Invasive Species Compendium

Detailed coverage of invasive species threatening livelihoods and the environment worldwide

Datasheet

channel catfish virus disease

Toolbox

Datasheet

channel catfish virus disease

Summary

  • Last modified
  • 14 July 2018
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • channel catfish virus disease
  • Overview
  • 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 af...

Don't need the entire report?

Generate a print friendly version containing only the sections you need.

Generate report

Pictures

Top of page
PictureTitleCaptionCopyright
External signs of channel catfish virus disease in fingerlings. A: Lateral view: distended abdomen and urogenital vent, bleedings at the bases of fins. B: Dorsal view: bilateral exophthalmia, abdominal distension and haemorrhage in anal fin.
TitleChannel catfish virus disease
CaptionExternal signs of channel catfish virus disease in fingerlings. A: Lateral view: distended abdomen and urogenital vent, bleedings at the bases of fins. B: Dorsal view: bilateral exophthalmia, abdominal distension and haemorrhage in anal fin.
CopyrightN. Fijan
External signs of channel catfish virus disease in fingerlings. A: Lateral view: distended abdomen and urogenital vent, bleedings at the bases of fins. B: Dorsal view: bilateral exophthalmia, abdominal distension and haemorrhage in anal fin.
Channel catfish virus diseaseExternal signs of channel catfish virus disease in fingerlings. A: Lateral view: distended abdomen and urogenital vent, bleedings at the bases of fins. B: Dorsal view: bilateral exophthalmia, abdominal distension and haemorrhage in anal fin.N. Fijan
Posterior kidney from channel catfish fingerling 3 days after injection with CCV. Large number of lymphoid cells and necrotic tubules (T). x 280. Courtesy of J.A. Plumb.
TitlePosterior kidney from channel catfish
CaptionPosterior kidney from channel catfish fingerling 3 days after injection with CCV. Large number of lymphoid cells and necrotic tubules (T). x 280. Courtesy of J.A. Plumb.
CopyrightN. Fijan
Posterior kidney from channel catfish fingerling 3 days after injection with CCV. Large number of lymphoid cells and necrotic tubules (T). x 280. Courtesy of J.A. Plumb.
Posterior kidney from channel catfishPosterior kidney from channel catfish fingerling 3 days after injection with CCV. Large number of lymphoid cells and necrotic tubules (T). x 280. Courtesy of J.A. Plumb.N. Fijan
Negatively stained virions of channel catfish virus (CCV). The membrane-bound envelope is very distinct. Nucleocapsid is located somewhat excentrically. x 298,000. Courtesy of R.C. Bird, K.E. Nusbaum and M. Toivio-Kinnucan.
TitleNegatively stained virions of channel catfish virus (CCV)
CaptionNegatively stained virions of channel catfish virus (CCV). The membrane-bound envelope is very distinct. Nucleocapsid is located somewhat excentrically. x 298,000. Courtesy of R.C. Bird, K.E. Nusbaum and M. Toivio-Kinnucan.
CopyrightN. Fijan
Negatively stained virions of channel catfish virus (CCV). The membrane-bound envelope is very distinct. Nucleocapsid is located somewhat excentrically. x 298,000. Courtesy of R.C. Bird, K.E. Nusbaum and M. Toivio-Kinnucan.
Negatively stained virions of channel catfish virus (CCV)Negatively stained virions of channel catfish virus (CCV). The membrane-bound envelope is very distinct. Nucleocapsid is located somewhat excentrically. x 298,000. Courtesy of R.C. Bird, K.E. Nusbaum and M. Toivio-Kinnucan.N. Fijan
Intranuclear channel catfish virus in spleen cell of channel catfish. The virus has migrated to the nuclear membrane, which in some places has been destroyed. Intranuclear lamellar-like inclusions are also present. x 22,000. Courtesy of J.A. Plumb.
TitleIntranuclear channel catfish virus
CaptionIntranuclear channel catfish virus in spleen cell of channel catfish. The virus has migrated to the nuclear membrane, which in some places has been destroyed. Intranuclear lamellar-like inclusions are also present. x 22,000. Courtesy of J.A. Plumb.
CopyrightN. Fijan
Intranuclear channel catfish virus in spleen cell of channel catfish. The virus has migrated to the nuclear membrane, which in some places has been destroyed. Intranuclear lamellar-like inclusions are also present. x 22,000. Courtesy of J.A. Plumb.
Intranuclear channel catfish virusIntranuclear channel catfish virus in spleen cell of channel catfish. The virus has migrated to the nuclear membrane, which in some places has been destroyed. Intranuclear lamellar-like inclusions are also present. x 22,000. Courtesy of J.A. Plumb.N. Fijan
Formation and contraction of syncytia in CCO cells about 14 h after inoculation with CCV and incubation at 30°C. Wright stain. x 230.
TitleSyncytia in CCO cells
CaptionFormation and contraction of syncytia in CCO cells about 14 h after inoculation with CCV and incubation at 30°C. Wright stain. x 230.
CopyrightN. Fijan
Formation and contraction of syncytia in CCO cells about 14 h after inoculation with CCV and incubation at 30°C. Wright stain. x 230.
Syncytia in CCO cellsFormation and contraction of syncytia in CCO cells about 14 h after inoculation with CCV and incubation at 30°C. Wright stain. x 230.N. Fijan

Identity

Top of page

Preferred Scientific Name

  • channel catfish virus disease

English acronym

  • CCVD

Overview

Top 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.

(OIE, 2003)

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 Affected

Top 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.

Distribution

Top 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 Table

Top 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/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

North America

USAPresent Invasive Plumb, 1994

Central America and Caribbean

HondurasPresent Invasive Plumb, 1994

Europe

Russian FederationPresent Invasive Plumb, 1989
UKPresent

Pathology

Top 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.

Diagnosis

Top of page

Clinical Signs

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.

Direct Methods

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/Signs

Top of page
SignLife StagesType
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 Course

Top 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.

Survivors of experimental CCV infection have a retarded growth rate (McGlamery and Gratzek, 1974), but this is not obvious in natural CCVD outbreaks in commercial operations (Plumb, 1989).

Pathogenesis and Immunity

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).

Epidemiology

Top 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 Summary

Top of page
CategoryImpact
Fisheries / aquaculture Negative

References

Top of page

Amend DF; McDowell T, 1983. Current problems in the control of channel catfish virus. Journal of the World Mariculture Society, 14:261-267.

Amend DF; McDowell T, 1984. Comparison of various procedures to detect neutralizing antibody to the channel catfish virus in California brood channel catfish. Progressive Fish-Culturist, 46(1):6-12.

Amend DF; McDowell T; Hedrick RP, 1984. Characteristics of a previously unidentified virus from channel catfish (Ictalurus punctatus). Canadian Journal of Fisheries and Aquatic Sciences, 41:807-811.

Arkush KD; McNeill C; Hedrick RP, 1992. Production and initial characterization of monoclonal antibodies against channel catfish virus. Journal of Aquatic Animal Health, 4(2):81-89.

Awad MA; Nusbaum KE; Brady YJ, 1989. Preliminary studies of a newly developed subunit vaccine for channel catfish virus disease. Journal of Aquatic Animal Health, 1(3):233-237.

Baek YS; Boyle JA, 1996. Detection of channel catfish virus in adult channel catfish by use of a nested polymerase chain reaction. Journal of Aquatic Animal Health, 8(2):97-103.

Bird RC; Nusbaum KE; Screws EA; Young-White RR; Grizzle JM; Toivio-Kinnucan M, 1988. Molecular cloning of fragments of the channel catfish virus (Herpesviridae) genome and expression of the encoded mRNA during infection. American Journal of Veterinary Research, 49(11):1850-1855.

Boon JH; McDowell T; Hedrick RP, 1988. Resistance of the African (Clarias gariepinus) and the Asian catfish (Clarias batrachus) to channel catfish virus. Aquaculture, 74:191-194.

Booy FP; Trus L; Davidson AJ; Steven AC, 1996. The capsid architecture of channel catfish virus, an evolutionary distinct herpesvirus, is largely conserved in the absence of discernible sequence homology with herpes simplex virus. Virology, 215:134-141.

Bowser P; Plumb JA, 1980. Fish cell lines: establishment of a line from ovaries of channel catfish. In Vitro, 16:365-368.

Bowser PR; Munson AD, 1986. Seasonal variation in channel catfish virus antibody titers in adult channel catfish. Progressive Fish-Culturist, 48(3):198-199.

Bowser PR; Munson AD; Jarboe HH; Francis-Floyd R; Waterstrat PR, 1985. Isolation of channel catfish virus from channel catfish, Ictalurus punctatus (Rafinesque), broodstock. Journal of Fish Diseases, 8(6):557-561.

Bowser PR; Plumb JA, 1980. Channel catfish virus: comparative replication and sensitivity of cell lines from channel catfish ovary and the brown bullhead. Journal of Wildlife Diseases, 16(3):451-454.

Bowser PR; Plumb JA, 1980. Growth rates of a new cell line from channel catfish ovary and channel catfish virus replication at different temperatures. Canadian Journal of Fisheries and Aquatic Sciences, 37(5):871-873.

Boyle J; Blackwell J, 1991. Use of polymerase chain reaction to detect latent channel catfish virus. American Journal of Veterinary Research, 52(12):1965-1968.

Brady YJ; Ellender RD, 1982. The role of sediment in transmission of channel catfish virus disease. Mississippi, USA: Mississippi-Alabama Sea Grant Consortium, University of South Mississippi, 67:111.

Buck CD; Loh PC, 1985. Liquid overlay plaquing of channel catfish virus. Journal of Fish Diseases, 8(3):325-328.

Cebrian J; Buccini D; Sheldrick P, 1983. Endless viral DNA in cells infected with channel catfish virus. Journal of Virology, 46:405-412.

Chinchar VG; Rycyzyn M; Clem LW; Miller NW, 1993. Productive infection of continuous lines of channel catfish leukocytes by channel catfish virus. Virology (New York), 193(2):989-992.

Chousterman S; Lacasa M; Sheldrick P, 1979. Physical map of the channel catfish virus genome: location of sites for restriction endonucleases EcoRI, HindIII, HpaI, and Xbal. Journal of Virology, 31:73-85.

Chumnongsitathum B; Plumb JA; Hilge V, 1988. Histopathology, electron microscopy and isolation of channel catfish virus in experimentally infected European catfish, Silurus glanis L. Journal of Fish Diseases, 11(4):351-357.

Clem LW; Bly JE; Miller NW, 1996. Vaccination strategies for carp and catfish. In: Book of Abstracts, International Symposium on Fish Vaccinology, Oslo, 5-7 June 1996, 53.

Colyer TE; Bowser PR; Doyle J; Boyle JA, 1986. Channel catfish virus: use of nucleic acids in studying viral relationships. American Journal of Veterinary Research, 47(9):2007-2011.

Davis KB; Griffin BR; Gray WL, 2002. Effect of handling stress on susceptibility of channel catfish Ictalurus punctatus to Ichthyophthirius multifiliis and channel catfish virus infection. Aquaculture, 214(1/4):55-66.

Davis KB; Griffin BR; Gray WL, 2003. Effect of dietary cortisol on resistance of channel catfish to infection by Ichthyopthirius multifiliis and channel catfish virus disease. Aquaculture, 218(1/4):121-130.

Davison AJ, 1992. Channel catfish virus: a new type of herpesvirus. Virology, 186:9-14.

Davison AJ, 1994. Fish herpesviruses. In: Webster RG, Granoff A, eds. Encyclopedia of Virology. London, UK: Academic Press, 470-474.

Davison AJ; Davison MD, 1995. Identification of structural proteins of channel catfish virus by mass spectrometry. Virology, 206:1035-1043.

Dixon RAF; Farber FE, 1980. Channel catfish virus: physiochemical properties of the viral genome and identification of viral polypeptides. Virology, 103(2):267-278.

Fernandez RD; Yoshimizu M; Kimura T; Ezura Y; Inouye K; Takami I, 1993. Characterization of three continuous cell lines from marine fish. Journal of Aquatic Animal Health, 5(2):127-136.

Fijan N, 1999. Spring viraemia of carp and other viral diseases and agents of warm-water fish. Fish diseases and disorders. Volume 3: viral, bacterial and fungal infections., 177-244; 19 pp of ref.

Fijan NN, 1968. Progress report on acute mortality of channel catfish fingerlings caused by a virus. Bulletin de l’Office International des Épizooties, 69:1167-1168.

Fijan NN; Wellborn TJ; Naftel JP, 1970. An acute viral disease of channel catfish. Technical Paper, Bureau of Sport Fisheries and Wildlife, No. 43, Washington, DC, USA. 11 pp.

Goodheart CR; Plummer G, 1975. The densities of herpesviral DNAs. Progress in Medical Virology, 19:324-352.

Gratzek JB; McGlamery MH; Dawe DL; Scott T, 1973. Microcultures of brown bullhead (Ictalurus nebulosus) cells: their use in quantitation of channel catfish (Ictalurus punctatus) virus antibody. Journal of the Fisheries Research Board of Canada, 30:1641-1645.

Gray WL; Williams RJ; Jordan RL; Griffin BR, 1999. Detection of channel catfish virus DNA in latently infected catfish. Journal of General Virology, 80(7):1817-1822.

Hanson LA; Kousoulas KG; Thune RL, 1994. Channel catfish herpesvirus (CCV) encodes a functional thymidine kinase gene: elucidation of a point mutation that confers resistance to Ara-T. Virology (New York), 202(2):659-664.

Hanson LA; Rudis MR; Petrie-Hanson L, 2004. Susceptibility of channel catfish fry to channel catfish virus (CCV) challenge increases with age. Diseases of Aquatic Organisms, 62:27-34.

Hanson LA; Thune RL, 1993. Characterization of thymidine kinase encoded by channel catfish virus. Journal of Aquatic Animal Health, 5(3):199-204.

Heartwell CM III, 1975. Immune Response and Antibody Characterization of the Channel Catfish (Ictalurus punctatus) to a Naturally Pathogenic Bacterium and Virus. Technical Paper. Washington, DC, USA: Bureau of Sport Fisheries and Wildlife 85, 34 pp.

Hedrick RP; Groff JM; McDowell T, 1987. Response of adult channel catfish to waterborne exposures of channel catfish virus. Progressive Fish-Culturist, 49(3):181-187.

Hedrick RP; McDowell T, 1987. Passive transfer of sera with antivirus neutralizing activity from adult channel catfish protects juveniles from channel catfish virus disease. Transactions of the American Fisheries Society, 116(2):277-281.

Hogan RJ; Stuge TB; Clem LW; Miller NW; Chinchar VG, 1996. Anti-viral cytotoxic cells in the channel catfish (Ictalurus punctatus). Developmental and Comparative Immunology, 20(2):115-127.

Kancharla SR; Hanson LA, 1996. Production and shedding of channel catfish virus (CCV) and thymidine kinase negative CCV in immersion exposed channel catfish fingerlings. Diseases of Aquatic Organisms, 27(1):25-34.

Kimura T; Suzuki S; Yoshimizu M, 1983. [I] In vitro antiviral effect of 9-(2-hydroxyethoxymethyl) guanine on the fish herpesvirus, Oncorhynchus masou virus (OMV). [II] In vivo antiviral effect of 9-(2-hydroxymethyl) guanine on experimental infection of chum salmon (Oncorhynchus keta) fry with Oncorhynchus masou virus (OMV). Antiviral Research, 3(2):93-101, 103-108.

Koment RW; Haines H, 1978. Decreased antiviral effect of phosphonacetic acid on the poikilothermic herpesvirus of channel catfish disease. Proceedings of the Society for Experimental Biology and Medicine, 159:21-24.

Lacasa M, 1990. A protein kinase-related gene within the channel catfish herpesvirus genome. Nucleic Acids Research, 18:3050.

Major RD; McCraren JP; Smith CE, 1975. Histopathological changes in channel catfish (Ictalunes punctatus) experimentally and naturally infected with channel catfish virus disease. Journal of the Fisheries Research Board of Canada, 32(4):563-567.

McConnell S; Austen JD, 1978. Serologic screening of channel catfish virus. Marine Fisheries Reviews, 40:30-32.

McGlamery MH Jr; Gratzek JB, 1974. Stunting syndrome associated with young channel catfish that survived exposure to channel catfish virus. Progressive Fish Culturist, 36:38-41.

Noga EJ; Hartmann JX, 1981. Establishment of walking catfish (Clarias batrachus) cell lines and development of a channel catfish (Ictalurus punctatus) virus vaccine. Canadian Journal of Fisheries and Aquatic Sciences, 38:925-930.

Nusbaum KE; Grizzle JM, 1987. Adherence of channel catfish virus to sperm and leukocytes. Aquaculture, 65:1-5.

Nusbaum KE; Grizzle JM, 1987. Uptake of channel catfish virus from water by channel catfish and bluegills. American Journal of Veterinary Research, 48(3):375-377.

Nusbaum KE; Smith BF; DeInnocentes P; Bird RC, 2002. Protective immunity induced by DNA vaccination of channel catfish with early and late transcripts of the channel catfish herpesvirus (IHV-1). Veterinary Immunology and Immunopathology, 84(3/4):151-168.

Office International des Épizooties, 1995. Diagnostic manual for aquatic animal diseases. Diagnostic manual for aquatic animal diseases., Ed. 1:xiv + 195 pp.

OIE, 2003. Diagnostic Manual for Aquatic Animal Diseases. Paris, France: Office International des Épizooties.

Plumb JA, 1971. Channel catfish virus disease in southern United States. Proceedings of the Annual Conference, Southeastern Association of Game and Fish Commissioners, 25:489-493.

Plumb JA, 1971. Channel Catfish Virus Research at Auburn University. Progress Report Series, No. 95, Agricultural Experimental Station, Auburn University, Alabama.

Plumb JA, 1971. Tissue distribution of channel catfish virus. Journal of Wildlife Diseases, 7:213-216.

Plumb JA, 1973. Effects of temperature on mortality of fingerling channel catfish (Ictalurus punctatus) experimentally infected with channel catfish virus. Journal of the Fisheries Research Board of Canada, 30(No.4):568-570.

Plumb JA, 1973. Neutralization of channel catfish virus by serum of channel catfish. Journal of Wildlife Diseases, 9(No.4):324-330.

Plumb JA, 1974. Viral diseases of fishes of the Gulf of Mexico region. In: Amborski RL, Hood MA, Miller RR, eds. Gulf Coast Regional Symposium on Diseases of Aquatic Animals. LSU-SG-74-05, Louisiana State University, Baton Rouge, 55-75.

Plumb JA, 1978. Epizootiology of channel catfish virus disease. Marine Fisheries Review, 3:26-29.

Plumb JA, 1988. Vaccination against channel catfish virus. Fish vaccination., 216-223.

Plumb JA, 1989. Channel catfish herpesvirus. Viruses of lower vertebrates., 198-216; [1st International Symposium on Viruses of Lower Vertebrates, Munich, August 1988].

Plumb JA, 1994. Channel catfish virus disease. In: Thoesen JC, ed. Suggested Procedures for the Detection and Identification of Certain Finfish and Shellfish Pathogens, 4th edition, Version 1. Fish Health Section. Bethesda, Maryland, USA: American Fisheries Society, 3 pp.

Plumb JA, 1999. Health maintenance and principal microbial diseases of cultured fishes. Health maintenance and principal microbial diseases of cultured fishes., vx + 328 pp.

Plumb JA; Gaines JL Jr, 1975. Channel catfish virus disease. In: Ribelin WE, Migaki G, eds. The Pathology of Fishes. Madison, USA: Wisconsin Press, 287-301.

Plumb JA; Gaines JL; Mora EC; Bradley GG, 1974. Histopathology and electron microscopy of channel catfish virus in infected channel catfish, Ictalurus punctatus (Rafinesque). Journal of Fish Biology, 6(No.5):661-664; [4 plates].

Plumb JA; Green OL; Smitherman RO; Pardue GB, 1975. Channel catfish virus experiments with different strains of channel catfish. Transactions of the American Fisheries Society, 104(1):140-143.

Plumb JA; Hilge V; Quinlan EE, 1985. Resistance of the European catfish (Siluru glanis) to channel catfish virus. Journal of Applied Ichthyology, 1(2):87-89.

Plumb JA; Jezek DA, 1983. Channel catfish virus disease. Les antigènes des micro-organismes pathogènes des poissons, symposium international. [Antigens of fish pathogens, international symposium] Talloires, France, 10-12 May 1982., 33-49; [Discussion p.50].

Plumb JA; Thune RL; Klesius PH, 1981. Detection of channel catfish virus in adult fish. Developments in Biological Standardization, 49:29-34.

Plumb JA; Wright LD; Jones VL, 1973. Survival of channel catfish virus in chilled, frozen, and decomposing channel catfish. Progressive Fish Culturist, 35:170-172.

Robin J; Rodrigue A, 1980. Isolation and preliminary characterization of herpes channel catfish virus DNA. Canadian Journal of Microbiology, 26(2):130-134.

Robin J; Rodrigue A, 1980. Resistance of herpes channel catfish virus (HCCV) to temperature, pH, salinity and ultraviolet irradiation. Revue Canadienne de Biologie, 39(3):153-156.

Silverstein PS; Bird RC; van Santen VL; Nusbaum KE, 1995. Immediate- early transcription from the channel catfish virus genome: characterization of two immediate-early transcripts. Journal of Virology, 69:3161-3166.

Tham KM; Moon CD, 1996. Polymerase chain reaction amplification of the thymidine kinase and protein kinase-related genes of channel catfish virus and a putative pilchard herpesvirus. Journal of Virological Methods, 61(1/2):65-72.

Thune RL, 1993. Catfish viruses. In: Stoskopf MK, ed. Fish Medicine. Philadelphia, USA: WB Saunders, 521-524.

Vanderheijden N; Hanson LA; Thiry E; Martial JA, 1999. Channel catfish virus gene 50 encodes a secreted, mucin-like glycoprotein. Virology (New York), 257(1):220-227.

Walczak EM; Noga EJ; Hartmann JX, 1981. Properties of a vaccine for channel catfish virus disease and a method of administration. Developments in Biological Standardization, 49:419-429.

Wise JA; Bowser PR; Boyle JA, 1985. Detection of channel catfish virus in asymptomatic adult channel catfish, Ictalurus punctatus (Rafinesque). Journal of Fish Diseases, 8(6):485-493.

Wise JA; Boyle JA, 1985. Detection of channel catfish virus in channel catfish, Ictalurus punctatus (Rafinesque): use of a nucleic acid probe. Journal of Fish Diseases, 8(5):417-424.

Wise JA; Harrell SF; Busch RL; Boyle JA, 1988. Vertical transmission of channel catfish virus. American Journal of Veterinary Research, 49(9):1506-1509.

Wolf K, 1988. Fish viruses and fish viral diseases. Fish viruses and fish viral diseases., xii + 476 pp.

Wolf K; Darlington RW, 1971. Channel catfish virus: a new herpesvirus of ictalurid fish. Journal of Virology, 8(No.4):525-533.

Wolf K; Herman RL; Carlson CP, 1972. Fish viruses: histopathologic changes associated with experimental channel catfish virus disease. Journal of the Fisheries Research Board of Canada, 29(No.2):149-150; [2 plates].

Yoshimizu M; Takizawa H; Sami M; Kataoka H; Kugo T; Kimura T, 1989. Disinfectant effects of ultraviolet irradiation on fish pathogens in hatchery water supply. In: Hirano R, Hanyu I, eds. Proceedings of the Second Asian Fisheries Forum, Tokyo, Japan, 17-22 April 1989. Manila, Philippines: Asian Fisheries Society, 643-646.

Zhang HG; Hanson LA, 1995. Deletion of thymidine kinase gene attenuates channel catfish herpesvirus while maintaining infectivity. Virology (New York), 209(2):658-663.

Zhang HG; Hanson LA, 1996. Recombinant channel catfish virus (Ictalurid herpesvirus 1) can express foreign genes and induce antibody production against the gene product. Journal of Fish Diseases, 19(2):121-128; 18 ref.

Contributors

Top of page

Main Author
Kenneth Nusbaum
Department of Pathobiology, College of Veterinary Medicine, Auburn University, AL 36849, USA

Joint Author
R Curtis Bird

Distribution Maps

Top of page
You can pan and zoom the map
Save map