Xenoma Formation Research Articles

Regulatory Effects of Water Temperature onLoma salmonae(Microspora) Development in Rainbow Trout

Abstract Water temperature, a pivotal factor influencing interactions between teleosts and pathogens, was examined to determine its effects on the kinetics of xenoma formation and dissolution subsequent to experimental exposure of rainbow trout Oncorhynchus mykiss to the microsporidian gill pathogen Loma salmonae. The permissive water temperature range in which xenomas developed was between 9° and 20°C. Parasite development was arrested at temperatures outside this range, as indicated by the absence of visible xenomas among exposed fish. In addition, when these trout were subsequently moved to temperatures within the permissive range, xenomas failed to develop. Water temperature, within the permissive range, had no significant effect on either the number of xenomas that formed or the proportion of fish that developed xenomas following gastric intubation with a standard dose of spores. The relationship between water temperature and xenoma onset-time was best described (R 2 = 88.3%) by polynomial regression...

Effect of water temperature manipulation on a thermal unit predictive model for Loma salmonae

Loma salmonae is an important microsporidian pathogen affecting the mariculture of Pacific salmon, Oncorhynchus tshawytscha (Walbaum). Clinical signs associated with infection arise when the parasite enters sporogony and forms xenoparasitic complexes (xenomas) within the gill. The present study tested a thermal unit (TU) model, which was devised to predict the timing of xenoma formation, under conditions in which water temperature changed during the course of infection. In vivo trials with juvenile trout showed that the model [TU for xenoma onset = (days post exposure) × ( °C above 7 °C)] accurately predicted the onset time for xenomas when fish were moved from either 11 or 5 °C to 15 °C at various intervals after exposure. These findings suggest that the TU model may allow aquaculturists to predict disease onset. However, the model failed when fish were moved from 15 to 5 °C at intervals after exposure. This finding suggests that the temperature‐constrained phase of the life‐cycle of L. salmonae occurs early on after the spore is ingested by the fish.

Redescription of Glugea caulleryi, a microsporidian parasite of the greater sand‐eel, Hyperoplus lanceolatus (Le Sauvage), (Teleostei: Ammodytidae), as Microgemma caulleryi comb. nov.

A detailed study of a microsporidian parasite detected in the liver of the greater sand-eel, Hyperoplus lanceolatus (Le Sauvage), is reported. The parasite, originally described as Glugea caulleryi, invades hepatocytes, inducing xenoma formation and marked hypertrophy of the host-cell nucleus. Macroscopically, the infection is characterized by the presence of fibrous whitish structures of about 5 mm in length, each containing several xenomas. The final merogonic stages are rounded plasmodia, about 5 μm in length, which divide by plasmotomy. Meronts are characterized by the abundant membranous structures present in their cytoplasm. It was not possible to characterize the transition from merogonic to sporogonic plasmodia. During sporogony, the parasite remains in direct contact with the host-cell cytoplasm and sporonts produce uninucleate sporoblasts by exogenous budding. The spores are ovoid and uninucleate with a mean size of 1.2 x 2.6 μm, a polar tube coiled between seven and nine times and only a laminar-type polaroplast. In view of these characteristics, it is proposed that this species should be transferred to the genus Microgemma, with the name Microgemma caulleryi comb. nov.

Quinine hydrochloride treatment delays xenoma formation and dissolution in rainbow trout challenged with Loma salmonae

An experiment was designed to study the effect of dietary quinine hydrochloride (61 mg/kg of fish/day), on the rate of xenoma formation in the gills of Loma salmonae-infected juvenile rainbow trout maintained at a water temperature of 15 degrees C. Almost all (90.9%) control fish had developed xenomas by week 6 post-exposure (PE), but significantly fewer (18.2%) of the medicated fish were similarly affected (P < 0.0001). By week 8 PE, 100% of control fish had xenomas, but only 57.5% of quinine-treated had xenomas (P < 0.0001). However, by week 9 there was no difference between treated and control fish. Xenoma dissolution and branchitis, two crucial events in the pathogenesis of L. salmonae infection in farm-reared Pacific salmon, were present at week 10 in control fish. In contrast, comparable lesions did not develop in treated fish until week 14. These findings are of potential significance for the control of L. salmonae infection in farmed salmon.

Loma salmonae‐associated growth rate suppression in rainbow trout, Oncorhynchus mykiss (Walbaum), occurs during early onset xenoma dissolution as determined by in situ hybridization and immunohistochemistry

AbstractExperimental infection of rainbow trout, Oncorhynchus mykiss (Walbaum), juveniles with Loma salmonae at a water temperature of 15 °C yielded detectable parasite DNA within the gills by week 2 post‐exposure (PE) and detectable spore‐wall antigen within developing xenomas by week 3 PE, as determined by in situ hybridization and monoclonal antibody (Mab) based immunohistochemistry, respectively. The microsporidian was most commonly located within endothelial cells of lamellar basal channels. Whereas the onset of xenoma formation appeared to be relatively synchronous, as expected from previous studies, xenoma dissolution followed an unexpected biphasic pattern with peaks at weeks 4 and 9 PE. The onset of significant growth rate suppression, at week 4 PE in exposed fish, was temporally associated with the appearance of gill lesions which, in turn, were centred about sites of premature xenoma dissolution. The latter was determined by the detection of spore‐wall antigen within lesions. Co‐habitant control fish began developing xenomas by week 10, indicating the infective potential of those spores released from the principal fish during early xenoma dissolution. Although infection with L. salmonae significantly affects fish growth rates, the time‐course of this suppression is limited, and as an unexpected finding, growth rate recovery commences prior to the infection’s resolution.

Johenrea locustaen.g., n.sp. (Microspora: Glugeidae): A Pathogen of Migratory Locusts (Orthoptera: Acrididae: Oedipodinae) from Madagascar

A new microsporidium was isolated from the migratory locust,Locusta migratoria capito,collected in Madagascar. This new species was found to be haplokaryotic throughout development, produced polysporophorous vesicles of parasite origin, and there was conspicuous xenoma formation. The xenoma was a complex structure composed primarily of fat body cells. The wall of the xenoma was bound by a basement membrane beneath which was a region of collagen-like fibers. Multiplication of the parasite occurred by way of both a schizogonic phase and by a sporulation phase. Schizonts divided either directly or with the intervention of paucinucleate plasmodia into additional schizonts. At some point, plasmodia developed (with an increase in size and number of nuclei) into sporogonial plasmodia with typically 16 nuclei. Sporogonial plasmodia elaborated an interfacial envelope within which they underwent sporogony. Sporophorous vesicles normally contained 16 spores but also 8 and rarely 32 spores were formed. Spores were elongate ovoid (sometimes slightly curved) and measured 8.3 by 3.8 μm (fresh) and 6.9 by 4.2 μm (fixed). Based on the development of the microsporidium and the features of the xenoparasitic complex, a new species and genusJohenrea locustaen.g., n.sp. is proposed.

Myxosporea-induced xenoma formation in pike ( Esox lucius L.) renal corpuscles associated with Myxidium lieberkuehni infection

Myxidium lieberkuehni infection of the urinary tract of the pike (Esox lucius L.) is in most cases associated with the presence of cystic structures in renal corpuscles. These structures are greatly hypertrophic host cells constituting xenomas with the cytoplasm replete with proliferating myxosporean cells. Their development results in primary cells each enclosing one secondary and two tertiary cells. Eventually the cell structure assumes an appearance which suggests that the stages are no longer viable and most xenomas are destroyed by host tissue reaction. Some cells, however, may be released into the tubule lumen, suggesting a possible further sporogonic development of M. lieberkuehni. Circumstantial evidence points at the identity of the xenoma stages (designated Nephrocystidium pickii by Weissenberg in 1921, referenced in Weissenberg, 1923 [26]) with M. lieberkuehni, and this applies also to intracellular stages found in the epithelium of the collecting renal ducts. The latter have the same cell-in-cell arrangement of primary, secondary and tertiary cells, but were not observed to show any signs of cell degradation.