SBP is thought to result from a combination of factors inherent in cirrhosis and ascites, such as prolonged bacteremia secondary to compromised host defenses, intrahepatic shunting of colonized blood, and defective bactericidal activity within the ascitic fluid.[7] Suppression of the stomach's secretion of acid, such as by proton pump inhibitor medications, has also been associated with SBP in patients with advanced cirrhosis.[8][9][10] Contrary to earlier theories, transmucosal migration of bacteria from the gut to the ascitic fluid is no longer considered to play a major role in the etiology of SBP.[11]