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Fish viral pathogens

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Introduction

Viral pathogens are particularly challenging since there are few, if any, effective treatments, and the development of vaccines for delivery in aquatic systems remains elusive. Because of this, good husbandry practices are the best preventative measure for the disease. These practices include maintaining proper water quality, minimizing stress, and a proper quarantine protocol. Stocking density may impact disease levels.

Fish are susceptible to many viral pathogens, some of which are readily identifiable, whereas others remain obscure. Identification is not always possible owing to lack of resources or inability of the virus to grow in available fish cell lines. In many instances viral infection may remain latent until adverse environmental conditions, such as poor water quality, overcrowding, or rough handling, trigger the onset of disease. Frequently the only course is to destroy the fish and effectively disinfect all equipment.

Transmission of disease agents among susceptible fish is not necessarily restricted to water-borne routes. Fish-eating birds such as the Gray Heron (Ardea cinerea) have been shown to transmit viral pathogens via their feces (Infectious Pancreatic Necrosis Virus [IPNV]) or by regurgitation of food (SVCV and Viral Hemorrhagic Septicemia Virus [VHSV]). Blood-sucking parasites such as carp lice (Argulusfoliaceus) and the leech (Piscicola geometra) can serve as mechanical vectors for SVCV. It is possible that similar mechanisms are involved in the transmission of other viral pathogens.

Response to any systemic viral or bacterial infection often results in several nonspecific clinical signs that include lethargy, inappetence, darkening of the skin, exophthalmia, dropsy, respiratory distress, uncoordinated swimming movements, hemorrhages in the skin (especially at the base of the fins and around the vent), and pseudofeces (material including mucus and intestinal epithelium which, caused by the infection, has sloughed off into the gut lumen and is often observed trailing from the vent). Such signs by themselves cannot be used to identify the causative agent of an ongoing infection.

There are no cures available for viral infections in fish, nor are there any vaccines available for their prevention. Rarely (eg, lymphocystis disease), surgical removal of affected areas may be an option, such as when lesions in the mouth region interfere with feeding. However, currently the only effective means of preventing viral disease is to restrict importation of exotic fish species, to comply with quarantine regulations and/or recommendations, to implement disinfection, to observe other hygienic practices in a strict manner, and to optimize living conditions. Generally, the only possible means to eliminate viral disease is to remove the clinically infected fish, as well as any other fish suspected to be a carrier, in a way that prevents further spread of the agent and desinfect all equipment.

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dsDNA viruses, no RNA stage

Cyprinid herpesvirus 2

Taxonomy

viruses - dsDNA viruses, no RNA stage - Herpesvirales - Alloherpesviridae - Cyprinivirus - Cyprinid herpesvirus 2

Synonym: Haematopoietic necrosis herpesvirus of goldfish

Acronym: CyHV-2

Brief facts

CyHV-2 (goldfish herpesvirus or herpesviral hematopoietic necrosis virus) was first described as a herpesvirus from an outbreak of disease in goldfish (Carassius auratus) in the autumn of 1992 and the spring of 1993 in western Japan. Since then, the virus has been isolated from goldfish collections worldwide. This disease can go undetected in latent carriers or undiagnosed because of the limited availability of confirmatory diagnostic tests.

Clinical signs

Clinical signs of CyHV-2 infection are largely nonspecific, and infections may only be suspected because of high mortality rates in farmed goldfish. When present, common antemortem clinical signs include lethargy, anorexia, inappetence, and respiratory signs; but they are often lacking, and mortalities may be the first and only clinical sign of infection. Goldfish of any age may be infected with higher mortalities in juvenile fish. Mortalities may be acute and widespread or chronic with low-grade mortalities persisting over subsequent years. In most reported cases, the onset of clinical signs was correlated with the change to spring or autumn temperatures (15°C– 25°C).

Diagnosis

The initial diagnosis of the disease can be made from gross necropsy and histopathology. Major postmortem lesions include pale gills, coelomic effusion, splenomegaly with white nodules, and swollen kidneys.

Treatment/prevention

There is no known treatment of CyHV-2 infection. Because of the apparent worldwide prevalence of the virus, the best way to control the disease is through prevention of outbreaks. Good husbandry and quarantine protocols are recommended to reduce the chance of a viral outbreak. Fish that recover from infection are considered carriers.

Cyprinid herpesvirus 2 in PubMed

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Cyprinid herpesvirus 3

Taxonomy

viruses - dsDNA viruses, no RNA stage - Herpesvirales - Alloherpesviridae - Cyprinivirus - Cyprinid herpesvirus 3

Synonyms: Koi herpesvirus; Carp nephritis and gill necrosis virus

Acronyms:CyHV-3, KHV

Other names: carp pox, Epithelioma Papillosum

Brief facts

KHV (CyHV-3, carp interstitial nephritis, and gill necrosis virus) infects and causes massive mortality in koi and common carp (Cyprinus carpio). KHV was first reported as a cause of massive fish mortality in Israel in 1998 and is now global in distribution.

Clinical signs

Presumptive diagnosis is based on clinical signs (i.e., macroscopically visible milky-white/ grey plaques), sometimes with a gelatinous appearance, which occur on the body surface, including the fins, and are comparable with drops of candlewax. Individual lesions can be as large as 3 x 7 mm in Koi Carp and they gradually increase in size, the lesions may coalesce to cover large areas. The lesions are unsightly and can develop into tumors after several weeks or months.

Clinical signs include piping (gasping at water surface), elevated opercular rate, gathering near the surface and in well-aerated areas, such as near waterfalls/filter input, excessive mucus from the gills, mottled areas of gill necrosis/discoloration, skin changes, including ulcers, hemorrhages, sloughing of scales, and increased or decreased mucus production, lethargy, anorexia, sunken eyes (enophthalmos),  notched nose, erratic swimming, hanging with a head-down position in the water column.

On postmortem examination, all fish have gill necrosis, which often presents as patchy regions of white discoloration. Other gross necropsy changes are nonspecific and may include darkening or mottling of internal organs (e.g., the spleen, kidney, or liver) and coelomic fluid accumulation. Secondary skin and gill parasitic and bacterial infections are extremely common.

Transmission

Virulent virus is shed via the feces, urine, and skin/gill mucus. The main portal of entry for KHV in koi has been shown to be the skin, with systemic spread of the virus from the skin and gills through the bloodstream (via white blood cells) to the kidney and other organs, such as the spleen, liver, and intestines. Branchitis (gill damage) and interstitial nephritis are seen histologically as early as 2 days after infection, but mortality does not typically occur until 6 to 8 days after infection. Typically, mortality approaches 70% to 100% over a course of 7 to 21 days. Common carp that recover from KHV infection can become persistently infected and may shed the virus to infect naive fish at water temperatures greater than 20°C (68°F).

Treatment/prevention

There is no effective treatment of KHV. Depopulation and disinfection is recommended because fish that survive infection are considered carriers. In private collections, some owners may elect to treat their pet fish. The water temperature can be increased to greater than 29°C (84°F) to help reduce morbidity and mortality. Secondary bacterial and parasitic infections are extremely common and must be treated accordingly. Prolonged bath immersion with salt (0.1%–0.3%) can be used to decrease osmotic stresses associated with gill necrosis and cutaneous ulceration. Surviving fish are considered carriers and should not be mixed with naive fish.

Clinical signs in cyprinid herpesvirus 3–infected fish.
A) Severe gill necrosis; B) hyperemia at the base of the caudal fin; C) herpetic skin lesions on the body and fin erosion.
Cyprinid Herpesvirus 3. Michel B. et al. Emerg Infect Dis. Dec 2010; 16(12): 1835–1843.

Cyprinid herpesvirus 3 in PubMed

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Epizootic hematopoietic necrosis virus (EHNV)

Taxonomy

viruses - dsDNA viruses, no RNA stage - Iridoviridae - Ranavirus - Epizootic haematopoietic necrosis virus

Acronym: EHNV

Brief facts

Ranaviruses, unlike the alloherpesviruses, lack host specificity. This lack of host specificity allows them to cause disease across many species, although the clinical signs of disease may vary by species. For example, EHNV, the first iridovirus to cause epizootic mortality in vertebrates, was discovered in Australia in 1985. Outbreaks of this disease caused mortality in wild redfin perch (Perca fluviatilis) but less severe disease in rainbow trout (Oncorhynchus mykiss).

Clinical signs

All ranaviruses in fish, except for Santee-Cooper ranavirus, produce a systemic necrotizing infection. Epizootic hematopoietic necrosis virus produces an often-fatal systemic disease in redfin perch and rainbow trout. On postmortem examination, there is often multifocal necrosis of the liver, spleen, and renal hematopoietic tissue. Grossly, the kidney and spleen may be swollen, and the liver will have miliary (resembling millet seed) pale foci. There may be petechial hemorrhage at the base of the fins.

Transmission

Natural transmission is assumed to be through direct contact with infected fish or ingestion of viral particles in food or water.

Epizootic haematopoietic necrosis virus in PubMed

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Santee-Cooper ranavirus

Taxonomy

viruses - dsDNA viruses, no RNA stage - Iridoviridae - Ranavirus - Santee-Cooper ranavirus

Brief facts

Unlike other ranaviruses, Santee-Cooper ranaviruses do not produce a systemic necrotizing infection. Santee Cooper ranavirus infection may be subclinical or cause mortalities. Clinical signs include erratic swimming or hyperbuoyancy caused by effects on the swim bladder, but this is uncommon. Experimentally, the mortality rate of infection varies based on the isolate of SCV used and the route of infection.

Clinical signs

Transmission

Natural transmission is assumed to be through direct contact with infected fish or ingestion of viral particles in food or water.

Santee-Cooper ranavirus in PubMed

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Lymphocystivirus

Taxonomy

viruses - dsDNA viruses, no RNA stage - Iridoviridae - Lymphocystivirus

Brief facts

Lymphocystis disease, caused by iridoviruses belonging to the genus Lymphocystivirus, is a chronic disease that occurs worldwide and is found in a broad range of warm- and cold-water and freshwater and saltwater fish species.

Clinical signs

The disease is characterized by the occurrence of macroscopically visible pearl-like or wart-like nodules on the skin and fins and sometimes in the mouth region, gills, or eye. The nodules are normally 0.3 to 2.0 mm in diameter. They can vary in color and appear either white, cream, brown, grey, or pink, depending on the overlying epithelium and state of vascularization. Normally the nodules take 1 to 3 months or, sometimes, up to a year to develop and are caused by infection of connective tissue fibroblasts, usually in the skin but sometimes on internal organs such as the spleen. These lymphocysts develop as the grossly hypertrophic infected cells are encapsulated by proliferating fibroblasts and the cysts are invaded by inflammatory cells (lymphocytes, plasma cells, macrophages, and polymorphonuclear leucocytes). This inflammatory response marks the beginning of the healing process that can take up to 9 months. The cysts eventually turn necrotic and slough off leaving an intact epidermis. Although the infection is seldom fatal, it is unsightly and can interfere with feeding when the lesions are in the mouth region.

Transmission

It is probable that infection occurs via skin abrasions, gills, or by ingestion of infected cells, and dissemination of virus occurs when cysts slough off and/or rupture.

Diagnosis

The disease is diagnosed by the appearance of the nodules but can sometimes be confused with other infections such as "white spot" caused by Ichthyophthirius multifiliis. Definitive diagnosis of lymphocystic disease is made by histological examination, isolation of the causative virus in cell culture when possible, and/or examination by electron microscopy.

Lymphocystis+fish in PubMed

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Megalocytiviruses

Taxonomy

viruses - dsDNA viruses, no RNA stage - Iridoviridae - Megalocytivirus

Brief facts

There are currently three well-described viruses within the Megalocytivirus genus, including infectious Spleen and Kidney Necrosis Virus (ISKNV), Red Sea Bream Iridovirus (RSIV), Turbot Reddish Body Iridovirus (TRBIV), or Turbot Iridiovirus. ISKNV and closely related viral strains have caused disease in numerous species of freshwater and marine fish, including grouper, gourami, cichlid, red sea bream, angelfish, sea bass, and lamprey. RSIV was first discovered in the early 1990s in Japan and has been reported in Asian marine finfish. TRBIV mainly affects Asian flounder species. Megalocytivirus infections have been reported in several common ornamental fish, including Banggai cardinalfish (Pterapogon kauderni), freshwater angelfish (Pterophyllum scalare), other freshwater cichlids, sailfin mollies (Poecilia latipinna), other common live-bearers, and numerous gourami species.

Clinical signs

Fish infected with any of the megalocytiviruses show nonspecific signs of disease, including lethargy, loss of appetite, darkening, abnormal swimming or position in the water column, increased respiration, coelomic distension, ulceration/ hemorrhages, pale gills/anemia, fin erosion, white feces, and death. Mortality may be up to 100% in some outbreaks. On postmortem examination, there will be necrosis of internal organs, especially the spleen, kidney, and liver. Other affected organs include the muscles, gonad, heart, gills, and GI tract. There may be amber or hemorrhagic fluid in the coelomic cavity. The onset of clinical signs for megalocytiviruses has been correlated with environmental stressors that weaken the immune system and warmer temperatures. Megalocytiviruses have been reported to cause disease at water temperatures ranging from 20°C to 32°C (68°F-90°F). In a study of RSIV in rock bream (Oplegnathus fasciatus), no infections were seen in temperatures less than 12°C (54°F), and the incubation period for disease decreased as the temperature was increased to 30°C (86°F).

Transmission

Natural transmission is assumed to be through direct contact with infected fish or ingestion of viral particles in food or water.

Megalocytivirus+fish in PubMed

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ssRNA positive-strand viruses, no DNA stage

Betanodavirus

Taxonomy

viruses - ssRNA viruses - ssRNA positive-strand viruses, no DNA stage - Nodaviridae - Betanodavirus

Brief facts

Viruses in the family Nodaviridae are non-enveloped RNA viruses with an icosahedral capsid roughly 29 to 35 nm in diameter. Family Nodaviridae is divided into 2 major genera or clades: Alphanodavirus, which primarily affect insects, and Betanodavirus, which primarily affect fish. The terms Viral Nervous Necrosis, Encephalopathy, and Vacuolating Encephalopathy and Retinopathy (VER) have all been used to describe the signs of betanodaviral infections.

The virus infects a large range of host species - at least 40 species of marine and freshwater fish world-wide - and the known host range continues to expand as new species of fish are used for aquaculture. Several betanodaviruses have been described and have been found on all continents except Africa.

Clinical signs

Most fish are affected as larvae or juveniles, although outbreaks of disease have been seen in older fish in association with high water temperatures and other environmental stressors. Mortality may be up to 100%. Infected fish show signs correlated to the lesions in the brain and retina, including abnormalities in movement, sight, and coloration. Larval barramundi and halibut become pale, whereas groupers, juvenile halibut, European sea bass, and turbot become dark. Fish will seem to be uncoordinated and darting can be seen. Flatfish may show looping swimming behavior and rest upside down.

Diagnosis

Tentative diagnosis is made on histologic examination of the central nervous system. The consistent finding on histology among all species is the vacuolization and necrosis of the central nervous system.

Betanodavirus in PubMed

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ssRNA negative-strand viruses

Spring viraemia of carp virus

Taxonomy

viruses - ssRNA viruses - ssRNA negative-strand viruses - Mononegavirales - Rhabdoviridae - Vesiculovirus - Spring viraemia of carp virus

Synonyms: Spring viremia of carp virus; Rhabdovirus carpio

Acronym: SVCV

Brief facts

Spring Viraemia of Carp, caused by the rhabdovirus Rhabdovirus carpio, is quoted as "undoubtedly the most important virus disease of ornamental, as well as wild and farmed carp". It has a worldwide distribution except for North America and Australia and occurs mainly in young fish (less than 1 year old) of all major cyprinid species. In addition, guppies have been shown to be experimentally susceptible. Between 1998 and 2002, outbreaks of SVC were reported in ornamental and wild fish in Europe and America.

Clinical signs

A variety of clinical signs have been described, most of which are nonspecific. These include lethargy, darkening of the skin, respiratory distress, exophthalmia, petechial hemorrhages of the skin and gills, pseudofeces, inflamed and protruding vent, and loss of balance (sometimes fish appear to stand on their heads or their tails). Internal signs include those typical of a viral septicemia with all organs affected, i.e. inflammatory edema, necrosis in all organs (liver, pancreas, kidney, heart, brain, intestine, swimbladder), visceral hemorrhages and serosanguineous (blood cells with serum) fluid in the abdominal cavity. Inflammation of the swimbladder is the cause of loss of balance; in cases where only one chamber of the swimbladder is involved, head/tail standing is often exhibited, depending on whether the posterior or anterior chamber is affected.

Spring Viraemia of Carp in PubMed

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dsRNA viruses

Aquabirnavirus

Taxonomy

viruses - dsRNA viruses - Birnaviridae - Aquabirnavirus - Infectious pancreatic necrosis virus

Brief facts

Aquabirnavirus is the largest and most diverse of the three genera within the family Birnaviridae - non-enveloped viruses with a bi-segmented, double-stranded RNA genome. The type species, Infectious Pancreatic Necrosis Virus (IPNV), was the first fish virus isolated in cell culture and until recently has remained one of the most intensely studied viruses of fish. The associated disease in farmed trout was recognized as early as the 1940s. Infectious pancreatic necrosis in its acute form can cause up to 100% mortality in young salmonids and remains one of the most significant diseases of major concern to the salmonid aquaculture industry. A vast range of IPNV and IPN-like viruses has been isolated from a very wide host range of diseased and non-diseased salmonid and non-salmonid fish species and invertebrates world-wide. An example of a pathogenic marine aquabirnavirus (MABV) is Yellowtail Ascites Virus (YAV), which was the first aquabirnavirus isolated from marine fish, yellowtail (Seriola quinqueradiata) in Japan. Since then MABV have been detected in various marine hosts. This diversity within the Aquabirnavirus genus makes classification down to the species level difficult.

IPN was first recognized as an acute contagious disease of young salmonid fry in the freshwater phase of production that could cause up to 100% mortality. More recently, disease associated with significant mortality has emerged in the post-smolt, seawater stages.

Transmission

In salmonids, the mode of virus transmission by shedding via the feces, and excretory and sexual products (ie, both horizontal and vertical routes) with viral entry occurring via the gills, or lateral line pores or by ingestion of contaminated food is well established. In ornamental fish, vertical transmission has been confirmed experimentally in zebra fish (Danio rerio). The majority of fish that survive a disease outbreak become sub-clinical carriers—fish that are persistently infected with no clinical signs. These sub-clinical carriers are a source of horizontal transmission, shedding virus in their feces particularly under stressful conditions such as spawning.

Aquabirnavirus in PubMed

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References

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