Normal and aberrant tissue distribution of <i>Loma salmonae</i> (Microspora) within rainbow trout, <i>Oncorhynchus mykiss</i> (Walbaum), following experimental infection at water temperatures within and outside of the xenoma‐expression temperature boundaries

Sánchez, J. G.; Markham, R. J. Frederick

doi:10.1046/j.1365-2761.2000.00222.x

Cited by 31 publications

(27 citation statements)

References 19 publications

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“…Beaman et al (1999) found that normal development of Loma salmonae is interrupted by temperatures below 9°C as well as above 20°C, when xenoma formation in the gills is inhibited. At low temperature, the parasite arrives in the heart where an initial merogony normally occurs, but xenoma formation in the gills does not occur and the gills eventually become PCR-negative by 4 wk post-challenge (Sanchez et al 2000(Sanchez et al , 2001. Apparently, normal proliferation in the heart is arrested by low temperatures.…”

Section: Discussionmentioning

confidence: 99%

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Paranucleospora theridion (Microsporidia) infection dynamics in farmed Atlantic salmon Salmo salar put to sea in spring and autumn

Sveen

Øverland²,

Karlsbakk³

et al. 2012

Dis. Aquat. Org.

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The microsporidian Paranucleospora theridion (syn. Desmozoon lepeophtheirii) is a parasite of Atlantic salmon Salmo salar and also a hyperparasite of the salmon louse Lepeophtheirus salmonis. The parasite develops 2 types of spores in salmon, cytoplasmic spores in phagocytes and intranuclear spores in epidermal cells. The former type of development is assumed to be propagative (autoinfection), while the epidermal spores transfer the parasite to lice. Development in lice is extensive, with the formation of xenoma-like hypertrophic cells filled with microsporidian spores. We show that salmon are infected in the absence of lice, likely through waterborne spores that initiate infections in the gills. During summer and autumn the parasite propagates in the kidney, as evidenced by peaking normalised expression of P. theridion rRNA. Lice become infected during autumn, and develop extensive infections during winter. Lice mortality in winter and spring is likely responsible for a reservoir of spores in the water. Salmon transferred to sea in November (low temperature) did not show involvement of the kidney in parasite propagation and lice on such fish did not become infected. Apparently, low temperatures inhibit normal P. theridion development in salmon.

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Section: Discussionmentioning

confidence: 99%

“…Microsporidian development may be highly temperature-dependent (see Sanchez et al 2000). Kaba -tana takedai infections in salmonids do not develop at 9°C, and are reduced at 11°C.…”

Section: Discussionmentioning

confidence: 99%

Paranucleospora theridion (Microsporidia) infection dynamics in farmed Atlantic salmon Salmo salar put to sea in spring and autumn

Sveen

Øverland²,

Karlsbakk³

et al. 2012

Dis. Aquat. Org.

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“…1). The parasite is likely transported from the gut in leucocytes (Rodríguez-Tovar et al 2002), and early merogonic stages have been observed by ISH (Sánchez et al 2001a) or PCR (Sánchez et al 2000) in the heart endocardium a few days after infection. Loma salmonae is first detected in the gills about 2-3 wk p.e.…”

Section: Sequential Developmentmentioning

confidence: 99%

Review of the sequential development of Loma salmonae (Microsporidia) based on experimental infections of rainbow trout (Oncorhynchus mykiss) and Chinook salmon (O. tshawytscha)

Kent¹,

Speare²

2005

FOLIA PARASIT

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Abstract. Loma salmonae (Putz, Hoffman et Dunbar, 1965) is a common gill parasite of salmonids, and essentially all species in the genus Oncorhynchus are susceptible. Infections occur in both fresh and salt water. Loma salmonae is directly transmissible by ingestion of spores or infected tissue. The parasite infects the wall of blood vessels of various organs, but the gill is the primary site of infection. Initial infection occurs in the intestine, and xenomas are easily detected in the gills by standard histology at 4-6 wk post-exposure. A few presporogonic stages of the parasite are found in the heart endothelium prior to xenoma formation in the gills. Ultrastructure studies of early infections demonstrated that wandering blood cells transport the meronts to the gills, and that merogony occurs in pillar cells and other cells underlying the gill endothelium. Xenomas develop in these cells, resulting in hypertrophied host cells filled with spores. Xenomas ultimately rupture, and are associated with severe inflammation in which free spores are found in macrophages. The parasites are most pathogenic during this phase of the infection, resulting in severe vasculitis and clinical disease. Both rainbow trout (Oncorhynchus mykiss) and Chinook salmon (Oncorhynchus tshawytscha) recover from infections, but free spores persist in kidney and spleen phagocytes for many months after xenomas are absent in Chinook salmon. Fish that have recovered from the infection show strong immunity against the parasite, lasting up to 1 year. Fish are susceptible to infection by other routes of exposure by spores; co-habitation, anal gavage, and intramuscular, intraperitoneal and intravascular injection. Autoinfection probably occurs following release of spores in blood vessels after xenomas rupture. The optimal temperature for L. salmonae infections is 15-17°C, with a permissive range of 11-20°C.

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“…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. Development to the xenoma stage has been effectively modelled relative to the effects of temperature on the rate of xenoma formation.…”

Section: Introductionmentioning

confidence: 99%

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

Becker

2004

Dis. Aquat. Org.

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Previous studies have modelled the relationship between water temperature and the rate of sporulation as defined by xenoma formation during microsporidial gill disease (MGD) in salmon caused by Loma salmonae. Although offering insight into the epidemiology of MGD, a key unexplored area is the role of temperature in the rate of xenoma dissolution including spore release into the environment, and this is crucial to our ability to model horizontal transmission of MGD within confined net-pen populations of farmed salmon. Results from a previous trial suggested that xenoma dissolution may be dramatically hastened as water temperature declines, thus introducing a critical anomaly into any predictive exercise. The data generated herein was evaluated using the statistics of survival analysis to re-establish the baseline relationship of xenoma formation and dissolution relative to water temperature and to compare these results with those of previous studies. We infected 30 individuals of Oncorhynchus mykiss (Walbaum) with macerated xenoma-laden gill material, and afterwards allocated them to tanks with water temperatures of 11, 15, or 19°C and monitored them through a disease cycle. Xenoma onset and clearance times were similar to previous findings with both events being accelerated at higher water temperatures, thereby suggesting a similar temperature response in the current strain to those used in previous studies. Another group of 45 fish was infected with L. salmonae and held at 15°C until xenomas formed, and were subsequently shifted to 11, 15, or 19°C. The median xenoma dissolution time in these tanks was 49, 35 and 28 d, respectively, similar to rates observed when water temperature remained constant. Thus we rejected the hypothesis that a sudden change in water temperature triggers rapid or anomalous xenoma dissolution.

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Normal and aberrant tissue distribution of Loma salmonae (Microspora) within rainbow trout, Oncorhynchus mykiss (Walbaum), following experimental infection at water temperatures within and outside of the xenoma‐expression temperature boundaries

Cited by 31 publications

References 19 publications

Paranucleospora theridion (Microsporidia) infection dynamics in farmed Atlantic salmon Salmo salar put to sea in spring and autumn

Paranucleospora theridion (Microsporidia) infection dynamics in farmed Atlantic salmon Salmo salar put to sea in spring and autumn

Review of the sequential development of Loma salmonae (Microsporidia) based on experimental infections of rainbow trout (Oncorhynchus mykiss) and Chinook salmon (O. tshawytscha)

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

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