Fish are susceptible to a wide variety of bacterial pathogens. Many of these bacteria capable of causing disease are
considered by some to be saprophytic in nature.
This bacteria only become pathogens when fishes are physiologically
unbalanced, nutritionally deficient, or there are other stressors, i.e., poor
water quality, overstocking, which allow opportunistic bacterial infections to
proceed. Some of these bacterial
pathogens of fishes are fastidious and require special growth media for
laboratory culture. Others grow at
different temperatures, dependent upon the aquatic environmental temperature of
the fish. Some of the more common
bacterial pathogens are listed below.
Aeromonas salmonicida: This is the most common bacterial pathogen of fishes worldwide. This bacteria can cause the following diseases:
(a) Furunculosis of salmonids,
(b) Goldfish Ulcer Disease, (c) Carp Erythrodermatitis, and (d) Trout Ulcer
Disease. Additionally, several
other species of Aeromonas, including:
A. hydrophila, A. formicans, A.
liquefaciens, and A. hydrophila complex
are capable of causing a disease known as “Motile Aeromonas Septicemia” or
“Bacterial Hemorrhagic Septicemia”. Each
of the following diseases is discussed briefly below.
Furunculosis of Salmonids
Typical furunculosis in salmonids may occur in one of several forms:
Peracute form in fingerlings: These
fish usually have a dark discoloration and die rapidly without any other premonitory signs.
gross lesions may resemble those observed in the acute form of the disease.
Acute form: Premonitory signs of anorexia occur 2-3 days prior to death. Gross lesions include hemorrhage of the liver and splenomegaly.
Subacute: This form has
a much slower onset of clinical signs with petechial hemorrhages being observed in the skin and around the fins.
Fish exhibit focal discolorations and
anorexia and die approximately 4-6 days after the onset of clinical
signs. Gross lesions include
typical “furuncles” as well as internal lesions listed above for the acute
Chronic: This form is observed in fish which survive the subacute form and is manifested by healing of the furuncles and scarring. Affected and recovered fish may exhibit poor weight gain and be focally discolored.
Histologic lesions observed in the peracute and acute form will demonstrate necrosis, hemorrhage and bacterial microcolonies within affected organs. Furuncles classically are described a dark, raised tumefaction involving the skin, subcutis and underlying skeletal musculature. These lesions will ulcerate and drain a serosanguinous fluid. These lesions develop from localization of hematogenous bacteria in the muscle or skin, not from an external skin leison. The lesion histologically is characterized by marked necrosis of the skin, subcutis and skeletal muscle with mild to minimal acute inflammatory infiltrates in the acute stage. In the chronic form, scarring with be characterized by the replacement of muscle tissue with fibrous connective tissue. Culture of acute lesions will often recover the organism in pure culture.
Cutaneous Ulcerative Disease of Goldfish
This disease, although it is most common in goldfish, also affects other non-salmonid fishes. It is caused by Aeromonas salmonicida, and the disease is also referred to as “furunculosis”. However, unlike furunculosis as discussed above, this disease is typically localized to the skin and only becomes systemic late in the disease. The skin lesions range from whitish discolorations to shallow hemorrhagic ulcers to deep lesions which may expose underlying muscle or bone. These lesions can become secondarily infected with fungi, protozoa, or other bacterial agents. Fish may exhibit hemorrhage on the body as well as the base of the fins.
Diagnosis of this disease is dependent upon culture of the etiologic
agent from the lesions. Histologically,
the lesions have a mild to moderate primarily mononuclear inflammatory
infiltrate. Large numbers of
bacterial microcolonies are observed in many of the lesions.
Motile Aeromonas Septicemia (MAS)
This is the third manifestation of disease caused by Aeromonas sp. This is probably the most common bacterial disease of freshwater fish. This disease has been associated with several members of the genus Aeromonas, including A. hydrophila, A. sobria, A. caviae, A. schuberti, and A.veronii. Clinical signs of motile aeromonas septicemia range from sudden death with high morbidity in peracute cases to superficial to deep skin lesions. Skin lesions include variously sized areas of hemorrhage and necrosis and the base of the fins. These lesions may progress to reddish to gray ulcerations with necrosis of the underlying musculature. Ulcers may be observed in conjunction with a hemorrhagic septicemia which can produce non-specific lesions and clinical signs of exophthalmos, ascites, visceral petechiation, and a hemorrhagic and swollen lower intestine and vent. Anorexia and cutaneous discoloration are also observed with the septicemia.
Histopathological lesions include acute-to-chronic dermatitis and myositis. With the septicemia, there may be depletion and necrosis of the renal and splenic hematopoietic tissue, as well as necrosis in the intestinal mucosa, heart, liver, pancreas and gonad.
Definitive diagnosis of MAS requires biochemical identification of the
suspected bacterial agent within the target tissues, with attendent clinical
signs and lesions. The kidney is
probably the best target tissue for culture, however, clinical lesions should
also be cultured.
This disease is also known by the following synonyms: Enteric Redmouth Disease, Redmouth, and Blood Spot Disease. This disease is caused by the pathogen Yersinia ruckeri. This is an important pathogen of salmonids, particularly rainbow trout. Outbreaks of this disease usually begin with chronic, low mortality which slowly escalates. Severity of yersiniosis is dependent mainly on strain virulence and the degree of environmental stress. There are six serovars of Y. ruckeri classified as Strains I through Strain VI, with Strain I being the most common. However, not all Strain I serovars are pathogenic, but all of the other strains are highly lethal. The early stages of this disease may resemble MAS with petechial hemorrhages observed around the fin and on the skin. Additionally, there is discoloration of the dorsum of the fish, as well as anorexia and lethargy. With chronic disease, there is ascitic fluid and unilateral or bilateral exophthalmos and hyphema (hence the term, “blood spot disease”). The characteristic gross lesions of this disease include hemorrhage of the oral cavity and skin erosions of the mouth. Histopathology includes bacterial colonization of well-vascularized tissues and hemorrhage of the gills, kidney, liver, spleen, and heart, as well as muscle. Definitive diagnosis of this disease involves culture of the target organ (kidney) as well as attendent clinical signs and lesions.
This is probably the most important bacterial disease of catfish.
It has a very high predilection for channel catfish, but has been
occasionally reported in other ictalurids such as brown bullhead, blue and white
catfish. This is a markedly
seasonal disease, with outbreaks occurring when water temperatures are in the
range of 24 - 28 oC.
Therefore it is most prevalent during May to June and September to
October in the southeastern United States.
There are two forms of ESC which are directly related to the route of
Bacteria are ingested into the gastrointestinal tract and enter the
bloodstream through the intestine with subsequent colonization of internal
organs with resultant necrosis of these organs.
There is usually a very high mortality and in some cases, very few
premonitory clinical signs are observed. Clinical
signs may include corkscrew spiral swimming, abdominal distention, exophthalmos,
or pale gills. Petechial
hemorrhages may be observed on dark areas of the skin as small (1 to 3 mm)
depigmented foci (called “false spots”).
Internally, the peritoneal cavity contains a bloody or clear fluid,
hemorrhage and necrosis of the liver, as well as splenic and renal hypertrophy.
Bacteria enter the catfish via the nervous system, by invading the
olfactory organ via the nasal opening and migrate up the olfactory nerve to the
brain, where the infection spreads from the meninges to the skull and finally to
the skin, forming the classic “hole-in-the-head” lesion.
This is a raised or open ulcer on the frontal bone of the skull (photo).
Histologically, enteritis, hepatitis, myositis, and interstitial nephritis begin as acute lesions and develop into chronic foci. Fish with the nervous form develop neuritis of the olfactory nerve with meningoencephalitis developing in the late stages. Definitive diagnosis of ESC requires identification of the gram negative bacteria in target tissues, with attendant clinical signs. In the acute form, the kidney is the target organ for culture, whereas in the chronic form, the brain is the target organ for culture.
This disease is also known as Emphysematous Putrefactive Disease (EPD) and is caused by Edwardsiella tarda. This disease is much less common than ESC and is more of a problem in older channel catfish, but fingerlings are still susceptible. Clinically, lesions are initially observed as 3 to 5 mm red cutaneous foci on the flanks and caudal peduncle. They are caused from fistulas originating deep in the skeletal muscle. There is petechiation and malodorous liquefactive necrosis of the viscera with fibrinous peritonitis. Catfish affected with this disease will continue to eat even if they are severely affected. There may be posterior paresis in the later stages of the disease. Definitive diagnosis is based on identification of the bacterium within the lesions and the attendent clinical findings. A fluorescent antibody test is available for identification of the bacterial agent, using kidney as the target tissue.
Bacterial Kidney Disease
This disease is caused by Renibacterium salmoninarum and primarily affects salmonids, especially rainbow, chinook, coho, brown and brook trout. Any age fish is susceptible to this disease, but losses may not occur until the fish are well grown. Vertical transmission of the disease from parent to offspring is thought to be the most common route of infection, however, horizontal transmission can also occur. Clinical disease is most likely to occur during times of stress, especially during transfer of salmonids from freshwater to seawater, or during spawning. Fish with BKD may have no external lesions, however, they may also present with cutaneous discoloration, exophthalmos, pale gills, abdominal distention or hemorrhages at the vent or base of the fins. Small vesicles on the flanks (often called “spawning rash”) filled with fluid, rupture to form cutaneous ulcers. The major target organ is the kidney, which may have large white, raised coalescing granulomas. These granulomas may also be observed in the spleen in severe cases. Histopathologic evaluation of these granulomas reveals large numbers of macrophages with phagocytized Renibacterium salmoninarum. Definitive diagnosis of clinical BKD requires identification of the bacteria within target tissues. Renibacterium salmoninarum is an extremely fastidious organism and may require up to twelve weeks to culture using selective media. Other methods of identification may include ELISA and/or FA testing or immunohistochemistry (Photomicrograph demonstrates a kidney which was positive for BKD using immunohistochemistry).
This is probably the most common chronic disease of aquarium fish, as well as other freshwater and marine fishes (photo demonstrates emacation in two Tang fish with mycobacteriosis). Clinical signs include emaciation, poor growth or retarded sexual maturation. Lesions include skeletal deformities, chronic nonhealing shallow to deep ulcers or fin erosions. Internally, 1 to 4 mm white nodules may be present on the viscera including the liver and kidney. Histopathology reveals a chronic inflammatory response with large numbers of of epithelioid macrophages surrounding the bacteria. This disease can be strongly suspected based on the presence of acid-fast staining bacteria within the lesions. Confirmation of this disease requires culture of the organism.
Columnaris, is a common bacterial disease that affects the skin or gills of freshwater fish and is caused most commonly by Flexibacter columnaris. This disease is also known by a wide variety of synonyms including the following: mxyobacterial disease, peduncle disease, saddleback, fin rot, cotton wool disease, and black patch necrosis. This bacteria is usually pathogenic at temperatures greater than 59 oF. Both mortality and acuteness of the disease will increase at higher water temperatures. Virulence mechanisms associated with this disease are not well understood, however, the mineral content of the water is thought to be important, since this bacteria has been shown to be less pathogenic in soft water as compared to hard water. Other risk factors include physical injury, low dissolved oxygen, organic pollution and high nitrite levels.
This is primarily an epithelial disease, i.e., it causes erosions and
necrosis of the skin and gills which may become systemic.
It often presents as whitish plaques that may have a red peripheral zone
on the head or back (hence the name saddleback)
and/or the fins (hence, fin rot) and
especially the caudal fin (hence, peduncle
disease). Fragments of the fin
rays may remain after the epithelium has sloughed, leaving a ragged appearance.
Lesions rapidly progress to ulcers, which may be yellow or orange due to
masses of pigmented bacteria. Ulcerations
spread by radial expansion and may penetrate into deeper tissues, producing a
septicemia. Gill infections are
less common but more serious. Columnaris
begins at the tips of the lamellae and causes a progressive necrosis that may
extend to the base of the gill arch. Definitive
diagnosis is dependent upon the isolation of the bacterial agent in the presence
of attending clinical lesions. It
should be noted that a presumptive identification of Flexibacter columnaris can be made by examination of wet mounts and
observation of long thin bacterial rods which a characteristic flexing or
gliding motion. In addition to Flexibacter
columnaris, other bacterial agents which have been implicated in this
disease include: Flexibacter
psychrophilia as well as Cytophaga
and Flavobacterium branchiophila.