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Edwardsiella septicaemia (Edwardsiella tarda infection)

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Edwardsiella septicaemia (Edwardsiella tarda infection)

Summary

  • Last modified
  • 09 November 2017
  • Datasheet Type(s)
  • Animal Disease
  • Preferred Scientific Name
  • Edwardsiella septicaemia (Edwardsiella tarda infection)
  • Overview
  • The genus Edwardsiella includes two species of bacteria that cause major diseases in fish: Edwardsiella tarda (Ewing...

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Pictures

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PictureTitleCaptionCopyright
(A) Edwardsiella tarda infection in channel catfish. The muscle tissue is necrotic, has lost its firmness and has open lesions (arrow). (Photo by Ahmad Darwish.) (B) A juvenile largemouth bass with necrotic E. tarda lesion on the caudal peduncle (arrow).
TitleEdwardsiella tarda infection
Caption(A) Edwardsiella tarda infection in channel catfish. The muscle tissue is necrotic, has lost its firmness and has open lesions (arrow). (Photo by Ahmad Darwish.) (B) A juvenile largemouth bass with necrotic E. tarda lesion on the caudal peduncle (arrow).
CopyrightJ. A. Plumb
(A) Edwardsiella tarda infection in channel catfish. The muscle tissue is necrotic, has lost its firmness and has open lesions (arrow). (Photo by Ahmad Darwish.) (B) A juvenile largemouth bass with necrotic E. tarda lesion on the caudal peduncle (arrow).
Edwardsiella tarda infection(A) Edwardsiella tarda infection in channel catfish. The muscle tissue is necrotic, has lost its firmness and has open lesions (arrow). (Photo by Ahmad Darwish.) (B) A juvenile largemouth bass with necrotic E. tarda lesion on the caudal peduncle (arrow).J. A. Plumb
(A) Edwardsiella tarda infection in Japanese eel with haemorrhagic and congested anal fin (arrow). (B) Cross-sections of body of Japanese eel with inflamed and necrotic muscle lesions (arrows).
TitleEdwardsiella tarda infection
Caption(A) Edwardsiella tarda infection in Japanese eel with haemorrhagic and congested anal fin (arrow). (B) Cross-sections of body of Japanese eel with inflamed and necrotic muscle lesions (arrows).
CopyrightJ. A. Plumb
(A) Edwardsiella tarda infection in Japanese eel with haemorrhagic and congested anal fin (arrow). (B) Cross-sections of body of Japanese eel with inflamed and necrotic muscle lesions (arrows).
Edwardsiella tarda infection(A) Edwardsiella tarda infection in Japanese eel with haemorrhagic and congested anal fin (arrow). (B) Cross-sections of body of Japanese eel with inflamed and necrotic muscle lesions (arrows).J. A. Plumb
Histopathology of Edwardsiella tarda infection in several different fish. (A) Abscess (arrow) in kidney of Japanese eel (haematoxylin and eosin (H & E), x 31). (B) Early E. tarda infection in liver of tilapia. Affected hepatic cells are necrotized (N) which is followed by macrophage infiltration (arrow) (Giemsa, x 80). (C) Granuloma (arrow) formation in liver of E. tarda-infected red sea bream (Giemsa, x 200). (D) Neutrophils gorged with E. tarda (arrow) from abscess in the kidney of eel (Giemsa, x 1000). (All photographs by T. Miyazaki.)
TitleHistopathology of Edwardsiella tarda infection
CaptionHistopathology of Edwardsiella tarda infection in several different fish. (A) Abscess (arrow) in kidney of Japanese eel (haematoxylin and eosin (H & E), x 31). (B) Early E. tarda infection in liver of tilapia. Affected hepatic cells are necrotized (N) which is followed by macrophage infiltration (arrow) (Giemsa, x 80). (C) Granuloma (arrow) formation in liver of E. tarda-infected red sea bream (Giemsa, x 200). (D) Neutrophils gorged with E. tarda (arrow) from abscess in the kidney of eel (Giemsa, x 1000). (All photographs by T. Miyazaki.)
CopyrightJ. A. Plumb
Histopathology of Edwardsiella tarda infection in several different fish. (A) Abscess (arrow) in kidney of Japanese eel (haematoxylin and eosin (H & E), x 31). (B) Early E. tarda infection in liver of tilapia. Affected hepatic cells are necrotized (N) which is followed by macrophage infiltration (arrow) (Giemsa, x 80). (C) Granuloma (arrow) formation in liver of E. tarda-infected red sea bream (Giemsa, x 200). (D) Neutrophils gorged with E. tarda (arrow) from abscess in the kidney of eel (Giemsa, x 1000). (All photographs by T. Miyazaki.)
Histopathology of Edwardsiella tarda infectionHistopathology of Edwardsiella tarda infection in several different fish. (A) Abscess (arrow) in kidney of Japanese eel (haematoxylin and eosin (H & E), x 31). (B) Early E. tarda infection in liver of tilapia. Affected hepatic cells are necrotized (N) which is followed by macrophage infiltration (arrow) (Giemsa, x 80). (C) Granuloma (arrow) formation in liver of E. tarda-infected red sea bream (Giemsa, x 200). (D) Neutrophils gorged with E. tarda (arrow) from abscess in the kidney of eel (Giemsa, x 1000). (All photographs by T. Miyazaki.)J. A. Plumb
Edwardsiella ictaluri, E. tarda, Aeromonas hydrophila and Pseudomonas fluorescens on Edwardsiella isolation media incubated at 25°C for 48 h. (Photo by D. Earlix.)
TitleEdwardsiella septicaemia
CaptionEdwardsiella ictaluri, E. tarda, Aeromonas hydrophila and Pseudomonas fluorescens on Edwardsiella isolation media incubated at 25°C for 48 h. (Photo by D. Earlix.)
CopyrightJ. A. Plumb
Edwardsiella ictaluri, E. tarda, Aeromonas hydrophila and Pseudomonas fluorescens on Edwardsiella isolation media incubated at 25°C for 48 h. (Photo by D. Earlix.)
Edwardsiella septicaemiaEdwardsiella ictaluri, E. tarda, Aeromonas hydrophila and Pseudomonas fluorescens on Edwardsiella isolation media incubated at 25°C for 48 h. (Photo by D. Earlix.)J. A. Plumb

Identity

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Preferred Scientific Name

  • Edwardsiella septicaemia (Edwardsiella tarda infection)

International Common Names

  • English: Edwardsiella tarda infection; edwardsiellosis; emphysematous putrefactive disease of catfish; fish gangrene

Local Common Names

  • Japan: red disease

Overview

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The genus Edwardsiella includes two species of bacteria that cause major diseases in fish: Edwardsiella tarda (Ewing et al., 1965) infects fish and other animals and Edwardsiella ictaluri (Hawke, 1979) infects fish only. A third species, Edwardsiella hoshinae (Grimont et al., 1980), infects birds and reptiles. Edwardsiella tarda produces the disease commonly known as fish gangrene, emphysematous putrefactive disease of catfish or red disease of eels and hereafter known in this text as Edwardsiella septicaemia (ES), and E. ictaluri causes ‘enteric septicaemia of catfish’ (ESC). Because E. tarda and E. ictaluri produce distinctively different diseases, they are discussed separately.

Edwardsiella septicemia is a serious systemic bacterial infection of cultured channel catfish (Ictalurus punctatus) in the USA (Meyer and Bullock 1973). In Japan and Taiwan it is a serious infection, called red disease, of cultured Japanese eels (Anguilla japonica) (Egusa, 1976) and Japanese flounder (Paralichthys olivaceous) (Nakatsugawa, 1983). In addition E. tarda occasionally produces infection in a variety of other fish species in the USA, Asia and elsewhere. Edwardsiella tarda infects freshwater and marine fishes, reptiles and amphibians and mammals throughout the world.

Edwardsiella septicemia in fish is characterized by necrotic abscesses in the muscle that emit a putrid odor when incised. The skin that covers muscle abscesses can be pale or have petechia. Mortality of infected fish may be acute but is often chronic depending upon the degree of stressful environmental conditions under which E. tarda infections occur. Edwardsiella tarda commonly resides in the intestine of fish and other aquatic animals and may be found in many environs where a host is not required for survival. The bacterium may also be present in the bottom mud of many bodies of water. Edwardsiella tarda is a typical member of the Enterobacteriacae; it is a Gram negative motile rod that is cytochrome oxidase negative and ferments glucose.

[Based upon material originally published in Woo PTK, Bruno DW, eds., 1999. Fish diseases and disorders, Vol. 3 Viral, bacterial and fungal infections. Wallingford, UK: CABI Publishing.]

Hosts/Species Affected

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Edwardsiella tarda infects a wide variety of fish. The most prominent hosts are Japanese eel (Anguilla japonica) in Japan (Egusa, 1976) and channel catfish (Ictalurus punctatus) in the USA (Meyer and Bullock, 1973). However, many other fish groups are also susceptible; for example Japanese flounder (Paralichthys olivaceus) in Japan (Nakatsugawa, 1983), and tilapia (Oreochromis spp.) are significantly affected and isolations from tropical ornamentals have been reported (Vandepitte et al., 1983; Bullock and McCraran, 1989; Dixon and Contreras, 1992). Most diseases associated with E. tarda occur in cultured fish in either fresh or marine waters; at least 30 species of fish are known to have been infected and probably all species are susceptible under certain conditions. Edwardsiella tarda generally causes disease only in warm-water fish, but infections have also occurred in migrating chinook salmon (Oncorhynchus tshawytscha) in the Rogue River, Oregon, USA (Amandi et al., 1982), spawning Atlantic salmon (Salmo salar) in Nova Scotia, Canada (Martin, 1984), farmed rainbow trout (Onchorhynchus gairdneri) in Australia (Reddacliff et al., 1996) and brook trout (Salvelinus fontinalis) broodstock in Quebec, Canada (Uhland et al., 2000). Other marine species such as turbot (Scophthalmus masimus) (Nougayrede et al., 1994) and sea bass (Dicentrarchus labrax) (Blanch et al., 1990) have also been reported to be infected with E. tarda.

Edwardsiella tarda infections are not limited to fish and in some instances other animals may simply be carriers and/or reservoirs of the pathogen. E. tarda can be found in reptiles (snakes, turtles and alligators) (Wallace et al., 1966; Nagel et al., 1982; Sugita and Deguchi, 1983), birds (White et al., 1969, 1973; Berg and Anderson, 1972), cattle (Ewing et al., 1965), swine (Arambulo et al., 1967), marine mammals (Coles et al., 1978) and other warm-blooded animals (Van Damme and Vandepitte, 1984). In many instances, E. tarda is part of the normal intestinal microflora of aquatic animals (Wyatt et al., 1979; Van Damme and Vandepitte, 1980; Kanai et al., 1988). Bauwens et al. (1983) found E. tarda in the intestine of a variety of zoo animals, especially fish-eaters and water-loving species. Edwardsiella tarda has also been associated with several different manifestations in humans (King and Adler, 1964; Jordan and Hadley, 1969; Bockemuhl et al., 1971; Van Damme and Vandepitte, 1980,1984; Vandepitte et al.,1983; Janda and Abott, 1993b).

Although environmental stressors are not essential precursors to E. tarda infections in fish, high temperature, poor water quality and high organic fertility probably contribute to the onset and severity of the disease. Juvenile channel catfish that were experimentally infected with Aeromonas hydrophila and then exposed to environmental stressors (low dissolved oxygen, high ammonia and high carbon dioxide) developed E. tarda infections in 25-50% of the fish (Walters and Plumb, 1980). This compared to 4.5-12.5% E. tarda infections in the non-A. hydrophila injected or otherwise non-stressed fish. Indications were that environmentally induced stress and other bacterial infections could predispose channel catfish to endemic E. tarda. Cultured tilapia under stress are also susceptible to E. tarda (Benli and Yildiz, 2004). On several occasions, intensively cultured and environmentally stressed Nile tilapia (Oreochromis niloticus) in recirculating systems that had a moderate to heavy Trichodina (protozoan parasite) infestation, were also infected with E. tarda and Streptococcus spp. While stressed, neither bacterial infection responded to chemotherapy, but, as soon as the stressor was relieved and parasites were eliminated, the E. tarda infection disappeared. Many epizootics of E. tarda occur in fish predisposed to fluctuating water temperatures (Liu and Tsai, 1980; Amandi et al., 1982) or fish in highly enriched waters (Meyer and Bullock, 1973; Baya et al., 1997; Uhland et al., 2000). Other fish species susceptible by stress are striped bass (Morone saxatilis) (Herman and Bullock, 1986; Baya et al., 1997) and rainbow trout (Redacliff et al., 1996)

Distribution

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Edwardsiella tarda is a ubiquitous organism, having been isolated from animals or the environment of most continents and occurs in both freshwater and marine waters. The list of countries in which E. tarda has been found is lengthy but includes predominantly the USA, Japan, Taiwan, Thailand, Israel and many developing countries.

Distribution Table

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The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.

Continent/Country/RegionDistributionLast ReportedOriginFirst ReportedInvasiveReferenceNotes

Sea Areas

Atlantic, NortheastPresentTaksdal and et al. , 1989
Atlantic, Western CentralPresentHerman and Bullock , 1986
Pacific, SouthwestPresentHumphrey and et al. , 1986; Eaves and et al. , 1990
Pacific, Western CentralPresentHoshinae , 1962

Asia

BangladeshPresentChowdhury and Wakabayashi , 1990
ChinaPresentZheng , 1987
IndiaPresentKoshi and Lalitha , 1976
-Andhra PradeshPresentSwain and Nayak, 2003
IsraelPresentSechter and et al. , 1983
JapanPresentHoshinae , 1962; Sano et al., 2001
Korea, Republic ofPresentKokuska , 1973
PhilippinesPresentTacal and Menez , 1968
SingaporePresentTan and Lim , 1977
TaiwanPresentLiu and Tsai , 1980
ThailandPresentBoonyaratpalin , 1983

Africa

Congo Democratic RepublicPresentDamme and Vandepitte , 1980
MadagascarPresentFourquet and et al. , 1975
MaliPresentVandepitte and et al. , 1980
NigeriaPresentGugnani and et al. , 1986

North America

CanadaPresentMartin , 1984
-Nova ScotiaPresentMartin , 1984
-QuebecPresentUhland et al., 2000
USAPresentMeyer and Bullock , 1973
-AlabamaPresentPlumb , 1999a
-ArkansasPresentMeyer and Bullock , 1973
-FloridaPresentFrancis-Floyd et al., 1993
-MarylandPresentBaya et al., 1997
-OregonPresentAmandi and et al. , 1982

Central America and Caribbean

PanamaPresentKourany and et al. , 1977

South America

BrazilPresentMuratori et al., 2000
VenezuelaPresentClavijo et al., 2002

Europe

BelgiumPresentBauwens and et al. , 1983
Czech RepublicPresentVladick and et al. , 1983
GermanyPresentBockemuhl and et al. , 1983
ItalyPresentMaserati and et al. , 1985
NorwayPresentBergen and et al. , 1988
Russian FederationPresentKalina , 1980
SpainPresentMarinez , 1987; Nougayrede et al., 1994

Oceania

AustraliaPresentHow and et al. , 1983
-New South WalesPresentReddacliff et al., 1996

Pathology

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Most pathogenesis and pathology studies of E. tarda have been in Japanese eels. This is in contrast to limited histopathological information in channel catfish; however, there are some reports describing E. tarda infections in other fish. Egusa (1976) described E. tarda infections of eels that spread from lesions in visceral organs into the musculature and then to the dermis. Miyazaki and Egusa (1976a,b) described histopathology of the suppurative interstitial nephritis forms of edwardsiellosis in adult eels, in which the haematopoietic tissue of the kidney has masses of neutrophils, which contain phagocytized bacteria. Small abscesses, which develop from primary foci of neutrophils in haemopoietic tissue and nephrons, are present in the early stages of infection. Enlarged abscesses become liquefied, from which bacteria spread to surrounding tissues, where blood-vessels form emboli, that produce additional abscesses. Peripheral abscesses progress into ulcers in the epidermis. Generalized infections show ulcerative and necrotic (serous-exudative and liquefactive) lesions in the spleen, liver, epicardium, stomach, gill and musculature. As result of experimental infection by immersion in E. tarda after mechanical skin injury, channel catfish develop a generalized congestion of internal organs and severe multifocal necrotizing inflammation of the liver, head and trunk kidney, and spleen (Darwish et al., 2000)

In the hepatitis form, micro-abscesses, which contain bacteria-laden macrophages, develop in the liver. As the disease progresses, abscesses enlarge and hepatic cells become necrotic. This is followed by extensive liquefaction of abscesses and bacterial multiplication in blood-vessels in various parts of the liver. Hepatic cells have fatty degeneration, while ulcers develop in the body musculature adjacent to the diseased liver (Miyazaki and Egusa, 1976b).

Histopathology of E. tarda in Japanese flounders, red sea bream Japanese eels and tilapia (were compared (Miyazaki and Kaige, 1985). The major difference from infections in eels is the predominance of granulomatous inflammation in the Japanese flounder and red sea bream. In infected tilapia, the abscesses in internal organs also progressed to granulomas (Kubota et al., 1982). Histopathology of age 0 hatchery raised striped bass includes epithelial hyperplasia, necrosis associated with the lateral-line canals and abscess formation in the anterior kidney and other internal organs (Herman and Bullock, 1986).

At least some E. tarda isolates produce toxic extracellular products (ECP). Ullah and Arai (1983) isolated an exotoxin from E. tarda culture media and found no evidence of endotoxins, therefore postulating that the exotoxin was responsible for pathogenicity. However, factors that regulate pathogenicity of E. tarda are unclear. Suprapto et al. (1995; 1996) detected a heat-labile ECP in a virulent strain of E. tarda belonging to serogroup A, which was lethal to Japanese eel and Japanese flounder. The optimum incubation temperature for ECP production was 25-30°C, which coincides with most reports of optimum temperature for fish susceptibility. An intracellular component (ICC) was also detected in bacteria, associated with cell lysis. Japanese flounder appeared to be more susceptible to E. tarda (about 15 times higher) than the Japanese eel. Results of these studies suggest that the toxin produced by E. tarda plays an important role in its virulence.

The ability of E. tarda to infect warm blooded animals, humans in particular, was shown by Janda et al. (1991), who demonstrated its ability to invade HEp-2 cell monolayers, produce cell-associated haemolysin and siderophores and express mannose-resistant hemagglutination against guinea-pig erythrocytes. Some strains of E. tarda were virulent to mice. Janda and Abbott (1993a) showed that strains of E. tarda, a known pathogen of warm-blooded animals, produced 30-40% higher levels of cell-associated haemolytic activity (haemolysins) than strains of E. ictaluri, known only from fish. The increased haemolytic activity could contribute to the pathogenicity of E. tarda to humans. When grown under iron-restricted conditions in the presence of ethylenediamine di (o-hydroxyphenylacetic acid), haemoglobin, haematin and haemin stimulated bacterial growth in both liquid and agar bioassays. Haemolysin activity under these conditions was increased three- to > 40-fold. All of these studies indicate that, in addition to its invasive capabilities, E. tarda produces a haemolysin, which is partially regulated by availability of iron and may also play a role in human disease (Igarashi et al., 2002).

Diagnosis

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Edwardsiella septicemia in fish is characterized by necrotic abscesses in the muscle that emit a putrid odor when incised. The skin that covers muscle abscesses can be pale or have petechia. Mortality of infected fish may be acute but is often chronic depending upon the degree of stressful environmental conditions under which E. tarda infections occur. Edwardsiella tarda commonly resides in the intestine of fish and other aquatic animals and may be found in many environs where a host is not required for survival. The bacterium may also be present in the bottom mud of many bodies of water. Edwardsiella tarda is a typical member of the Enterobacteriacae; it is a Gram negative motile rod that is cytochrome oxidase negative and ferments glucose.

Clinical signs of E. tarda infections vary between species of fish; therefore, are generally of little use, except to indicate the likely presence of a bacterial infection. Nishibuchi et al. (1980) pointed out that, for diagnostic purposes, it is necessary to isolate bacteria from diseased eels, as well as other species of fish, because clinical signs of E. tarda, A. hydrophila, Vibrio anguillarum and Pseudomonas anguilla septica infections generally cannot otherwise be differentiated. Edwardsiella tarda can be isolated on brain–heart infusion (BHI) agar or trypton soya agar (TSA) with inocula from internal organs or lesions in the muscle of clinically infected fish. When incubated at 26-30°C, small, round, convex transparent colonies of approximately 0.5 mm in diameter are visible in 24-48 h. Amandi et al. (1982) improved isolation incidence (from 2% to 19%) from brain of chinook salmon by first inoculating thioglycolate media and, after incubation, transferring an inoculum to BHI agar. Edwardsiella tarda forms small green colonies with black centres on Edwardsiella isolation media (EIM) (Shotts and Waltman, 1990). In addition to conventional isolation and identification with biophysical and biochemical characterisltics, serological (fluorescent antibody technique (FAT), or enzyme-linked immunosorbent assay (ELISA) may be satisfactory for diagnosis and identification (Meyer and Bullock, 1973; Amandi et al., 1982; Swain and Naykak, 2003). Also, Toranzo et al., 1987 used specific slide agglutination for detecting and identifying several different bacterial pathogens including E. tarda.

Important characteristics of E. tarda that are of presumptive diagnostic value are motility, indole production, reaction on TSI agar, citrate and methyl red media, and salt and temperature tolerance. Using the Minitek numerical identification system, Taylor et al. (1995) correctly identified E. tarda 100% of the time compared with 83% positive identification with the API 20E system. Positive identification can be made using specific serum agglutination or FAT. There is no evidence of serological cross-reactivity between E. tarda and E. ictaluri (Rogers, 1981; Klesius et al., 1991).

More recently, a loop-mediated isothermal amplification (LAMP) for rapid and sensitive detection of E. tarda was developed by Savan et al. (2004). This method detected E. tarda in the kidney and spleen of infected Japanese flounder. Sea water samples from infected flounder culture ponds were also LAMP positive. In conclusion, a variety of new or improved diagnostic methods are becoming available for rapid and sensitive detection of edwardsiellosis in fish and culture environments.

List of Symptoms/Signs

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SignLife StagesType
Finfish / Build up of bloody fluids - Body Cavity and Muscle Aquatic:Adult Sign
Finfish / Bursts of abnormal activity - Behavioural Signs Aquatic:Adult Sign
Finfish / Bursts of abnormal activity - Behavioural Signs Aquatic:Adult Sign
Finfish / Bursts of abnormal activity - Behavioural Signs Aquatic:Adult Sign
Finfish / Change in cloudiness - Eyes Aquatic:Adult Sign
Finfish / Change in cloudiness - Eyes Aquatic:Adult Sign
Finfish / Cysts (clumps of white spheres) - Body Cavity and Muscle Aquatic:Adult Sign
Finfish / Haemorrhagic lesions - Skin and Fins Aquatic:Adult Sign
Finfish / Haemorrhagic lesions - Skin and Fins Aquatic:Adult Sign
Finfish / Haemorrhaging - Body Cavity and Muscle Aquatic:All Stages Sign
Finfish / Increased food consumption - Behavioural Signs Aquatic:Adult Sign
Finfish / Increased food consumption - Behavioural Signs Aquatic:Adult Sign
Finfish / Increased food consumption - Behavioural Signs Aquatic:Adult Sign
Finfish / Kidney - white-grey patches (haemorrhage / necrosis / tissue damage) - Organs Aquatic:Adult,Aquatic:Broodstock,Aquatic:Larval,Aquatic:Fry Sign
Finfish / Liver - white / grey patches (haemorrhage / necrosis / tissue damage) - Organs Aquatic:Adult,Aquatic:Broodstock,Aquatic:Larval,Aquatic:Fry Sign
Finfish / Loss of balance - Behavioural Signs Aquatic:Adult Sign
Finfish / Loss of balance - Behavioural Signs Aquatic:Adult Sign
Finfish / Loss of balance - Behavioural Signs Aquatic:Adult Sign
Finfish / Mortalities -Miscellaneous Aquatic:Adult Sign
Finfish / Necrotic musculature - Body cavity and muscle Aquatic:Adult Sign
Finfish / Necrotic musculature - Body cavity and muscle Aquatic:Adult Sign
Finfish / Necrotic musculature - Body cavity and muscle Aquatic:Adult Sign
Finfish / Paleness - Gills Aquatic:Adult Sign
Finfish / Pop-eye - Eyes Aquatic:Adult Sign
Finfish / Pop-eye - Eyes Aquatic:Adult Sign
Finfish / Red spots: larger patches - Skin and Fins Aquatic:Adult Sign
Finfish / Red spots: larger patches - Skin and Fins Aquatic:Adult Sign
Finfish / Red spots: larger patches - Skin and Fins Aquatic:Adult Sign
Finfish / Skin erosion - Skin and Fins Aquatic:Adult Sign
Finfish / Skin erosion - Skin and Fins Aquatic:Adult Sign
Finfish / Skin erosion - Skin and Fins Aquatic:Adult Sign
Finfish / Splenomegaly - spleen swelling / oedema - Organs Aquatic:Adult Sign
Finfish / Swelling - Organs Aquatic:Adult
Finfish / White-grey patches (necrosis / tissue damage) - Organs Aquatic:All Stages Sign

Disease Course

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Edwardsiella septicaemia, caused by E. tarda, is a mild to severe condition, but clinical signs of infection differ slightly between species of fish. In channel catfish, E. tarda initially produces small, 1-5 mm, cutaneous lesions, which are located dorsolaterally in the muscle (Meyer and Bullock, 1973). These small lesions progress to larger necrotic abscesses within the flank muscle or caudal peduncle, where they form obvious convex swollen areas and the skin loses its pigmentation. Lesions in the muscle, which contain large amounts of necrotized tissue, emit a putrid odour when incised, hence the name emphasymetous putrefactive disease of catfish (Meyer and Bullock, 1973). As infection progresses, affected fish lose mobility of the caudal portion of the body and a generalized internal hyperaemia, similar to other bacterial septicaemias, is evident. The kidney, in particular, is enlarged and the liver is mottled; both organs are soft. Initially, it was believed that E. tarda caused disease in only larger channel catfish (i.e. over 0.4 kg); however, there seems to be no distinct size or age differential in susceptibility of any species of fish (Herman and Bullock, 1986). Edwardsiella septicaemia of catfish in the USA occurs mostly during the warm summer months.

Japanese eels with acute infection of E. tarda develop severe hyperaemia, with bloody congestion of fins, ecchymosis or petechial haemorrhage on various body surfaces, gas-filled pockets in the skin and large bloody necrotic lesions in the muscle. The anal region is swollen and hyperaemic. Internally, there is a general hyperaemia of the peritoneum; the liver is mottled, oedematous and abscessed. Although Egusa (1976) reported that E. tarda infections of eels in Japan were more prevalent during the summer, Liu and Tsai (1980) found that infections of eels in Taiwan were most common when water temperatures were 10-18°C, during January to April.

A variety of clinical signs occur in other species of fish. For example, E. tarda causes exophthalmia and cataracts in tilapia and striped bass, as well as abscesses in internal organs (Kubota et al., 1982; Baya et al., 1997). Japanese flounders, naturally infected with E. tarda, develop ulcerative lesions and loss of skin, which expose underlying muscle, haemorrhage in fins, rectal protrusion and swelling of the spleen. Infected cage-cultured largemouth bass developed necrotic lesions on the caudal peduncle.

Epidemiology

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The source of E. tarda is presumably the intestinal contents of carrier animals, but it may be a common inhabitant of the aquatic environment. In the USA, E. tarda was isolated from 75% of water samples, 64% of pond-mud samples and 100% of frogs, turtles and crayfish from catfish ponds (Wyatt et al., 1979). Following processing E. tarda was also isolated from as high as 88% of fillets from cultured channel catfish and from 30% of imported fish fillets in the USA. In an ecological study of E. tarda in a salt-water flounder farm, Rashid et al. (1994a) isolated the bacterium from 86% of water samples from one pond and 22% of water samples from a second pond. The organism was present in 44% of sediment samples and 14% of fish from the first pond, and 0% of sediment samples and 2% of fish from the second pond. Ironically, clinical ES did not occur in the fish in either pond, but the data indicate that the incidence of E. tarda in fish is associated with its presence in the environment. However, the high incidence in the environment may have been a function of the organism’s presence in the fish. Hidaka et al. (1983) showed that E. tarda cell counts in eel-pond water at 22-26°C were four times higher when clinical disease was present than when there was no disease.

In spite of the apparent extensive presence of E. tarda in fertile channel catfish ponds, infections in these fish are not common. When deaths do occur, mortality seldom exceeds 5%; however, if the fish are moved into confined holding tanks, the rate of infection may quickly accelerate to 50%, with concomitant deaths (Meyer and Bullock, 1973). Mortality data of E. tarda infected cultured eels in Asia indicate potentially high losses. Ishihara and Kusuda (1981) induced up to 60% mortality in 100 g eels experimentally infected by immersion in water containing E. tarda. In a naturally infected Japanese eel population, the mortality was 80% (Kodoma et al., 1987). Cumulative mortality of spontaneously infected Nile tilapia in confinement reached 83% in 4 days (Benli and Yildiz, 2004).

Transmission of the Disease

Edwardsiella tarda is transmitted through the water from an infected source (carrier animal faeces, water or mud) to susceptible fish. Fish can be experimentally infected with E. tarda by intraperitoneal (i.p.) and intramuscular (i.m.) injection, stomach gavage or immersion in a bath containing the pathogen; however, infection is not guaranteed simply by introducing the fish to the pathogen. Huang and Liu (1986) killed 100% of i.p. injected eels when E. tarda was mixed with A. hydrophila, but water-borne exposure to the same mixture failed to induce mortality unless sublethal concentrations of nitrogenous compounds were present. A disease identical to natural infections in tilapia was also reproduced by i.m. injection by Miyashita (1984). Most probably, fish become naturally infected via injuries to the epithelium or through the intestine. Miyazaki et al. (1992) injured the intestine with hydrogen peroxide prior to introducing E. tarda into the lumen via a silicon tube. This procedure resulted in death 5-23 days later and the infected fish developed pathological lesions in kidneys and livers that were nearly identical to those observed in natural infections. Similarly Darwish et al. (2000) produced Edwardsiella septicemia by first mechanically injuring the skin prior to immersion in a solution containing E. tarda.

Transmission of E. tarda in catfish, eels and most other fish species appears to be enhanced at water temperatures from 20 to 30°C. Japanese flounder were most susceptible at 20-25°C by i.m. injection, in which a median lethal dose (LD50) of 7.1 x 101 colony-forming units (cfu) was established (Mekuchi et al., 1995a). This compared with an LD50 of 1.7 x 102 cfu for i.p. injection and 3.6 x 106 cfu ml-1 and 1.3 x 106 cfu fish-1 for immersion and oral exposure, respectively, at the same temperatures. In experimental studies, gilthead seabream, turbot and hybrid striped bass had LD50 of 3, 4 and 7 x 105 cfu, respectively following injection.

Impact Summary

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CategoryImpact
Biodiversity (generally) Negative
Fisheries / aquaculture Negative
Human health Negative
Native flora Negative

Impact: Economic

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The economic impact of E. tarda on mortality and morbidity of Japanese flounder and red sea bream (Pagrus major) culture is severe (Igarashi and Iida 2002). Mortality and morbidity are reported to range from 5% to 30% and between 5% to 70% in these cultured fish, respectively (Pastor, 1981; Pavanelli et al., 1998). While E. tarda infection occurs in a variety of cultured and wild fish populations, little or no information is available regarding its rate of incidence, fish mortality and morbidity estimates, or chemotherapeutic costs to assess economic impact due primarily to the lack of reliable, sensitive and widely used detection assays. An epidemiological and ecological investigation of E. tarda on two Japanese flounder farms in Japan revealed that culture water, sediment and fish were frequently positive for E. tarda (Rashid et al., 1994a). Edwardsiellosis is often a chronic problem that may not only increase mortality, but may increase production costs, lower feed conversion and delay harvest.

Accumulative losses of fish due to E. tarda may be moderate to high thus resulting in reduced availability of fish to the market and loss of revenue to the producer. This is exacerbated by the fact that the infection most often affects market size fish but it is not confined to this age/size group. Generally, E. tarda has a mild impact on cultured channel catfish, however, stressful environmental conditions can cause a non-clinical infection to progress into a clinical infection resulting in significant mortality (Meyer and Bullock, 1973).

The impact of E. tarda in wild fish populations is unknown due to the absence of routine spatial and temporal E. tarda environmental disease monitoring and effects of E. tarda on fish populations. Epizootics in two commercially and recreationally valuable warm water species, largemouth bass (Micropterus salmoides) and striped bass, have occurred in the USA (Francis-Floyd et al., 1993; Baya et al., 1997). Seasonal mortality of largemouth bass may reduce annual revenues of $600 million, the reported value for this freshwater game fish indigenous to Florida lake systems (Hardin et al., 1987). Edwardsiella tarda has little economic impact on salmonids as it is not considered a common pathogen (Amandi et al., 1982; Martin, 1984).

An additional negative effect may result from undetected infected fish contaminating processing plants, requiring shutting down operations and disinfecting all equipment that had come in contact with the infected fish (Meyer and Bullock, 1973). Also, gulls with E. tarda in their feces could contaminate fish processing plants along the coast (Berg and Anderson, 1972).

Impact: Environmental

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Only minor environmental impact results from E. tarda because this bacterium is rather common in the environment (Wyatt et al., 1979; Rashid et al., 1994a). Ecological changes resulting from its introduction have not been reported perhaps due to the lack of cross disciplinary studies.

Impact: Social

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Edwardsiella tarda may cause social impact because of its potential infectious nature to humans and other warm blooded animals (Bockemuhl et al., 1971). Edwardsiella tarda sometimes produces an undiagnosed sub-clinical infection in fish intended for human consumption, where it may create problems during processing (Meyer and Bullock, 1973). When sub-clinically infected fish are cleaned, the equipment becomes contaminated and requires interrupting processing, disinfecting equipment, and disposing of infected fish. Human infections have been contracted from infected fish when handling or by consuming uncooked contaminated fish.

Human infections are usually of the digestive tract resulting from consuming improperly cooked fish (Claridge et al., 1980; Noga, 2000), or infections in muscle tissue of healthy persons via puncture wounds by spines of infected catfish (Hargraves and Lucey, 1990; Vartian and Septimus, 1990). Janda and Abbott (1993a) cited additional human risk factors in E. tarda zoonoses including occupational and recreational exposure to aquatic environments or exotic animals and dietary preferences such as ingestion of raw fish. In addition, age (adults over 50 and children), geographical distribution (tropical and subtropical regions) and pre-existing liver disease and underlying iron overload states (cirrhosis, red cell sickling, and leukemia) may predispose humans to E. tarda infection (Bockemuhl et al., 1971; Janda and Abbott, 1993b). Because E. tarda is also an emergent bacteria for food borne disease of humans (Stiles, 1989), its potential impact on food production and safety must be considered to be significant. Bernoth (1991) reported that E. tarda is a potential pathogen transmitted from fish to other animals and their environments. Recently, E. tarda was demonstrated to be transmitted from the faeces of pigs to culture fish on an integrated fish farm (Muratori et al., 2000) suggesting that the high incidence of E. tarda was a potential risk for food contamination.

Due to the unaesthetic appearance of fish infected with E. tarda, a poor perception of fishery products from areas where infection has been reported may deter their purchase and consumption by humans for fear of sickness. Tourism may also be impacted as a result of human perception of an unclean environment.

Zoonoses and Food Safety

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Edwardsiella tarda is a health threat to other animals, including humans (Bockemuhl et al., 1971; Boehrer et al., 1977; Kourany et al., 1977; Clarridge et al., 1980). In fact, some of the first isolates of E. tarda were from human faeces (Ewing et al., 1965). In humans, the bacterium usually causes diarrhoea and gastroenteritis (King and Adler, 1964; Jordan and Hadley, 1969; Bockemuhl et al., 1971; Van Damme and Vandepitte, 1980), while extraintestinal infections may produce a typhoid-like illness, peritonitis with sepsis and cellulitis (Fields et al., 1967). Occasionally, E. tarda-induced abscesses have been seen in liver (Zighelboim et al., 1992). Several other clinical conditions in humans have been associated with E. tarda, including meningitis (Sonnenwirth and Kallus, 1968; Sachs et al., 1974). Funada et al. (1988) found E. tarda septicaemia complicating an acute leukaemia patient in Japan while Gilman et al. (1971) thought that the organism was involved with jungle diarrhoea and possibly associated with Entamoeba histolytica (protozoan) infection in Thailand. Van Damme and Vandepitte (1980) reported that sporadic cases of tropical diarrhoea in humans with E. tarda were traced to consumption of freshwater fish in Zaïre. Serious and/or life-threatening infections of E. tarda in the muscle, which resulted from wounds received while fishing or puncture wounds caused by catfish spines, have been described in humans (Clarridge et al., 1980; Hargraves and Lucey, 1990). Wyatt et al. (1979) could not correlate or substantiate E. tarda in aquatic animals to human infections. However, there is sufficient evidence to indicate that the organism can be a public-health problem, as well as a threat to other animals such as pigs and cattle (Arambulo et al. 1967; Ewing et al., 1965). According to Nucci et al. (2002)E. tarda isolates from fish are similar to those of human origin, therefore, isolates from fish are potential human pathogens. Because E. tarda has such a wide host susceptibility and environmental adaptation it may enter the human food chain through fish processing plants and/or poor sanitation.

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