Experimental Intra-Abdominal Abscesses in Rats: Development of an Experimental Model

Abstract

An animal model has been developed to study the evolution of intra-abdominal abscesses. Gelatin capsules containing pooled colonic contents and barium sulfate were prepared in an anaerobic chamber and implanted into the pelvic region of Wistar rats. The natural course of the ensuing disease was studied in various groups according to the source of the inoculum and sex of the recipient. Colonic contents derived from rats fed a grain diet produced a highly lethal disease with an 80% mortality rate for males and 100% for females. Most deaths occurred within 3 days of implantation, and autopsies showed generalized peritonitis. The addition of blood to the inoculum caused a rapidly fatal peritonitis in all animals. With an inoculum derived from meat-fed rats implanted in male recipients, there was a biphasic disease. Initially, there was peritonitis associated with 43% mortality. All animals that survived this acute period developed discrete intra-abdominal abscesses by the seventh postoperative day. The latter stage was characterized by an indolent course and progressive enlargement of abscesses.

The disconnect between animal models of sepsis and human sepsis

“…administration of feces [36]. A pellet most commonly within a fibrin clot is used [37,38]. Without additives, feces instillation leads to rapid death or recovery of the animals [39].…”

Microbiology and management of intra‐abdominal infections in children

“…The Weinstein and Onderdonk group were the first to study the pathogenicity and principles of management of infection after perforated viscus. [31][32][33][34] Peritonitis was induced by introducing capsules of cecal material into the abdominal cavity of rats. A biphasic disease emerged, and about 40% of the rodents died within the first week from peritonitis and sepsis, and 100% of the survivors developed intra-abdominal abscesses.…”

“…The proper management of mixed aerobic and anaerobic infections requires the administration of antimicrobials that are effective against both aerobic and anaerobic components of the infection. 31 If such therapy is not delivered, the infection may progress, and more serious complications may develop. 15 Failure of the antimicrobial therapy may occur because of the development of bacterial resistance, achievement of insufficient tissue levels, incompatible drug interaction, or the development of an abscess.…”

Inflammatory processes in a murine model of intra-abdominal abscess formation

“…A typical abscess-inducing mixture comprises 5 ϫ 10 8 B. fragilis, 5 ϫ 10 6 E. coli, and 0.1 mg of ACC or 1 mg of bran [10]. Abscess-potentiating agents have also included a fibrin clot, in which the bacteria are enmeshed in vitro before inoculation [12], as well as barium sulfate plus ACC in a gelatin capsule that encapsulates the bacteria [13]. Other agents include mucin [14] and agarose [15].…”

“…Fibrinolytic agents administered at the time • A microbial challenge that leads to fibrin deposition in the peritoneal cavity is necessary for abscess formation [5,12,37]. • Addition to the inoculum of a ''potentiating agent'' such as autoclaved cecal contents, bran, or other (e.g., mucin, agarose) is typically required [9][10][11][12][13][14][15]. • A major role of the potentiating agent is to deplete complementderived opsonins at the site of infection, thereby impairing phagocytic killing and clearance [11].…”