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major viral diseases of present developing aquaculture sector

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VIRAL DISEASES IN FISHES:

VIRAL DISEASES IN FISHES SUBMITTED BY DIVYA MOL K K MFSc , AAHM KUFOS

MAJOR VIRAL DISEASES….:

MAJOR VIRAL DISEASES…. Infectious haematopoietic necrosis virus (IHNV ) Infectious haematopoietic necrosis virus (IHNV) Infectious salmon anaemia virus (ISAV ) Infectious pancreatic necrosis virus (IPN ) Spring viraemia of carp virus (SVCV )

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Koi herpesvirus (KHV ) Channel catfish viral disease .( CCV ) Lymphocystis disease Viral erythrocytic necrosis (VEN ) Viral encepalopathy and retinopathy virus (VERV) also known as viral nervous necrosis virus (VNNV ) Oncorhynchus masou virus (OMV )

1.KOI HERPES VIRUS DISEASE:

1.KOI HERPES VIRUS DISEASE CLASSIFICATION Family : alloherpesviridea Genus : cyprinivirus Causative agent : cyprinid herpes virus - 3

INTRODUCTION :

INTRODUCTION Most serious threat to carp farming in Europe and Asia  Caused by a highly contagious enveloped, circular double-stranded DNA virus

GEOGRAPHICAL DISTRIBUTION:

GEOGRAPHICAL DISTRIBUTION KHVD first reported from Israel and Germany in 1998 and detection of KHV DNA in tissue samples taken during a mass mortality of carp in the UK in 1996 . The disease has been spread to many countries worldwide, predominantly through the trade of infected in koi carp. It is now known to occur in at least 28 different countries . It is reported from Asia, China ,Indonesia , Japan, Korea, Malaysia , Singapore and Thailand etc…

SUSCEPTIBLE HOST SPECIES:

SUSCEPTIBLE HOST SPECIES Major host is common carp ( Cyprinus carpio ) and varieties of this species especially koi carp . Goldfish × common carp hybrids have been reported to show some susceptibility to KHV infection . Recent studies have provided increasing evidence to indicate that goldfish ( Carassius auratus ) are susceptible to KHV infection.

ENVIRONMENTAL FACTORS :

ENVIRONMENTAL FACTORS Disease patterns are influenced by water temperature virulence of the virus Age and condition of the fish Population density and stress factors

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Clinical disease occurs at water temperatures of 22–27°C . maximum mortality at temperatures of 22–25.5°C. Mortality rates can reach 80–100 %. Although mortality decreases or stops as water temperature approaches 30°C, survivors will remain as carriers .

HOST FACTORS:

HOST FACTORS Fish of any age are susceptible. Mortality rates may be higher in younger fish, especially fry. The skin covering the fins and body of the carp is the major portal of entry for KHV. There is then a systemic spread of the virus from the skin and gills to the internal organs. High levels of KHV DNA have been detected in kidney, spleen, liver and gut tissue.

CLINICAL SIGNS:

CLINICAL SIGNS Gill, kidney, and spleen are the organs in which KHV is most abundant during the course of infection. Major clinical signs include : Pale discolouration or reddening of the skin. Little or total loss of epidermis. Over- or under-production of mucus on the skin and gills. Pale discoloration of the gills. Enophthalmia (sunken eyes) Haemorrhages on the skin and base of the fins, and fin erosion.

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Skin hemorrhages. Pale gill.

Transmission mechanisms:

Transmission mechanisms The mode of transmission of KHV is horizontal but ‘ vertical’ transmission cannot currently be ruled out . Horizontal transmission may be direct or via vectors . Water is the major abiotic vector. Animate vectors (e.g. other fish species, parasitic invertebrates and piscivorous birds and mammals) and fomites may also be involved in transmission . The reservoirs of KHVD are clinically infected fish and carriers. Virulent virus is shed via faeces , urine, gills and skin.

DIAGNOSIS :

DIAGNOSIS It include field diagnosis method, clinical methods and agent detection and identification. Field diagnosis method include clinical signs and behavioral changes. Clinical methods include gross pathology and microscopy etc… Agent detection and identification include immunofluorescence (IF ). ELISA-based are under development but no validated methods have been published.

CONTROL AND PREVENTION :

CONTROL AND PREVENTION It mainly rely on avoiding exposure to the virus coupled with good hygiene and biosecurity practices. A safe and effective vaccine is not currently widely available. Disinfection of eggs can be achieved by iodophor treatment. KHV has been shown to be inactivated by iodophor at 200 mg litre–1 for 30 seconds at 15°C .

   2. CHANNEL CAT FISH VIRUS DISEASE ( CCVD) :

   2 . CHANNEL CAT FISH VIRUS DISEASE ( CCVD)   Channel Catfish virus ( Ictalurid herpesvirus 1 ) causes disease in channel catfish ( Ictalurus punctatus ) in the USA. Infection with CCV can cause significant economic loss in channel catfish farms.

CLASSIFICATION:

CLASSIFICATION ORDER : HERPESVIRALES FAMILY : ALLOHERPESVIRIDAE GENUS : ICTALURI VIRUS CAUSATIVE AGENT : Ictalurid herpes virus 1(IcHV1) CCV is a ds DNA virus.

GEOGRAPHIC DISTRIBUTION:

GEOGRAPHIC DISTRIBUTION The disease is endemic in the USA and there are reports of the virus in Honduras and Russia.

SUSCEPTIBLE SPECIES:

SUSCEPTIBLE SPECIES Channel catfish and blue catfish are the only fish that are susceptible to CCVD . Reservoirs of disease are clinically affected fish and recovered covert carriers . Disease occurs in fish less than 1 year old ( fry and fingerlings ) that weigh less than 10 grams . As fish age, mortality decreases, and clinical infection in fish >1 yr old is rare .

Host factors &TRANSMISSION:

Host factors &TRANSMISSION The reservoirs of CCV are clinically infected fish and asymptomatic carriers. Infectious CCV is shed via faeces , urine and the sexual products . kidney, spleen, intestine and encephalon are the sites in which virus is the most abundant during the course of overt infection .

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The transmission of CCV is horizontal and possibly vertical . Horizontal transmission may be direct or vectorial . Water is the major abiotic vector. Animate vectors and fomites also act in CCV transmission. Fish that survive the infection have lifelong protective immunity but remain latent carriers of CCV.

ENVIRONMENTAL FACTOR:

ENVIRONMENTAL FACTOR Water temperature is the critical environmental factor : the mortality rate is high at 25°-30°C but readily decreases and ceases below 18°C.

CLINICAL SIGNS:

CLINICAL SIGNS Erratic swimming or spiraling Lethargy. Mortality is very high.. Hemorrhage at the base of the fins and skins Exophthalmos Pale gills  Kidneys swollen and pale with hemorrhage  Spleen is enlarged and dark red.

DIAGNOSIS:

DIAGNOSIS CCV can be detected in water containing infected fish and organs of diseased fish by : virus neutralization fluorescent antibody testing ( FAT ) ELISA PCR . FAT and ELISA should be used for diagnosis of clinically infected fish. While virus neutralisation or PCR should be used to detect carrier fish.

TREATMENT AND CONTROL :

TREATMENT AND CONTROL There is no available treatment . Avoid Stress and high stocking densities . Appropriate quarantine and hygiene measures should be employed. The virus is sensitive to acidic pH ,heat and UV light.

    3. LYMPHOCYSTIS:

      3 . LYMPHOCYSTIS This typically chronic, viral infection of wild or captive marine and freshwater fish . CLASSIFICATION AND STRUCTURE Family : Iridoviridae Virus : Lymphocystis virus Icosahedral dna virus

GEOGRAPHICAL DISTRIBUTION:

GEOGRAPHICAL DISTRIBUTION First reported in 1874. The disease affects a wide range of fish and is generally considered global.

Susceptible host species.:

Susceptible host species. Lymphocystis disease has been reported in over 125 different marine and freshwater fish species from 34 different families . It affects advanced orders of bony fishes ( teleosts )including cichlids ( Cichlidae ) killifishes ( Cyprinodontidae ) gouramies ( Osphronemidae ), sunfishes ( Centrarchidae sea basses ( Serranidae ), and many others.

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Lymphocystis does not affect less advanced orders, including : catfish (Order Siluriformes ) cyprinids (such as goldfish, koi, barbs, or danios ; Family Cyprinidae ) salmonids (Family Salmonidae ).

CLINICAL SIGNS:

CLINICAL SIGNS The most obvious sign is the appearance cauliflower-like lesions or nodules typically located on fins and also present on gills. The nodules are actually clustered groups of greatly enlarged, infected cells known as fibroblasts. Initially fish starts growing small white pin-prick like growths on their  fins  or skin and this is often mistaken for Ich ( Ichthyophthirius multifiliis ) in the early stages but It soon clumps to form a cauliflower-like growth. Pop-eye ( exophthalmia).

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Pop eye

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Wet mount. Microscopic view of nodules on fins of blue gourami. Clownfish with lymphocystis nodules on fins and body.

TRANSMISSION :

TRANSMISSION Lymphocystis is spread by horizontal transmission. In addition, crowding, shipping, and other stressors trigger disease outbreaks . there is no vertical transmission of the disease. Lymphocystis virus shows host specificity. Specific strain of virus will affect specific host species.

DIAGNOSIS:

DIAGNOSIS By clinical signs. Fishes with internal nodules the disease is diagnosed by : Microscopic examination of a wet mount (fresh) biopsy of suspected infected tissues Histopathology Electron microscopy Molecular methods.

TREATMENT :

TREATMENT There is no known cure for this virus. A privately owned fish research & breeding facility from USA has reportedly been able to suppress the virus using the human antiviral "Acyclovir" at the rate of 200 mg per 10 US gallons for 2 days . Usually the best cure is to simply give the fish a stress free condition and the virus will slowly reduced and the fins will repair themselves.

4. VIRAL ENCEPHALOPATHY AND RETINOPATHY (VER ) or VIRAL NERVOUS NECROSIS (VNN):

4. VIRAL ENCEPHALOPATHY AND RETINOPATHY (VER ) or VIRAL NERVOUS NECROSIS ( VNN ) Family : nodaviridae Genus : betanoda virus Structure Non enveloped Icosahedral ssRNA virus 30 nm diameter

Betanodavirus genotypic and phenotypic variants:

Betanodavirus genotypic and phenotypic variants Genotype Serotype Target host Optimum growth temperature SJNNV A Striped jack 20–25°C TPNNV B Tiger puffer 20°C BFNNV C Cold-water fish: Atlantic halibut, Atlantic cod, flounders, etc. 15–20°C RGNNV C Warm-water fish: Asian sea bass, European sea bass , groupers , etc. 25–30°C

GEOGRAPHIC DISTRIBUTION:

GEOGRAPHIC DISTRIBUTION The virus was reported for the first time during the years 1989-1991 .  It was discovered almost simultaneously in Australia, Norway, France and Japan. the disease has been officially reported from many regions. these include countries in south and east asia (china, India , Indonesia, Iran, japan, Korea, Malaysia ), UK, Norway… VNN has been reported as a serious disease of larval and juvenile and sometimes older marine fish .

SUSCEPTIBLE SPECIES:

SUSCEPTIBLE SPECIES The disease has been reported in at least 40 fish species.  Most of them marine. The disease is more likely to occur in larvae or juveniles but it can also affect adults. Major host species are: Sea bass ( Lates calcarifer and Dicentrarchus labrax ) Groupers ( Epinephelus spp ) Parrotfish ( Oplegnathus fasciatus ) Puffer fish ( Takifugu rubripes ) etc….

TRANSMISSION :

TRANSMISSION Disease spread mainly through horizontal transmission. Dead decomposed fish may spread the virus in the environment. Water is the most important abiotic vector . E vidence exists for vertical transmission from brood stock to offspring in striped jack, European sea bass, Asian sea bass .

TARGET ORGANS AND INFECTED TISSUE. :

TARGET ORGANS AND INFECTED TISSUE. The virus most likely invades the host through the intestinal epithelium and peripheral nervous system. Very soon reaching the central nervous tissues where it may induce the death of the host or remain for several years in survivors . Brain , spinal cord and retina are considered the target organs in which the virus actively replicates

MORTALITY AND ENVIRONMENTAL FACTORS:

MORTALITY AND ENVIRONMENTAL FACTORS The mortality rate is age-dependent. When larval stages are affected, highest mortality, often reaching 100 %. In juveniles and older fish lower losses have been generally reported . Water temperature is an important factor . Betanodaviruses are highly resistant in the aquatic environment and can survive for a long time in sea water at low temperatures . At 25°C or higher, the survival rate is significantly affected. The effect of temperature is particularly well known in sea bass farming .

CLINICAL SIGNS & BEHAVIOURAL CHANGES :

CLINICAL SIGNS & BEHAVIOURAL CHANGES There are no external signs on the body surface and gills of infected fish except a progressive change in pigmentation. Infected fish show a variety of erratic swimming behavior patterns such as Spiraling. Whirling . Belly-up at rest (sometimes with inflation of the swim bladder).

DIAGNOSIS :

DIAGNOSIS For several years the “gold standard” method to detect VNN was isolation of viral agents in cell culture followed by immunological or molecular identification. Diagnosis methods include: Field diagnostic methods Clinical methods 1.GROSS PATHOLOGY No macroscopic lesions have been associated with the infection except hyperinflation of the swim bladder, which has been frequently observed in different species.

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2.MICROSCOPIC PATHOLOGY The most common microscopic findings detected consist of vacuolation and necrosis of nervous cells of the spinal cord, brain and/or retina. 3.Electron microscopy/cytopathology Sub spherical viral particles can be visualized in brain, spinal cord and retina of heavily infected animals . Agent detection and identification methods ELISA Immunofluorescence (IF ) Immunohistochemistry ( IHC) on brain and retina . PCR

CONTROL AND PREVENTION:

CONTROL AND PREVENTION Prevention of the disease may only be obtained avoiding the exposure of farmed population to the causative agents. Common disinfectants such as sodium hypochlorite, iodine, hydrogen peroxide, and benzalkonium chloride are very useful for inactivating betanodaviruses . Ozone has also been used to avoid or reduce virus contamination on egg shell surface. virus contaminated water may be effectively sterilized by UV exposure

5. ONCORHYNCHUS MASOU VIRUS DISEASE :

5. ONCORHYNCHUS MASOU VIRUS DISEASE CLASSIFICATION Family : herpesviridae Virus : onchorhyncus masou virus

GEOGRAPHIC DISTRIBUTION :

GEOGRAPHIC DISTRIBUTION First reported from japan There are no reports of disease occurrence outside Japan. Salmonids are the only fish species susceptible to OMV infection .

SUSCEPTABLE SPECIES :

SUSCEPTABLE SPECIES Fish species that are susceptible to OMV include : masu salmon ( O. masou ) coho salmon ( O. kisutch ) rainbow trout ( O. mykiss ). The age of the fish is critical 1-month-old alevins are the most susceptible target for virus infection The main environmental factor favouring OMV infection is low water temperature , below 15°C .

TRANSMISSION :

TRANSMISSION The transmission of OMV is horizontal and possibly vertical. Horizontal transmission may be direct or vectorial . water is the major abiotic factor . Under natural conditions, survivors of OMVD are persistently infected with virus and they shed the virus and fish retain the virus until maturation .

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The reservoirs of OMV are clinically infected fish and covert carriers. Infectious virus is shed via faeces , urine, sexual products and probably skin mucus. while the kidney, spleen, liver and tumours are the sites where virus is the most abundant during the course of overt infection.

CLINICAL SIGNS :

CLINICAL SIGNS Clinically, the initial infection by OMV appears as oedema and haemorrhages . Virus multiplication in endothelial cells of blood capillaries, haematopoietic tissue and hepatocytes are the clinical signs . Four months after this first clinical condition , a varying number of surviving fish exhibit epithelioma occurring mainly around the mouth and, to a lesser extent, on the caudal fin, operculum and body surface . This neoplasia may persist for up to 1 year post-infection.

OMV infected fish:

OMV infected fish

DIAGNOSIS :

DIAGNOSIS Major 3 methods Field diagnosis method Clinical methods Gross pathology Gross signs in infected fish are inappetence and exophthalmia, and petechiae on the body surface,especially beneath the lower Microscopic pathology Kidney of the infected fish is the major site of histopathological studies in early stage. It shows necrosis of kidney. Liver is the site for histopathological studies in later stages. Agent detection and identification method

CONTROL AND PREVENTION:

CONTROL AND PREVENTION OMV is sensitive to ultraviolet irradiation, ozone or iodophor treatment. Nowadays, all eggs and facilities had been disinfected by iodophor just after fertilization and again at the early eyed stage . Vaccination of mature rainbow trout with formalin-inactivated OMV could reduce OMV disease .

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Hybrids represent a potential control method to prevent serious losses from OMVD. Studies on a population of triploid hybrid salmonid (tetramer rainbow trout × brown trout) found them to be resistant to OMVD. Disinfection of eggs can be achieved by iodophor treatment. OMV has been shown to be inactivated by iodophor at 50 mg litre –1 for 15 minutes at 15°C or 25 mg litre –1 for 20 minutes at 15°C

6. VIRAL ERYTHROCYTIC NECROSIS :

6. VIRAL ERYTHROCYTIC NECROSIS Family : iridoviridae Virus : Viral erythrocytic necrosis virus ( VENV)

Geographical Range :

Geographical Range The geographic range of VEN is potentially global in the marine environment. majority of reports from anadromous fish collected from coastal areas of the North Atlantic and North Pacific Oceans.

Host Species :

Host Species The host range of ENV has been reported to extend through Hagfish lampreys sharks, skates and rays Teleost. Among teleosts , virions or cytoplasmic inclusions typical of ENV have been observed in the RBCs of more than 20 marine or anadromous species .

DISEASE SIGNS :

DISEASE SIGNS The most common and consistent disease sign is anemia, which can be observed externally as pale gills and pale internal organs. Fish with clinical VEN also show greatly reduced stamina and losses are often associated with secondary infections . In severe cases, hematocrits may be as low as 2 to 10%.

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Stained blood smears reveal severe blood disorders characterized by : Erythroblastosis leukocytosis erythroid cell destruction cytoplasmic inclusions of differing morphology in erythrocytes and erythroblasts. The percentage of erythrocytes demonstrating inclusions can range from less than 1% in normal-appearing fish to 100% in fish experiencing severe anemia.

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Gills of Pacific herring experimentally infected with ENV (top); note the pale color due to the severe anemia. Bottom fish is an uninfected control. ENV infected fish.

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Red blood cells of Pacific herring experimentally infected with ENV. Note the presence of inclusion bodies (arrows) in a high percentage of erythrocytes.

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Ultrathin section of a red blood cell viewed by transmission electron microscopy. Note the electron-dense core of the icosahedral virions typical of iridoviruses VIRIONS Nucleus Inclusion boies

TRANSMISSION :

TRANSMISSION Vertical transmission is suspected due to the high prevalence of infection in fry from infected brood stock.

DISEASE DIAGNOSTIC PROCEDURES :

DISEASE DIAGNOSTIC PROCEDURES 1 . Presumptive Diagnosis the presumptive diagnosis of VEN depends on observation of inclusion bodies in the cytoplasm of infected erythrocytes. 2. Confirmatory Diagnosis confirmed diagnosis of VEN depends on transmission electron microscopy (TEM) to observe iridovirus -like particles within the cytoplasm of erythrocytes 3. Molecular Assays A standard PCR assay has been developed using genomic sequences of a strain of ENV from Pacific herring .

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