February 1986

Antibiotics Fail to Prevent Abscess Formation Secondary to Bacteria Trapped in Fibrin Clots

Author Affiliations

From the Department of Surgery, Case Western Reserve University, Cleveland. Dr Hau is now with St Willehad Hospital, Wilhelmshaven, West Germany.

Arch Surg. 1986;121(2):163-168. doi:10.1001/archsurg.1986.01400020049005

• We inoculated 120 rats with 2×109Escherichia coli or 2×109Bacteroides fragilis suspended in normal saline solution or incorporated into fibrin clots. In the control group, all animals died after inoculation with E coli, but none died after the inoculation with B fragilis; both were suspended in normal saline solution. Escherichia coli entrapped in fibrin did not cause mortality but did result in abscess formation in all animals. Bacteroides fragilis incorporated into fibrin clots resulted in abscess formation in the majority of animals. Treatment with gentamicin sulfate, ampicillin sulfate, and cefoxitin sodium completely abolished the mortality secondary to E coli suspended in normal saline solution but did not influence the rate of abscess formation secondary to E coli incorporated into fibrin clots. Similarly, cefoxitin and clindamycin phosphate did not significantly change abscess formation secondary to B fragilis incorporated into fibrin clots. We conclude that systemic antibiotics are ineffective in the prevention of abscesses secondary to bacteria trapped in fibrin, either because they do not reach bactericidal levels in the fibrin clot, as in the case of gentamicin, ampicillin, and clindamycin, or, as in the case of cefoxitin, because of the inoculum effect caused by the high number of bacteria. Fibrinogen or fibrin itself do not afford any protection of bacteria against the action of antibiotics.

(Arch Surg 1986;121:163-168)