaw, Ross W.; Kent, Michael L.; Adamson, Martin L.
The viability of the fish-infecting microsporidian Loma salmonae Morrison and Sprague, 1981 was determined under laboratory conditions by polar filament extrusion and infectivity to chinook salmon (Oncorhynchus tshawytscha). Extrusion rates of isolated spores decreased from 51.0% to 0.0% by 100 days after storage in fresh or sea water at 4 °C. Spores stored up to 95 days in either solution infected 80.0–100.0% of exposed chinook, although no spores infected fish at 100 days in one trial. Viability in Earl's balanced salt solution was tested up to 50 days, with 23.7% of spores extruding filaments and 80.0% of exposed chinook becoming infected. Spores frozen to −20 °C or −70 °C were unable to infect fish.

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