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Pathogenesis of spontaneous bacterial peritonitis

Bruce A Runyon, MD
Section Editor
Keith D Lindor, MD
Deputy Editor
Kristen M Robson, MD, MBA, FACG


Spontaneous bacterial peritonitis (SBP) is defined as an ascitic fluid infection without an evident intra-abdominal surgically treatable source [1]. The presence of infection is documented by a positive ascitic fluid bacterial culture and an elevated ascitic fluid absolute polymorphonuclear leukocyte (PMN) count (≥250 cells/mm3). The absolute PMN count is calculated by multiplying the total white blood cell count (or total "nucleated cell" count) by the percentage of PMNs in the differential. The cell count and differential are performed manually without formal quality control. The accuracy of these tests is totally dependent upon the skill and interest of the medical technologist. (See "Spontaneous bacterial peritonitis in adults: Diagnosis".)

Our current understanding of the pathogenesis of SBP will be reviewed here. The clinical manifestations, diagnosis, and treatment of SBP are discussed separately. (See "Spontaneous bacterial peritonitis in adults: Clinical manifestations" and "Spontaneous bacterial peritonitis in adults: Diagnosis" and "Spontaneous bacterial peritonitis in adults: Treatment and prophylaxis".)


When the phrase spontaneous bacterial peritonitis was coined in 1964, the descriptor "spontaneous" was used because the pathogenesis of the infection was not apparent [1]. Over the past decades, this void of information has been at least partially filled [2] (figure 1).

Microbiology and bacterial entry into ascites — One of the early steps in the development of SBP is a disturbance in gut flora with overgrowth and extraintestinal dissemination of a specific organism, most commonly Escherichia coli (table 1) [3,4]. Cirrhosis predisposes to the development of bacterial overgrowth, possibly because of altered small intestinal motility [5], and the presence of hypochlorhydria due to use of proton pump inhibitors [6]. In addition, patients with cirrhosis may have increased intestinal permeability [7].

However, the role of bacterial overgrowth in the pathogenesis of SBP remains unsettled. In one study, small bowel motility and bacterial overgrowth were compared in 20 patients with cirrhosis and a history of SBP and 20 patients with cirrhosis without a history of SBP [8]. The prevalence of bacterial overgrowth was higher in the patients with a history of SBP (70 versus 20 percent); these patients also exhibited more severe small intestinal motility disturbances. In contrast, in another study, the presence of bacterial overgrowth was not associated with the development of SBP [9]. (See "Small intestinal bacterial overgrowth: Clinical manifestations and diagnosis".)

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Literature review current through: Nov 2017. | This topic last updated: Aug 11, 2016.
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