THE MERCK VETERINARY MANUAL
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Viral Diseases of Fish

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Descriptions of viral diseases of fish are rapidly expanding. Viruses are being reported in new species, and interpretation of the significance of findings is also changing. Several viral diseases of ornamental fish are reportable (see Fish Diseases of Regulatory Concern in the USATables).

While viruses of homeothermic animals are cultured at uniform temperatures, fish viruses have wider, but specific, temperature tolerances in fish cell cultures at lower temperatures. Because of this relatively defined temperature range, variation in temperature may enable control, although often it merely induces latency. Because many viral diseases of fish are geographically limited, regulatory agencies and fish farms in disease-free areas consider them exotic diseases and require certification of introduced stocks. Many produce high mortality in young fish and little or no losses in adults, which may become carriers. For these reasons, avoidance of carriers and certification of SPF replacement stocks are frequently required. Specific testing procedures are available. Most vaccines used for control of fish diseases are for bacterial agents; however, use of vaccines to control some viral diseases is being introduced. Drugs are not effective, although antibiotics and other drugs may be used to control secondary bacterial infections. Management techniques that minimize stress and crowding, biosecurity measures, and temperature manipulation hold the greatest promise for control of piscine viral diseases.

One of the oldest recognized fish diseases, carp pox is caused by cyprinid herpesvirus-1. Pox lesions may occur on other species of fish, and are sometimes referred to as fish pox. Lesions typically are smooth and raised and may have a milky appearance. They are benign, non-necrotizing areas of epidermal hyperplasia. Severe cases may result in development of papillomatous growths, and these may be a site of complicating bacterial infection. Generally, lesions are self-limiting and of minimal clinical significance. Carp pox can be a significant problem with koi because the aesthetic quality, and hence the market value, of the animal is severely compromised. For the serious koi enthusiast, carp pox-affected fish should be culled, preferably during quarantine. Surgical removal of pox lesions has not been rewarding.

Koi herpesvirus (KHV), caused by cyprinid herpesvirus-1, was first recognized in 1996. It is currently widespread in the USA and is considered endemic. Confirmed cases must be reported to the state veterinarian and USDA Area Veterinarian in Charge. Because the disease is endemic, regulating bodies report its occurrence to the OIE, but they do not require specific action, such as depopulation, when the disease is reported.

KHV causes clinical disease in koi and common carp. Goldfish and grass carp are refractory to clinical disease but may serve as carriers. Koi that are exposed, but survive, may also serve as carriers. Clinical disease occurs at water temperatures of 72–81°F (22–27°C), with maximum mortality at temperatures of 72–78°F (22–25.5°C). Mortality rates can reach 80–100%. Fish of any age are susceptible, but mortality rates may be higher in younger fish, especially fry. The most obvious lesions are seen on gill tissues, which are severely affected and develop a mottled red and white appearance, with obvious hemorrhage in some cases. An important differential diagnosis is columnaris disease (see Bacterial Diseases of Fish). Affected fish are lethargic, swim at the surface, and may show behavioral signs of respiratory distress. The presence of severe bacterial or parasitic disease may mask the fact that KHV is the primary cause of gill lesions. The disease is transmitted horizontally by exposure to sick or carrier fish and also by exposure to contaminated water, substrate, or equipment.

When KHV is suspected, affected fish can be shipped to a laboratory for confirmation. Freshly dead specimens shipped on ice and received within 24 hr should be adequate. PCR or virus isolation and identification can be used to confirm the infection in dead animals. Because of the value of koi, there is significant demand for nonlethal testing protocols. Blood, gill tissue from biopsy, feces, or mucus may be used to assess the status of suspect fish. A positive cell culture from any of these samples indicates active infection. A positive PCR test indicates virus is present; infection may be active or the fish may be a carrier. Indirect tests using blood samples, including ELISA or virus neutralization, are less straightforward. Negative test results could indicate a true negative or alternatively that the infection is in its early stages and the fish has not yet developed a measurable antibody response. A negative test result could potentially be obtained from a previously infected animal that has had a decrease in circulating antibody; however, such an animal could still function as a carrier. There is a misperception among some hobbyists that a negative blood test is an adequate screening test to rule out carrier status. Practitioners should communicate this clearly to clients, as it is easily misunderstood.

If KHV infection is confirmed in a population of koi, depopulation is strongly recommended. Surviving fish are carriers and can serve as a source of infection for naive fish. Although mortality decreases or stops as water temperature approaches 86°F (30°C), survivors are likely to retain carrier status and therefore put other populations at risk.

Prevention of KHV is best accomplished with careful quarantine protocols. A minimum quarantine of 30 days at 75°F (24°C) is recommended to minimize the chance of introducing KHV to an established population of koi. If disease develops during the quarantine period, fish should be worked up with special consideration for ruling out KHV. Blood tests for KHV antibody can augment but should never replace quarantine. After quarantine, a new fish may be placed in an isolated area with a few fish from the established population and monitored for signs of disease for at least 2 wk as an added precaution. If koi are taken to shows, quarantine protocols should be followed every time they return. Koi enthusiasts should be strongly encouraged to attend English-style shows (as compared to Japanese-style shows) where competing fish are not placed in a common container.

This acute, virulent herpesvirus infection of fry and fingerling channel catfish can cause mortality of >80% at water temperatures ≥25°C in small fish (≤5 cm). As fish age, mortality decreases, and clinical infection in fish >1 yr old is rare. Acute infection often includes a recent history of a stressful event such as handling or transport, low dissolved oxygen, or chemical treatment. Infected fish show signs of ascites, exophthalmos, and hemorrhages in fins. The cell line of choice for virus isolation is channel catfish ovary, followed by serum neutralization to confirm identification. Typical cytopathic effects include cell fusion, syncytia formation, and intranuclear inclusions. There is evidence for vertical transmission of CCV; consequently, survivors of an epizootic should not be used for broodstock. Although CCV can cause severe mortality when an outbreak is in progress, the annual number of cases of CCV in the catfish industry is relatively low.

This disease is caused by a novirhabdovirus in the family Rhabdoviridae, and is listed as an OIE notifiable disease. It is endemic in salmonid (Oncorhynchus spp) populations in the Pacific Northwest and Alaska and has been reported in Atlantic, chum, chinook, sockeye, and kokanee salmon and in cutthroat, steelhead, and rainbow trout. Lake trout and Arctic char, members of the genus Salvelinus, appear resistant. The disease has also been reported in parts of Europe and Asia. Most epizootics have been attributed to importation of infected eggs or fry.

Acute disease in fry < 2 mo old may result in high mortality (> 90%) with few external signs. Disease usually occurs at water temperatures of 10–12°C, although outbreaks occasionally occur at temperatures >15°C. Typical signs include lethargy with sporadic hyperexcitability, including whirling. Sick fish may be darkened with distended abdomens, exophthalmia, pale gills, and mucoid fecal casts. Important differential diagnoses include infectious pancreatic necrosis and viral hemorrhagic septicemia. Hematopoietic tissue in the kidney and spleen are most severely affected by necrosis.

Risk factors include age (fish < 2 mo old are more susceptible), density, and water temperature. Hauling young fish around dams in trucks may be a significant risk factor because of crowding during transit. Although most disease outbreaks have been reported in freshwater, active disease has occurred in Atlantic salmon housed in sea cages. Diagnosis is by viral isolation (from kidney and spleen of young fish and ovarian fluid of broodstock), with confirmation by serum neutralization. Rapid serologic tests are becoming more available. A nonlethal test involving viral isolation from mucus has been reported. The disease is transmitted horizontally through the water, and vertical transmission is suspected. Asymptomatic carrier fish serve as reservoirs of infection.

This disease is caused by a novirhabdovirus in the family Rhabdoviridae, and is a highly regulated disease in the USA. The disease causes marked necrosis of hematopoietic tissue in the kidney, particularly the anterior kidney, but largely spares excretory tubules in the posterior kidney. Rainbow, brook, and lake trout (genus Salvelinus), and Atlantic salmon and brown and golden trout (genus Salmo) are susceptible. The virus also causes disease in a variety of freshwater and marine coldwater fish including pike, turbot, white fish, and sea bass. Viral hemorrhagic septicemia also is found in free-ranging marine fish in the Pacific Northwest, including anadromous salmon (coho and chinook), as well as haddock and cod in the North Sea.

The disease occurs in 3 forms: acute, chronic, and nervous. Acute mortalities occur in rainbow trout fry < 3 g and < 30 days old. In these fish, the kidney is swollen and the anterior segment is necrotic and pale. The liver may be pale with hemorrhagic mottling, and systemic hemorrhage may be visible in the eyes, skin, skeletal muscle, and viscera. The most notable lesion is widespread hemorrhage in the liver, adipose tissue, and within skeletal muscle. Moribund fish lie on the bottom of the tank and may exhibit sporadic flashing and corkscrew swimming behavior. As fish age, mortalities drop from 80–100% to 10–50%. The chronic form is a persistent infection with low red and white blood cell counts; virus can be isolated from all tissues. Chronically infected fish may exhibit few visible external signs. The nervous form of the disease has been reported primarily in cultured freshwater fish but has also been reported in marine fish.

The optimal temperature for active infection is 9–12°C; the virus is unable to replicate at temperatures >15°C. The cell line of choice for virus isolation is bluegill fry (BF-2). Viral identification is confirmed by serum neutralization. Newer diagnostic tests include immunofluorescence, ELISA, and PCR. Viral hemorrhagic septicemia is a heavily regulated disease with disease-free geographic regions defined in Europe. No vaccine is commercially available. Veterinarians working with zoologic collections must ensure that susceptible species received from endemic areas are properly tested and certified disease-free.

This acute, virulent, usually hemorrhagic disease of cultured carp is caused by Rhabdovirus carpio. The disease is listed as notifiable by the OIE. Historically, it was reported in Europe and the former USSR; however, several outbreaks have been reported in the USA between 2002–2007, in both wild fish and cultured ornamental koi. The disease is considered a foreign animal disease in the USA and must be reported. SVC causes disease in common carp, including koi, as well as grass, bighead, silver, and crucian carp. Limited experience suggests that common goldfish may be susceptible.

Clinical signs are nonspecific and may include darkening of the skin, exophthalmia, ascites, pale gills, hemorrhage, and a protruding vent with thick mucoid fecal casts. Pinpoint hemorrhage in the swim bladder is indicative of SVC, if present. Coinfection with Aeromonas or other systemic bacteria may obscure the presence of the virus. The bacterial component of the infection can be controlled with antibiotics; however, depopulation of affected or exposed fish is required in the USA. The disease causes death in both adult and young fish. Clinical disease occurs at cool temperatures, 54–72°F (12–22°C), an important distinction from KHV. The virus is readily isolated in common fish cell lines and identified by serum neutralization and fluorescent antibody tests.

This typically chronic, viral infection of wild or captive marine and freshwater fish is caused by an icosahedral DNA virus of the Iridoviridae family. Infection may be manifest by benign cauliflower-like lesions typically located on fins. The disease affects a wide range of fish and is generally considered global. Within the aquarium trade, painted glass fish are commonly infected. Presumptive diagnosis is based on the presence of enlarged fibroblasts (up to 1 mm), which are easily visualized with a light microscope. Microscopic examination typically reveals the appearance of grape-like clusters of virus-laden cells. Diagnosis is confirmed histologically. Feulgen-positive cytoplasmic inclusions and a hypertrophied nucleus are pathognomonic. The disease is usually self-limiting but is of aesthetic concern.

This is an OIE-notifiable disease. It has been reported in >20 species of marine and anadromous fish (both cultured and free ranging) and is characterized by erythrocytic degeneration. Affected species include Pacific herring, Atlantic cod, and Pacific salmonids (chum, pink, coho, and chinook), steelhead trout, and cultured eels in Taiwan. The disease is chronic, and external signs may be subtle or nonexistent. Sick fish are anemic, which may result in pale gills and internal organs. Severity of the disease is related to age and species of fish, with juveniles <1 g most severely affected.

The characteristic lesion is a single eosinophilic cytoplasmic inclusion body in the circulating erythrocytes of anemic fish. The inclusions are best visualized from Giemsa-stained fresh blood smears. To date, the agent has not been successfully isolated. Histologically, increased hematopoietic activity may be evident in the kidney, and round cytoplasmic inclusions (0.8–4 μm) are found in circulating RBC. Inclusions stain pink or magenta with Giemsa. Other degenerative changes may be evident in RBC, including cytoplasmic vacuolation and margination of nuclear chromatin. Hemolytic anemia with concurrent hemosiderosis and erythroblastosis has been reported in moribund Pacific herring. Multinucleated giant erythroblasts may occasionally be seen in peripheral blood, and macrophages may phagocytize abnormal erythroblasts. A presumptive diagnosis is based on the presence of typical cytoplasmic inclusions in circulating erythrocytes of anemic fish. Confirmation requires visualization of hexagonal virus particles in cytoplasm of affected erythrocytes using transmission electron microscopy. A marine reservoir is suspected but has not been identified. Vertical transmission is suspected due to the high prevalence of infection in fry from infected broodstock.

The ranaviruses are an important group within the family Iridoviridae that affect fish. One of these causes EHN, listed as a notifiable disease by OIE. It was first reported in redfin perch in Australia in the spring of 1984, but has also been shown to cause disease, albeit less severe, in rainbow trout. Similar viruses have been reported in sheatfish in Germany and black bullhead catfish in France and Italy.

EHN is endotheliotropic, producing necrotic lesions in the endothelium of blood vessels and some visceral lesions. Behavioral signs include lethargy, darkening, and erratic swimming. Mortality occurs after 4–5 days. The most consistent lesion associated with EHN is focal necrosis of hematopoietic tissue in the anterior kidney and liver. Necrotic hematopoietic cells may be visible within blood vessels. Presumptive diagnosis is based on clinical signs and isolation of the suspect agent in cell culture. Bluegill fry (BF-2) is the cell line of choice. Detection may also be accomplished using ELISA, immunofluorescence, or electron microscopy. Epizootics of EHN in redfin perch are most common in the spring and summer and almost exclusively involve juvenile fish. Survivors seem to be resistant to future infection. There is no evidence of vertical transmission of EHN, and redfin perch carriers have not been detected. An unidentified reservoir and carrier host is suspected. Fomite transmission of EHN has been demonstrated, and birds have also been shown to carry infected material.

This ranavirus was isolated from moribund largemouth bass in South Carolina in 1995. It was previously isolated from largemouth bass in several Florida lakes but had not been directly associated with disease. It has been found in largemouth bass in most southeastern and many midwestern states. The disease is not well understood because the virus is commonly isolated from tissues of clinically normal fish. In the 1995 fish kill, ∼1,000 fish died over a 2- to 3-mo period in an area that encompasses > 66,000 hectares. Lesions were nonspecific and are still poorly described. Fat-head minnow (FHM) is the cell line of choice for isolation of virus.

Several other iridoviruses have been described in ornamental fish. Two of these were initially reported as being closely related to largemouth bass virus, but more recent work indicates that the isolates from guppy and doctor fish are not as closely related as originally thought. An iridovirus has been described in freshwater angelfish (Pterophyllum scalare) showing signs of systemic disease, but the agent has not been isolated. An iridovirus has been isolated from gouramis in the genus Trichogaster using a tilapia heart cell line. This virus does not grow on FHM cells or other common cell lines used for isolation of fish viruses. The gourami virus has been associated with systemic disease and mortality of Trichogaster spp gouramis. Efforts to fulfill River's postulates were supportive though not conclusive. Clinical disease with largemouth bass virus and the gourami iridovirus seems more severe at water temperatures ≥30°C, based on very limited information.

This is an emerging disease in USA aquaculture. It is classified as a significant disease by OIE, but the USDA has listed it as a federally notifiable disease in the USA. The first report was from farmed Atlantic salmon on the west coast of Norway in 1984. Affected fish were lethargic and severely anemic (PCV <5% in moribund fish). The causative agent is an orthomyxovirus. Acute outbreaks result in high mortality. Initial signs include lethargic fish hanging around the edges of the cage. As the disease progresses, moribund animals lie on the bottom.

The most obvious external lesions are pale gills and hemorrhage in the anterior chamber of the eye. Internally, the liver appears dark and hemorrhagic, an important indication of infectious salmon anemia. Other lesions may include a fibrinous capsule around the liver, a distended stomach filled with viscous mucus, and sometimes hemorrhagic areas on the mucosa. Infected fish often have obvious ascites, and hemorrhage may be present in skeletal muscle. Histologically, the most important lesion is multifocal, hemorrhagic hepatic necrosis, which may appear zonal; hepatocytes may be dark and swollen and necrotic areas are eosinophilic. Circulating RBC are small, and evidence of cytoplasmic vacuolation, nuclear degeneration, and cell fragmentation may be seen. Affected fish may develop lymphocytopenia and thrombocytopenia and an apparent increase in immature RBC in the peripheral circulation. Signs of chronic infection are more subtle but may include hemorrhage in the swim bladder and skin.

Diagnosis is based on clinical signs, with emphasis on anemia (PCV <10%), the gross appearance of a dark liver, and hepatic necrosis. Confirmation can be by viral isolation using the SHK-1 cell line. Virus may be visualized in endothelial cells of cardiac blood vessels using transmission electron microscopy. The agent is enveloped, slightly pleomorphic, and ∼100 nm in size. Suspected cases can also be verified using an immunofluorescent antibody technique on frozen tissue. Transmission is horizontal and virus is shed in skin, mucus, feces, and urine. Sea lice (Lepeophtheirus salmonis) may be a vector; disease outbreaks seem worse when sea lice are present. Currently there is no evidence of vertical transmission. Sea trout have been proposed as a possible reservoir of infection. Protective immunity has been demonstrated in salmon that survive an outbreak. The disease is heavily regulated in Norway and now in the USA, where the USDA should be notified immediately of any suspected cases.

This acute, systemic, contagious disease of salmonid fry and fingerlings is caused by a birnavirus. The virus is the archetype of the aquatic birnaviruses, which are further subdivided into 2 serotypes, A and B, that do not crossreact using serum neutralization. The serotype B group currently consists of only 10 isolates, all European in origin. In contrast, the A serotype contains >200 isolates that have been further subdivided into 9 serotypes, A1–A9. Morbidity and mortality occur only in young animals, usually <3 g; however, virus can be isolated from survivors for the duration of their lives, resulting in a persistent carrier state. Recrudescence of disease in survivors has not been reported. The virus is vertically and horizontally transmitted, widespread, and reported worldwide, except in Iceland and Australia. Rainbow trout are highly susceptible to disease. In the USA, striped bass and their hybrids are recognized as potential carriers. Other species affected include freshwater eels (Anguilla spp), yellowtail, turbot, sea bass, and menhaden, as well as aquatic invertebrates including molluscs and crustaceans. Brook trout are believed to be reservoirs of infection in the USA.

Clinical infection is nonspecific. Diseased fish may be anorectic, ataxic, and display a corkscrew swimming pattern. Externally, fish are darkened; exophthalmia and external petechiation may be evident. Internally, petechiae may be visible on viscera; the gut is typically empty and may contain a yellow exudate. Fecal pseudocysts may be evident in the water column. Histologically, focal areas of coagulative necrosis involve acinar and islet cells of the pancreas and hematopoietic cells of the kidney. Intracytoplasmic viral inclusions may be visible in pancreatic acinar cells. Infection should be confirmed with viral isolation followed by serum neutralization. Most fish cell lines are susceptible. The virus can also be identified using fluorescent antibody, complement fixation and ELISA techniques. There is no treatment for infected fish, but avoidance can be accomplished by purchase of SPF stocks, quarantine, and disinfection of eggs with iodophores (20–50 mg/L). Infectious pancreatic necrosis is not regulated by the USDA, but state regulations exist in various parts of the country.

Last full review/revision July 2011 by Ruth Francis-Floyd, DVM, MS, DACZM

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