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 ( 22 ) or Plumb ( 15 ) .
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 interstitial 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-detection means, 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 between isolates ( 1 ) . 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 ( 7, 18 ) .
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, gills, spleen and intestine, respectively, in decreasing magnitude ( 12, 13 ) . The transmission of CCV is horizontal and vertical. Horizontal transmission may be direct or vectorial with water being the main abiotic vector. The virus has been shown to readily adsorb to pond sediments ( 6 ) and interaction with suspended clay particles in pond water may influence horizontal transmission. Animate vectors and inanimate objects 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 ( 11 ) , 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 proteins 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 is 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 to 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 ( 2, 5, 9, 21 ) . Vaccination, although experimentally promising ( 19, 20, 23, 24 ) , is not in use at this time.