Difference between revisions of "Channel Catfish Virus"
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| − | Also Known As | + | Also Known As: '''''CCV — Channel Catfish Viral Disease — CCVD''''' |
==Introduction== | ==Introduction== | ||
| − | [[File:Channel Catfish.jpg|thumb|200px|right| | + | [[File:Channel Catfish.jpg|thumb|200px|right|Channel Catfish - the primary species affected by CCVD. Wikimedia Commons]] |
Channel Catfish Viral Disease (CCVD) is caused by a '''[[Herpesviridae|herpesvirus]]''' and causes significant economic losses in channel catfish farming. '''High mortalities in fry and young fish''' are the biggest direct loss. | Channel Catfish Viral Disease (CCVD) is caused by a '''[[Herpesviridae|herpesvirus]]''' and causes significant economic losses in channel catfish farming. '''High mortalities in fry and young fish''' are the biggest direct loss. | ||
==Distribution== | ==Distribution== | ||
| − | CCVD is '''endemic in the USA''', where at least | + | CCVD is '''endemic in the USA''', where at least two catfish farms have been closed partially because of the virus. Imported fish may have also introduced the disease to Honduras <ref> Plumb, J. A (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'', pp 3</ref> and Russia. <ref> Plumb, J. A (1989) '''Channel catfish herpesvirus. Viruses of lower vertebrates'''. 198-216; ''1st International Symposium on Viruses of Lower Vertebrates, Munich'', August 1988</ref> CCVD is also present in the '''UK'''. |
Reservoirs of disease are clinically affected fish and recovered covert carriers – see below for more details. | Reservoirs of disease are clinically affected fish and recovered covert carriers – see below for more details. | ||
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Disease occurs almost exclusively in fish '''less than a year old''', and is '''most common in those under 4 months''' of age. Natural clinical disease is generally confined to fish '''weighing less than 10g.''' | Disease occurs almost exclusively in fish '''less than a year old''', and is '''most common in those under 4 months''' of age. Natural clinical disease is generally confined to fish '''weighing less than 10g.''' | ||
| − | The critical environmental factor is water temperature, with '''mortality highest above | + | The critical environmental factor is water temperature, with '''mortality highest above 27⁰C and zero when below 18⁰C'''. Thus, disease occurs during warm weather in May to September. |
==Clinical Signs== | ==Clinical Signs== | ||
| − | Affected fish have '''marked ascites giving them a pot bellied appearance, show exopthalmos and have multiple haemorrhages of the fins and musculature'''. The '''vent may be swollen''' and protrusive and the gills pale. Opercular movements are often | + | Affected fish have '''marked ascites giving them a pot-bellied appearance, show exopthalmos and have multiple haemorrhages of the fins and musculature'''. The '''vent may be swollen''' and protrusive and the gills pale. Opercular movements are often increased. Affected fish may seem to be '''off balance, swimming erratically''' or close to the surface and eventually sinking to the bottom. Up to 50% of moribund fish may '''hang head upwards''' at the surface. |
| − | Fish that survive CCVD have '''strong protective immunity for the remainder of their lives but remain in a covert latent carrier state''' which is undetectable antigenically and difficult at best. This is a significant source of disease for vulnerable fish. It is unclear how these fish shed the | + | Fish that survive CCVD have '''strong protective immunity for the remainder of their lives but remain in a covert latent carrier state''' which is undetectable antigenically and difficult at best. This is a significant source of disease for vulnerable fish. It is unclear how these fish shed the virus. |
==Diagnosis== | ==Diagnosis== | ||
Increased fry or fingerling mortality in catfish in warm weather, especially after stress, should raise suspicion of CCVD. | Increased fry or fingerling mortality in catfish in warm weather, especially after stress, should raise suspicion of CCVD. | ||
| − | CCV can be detected in '''water''' containing infected fish and organs of | + | CCV can be detected in '''water''' containing infected fish and organs of diseased fish, particularly the '''kidneys'''. All viscera should be taken from fish of 4-6cm, whole fish if smaller and kidney, spleen and encephalon if larger than 6cm. All should be transported cooled or on ice but not frozen. The virus can be '''isolated in cell culture and identified by virus neutralisation, [[FAT|fluorescent antibody testing]] (FAT), [[ELISA testing|ELISA]] and PCR'''. FAT and ELISA are best for diagnosis of clinically infected fish while carrier fish can only be detected by neutralisation or PCR. The formation of '''syncytia''' in ovary cell cultures is also specific for CCV. |
At necropsy, the '''peritoneal cavity is hyperaemic and a serosanguinous fluid''' often present. The liver and kidneys may be pale and petechiated. Yellow mucoid material is found within the digestive tract. | At necropsy, the '''peritoneal cavity is hyperaemic and a serosanguinous fluid''' often present. The liver and kidneys may be pale and petechiated. Yellow mucoid material is found within the digestive tract. | ||
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'''Control policies and hygiene practices''' are also often implemented n the catfish industry. The virus is sensitive to acidic pH, heat and UV light and is inactivated immediately by pond mud as soil sediments rapidly absorb the virus. It is also unstable in sea water. | '''Control policies and hygiene practices''' are also often implemented n the catfish industry. The virus is sensitive to acidic pH, heat and UV light and is inactivated immediately by pond mud as soil sediments rapidly absorb the virus. It is also unstable in sea water. | ||
| − | Fry should be '''reared and eggs | + | Fry should be '''reared and eggs incubated in a separate facility''' from any potential carrier population to maintain CCV-free status. |
No vaccination is available at present. Juvenile catfish can however be '''passively immunised by injection of antiserum from adults'''. | No vaccination is available at present. Juvenile catfish can however be '''passively immunised by injection of antiserum from adults'''. | ||
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Animal Health & Production Compendium, '''Channel Catfish Disease Virus datasheet''', accessed 11/07/2011 @ http://www.cabi.org/ahpc/ | Animal Health & Production Compendium, '''Channel Catfish Disease Virus datasheet''', accessed 11/07/2011 @ http://www.cabi.org/ahpc/ | ||
| − | [[Category: | + | |
| + | {{review}} | ||
| + | [[Category:CABI Expert Review]] | ||
| + | [[Category:Herpesviridae]] | ||
| + | [[Category:Fish Diseases]] | ||
Revision as of 23:08, 18 July 2011
Also Known As: CCV — Channel Catfish Viral Disease — CCVD
Introduction
Channel Catfish Viral Disease (CCVD) is caused by a herpesvirus and causes significant economic losses in channel catfish farming. High mortalities in fry and young fish are the biggest direct loss.
Distribution
CCVD is endemic in the USA, where at least two catfish farms have been closed partially because of the virus. Imported fish may have also introduced the disease to Honduras [1] and Russia. [2] CCVD is also present in the UK.
Reservoirs of disease are clinically affected fish and recovered covert carriers – see below for more details.
Transmission is both horizontal and vertical. Horizontal transmission can be direct or via water.
Signalment
Channel catfish and the closely related blue catfish are the only fish known to be susceptible to CCVD. Natural outbreaks are seen almost exclusively in cultivated channel catfish.
Disease occurs almost exclusively in fish less than a year old, and is most common in those under 4 months of age. Natural clinical disease is generally confined to fish weighing less than 10g.
The critical environmental factor is water temperature, with mortality highest above 27⁰C and zero when below 18⁰C. Thus, disease occurs during warm weather in May to September.
Clinical Signs
Affected fish have marked ascites giving them a pot-bellied appearance, show exopthalmos and have multiple haemorrhages of the fins and musculature. The vent may be swollen and protrusive and the gills pale. Opercular movements are often increased. Affected fish may seem to be off balance, swimming erratically or close to the surface and eventually sinking to the bottom. Up to 50% of moribund fish may hang head upwards at the surface.
Fish that survive CCVD have strong protective immunity for the remainder of their lives but remain in a covert latent carrier state which is undetectable antigenically and difficult at best. This is a significant source of disease for vulnerable fish. It is unclear how these fish shed the virus.
Diagnosis
Increased fry or fingerling mortality in catfish in warm weather, especially after stress, should raise suspicion of CCVD.
CCV can be detected in water containing infected fish and organs of diseased fish, particularly the kidneys. All viscera should be taken from fish of 4-6cm, whole fish if smaller and kidney, spleen and encephalon if larger than 6cm. All should be transported cooled or on ice but not frozen. The virus can be isolated in cell culture and identified by virus neutralisation, fluorescent antibody testing (FAT), ELISA and PCR. FAT and ELISA are best for diagnosis of clinically infected fish while carrier fish can only be detected by neutralisation or PCR. The formation of syncytia in ovary cell cultures is also specific for CCV.
At necropsy, the peritoneal cavity is hyperaemic and a serosanguinous fluid often present. The liver and kidneys may be pale and petechiated. Yellow mucoid material is found within the digestive tract.
Histologically, extensive tubular and interstitial tissue necrosis is evident in the kidneys of infected fish. Haematopoeitic tissues show lymphoid aggregation, oedema, necrosis and macrophage accumulation. Similar congestion, oedema, macrophage infiltration and focal haemorrhage is seen in the liver, spleen, gastrointestinal mucosa and infrequently, heart. Occasional eosinophilic inclusions may be seen in hepatocytes.
Treatment
No treatment is available for fish once infected.
Control
Maintaining low stocking density and avoiding stressful handling of young fish will help to reduce prevalence of infection.
Control policies and hygiene practices are also often implemented n the catfish industry. The virus is sensitive to acidic pH, heat and UV light and is inactivated immediately by pond mud as soil sediments rapidly absorb the virus. It is also unstable in sea water.
Fry should be reared and eggs incubated in a separate facility from any potential carrier population to maintain CCV-free status.
No vaccination is available at present. Juvenile catfish can however be passively immunised by injection of antiserum from adults.
| Channel Catfish Virus Learning Resources | |
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 Test your knowledge using flashcard type questions |
Channel Catfish Virus Flashcards |
References
- ↑ Plumb, J. A (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, pp 3
- ↑ Plumb, J. A (1989) Channel catfish herpesvirus. Viruses of lower vertebrates. 198-216; 1st International Symposium on Viruses of Lower Vertebrates, Munich, August 1988
Animal Health & Production Compendium, Channel Catfish Disease datasheet, accessed 11/07/2011 @ http://www.cabi.org/ahpc/
Animal Health & Production Compendium, Channel Catfish Disease Virus datasheet, accessed 11/07/2011 @ http://www.cabi.org/ahpc/
 |
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