Review Article

Spontaneous Bacterial Peritonitis – Bacteriology, Diagnosis, Treatment, Risk Factors and Prevention

J. B. Dever; M. Y. Sheikh


Aliment Pharmacol Ther. 2015;41(11):1116-1131. 

In This Article


In a healthy individual, the variety and density of bacteria increases exponentially from the stomach to the colon with up to a 1000 or more different species and a trillion bacteria per gram of faecal material in the caecum.[16] A symbiotic relationship usually exists. However, in advanced liver disease, normal intestinal flora can cause deleterious effects to the host through a variety of mechanisms leading to SBP including bacterial overgrowth,[17,18] increased intestinal permeability[19] so-called leaky gut and pathological bacterial translocation[20] – all in the setting of immune dysregulation pervasive in patients with cirrhosis.

Gram-negative bacilli (GNB) are the major cause of SBP (Table 2). The three most common isolates from 263 ascitic fluid cultures, compiled in 1994 from various studies published between 1971 and 1991, included E. coli (46%), Streptococcus (30%) and Klebsiella (9%).[21] Similar results were demonstrated in 1992 from numerous studies encompassing 746 cases of SBP: E. coli (47%), Streptococcus (19%) and Klebsiella (13%).[22]E. coli was found in the majority of patients with SBP as reported by Conn et al. (66%)[4] and Kerr et al. (72%)[3] and consistently remains most common isolate in recent literature albeit with lower prevalence. E. coli was the predominant strain to cause of SBP reported by Fernandez et al. from data obtained between 1998 and 2000 accounting for 34 of 138 cases (25%) of SBP.[23] Likewise, E. coli represented 31 of 140 cases (22%) as reported by Novovic et al. from data gathered between 2000 and 2006.[24]

Gram-positive cocci (GPC) have generally accounted for less than 25% of cases of SBP.[25,26] Infections with GPC including pneumonia and urinary tract infections have markedly increased in patients with cirrhosis in recent years and have been linked to therapeutic interventions[23] and chronic antibiotic usage.[25] The increasing trend of GPC-related SBP has also been demonstrated and represents a changing paradigm in the known bacteriology of SBP. Notably, 229 GPC were identified on ascitic fluid culture compared to 151 GNB out of 411 strains from 325 subjects. The most frequently encountered bacteria were coagulase-negative staphylococci (n = 85), E. coli (n = 75), enterococci (n = 54), streptococci (n = 50), Klebsiella (n = 33), Enterobacter (n = 33), Serratia (n = 33) and S. aureus (n = 33).[27] An observational French study from the same affiliate acquired 268 positive culture results from patients with cirrhosis, and GPC-related SBP was the predominate group representing 65% (coagulase-negative Staphylococcus 27%, Enterococcus 24%) of SBP cases validating prior findings.[28] The spectrum of bacteria causing SBP in in-patients from nine studies with ascitic fluid samples collected since 1998 has demonstrated comparable results in an original table herein. However, GNB and foremost E. coli remain the most common class of bacteria and isolate respectively.

The prevalence of SBP generally remains low in the out-patient setting especially in asymptomatic patients. Culture results from 427 out-patients demonstrated 1% prevalence of SBP which was predominately GPC [Staphylococcus aureus (n = 1), Streptococcus viridans (n = 3) and Staphylococcus saccharolyticus (n = 1).[29]

The emergence of extended spectrum β-lactamase-producing (ESβL) GNB, methicillin-resistant Staphylococcus aureus (MRSA), flouroquinolone-resistant (QR) GNB,[30] vancomycin-resistant Enterococcus[31] and other resistant microorganisms have also changed prior perceptions about SBP bacteriology and its treatment.[32] MRSA was found to cause 9 of 87 SBP cases (10%) in a prospective study.[33] In another study, the same research group found SBP was due to GPC in 34 of 60 cases (57%) when patients received norfloxacin (Noroxin; Merck & Co., Inc., White House Station, NJ, USA) for more than 1 month, and MRSA was the most common isolate (77%).[34] Extended spectrum β-lactamase-producing (ESβL) GNB (E. coli and Klebsiella) were the most common multi-drug resistant bacteria (73%), especially among nosocomial infections, followed by fluoroquinolone resistant GNB in patients who were receiving norfloxacin prophylaxis.[30]

One bacterium (monomicrobial) is the cause in more than 90% of cases, yet the probability of identifying a pathogen is mediocre as ascitic fluid cultures are positive in 50–60% of patients with SBP.[31] Rare isolates reported in the literature include anaerobes, Aeromonas,[35]Listeria,[36]Streptococcus bovis,[37]Bordetella bronchiseptica,[38]Candida,[39]Pasteurella multocida,[40]Leclercia adecarboxylata,[41] and Salmonella paratyphi A.[42]