DISEASES OF FISH

I. NORMAL ANATOMY AND HISTOLOGY OF FISH — SOME UNIQUE ASPECTS

 
1. Gills: Most fish have four pairs of gill arches. From each gill arch are two
hemibranchs that consist of a row of primary lamellae. Secondary lamellae are found on each
primary lamalla. The purpose of these structures is to establish a large surface area that
supports respiratory and excretory functions. A pseudobranch may also be found in the dorsal
area immediately under the operculum. It is made up of closely placed capillaries that resemble
seconday lamellae. The function of this network of capillaries is thought to be the supplying of
the retina and optic choroid with well oxygenated blood.
 
2. Kidneys: The kidneys may be one continuous organ (eg. Salmonids), found dorsal to
the swim bladder or it may be two unique organs (eg. Ictalurids) found anterior to and posterior
to the swim bladder. As a generalization, the anterior (head) kidney functions as a
hematopoietic and endocrine organ while the posterior kidney functions as an osmoregulatory
and to some extent excretory organ. It is worth noting that the majority of the nitrogenous
waste products of a fish are eliminated by excretion across the gills.
In a freshwater fish the kidney conserves ions and excretes water. In a saltwater fish the
kidney conserves water and excretes ions.
 
3. Corpuscles of Stannius: The Corpuscles of Stannius are islands of eosinophilic cells
that are typically found on the latero-ventral surface of the kidneys. Typically they are paired.
They secrete hypocalcin (teleocalcin) which acts with calcitonin to regulate calcium metabolism.
The Corpuscle of Stannius functions as the parathyroid gland (not found in fish) would in
higher animals.
 
4. Ultimobranchial Gland: This gland is a small group of cells that lie centrally in the
fish on the septum separating the heart from the abdominal cavity. The ultimobranchial gland
secretes calcitonin (lowers serum calcium concentrations) which acts with hypocaclin to
regulate calcium metabolism.
 
5. Interrenal Cells: Interrenal cells found in the anterior kidney have the function of the
adrenal cortical tissue in higher animals. (Most fish do not have an adrennal gland.) These cells
are pale eosinophilic cells found interspersed between hemopoietic tissue near major blood
vessels of the anterior kidney. Interrenal cells secrete glucocorticoid and mineralocorticoid.
 
6. Chromaffin Cells: Chromaffin cells in fish are the equivalent of adrenal medullary
cells in higher animals. These cells are typically found closely intermingled with the interrenal
tissue and are also associated with the major blood vessels of the anterior kidney. They get their
name from their affinity for chromate salts. The potassium dichromate method is used to
demonstrate brown colored granules in these cells; differentiating them from interrenal cells.
Chromaffin cells secrete adrenalin and noradrenalin.
 
7. Thyroid Gland: Thyroid follicles appears similar to those found in higher animals.
They are typically found in the pharyngeal region, but may also be found in other areas.
 
8. Endocrine Pancreas: The endocrine pancreas is found as islets of Langerhans and is
typically found in close association with the exocrine pancreas located in discrete foci in the
mesenteries near the small intestine or near pyloric cecae if they are present.
 
9. Digestive System: The digestive system displays some variation between different
species of fish. In general, carnivorous fish have a shorter digestive system than herbivorous
fish. Pyloric cecae may be found in some species of fish (more commonly carnivorous fish).
These are typically found near the junction of the stomach and intestine. They secrete enzymes
that participate in digestion.
 
10. Liver: Distinct lobules, portal triads and hepatic cords are not readily apparent.
Exocrine pancreas may be found in the liver in some species of fish. This tissue is normally
found in close association with the branches of the hepatic portal vein.
 
11. Heart: Various references describe the heart as either a 2-chamber or 4-chamber
organ. The primary chambers are a single atrium and a single ventricle. The blood is collected
by the sinus venosus prior to entering the atrium. Once pumped by the muscular ventricle the
blood moves through the bulbus arteriosus. A major component of the bulbus arteriosus is
fibrous connective tissue, which acts as a “shock absorber” when the blood is pumped by the
ventricle.
 
12. Lateral Line System: The lateral line system is a special sense organ of fish. The
organ is sensitive to changes in hydrostatic stimuli and sound.

13. Skin: Fish do not have a keratonized skin. The outermost living cells of the skin are
covered by a cuticle that is made up of mucus, mucopolysaccharides, immunoglobulins and
free fatty acids. The epidermins is composed of stratified squamous cells and may be from 4-20
cells thick. The dermis is immediately below the epidermis and is the location of the pigment
cells (melanophores, xanthophores, iridophores). The scales are calcified plates that originate in
the dermis and extend toward the exterior of the fish in an overlapping fashion and are covered
by the epidermis.
The skin is extremely important the ability of fish to maintain proper osmoregulatory
function. The skin also acts as the initial barrier to infection. It contains leukocytes and
macrophages in addition to immunoglobulins.
 
 II. FISH DISEASE TREATMENTS

In the United States, the U.S. Food and Drug Administration has regulatory authority over the
use of therapeutic compounds in animals. Very few compounds have a label, or FDA approval,
for use in fish. A label will specify the species of animal (in this case, species of fish), the disease
to be treated, the method of administration and dose, and any withdrawal time for food
animals. Individuals involved with the treatment of fish disease should become fully aware of
the most current information regarding disease treatment compounds, especially when treating
food animals.

There are two broad strategies when administering fish disease treatments. Compounds such
as copper sulfate, potassium permanganate, and formalin are added to the water to treat
external parasite infections, external fungal infections and external bacterial infections (most
commonly those diseases caused by the Flavobacterium). The compounds are added to the
water to achieve a particular concentration in terms of mg/L (= ppm). Most commonly the
treatments are administered as prolonged treatments; ie. they are placed in the water and
allowed to dissipate with time. The second strategy in disease treatment is the incorporation of
an antibacterial compound into the feed. This is done to treat systemic bacterial infections.
Currently there are two antibacterials that have a label for use in fish an are available:
Terramycin (Pfizer) and Romet-30 (Sulfadimethoxine/Ormetoprim, Hoffman-LaRoche).
Sulfamerazine (American Cyanimide) has a label but is no longer available. The antibacterial is
fed to the fish to provide a quantity of drug/fish weight per day for a specified number of days.
The administration of medication via the feed necessitates that the fish are still actively feeding.
Antibiotics are rarely administered as water baths in aquaculture, due to the large volume of
water to be treated. Because of problems with resistance to the two available antibacterials,
most fish health specialists consider it necessary to determine the antibiotic resistance pattern of
particular bacterial isolate before the antibacterial treatment is applied.

III. PATHOLOGY — COMMON PARASITES

 
PROTOZOA
 
1. Ichthyophthirius multifiliis (Cryptocaryon = saltwater)
“Ich” or “White Spot Disease” is an external parasite infestation caused by a large ciliate
protozoan. The parasite is characterized by its large horseshoe-shaped nucleus. The white
spots observed on fish are the adult trophozoite which is a feeding stage that are embedded in
the skin or gill epithelium. The trophozoite breaks through the skin, leaving the host to form an
encysted tomont stage, which may undergo numerous divisions. Numerous theronts break out
of the tomont to search for a fish to infect. The theronts burrow into the epithelium and form
the trophozoite. Depending on the water temperature, this life cycle may require 7-14 days.
The pathology caused by the trophozoite include epithelial hyperplasia and necrosis.
Considerable damage to the integredity of the epithelium may be caused by entrance and exit of
the parasite from the fish.
Diagnosis is made by observation of the numerous white spots on the surface of the fish.
The presence of the trophozoite can be confirmed by microscopic examination of fresh skin
scrapings, gill clippings, or fin clippings. The large ciliate protozoan with a characteristic C-
shaped macronucleus will be seen. The parasite can also be seen during histological evaluation
of skin and gill tissues.
Treatment may consist of formalin or copper sulfate. It is important to note that the
treatment protocol for Ich requires at least 3-4 treatments at 3-day intervals. This is because the
treatment is only effective against the free swimming theront after it leaves the fish and the free
swimming theronts as they are in search of a host. The treatment to effect the trophozoite
embedded in the skin would likely be toxic to the fish. Also, the encysted tomont stage is
usually resistant to the chemical.
 
2. Ichthyobodo necratix (Costia = former name)
Ichthyobodo is a small flagellate that infects the external
surface of the body and gills of fish. The disease has the common name “Blue Slime Disease”
due to the increased production of mucus in response to heavy infections. Epithelial
hyperplasia may also be present.
Diagnosis is made by microscopic examinations of fresh skin scrapings or gill clippings.
The characteristic rapid movement of the parasite at its attached point to the epithelium may
aid in identification. The parasite may also be seen on skin and gill tissues prepared for
histological evaluation. Treatment may include the use of formalin or copper sulfate.

3. Trichodina sp. (Also Trichodinella, Tripartiella)

These parasites are peritrichal ciliated protozoans that have the appearance of a disk.
Severity of an infection is usually associated with poor water quality and high numbers of the
parasites. The parasites are free swimming. The primary lesion observed will be a necrosis of
epithelial tissue.
Diagnosis is made by the microscopic examination of fresh skin scrapings or gill
clippings for the presence of the parasites.
Treatment may include such compounds as formalin or copper sulfate. It is also
appropriate to alleviate any less than optimal water quality conditions.
 
4. Dinoflagellates (Oodinium, Amylodinium)
These parasites are dinoflagellate algae that cause diseases known as “Velvet Disease”
(Oodinium) and “Coral Reef Disease” (Amylodinium). These dinoflagellates are particularly
problematic in marine fish. Amylodinium has a life cycle that is virtually identical to that of
Ichthyophthirius. These organisms usually infect the gills, but may also infect the skin. Severe
infections may cause epithelial hyperplasia, inflammation, hemorrhage and necrosis.
A valuable gross observation may be made by examination of the fish in its tank using
indirect light. This can be done by shining a flashlight on top of the fish in a darkened room
while examining the fish from the side. The fish will appear to have a “gold dust” or “velvet”
appearance. Diagnosis is made by the microscopic examination of fresh skin scrapings or gill
clippings for the presence of the parasites.
 
5. Epistylis
Epistyis is a branched, stalked, ciliate protozoan. This organism is most likely to cause
disease when there are conditions of eutrophic (fertile) water. The common name of the disease
caused by Epistylis is “Red Sore Disease.” Grossly, fish are observed to have white or
hemorrhagic lesions on the body. The parasite causes an ulceration at the site of attachment to
the fish. This ulceration may serve as a sight of secondary bacterial or fungal infection.
Diagnosis is made by the microscopic examination of fresh skin scrapings or gill
clippings for the presence of the parasites. Treatment may include formalin, potassium
permanganate or salt (NaCl).
 
6. Ambiphrya (Scyphidia = former name) and
Apiosoma (Glossatella = former name)
These protozoa are barrel-shaped or urn-shaped organisms that can be found attached
to the gills or body surface. When present in large numbers combined with deteriorating water
quality, they can become problematic. These organisms use the fish as a site for attachment as
they feed on bacteria and suspended organic matter in the water. In high numbers they can
reduce the functional capabilities of the gills.
Diagnosis is made by the microscopic examination of fresh skin scrapings or gill
clippings for the presence of the parasites. Treatment may include copper sulfate or formalin.
 
7. Capriana (Trichophrya = former name)
Capriana is a suctorian parasites found on the gills of fish. Heavy infections can cause
severe swelling, anemia and erosion of gill tissues. Copper sulfate is the only chemical
treatment found to be effective in controlling this parasite.
Diagnosis is made by the microscopic examination of fresh skin scrapings or gill
clippings for the presence of the parasites.
 
8. Henneguya
Henneguya is a myxosporidian parasite with two polar capsules and a long tail-like
extension of the spore shell. It can be found in cysts on the skin, fins and gills of fish. It can
become problematic when present in large numbers on the gills by reducing the functional
capabilities of the gills. On some fish, discrete white cysts may be seen on the gills or skin. If
these cysts are broken open and examined microscopically, numerous elongate myxosporidia
will be visible. Diagnosis may require histological evaluation of tissues.
A disease that has been associated with Henneguya is Proliferative Gill Disease. At
present the specific etiology of Proliferative Gill Disease remains open. This is a disease that is
characterized by a severe gill epithelial hyperplasia with granulocytic infiltrate around cysts of
what are considered immature parasites. Necrosis of the cartilage of the primary lamellae may
also be observed. Although this is a disease primarily of the gills, the immature parasite cysts
have occasionally been observed histologically in internal organs. There is some evidence that
the parasite causing Proliferative Gill Disease may have a life cycle similar to the
Myxosporidian (Myxobolus cerebralis) that caused Whirling Disease (see below). In the case of
Proliferative Gill Disease, the aquatic worm Dero digitata may serve as an intermediate host
and release an infectious form termed Aurantiactinomyxon sp. that infects the fish causing the
disease. Mature spores have not been observed in Proliferative Gill Disease. Some fish health
specialists feel that the parasite may be in an aberrant host when it is found in the channel
catfish.
 
9. Myxobolus cerebralis (Myxosoma cerebralis = former name)
Myxobolus cerebralis is the causative organism of whirling disease. This myxosporidian
has a tropism for cartilage and bony tissues. It is particularly problematic in young salmonid
fishes, during the first three months of life before ossification is complete. The parasite feeds
upon cartilagenous tissue. Disease signs include a “black tail” condition in young fish and a
tail-chasing swimming behavior. The “black tail” condition is caused by vertebral instability
that effects the sympathetic nerves controlling the melanocytes of the tail. The impact on the
nervous system also causes the erratic swimming behavior.
Because the sporozoa are embedded in the cartilage and bone, diagnosis is made by
histological examination of those tissues, particularly of the skull and gill arches. The mature
myxosporidian can be seen in the tissues. A giemsa stain will allow for an easier visualization
of the parasites.
The parasite has a life cycle that includes the fish for the mature myxosporidian and the
aquatic worm Tubifex tubifex as an intermediate host. When the infected fish dies, the spores
are ingested by the tubifex worm where they metamorphose and are released from the worm as
a form termed a Triactinomyxon. The Triactinomyxon is thought to adhere to and penetrates
the gills or is ingested by the fish. The sporoplasm is released and migrates to the cartilagenous
tissue.
There is no treatment for the Whirling Disease organism.
 
10. Microsporidia (Glugea, Plistophora, Nosema, Thelohania)
Microsporidia represent a large group of sporozoan parasites of fish. Some species of
these organisms are particularly pathogenic, while others do not pose any great health risk to
the infected fish. The microsporidia are sometimes present in large cysts or xemonas. In the
case of large abdominal xenomas, a pressure necrosis may be observed in the abdominal organs
that are displaced from their usual location.
There are no treatments for the microsporidia.

METAZOA
 
1. Monogenetic Trematodes (e.g. Gyrodactylus, Dactylogyrus)
Monogenetic trematodes are a group of flat worms that complete their life cycle on a
single host. A major identifying characteristic of these helminths is their organ of attachment,
the haptor. This is at the posterior end and may have 0, 1 or 2 pair of anchors and a number of
small hooklets around the periphery. Other identifying characteristics include the presence or
absence of “eye spots.”
Lesions observed are primarily hemorrhage and necrosis of epithelial tissue of the gill
and skin.
Diagnosis is made by the microscopic examination of fresh skin scrapings or gill
clippings for the presence of the parasites. Treatment may include bath applications of formalin
or potassium permanganate.
 2. Digenetic Trematodes
Digenetic trematodes are helminths that require several hosts on which to complete their
life cycle. The majority of digenetic trematodes that infect fish do so as a metacercaria or “grub”
stage. In general, the life cycle of these digenetic trematodes consists of the adult worm living
in the gut of a fish-eating bird. Eggs from the worm are shed into the water with the bird feces.
These eggs hatch to form a free swimming larva (miracidium). The miracidium must find an
appropriate snail or clam host to infect. Once in the snail or clam, the miracidium goes through
several developmental stages and emerges as a free-swimming larva (cercaria). The cercaria
find a fish host, penetrate the fish and migrate to a specific part of the fish where they encyst
and become the metacercaria (grub). The fish containing the metacercaria must be eaten by a
fish-eating bird for the parasite to complete its life cycle.
Some metacercaria are very specific with respect to the location (organ/tissue) they infect
on the fish host. Others are not so specific. Usually the presence of digenetic trematodes does
not have serious health consequences to the fish host. However, in very heavy infections or
infections of specific organs (e.g. Diplostomum, the eye fluke may cause blindness), the fish may
be adversely effected.
Diagnosis is based on microscopic examination of fresh materials or materials prepared
for histological examination. Identification to genus and species may require a knowledge of
the life cycle and primary hosts present in a particular environment.
There are not treatments for digenetic trematodes.
 
3. Acanthocephalans
Acanthocephalans are spiny-headed worms that are found as adults in the intestine of
the fish. Larval worms may be found in the internal organs. Acanthocephalans have a complex
life cycle which includes an amphipod as the first intermediate host and may include a fish as a
second intermediate host.
In spite of heavy infections in the intestine, fish may not show signs of disease.
Occasionally a worm may perforate the intestine, leading to an abdominal peritonitis.
Diagnosis is based on microscopic examination of fresh materials or materials prepared
for histological examination.
There are no treatments for acanthocephalans.
 
4. Cestodes
Cestodes can be found as parasites of fish as adult worms in
the digestive tract or as larval worms in various organs and tissues of fish. Cestodes have a
complicated life cycle which involves and arthropod (copepod) intermediate host and
sometimes a second intermediate host, such as a fish.
The most serious impact on fish is usually due to a heavy infection of larval tissue
dwelling forms. As these larvae migrate through the tissues, they leave a tract of scar tissue.
Diagnosis is based on microscopic examination of fresh materials or materials prepared
for histological examination.
There are no compounds that have a label as treatments for cestodes in fish.
 
5. Nematodes
Nematodes have a complicated life cycle which may require one or two intermediate
hosts. Sometimes the fish is the final host, with the nematode being found in the intestine.
Larval forms of nematodes are found encysted in various organs and tissues.
Diagnosis is based on microscopic examination of fresh materials or materials prepared
for histological examination.
There are no compounds that have a label as treatments for nematodes in fish.
 
6. Crustaceans: Copepods and Branchiurans
A number of Crustacean Copepods are parasites of fish. Lernea, the anchor worm, is the
adult female of the species. As immature forms, the male and female are free-swimming
aquatic invertebrates. Once mating occurs, the male dies and the female searches for a fish host.
The organism attaches to the fish by a “anchor” structure that develops below the skin, usually
in the underlying muscle. The body of the parasite (“the worm”) trails outside the fish. There
may be two egg sacs on a gravid female.
Another common copepod parasite is Ergasilus. Ergasilus usually infect the gills of fish. They
attach by a pair of modified appendages that look like “ice tongs.”
The Branchiuran Argulus, also known as the fish louse, has a flattened disk-like
appearance. It infects the external surface of the fish, often being found underneath the
operculum. When present in large numbers, it can cause extensive skin necrosis.
Diagnosis is based on microscopic examination of fresh materials.
There are no compounds that have a label as treatments for crustacean parasites of fish.
 
IV. Pathology — Common Bacterial Diseases
 
1. Motile Aeromonad Septicemia
(Aeromonas hydrophila, Pseudomonas fluorescens)
Motile Aeromonad Septicemia, also known as Bacterial Hemorrhagic Septicemia is an
infection caused by the motile, gram negative bacteria Aeromonas hydrophila, Aeromonas
sobria, and others. For purposes of this presentation, Pseudomonas fluorescens is included in
this bacterial disease. Infection by these ubiquitous organisms is usually associated with stress
from such factors as crowding, elevated/changing water temperatures, reproduction/spawning,
and water quality. Signs of disease and lesions can be variable. They can include hemorrhage
at the base of the fins and on the skin, shallow to deep skin ulcers, swollen abdomen,
exophthalmia, and red colored ascites.
In some cases the internal organs can be liquified. Histologically, renal and splenic hemopoietic
tissue is reduced. Focal necrosis may be found in the cardiac muscle, liver, gonad an pancreatic
tissue. A serosanguinous exudate may also be present.
Diagnosis is based on culture and identification of the organism. Treatment often
consists of antibiotic therapy, usually delivered via the feed.
 
2. Furunculosis
 (Aeromonas salmonicida)
Furunculosis is an infection caused by the non-motile, gram negative bacterium
Aeromonas salmonicida. This is most often considered to be a disease of salmonids, but the
bacterium is known to infect other species of fish. A particular characteristic of the bacterium is
that it produces a brown diffusible pigment on a bacterial agar that is rich in the amino acids
tyrosin an phenylalanine. A variant of Aeromonas salmonicida, termed achromogenic (does
not produce the brown diffusible pigment), causes Goldfish Ulcer Disease.
Considerable variation can be seen in the clinical presentation of this disease. The
chronic form of Furunculosis is characterized by a deep necrotic lesion of the muscle, the
“furuncle.” The acute form of the disease may be characterized by a diffuse hemorrhagic
condition. Histologically, hemorrhage and foci of bacteria can be seen in cardiac, hemopoietic,
hepatic and gill tissue. These foci or colonies of bacteria may be seen with or without a cellular
infiltrate. The lack of the infltrate is due to the leukocytlytic exotoxin produced by the
bacterium.
Diagnosis is based on gross and microscopic lesions and culture and identification of the
orgnanism. Treatment often consists of antibiotic therapy, usually delivered via the feed.
 
3. Enteric Septicemia of Catfish
(Edwardsiella ictaluri)
Enteric septicemia of catfish is caused by the gram negative
bacterium Edwardsiella ictaluri. This disease has been, for at least the past 15 years, the most
serious disease faced by the commerial cafish farmer. The bacterium will also infect a number
of other fish species. Although the clinical presentation of this disease can be variable, the
distribution of the lesions tend to be multifocal. Also, there may be a lesion on the head of the
fish, along the fissure between the frontal bones that has given rise to the common name “Hole
in the Head Disease” (Not to be confused with the Hole in the Head Disease in aquarium fishes
that has historically been associated with Hexamita — although there is little scientific basis for
this association).
Additional lesions that may be found in fish with Enteric Septicemia of Catfish include
hepatomegaly, splenomegaly, renomegaly; hemorrhagic enteritis; necrohemorrhagic hepatic
foci; necrotizing enteritis of the intestinal villi and presence of a serosanguinous exudate.
Field outbreaks of this disease tend to follow a unique temperature pattern; occurring
most commonly at water temperatures between 22-28C.
Diagnosis is based on presence of gross and microscopic signs and culture and
identification of the bacterium. It is important to note that this bacterium is particularly slow
growing. Very small colonies may be seen after 72-96 hrs of culture (most other bacterial fish
pathogens produce heavy growth within 24-48 hrs). Treatment may consist of antibiotic
therapy delivered via the feed. More recently the practice has been to take the fish off feed. The
benefits observed from doing this are thought to occur due to the reduction of the fecal to oral
route of transmission of the bacterium.
 
 
 
 4. Bacterial Gill Disease
(Flavobacterium branchiophilum)
Bacterial gill disease is caused by the gram negative Myxobacter Flavobacterium
branchiophilum. This disease is also termed Environmental Gill Disease. The disease is
considered to be caused by a combination of a number of factors: small fish in crowded
conditions, poor water quality, overfeeding of a fine (dust-like) ration and presence of the
ubiquitous bacterium. These conditions are also characteristic of the environment for rearing
fry and small fingerling fish.
Signs of the disease include reduced feeding and crowding of the fish near the water
inlet. This is due to the compromised condition of the gills. The lesion caused by this bacterium
is a proliferation of the gill epithelium. Diagnosis of this disease is based primarly on
histological finding. The gill tissue may exhibit a moderate to severe diffuse proliferation of the
epithelial tissue that is most pronounced at the distal end of the primary lamellae. Secondary
lamellae may be fused. A Brown and Bren stain or a Gram stain may reveal long rod-shaped
bacteria that tightly adhere to the gill tissue.
Treatment and/or management of this disease is problematic. Losses may be reduced by
elimination of some of the above stresors. Some benefit has been achieved by taking the fish off
feed. Several compounds with potential therapeutic value are currently being evaluated to
satisfy FDA label requirements. These compounds, primarily chloramine-T an hydrogen
peroxide, are considered to act as “disinfectants” to reduce the number of pathogenic bacteria
present. Any managment strategy for this disease must also consider ways to reduce the stress
inherent in the culture system.
 
5. Columnaris
(Flavobacterium columnare)
Columnaris is caused by the gram negative Myxobacteria Flavobacterium columnare.
Previous names for this bacterium have included Flavobacterium columnaris, Flexibacter
columnaris, Cytophaga columnaris, Chondrocccus columnaris and others. The infection is most
commonly and external infection found on the body and/or gills. In some instances a systemic
infection is also found. The bacterium is a ubiquitous bacterium and the disease is often
associated with stress of the fish.
The clinical presentation of the fish may include shallow erosions of the skin, frayed fins,
and eroded gills. Lesions may take on a yellow color; the bacterium is a member of the yellow
pigmented bacteria (Flavobacterium).
Histologically, lesions found in the skin and gills are characterized by necrosis. Wet
mounts of scrapings of lesions will reveal long flexing rod-shaped bacteria that may aggregate
into a characteristic “haystack” which gave rise to the “Columnaris” name.
Diagnosis is often based on gross signs an presence of the characteristic “haystack”
aggregations of the bacteria. The bacterium can be cultured, but is usually most successful
when either Cytophaga agar or Ordal’s medium are used. The colonies have been described as
yellow rhizoid colonies that tightly adhere to the agar.
Treatment/management of this disease includes reduction of stress and application of
potassium permanganate or formalin to reduce the number of bacteria associated with external
infection. Antibiotic medicated feeds have been used for systemic infections, although there is
not an FDA lable for such an application.
 
6. Fish Mycobacteriosis
(Mycobacterium marinum, M. forituitum, and M.chelonei)
Fish mycobacteriosis is considered a chronic bacterial infection caused by one of the
acid-fast bacteria of the genus. Species such as M. marinum, M. forituitum, and M.chelonei are
among the most common species involved with infection of fish. These bacterium are capable
of infection in a wide range of fish species. Mycobacteriosis appears to be particularly
problematic in closed aquatic water recirculation systems, such as aquaria and recirculation
aquaculture systems.
The clinical presentation of Fish Mycobacteriosis can be extremely variable. Signs can
include anorexia, emaciation, ulceration of the skin, spinal curvature, exophthalmia, lethargy,
and loss of equilibrium. In some cases the only observable sign is lethargy. Internal
examination may reveal grossly visible nodules (granulomas) in various internal organs.
Diagnosis is based on histological finding of granulomas with acid fast organisms.
Culture of the organisms on artificial media may be difficult.
Management of the disease often required depopulation of the infected population and
disinfection of the holding facility. Although various therepeutic protocols have been proposed
(most in the non-refereed literature), there is little scientific information supporting the efficacy
of any therepeutic treatment.
Of particular note is the fact that Fish Mycobacteriosis is a zoonotic disease. The bacterium is
thought to infect humans by gaining entry through cuts or abrasions in the skin. The bacterium
appears to be cold adapted, as is tends to localize in the skin of humans causing skin nodules.

7. Emphasematous Putrefactive Disease of Catfish

(Edwardsiella tarda)
Emphasematous Putrefactive Disease of Catfish or “Fish Gangrene” is caused by the
gram negative bacterium Edwardsiella tarda. The bacterium has been associated with disease
in a number of species of fish other than the channel catfish. The disease is often found in large
channel catfish held in eutrophic waters.
Although clinical signs tend to be similar to those found in other bacterial infections,
there may be the presence of a deep necrotic lesion into the musculature. This necroic foci may
be filled with a malodorous gas.
Diagnosis is based on culture and identification of the organism. Treatment may consist
of antibiotic therapy delivered via the feed, although such an application does not have an FDA
label.
 
8. Vibriosis
(Vibrio anguillarum, V. alginolyticus)
A variety of species of Vibrios infect fish, typically in the marine environment. Species
such as Vibrio anguillarum and V.alginolyticus are often involved. Clinical presentation and
histological findings are similar to those of Motile Aeromonad Septicemia.
 
9. Enteric Redmouth Disease
(Yersinia ruckeri)
Enteric Redmouth Disese is caused by the gram negative bacterium Yersinia ruckeri.
This disease is most commonly a disease of salmonids and is particularly problematic in
rainbow trout and brook trout.
The clinical presentation is characterized by hemorrhage and ulceration of the region
around the mouth and operculum. Histologically, bacterial colonies and inflammatory cells
may be observed in the liver, kidney and spleen.
Diagnosis is based on culture and identification of the orgnanism. Treatment may
consist of antibiotic therapy delivered via the feed, although an FDA label does not exist for
such a use.
 
10. Bacterial Kidney Disease
(Renibacterium salmoninarum)
Bacterial Kidney Disese is caused by the gram positive diplobacillus Renibacterium
salmoninarum. This is considered a chronic disease of salmonids that is most problematic in
waters with low alkalinity (carbonate, bicarbonates and silicates). Fish may exhibit such signs
as exophthalmia, darkening of the skin and hemorrhage at the base of the fins. Upon internal
examination, gray to white nodules (granulomas) may be present on the kidneys. Similar
nodules may be observed on other organs (liver, spleen, heart). Histologically, the nodules are
characterized as granulomas; numerous gram positive bacteria may be visible with a gram stain
of the granuloma.
The bacterium is particularly difficult to culture, even on a high nutrient agar (KDM-2
medium, Kidney Disease Medium). The bacterium is very slow growing. Some fish health
specialists do not score a culture as negative for growth until day 42 of incubation. Due the the
slow growing characteristic of Renibacterium salmoninarum, diagnosis is usually based on
observation of gross signs and microscopic lesions and use of an specific antibody-based test,
such as fluorescent antibody or ELISA.

 
 
11. Coldwater Disease
(Flavobacterium psychrophilum)
Coldwater Disease is caused by the gram negative Myxobacter Flavobacterium
psychrophilum. This disease is observed in fry and fingerling salmonids and is most commonly
observed when the fish are held at temperatures between 4.4 - 10C. Lesions may include open
lesions and erosion of the skin on the caudal peduncle, erosion of muscle on the caudal
peduncle, and loss of the caudal fin.
Diagnosis is based on observation of gross and microscopic lesions. Treatment is similar
to that practiced for Bacterial Gill Disease.

12. Streptococcus Infection

 (Streptococcus iniae)
Bacteria of the genus Streptococcus have been documented occasionally as pathogens of
a variety of fish species. More recently, this bacterial infection has taken on more importance.
In 1997, zoonotic infections occurred in members of the Asian population of Toronto, Ontario,
Canada, when they purchased live tilapia that apparently carried a particular strain of
Streptococcus iniae. The infection apparently occurred when the individuals suffered wounds
from the fish spines or cut themselves with the knife used to clean the fish.
In fish this disease is characterized as a gram positive bacterial hemorrhagic enteritis.
Externally, hemorrhage may be observed on the abdomen and at the base of the fins. Kidney,
liver and spleen may be enlaraged.
In the past several years, several cases of Steptococcus infections have been reported for
a variety of fish cultured in closed recirculation aquaculture systems, including tilapia and
hybrid striped bass. Whether this infection will be particulary problematic in this unique
culture environment has yet to be seen.
Diagnosis is made by observation of clinical signs and culture and identification of the
organism. At present there is no FDA label for any therapeutic treatment. The literature does
contain reports of successful therapy through the use of antibiotic medicated feeds.
 
V. Pathology — Common Viral Diseases
 
1. Channel Catfish Virus Disease
Channel Catfish Virus Disease is a herpesvirus infection of fry and fingerling channel
catfish. The disease is often associated with stress. Losses can be high, approaching 100% of the
population of fish in a pond, under conditions of high water temperatures, low dissolved
oxygen and handling of the young susceptible fish. If an rapid onset of high mortalities are
observed in fry and fingerling channel catfish during hot summer weather, Channel Catfish
Virus Disease should be considered on the rule out list.
Signs of the disease include erratic swimming or spiralling, abdominal distension,
exophthalmia, hemorrhage at the base of the fins and on the abdomen. The gills may appear
pale. Internally, a clear “straw colored” ascites may be seen in the abdominal cavity. The
kidney and liver may be pale. Of particular note is the dark red (almost black) color of the
enlarged spleen. Necrosis and hemorrhage are observed during microscopic examinarion of the
liver, kidney, spleen and digestive tract.
Diagnosis is made by observation of disease signs and culture of the virus. It is not
uncommon for a syncytial cytopathic effect to be observed on brown bullhead (BB) or channel
catfish ovary (CCO) cell cultures within 24 hours of inoculation with a cell free filtrate from
internal organs of infected fish.
Management centers around reduction of stress that is inherent in the culture
environment. In particular, netting or other handling of susceptible fry and fingerling catfish is
limited or not done during times of high water tempertures. Other practices include use of
serum negative brood fish and elimination of known positive fish from a facility.
 
2. Lymphocystis
 Lymphocystis is a disease caused by an iridovirus that is characterized by a hypertrophy
of fibroblasts. The lesion observed appears as a large nodule that is made up of a number of
these hypertrophied cells. The disease occurs in a wide variety of freshwater and marine fish
species. Although the disease is normally external, found of the skin and fins, on rare occasions
it has been reported as an internal infection. The disease has been observed to have a seasonal
incidence in wild fish, being most commoly observed during the cooler months of the year.
Histologically the cells appear hypertrophied and may have cytoplasmic and nuclear
inclusions. Each cell is surrounded by a hyaline capsule.
Diagnosis is based on gross an histological findings. There is no treatment for this
disease.
 
3. Infectious Hematopoietic Necrosis
Infectious Hematopoietic Necrosis is a severe rhabdoviral disease of salmonid fishes.
Mortalities may approach 100% of the fish in an effected population. Signs of the disease may
include lethargy or excitibility, darkening color, exophthalmia, abdominal distension,
hemorrhage, and anemia. Of particular note may be the presence of a fecal cast that trails from
the anus of infected fish.
As the name implies, the most notable histological lesion is a necrosis of the
hematopoietic tissue found in the kidney and spleen. The eosinophilic cells of the intestinal
submucosa also appear necrotic.
Diagnosis is based on observation of clinical signs and culture and/or identification of
the virus. A number of immunological and molecular diagnostic reagents have been developed
in various fish health research laboratories.
The disease is most severe at water temperatures of 10C. Although there is no treatment
for this disease, one management option has been to increase the water temperature to above
19C, if that is possible. Other management practices include avoidance.
 
4. Infectious Pancreatic Necrosis
Infectious Pancreatic Necrosis is a birnavirus infection, primarily of salmonids. Signs of
disese include a sudden rise in mortallities, fish spiralling around their long axis, abdominal
distension, exophthalmia, darken color, and presence of a mucoid material in the stomach and
anterior intestine. Within a population, the larger fish appear to be infected first.
As the name implies, a notable histological lesion is a necrosis of the pancratic acinar
tissue. This tissue is found in nodules in the mesenteries, near the junction of the stomach and
the intestine. Other lesions include a necrosis of the mucosa of the digestive tract and
hematopoietic tissue of the kidney.
Diagnosis is based on observation of signs of diseas and culture of the virus.
Management centers around avoidance.
 
5. Viral Hemorrhagic Septicemia
Viral Hemorrhagic Septicemia is a severe rhabdovirus infection of salmonids, paticularly
the rainbow trout. Historically, this disease has been known as a severe fish disease found in
Europe but not in North America. The first isolation of Viral Hemorrhagic Septicemia in North
America occurred in 1988, when it was isolated from asymptomic adult salmonids to be used as
brood fish when they returned to the Puget Sound region to spawn. Further evaluation of these
findings lead to the identification of the virus in Pacific Cod. The isolate from the salmonids
was further found to have low virulence to salmonids following challenge studies. All fish
associated with the 1988 findings, as well as several additional isolations in 1989, were
destroyed. No cases of clinical Viral Hemorrhagic Septicemia have been documened in North
America to date.
Although a variety of disease signs may be present, the most notable are those of
hemorrhage. Fish also appear anemic. Histologically, hemorrhage may be observed under the
skin and in the musculture.
Diagnosis of Viral Hemorrhagic Septicemia is done by observation of disease signs an
culture and identification of the virus. There is no treatment for this disease. Management
center around avoidance.
 
 
 
 
 
 
 
VI. Non-Infectious Diseases
1. Nitrite Toxicity
Nitrite Toxicity, Methemoglobinemia or Brown Blood Disease is a disease caused by
high nitrite concentrations in the water. The source of the nitrite is the metabolic wastes
produced by fish when they metabolize the protein in their diet. The primary nitrogenous
waste product of fish is ammonia. When this is excreted into the water it is oxidized by the
Nitrosomonas genus of bacteria to form nitrite. The nitrite is subsequently oxidized by the
Nitrobacter genus of bacteria to form nitrate. If fish are heavily fed and/or if the Nitrobacter do
not efficiently oxidize the nitrite to nitrate, the nitrite concentration can increase to problematic
concentrations. Although a number of other factors are involved, nitrite can become toxic to
fish at concentrations as low as 0.5 mg/L (= ppm). The nitrite is hypothesized to cross the gills
and oxidize the hemoglobin in the fish erythrocytes to form methemoglobin. Methemoglobin is
brown, giving rise to the common name “Brown Blood Disease.” The blood of effected fish
takes on a characteristic brown color. When the hemoglobin is converted (oxidized) to
methemoglobin, it is incapable of transporting oxygen. The fish behave as if there is an oxygen
depletion in the water. Fish can be observed to be lethargic and may gasp at the water surface
or crowd near water inlets. The disease, in effects, reduces the respiratory capabilities of the
fish.
The two primary environments in which methemoglobinemia has been observed are: (1)
channel catfish ponds in the cooler months of the year, (2) closed water recirculation systems
(aquaculture production or aquaria). In cafish ponds the elevated nitrites are though to
originate due to combination of high feeding rates and the depressed metabolic activities of the
Nitrobacter bacteria during the cooler months of the year. It is hypothesized that the metabolic
activities of the Nitrobacter are suppressed to a greater extent than are those of the
Nitrosomonas. This results in a greater reduction in the rate of oxidization of nitrite to nitrate
than is occurring for ammonia being oxidized to nitrite. In closed water recirculation systems
the buildup of nitrite is associated with a less than efficient biological filter and overfeeding.
Treatment of methemoglobinemia may consist of adding chloride (usually as sodium
chloride) to the water. The rationale is that the chloride ion and nitrite ion are competing
monovalent anions for limited number of uptake sites across the gill epithelium. The
management strategy is to establish a ration of Cl:NO2 of at least 5:1. This is thought to reduce
the uptake of nitrite by the fish to the extent where the natural methemoglobin reductase
enzyme system in the fish can convert the methemoglobin back to hemoglobin. An additional
managment practice may be to reduce the amound of feed given to the fish.
 
2. Ammonia Toxicity
Ammonia Toxicity occurs in a manner similar to that described above, except that it is
primarily a function of over feeding of the fish. Elevated ammonia concentrations are the result
of large amounts of ammonia being excreted by the fish and an inadequate number of bacteria
in the biological filtration of the fish holding facility. The toxicity of ammonia is greatly
influenced by the pH and temperature of the water. Ammonia toxicity increases with both pH
an temperature. Actually, the ammonia exists in two species, unionized ammonia (NH3) and
the ammonium ion (NH4+) as described by the following equilibrium equation:
 
NH4+ <-----> NH3 + H+
 
High pH shifts equation ----->
High water temperature shifts equation ----->

Unionized ammonia (NH3) is the toxic species that is capable of crossing the gill epithelium.
Chronic low concentrations of elevated unionized ammonia will result in a diffuse gill
epithelian proliferation. An acute, high concentration of ammonia will result in an ascites that
will lift the gill epithelium from the supporting primary and secondary lamellae. Compromised
gills result in reduction of the ability of the fish to conduct respiration and to excrete metabolic
wastes (ammonia).
Treatment of elevated ammonia may consist of reducing stocking rate, reducing feeding
rate and water changes to dilute the existing ammonia.
 
3. Gas Bubble Disease
Gas Bubble Disease is a condition when gases, present in the water at supersaturation
concentrations come out of solution to form gas emboli in the fish. These emboli may be under
the skin or in the blood vasculature. Emboli under the skin destroy the integrity of the skin as a
barrier to infection and as a tissue important for proper osmotic balance. Emboli in the blood
vasculature may block flow of blood, especially in the gills.
Supersaturation of gases can be the result of:
1. A rapid water temperature rise. The ability of water to hold dissolved gases
decreases as water temperature rises.
2. Algal bloom and photosynthetic activity
3. Imperfections in fittings and joints in plumbing systems. Small imperfections may
allow for air to be “sucked into” (cavitate into) the pipes supplying water to a fish holding
system.
4. Water from deep wells. When the water is drawn to the surface of the earth, the
pressure on that water is reduced.
5. Water released from the bottom of dams/water impoundments. Pressure on that
water is reduced similar to (4.) above.
 
4. Vitamin C Deficiency
Vitamin C is a necessary vitamin that most fish cannot produce themselves. It must be
provided in the diet. Diets with insufficient Vitamin C may result in a condition known as
“Broken Back Syndrome.” Vitamin C is important in the conversion of cartilage to bone. With
insufficient Vitamin C, proper ossification of cartilage does not occur. At locations of major
muscle mass on the fish, muscle tension may cause the vertebral column to take on a curved
appearance, giving rise to the common name.
A less visible impact of low dietary Vitamin C is a reduction of the functional
capabilities of the immune system. Fish fed a deficient diet may suffer from a variety of
facultative pathogens (pathogens normally present in the aquatic environment that become
problematic when the fish are stressed).
Diets are deficient in Vitamin C due to manufacture error or to improper storage.
Vitamin C is very labile at high temperatures. Long term storage of feeds may result in
degredation of the Vitamin C present.
Management of this condition is to feed diets with adequate Vitamin C. This can be
done by proper storage of feeds to prevent degredation of this vitamin.
 
5. Pantothenic Acid Deficiency
Pantothenic Acid Deficiency is a dietary vitamin deficiency disease that is characerized
by a gill tissue proliferation. Signs of the disease include respiratory distress and mortalities.
The gills may appear swollen. Diagnosis of the disease is based on observation of disease signs
and histological evaluation of the gills. The gills of effected fish will have a proliferation of the
gill epithelium that is most pronounced at the distal end of the primary lamellae. Care must be
taken to differentiate this condition from a number of other causes of gill epithelial
proliferation, including Bacterial Gill Disease (in which long gram negative rod-shaped bacteria
will be seen with a gram stain) and chronic unsatisfactory water quality.
Management includes proper storage of feeds to avoid deterioration of pantothenic acid
content.
Appendix 1

Metazoan Parasite Characteristics Used in Identification of Metazoan Parasites in Tissue

Sections

Group Shape Cavity Tract Features

Nematoda Spherical 1. cuticle
+ +
2. musculature
Acantho Spherical 1. hypodermis
cephala 2. Lemniscus
+ -
3.muscle layers
4. proboscis
Trematoda Flattened 1. suckers
- + 2. tegument
3. blind cecae
Arthropod Tend to be 1.Chitinous Cuticle
spherical 2.Striated Muscle Bands
+ +
3. Appendages
4. Tracheal Tubes
Cestoda Flattened Dorso 1. Calcareous Cuticle
ventrally - - 2. Scolex
3. Tegument
Pentastomes Spherical 1. Chitinous Cuticle
2. Striated Muscle Bands
+ + 3. Sclerotized Openings
4. Digestive Glands
5.Hooks