Viral Diseases of Fish

One of the oldest recognized fish diseases, carp pox is caused by Cyprinid herpesvirus-1 (CyHV-1). Pox lesions may be seen 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, which 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 in koi because their aesthetic quality, and hence market value, is severely compromised. For the serious koi enthusiast, fish affected with carp pox should be culled, preferably during quarantine. Surgical removal of the lesions has not been rewarding.

Koi herpesvirus (KHV), caused by Cyprinid herpesvirus-3 (CyHV-3), was first recognized in 1996. It is widespread in the USA and considered endemic. Confirmed cases must be reported to the State Veterinarian and the 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 is seen at water temperatures of 72°–81°F (22°–27°C), with maximal 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. 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 moribund fish. It is important to note these tests can result in false-negatives if performed on clinically normal fish. 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 fish that has had a decrease in circulating antibody; however, such a fish could still function as a carrier. There is a misconception among some hobbyists that a negative blood test is an adequate screening test to exclude carrier status. Practitioners should communicate this clearly to owners, because 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 will 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 evaluated with special consideration for excluding KHV. 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 (versus Japanese-style shows), where competing fish are not placed in a common container.

This condition of goldfish is caused by Cyprinid herpesvirus-2 (CyHV-2). It is probably widespread throughout the USA, but it is not a reportable disease. Clinically ill goldfish often are anorectic and exhibit pale gills and ascites. At necropsy, the spleen and kidneys (anterior and posterior) are often enlarged. As is typical for herpesviruses, survivors can be carriers and exhibit clinical signs of disease if subjected to stressors. Water temperatures between 10° and 22°C will result in replication of the virus that can be detected with quantitative PCR. There is no treatment.

A herpesvirus of angelfish (Pterophyllum spp) has been detected by electron microscopy of skin from moribund angelfish. Affected fish produce copious amounts of skin mucus that gives affected fish a grey sheen. Often, these fish have multiple parasitic infestations and bacterial infections, similar to that of KHV in koi. It is suspected that survivors are carriers.

This reportable disease is caused by a Novirhabdovirus and is a member of the family Rhabdoviridae. This disease is listed by OIE as notifiable. Most of the reported hosts are not ornamental fishes, but koi were shown to be susceptible experimentally to genotype IVb. This genotype affects a diverse group of fishes in the Great Lakes region of North America.

This acute, virulent, usually hemorrhagic disease of cultured carp is caused by a Vesiculovirus that, like VHS, is a member of the Rhabdoviridae family. 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. SVC is considered a foreign animal disease in the USA and must be reported. It 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 to have a global distribution. Within the aquarium trade, painted glass fish and marine tropical fishes such as the anemonefishes (Pomacentridae), marine angels (Pomacanthidae), and butterflyfishes (Chaetodontidae) are susceptible. 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.

Several other iridoviruses have been described in ornamental fish. Megalocytiviruses consist of two major groupings, red sea bream iridovirus (RSIV) and infectious spleen and kidney necrosis virus (ISKNV). RSIV has been found in >30 other marine fishes so far; many of the affected species include some tropical fishes kept in aquaria. RSIV is a reportable disease. ISKNV includes megalocytiviruses that primarily affect ornamental freshwater fishes. ISKNV is not currently reportable.

A megalocytivirus has been described in freshwater angelfish (Pterophyllum scalare), but the agent has not been isolated. It can result in high mortality. An iridovirus has also been isolated in the USA from gourami 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 T trichopterus and T leeri gourami. Efforts to fulfill River’s postulates were supportive although not conclusive. Clinical disease with the USA gourami megalocytivirus appears to be more severe at water temperatures ≥30°C, based on very limited information. A megalocytivirus is known from dwarf gourami Trichogaster spp, but it is not known whether it is the same virus that affects gourami in the USA.