The production of fibrinous exudates plays an important role in determining the outcome of peritoneal infection. Large numbers of bacteria are sequestered within fibrin matrices, thereby retarding bacterial spread throughout the peritoneal cavity and into the bloodstream. This walling-off process is teleologically advantageous in that it lessens early rapid mortality. Recent studies have documented that this same process is probably integral to the development of residual infection in the peritoneum. Bacteria sequestered within fibrin deposits are protected from normal host clearance mechanisms, thereby permitting unopposed proliferation and ultimately the establishment of an abscess. A complete understanding of the cellular and noncellular aspects of the host response to peritoneal infection will suggest novel strategies both to treat and to prevent the development of intraabdominal abscesses and their attendant consequences.