Submitted to: Journal of Aquatic Animal Health
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/12/2000
Publication Date: 12/1/2000
Citation: DARWISH, A.M., PLUMB, J., NEWTON, J. PATHOLOGY OF EXPERIMENTAL EDWARDSIELLA TARDA INFECTION IN CHANNEL CATFISH ICTALURUS PUNCTATUS. JOURNAL OF AQUATIC ANIMAL HEALTH. 2000. v.12. p.255-266. Interpretive Summary: Edwardiella tarda is a pathogen that infects channel catfish. The infection rate can reach 50% when fish are held in confinement prior to processing. This pathogen can also infect humans causing different kinds of symptoms such as diarrhea with salmonella-like food poisoning and wound infections. Despite the importance of the infection and its potential health hazard to humans, the histopathology of the infection in channel catfish has not been studied. In this research, channel catfish were experimentally infected with E. tarda and the progression of the clinical signs, gross and microscopic lesions, and bacterial counts was studied. This information will provide indispensable understanding needed for developing effective strategies to control this infection.
Technical Abstract: The histopathology and pathogenesis of Edwardsiella tarda induced edwardseillosis in juvenile channel catfish (Ictalurus punctatus) was characterized. The lateral body surface of fish were scraped before infection by immersion in a bath of E. tarda for 30 minutes. Scattered cutaneous petechiae and ulcerations were seen on the mouth, operculum,isthmus, abdomen and lateral body following infection. Injured skin developed focal ulcerative necrotizing dermatitis, increased mucus, and irregular areas of skin depigmentatin scattered over the entire body. Internal organs were congested and livers showed patchy discoloration and petechiae. Histologically the liver, head kidney, trunk kidney, and spllen had severe multifocal necrotizing inflammation. Bacteria in the hepatic lesions were specifically identified by immunohistochemistry using rabbit anti-E. tarda serum. Colony forming units of E. tarda per gram of tissue or milliliter of blood peaked 3 post infection (PI) in the liver, trunk kidney and blood. No bacteria were isolated from infected fish after 6 d PI. Clinical signs and internal gross lesions declined by 8 d PI and were absent thereafter. No histological lesions were observed in the intestine, stomach, heart, gills, or brain. Infected fish were sluggish with rapid opercular movements and pale gills prior to death.