Written by: Robert B. Moeller Jr., DVM
March 22, 2000 part III
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.
- B. Problem in many cultured freshwater fish; channel catfish can be
- 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).
|2) Proliferative gill disease (Hamburger gill disease)
- 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
- E. Survivors are believed to be resistant to reinfection.
|3) Myxobolus cerebralis (Myxosoma cerebralis or Whirling
- A. Myxosporidean parasite with a 10 micron oval spore with 2 piriform
- B. Parasite affects primarily young salmonids (rainbow trout most
- 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.
|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
- 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
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
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
- 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.
|6) Hexamita salmonis
- A. Binucleated piriform protozoan with 6 anterior and 2 posterior
- 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.
|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 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 (15?
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.
|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 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
- 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.
|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
- 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
|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.
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 which 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
|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/Neurofibroma's of the bicolored damselfish (Damselfish
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
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
|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.
Robert B. Moeller Jr., DVM
California Animal Health and
Food Safety Laboratory System
University of California
18830 Road 112
Tulare, California 93274
- Roberts R.J: Fish Pathology, Bailliere Tindall, London, Second edition,
- Ferguson H.W.: Systemic Pathology of Fish, Iowa State Press, Ames,
- Anderson B.G.: Atlas of Trout Histology, Wyoming Department of Fish
and Game, 1974.
- Fox J.C.: Laboratory Animal Medicine, Academic Press, 1984.
- Migaki G., Rebelin W.E.: The Pathology of Fishes, The University of
Wisconsin Press, 1975.
- Wolf K.: Fish Viruses and Fish Viral Diseases, Cornell University
Press, London 1988.
- Tucker C.S.: Channel Catfish Culture, Elsevier Science Publishers,
- Principal Diseases of Farm Raised Catfish, Southern Cooperative
Series Bulletin No 225, 1985.
- Wales J.H.: Microscopic Anatomy of Salmonids. An Atlas, United
States Department of the Interior, Resource Publication 150, 1983.
- Grizzle J.M.: Anatomy and Histology of the Channel Catfish, Auburn
Printing Co, 1976.
- Reichenbach-Klinke H. H.: Fish Pathology, T.F.H. Publications, Inc.
Neptune City, NJ. 1973.
- Stoskopf, M.K.: Fish Medicine, W.B. Saunders Co. 1993.
- DeTolla, L.J., Srinivas, S.: Guidelines for the Care and Use of
Fish in Research. Institute of Laboratory Animal Resources Journal. Vol
- 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.
- Lewbart G.A. Self-Assessment Color Review of Ornamental Fish, Iowa
- Bruno D.W., Poppe T.T., A color atlas of Salmonid Diseases.
Academic press, 1996.