Characteristics of pathogenic mechanisms of Edwardsiella ictaluri in the channel catfish, Ictalurus punctatus.

摘要

Edwardsiella ictaluri, a gram negative rod shaped enteric bacterium, is the etiological agent of enteric septicemia of catfish (ESC). Little is known about the pathogenic mechanisms operative in the disease. However, E. ictaluri extracellular products seem to play a major role in the pathology. Bacterial surface morphology and pathogenicity were examined by studies of congo red binding, capsule production, and degradation of chondroitin sulfate. Electron microscopy revealed a fibrilar network for virulent isolates that appeared to connect the bacterial cells. Virulent isolates also had a greater amount of capsular material, demonstrated a greater ability to degrade chondroitin sulfate, and had a greater congo red dye binding capability than the avirulent forms.; It has been previously shown that an extract of a marine tunicate, Ecteinascidia turbinata was capable of suppressing humoral and cellular immune responses in vivo and in vitro. In this study mechanisms of action and effects of the extract (Ete) on the immune response of channel catfish exposed to E. ictaluri were investigated. Ete dramatically decreased survival of channel catfish challenged with a virulent strain of E. ictaluri. Decreased resistance was seen two days prior, two post, and when administered on the day of challenge. Mitogenic responses of peripheral blood leucocytes to concanavalin A, Salmonella typhimurium lipopolysaccharide, and pokeweed mitogen were diminished for both in vivo and in vitro trials. Treatment with Ete resulted in enhanced in vitro phagocytic activity of anterior kidney cells and peripheral blood leucocytes.; Phagocytosis of E. ictaluri by macrophages isolated from the pronephros of channel catfish was examined in vitro. For virulent strains of E. ictaluri more bacteria were engulfed per macrophage and the association occurred more readily than for an avirulent strain. Avirulent bacteria seemed to be degraded within the phagolysosome, whereas virulent forms seemed to survive within the phagocytic cells. It is postulated that the virulent forms may have some surface structure which helps confer resistance to lysosomal degradation.