The following statement(s) is/are true concerning host defense mechanisms to intraabdominal infection

a. Bacterial clearance can occur via translymphatic absorption

b. Phagocytic activity and bacterial killing can occur via resident phagocytic cells and an influx of PMNs

c. A fibrinogen-rich inflammatory exudate is released into the peritoneal cavity, trapping large numbers of bacteria and other particulate matter

The introduction of microorganisms into the normally sterile peritoneal environment invoke several potent specialized host antimicrobial defense mechanisms. Bacterial clearance, also termed translymphatic absorption, occurs through specialized structures found only on the peritoneal mesothelium on the underside of the diaphragm that act as conduits for both fluid and particulate matter. Lymphatic channels eventually form which drain into the venous circulation via the thoracic duct. Bacteria not cleared via translymphatic absorption are rapidly engulfed by resident and recruited phagocytic cells including resident macrophages on the peritoneal surface and omentum and attracted PMNs. The final primitive host defense mechanism is sequestration by which a fibrinogen-rich exudate containing plasma oposonins appears during peritoneal infection and fibrin polymerization occurs. Fibrin has the capacity to trap large numbers of bacteria and other particulate matter. Acting in conjunction with omentum and other mobile viscera, perforations are sealed and the contaminated enteric contents walled off, preventing continued soilage of the peritoneal cavity.