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Diseases of Fish
by Robert B. Moeller Jr., DVM

California Animal Health and Food Safety Laboratory System
University of California











Adrenal Gland



Thyroid Gland


Endocrine Pancreas


Parathyroid Glands


Ultimobranchial Gland


Corpuscles of Stannius




Pineal Gland















Lateral line system



Necropsy and Biopsy Procedures​

Fish, like other vertebrates, have a complex nervous system and when handled, can experience stress. When performing most diagnostic procedures, fish should be anesthetized before handling. If a fish is to be submitted for pathology, euthanasia should be done prior to placing the animal into 10% formalin or other fixative. It would be considered inhumane to place a fish in 10% neural buffered formalin or other fixative without euthanasia.

The 1993 AVMA Report of the AVMA Panel on Euthanasia states that acceptable anesthetics to be used for the euthanasia of fish are tricaine methane sulfonate, benzocaine and barbiturates. A conditionally acceptable method for euthanasia is a blow to the head followed by decapitation. Other commonly used methods are carbon dioxide (four alka-selzer tablets to 500 ml of water), electrocution and hypothermia. Other anesthetic agents are available for immobilizing fish for euthanasia; an excellent review of these agents and their mechanism of action can be found in Stoskopf's book, Fish Medicine (1993).

The preferred method of euthanasia would be to anesthetize the fish to a deep plane of anesthesia (stage III or stage IV) and then sever the spinal cord just caudal to the brain. The most common and practical way to anesthetize a fish is to place the anesthetic agent in water. The fish will go through all four stages of anesthesia prior to death. The four stages of anesthesia and the clinical presentation of each are as follows:

Stage I; Induction and light sedation: The fish goes through an excitement phase with erratic swimming followed by reduced activity. The respiratory rate increases and there is a loss of some response to tactile stimulation.

STAGE II; Sedation: Fish swim slowly; have decreased gill movement (respiration), and a loss of equilibrium.

STAGE III; Anesthesia: Fish have a complete loss of equilibrium and are unable to swim. Gill movement (respiration) becomes very slow. The fish is unresponsive to external stimuli.

Stage IV; Anesthetic overdose: The fish has a total loss of gill movement and the opercules become distended. The fish goes into cardiac arrest.

Collecting Samples for Bacteria and Fungi​

Sampling for bacteria and fungi should be done on fish that are brought in for examination alive or from fresh fish that had died only recently (usually less than 6 hours).

Ideally, the fish is alive when sampling cutaneous lesions. The area to be cultured should not be handled prior to culturing. Like cutaneous smears, large ulcerated areas should be avoided and small developing lesions cultured. The sterile loop or culturette should be rubbed into the lesion.

As with cutaneous lesions, gills from live fish are the best to culture. Gills are cultured by gently rubbing and rolling the sterile culturette through the gill arches. The culturette should pick up abundant mucus on the tip of the culturette. Since the gills and cutaneous lesions are exposed to the aqueous environment, a mixed bacterial culture should be expected. If a pure culture of potential pathologic bacteria is obtained, this should be considered a possible cause of disease in this fish.

The kidney is one of the most important internal organs to culture. There are two methods of culturing the kidney. The first method is to cut the dorsal fin off, sterilize the open area with heat, cut the vertebra with a sterile scissors or scalpel and snap the fish by bringing the head and tail together. This exposes the kidney for culturing. The second method, can allow for possible contamination of internal organs. Here the fish is dipped into 70% alcohol and the abdominal cavity opened aseptically to allow all organs to be exposed. Sterilize with heat, the desired internal organs to be cultured, cut open the organ with a sterile scalpel and culture.

Another method for culturing, particularly in cases where a bacterial septicemia is suspected, is to examine heart blood. Collection of heart blood from the atrium is most productive since the atrium contains phagocytic cells that assist in clearing bacteria from the blood.

Biopsy Procedures​

For biopsy specimens and bacterial cultures, a fish does not need to be killed. The fish should be anesthetized prior to performing most clinical examinations and biopsies. Biopsy procedures on fish usually are cutaneous smears, fin biopsies and gill biopsies.

Cutaneous smears are done primarily for ectoparasites. Large ulcerated lesions should be avoided; Try to find smaller developing lesions for sampling. Prior to performing cutaneous smears, bacterial cultures should be taken. The procedure for cutaneous smears involves passing several clean microscope slides over the area of interest. Only light pressure on the glass slide needs to be used to remove some epidermis and mucus. On one slide, a drop of water is placed on the smear and a cover slip is placed on the slide for examination. The other slides should be air-dried or fixed in alcohol. These are stained with either new methyl blue stain or Diff-Quick stain.

A fin biopsy is accomplished by spreading out the fin and a triangular wedge shaped piece of tissue is cut between the rays of the fin. Place the fin biopsy on a slide with water and cover slip for examination.

A gill biopsy is performed by cutting a few tips of the primary lamella with the blades of the scissors. Place the lamellar tips on the slide with a drop of water, cover slip and examine. Both fin and gill biopsies should not cause undue harm to a fish.

Necropsy Procedure​

Ideally, the fish should be submitted alive for the post mortem examination. This gives the pathologist a chance to observe the fish prior to euthanasia and note any important clinical signs. Unfortunately, some situations do not allow the pathologist to evaluate the fish while they are alive. Fish should be dead less than 6 hours. Fish found floating in a tank longer than 6 hours are poor candidates for necropsying due to post mortem autolysis. Dead fish should be wrapped in paper or gauze and refrigerated. Do not freeze the fish.

Prior to performing the necropsy, insure that all necropsy tools, sterile loop or culturettes, glass slides for impression smears, 70% alcohol and 10% neutral buffered formalin or Bouin's solution (I prefer Formalin) are available. A systematic approach should be used when performing the necropsy. Evaluate the external surface and note the general body condition of the fish, identify and note lesions on the skin, fins, eyes, oral cavity and anus. Take cultures of the desired lesions.

After completion of the external examination, place the fish in lateral recumbency on a disposable towel. Remove the eyes and then the operculum with the pseudobranch; place these in formalin. Remove the second and third gill arches being careful not to crush the primary lamella. Take several primary lamella from one of the gill arches and place on the glass slide for parasitic examination. Place the remaining gills into the fixation solution.

Using aseptic techniques, open the abdominal cavity by cutting through the pectoral girdle to the spine and follow the abdominal cavity to the anus, extend this cut along the ventral midline from the gills to the anus and remove the body wall. Remove the body organs (heart, liver, intestines, spleen, gonads and swim bladder) for examination. When submitting the swim bladder for histopathology, insure that the red gas-forming organ is present. Sample both the anterior and posterior kidney in fish with both kidneys. In fish with fused kidneys, insure that anterior and posterior sections are submitted for examination.

Remove the brain by opening the skull just dorsal to the eyes and removing the bones over the brain. Sample all cutaneous lesions for histopathology. Insure that normal tissue from the margin of the lesion are submitted with the lesions. Cut into the skeletal muscle and look for parasitic cysts. Finally, open the stomach and intestine and examine food material.

If toxicology is desired, be sure to submit gills, kidney, liver, skeletal muscle, and fat. Toxicologic samples should be immediately frozen and stored in at -70 degrees C. Analysis of the tissue should occur as soon as possible after collection.

Viral Diseases

1) Lymphocystis Disease

A) Iridovirus

B) Observed in most freshwater and saltwater species.

C) Clinically, fish are presented with variably sized white to yellow cauliflower-like growths on the skin, fins, and occasional gills. Occasionally, this virus may go systemic with white nodules on the mesentery and peritoneum.

D) Histopathology: Fibroblast undergoes cytomegaly with many basophilic cytoplasmic inclusion bodies and a thick outer hyalin capsule. The inflammatory response is variable but is usually a chronic lymphocytic inflammatory infiltrate.

E) The disease gains entry through epidermal abrasions. The virus infects dermal fibroblasts.

F) The disease is self limiting and refractory to treatment. Nodules may last several months and cause infected fish to be susceptible to secondary bacterial infections. Reinfection can occur.

2) Herpesvirus salmonis (Herpesvirus disease of Salmonids)

A) Herpesvirus

B) Disease is observed primarily in the fry of rainbow trout.

C) Clinically the fish are lethargic with prominent gill pallor. Mucoid fecal casts are commonly observed trailing from vent.

D) Lesions: 1) Exophthalmus and ascites
2) Low hematocrit and numerous immature
3) Hemorrhage in eyes and base of fins

E) Histopathology:

1) Multifocal areas of necrosis of the
myocardium, liver, kidney, and posterior
gut (leading to cast formation)

2) Syncytial cells involving the acinar cells of the pancreas is considered to be pathognomonic sign.

F) Transmission of the virus is believed to be direct.

G) Control is by avoiding exposing susceptible trout to the virus. If the disease occurs, raising the water temperature to 15 C or more will minimize losses.

3) Channel Catfish Virus

A) Herpesvirus

B) Observed in fry or fingerling channel catfish (less than 10-gram weight) during the summer when water temperatures are above 22oC.

C) Clinically these fish usually show erratic swimming or spiraling followed by terminal lethargy. Mortality is very high.

D) Lesions: 1) Hemorrhage at the base of the fins and skins;
2) Ascites; exophthalmos; and pale gills;
3) Kidneys swollen and pale with hemorrhage;
4) Spleen is enlarged and dark red;
5) Gills usually pale;

E) Histopathology: Multifocal areas of necrosis and hemorrhage
are observed in the posterior kidney, liver, intestines, and spleen.

F) Infection is direct with transmission of the virus in the water or feed. Piscivorous birds, snakes, or turtles may mechanically carry the virus from pond to pond. Transovarian transmission has not been conclusively demonstrated but is suspected. Survivors are persistently infected and become carriers for life.

G) Control of the disease is by sanitation, purchasing of virus free brood stock and lowering water temperature to less than 19 C during an outbreak to lessen the mortality.

4) Epithelioma papillosum (Fish Pox)

A) Herpesvirus cyprini (Cyprinid herpesvirus 1)

B) Non-fatal disease is observed in carp and other cyprinids

C) Lesions: Elevation of the epidermis with the formation of white to yellow plaques over the body of the fish. Healed lesions usually turn black.

D) Histopathology: There is epidermal hyperplasia with the epithelial cells occasionally demonstrating intranuclear inclusion bodies.

E) Transmission is unknown, however, it is probably direct.

5) Infectious Hematopoietic Necrosis (IHN)

A) Rhabdovirus

B) The disease is observed in the fry of trout (rainbow) and salmon (Chinook and sockeye) with mortality up to 100%.

C) Clinical signs and lesions:

1) Fish become lethargic or hyperactive.
2) The fish become dark due to increase in pigmentation.
3) Exophthalmus, abdominal distension, and fecal cast.
4) Hemorrhage on skin and viscera primarily at base of
fins, behind the skull, and above the lateral line.
5) Anemia with pale gills.
6) Surviving fish may develop scoliosis.

D) Histopathology: There is prominent necrosis of hematopoietic tissue including melanomacrophages of the kidney, red pulp of the spleen and hepatic parenchyma. Necrosis of the submucosal eosinophilic granular cells is considered pathognomonic for IHN. (This lesion is observed in other systemic viral diseases.) Intranuclear and intracytoplasmic inclusions are occasionally observed in acinar and islet cells of pancreas.

E) The virus is transmitted by direct contact with infected
survivors or by feeding contaminated feed. The virus is probably shed in contaminated semen and eggs. The disease is most severe at 10oC and rare at temperatures above 15oC.

6) Viral Hemorrhagic septicemia

A) Rhabdovirus

B) Widespread and very contagious viral disease of rainbow trout. This is a serious disease of trout in Europe. Affects both salmonids in fresh water and seawater. Disease occurs in temperatures below 14oC.

C) Two forms of the Disease --- Acute and Chronic

1) Acute disease: High mortality in affected fish. Fish have pale gills, dark body coloration, ascites, exophthalmus and erratic swimming behavior (spiraling). Hemorrhage is a common finding in the eyes, skin, serosal surfaces of the intestines and muscles. Necrosis of the hematopoietic and lymphoid elements of the anterior kidney and congestion and necrosis of the hepatic parenchyma are histopathologic findings.

2) Chronic disease: See a slower prolonged mortality. Fish become lethargic, have pale anemic gills, darken skin coloration, exophthalmus, and distention of the abdominal cavity. Internal organs are commonly involved with splenomegaly, hepatomegaly, and swollen kidneys.

D) Turbot, sea bass, and Atlantic salmon are commonly affected by similar viruses.

E) Transmission is believed to be direct with contact of carriers and contaminated water and feed. Vertical transmission via the egg is not reported.

7) Spring Viremia of Carp (SVC) and Swim Bladder Infection virus (SBI)

A) Caused by several subtypes of Rhabdovirus carpio.

B) Disease occurs in carp and other cyprinids.

C) Clinical Signs and Lesions:

1) Loss of coordination and equilibrium.
2) Exophthalmus and abdominal distension (ascites).
3) Inflamed and swollen vent.
4) Edema and hemorrhage in many organs.
5) In SBI see pronounced inflammation and hemorrhage of swim bladder.

D. Transmission: Virus shed in feces and found in contaminated eggs.

8) Infectious Pancreatic Necrosis (IPN)

A) Birnavirus

B) Affects most salmonids primarily rainbow trout and brook trout. IPN has also been implicated in disease among several nonsalmonid fish.

C) Clinical signs and lesions:

1) IPN is characterized by a sudden explosive outbreak with high mortality.
2) Affected fish become dark and rotate their bodies while swimming.
3) Diseased fish usually have distended abdomens and exophthalmus.
4) The presence of a gelatinous material in the stomach and anterior intestine is highly suggestive of IPN; mucoid fecal casts are common.
5) Infected fish commonly have a low hematocrit and hemorrhage in gut, primarily in the area of the pyloric ceca.

D) Histopathology:

Histologically, there is necrosis of the pancreatic acini, gut mucosa, and renal hematopoietic elements. A moderate inflammatory infiltrate is usually observed around the pancreatic acini. Hyalin degeneration of skeletal muscle is also observed.

E) Virus can be transmitted vertically in the eggs.

Bacterial Disease

1) Aeromonas hydrophila (Bacterial Hemorrhagic Septicemia)

A) Gram negative motile rods

B) Effects many freshwater species and usually is associated with stress and overcrowding.

C) The clinical signs and lesions are variable. The most common finding is hemorrhage in skin, fins, oral cavity and muscles with superficial ulceration of the epidermis. Occasionally cavitary ulcers (similar to A. salmonicida) are observed. Exophthalmus and ascites are commonly observed. Splenomegaly and swollen kidneys are common. Histologically, multifocal areas of necrosis in the spleen, liver, kidney and heart with numerous rod shaped bacteria are observed.

D) Diagnosis is rendered by culturing the organism from affected animals: Remember this is a common water saprophyte with a great variation in virulence in serotypes.

E) Disease is transmitted via contaminated water or diseased fish.

2) Pseudomonas fluorescens

A) Short motile Gram-negative rods with polar flagella.

B) Lesions similar to Aeromonas hydrophila with a hemorrhagic septicemia resulting in hemorrhage of the fins and tail and ulceration of the skin.

C) Pseudomonas anquilliseptica causes a serious problem in Japanese eels with a septicemia resulting in petechial hemorrhage on fins and tail and ulceration of the skin.

3) Vibrio

A) Gram negative rod, lives primarily in a marine environment

B) Vibrio septicemia: V. alginolyticus / V. anquillarum / V. salmonicida

1. Septicemia has similar lesions to Aeromonas hydrophila.

2. See hemorrhage in the skin of the tail and fins, ulceration of the skin, hemorrhage in the muscles and serosal surfaces. The spleen may be enlarged and bright red. Histologically may see necrosis of the liver, kidney, spleen and occasionally the gut mucosa.

c) Ulcer Disease of Damselfish: V. damsela
1. Deep skin ulcers and necrotizing myositis.

2. Lesions similar to Aeromonas salmonicida.

D) Vibrio salmonicida: Hitra disease or Cold water vibriosis

4) Edwardsiella tarda (Edwardsiella septicemia)

A) Gram negative motile pleomorphic curved rod

B) The disease affects primarily channel catfish but also observed in goldfish, golden shiners, largemouth bass, and the brown bullhead. This organism is the most serious disease involving the eel culture of Asia.

C) The lesions are similar to A. hydrophila with small cutaneous ulcers and hemorrhage observed both in the skin and muscle. Muscle lesions often develop into large gas filled (malodorous) cavities. Diseased fish lose control over the posterior half of their body yet continue to feed.

5) Edwardsiella ictaluri (Enteric septicemia of catfish)

A. Gram negative motile pleomorphic curved rod

B. Disease affects primarily fingerlings and yearling catfish

C. Clinical signs of enteric septicemia of catfish closely resembles those of other systemic bacterial infections. The most characteristic external lesion is the presence of a raised or open ulcer on the frontal bone of the skull between the eyes (Hole in the head disease).

6) Aeromonas salmonicida (Furunculosis, Ulcerative disease of goldfish)

A. Gram negative non-motile short rod

B. Bacteria affects primarily salmonids but other freshwater fish can be affected.

C. Clinically the disease may present as a septicemia with hemorrhage in the muscles and other sites. The major lesion is a subcutaneous swelling that often causes an ulcerative dermatitis. In chronic disease these lesions may cavitate into the adjacent musculature. In the septicemic disease, there is splenomegaly, ascites, and swelling of the kidneys. Histologically, there is necrosis of the affected tissue with abundant colonies of bacteria and few inflammatory cells due to the bacteria's leukocytolytic exotoxin.

D. The disease is transmitted by contact with diseased fish, contaminated water, fomites, and infected eggs.

7) Yersinia ruckeri (Enteric red mouth)

A. Gram negative motile rod

B. The bacteria affects salmonids; rainbow trout are the most susceptible.

C. Clinically this disease manifest itself as a septicemia with exophthalmus, ascites, and hemorrhage and ulceration of the jaw, palate, gills and operculum. Hemorrhage of the musculature and serosal surfaces of the intestines, splenomegaly, and kidney swelling are common. Histologically numerous bacterial colonies admixed with inflammatory cells are observed in many areas of necrosis involving the liver, spleen and kidney.

D. The disease is transmitted by contact with diseased or carrier fish, and contaminated water. Bacteria persist in asymptomatic non-salmonid fish and in some birds.

8) Streptococcus iniae

A. Beta-hemolytic Streptococcus (Note: Beta hemolysin may not be present in culture media in all cases leading to the possible believe that this bacteria is a non-pathogen.)

B. Disease of tilapia, hybrid striped bass and rainbow trout.

C. Major problem in the tilapia industry. Streptococcus iniae presents either as an acute fulminating septicemia or in a chronic form limited primarily to the central nervous system. The septicemic form may present with hemorrhage of the fins, skin, and serosal surfaces. Ulcers may appear. Microscopically, one observes a meningoencephalitis, polyserositis, epicarditis, myocarditis and/or cellulitis. Cocci/diplococci are present in the inflammation. In the chronic form, granulomas or granulomatous inflammation are evident in the liver, kidney, and brain(meningoencephalitis). In the chronic disease, the brain is the best organ to culture.

D. Streptococcus iniae is a problem primarily of closed recirculating culture system. Probably associated with overcrowding and poor water quality - high nitrates. Depopulation, disinfection and restocking with disease free fish are the best means of elimination of the organism.

E. The bacteria is known to be a zoonotic agent. Individuals who have handled infected fish have developed cellulitis of the hands and endocarditis.

9) Flexibacter columnaris (Columnaris disease or Saddleback disease)

A. Gram negative slender rods (3-8 microns)

B. The disease is a serious disease of young salmonids, catfish and many other fish.

C. This is a highly communicable disease. Lesions usually first appear as small white spots on the caudal fin and progresses towards the head. The caudal fin and anal fins may become severely eroded. As the disease progresses, the skin is often involved with numerous gray white ulcers. Gills are a common site of damage and may be the only affected area. The gill lesions are characterized by necrosis of the distal end of the gill filament that progresses basally to involve the entire filament.

D. Flexibacter columnaris infections are frequently associated with stress conditions. Predisposing factors for Columnaris disease are high water temperature (25oC-32oC.), crowding, injury, and poor water quality (low oxygen and increased concentrations of free ammonia).

E. Flexibacter maritimus: cause similar problems in salt-water environment.

F. Flexibacter psychrophilus causes Cold Water Disease or Peduncle disease. Fish develop dark skin, hemorrhage at the base of fins, and anemia with pale gills with increase mucus. Hemorrhage into the muscles is common. Periostitis of cranial and vertebral bones is common in chronic cases. A chronic meningoencephalitis occasionally is observed with abnormal and erratic swimming.

10) Bacterial Gill Disease

A. Bacterial gill disease is caused by a variety of bacteria. Flexibacter columnaris, Flexibacter psychrophilus, Cytophagy psychrophila and various species of Flavobacterium (all are gram negative rods) are the primary bacteria involved in this disease.

B. Fry are the most susceptible to the disease, however, all ages may be affected. Clinically the fish become anorectic, and face the water current. Prominent hyperplasia (mucus and epithelial) of the gills is evident on gross and microscopic examination. Microscopically one observes proliferation of the epithelium that result in clubbing and fusion of the lamella. Necrosis of the gill lamella occurs in serious cases.

C. Overcrowding, accumulation of metabolite waste products (particularly ammonia), organic matter in the water, and an increase in water temperature may all be predisposing factors.

11) Cytophaga psychrophila (Rainbow Trout Fry Anemia)

A. Gram negative filamentous bacteria

B. Occurs primarily in rainbow trout fry. Fish develop abdominal distention, exophthalmus, increased pigmentation, lethargy, loss of balance, pale gills, and occasional cutaneous ulcers and necrosis of tail fins. Epidermal hyperemia and increase mucus secretions are common. Splenomegaly and hepatomegaly are common with multifocal necrosis of the liver spleen and kidney.

C. Transmission is believed to be by direct contact with contaminated water and is an indication of poor water quality and overcrowding.

12) Renibacterium salmoninarum (Bacterial Kidney Disease)

A. Gram positive nonmotile diplobacillus.

B. This is a serious disease of salmonids. Brook trout are the most severely affected species.

C. The disease follows a slow course with clinical signs not present until the fish is well grown. The fish may exhibit exophthalmus, skin darkening, and hemorrhage at the base of the fins. Cutaneous vesicles and ulcers may develop in mature trout "spawning rash". Abscesses, cavitation and contraction of muscles is occasionally observed. Splenomegaly and swelling of the kidney and liver with abundant ascites fluid is commonly observed. The large swollen kidney and spleen have numerous white nodules visible in the parenchyma. Numerous granulomas (containing gram positive bacteria) are observed in the kidney and may be also present in the spleen, heart and liver.

D. Transmission of the disease is believed to be via direct contact with contaminated fish. It is believed that the organism enters through the epidermis and then becomes a systemic disease.

13) Mycobacterium species (Tuberculosis)

A. Gram positive, acid fast rods (M. marinum, M. chelonei and M. fortuitum are the most common Mycobacterium species involved.)

B. All species of fish are affected. This disease affects both saltwater and freshwater aquariums as well as fish raised for food (up to 10 to 25% of pen raised fish).

C. Clinical signs of tuberculosis are quite variable. The most common signs are anorexia, emaciation, vertebral deformities, exophthalmus, and loss of normal coloration. Numerous variably sized granulomas are often observed in various organs throughout the body. Often numerous acid fast bacteria are observed in the granulomas.

D. The aquatic environment is believed to be the source of initial infection with fish becoming infected by ingestion of bacterial contaminated feed or debris. Once an aquarium is infected with this disease, it is difficult to remove except by depopulation of the aquarium and disinfecting the tank. Remember this is a zoonotic disease (atypical mycobacteriosis).

E. Atypical mycobacteriosis may manifest itself as a single cutaneous nodule on the hand or finger or may produce a regional granulomatous lymphadenitis of the lymphatics near the original nodule. Occasional local osteomyelitis and arthritis may also occur.

14) Nocardia sp.

A. Gram positive filamentous rod (weakly acid fast positive)

B. The organism is a problem with mostly aquarium fish. However, it is occasionally observed in cultured salmonids.

C. Clinically this is a chronic disease characterized by raised granulomatous masses in the mouth, jaw, gills and skin (The mouth and jaw are the most common sites). Dermal masses eventually ulcerate. Numerous white raised nodules (granulomas) are often observed in the viscera.

D. The exact route of transmission is unknown. However, it is felt that entry through wounds and abrasions is the most common source of infection. (Ingestion of the bacteria has been known to cause the disease.)

15) Flavobacterium sp.

A. Gram negative rods

B. Usually a problem for individual fish. This disease is a cause of concern to primarily hobbyist and producers of ornamental fish. (Mollie granuloma, Mollie madness, Mollie popeye)

C. Infected fish are usually emaciated and pale. Multifocal white nodules are observed in the visceral organs, the retina and choroid and the brain. These nodules may be cystic or mineralized. Histologically the nodules are granulomas with a caseous center, a thin peripheral rim of macrophages and lymphocytes and a fibrous capsule.(Must be differentiated from Mycobacterium)

D. The mode of transmission is unknown.

16) Epitheliocystis (Chlamydial infection)

A. Obligated intercellular parasite. Organisms stain red with Macchiavello stain.

B. These organisms have been observed in many species of fresh water and marine fish. Mortality occurs most commonly in heavily infected juvenile fish.

C. Clinically infected fish may be asymptomatic or show respiratory distress or excessive mucus secretions. Multiple white cysts are observed on the gill lamella and skin. Histologically, the cyst consists of distended epithelial cells with numerous basophilic organisms.

D. The means of transmission is unknown.

Mycotic Diseases

1) Saprolegniasis

A. Caused by various groups of aquatic fungi; primarily Saprolegnia, Achlya, and Aphanomyces.

B. Saprolegniasis affects all species and ages of freshwater and estuarine fish.

C. Clinically, affected fish develop white to brown cotton like growths on skin, fins, gills and dead eggs. This organism is an opportunist that will usually grow over previous ulcers or lesions. Diagnosis is by finding broad nonseptate branching hyphae that produce motile flagellated zoospores in the terminal sporangia.

D. In the Atlantic menhaden, gizzard shad, and some other marine fishes, this fungus may present as an ulcerative mycosis that may progress to a deep necrotic lesion involving the muscle. Histologically there is an intense granulomatous inflammation with broad (7 to 14 micron), nonseptate hyphae.

D. Most fish die due to osmotic or respiratory problems if the affected area of skin or gills is large.

E. The fungi are normal water inhabitants that invade the traumatized epidermis. Improper handling, bacterial or viral skin diseases, and trauma are the major causes of the disease. It is interesting to note that temperature has a significant effect on the development of infections. Most epizootics occur when temperatures are below the optimal temperature range for that species of fish.

2) Branchiomycosis (Gill rot)

A. Caused by two species Branchiomyces sanguinis and B. demigrans.

B. Primarily a problem in carp, rainbow and brown trout, and eels.

C. Affected fish usually show respiratory distress. There is prominent gill necrosis caused by thrombosis of blood vessels in the gills. Histologically, the identification of nonseptate branching hyphae with an intrahyphal eosinophilic round body (apleospores) in and around blood vessels of the gill is diagnostic.

D. The disease occurs most commonly in overcrowded ponds with abundant organic matter and high ammonia levels. Usually warm water temperatures (20 25 C) bring about the disease.

3) Ichthyosporidiosis

A. Ichthyophonus hoferi; large 10 250 micron spores which may germinate to form large hyphae (similar to the hyphae of Saprolegnia).

B. This fungus infects all species of fish.

C. Clinically the fish are emaciated with small round occasionally ulcerated black granulomas in the skin. Scoliosis is occasionally observed. Internally, numerous granulomas are observed in many visceral organs. Microscopically, the lesion consists of granulomas with encysted large PAS positive spores. Occasionally large irregular shaped hyphae are observed.

D. Transmission is unknown, but believed to be due to ingestion of contaminated feed.

4) Exophiala sp.

A. Exophiala salmonis and E. psychrophila; these fungal organisms have hyphae that are septated, irregular in width and branched.

B. This disease is observed in many species of fresh and saltwater fish. E. salmonis has become an organism of increased importance in caged cultured salmonids.

C. Clinically the fish become darker and lethargic, with erratic and whirling swimming behavior. Occasionally dermal nodules are present. Numerous round yellow to white granulomas are present in visceral organs (liver, kidney, spleen) with prominent enlargement of the posterior kidney common. Histologically, branched, irregular width, septated hyphae are present in the lesions.

D. Transmission is unknown.

External Protozoal Diseases

1) Ichthyophthirius multifiliis ("Ich" or White Spot Disease)

A. The largest protozoan parasite of fish. The trophozoite are up to 100 microns diameter, ciliated and contain an oval horseshoe shaped nucleus.

B. This is a disease of aquarium and hatchery reared fish.

C. Clinically fish become hyperactive with fish flashing and cutting against rocks or sides of aquariums. As the trophozoites enlarge they cause hyperplasia of the epidermis with white spots forming on the skin and gills. Severely infected fish may have respiratory problems and die. Histologically there is epidermal hyperplasia with the encysted trophozoite present in the epidermis.

D. The life cycle is direct. Encysted trophozoites (trophonts) leave the fish and settle to the bottom of the tank. The trophozoites (tomonts)divide into numerous tomites (theronts) that are released to infect the skin of the fish. The life cycle takes approximately 4 days to complete. However, it can be sped up by increasing the water temperature.

E. The only way to treat the disease is by interrupting the life cycle of the parasite. Removal of fish from the infected water for 3 days (25 C) will usually interrupt the life cycle (Tomites live only 48 hours at 26 C). One must treat the water to kill the tomites to prevent spread of the disease (Malachite green, formalin, methylene blue, or KMnO4). Remember, these treatments only kill the tomites and not the trophozoites that are encysted in the fish.

F. Cryptocaryon irritans is the salt water equivalent to Ichthyophthirius.

2) Ichthyobodo necator (Costiasis)

A. Piriform shaped protozoa 6 12 microns long with two short and two long flagella. These are stalked protozoa that attach to the skin or gills.

B. This disease is observed in most aquariums and hatchery raised fish. This disease occurs primarily in cold waters (10 C) and affects very young fish when they are just beginning to eat food.

C. Clinically the fish may flash, produce abundant mucus over the skin (blue slime disease) and/or show respiratory distress (flaring of gills). Histologically the parasites are attached to the epithelial surface of the skin or gills.

D. Transmission of the parasite is by direct contact with the protozoa. This protozoon is a free swimmer so it can swim and then attach to the host where it undergoes binary fusion for reproduction.

3) Trichodina sp. (Trichodiniasis)

A. This disease is caused by a group of peritrichal ciliated protozoans. The organisms are saucer shaped, 50 microns diameter, with rows of cilia at both ends and a macro and micronucleus. When viewed dorsoventrally, the parasite appears as an ornate disk with a characteristic ring of interlocking denticles forming a circle in the middle of the organism. (Trichodina truttae is considered to be a specific pathogen for salmonids).

B. These are observed on most fresh and saltwater fish. This protozoon is relatively common on many fish and is not always associated with disease.

C. Clinically fish usually exhibit flashing and become lethargic. There is an increase in mucus production causing a white to bluish haze on the skin. The skin may develop ulcers and the fins may fray. If the gills are involved, the fish may have severe respiratory distress. Histologically, masses of organisms are attached by adhesive discs and denticles of exoskeleton to the epidermis. The underlying epithelial cells undergo necrosis. There is secondary hyperplasia and hypertrophy of the gill epithelium.

D. Transmission is by direct contact with infected fish and or contaminated water.

4) Tetrahymena corlissi and Tetrahymena pyriformis

A. Normally a free living oval ciliated 50 70 micron long protozoa.

B. The organism has been known to affect the fry of various cultured fish (Guppy "Guppie killer" and Northern pike).

C. Clinically, one may observe necrosis and hemorrhage of the skin. In severe cases the fish have rupture of the body walls and the fish eviscerate. Histologically one observes massive invasion of the musculature by this organism. (The ventral abdominal wall is severely affected.)

D. This is a free living protozoan that only becomes a problem at times of overcrowding and poor water quality.(water having a high organic matter content)

5) Dinoflagellates (Velvet disease, Coral fish disease)

A. Dinoflagellate 100 microns diameter containing chromatophores and a single eccentric nucleus. When free swimming they are 20 microns diameter contain a transverse flagellum in the transverse furrow and a longitudinal flagellum in the longitudinal sulcus. Several species of dinoflagellate are involved:

1) Oodinium Velvet disease
2) Amyloodinium Coral fish disease

B. Problem in aquarium and cultured fish.

C. Clinically, fish flash in the water and become depressed with lateral opercular movement. A shimmering heavy yellow colored mucus secretion over the skin and gills is observed. Histologically, large oval organism (80 microns diameter) with multiple chromatophores and a single eccentric nucleus are attached to epithelial cells by pseudopodia.

D. Transmission is by direct contact with infected fish, and contaminated water.

6) Epistylis (Heteropolaria sp.; Red sore disease)

A. Branched stalked ciliated protozoan (Heteropolaria colisarum).

B. Found primarily in wild populations of scaled fish.

C. Clinically, one observes ulcers or cotton-like growth on the skin, scales and spine resulting in a red colored lesion. In catfish the lesion involves the spines and bones that underlie the skin of the head and pectoral girdle. This protozoan parasite has also been observed on eggs.

D. This ciliated protozoan is primarily a free-living protozoan that lives on aquatic plants and is believed to be an opportunist. Outbreaks have occurred in catfish and salmon that have been maintained in water high in organic content.

7) Glossatella

A. This disease is caused by the ciliated protozoan Apiosoma that has a barrel shaped body with cilia at the distal end and a large rounded macronucleus.

B. This organism usually is not a problem but can affect many species of fish.

C. The organism can appear on the gills or skin causing increased mucus production and hyperplasia. Severe infections of the gills will cause respiratory problems.

D. This disease is a problem when fish are exposed to poor water quality.

Internal Protozoal Diseases

1) Henneguya (Blister disease, Myxosporidiosis)

A. Myxosporidean parasite (6 Henneguya sp.)with two polar capsules and a long tail like extension of the spore shell. This parasite is believed to be a Myxosporidean in the fish and an Aurantiactinomyxoa in the mud worm.

B. Problem in many cultured freshwater fish; channel catfish can be heavily infected.

C. Clinically, fish are presented with numerous white cysts on the skin and gills. Cyst can become very large. Cysts may lead to gill epithelial hyperplasia leading to anoxia. Interlamellar forms may cause some necrosis of gills and occasional death. Treating affected fish with chemotherapeutic agents is usually ineffective and may cause more deaths.

D. The life cycle is unknown. It is felt that a mud worm (Oligochaete sp.) is involved in an indirect life cycle with asexual and sexual stages in the mud worm (Aurantiactinomyxoa sp.)and catfish (Myxosporidean).

E. Henneguya exilis kudo was once believed to be the cause of Proliferative Gill Disease. However, the evidence suggests that the interlamellar form of the parasite that evokes a serious inflammatory response is probably due to another Myxosporidean(Aurantiactinomyxoa sp. or the extrasporogenic stage of the myxozoan Sphaerospora ictaluri).

2) Proliferative gill disease (Hamburger gill disease)

A. Myxosporidean parasite; most likely an Aurantiactinomyxoa sp. (Triactinomyxid myxozoan). Note: some feel that this may represent the extrasporogenic stage of the myxozoan Sphaerospora ictaluri.

B. Problem in many cultured freshwater fish (primarily catfish) and usually involves new ponds.

C. Clinically there is rapid onset with the disease killing 10% to 95% of the fish. Water temperatures between 16 and 20 degrees centigrade favor optimal growth of the organism. Fish are presented in severe respiratory distress. Grossly there is intense granulomatous inflammation and swelling of the gills with epithelial hyperplasia and gill necrosis. Histologically, the cyst observed in the gill lamella cause necrosis of the cartilage, distortion of the gill lamella and an intense inflammatory response with numerous macrophages infiltrating the gill lamella around the cysts. Cyst have been observed in other organs (brain, spleen, liver, kidney).

D. The life cycle is unknown. The parasite is believed to maintain mild subclinical infections in some fish host or has an indirect life cycle involving a mud worm (Oligochaete of the Duro sp.(Duro digitata)). Infected oligochaetes release Aurantiactinomyxoa spores that infect more oligochaete and the channel catfish. Transmission of the spores from the fish to the oligochaete have not been observed. This suggests that the catfish may be an abnormal host for this parasite.

E. Survivors are believed to be resistant to reinfection.

3) Myxobolus cerebralis (Myxosoma cerebralis or Whirling Disease)

A. Myxosporidean parasite with a 10-micron oval spore with 2 piriform polar capsules.

B. Parasite affects primarily young salmonids (rainbow trout most susceptible; Brown trout and Coho salmon resistant).

C. Clinically, fish develop blackened tails and become deformed about the head and spine (scoliosis) with the fish swimming erratically (whirling). Histologically, there is necrosis of the cartilage, particularly of the head and spine, with numerous spores present in the area of inflammation. The necrosis of the cartilage is the cause of the deformation.

D. Transmission is believed to be by ingestion of spores or spore attachment and penetration. The life cycle of this organism is not completely known. A tubificid oligochaetes (tubifex mud worm, Tubifex tubifex) is an important intermediate or transport host. It is believed that the parasite undergoes sporulation in the tubifex worm were the organism takes on the form of a Triactinomyxon sp. It is believed that this parasite is then released from the tubifex worm and infects the trout. Tubifex worms are infected for life. Trout are believed to become infected by the ingestion of Triactinomyxon spores by eating the mud worms, by the ingestion of spores free in the water or by free spores penetrating the epithelial surface of the fish. Released spores may attach and penetrate the epithelial surface of the fish (body, tail, gills, causal fin, or mouth). Spores develop into sporoplasms and invade epidermal cells (goblet or mucosal cells). These parasites then multiply and progressively migrate to the peripheral nerves by day 4-post infection. Later they migrate to the bone and cartilage. In the cartilage, the sporoplasms develop into trophozoites that undergo asexual mitosis forming numerous spores that infect the cartilage. Spore development is substantially influenced by temperature with lower temperatures causing spore development to take longer.

E. Spores are very resistant to environmental conditions and can with stand freezing and thawing, temperatures as high as 66oC, passing through the gut of birds and fish, and survive in sediment for up to 30 years. Control is done by removal of all dead or infected fish and disinfecting the pond with Calcium Cyananide, lime, or chlorine. Decreasing the Oligocheate in the water can also be accomplished by concrete lining of ponds and raceways. Spores can be reduced in water by ultraviolet treatment of the water. Infected fish can be treated with Fumagillin in feed at 0.5g/kg of feed for two weeks.

4) Microsporidians (Glugea, Pleistophora, Loma)

A. Microsporidian parasites form cysts in various organs. The cysts are filled with small 1 to 2 micron spores. Parasitic cyst may induce hypertrophy of the infected cell (Glugea, Loma, Spraguea, and Ichthyosporidium) or does not cause hypertrophy of infected cells (Pleistophora).

B. Microsporidian parasites are found in numerous fresh and saltwater fish.

C. Clinically microsporidian present themselves as individual or multiple cysts that can become quite large and may give the appearance of neoplasms (xenomas). These cysts are filled with numerous refractile spores.

1) Glugea and Loma: Infect macrophages and other mesenchymal tissues which then undergo massive hypertrophy causing deformity of visceral organs (liver, gut, ovaries) as well as infections in the muscle and subcutis.

2) Pleistophora hyphessobryconis (Neon tetra disease): This microsporidian infect the sarcoplasm of muscle fibers causing these fibers to be filled with these organisms. There is no inflammatory reaction around the cyst.

D. Transmission of the disease is most likely direct.

5) Coccidiosis

A. Primarily of the genus Eimeria. Various species of Eimeria are observed in the different fish.

B. Affects both fresh and saltwater fish. The coccidia not only infects the epithelium but also many other organs including the gonads. This is a very important problem in the carp and goldfish culture.

C. 1) Eimeria subepithelialis; carp: Nodular white raised areas in the middle and anterior gut.

2) Eimeria carpelli; carp: Ulcerative, hemorrhagic enteritis.

3) Eimeria sardinae; marine fish: Granulomatous reaction in the liver and testicles.

6) Hexamita salmonis

A. Binucleated piriform protozoan with 6 anterior and 2 posterior flagella.

B. Infects young salmonids.

C. Clinically the young fish have anorexia, and become debilitated with reduced growth. The fish develop acute enteritis with numerous organisms present in the feces.

D. In farmed Chinook and Atlantic salmon the disease can become systemic with fish becoming anemic with swollen kidneys and exophthalmus. Boils on the dorsal skin and numerous granulomas with organisms present have been observed.

E. Transmission is by ingestion of infective cyst.

7) Proliferative Kidney Disease ( PKD, PKX, X Disease)

A. Believed to be caused by a myxosporan parasite (Sphaerospora sp), however, the taxonomy of the parasite is not completely worked out.

B. Parasite causes a serious problem in cultured salmonids (Rainbow trout and salmon) in Europe and North America. Infected ponds can see a mortality between 10% and 95%. Outbreaks tend to occur in fingerlings with rising water temperatures. Water temperatures of 16 degrees centigrade seem to favor growth of the organism.

C. Clinically infected fish have a darker body pigmentation, exophthalmos, ascites and pale gills. Internally, the kidneys are swollen and have numerous grey white area of granulomatous inflammation scattered throughout. Diseased fish also develop anemia and hypoproteinemia. Histologically, the kidney has a granulomatous interstitial nephritis with macrophages and lymphocytes surrounding the amoeboid parasites (15µ diameter and usually with multiple daughter cells). There is usually prominent tubular and hematopoietic tissue loss. The parasite may also be identified in the spleen, liver, muscle, gills and intestines.

D. The life cycle of the parasite is unknown. The marked inflammatory response observed in the infected fish and the lack of mature spores suggests that the fish may be an aberrant host.

8. Cryptosporidiosis

a. Intercellular extracytoplasmic protozoan

b. Cryptosporidium infects the intestine of several species of fish. (Carp; Naso tang, Naso litatus; tropical freshwater catfish, Plecostomus sp.; and cichlids)

C. The importance of cryptosporidiosis as a pathogen in fish is unknown. May cause some debilitation; believed to be a secondary invader after the immune system is depressed. Infected fish usually are presented emaciated and not doing well.

d. The importance of this organism as a reservoir for infection in other animals and man is unknown.

Miscellaneous Parasites

1) Lernea Anchor worm (Also Salmincola and Lepeophtheirus sp.)

A Copepod

B. Infects all freshwater fish and is a serious problem in cyprinids (bait minnows, goldfish, and carp).

C. Clinically the parasite invades the skin, usually at the base of a fin. The head develops into an anchor that holds the female in place. The female then develops egg sacs (two finger like projections attached to the end of the body). The ulcers are slow to heal.

D. Other copepods such as Ergasilus sp. are found on the gills and cause serious gill damage.

2) Argulus - Fish louse (Branchiura)

A. Parasite of the skin and occasionally buccal cavity.

B. Cutaneous ulcers due to piercing of epidermis by the retractile preoral stylet (a proboscis-like mouth) for sucking blood from the fish.

3) Gyrodactylus sp.

A. Monogenetic trematode; flattened and leaf-like, no eyespot, cephalic end V shaped, has an attachment organ (haptor) and two large anchors with 16 marginal hooklets.

B. Affects most species of fish.

C. Fluke anchors itself to skin, fins, and gills that may cause excessive mucus secretions over gills and skin. Fish may undergo flashing and have fraying of fins. Severe infection (gills) may cause the fish to become dyspneic and die.

D. Life cycle is direct. The larva are released and attach almost immediately to the host.

4) Dactylogyrus

A. Monogenetic trematode; flattened and leaf-like, four anterior eyespots, cephalic end scalloped, ova present, has an attachment organ (haptor).

B. Affects most freshwater species, particularly carp and goldfish.

C. Fluke anchors to gills causing excessive mucous secretions, and frayed edges. Fish become anoxic with flaring of the gill opercula.

D. Life cycle is direct. The adults are oviparous and produce eggs with long filaments. The eggs are usually attached to the gills. The eggs develop into a onchomiricidium that then attaches to the fish.

5) Diplostomum spathaceum (Eye fluke)

A. Digenetic fluke; metacercaria is infective state in fish.

B. Gulls and pelicans are the definitive host. Snails (Lymnaea sp.) are the first intermediate host. Fish (salmonids) are the second intermediate host.

C. Clinically, the metacercaria are presented as white dots; later the eye becomes opaque. Blindness occurs in severe infections. The metacercaria are found in the anterior chamber, vitreous body, and lens causing cataracts.

6) Uvulifer ambloplitis (Black spot disease)

A. Digenetic fluke; metacercaria infect fish.

B. Herons and kingfishers are the definitive host, snails are the first intermediate host. Fish are the second intermediate host.

C. Clinically the fish have numerous black to brown spots up to 1 mm (dia) over the skin, gills and eyes. The spots contain a metacercaria surrounded by heavily pigmented fibrous connective tissue.

7) Acanthocephalus (Thorny headed worm)

A. Pomphorhynchus sp. and Acanthocephalus sp.

B. Acanthocephalans are observed in many species of fresh water and marine fish. Adult parasites live in the intestine. The larval second intermediate stage may encyst in the liver, spleen or mesentery.

C. Heavy infections are observed in feral fish. Infected fish may not show signs. However, some fish are emaciated and have swollen abdomens. In heavy infections, raised subserosal nodules may be observed in the gut. These nodules may have the proboscis attached. Histologically, a severe granulomatous reaction is associated with the nodules. If the parasite penetrates the serosa, a peritonitis may occur.

D. The life cycle is complex; an amphipod is the first intermediate host. In the amphipod, the acanthor develops into a cystacanth. Small fish are believed to be the second intermediate host (paratenic host)for the cystacanth. The life cycle is then completed with the ingestion of the cystacanth and development of the adult worm.

8) Anisakis

The parasite causes little problem in fish. However, in man, it can be a serious public health threat. Brown and white larva (third stage) are observed in the viscera and musculature of fish. Many marine mammals are the definitive host with this nematode living in the stomach.


1) Melanoma in Platyfish/Swordtail hybrids

Unique invasive melanoma that occurs in the offspring from F1 hybrid platyfish/swordtail with the spotting traits that are crossed with swordtails. F1 hybrids with the spotting trait develop premelanosomes. F1 X swordtail cross will produce frank melanomas. The reason for these melanomas is believed to be due to enhancement of the macromelanophore gene due to a deficiency of modifier genes that leads first to melanosis and finally to invasive melanomas.

2) Hepatoma and hepatocellular carcinoma in rainbow trout

The fry of rainbow trout are very susceptible to aflatoxins in the feed. These hepatic neoplasms are associated with the ingestion of aflatoxins in the feed. Acute aflatoxicosis causes acute massive liver necrosis with bile duct proliferation.

3) Stomatopapilloma of eels (Cauliflower disease)

These are large firm cauliflower like masses that are attached to the mouth. Tumors tend to proliferate in the summer and degenerate in the winter. A birnavirus, similar to infectious pancreatic necrosis virus, has been reported to have been isolated from the affected eel (Anguilla anguilla). However, initiation of the tumor with cell free extracts has been unsuccessful.

4) Papilloma of the Brown bullhead

Papillomas are common in the brown bullhead with occurrence on the head and lip. Viral particles have been observed ultrastructurally in the papillomas, but a virus has not been isolated. Some of these papillomas may progress and become locally invasive squamous cell carcinomas.

5) Lip Fibroma (Fibropapilloma) of Angel Fish

Tumor of the mucocutaneous junction of the lip near the midline. Adult female fish are the only effected fish. Tumors begin as small white vesicles that enlarge over several weeks. The tumors are firm, lobulated, and elevate the epidermis. On cut sections, the tumors are white with some having cavernous centers filled with clear fluid.

Histologically, the tumors consist of dense fibrovascular connective tissue arranged in whorls, streams and bundles and covered by a thick stratified squamous epithelium. Cause is unknown. A type "A" retrovirus has been isolated from affected tissue. Laboratory transmission of the disease to other fish has not occurred.

6) Dermal Fibrosarcomas of Walleye pike

Fibrosarcomas are a common neoplasm affecting a large variety of fish. Dermal fibrosarcomas of Walleye pike arise in the dermis and cause multifocal nodules over the entire body. They can be very large and locally invasive. A type-C retrovirus has been associated with this disease. Occasionally, this neoplasm has also been associated with a herpesvirus induced epidermal hyperplasia or lymphocystis disease.

7) Lymphosarcoma of Pike

This is an epizootic condition in northern pike and muskellunge in certain regions (i.e. Lake Ontario). The lesion develops as a purple ulcerative cutaneous mass on the head, mouth and flank with invasion into the adjacent muscle and metastasis to spleen, liver and kidney. A type-C Retrovirus is believed to be the cause of this disease.

8) Schwannoma/Neurofibromas of the bicolored damselfish (Damselfish Neurofibromatosis DNF)

Neurofibromas have been reported in numerous species of fish. The bicolored damselfish has gained notoriety in that some of these fish develop multiple cutaneous schwannomas. This neoplasm is believed to possibly represent an animal model for von Recklinghausen Neurofibromatosis (NF type 1) in man. The similarities and differences between these two diseases are as follows: The primary lesion in both NF type 1 and DNF are neurofibromas, many of which are plexiform in nature. The fish tumors are often malignant. DNF the pigment lesions can be neoplastic and quite invasive, while the cafe au lait spots of NF type 1 are benign. NF type 1 appears to be genetically transmitted while DFN appears to be horizontally transmitted.

9) Plasmacytoid Leukemia (Marine anemia) of Chinook salmon

Plasmacytoid leukemia virus is observed in farmed raised Chinook salmon (Experimentally in Sockeye, Coho and Atlantic salmon). It is believed to be caused by a retrovirus (Salmon leukemia virus). Affected fish become lethargic, have dark skin, pale gills (anemia), and exophthalmus. The spleen, kidney, and retrobulbar tissues are enlarged and mottled. Petechial hemorrhage of the serosa is common. Infiltration of the liver, spleen, and kidneys with plasmablastic cells is noted. Plasmablast have a slightly lobulated nucleus with a central nucleoli.

Nutritional Deficiencies

1) Iodine Deficiency

Iodine deficiency cause hyperplasia (goiter) of the thyroid tissue. The cause is not always known. Some goiters may be due to iodine deficiency (very difficult to produce). However, the most likely cause may be due to the affects of goitrogenic substances in the feed or due to the presence of goitrogenic pollutants in the water.

2) Fatty Acid Deficiency (Linolenic and linoleic acid deficiency)

Fish are capable of synthesizing most fatty acids but not the linolenic or linoleic acid series. Deficiencies of these fatty acids lead to depigmentation, fin erosion, cardiomyopathy, fatty infiltration of the liver, and myxomatous degeneration of fat.

3) Vitamin C Deficiency

Ascorbic acid is an essential vitamin of fish. Deficiencies of this vitamin lead to poor wound healing, ulceration of the skin on fins, hemorrhage, and skeletal deformity. This vitamin is very temperature sensitive and oxidizes readily in stored feed.

4) Vitamin E Deficiency

Vitamin E deficiency is associated with necrosis and degeneration of skeletal and cardiac muscle, steatitis, and lipoidal liver disease.

5) Pantothenic Acid Deficiency

Pantothenic acid is a coenzyme need in the metabolism of fats and carbohydrates. Deficiencies lead to anorexia due to hyperplasia of the gill lamellar epithelium and fusion of secondary lamella (nutritional gill disease). Anemia is usually associated with the disease.

6) Methionine Deficiency

Methionine deficiency (primarily in salmonids) leads to reduced growth rate with the development of bilateral cataracts. (Zinc, and cystine deficiencies can also cause cataracts) It is felt that deficiencies of vitamin A and riboflavin also play a role in this lesion.

The author of this lecture wishes to thank Drs. Floyd, Bowser, Plumb, Herman, Wolke, Magaki, Harshbarger, Schmale, Smith, Colorni Leard, Chen, Muench, Hedrick and Wedemyer for supplying photographs of the various fish diseases to the Registry of Veterinary Pathology.














13. DeTolla, L.J., Srinivas, S.: Guidelines for the Care and Use of Fish in Research. Institute of Laboratory Animal Resourses Journal. Vol 37:4(1995), pp 159-173.

14. Kane, A.J., Gonzalez, J. F., Reimschuessel, R: Fish and Amphibian Models Used in Laboratory Research. Laboratory Animal. Vol 25:6(1996), pp 33-38.


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