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In the present series, the primary site of disease was associated with particular clinicopathologic features and outcome, though the latter largely depended on other factors.

Bacterial translocation occurs in ascitic cirrhotic rats, but its association with ascites infection is unknown. The aim of this study was to assess the relation between bacterial translocation and ascites infection in cirrhotic rats. Male Sprague-Dawley rats were induced to cirrhosis with intragastric CC14. Ascitic fluid, portal and peripheral blood, mesenteric lymph nodes, liver and spleen samples were cultured before death in those cirrhotic rats with less (group A) or more (group B) than 250 polymorphonuclear neutrophils/mm3 in ascitic fluid, as well as in healthy control rats. Histological examination of jejunum, ileum, and caecum was also performed. Bacterial translocation occurred in 45% of ascitic rats (without differences between groups A and B), but in 0% controls (p=0.01). Bacterial translocation was associated with positive ascitic fluid culture in 60% of the cases. In all of them the same bacterial species was isolated in both mesenteric lymph node and ascitic fluid. Submucosal caecal oedema (100%), ileal lymphangiectasia (410/%), and caecal inflammatory infiltrate (41%) occurred in ascitic rats, the last being associated with ascitic fluid positive culture (p=0.04). These results suggests that bacterial translocation occurs frequently in ascitic cirrhotic rats, and may play a permissive, but not unique, part in a number ofascites infections. Whether histological changes seen in cirrhotic ascitic rats favour bacterial translocation remains to be elucidated. (Gut 1994; 35: 1648-1652 Cirrhotic patients have increased susceptibility to severe infections, mainly spontaneous bacterial peritonitis and bacteraemia. Most of them (75%) are caused by aerobic organisms of enteric origin. [1][2][3] In the pathogenic hypothesis for spontaneous bacterial peritonitis two complementary mechanisms have been proposed. Firstly, the passage of enteric bacteria into the bloodstream after crossing the gut barrier,3 4 and secondly, the inability of the systemic and local -that is, peritoneal-host defences to eradicate them. Enough data on this second mechanism are available. In fact, both hepatic reticuloendothelial system impairment5 and systemic immune alterations6 have been reported in cirrhotic patients. Moreover, a facilitating role of decreased opsonic and bactericidal activities, C3 concentrations, and protein concentration in ascitic fluid upon the appearance of spontaneous bacterial peritonitis has been shown.7-1

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