Edwardsiella tarda

Edwardsiella tarda
Kingdom	Bacteria
Phylum	Proteobacteria
Class	Gammaproteobacteria
Order	Enterobacteriales
Family	Enterobacteriaceae
Genus	Edwardsiella
Species	Edwardsiella tarda

Also known as: Edwardsiella septicaemia — Edwardsiella tarda infection — Edwardsiellosis— Emphysematous putrefactive disease of catfish — Fish gangrene— Red disease.

Introduction

Edwardsiella tarda belongs to the Enterobacteriaceae family and is a motile Gram negative, small, straight rod with peritrichous flagella and measures 1 × 2-3mm. It is cytochrome oxidase negative, and ferments glucose and is classified as facultatively anaerobic.

Edwardsiella tarda infects freshwater and marine fishes, reptiles and amphibians and mammals throughout the world. It causes Edwardsiella septicemia (ES) which is also known as fish gangrene, emphysematous putrefactive disease of catfish or red disease in eels. It causes serious systemic infection in cultured channel fish in the USA and in eels and flounders in Japan. Pale skin, petechiation and necrotic abscesses within the muscle of fish (that have a putrid odour when incised) are characteristic of ES. Mortality rates can depend on the amount of stress that the fish are kept under and high temperature, poor water quality and high organic fertility probably contribute to the onset and severity of the disease.

Unlike E.ictaluri, E.tarda is zoonotic and can infect humans. E.ictaluri causes enteric septicaemia of catfish (ESC) and only infects fish species, whereas Edwardsiella hoshinae infects birds and reptiles.

Signalment

Wild hosts include European and Japanese eels, largemouth bass, striped sea bass, Atlantic salmon, Marble goby, snakes and birds.

Domestic hosts include Japanese Eels, Siamese fighting fish, carp species including catla and rosy barb, crimson and European seabass, black tetra, Asian seabass (barramundi ), rainbow trout, chinook salmon, Nile tilapia, red seabream, turbot, and Angel fish.

Other fish hosts that have been documented are perch-like species including Cichlidae, Chrysophrys unicolor, flathead mullet , bastard halibut, flounders, and mozambique tilapia. E.tarda can also be found in zoo animals, zebu, cattle, pigs, reptiles, marine mammals, members of the Alligatoridae family (alligators and caimans) and humans.

Clinical Signs

All stages of fish are affected by E.tarda and haemorrhaging of the body cavity, muscle, and organs including liver and kidneys are commonly seen. Within the kidneys and spleen, necrotic white/grey lesions can be seen on the surface of the organs.

In adult fish a variety of clinical sign can be seen including organomegaly, pale inflamed gills, exophthalmia, and cataracts, haemorrhagic red lesions (ecchymosis) on the skin and fins, erosion of the skin, systemic oedema, and ascites. The anal region of certain species can become swollen and hyperaemic and rectal prolepses can occur. General behavioural changes include loss of balance, bursts of abnormal activity, and increased food consumption.

In humans it causes diarrhoea, gastroenteritis and can casue typhoid-like illness, peritonitis with sepsis,cellulitis,and meningitis.

Epidemiology

E.tarda commonly resides in the intestine of fish and other aquatic animals and in the bottom mud of many bodies of water. Within the USA E.tarda has been isolated from the mud, water samples and frogs, turtles and crayfish from catfish ponds. The bacteria are transmitted through infected water and mud from carrier animal faeces, and most probably infect susceptible fish through trauma of the epithelium or via the intestines and can be enhanced by water temperatures of 20-30°C. Humans have been known to be infected with E.tarda by eating infected fish meat.

Distribution

E.tarda is a ubiquitous organism and predominantly found in the USA, Japan, Taiwan, Thailand, Israel and many developing countries including Africa and South and Central America. It has also been found in parts of Europe and Australia.

Pathology

Histopathology shows suppurative interstitial nephritis in adult eels, with masses of degenerate neutrophils containing bacteria. Within early stages of infection small abscesses are present. These enlarge and liquefy, spreading bacteria to surrounding tissues and vessels, causing ulceration of the dermis and emboli and infecting the spleen, liver, epicardium, stomach, gill and musculature.

In the hepatitis form, micro-abscesses can also develop in the liver and in different species such as Japanese flounders, red sea bream Japanese eels and tilapia show predominantly granulomatous inflammation.

At least some E. tarda isolates produce toxic extracellular products (ECP) which may play a role in its virulence. 'E.tarda' haemolytic activity which is partially regulated by iron concentration could contribute to the pathogenicity of this bacteria to humans.

Diagnosis

'E. tarda' can be isolated on brain–heart infusion (BHI) agar or trypton soya agar (TSA) with inocula from infected internal organs or muscle and form small, round, convex transparent colonies (0.5 mm in diameter)after 24-48 hours. On Edwardsiella isolation media (EIM), it forms small green colonies with black centres.

Indirect FAT (detecting antibodies) and enzyme-linked immunosorbent assay (ELISA) test is used to confirm the presence of E. tarda. There is no serological cross-reactivity between E. tarda and E. Ictaluri. More recently, a loop-mediated isothermal amplification (LAMP) for rapid and sensitive detection of E. tarda has been developed(Savan et al. (2004)

Treatment

Oxytetracycline, sulfadimethoxine or methoprim have been used to treat ES. The latter two can cause cessation of feeding in some fish species.

Control

ES may be controlled by the immersion of fish in formalin-killed whole cells (FKC), Lipopolysaccharide (LPS) culture filtrates or Whole cell bacterins vaccines. The two former vaccination may be administered via intramuscular injection and can cause death to some fish species.

References

Edwardsiella tarda Learning Resources
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