To assess the risk of development of spontaneous bacterial peritonitis in relation to ascitic fluid opsonic activity, routine admission abdominal paracentesis was performed on 119 patients during 141 hospitalizations. Paracentesis was repeated if evidence of peritonitis developed during the hospitalization. The ascitic fluid opsonic activity (0.2 f 0.5 log kill) of 24 spontaneously infected specimens was significantly (p < 0,001) lower than that of the group with sterile portal hypertensionrelated ascites (0.8 f 1.1 log kill), and significantly lower than the group with ascites of miscellaneous type (2.4 f 1.0 log kill, p < 0.001). The C3 and C4 concentrations of the spontaneous peritonitis specimens were also significantly lower than in the specimens from the other groups. Of the 56 patients whose initial sterile ascitic fluid opsonic activity was <0.2 log kill, 8 (14.5%) developed spontaneous bacterial peritonitis during the hospitalization; whereas none of the 70 patients with sterile ascitic fluid opsonic activity 20.2 log kill developed spontaneous peritonitis. This difference in the risk of development of peritonitis was significant (p < 0.01).
Patients with deficient ascitic fluid opsonic activity are predisposed to spontaneous bacterial peritonitis.
Recently, the pathogenesis of spontaneous bacterial peritonitis (SBP) has become more clear. The evidence favors colonization of "susceptible ascites" as a result of "spontaneous bacteremia" (1). The purpose of this study is to determine if the endogenous antimicrobial activity (opsonic activity) of ascitic fluid plays a role in determining the susceptibility of ascites to spontaneous infection.
Bacteremia is common among patients with severe acute and/or chronic liver disease (e.g., at the time of spontaneous ascitic fluid infection, blood cultures are found to grow bacteria in 54% of patients) (1, 2). Many patients with cirrhosis, especially those with ascites, are complement-deficient (3-5). These patients also have neutrophil dysfunction as well as poor reticuloendothelial system function (6, 7). Such abnormalities in host defense would be expected to result in frequent and prolonged bacteremia (8). In fact, cirrhotic rats with ascites have been shown to uniformly develop bacteremia