• ascites
• bacterial peritonitis
• bacterial translocation
• cirrhosis
• cytokines

The database regarding spontaneous bacterial peritonitis (SBP) has increased dramatically in the past 33 years since this phrase was first coined by Harold Conn.¹ In the remote past this easily treatable cause of deterioration of patients with advanced cirrhosis was underdiagnosed and undertreated. This undoubtedly led to many unnecessary deaths, which were probably viewed as mysterious at the time.

Now we know that SBP is quite common, with a prevalence of >20% on admission to the hospital, prior to the era of prevention.² We know who is at high risk—patients with cirrhosis and (a) prior SBP, (b) low protein ascites, or (c) gastrointestinal bleeding.³ We also know how to diagnose, treat, and even prevent this potentially fatal infection.^3,4

Even the “spontaneous” nature of this infection has been largely resolved in recent years. We now know that the gut is the source of most of the bacteria that eventually cause SBP.⁵ As cirrhosis develops in animals, gram negative bacteria increase in numbers in the gut.⁵ We know that the gut of animals and patients with advanced cirrhosis is more permeable to bacteria than the normal gut and more permeable than the gut in less advanced cirrhosis.^6,7 Once bacteria reach a critical concentration in the gut lumen, they “spill over”, and escape the gut, “translocating” to mesenteric lymph …