channel catfish virus disease
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IdentityTop of page
Preferred Scientific Name
- channel catfish virus disease
OverviewTop of page
Channel catfish virus disease (CCVD) is caused by a herpesvirus designated Ictalurid herpesvirus 1 by the International Committee on Taxonomy of Viruses, but the commonly used name is channel catfish virus (CCV). CCV affects channel catfish (Ictalurus punctatus) in the United States of America. For more detailed reviews of the condition, see Wolf (1988) or Plumb (1999).
CCVD is of importance because of its clinical and economic consequences in channel catfish farming. CCVD results in high mortality rates in populations of fry and juvenile catfish. Diseased fish demonstrate ascites, exophthalmia and haemorrhage in fins and musculature. Histologically the most remarkable damage occurs in the kidney with extensive necrosis of renal tubules and intersititial tissue.
In survivors, CCVD results in a strong protective immunity, the synthesis of circulating antibodies to the virus, and a covert latent carrier state. During this latent carrier state the virus is undetectable by traditional culture or antigen-detecting methods, even when adults are immunosuppressed during spawning.
On the basis of antigenic studies conducted with polyclonal rabbit antibodies, CCV isolates form a homogeneous group. However, the use of monoclonal antibodies shows some variation in antigenic determinants among isolates (Arkush et al., 1992). Some variation in the virulence of CCV strains has been recorded during natural outbreaks of disease and has been demonstrated experimentally. Additionally, molecular data indicate genetic variation within this species (Coyler et al., 1986; Vanderheijden et al., 1999).
Reservoirs of CCV are clinically infected fish and covert carriers. Infectious CCV can be detected in the water from tanks of experimentally infected fish, but the route of shedding has not been determined. The sites where the virus is most abundant during the course of overt infection are: posterior kidney, skin, gill, spleen and intestine, respectively, in decreasing magnitude (Plumb, 1971; Kancharla and Hanson, 1996). The transmission of CCV is horizontal and vertical. Horizontal transmission may be direct or vectorial with water being the main abiotic vector. Animate vectors and fomites could also act in CCV transmission. Vertical transmission is thought to be common, but the mechanism of vertical transmission is not known as infectious virus has not been detected on the skin or in the sexual products of spawning adults. Once CCVD occurs in a fish population, survivors of the disease become covert carrier fish.
Channel catfish and the closely related blue catfish (Ictalurus furcatus) have been the only fish found to be infected with CCV, and variations in susceptibility to CCV have been recorded depending on fish strain. The age of the fish is extremely important for overt infection. Although experimental data suggest that older fish are susceptible to natural outbreaks of acute CCVD (Hedrick et al., 1987), the disease occurs almost exclusively in fish that are less than 1 year of age, and generally less than 4 months of age. Water temperature is the critical environmental factor. The mortality rate is high - above 27°C, but readily decreases and ceases below 18°C.
Diagnosis of CCVD is based on virus isolation in cell culture. Confirmatory testing is by immunological identification by neutralisation, immunofluorescence, enzyme-linked immunosorbent assay (ELISA) or polymerase chain reaction (PCR). Rapid techniques by immunofluorescence tests or ELISA are suitable mainly for diagnosis in clinically infected fish. Because virus protein or infectious virus is not produced, culture methods or antigen-based testing is of little use for carrier screening. Instead, detection of neutralising antibodies in a population of fish and, more recently, the use of PCR to detect latent CCV genomic DNA, are of more use.
Control methods currently rely on maintaining relatively low stocking densities and avoiding stressful handling of young fish during the summer months. Also, control policies and hygiene practices have been used, where practical, in catfish husbandry. The incubation of eggs and rearing of fry and juveniles in facilities separated from carrier populations are critical for preventing the occurrence of CCVD in a CCV-free fish production site. Because virus is only detected during active outbreaks, defining CCV-free status has been done largely from historical data or identifying populations that are seronegative to the virus. Recent use of PCR and hybridisation probes to detect latent CCV genomic DNA suggests that CCV is present in many populations that have no history of the disease (Wise and Boyle, 1985; Boyle and Blackwell, 1991; Baek and Boyle, 1996; Gray et al., 1999). Vaccination, although experimentally promising (Walczak et al., 1981; Zhang and Hanson, 1995, 1996), is not in use at this time.
Historically, awareness of a viral disease affecting fry and fingerlings began when the channel catfish industry expanded in the mid-1960s. Severe hatchery mortality occurred in the southern USA. Evidence for a herpesvirus aetiology and a proposed name of the disease were discussed by Fijan (1968) and Fijan et al. (1970). The virus was described in more detail by Wolf and Darlington (1971). Reviews are presented by Wolf (1988), Plumb (1989) and Davison (1994).
Channel catfish virus disease can be economically devastating and is considered a serious problem. It has been partially responsible for the closing of at least two catfish farms in the USA and causing decreased production in others (Plumb, 1988). Precise data on economic damage inflicted by CCV are not available.
[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.]
Hosts/Species AffectedTop of page
Natural outbreaks of CCVD occur almost exclusively in cultivated channel catfish. There is only one brief account of a natural outbreak in blue catfish (Ictalurus furcatus) fingerlings (Plumb, 1989). The virus has not been reported from wild channel or any other wild catfish.
Experimental induction of disease by i.p. injection of virus is possible in fingerlings of blue catfish and of channel catfish x blue catfish hybrids. However, CCVD could not be induced in these fish by oral administration of virus or by cohabitation with infected channel catfish. White catfish (Ictalurus catus) is susceptible to experimental infection, but disease incidence and mortality are low (Plumb, 1971a). Fingerlings of brown bullhead (Ameiurus nebulosus) and yellow bullhead (Ameiurus natalis) did not develop disease after injection of the virus (Plumb, 1989). Sheatfish, the African catfish (Clarias gariepinus), the Asian catfish (Clarias batrachus) and the bluegill (Lepomis macrochirus) are resistant to CCV (Plumb et al., 1985; Boon et al., 1988; Chumnongsitathum et al., 1988); the virus was detected in some specimens of these resistant species only within a few days of infection.
Plumb et al. (1975) found striking differences among strains of channel catfish fingerlings in their susceptibility to the virus. The interstrain hybrids can be significantly more resistant to infection than pure strains.
DistributionTop of page
Channel catfish virus and CCVD are endemic in reared channel catfish in most parts of the USA. Plumb (1994) listed 15 states as their range. Evidence suggests that there are infected local populations with no history of CCVD outbreaks. The CCVD status in other countries with channel catfish culture is not known. It is (or was) present in Honduras (Plumb, 1994) after a shipment of fry from the USA (J.A. Plumb, personal communication). After introduction of channel catfish into the former USSR, a syncytium-forming virus was isolated in BB cells from fish with the clinical signs of CCVD (A.E. Osadcaja, 1976, personal communication). Plumb (1989) reported similar information about CCVD and virus isolation after the import of channel catfish into Russia. Isolates from the two latter cases were not examined serologically, but they were most probably CCV.
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.
PathologyTop of page
At necropsy, the peritoneal cavity is hyperaemic and contains a clear, yellowish or slightly reddish fluid. Liver and kidney may be pale, with or without haemorrhage or petechiae. The spleen is congested and dark. A yellowish mucoid material, but no food, is found in the digestive tract.
The histopathology of CCVD is well documented (Wolf et al., 1972; Plumb et al., 1974; Major et al., 1975; Plumb and Gaines, 1975). Fish with natural and experimental infections show severe changes, consisting of oedema, haemorrhage and necrosis. Kidneys are the first and the most severely affected organ. The haematopoietic tissue shows an increase in lymphoid cells, oedema, necrosis and accumulation of macrophages. Necrosis and occasional haemorrhage develop in nephrons. The liver shows oedema, necrosis, haemorrhage and occasional eosinophilic cytoplasmic inclusions in the hepatocytes. The oedematous submucosa of the gastrointestinal tract shows multiple focal accumulations of macrophages and, in some specimens, haemorrhage. Necrosis and sloughing of intestinal lining are infrequent. The spleen is congested and its lymphoid tissue is reduced. Haemorrhage and mild necrosis are occasionally noted. Cardiac tissues may be affected by focal haemorrhage and/or necrosis.
The virus is most abundant in kidney, spleen, intestine and encephalon of overtly infected fish. Kancharla and Hanson (1996) found high virus quantities also in skin and gills of experimentally infected fingerlings.
DiagnosisTop of page
Infected fish swim convulsively, often in spirals. In terminal stages, they lie quietly on the bottom, respiring rapidly but superficially. Some or up to 50% of moribund fish may ‘hang’ head-up at the water surface, but this is not pathognomonic for CCVD.
External signs of disease can vary and depend on the degree of kidney dysfunction and capillary damage resulting from the replication of CCV. Some or all of the following signs are present: distension of abdomen, exophthalmia, swollen and protruding vent; haemorrhage at the base of ventral and caudal fins, in gills and skin (especially abdomen and peduncle); pale gills. Secondary infections with Flexibacter columnaris and/or aeromonads often occur at later stages of the disease and occasionally simultaneously, causing a combination of CCVD and secondary lesions as well as prolonged mortality.
The diagnosis of channel catfish virus disease (CCVD) is currently based on two direct methods: the isolation of channel catfish virus (CCV) in cell culture followed by its immunological identification (conventional approach), or the immunological demonstration of CCV antigen in infected fish tissues. The conventional approach is most common because the virus produces rapid cytopathic effect (CPE) in cell culture and there are no commercial sources of CCV-specific antiserum and custom produced antisera to CCV is often of low titre or has cross-reaction with fish tissue.
Due to insufficient knowledge of the serological responses of fish to virus infections, the detection of fish antibodies to viruses has not yet been recognised as a valuable diagnostic method for assessing the viral status of fish populations. However, the use of direct culture or detection of viral antigen is of little use in detecting carrier fish. Therefore, the identification of neutralising antibodies to CCV has more merit in screening carrier populations (Plumb, 1978). The antibody titres in carrier populations vary seasonally, with the lowest titres occurring in the late winter and early spring (Bowser and Munson, 1986). The validation of some serological techniques for diagnosis of certain fish virus infections could arise in the near future, rendering the use of fish serology more widely acceptable for diagnostic purposes.
Increased mortality among channel catfish fry or fingerlings during warm weather, especially after stress, warrants examination for CCVD and sampling for laboratory tests. Hydropic conditions in fish with external signs of columnaris disease or of other bacterial infections may also be an indication of primary involvement of CCVD. The OIE Manual (1995b) recommended the selection of a sample of ten moribund or clinically affected fish. Living or sacrificed specimens should be properly packed, labelled and transported under adequate cooling. They should not be frozen. It is preferable and recommended to collect viscera (including kidneys) from fish of 4-6 cm or kidney, spleen and encephalon from larger fish. Up to 1.5 g of such material from up to five fish should be pooled in a sterile vial with a fivefold volume of transport medium with antibiotics for suppression of bacterial contaminants. Whole fish shorter than 4 cm should be in such a transport medium. Material for examination should reach the laboratory at a time which allows processing within 24 or a maximum of 48 h after sampling.
Inocula for CCV isolation are prepared by homogenization of the sample, dilution 1:10, decontamination of supernatant with antibiotics or filtration and by making two additional tenfold dilutions. Channel catfish ovary cells are recommended for isolation (OIE Manual, 1995b). Aliquots of 100 ml from each of the three serial tenfold dilutions serve for inoculation of at least 2 cm2 of 24-hold and drained CCO cultures. After adsorption at 25-30°C for 0.5-1 h and addition of a medium buffered to maintain pH between 7.3 and 7.6, cultures are incubated at 25-30°C for 7 days. Positive and negative controls are mandatory. The cytopathic effect may become visible after 10-12 h in the form of focal cell granulation, which is soon followed by cell enlargement and formation of syncytia. If cultures inoculated with the test material remain negative, they should be subcultivated.
Formation of syncytia in CCO or BB cells is specific for CCV. Titres of CCV in infected fish may reach 105-106 TCID50 or pfu g–1 of tissue, but are usually lower, both in early and in late stages of an epizootic. Virus identification is carried out by virus neutralization, IFAT or ELISA, using positive and negative controls. The titre of neutralizing antibody solution for virus neutralization must be around 2000 in the 50% plaque reduction assay (OIE Manual, 1995b). The first monoclonal antibodies against CCV (Arkush et al., 1992) are opening better possibilities for identification, detection and quantification of CCV.
Attempts at viral isolation from survivors of CCVD outbreaks and from suspected brood-fish carriers were unsuccessful (Plumb and Jezek, 1983), until Bowser et al. (1985) examined a population suffering sustained mortality during the winter, using cocultivation of tissue extracts or leucocytes and blind passages of inoculated CCO cultures. Immunosuppression of brood fish by i.m. injection of dexamethasone increased the virus isolation rate by cocultivation of leucocytes to 100%. Using normal procedure and cocultivation, Wise et al. (1988) could not isolate virus from stressed, non-clinically infected fry. There are no further reports on testing of suspect carrier populations using the method described by Bowser et al. (1985).
The first indication of the CCV antigen in brood-fish ovaries was provided by Plumb et al. (1981), using an IFAT. Focal areas of fluorescence were recorded in spent ovaries from two immunosuppressed catfish and in the primary cell cultures from this tissue, but there was no virus replication in cultures. The authors believed the fluorescence to be a specific reaction, possibly with incomplete virus. Detection of latent CCV in clinically healthy catfish was successfully carried out by nucleic acid hybridization methods and by PCR. Wise and Boyle (1985) cloned the terminal fragment of the CCV genome and used it as a specific probe for detection of viral DNA. The probe demonstrated CCV DNA in liver and other soft tissues and in erythrocytes of some channel catfish with no history of CCVD (Wise et al., 1985). Bird et al. (1988) selected probes for detection of viral DNA expressed late in infection and one of them was highly sensitive for CCV-specific sequences. Boyle and Blackwell (1991) applied the PCR for detection of CCV DNA in latent carrier fish. Kancharla and Hanson (1996) developed a quantitative PCR which detected over 500 times more virus DNA molecules than the plaque assay of Buck and Loh (1985). Gray et al., (1999) used PCR to detect virus 140 days after infection and were able to determine the genome was present in circular or concatameric configurations. Refinements of these techniques may lead to the selection of appropriate testsfor diagnostic procedures. The OIE Manual (1995b) disclosed that ELISAs using certain monoclonal antibodies to virus nucleocapsid antigen may become the recommended procedure for the detection of virus carriers by screening fish for viral antigen in the encephalon.
List of Symptoms/SignsTop of page
|Finfish / Bursts of abnormal activity - Behavioural Signs||Aquatic:Larval,Aquatic:Fry||Diagnosis|
|Finfish / Bursts of abnormal activity - Behavioural Signs||Aquatic:Larval,Aquatic:Fry||Diagnosis|
|Finfish / Change in shape (e.g. distension) - Eyes||Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / 'Dropsy' - distended abdomen, 'pot belly' appearance - Body||Aquatic:Larval,Aquatic:Fry||Diagnosis|
|Finfish / Fish sinking to bottom - Behavioural Signs||Aquatic:Larval,Aquatic:Fry||Diagnosis|
|Finfish / Fish swimming near surface - Behavioural Signs||Aquatic:Larval,Aquatic:Fry||Diagnosis|
|Finfish / Fish swimming near surface - Behavioural Signs||Aquatic:Larval,Aquatic:Fry||Diagnosis|
|Finfish / Generalised lethargy - Behavioural Signs||Aquatic:Larval,Aquatic:Fry||Diagnosis|
|Finfish / Haemorrhagic lesions - Skin and Fins||Aquatic:Larval,Aquatic:Fry||Diagnosis|
|Finfish / Increased respiratory rate (increased opercular movements) - Behavioural signs||Aquatic:Larval,Aquatic:Fry||Diagnosis|
|Finfish / Loss of balance - Behavioural Signs||Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / Mortalities -Miscellaneous||Aquatic:Larval,Aquatic:Fry||Diagnosis|
|Finfish / Paleness - Gills||Aquatic:Larval,Aquatic:Fry||Diagnosis|
|Finfish / Pop-eye - Eyes||Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / Skin erosion - Skin and Fins||Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / Skin erosion - Skin and Fins||Aquatic:Larval,Aquatic:Fry||Sign|
|Finfish / Swollen or protruding vent - Body||Aquatic:Larval,Aquatic:Fry||Sign|
Disease CourseTop of page
The first sign of a CCVD outbreak in ponds is an increase in morbidity and mortality at temperatures above 25°C. The course of an outbreak without secondary infection is acute. Most fish die within 10 days and mortality normally ceases within 2-3 weeks. Mortality can vary from low to almost 100%, but 40-60% is common.
Radiolabelled CCV enters fish through gills and possibly also through the intestine and is concentrated in the liver (Nusbaum and Grizzle, 1987a). The kidney seems to be the primary site of virus replication, followed by other parenchymatous organs (Plumb, 1971b). A special (antiviral) class of cytotoxic cells from catfish peripheral blood leucocytes is capable of lysing virus-infected cells in vitro (Hogan et al., 1996). Fast virus replication in the host causes a short incubation time of about 3 days at 25-30°C and of about 10 days at 20°C. Destruction of infected cells leads to major damage of the circulatory system and of excretion causing osmotic imbalance as well as haemorrhage. Data on haematology and other clinical parameters are lacking.
The virus elicits a variable humoral immune response and resistance to reinfection. Plumb (1973b) was the first to recognize anti-CCV neutralizing antibodies in sera. Brood stock which had produced virus-infected fingerlings for 2 consecutive years had fairly constant neutralization indices throughout 1 year of examination. Gratzek et al. (1973) described virus neutralization in microcultures for quantitation of neutralizing antibodies. Heartwell (1975) characterized neutralizing antibodies as immunoglobulins. Virus neutralization activity can be found in juveniles 1 week after i.p. and i.m. infection (Plumb, 1973b; Heartwell, 1975) and at the same time after waterborne exposure of adults (Hedrick et al., 1987). Activity increases up to 9 weeks before declining. Survivors of experimental infection have anti-CCV activity in plasma 2 years after the last known exposure to virus (Hedrick et al., 1987). Under natural conditions, neutralizing antibodies can be found 4 weeks after the original disease outbreak (Bowser and Munson, 1986). Neutralizing antibodies may be absent in populations which suffer a low (0.1%) mortality (Amend and McDowell, 1983). Neutralizing antibody titres vary with water temperature and are highest during summer and lowest in winter (Bowser and Munson, 1986). Findings on farms with and without a history of CCVD indicate that vertical transmission with disease outbreaks in offspring occurs when brood stock have higher antibody titres and a higher percentage of positive sera (Plumb et al., 1981). Fish infected before 60 days post hatch may not develop protective immunity after surviving an initial challenge (Hanson et al., 2004) Continuing virus neutralization activity in sera seems to be stimulated by expression of certain viral antigens or periodic reactivation of virus (Hedrick et al., 1987). Concerning cellular immunity, Hogan et al. (1996) described a population of cytotoxic cells among peripheral blood leucocytes that killed CCV-infected cells. Even the early virus gene products rendered cells susceptible to lysis.
Juvenile catfish can be immunized passively by injection of antiserum from adults (Hedrick and McDowell, 1987).
EpidemiologyTop of page
Channel catfish virus disease occurs during warm weather (Fijan et al., 1970), from May to September (Plumb, 1971a). Outbreaks are more frequent in years with high water temperatures (Plumb, 1989). The importance of high temperatures for development of the disease is documented by experimental data. Virus-injected susceptible fingerlings suffer no or a low mortality when kept at or below 15°C and the moving of infected fish from 28 to 19°C markedly reduces mortality (Plumb, 1973a). Channel catfish virus disease affects up to 10 cm channel catfish in ponds, raceways or holding tanks. Adult channel catfish raised in the laboratory without contact with CCV as juveniles are susceptible to infection by bath and single fish are killed (Hedrick et al., 1987).
Virus infectivity is inactivated by ether, chloroform and glycerol. It is sensitive to acid pH, heat and UV light and is unstable in sea water (Robin and Rodrigue, 1980a). Under simulated farm pond conditions, CCV survives less than 24 h on dried concrete chips and less than 48 h on glass cover slips or dried fishnets and is immediately inactivated by pond mud (Plumb, 1974). The finding of Brady and Ellender (1982) that soil sediment rapidly absorbs the virus helps explain the immediate inactivation by pond mud. In pond water the virus persists for about 2 days at 25°C and about 28 days at 4°C, but somewhat longer in dechlorinated tap water (Plumb et al., 1973).
Reservoirs of virus are the overtly and the dormantly infected fish. Transmission is mostly horizontal but the claimed vertical or ‘egg associated’ transmission from carrier brood fish to eggs and fry seems to be important for virus survival and for perpetuation of infection in catfish culture.
Horizontal transmission occurs by contact and through water, and is easily demonstrable by cohabitation of virus-free catfish with infected fish. Channel catfish virus is probably shed via faeces and urine. Fingerlings infected by bath and kept at 28°C shed the virus from the second to the sixth day in considerable quantities (Kancharla and Hanson, 1996). Plumb (1988) assumed that fingerlings contracted the virus by cannibalizing dead or moribund fish with CCVD. The short CCV survival in pond water and mud and on tools indicates a low significance of vectorial transmission over long time intervals. The role of biological vectors has not been investigated. Nothing is known about potential virus reservoirs in natural catfish populations.
Plumb and Jezek (1983) never isolated the virus from suspected brood fish. Nusbaum and Grizzle (1987b) could not demonstrate the vertical transmission. Yet there is circumstantial epizootiological and other evidence for vertical transmission. Outbreaks of CCVD in progeny of brood stock with high titres of CCV-neutralizing antibodies were regular (Amend and McDowell, 1984), and the viral antigen was present in ovaries of spent females (Plumb et al., 1981). The virus was isolated from brood fish in the winter (Bowser et al., 1985) and the latent virus was detected in adult and in brood fish with no clinical signs and in their apparently healthy offspring, using hybridization methods or PCR (Wise and Boyle, 1985; Wise et al., 1985, 1988; Boyle and Blackwell, 1991). Hanson et al. (2004), found vertical transmission to occur at a rate of 40-75% in fry from carrier parents. Egg infection, if it occurs, is accomplished by different mechanisms from those involved in the surface infection of salmonid eggs by IHN virus (Nusbaum and Grizzle, 1987b).
The disease is easily induced in susceptible channel catfish fry and fingerlings by exposure to virus in water, swabbing the gills or feeding with virus, as well as by i.p. or i.m. injection (Fijan et al., 1970). However, some attempts to induce CCVD by exposure to virus in water have failed (Wolf et al., 1972; McConnell and Austen, 1978) for unknown reasons. Some adult fish can replicate CCV after water-borne exposure (Hedrick et al., 1987).
Strain and age of fish and water temperature are the decisive predisposing factors for outbreaks of CCVD. Hanson et al., 2004, found that fish under 60 days post hatch (dph) were resistant to immersion infection, and that only fish older than 60 dph developed antibodies. Resistance was greatest in fry from CCV positive parents.
Overt disease develops at an age between 2 weeks and 6 months. Natural overt infections are generally confined to fish weighing less than 10 g. Virus injection induces disease in fish of up to 50 g (Plumb, 1971a) and the virus has been occasionally isolated from 1-year-old fish (Plumb, 1989). Experimental water-borne infection of adult channel catfish with no prior viral contact resulted in very low mortality. Survivors become asymptomatic carriers, with specific neutralizing antibodies (Hedrick et al., 1987).
Impact SummaryTop of page
|Fisheries / aquaculture||Negative|
ReferencesTop of page
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ContributorsTop of page
Department of Pathobiology, College of Veterinary Medicine, Auburn University, AL 36849, USA
R Curtis Bird
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