Ultrastructural examination of the host inflammatory response within gills of netpen reared chinook salmon (Oncorhynchus tshawytscha) with Microsporidial Gill Disease.

The sequence of host changes following the rupture of spore-laden xenomas of the microsporidian Loma salmonae during Microsporidial Gill Disease of Salmon was deduced from ultrastructural examination of the gills of naturally infected, moribund, chinook salmon from a commercial aquaculture site. The gills contained many stages of parasite development suggesting fish were chronically exposed to the parasite. Intact xenomas were generally found beneath the endothelium in arteries and arterioles and were encapsulated by a layer of collagen containing fibroblasts sometimes joined by desmosomes. Xenoma dissolution was characterized by neutrophil infiltration and loss of the xenoma plasma membrane and encapsulation. The inflammatory responses associated with ruptured xenomas ranged from acute lesions, denoted by a marked neutrophil infiltration and vascular thrombosis, to chronic lesions with a macrophage-rich infiltrate variously accompanied by neovascularization and vascular remodelling. Dendritic-like cells and plasma cells were characteristic throughout. Basement membrane damage of the primary filament epithelium and subsequent transepithelial expulsion of spores were associated with severe inflammation. An unusual previously undescribed multifocal change, in which epithelial cells invaded deeply beyond the normal boundaries of the basement membrane, affected areas of gill filament epithelium with basement membrane damage. Some neutrophils that contained L. salmonae spores, or spore polar tube, displayed morphological changes that included irregular cell shape, cytoplasmic darkening associated with an abundance of free ribosomes, lysis of neighbouring cells, and type II nuclear clefts. Fusion of apparently intact neutrophils occurred in other areas of the lesion, where close contacts between neighbouring cells were established and in some areas plasma membrane fusion occurred. Closely associated neutrophils with intact plasma membranes were observed to contain type II nuclear clefts, abundant granules and rough endoplasmic reticulum. Other neutrophils in the lesion displayed type I nuclear pockets, which is suspected to be an early stage of apoptosis.

Whole body net ion fluxes, plasma electrolyte concentrations and haematology during a Loma salmonae infection in juvenile rainbow trout, Oncorhynchus mykiss (Walbaum).

Loma salmonae infections of salmonids culminate in the development of branchial xenomas and subsequent focal hyperplasia of the lamellar or filament epithelium following xenoma rupture and spore release. The effects of this acute branchial disruption upon net ionic flux rates and plasma electrolyte concentrations were determined in juvenile rainbow trout given an experimental oral exposure to L. salmonae. Mean numbers of branchial xenomas peaked at week 5 post-exposure (PE), which coincided with a reduction in the specific growth rate, although there were no significant differences in mass, length or condition of Loma-exposed fish compared with unexposed controls. Following exposure, negative net whole body Na(+) and K(+) fluxes decreased, whereas net Cl(-) fluxes remained unchanged compared with non-exposed control fish. At week 3 PE during the initial branchial xenoma formation stage, there was a significant negative whole body net K(+) flux in Loma-exposed trout compared with other points during the exposure and subsequent infection. Additionally, Loma-exposed fish had marginally elevated plasma Na(+) and Cl(-) concentrations, whilst K(+) levels remained unchanged, compared with control fish. Although there was a progressive decrease in leucocrit, haematocrit remained unchanged over the course of the Loma exposure and subsequent infection. These results suggest that ionic compensation can occur at the gills during the development of xenomas during exposure to L. salmonae and the resultant infection, therefore allowing defence of plasma electrolyte concentrations, unlike the acute ionic disturbances seen with some other parasitic diseases.

Interaction of water temperature and challenge model on xenoma development rates for Loma salmonae (Microspora) in rainbow trout, Oncorhynchus mykiss (Walbaum).

This study evaluated the regulatory effects of water temperature on the development of branchial xenomas caused by Loma salmonae using a high-dose per os-challenge model compared with a low-dose cohabitation-challenge model. Approximately 275 juvenile rainbow trout (RBT), Oncorhynchus mykiss, were randomly distributed to six tanks with two tanks each maintained at 11, 15 and 19 degrees C. Fish in one tank from each temperature setting were exposed per os to macerated L. salmonae-infected gill material and fish in the other tank from each temperature setting were exposed to L. salmonae using the cohabitation-challenge model. Fish were monitored for the development of branchial xenomas beginning at day 21 post-exposure. Survival analyses were used to evaluate the effect of water temperature and challenge model on the number of days until the first visible branchial xenoma was detected. The survivor curves for the per os-challenge model revealed that there was at least one significant difference, whereas the cohabitation challenge did not reveal any significant differences amongst the temperature settings. The proportional hazards model revealed a significant interaction between the challenge model used and water temperature. This indicated that the effect of water temperature was different depending on challenge model. Additionally, from the mean xenoma intensities, on average, the per os-challenged fish showed higher xenoma intensity compared with the cohabitation-challenged fish. Overall, the impact of water temperature on disease pathogenesis was greater when the RBT were per os challenged compared with using the cohabitation model.

Prevalence and influence of Loma branchialis (Microspora) on growth and mortality in Atlantic cod (Gadus morhua) in coastal Newfoundland.

A study was conducted to determine the prevalence, geographical distribution, and effects of a microsporan parasite, Loma branchialis, in Atlantic cod in coastal Newfoundland. The parasite was identified microscopically as opaque, ovoid xenomas, primarily in the gills, heart, and spleen. Although widely distributed in young fish inhabiting 7 coastal localities, prevalence was 1-7% in general, <0.01% in older and large fish, but 78% in market-size cod from a commercial farm. Some of the latter fish were emaciated, and approximately 2 mo after the parasite was detected, 63% succumbed with a massive infection. Condition factor and blood values were significantly lower than those in reference fish. An experimental study conducted over 2 yr revealed that mass gained and condition factor were significantly lower in infected cod than in controls at the termination of the study. Feed consumption, mass gained, feed conversion efficiency, and condition factor also were significantly lower in another group of infected cod of marketable size studied over 12 wk. Xenomas also were observed in the heart and gills of year class II cod reared in a hatchery. Loma branchialis is considered to be a potential pathogen in both hatchery-reared and net pen-cultured cod in Newfoundland.