Henneguya (Blister disease, Myxosporidiosis)
- Myxosporidean parasite (6 Henneguya spp.) 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.
- Problem in many cultured freshwater fish; channel catfish can be heavily infected.
- 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.
- 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).
- 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).
Proliferative gill disease (Hamburger gill disease)
- Myxosporidean parasite; most likely an Aurantiactinomyxoa sp. (Triactinomyxid myxozoan). Note: some feel that this may represent the extrasporogenic stage of the myxozoan Sphaerospora ictaluri.
- Problem in many cultured freshwater fish (primarily catfish) and usually involves new ponds.
- 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).
- 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.
- Survivors are believed to be resistant to reinfection.
Myxobolus cerebralis (Myxosoma cerebralis or Whirling Disease)
- Myxosporidean parasite with a 10-micron oval spore with 2 piriform polar capsules.
- Parasite affects primarily young salmonids (rainbow trout most susceptible; Brown trout and Coho salmon resistant).
- 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.
- 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.
- Spores are very resistant to environmental conditions and can with stand freezing and thawing, temperatures as high as 66°C, 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.
Microsporidians (Glugea, Pleistophora, Loma)
- 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).
- Microsporidian parasites are found in numerous fresh and saltwater fish.
- 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.
- 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.
- 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.
- Transmission of the disease is most likely direct.
- Primarily of the genus Eimeria. Various species of Eimeria are observed in the different fish.
- 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.
- Eimeria subepithelialis; carp: Nodular white raised areas in the middle and anterior gut.
- Eimeria carpelli; carp: Ulcerative, hemorrhagic enteritis.
- Eimeria sardinae; marine fish: Granulomatous reaction in the liver and testicles.
- Binucleated piriform protozoan with 6 anterior and 2 posterior flagella.
- Infects young salmonids.
- Clinically the young fish have anorexia, and become debilitated with reduced growth. The fish develop acute enteritis with numerous organisms present in the feces.
- 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.
- Transmission is by ingestion of infective cyst.
Proliferative Kidney Disease (PKD, PKX, X Disease)
- Believed to be caused by a myxosporan parasite (Sphaerospora sp), however, the taxonomy of the parasite is not completely worked out.
- 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.
- 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.
- 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.
1. Roberts R.J: Fish Pathology, Bailliere Tindall, London, Second edition, 1989.
- Intercellular extracytoplasmic protozoan
- Cryptosporidium infects the intestine of several species of fish. (Carp; Naso tang, Naso litatus; tropical freshwater catfish, Plecostomus sp.; and cichlids)
- 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.
- The importance of this organism as a reservoir for infection in other animals and man is unknown.
2. Ferguson H.W.: Systemic Pathology of Fish, Iowa State Press, Ames, Iowa, 1989.
3. Anderson B.G.: Atlas of Trout Histology, Wyoming Department of Fish and Game, 1974.
4. Fox J.C.: Laboratory Animal Medicine, Academic Press, 1984.
5. Magaki G., Rebelin W.E.: The Pathology of Fishes, The University of Wisconsin Press, 1975.
6. Wolf K.: Fish Viruses and Fish Viral Diseases, Cornell University Press, London 1988.
7. Tucker C.S.: Channel Catfish Culture, Elsevier Science Publishers, Amsterdam, 1985.
8. Principal Diseases of Farm Raised Catfish, Southern Cooperative Series Bulletin No 225, 1985.
9. Wales J.H.: Microscopic Anatomy of Salmonids. An Atlas, United States Department of the Interior, Resource Publication 150, 1983.
10. Grizzle J.M.: Anatomy and Histology of the Channel Catfish, Auburn Printing Co, 1976.
11. Reichenbach-Klinke H. H.: Fish Pathology, T.F.H. Publications, Inc. Neptune City, NJ. 1973.
12. Stoskopf, M.K.: Fish Medicine, W.B. Saunders Co. 1993.
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.
15. Lewbart G.A. Self-Assesment Color Review of Ornamental Fish, Iowa State Press,1998.
16. Bruno D.W., Poppe T.T., A color atlas of Salmonid Diseases. Academic press, 1996.