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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
International Common Names
- English: coho salmon syndrome; huito disease; parenthesis disease; Piscirickettsia salmonis infection; rickettsial infections of fish; salmon rickettsial disease; salmonid rickettsial septicaemia; salmonid rickettsial septicemia
OverviewTop of page
Piscirickettsiosis is a septicaemic condition of salmonids. The causative agent of the disease is Piscirickettsia salmonis (ATCC VR-1361), and the type strain is LF-89T (Fryer et al., 1992; Garcès et al., 1991). Thus far the disease has been described from Chile (Bravo and Campos, 1989; Fryer et al., 1990), Ireland (Palmer et al., 1997; Rodger and Drinan, 1993), Scotland (Birrell et al., 2003; Grant et al., 1996), Norway (Olsen et al., 1997), and both the west (Brocklebank et al., 1992; Evelyn, 1992) and east (Jones et al., 1998) coasts of Canada.
Piscirickettsia salmonis has been detected in coho salmon (Oncorhynchus kisutch), chinook salmon (O. tshawytscha), cherry salmon (O. masou), rainbow trout (O. mykiss), pink salmon (O. gorbuscha) and Atlantic salmon (Salmo salar). Coho salmon are believed to be most susceptible (Fryer et al., 1992; Smith et al., 1996). Mortality in seawater net pens was reported to be 30-90% among coho salmon reared in Chile (Bravo and Campo, 1989).
Piscirickettsiosis has been primarily reported in marine fish farms, but has also been observed in freshwater facilities (Bravo, 1994; Gaggero et al., 1995). Horizontal transmission occurs in saltwater and freshwater (Almendras et al., 1997; Cvitanich et al., 1991). The observations of P. salmonis (Chen et al., 2000) and P. salmonis-like organisms (Mauel and Miller, 2002) in marine fish suggest that reservoirs for the bacterium exist in the marine environment. The potential for vertical transmission has been demonstrated (Larenas et al., 2003,1996b), although the frequency of transmission by this route is not yet known.
Although antibacterial treatment provides some benefit, it is not entirely effective as a means of controlling the disease. Currently, oxalinic acid appears to be the drug of choice. Eggs may be disinfected as part of good hatchery practice.
The disease is a chronic, systemic infection that generally affects salmonids reared in seawater. All ages are susceptible, from smolts to market size fish. Signs of the disease both external and internal are well documented (Fryer and Lannan, 1996; Fryer and Hedrick, 2003; Cvitanich et al., 1991; Fryer et al., 1990; Olsen et al., 1997; Rodger and Drinan, 1993). The disease begins approximately 1 month after fish are introduced into the seawater net pens, and the organism was thought to be a marine bacterium.
A range of gross signs of infection may be present in salmonids infected with P. salmonis. Severely affected fish are dark, anorexic and lethargic. They often swim near the surface or edges of the cages. Fish with milder infections often show no abnormal external signs. Infections of the brain may cause erratic swimming behaviour (Skarmeta, 2000). Skin lesions, appearing as small white patches that can progress to shallow ulcers, may also be present on some fish. Perhaps the most consistent external signs observed during P. salmonis infections are pale gills resulting from a significant anaemia, but this is not pathognomonic for the disease.
Consistent with many systemic, chronic inflammatory diseases of salmonids, the internal signs are a swollen and discoloured kidney and an enlarged spleen. Ascites in the peritoneum may be present and haemorrhages on the visceral fat, stomach, swim bladder, and body musculature can also occur (Cvitanich, 1991; Schafer et al., 1990). Hallmark internal lesions of the disease are found in the liver, which may exhibit large, whitish or yellow, multifocal, coalescing, pyogranulomatous nodules. These lesions often rupture, resulting in shallow crater-like cavities in the liver. Whereas these liver lesions are somewhat unique to piscirickettsiosis, many fish with the disease do not exhibit them.
The most prominent histological changes are found in the liver, kidney, spleen and intestine, but pathological changes in the brain, heart, ovary and gill can also be observed (Branson and Nieto Diaz-Murroz, 1991; Chen et al., 2000; Cvitanich et al., 1991; Palmer et al., 1997; Schafer et al., 1990). Multifocal necrosis of hepatocytes, accompanied by a chronic inflammatory infiltrate of mononuclear cells, is observed in the liver. Vascular and perivascular necrosis are also evident in the liver, and intravascular coagulation resulting in fibrin thrombi within major vessels is a common finding. The focal areas of necrosis underlie the pale circular lesions observed grossly in more chronically infected fish. In more acute infections, the coalescence of areas of necrosis results in a more mottled appearance to the organ rather than discrete nodules. Granulomatous inflammation also occurs in the interstitium and parenchyma of the kidney and spleen, respectively. Vascular changes similar to those in the liver may also be observed in the kidney and spleen. Meningitis, endocarditis, peritonitis, pancreatitis, and branchitis may be observed with accompanying chronic inflammatory and vascular changes similar to those in the liver and haematopoietic organs. The ovary was reported to be involved in certain infections in coho salmon (Cvitanich, 1991).
High magnification examination of lesions reveals aggregates of the organism in the cytoplasm of degenerated hepatocytes and in macrophages. Infected macrophages are usually hypertrophied and replete with cellular debris. In tissue sections stained with haematoxylin and eosin (H&E), the organism appears as basophilic or amphophilic spheres, about 1 µm in diameter.
[Based upon material originally published in Woo PTK, Bruno DW, eds., 1999. Fish diseases and disorders, Vol. 3 Viral, bacterial and fungal infections. Wallingford, UK: CABI Publishing.]
Host AnimalsTop of page
|Animal name||Context||Life stage||System|
|Atractoscion nobilis||Domesticated host||Aquatic: Adult||Enclosed systems/Cages|Enclosed systems/Pens|
|Oncorhynchus gorbuscha (pink salmon)||Domesticated host||Aquatic: Fry||Enclosed systems/Cages|Enclosed systems/Pens|
|Oncorhynchus kisutch (coho salmon)||Domesticated host||Aquatic: All Stages||Enclosed systems/Cages|Enclosed systems/Pens|
|Oncorhynchus masou masou (cherry salmon)||Domesticated host||Aquatic: All Stages||Enclosed systems/Cages|Enclosed systems/Pens|
|Oncorhynchus mykiss (rainbow trout)||Domesticated host||Aquatic: All Stages||Enclosed systems/Cages|Enclosed systems/Pens|
|Oncorhynchus tshawytscha (chinook salmon)||Domesticated host||Aquatic: All Stages||Enclosed systems/Cages|Enclosed systems/Pens|
|Salmo salar (Atlantic salmon)||Domesticated host, Wild host||Aquatic: Adult||Enclosed systems/Cages|Enclosed systems/Pens|
Hosts/Species AffectedTop of page
Piscirickettsia salmonis and the disease it causes primarily affects members of the family Salmonidae. Although coho salmon seem to be the most susceptible species, the disease has been reported in cultured rainbow trout and Atlantic, Chinook and cherry salmon in Chile (Bravo, 1994). In Britsh Columbia, Canada, chronic losses have occurred in Chinook and juvenile pink salmon (Evelyn et al., 1992). A comparison of the virulence of P salmonis isolates from coho salmon from Chile, British Columbia and Norway demonstrated clear differences, with the Chilean isolate (LF-89) inducing the greatest losses and the isolate from Norway showing the lowest virulence (House et al., 1999).
The only non-salmonid host confirmed to be infected with P. salmonis are captive white seabass (Atractoscion nobilis) from California, USA (Chen et al., 2000). The isolate that caused disease in these fish was also found to possess virulence for coho salmon (Chen et al., 2000). Piscirickettsia-like organisms have been reported in additional nonsalmonid fish (Fryer and Hedrick, 2003; Mauel and Miller, 2002), but the relationship of these isolates to P. salmonis is not yet clear.
DistributionTop of page
Observation and/or isolation of P. salmonis is currently confined to salmonids from Chile, BC Canada, Norway, Ireland and Scotland. It is probable that the condition was first recognized in Canada during the early 1970s and referred to as ‘parenthesis disease’ (Evelyn, 1992). Numerous descriptive names for the disease include: coho salmon syndrome, piscirickettsiosis, salmonid rickettsial septicaemia, Huito disease and UA (unknown agent).
By the mid-1980s, the disease was recognized among cultured salmonids in Region X of Chile (Bravo and Campos, 1989). Here, recurring outbreaks resulted in losses of coho salmon exceeding 90% at numerous production fish farms. Piscirickettsia salmonis (ATL-4-91) was isolated in 1992 from diseased Atlantic salmon held in salt water in BC Canada (Brocklebank et al., 1992).
A bacterium similar to P. salmonis is associated with low-level mortality in Atlantic salmon held in salt-water net-pens in Norway (NOR-92; Olsen et al., 1993) and Ireland (Rodger and Drinan, 1993). These pathogenic microorganisms were all identified as P. salmonis by analysis of the 16S rRNA gene sequence (Mauel, 1996; Mauel et al., 1999), or by PCR (Mauel et al., 1996; House and Fryer, 2002).
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Atlantic, Northeast||Present||Olsen et al., 1993; Rodger and Drinan, 1993; Grant et al., 1996; Birrell et al., 2003|
|Atlantic, Northwest||Present||Jones et al., 1998|
|Pacific, Eastern Central||Present||Fryer et al., 1990; Garcés et al., 1991; Gaggero et al., 1995|
|Pacific, Northeast||Present||Evelyn, 1992|
|Canada||Present||Evelyn, 1992; Jones et al., 1998|
|-British Columbia||Present||Evelyn, 1992|
|USA||Present||Present based on regional distribution.|
|-California||Present||Chen et al., 2000|
|Chile||Present||Fryer et al., 1990; Garcés et al., 1991; Gaggero et al., 1995|
|Ireland||Present||Rodger and Drinan, 1993|
|Norway||Present||Olsen et al., 1993|
|UK||Present||Present based on regional distribution.|
|-Scotland||Present||Birrell et al., 2003|
PathologyTop of page
The histopathology associated with natural and experimental infections of P. salmonis has been described (Branson and Nieto Diaz-Munoz, 1991; Cvitanich et al., 1991; Garcès et al., 1991; Almendras et al., 2000). Pathological changes occur throughout internal organs, with the most severe manifestations of the disease in the intestine, kidney, liver and spleen. In the kidney and spleen, the normal haematopoietic and lymphoid tissues are replaced with chronic inflammatory cells and host-cell debris. Liver lesions are severe and rickettsiae are often seen in the cytoplasm of degenerating hepatocytes. Inflammation of the lamina propria of the large intestine is common and often results in necrosis and sloughing of the mucosal epithelium. Hyperplasia of gill epithelia results in fusion of the lamellae. Pathological changes in the heart and other organs are variable but disseminated intravascular coagulation is common.
The humoral response of rainbow trout experimentally infected with P. salmonis was investigated by Kuzyk et al. (1996). The infected fish did not produce a strong antibody response. The antibody response was directed against protein antigens (ranging from 10-70 kDa), a carbohydrate antigen and the OspA lipoprotein (Kuzyk et al., 2001a). Absence of a significant antibody mediated response is typical of infections caused by intracellular pathogens, and the role of cell mediated immunity against P. salmonis should be investigated.
DiagnosisTop of page
In Chile, mortality from P. salmonis usually occurs in the autumn, approximately 6-12 weeks after fish are transferred from freshwater to saltwater net-pens, and again the following spring (Bravo and Campos, 1989; Fryer et al., 1990; Cvitanich et al., 1991). Although PRS is usually associated with fish in estuaries or marine environments, there have been reports of the disease in juvenile salmonids held in freshwater (Gaggero et al., 1995).
External signs of disease are variable but include lethargy, anorexia, pale gills and darkened body coloration. Infected fish often have skin lesions that range from small areas of raised scales to shallow haemorrhagic ulcers (Branson and Nieto Diaz-Munoz, 1991). However, in acute infections, mortality may occur without gross signs of disease. Internally, the rickettsiae spread systemically, resulting in swollen kidneys and spleens. Although not common in infected fish (5-10%), the most diagnostic lesions occur in the liver as grey to yellow mottled areas or as ring-shaped foci (Cvitanich et al., 1991; Lannan and Fryer, 1993). Petechial haemorrhages also occur in visceral organs and adipose tissue. Microscopically, these changes are accompanied by extensive necrosis of haematopoietic tissues. Haematocrits generally fall below 25% and large numbers of macrophages containing P. salmonis cells and cellular debris can be detected in peripheral blood smears. The rickettsiae are seen within cytoplasmic vacuoles of cells from the kidney and other organs. Macrophages filled with rickettsial cells are common.
Isolation of P. salmonis in cell culture and microscopic observations of stained tissue imprints or smears are effective methods to detect rickettsiae in infected fish tissue. However, confirmation of P. salmonis must be made using serological or molecular methods.
Kidney tissue is recommended for isolating the rickettsia in cell culture. The tissue is aseptically removed and kept at 4°C, as the bacterium is sensitive to both elevated and freezing temperatures. Piscirickettsia salmonis replicates in a number of fish cell lines, including chinook salmon embryo (CHSE-214) (ATTC CRL 1681), chum salmon heart (CHH-1) (ATCC CRL 1680), rainbow trout gonad (RTG-2) (ATCC CCL 55), epithelioma papulosum cyprini (EPC) (Fijan et al., 1983) and fathead minnow (FHM) (ATCC CCL 71) (Wolf and Quimby, 1962; Fryer et al., 1990). Because the organism is sensitive to most of the antibiotics routinely used in cell culture, tissue is inoculated on to cells maintained in antibiotic-free medium. Inoculated cultures are incubated at the optimal growth temperature of 15-18°C and observed up to 28 days for appearance of CPE. Characteristic CPE appears as clusters of rounded cells with large vacuoles and, at primary isolation, may require 21 or more days to appear. In subsequent passages, CPE becomes apparent 4-7 days after inoculation.
Although isolation in cell culture provides a sensitive method for detection, there are disadvantages. Conditions in the field are rarely ideal for a septic necropsy and the incubation period further delays results. The necessary absence of antibiotics in the culture medium requires substantial efforts to prevent introduction of contaminating organisms.
A less sensitive but more rapid method for diagnosis of a rickettsial infection in fish is by microscopic examination of smears or imprints of kidney, liver or spleen tissue stained with Giemsa or acridine orange stain (Lauer et al., 1981; Lannan and Fryer, 1991). However, following initial detection in stained tissue smears or cell cultures, the identity of P. salmonis must be confirmed by means of serological methods, e.g. immunofluorescence (Lannan et al., 1991; Larenas et al., 1996a; Jamett et al., 2001), immunohistochemistry (Alday-Sanz et al., 1994), enzyme-linked immunosorbent assay (Aguayo et al., 2002) or molecular techniques (Mauel et al., 1996; Marshall et al., 1998; Heath et al., 2000; House and Fryer, 2002).
Gross and microscopic changes resulting from piscirickettsiosis are not are unique enough to allow for definitive diagnosis of the disease. Therefore, screening for and diagnosis of piscirickettsiosis is based on detection of the causative agent. Presumptive diagnosis can be achieved by the visualisation of the causative agent within macrophages or hepatocytes in histological sections or tissue imprints. Confirmatory diagnosis is achieved by isolation of Piscirickettsia salmonis in cell culture, but it does not grow on any known artificial bacteriological media. Confirmation of P. salmonis in culture may be made by indirect fluorescent antibody test (IFAT) or polymerase chain reaction (PCR) assay.
PCR assays can also be conducted directly on tissues (Marshall et al., 1998; Mauel et al., 1996; House and Fryer, 2002), and thus PCR assays on tissues along with the observation of suspect organisms within macrophages or hepatocytes are also suitable methods for confirmatory diagnosis. In an effort to provide a nonlethal sampling test for monitoring populations, Marshall et al. (1998) developed a PCR assay that utilized a small volume of fish serum. A variety of molecular methods have been developed that provide the ability to distinguish among groups of isolates of P. salmonis by analyzing the sequences of the ITS region of the rRNA gene and to assess the number of P. salmonids genome copies (Heath et al., 2000; Casanova et al., 2003). Alternatively, P. salmonis can be detected with Giemsa-stained tissue smears, followed by IFAT for positive identification. An enzyme-linked immunosorbent assay for detecting P. salmonis is commercially available.
Piscirickettsia-salmonis-infected fish tissues suitable for examination in cell culture, PCR, tissue imprints and histology are kidney, liver and blood, collected from diseased fish during either overt or covert infections (Lannan and Fryer, 1991). Due to sensitivity of P. salmonis to antibiotics in vitro, none should be used in media during collection of tissue or the culture of cells.
List of Symptoms/SignsTop of page
|Finfish / Cessation of feeding - Behavioural Signs||Aquatic:Adult,Aquatic:Broodstock,Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / Darkened coloration - Skin and Fins||Aquatic:Adult,Aquatic:Broodstock,Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / Generalised lethargy - Behavioural Signs||Aquatic:Adult,Aquatic:Broodstock,Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / Haemorrhagic lesions - Skin and Fins||Aquatic:Adult,Aquatic:Broodstock,Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / Haemorrhaging - Body Cavity and Muscle||Aquatic:Adult,Aquatic:Broodstock,Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / Intestines swelling / oedema - Organs||Aquatic:Adult,Aquatic:Broodstock,Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / Intestines white-grey patches (haemorrhage / necrosis / tissue damage) - Organs||Aquatic:Adult,Aquatic:Broodstock,Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / Kidney swelling / oedema - Organs||Aquatic:Adult,Aquatic:Broodstock,Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / Liver - white / grey patches (haemorrhage / necrosis / tissue damage) - Organs||Aquatic:Adult,Aquatic:Broodstock,Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / Mortalities -Miscellaneous||Aquatic:All Stages||Sign|
|Finfish / Paleness - Gills||Aquatic:Adult,Aquatic:Broodstock,Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / Spleen white-grey patches (haemorrhage / necrosis / tissue damage) - Organs||Aquatic:Adult,Aquatic:Broodstock,Aquatic:Larval,Aquatic:Fry||Sign|
EpidemiologyTop of page
Transmission of P. salmonis in natural infections is fish-to-fish and no vector is required. It has been demonstrated that P. salmonis can survive 14 days in seawater (Lannan and Fryer, 1994), but the bacterium is almost immediately deactivated in freshwater (Lannan and Fryer, 1994). This may explain why the disease is less common under freshwater culture conditions. Under experimental conditions, horizontal transmission has been demonstrated in both freshwater and saltwater (Almendras et al., 1997; Cvitanich et al., 1991). Infectivity trials exposing the skin and gills to bacterial cultures and intubating bacteria into the intestine demonstrated the skin as the most efficient site of entry (Smith et al., 1999, 2004).
Marine reservoirs for P. salmonis have been suspected since the first isolation from coho salmon in Chile as an explanation for the onset of infections after transfer to seawater. Recent observations of P. salmonis (Chen et al., 2000) and P. salmonis-like (Mauel and Miller, 2002) organisms from a variety of marine fish and from bacterioplankton from seawater (Mauel and Fryer, 2001) provide evidence for marine reservoirs for the bacterium.
Recent laboratory studies have demonstrated that vertical transmission of P. salmonis can occur by a mechanism where the bacterium attaches to the ova by means of an attachment complex (Larenas et al. 2003). The infrequency of infection reported in juvenile fish in freshwater suggests that vertical transmission may not be common for this pathogen (Lannan and Fryer, 1994). However, because of the implications for control of P. salmonis, the role of vertical transmission remains an important area of research.
Impact SummaryTop of page
|Fisheries / aquaculture||Negative|
Impact: EconomicTop of page
Piscirickettsiosis has caused substantial economic losses to the salmon aquaculture industry of southern Chile. During 1989, this disease was considered to be the cause of death of an estimated preharvest 1.5 million coho salmon, ranging from 200 g to market-sized fish (Bravo and Campus, 1989). In the following year, major losses were also attributed to P. salmonis among farmed Atlantic salmon. Although still a major problem in the Chilean salmon industry, loss from the disease has declined in recent years as a result of rearing more resistant Atlantic salmon and improved methods of prevention and control (Hedrick and Fryer, 2003; Smith, 2004). Mortalities typically develop 10-12 weeks after the transfer of fish to seawater, generally occur between March and August, and last approximately 10 weeks before they diminish. Outbreaks of piscirickettsiosis in other countries have not reached the importance and prevalence of the Chilean outbreaks. For example, 0.6-15% mortality has been reported in Canada, Norway and Scotland (Birrell, 2003; Brocklebank, 1992; Olsen et al., 1993).
Zoonoses and Food SafetyTop of page
This species is not a zoonosis.
ReferencesTop of page
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Almendras FE; Fuentealba IC; Markham RFF; Speare DJ, 2000. Pathogenesis of liver lesions caused by experimental infection with Piscirickettsia salmonis in juvenile Atlantic salmon, Salmo salar L. Journal of Veterinary Diagnostic Investigation, 12(6):552-557.
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Fryer JL; Lannan CN, 1996. Rickettsial infections of fish. Annual Review of Fish Diseases, 6:3-13; 30 ref.
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Mauel MJ, 1996. Evidence for molecular diversity of Piscirickettsia salmonis. PhD thesis. Oregon, USA: Oregon State University, 104 pp.
Mauel MJ; Fryer JL, 2001. Amplification of a Piscirickettsia salmonis-like 16S rDNA product from bacterioplankton DNA collected from the coastal waters of Oregon, USA. Journal of Aquatic Animal Health, 13(3):280-284.
Mauel MJ; Giovannoni SJ; Fryer JL, 1996. Development of polymerase chain reaction assays for detection, identification, and differentiation of Piscirickettsia salmonis. Diseases of Aquatic Organisms, 26(3):189-195.
Mauel MJ; Giovannoni SJ; Fryer JL, 1999. Phylogenetic analysis of Piscirickettsia salmonis by 16S, internal transcribed spacer (ITS) and 23S ribosomal DNA sequencing. Diseases of Aquatic Organisms, 35(2):115-123.
Mauel MJ; Miller DL, 2002. Piscirickettsiosis and piscirickettsiosis-like infections in fish: a review. Veterinary Microbiology, 87(4):279-289.
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