Enteric septicaemia of catfish ( ESC ) is caused by the bacterium Edwardsiella ictaluri , which belongs to the Enterobacteriaceae family ( 11 ) . ESC is one of the most important infectious disease problems in the commercial catfish industry in the United States of America ( USA ) . Most reported cases of disease caused by E. ictaluri are in channel catfish (Ictalurus punctatus) , but the bacterium has been isolated from related North American catfish including blue catfish (I. furcatus), white catfish (Ameiurus catus), and brown bullhead (A. nebulosus)( 11 ) . ESC has also been reported from Clarias batrachus in Thailand ( 12 ) and from several ornamental species ( 13, 37 ) . The susceptibility of other species including salmonids has been shown experimentally ( 4 ) . Edwardsiella ictaluri should not be confused with E. tarda , another member of the same genus that is frequently found in aquatic animals and is responsible for opportunistic infections in fish and mammals, including humans.
Several studies have shown that E. ictaluri is a very biochemically and antigenically homogeneous species ( 5, 21, 33, 38 ) .
Acute outbreaks of ESC occur within a limited temperature range, from 18 to 28°C. This critical temperature window makes spring and autumn the most common periods for outbreaks in regions where channel catfish are normally cultured. However, low-level mortality due to ESC can occur in carrier populations outside of this temperature range. Other environmental factors ( poor water quality, high stocking density and other stressors ) predispose the host to ESC. Edwardsiella ictaluri is considered to be a true obligate pathogen.
Two clinical forms of ESC occur in channel catfish, a chronic encephalitis and an acute septicaemia ( 20, 22, 30 ) . In the chronic form the bacterium infects the olfactory sacs, and migrates along the olfactory nerves to the brain, generating granulomatous inflammation. This meningo-encephalitis causes abnormal behaviour, with alternating listlessness and chaotic swimming. In late stages of this disease, swelling develops on the dorsum of the head as the inflammatory process erodes the connective tissue in this region. This swelling ulcerates exposing the brain. This has lead to the term 'hole in the head disease', used in the industry. In the acute form of ESC the bacterium is thought to infect through the intestinal mucosa ( 3 ) , and then to establish a bacteraemia. The affected fish display petechial haemorrhages around the mouth, on the throat, the abdomen and at the base of the fins. Multifocal distinct 2 mm diameter raised haemorrhagic cutaneous lesions that progress to depigmented ulcers also occur. Anaemia, moderate gill inflammation and exophthalmia are common signs. Internally, haemorrhages and necrotic foci are scattered in the liver and other internal organs. Haemorrhagic enteritis, systemic oedema, accumulation of ascitic fluid in the body cavity and enlargement of the spleen are nonspecific signs. Histological examination reveals a systemic infection of all organs and skeletal muscles, with the most severe changes being diffuse interstitial necrosis of the anterior and posterior kidney. Focal necrosis in the liver and spleen are also generally seen.
Fish from a population that has recovered from the disease are considered to be carriers. These fish will have protective immunity and may have high levels of E.-ictaluri- specific antibodies. Occasional losses due to recurrent ESC will occur in these populations, especially after a stress is induced. Edwardsiella ictaluri has been detected in the kidney of such fish well over 4 months after exposure ( 2, 14 ) , suggesting that carrier fish act as the natural reservoir for the organism. It is believed that shedding with faeces is the main means of dissemination into the environment. The pathogen persistence and the common practice of continual partial harvest and stocking within a production pond have contributed to the success of this pathogen and the prevalence of ESC in the industry. Moreover, the agent can survive in pond sediments for an extended period of time ( 27 ) , and this may be another important factor in disease recurrence in given areas. Researchers have found the bacterium in the gut of fish-eating birds by performing fluorescent antibody tests on ingesta, but generally no E. Ictaluri could be cultured indicating that the bacteria were not viable ( 34, 40 ) . This suggests that birds are not an important means of disseminating this pathogen.
ESC may be controlled through chemotherapy and/or prophylactic measures. The most common antimicrobial treatments are oral application of potentiated sulfonamide sulfadimethoxine ormethoprim or oxytetracycline, but plasmid-mediated resistance to these antibiotics does occur ( 6 ) . Many producers are now focusing on alternative methods to reduce losses. This relies on management to reduce stress in fish, the cessation of feeding when ESC-induced losses are detected ( 41 ) and on vaccination.