• A. Myxosporidean parasite ( 6 Henneguya sp.)with two polar capsules and a long tail like extension of the spore shell.
• 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 and catfish.
• E. Henneguya exilis kudo was once believed to be the cause of Proliferative Gill Disease. However, recent evidence suggests that the interlamellar form of the parasite which evokes a serious inflammatory response is probably due to another myxosporidean(Aurantiactinomyxo sp. or the extrasporogenic stage of the myxozoan Sphaerospora ictaluri).

• A. Myxosporidean parasite; most-likely an Aurantiactinomyxo 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.). Infected oligochaetes release 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.

• A. Myxosporidean parasite with a 10 micron oval spore with 2 piriform polar capsules.
• B. Parasite affects primarily young salmonids (rainbow trout most susceptible).
• 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 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) 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. Trout ingest the spores by eating the mud worms or by ingestion of spores free in the water. These spores may attach and penetrate the epithelial surface of the fish. Ingested spores develop into sporoplasms and penetrate the intestines and migrate to the bone and cartilage. In the cartilage, the sporoplasms develop into trophozoites that undergo asexual mitosis forming numerous spores which infect the cartilage. Spore development is substantially influenced by temperature with lower temperatures causing spore development to take longer.

• 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 cyst which 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 organism. There is no inflammatory reaction around the cyst.
• D. Transmission of the disease is most likely direct.

• 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.

• 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 an 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.

• 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 color, 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.

• 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.

• 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.

• 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.

• A. Monogenetic trematode; flattened and leaf-like, no eye spot, 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 which 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.

• 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 which then attaches to the fish.

• 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.

• 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.

• 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.

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.

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 which leads first to melanosis and finally to invasive melanomas.

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.

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.

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.

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.

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.

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.

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.

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 nucleolus with a central nucleoli.

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.

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.

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

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.

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.