Pathogenesis of Intraabdominal Abscess Formation: Abscess-Potentiating Agents and Inhibition of Complement-Dependent Opsonization of Abscess-Inducing Bacteria

Abstract

Bacteroides fragilis and Escherichia coli are synergistic in the production of intraabdominal abscesses. However, these bacteria initiate abscess formation only when inoculated with an agent such as autoclaved colonic contents (ACC) or bran (a fiber analogue). The mechanism of action of the abscess-potentiating agent was studied. Opsonins in normal mouse serum were determined for phagocytic killing by murine neutrophils of B. fragilis and E. coli. Opsonization required fixation of complement by the alternative pathway. ACC (0.2 mg/ml) and bran (1.0 mg/ml) inhibited phagocytic killing of Proteus mirabilis in the presence of normal but not immune serum. Assay of the alternative pathway of complement activation indicated that both bacterial components and abscess-potentiating agents in an abscess-inducing mixture activated complement. These findings suggest that abscess-potentiating agents inhibit opsonization and therefore the subsequent phagocytic killing of bacteria in the nonimmune host.

Candida glabrata Intra-Abdominal Candidiasis Is Characterized by Persistence within the Peritoneal Cavity and Abscesses

“…In human IAC, perforation or leakage of the GI tract is commonly associated with abscess formation but abscesses rarely result from infected peritoneal catheters. Sterile feces potentiates intra-abdominal infections by depleting complement-derived opsonins and impairing phagocytic killing (27,28). These effects likely account for our observation that tissue burdens and persistence of C. glabrata were increased in the presence of sterile feces, despite greater neutrophil counts.…”

Lesion Formation and Antibody Response Induced by Papillomatous Digital Dermatitis-Associated Spirochetes in a Murine Abscess Model

“…These data give evidence that, along with the genetic differences in these isolates (34), functional and/or antigenic differences involved in lesion induction are present. PDD spirochetes induce abscess formation in this model without the need for potentiating agents, as needed in experiments with Bacteroides fragilis and Escherichia coli (15). It was found that the potentiating agent used in those experiments interfered with complement activation and opsonization of the bacteria, allowing B. fragilis and E. coli to persist and initiate abscess formation.…”

In-vitro activity of peritoneal cells from rats after intra-abdominal infection with Bacteroides fragilis and Escherichia coli

“…"~ Specific combinations of facultatively and obligately anaerobic bacteria, e.g., Escherichia coli and Bacteroides fragilis, on the other hand often resulted in abscess formation when clinically " significant " inocula were used, whether combined with adjuvant or n~t .~-~ In the case of the fibrin clot model, originally described by Ahrenholz and Simmons,' the only '' adjuvant " required with E. coli and B. fragilis was fibrinogen. [2][3][4][5][6][7][8][9][10] In the present study this rat fibrin clot model was used to produce intra-abdominal abscesses. Previous work had shown that persistent abscesses formed when both E. coli and B. fragilis were present," but, individually, either B. fragilis or E. coli was cleared from the peritoneal cavity within 48 h and 2 weeks respectively.…”