Phagocytosis of Loma salmonae (Microsporidia) spores in Atlantic salmon (Salmo salar), a resistant host, and chinook salmon (Oncorhynchus tshawytscha), a susceptible host

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.     

Induction time for resistance to microsporidial gill disease caused by Loma salmonae following vaccination of rainbow trout (Oncorhynchus mykiss) with a spore-based vaccine

Resistance to re-infection of rainbow trout to Loma salmonae, a microsporidian gill parasite has been previously documented and this study examined how rapidly this resistance develops. Naive rainbow trout were inoculated intraperitoneally (IP) with an inactivated spore-based vaccine and were then given an oral challenge with a high dose of L. salmonae spores at various weeks after being vaccinated. Non-vaccinated naive fish (exposed group) were challenged alongside of each group of vaccinated fish to ensure that the challenges were relatively standardised. In each group of fish, four weeks after the challenge, numbers of xenomas were counted on a gill arch for all fish. Vaccinated trout were completely resistant to a L. salmonae challenge six weeks after vaccination, although the onset of resistance began at approximately week 3, as observed with a reduction in the percent infected and xenoma intensity. The maximum percent infected for the vaccinated fish was 83% following a challenge two weeks following vaccination, whereas for the exposed group the maximum prevalence of 100% was reached several times. With continued research, a spore-based vaccine for L. salmonae has the potential to become the first commercially available parasite vaccine for fish.     

Effects of dexamethasone on host innate and adaptive immune responses and parasite development in rainbow trout Oncorhynchus mykiss infected with Loma salmonae

The effects of dexamethasone (dex) treatment on infections with the microsporidian parasite, Loma salmonae and the effects of dex on initiation of the adaptive immune response were investigated in rainbow trout, Oncorhynchus mykiss experimentally infected with the parasite. Dex treatment resulted in significantly higher infections with the parasite in the gills and other internal organs, suggesting that dex inhibits aspects of the innate immune response to L. salmonae; the heavier infections in the gills and organs of rainbow trout resembled infections seen in Chinook salmon. Mean xenoma counts per microscope field in the gills of fish infected with L. salmonae treated with dex or left untreated were 169 and 30, respectively. Although higher numbers of xenomas were observed in dex treated fish, the xenomas were generally smaller in size than in infected control fish. The xenomas in dex treated fish showed morphological signs of degeneration including loss and degeneration of early parasite stages, accumulation of amorphous material in xenomas, and infiltration with phagocytic cells containing degenerated parasites. The xenomas in infected untreated fish had larger xenomas with a more uniform size and contained identifiable parasite stages in the cytoplasm. According to this study, once fish have developed an adaptive immune response to the parasite by previous exposure, then fish have 100% protection to reinfection even when treated with heavy doses of dex. L. salmonae immune fish treated or untreated with dex during reinfection with the parasite developed no xenomas in the gills 6 weeks post reinfection. These results indicate that once the cellular response is primed to L. salmonae, then dex related immunosuppression does not reduce the effectiveness of the adaptive immune response.     

Experimental vaccination of rainbow trout against Loma salmonae using a live low-virulence variant of L. salmonae

Prior exposure of rainbow trout Oncorhynchus mykiss juveniles to the low-virulence variant of Loma salmonae, L. salmonae SV, spores resulted in a xenoma intensity in the gill filaments fourteen times lower (0·044 v. 0·641 xenomas per filament; P=0·0001) than that observed in the naive controls, challenged with L. salmonae spores, as determined morphometrically by in situ hybridization at the peak of the disease (between 4 and 6 weeks post exposure). The marked degree of reduction in numbers of xenomas that formed after challenge suggests that use of the low-virulence variants should be further considered as a means to protect fish in regions where the parasite is endemic, to protect them during grow out periods.     

Effects of cortisol implants on the PKX myxosporean causing proliferative kidney disease in rainbow trout, Salmo gairdneri

The myxosporean (PKX) that causes proliferative kidney disease in salmonid fishes is found primarily in the kidney interstitium of clinically affected fish, where it invokes a severe inflammatory response. Incomplete spores are observed in the lumen of kidney tubules in recovering fish. PKX-infected rainbow trout, Salmo gairdneri, were immunosuppressed with cortisol implants to determine if a reduction in renal interstitial inflammation would enhance the development of the parasite. Immunosuppression of these fish was indicated by high plasma cortisol levels, chronic mortality due to opportunistic pathogens, and depressed leucocrits when compared to infected fish not receiving cortisol implants. Cortisol-treated PKX-infected fish had 20 times the density of interstitial PKX compared with nontreated fish, but showed less interstitial inflammation. All of the former group examined at 4 wk postimplantation exhibited intraluminal sporogonic forms of PKX, whereas no sporogonic forms were detected in the nontreated fish. Suppression of the inflammatory response clearly enhanced the parasite's ability to reach the sporogonic stage, but did not induce complete development of the spore. Possibly the kidney tubules of rainbow trout do not provide the proper physiological environment for complete sporulation of PKX and a nonsalmonid fish may be the primary host.     

Seasonal occurrence of the infectious stage of proliferative kidney disease (PKD) and resistance of rainbow trout, Salmo gairdneri Richardson, to reinfection

The seasonality of proliferative kidney disease (PKD) in rainbow trout, Salmo gairdneri Richardson, at the American River Hatchery, California was found to be primarily dependent on the presence or absence of the infectious stage in the water supply. This was determined by introducing sentinel trout into the hatchery water supply on a monthly basis, followed by their transfer to the laboratory for subsequent holding in 18° C, pathogen-free water for one month prior to examination. These exposures demonstrated that infections were obtained from April through October at ambient temperatures 12–20° C. Trout which had recovered from clinical infections were found to be resistant to reinfection. Resistance was induced by active infection and not just previous exposure to the infectious stage. Trout surviving PKD were also found to harbour later sporogonic stages of the parasite for at least one year following initial infection, but fully formed spores, as judged by well-developed valves, were not observed.     

Experimental susceptibility of turbot Scophthalmus maximus to viral haemorrhagic septicaemia virus isolated from cultivated turbot

Juvenile pathogen-free turbot were infected with a viral haemorrhagic septicaemia virus (VHSV) isolate recovered from turbot cultivated on the island of Gigha, West Scotland. Mortality of 100% was recorded in fish infected via the intra-peritoneal (i.p.) route. Horizontal transmission of VHSV in sea water was demonstrated by cohabitation of naive fish with i.p. infected fish at a ratio of 1:1. The total cumulative average mortality in cohabiting fish was 60% by 60 d post-infection. Turbot infected via an immersion route exhibited a cumulative average mortality of 71% by the end of the experiment. VHSV identified by enzyme-linked immunosorbent assay (ELISA) was recovered from both organ (kidney and spleen) and brain samples of individual fish that died following infection by all experimental routes. These findings pose significant implications regarding the persistence of VHSV and its role in limiting natural populations of marine fish species. In addition, the establishment of infection models for the transmission of VHSV in sea water is of fundamental importance to the development of anti-VHSV vaccines in important commercial species such as turbot.     

Mortality and kidney histopathology of chinook salmon Oncorhynchus tshawytscha exposed to virulent and attenuated Renibacterium salmoninarum strains

An isolate of Renibacterium salmoninarum (strain MT 239) exhibiting reduced virulence in rainbow trout Oncorhynchus mykiss was tested for its ability to cause bacterial kidney disease (BKD) in chinook salmon Oncorhynchus tshawytscha, a salmonid species more susceptible to BKD. Juvenile chinook salmon were exposed to either 33209, the American Type Culture Collection type strain of R. salmoninarum, or to MT 239, by an intraperitoneal injection of 1 x 10(3) or 1 x 10(6) bacteria fish(-1), or by a 24 h immersion in 1 x 10(5) or 1 x 10(7) bacteria ml(-1). For 22 wk fish were held in 12 degrees C water and monitored for mortality. Fish were sampled periodically for histological examination of kidney tissues. In contrast to fish exposed to the high dose of strain 33209 by either injection or immersion, none of the fish exposed to strain MT 239 by either route exhibited gross clinical signs or histopathological changes indicative of BKD. However, the MT 239 strain was detected by the direct fluorescent antibody technique in 4 fish that died up to 11 wk after the injection challenge and in 5 fish that died up to 20 wk after the immersion challenge. Viable MT 239 was isolated in culture from 3 fish that died up to 13 wk after the immersion challenge. Total mortality in groups injected with the high dose of strain MT 239 (12%) was also significantly lower (p < 0.05) than mortality in groups injected with strain 33209 (73 %). These data indicate that the attenuated virulence observed with MT 239 in rainbow trout also occurs in a salmonid species highly susceptible to BKD. The reasons for the attenuated virulence of MT 239 were not determined but may be related to the reduced levels of the putative virulence protein p57 associated with this strain.     

Susceptibility of captive adult winter-run Chinook salmon Oncorhynchus tshawytscha to waterborne exposures with infectious hematopoietic necrosis virus (IHNV)

Sexually mature female Chinook salmon Oncorhynchus tshawytscha with no prior history of exposure to infectious hematopoietic necrosis virus (IHNV) were susceptible to experimental infection induced by additions of virus to the water. The resulting infections resembled those observed among naturally infected hatchery and wild populations of Chinook salmon. Virus was detected as early as 4 d post-exposure (p.e.) and subsequently in all virus-exposed fish that died or that were examined at 14 d p.e. when the study was terminated. The greatest concentrations of virus, up to 10(8) plaque-forming units (pfu) ml(-1), were found in the ovarian fluid at 13 to 14 d p.e., but the virus was also found in high concentrations in the gill, kidney/spleen and plasma. In contrast, the virus was not recovered from unexposed control adult salmon that died or were sampled at the end of the study. Despite detecting concentrations of IHNV in excess of 10(7) pfu g(-1) of tissue, no specific microscopic lesions were found in IHNV-exposed compared to unexposed control salmon. The results of this initial study suggest that virus in the spawning environment, either from adult salmon or other sources, may contribute to its rapid spread among adult Chinook salmon, thereby considerably increasing the prevalence of IHNV infection in both wild and hatchery populations of adult Chinook salmon.     

Experimental mycobacteriosis in striped bass Morone saxatilis

Striped bass Morone saxatilis were infected intraperitoneally with approximately 10(5) Mycobacterium marinum, M. shottsii sp. nov., or M. gordonae. Infected fish were maintained in a flow-through freshwater system at 18 to 21 degrees C, and were examined histologically and bacteriologically at 2, 4, 6, 8, 17, 26, 36 and 45 wk post-infection (p.i.). M. marinum caused acute peritonitis, followed by extensive granuloma development in the mesenteries, spleen and anterior kidney. Granulomas in these tissues underwent a temporal progression of distinct morphological stages, culminating in well-circumscribed lesions surrounded by normal or healing tissue. Mycobacteria were cultured in high numbers from splenic tissue at all times p.i. Standard Ziehl-Neelsen staining, however, did not demonstrate acid-fast rods in most early inflammatory foci and granulomas. Large numbers of acid-fast rods were present in granulomas beginning at 8 wk p.i. Between 26 and 45 wk p.i., reactivation of disease was observed in some fish, with disintegration of granulomas, renewed inflammation, and elevated splenic bacterial densities approaching 10(9) colony-forming units g(-1). Infection with M. shottsii or M. gordonae did not produce severe pathology. Mild peritonitis was followed by granuloma formation in the mesenteries, but, with 1 exception, granulomas were not observed in the spleen or anterior kidney. M. shottsii and M. gordonae both established persistent infections in the spleen, but were present at densities at least 2 orders of magnitude less than M. marinum at all time points observed. Granulomas in the mesenteries of M. shottsii- and M. gordonae-infected fish resolved over time, and no reactivation of disease was observed.     

Two New Species of Plistophora (Microsporidea) from North American Fish with a Synopsis of Microsporidea of Freshwater and Euryhaline Fishes

SYNOPSIS. Two new species of Microsporidea, Plistophora salmonae from steelhead and rainbow trout (Salmo gairdntri) and Plistophora crpedianar from gizzard shad ( Dorosoma cepedianum) are described. Schizonts to spores of P. cepedianae were found at one time within the same cyst, while only sporonts and spores of P. salmonae were found within the cyst.
An illustrated synopsis of the known Microsporidea of freshwater and euryhaline fishes is given.     

Shedding of viral hemorrhagic septicemia virus (Genotype IVb) by experimentally infected muskellunge (<Emphasis Type="Italic">Esox masquinongy</Emphasis>)

Previous experimental infection demonstrated that juvenile muskellunge (Esox masquinongy) can survive experimental infection of viral hemorrhagic septicemia virus, Genotype IVb (VHSV IVb) at a low concentration of exposure. Herein we report that survivors of experimental infection with VHSV IVb shed the virus into the surrounding environment for an extended period of time. When muskellunge were exposed to VHSV IVb by immersion at a concentration of 1,400 plaque forming units (PFU)/ml, VHSV IVb was detected in the water of surviving fish for up to 15 weeks postexposure (p.e.) with the highest levels of shedding occurring between weeks 1 and 5 p.e. We estimated that each juvenile muskellunge can shed upwards of 1.36×10(5) PFU/fish/h after initial exposure signifying the uptake and amplification of VHSV to several orders of magnitude above the original exposure concentration. Muskellunge surviving low concentration exposure were re-infected with VHSV IVb by immersion at week 22 p.e. at concentrations ranging from 0 to 10(6) PFU/ml. Viral shedding was detected in all re-exposed fish, including mock rechallenged controls up to 15 consecutive weeks. Rates of viral shedding were substantially higher following rechallenge in the first 5 weeks. The highest rate of viral shedding was approximately 4.6×10(6) PFU/fish/h and shedding did not necessarily correspond to the re-exposure VHSV concentration. The results of this study shed new light into the dynamics of VHSV IVb shedding in a highly susceptible host and provide useful insights to fishery managers to design effective control strategies to this deadly virus.     

Development of Kudoa thyrsites (Myxozoa: Myxosporea) in netpen-reared Atlantic salmon determined by light microscopy and a polymerase chain reaction test.

The intramuscular phase of development of Kudoa thyrsites, the myxosporean associated with post-mortem myoliquefaction, or 'soft flesh syndrome', is described using histological preparations of the musculature of seawater netpen-reared Atlantic salmon Salmo salar. Hatchery-reared Atlantic salmon were naturally exposed to the infective stage while held in the experimental seawater netpens of the Pacific Biological Station in Nanaimo, British Columbia, Canada. In fish exposed during the summer of 1995, K. thyrsites infections were first detected in the somatic musculature at 13 wk post-exposure (p.e.) using only light microscopy. In the 1997 exposure, infections were first detected at 6 wk p.e. using a PCR test and at 9 wk p.e. using light microscopy. The earliest stage detected by histology was a small plasmodium containing 4 nuclei. No host response was observed that was directly related to the presence of intact plasmodia within muscle fibers. However, a response was associated with ruptured plasmodia, which was characterized by chronic, multifocal inflammation between the muscle fibers.     

Effect of repeated exposure to Plasmodium relictum (lineage SGS1) on infection dynamics in domestic canaries

Parasites are known to exert strong selection pressures on their hosts and, as such, favour the evolution of defence mechanisms. The negative impact of parasites on their host can have substantial consequences in terms of population persistence and the epidemiology of the infection. In natural populations, however, it is difficult to assess the cost of infection while controlling for other potentially confounding factors. For instance, individuals are repeatedly exposed to a variety of parasite strains, some of which can elicit immunological memory, further protecting the host from subsequent infections. Cost of infection is, therefore, expected to be particularly strong for primary infections and to decrease for individuals surviving the first infectious episode that are re-exposed to the pathogen. We tested this hypothesis experimentally using avian malaria parasites (Plasmodium relictum-lineage SGS1) and domestic canaries (Serinus canaria) as a model. Hosts were infected with a controlled dose of P. relictum as a primary infection and control birds were injected with non-infected blood. The changes in haematocrit and body mass were monitored during a 20 day period. A protein of the acute phase response (haptoglobin) was assessed as a marker of the inflammatory response mounted in response to the infection. Parasite intensity was also monitored. Surviving birds were then re-infected 37 days post primary infection. In agreement with the predictions, we found that primary infected birds paid a substantially higher cost in terms of infection-induced reduction in haematocrit compared with re-exposed birds. After the secondary infection, re-exposed hosts were also able to clear the infection at a faster rate than after the primary infection. These results have potential consequences for the epidemiology of avian malaria, since birds re-exposed to the pathogen can maintain parasitemia with low fitness costs, allowing the persistence of the pathogen within the host population.     

Infectivity of microsporidia spores stored in seawater at environmental temperatures

To determine how long spores of Encephalitozoon cuniculi, E. hellem, and E. intestinalis remain viable in seawater at environmental temperatures, culture-derived spores were stored in 10, 20, and 30 ppt artificial seawater at 10 and 20 C. At intervals of 1, 2, 4, 8, and 12 wk, spores were tested for infectivity in monolayer cultures of Madin Darby bovine kidney cells. Spores of E. hellem appeared the most robust, some remaining infectious in 30 ppt seawater at 10 C for 12 wk and in 30 ppt seawater at 20 C for 2 wk. Those of E. intestinalis were slightly less robust, remaining infectious in 30 ppt seawater at 10 and 20 C for 1 and 2 wk, respectively. Spores of E. cuniculi remained infectious in 10 ppt seawater at 10 and 20 C for 2 wk but not at higher salinities. These findings indicate that the spores of the 3 species of Encephalitozoon vary in their ability to remain viable when exposed to a conservative range of salinities and temperatures found in nature but, based strictly on salinity and temperature, can potentially remain infectious long enough to become widely dispersed in estuarine and coastal waters.     

Cryptobia salmositica: susceptibility of infected rainbow trout, Salmo gairdneri, to environmental hypoxia

Using the sealed jar technique (also called residual oxygen bioassay), rainbow trout fry infected with Cryptobia salmositica were more susceptible than non-infected fish to environmental hypoxia. The Winkler technique (azide modification) was used to determine the residual dissolved oxygen in the water. Susceptibility of infected fish increased with 1) time after infection and was most evident in 3-7 wk infections, 2) the severity of anemia, and 3) increasing parasitemia. In prolonged infections, susceptibility was reduced when there were decreases in anemia and parasitemia; however, these infected fish were still more susceptible than non-infected fish. The increase in susceptibility of infected fish to hypoxia may be an important contributing factor to mortality of fish in hatcheries where there is inadequate water flow and overcrowding. The sealed jar technique is recommended in future studies on the pathogenesis of parasitic fish diseases, especially if the metabolic and/or respiratory systems are affected by the infection.     

Depletion of eosinophils by anti-IL-5 monoclonal antibody treatment of mice infected with Trichinella spiralis does not alter parasite burden or immunologic resistance to reinfection.

Mechanisms of parasite killing by eosinophils are widely studied and are often implicated in mediating resistance to parasitic infection, especially in conjunction with specific antibodies. Evidence for the eosinophil as an anti-parasite killer cell in vivo is limited and may not justify the belief that eosinophils engage and/or kill infective helminths. We reexamined this question in a mouse model of trichinosis in which antisera to eosinophils were previously used to show the requirement for eosinophils in resistance to this nematode. The current studies used mAb to IL-5 to suppress eosinophil levels in CF1 mice infected with Trichinella spiralis. In mice given a primary infection and injected with an isotype control mAb or left untreated, the medullary and peripheral blood eosinophil numbers peaked at 3 wk postinfection (PI) and returned to baseline levels by 4 wk PI. Peripheral blood eosinophil numbers in infected mice injected with anti-IL-5 were maintained at levels below those of uninfected normal mice through 4 wk of infection. Histologically, there was a prominent eosinophil accumulation in infected, untreated, or control-mAb-treated mice associated with nurse cell complexes containing infective juveniles in skeletal muscle at 3 and 4 wk PI. This was largely eliminated in mice treated with anti-IL-5 mAb. However, the number of muscle stage juvenile worms recovered 3 and 4 wk PI after acid pepsin digestion was unaffected by eosinophil depletion. Challenge infections, in which mice were infected at day 0 with 125 muscle stage worms and challenged at day 28 PI with 350 muscle stage worms, developed peak eosinophil numbers in bone marrow and peripheral blood 3 wk after primary infection and 2 wk after challenge infection in mice receiving either no treatment or control mAb. In challenged mice receiving anti-IL-5 mAb, medullary and peripheral blood eosinophil numbers remained at or below those of uninfected animals. Although all groups exhibited significant resistance measured as muscle stage worm burdens 56 days PI, eosinophil depletion did not affect resistance of muscle worm recovery. These results suggest that eosinophils are not essential in the control of T. spiralis in either primary or challenge infections of CF1 mice. This in vivo study illustrates the questionable value of in vitro killing assays to assign effector function to any single inflammatory cell type.     

Involvement of Manayunkia speciosa (Annelida: Polychaeta: Sabellidae) in the life cycle of Parvicapsula minibicornis, a myxozoan parasite of Pacific salmon

A coelomic myxozoan infection was detected in freshwater polychaetes, Manayunkia speciosa from the Klamath River, Oregon/California, a site enzootic for the myxozoan parasites Ceratomyxa shasta and Parvicapsula minibicornis. The tetractinomyxon type actinospores had a near-spherical spore body 7.9 x 7.1 microm, with 3 spherical, protruding polar capsules, no valve cell processes, and a binucleate sporoplasm. Parvicapsula minibicornis-specific primers Parvi1f and Parvi2r amplified DNA from infected polychaetes in a polymerase chain reaction (PCR) assay. The small subunit 18S rRNA gene of the spores was sequenced (GenBank DQ231038) and was a 99.7% match with the sequence for P. minibicornis myxospore stage in GenBank (AF201375). Chinook salmon (Oncorhynchus tshawytscha) exposed to a dose of 1,000 actinospores per fish tested PCR positive for P. minibicornis at 14 wk postinfection and presporogonic stages were detected in the kidney tubules by histology at 20 wk. This life cycle is 1 of only about 30 known from more than 1,350 myxozoan species, and only the second known from a freshwater polychaete.     

Modulation of granulocyte responses in three-spined sticklebacks Gasterosteus aculeatus infected with the tapeworm Schistocephalus solidus

Leukocytes isolated from the head kidney and peripheral blood of 3-spined sticklebacks Gasterosteus aculeatus L. were analysed by means of flow cytometry during infection with the tapeworm Schistocephalus solidus (Müller, 1776). Although parasites increased their body weight continuously throughout the observation period (98 d), proportions of granulocytes increased in blood and head kidney only up to Day 63 post-infection (p.i.). Thereafter, declining proportions of granulocytes were observed in both organs. Thus the relative decrease in granulocyte number was not correlated to a decline in the parasitic load of the fish. To investigate a possible modulatory impact of S. solidus on granulocyte function, head kidney leukocytes were isolated at times before Day 63 p.i. and tested in vitro for their capacity to produce reactive oxygen species (ROS). Head kidney leukocytes from S. solidus-infected fish, analysed immediately after isolation (ex vivo, Day 40 p.i.), exhibited a higher ROS production when stimulated with phorbol myristate acetate (PMA), than leukocytes from naive, sham-treated control fish and fish that had resisted or cleared the infection (exposed but not infected). The latter showed an increased spontaneous ROS production that was not correlated to the numbers of granulocytes present in the head kidney isolates. In infected sticklebacks, spontaneous and PMA-induced ROS production was significantly correlated with numbers of granulocytes present in the head kidney isolates, suggesting that elevated ROS production was due to higher numbers of responding cells rather than an increased capacity of single cells. In vitro, after cultivation for 4 d in the presence of pokeweed mitogen (PWM) or extracts from S. solidus, head kidney leukocytes from control fish showed an increased ROS production and phagocytic activity compared with non-stimulated control cultures. In contrast, head kidney leukocytes from infected fish isolated on Days 48 and 44 p.i., failed to respond to S. solidus antigens in vitro. During S. solidus infection, granulocyte mobilisation resulted in elevated numbers of these cells in head kidneys, but the lack of an in vitro response to S. solidus antigens indicates an in vivo priming of granulocytes by the parasite. These observations may reflect the ability of S. solidus to impair the host's immune response once the parasite is developing in the body cavity of G. aculeatus.     

Marine netpen farming leads to infections with some unusual parasites

Marine netpen farming of salmonid fishes is a rapidly growing industry in several countries. With this relatively recent industry, new or unusual infections by parasitic pathogens have been observed. This is due to different hosts being reared in new geographic areas, or by indigenous species being reared in a different environmental condition, i.e. the marine netpen. Examples of the former include Kudoa thyrsites (Myxozoa) and Hemobaphes disphaerocephalus (Copepoda) infections in Atlantic salmon (Salmo salar) reared in the Pacific Northwest, Ceratothoa gaudichaudii (Isopoda) infections in Atlantic salmon reared in Chile, Neoparamoeba (=Paramoeba) sp. (Sacromastigophora) from salmonids reared in Tasmania, and Stephanostomum tenue (Digenea) infections in rainbow trout (Oncorhynchus mykiss) reared in Atlantic Canada. Chinook salmon (Oncorhynchus tshawytscha) reared in its native region, the Pacific Northwest, provides some examples of unusual or more severe infections than those normally seen in wild or freshwater reared chinook salmon. These include infections by Loma salmonae (Microsporidia), Gilguina squali (Cestoda) and the rosette agent, an undescribed fungus-like organism related to choanoflagellates. As the industry continues to expand, it is certain that more novel host-parasite relationships will be observed, providing challenges for fish farmers and parasitologists.