Patients with cirrhosis have altered immune defenses and are considered immunocompromised individuals. Changes in gut motility, mucosal defense and microflora allow for translocation of enteric bacteria into mesenteric lymph nodes and the blood stream. Additionally, the cirrhotic liver is ineffective at clearing bacteria and associated endotoxins from the blood thus allowing for seeding of the sterile peritoneal fluid. Thus, hospitalised cirrhotic patients, particularly those with gastrointestinal hemorrhage, are at high risk of developing bacterial infections, the most common being spontaneous bacterial peritonitis. Given the significant morbidity and mortality associated with spontaneous bacterial peritonitis and the fact that half of the cases are community acquired, all hospitalised cirrhotic patients should have a diagnostic paracentesis to exclude infection. Those admitted with gastrointestinal bleed and a negative paracentesis require short-term prophylaxis with norfloxacin. A third generation cephalosporin is the treatment of choice for spontaneous bacterial peritonitis and, once the acute infection is resolved, secondary prophylaxis with oral norfloxacin is warranted. Patients who develop renal dysfunction at the time of active infection have the highest mortality and require adjunctive albumin therapy. This article reviews the pathogenesis of SBP, the evidence behind the antibiotics used, the rationale for adjunctive albumin therapy in the setting of acute renal failure, and the role of prophylactic antibiotics in specific high-risk populations.