Protection Against Abscess Formation in a Model for Intraabdominal Sepsis

Abstract

Obligate anaerobes are known to play a significant role in the development of intraabdominal abscesses. Much of our knowledge about these organisms is based on observations made using an animal model developed by this laboratory in 1974 [1,2]. The basic model system employs Wistar rats surgically implanted with an inoculum of intestinal contents from other rats. The inoculum is prepared in a manner which simulates the microbiologic parameters of the human colon. This is accomplished by placing rats on a diet of lean ground beef for two weeks and then harvesting, homogenizing and freezing aliquots of prepared intestinal contents for subsequent use. Following implantation of the intestinal contents, animals develop a characteristic bi-phasic infection. The first phase of the disease is peritonitis associated with positive blood and peritoneal cultures, death of approximately 50% of implanted animals, free flowing peritoneal exudates and an increase in peripheral white blood cell counts. Animals that survive the initial stage of disease appear to recover within five days of surgery. However, all surviving recipients of the intestinal content inoculum develop intraabdominal abscesses. This second phase of the disease is more chronic and is characterized by the presence of abscesses, adhesions and negative blood cultures. Abscesses contain a polymicrobic flora consisting of both obligate anaerobes and facultative species. The clinical end points for evaluation in this model are mortality and abscess formation, while microbiologic end points include blood, peritoneal and abscess cultures. The two phases of this disease are associated with distinctly different bacterial populations. During the early, acute peritonitis stage, Escherichia coli and other Gram negative organisms are numerically dominant and are responsible for the early mortality. The second more chronic stage of the disease, abscess formation, requires the presence of obligate anaerobes, such as Bacteroides fragilis. It has also been shown that abscess development in this model is associated with either a synergistic combination of obligate anaerobes and facultative species [3], or can be experimentally reproduced with the capsular polysaccharide of B.fragilis [4]. The unique properties of the capsular polysaccharide of B.fragilis and it’s role in both the induction and prevention of abscesses has been well documented in the literature [5–15]. It is the second phase of this experimental disease process that will be discussed in this chapter.