Aetiology

The aetiology of SBP is infection of the ascitic fluid. More than 92% of all cases of SBP are monomicrobial.[16] The presence of polymicrobial infection significantly increases the risk for secondary peritonitis.

Gram-negative bacteria remain the most common pathogens in SBP. However, there has been an increase in infections due to gram-positive cocci. Studies have suggested that these changes are associated with long-term hospitalisation of patients with end-stage liver disease and the use of prophylactic antibiotics after an initial episode of SBP. Prophylactic antibiotics generally cover gram-negative organisms better than gram-positive organisms.[11][12][17] There has also been a case report of carbapenem-resistant Klebsiella pneumoniae, which is of particular concern due to the potential for widespread transmission of resistance due to its mobile genetic elements.[18]

The most common pathogens are:[19][20][21]

  • Escherichia coli (reported in 39% to 61% of cases)

  • Staphylococcus aureus (3% to 12%)

  • Streptococcus pneumoniae (2% to 11%)

  • Enterococcus faecalis (4% to 17%)

  • Klebsiella pneumoniae (4% to 20%)

  • Pseudomonas aeruginosa (3% to 9%).

Less common pathogens are:

  • Proteus species

  • Acinetobacter species

  • Citrobacter freundii

  • Bacteroides fragilis

  • Aeromonas hydrophila

  • Listeria monocytogenes[22]

  • Vibrio vulnificus.

Rare organisms noted in case reports include:

  • Haemophilus influenzae, non-typeable[23][24]

  • Haemophilus parainfluenzae[25]

  • Neisseria meningitidis[26]

  • Salmonella typhimurium[27]

  • Salmonella paratyphi A[28]

  • Leclercia adecarboxylata[29]

  • Leminorella grimontii[30]

  • Aerococcus urinae[31]

  • Gemella morbillorum[32]

  • Actinomyces species[33]

  • Streptococcus salivarius[34]

  • Ochrobactrum anthropi[35]

  • Arcanobacterium haemolyticum[36]

  • Cryptococcus neoformans (even in HIV-negative patients)[37][38]

  • Coccidioides immitis[39]

  • Candida species[40]

  • Brucella species[41]

  • Enterococcus hirae[42]

  • Enterococcus gallinarum[43]

  • Enterococcus casseliflavus[43]

  • Bordetella bronchiseptica[44]

  • Plesiomonas shigelloides[45]

  • Expanded dengue syndrome[46]

  • Edwardsielle tarda[47]

Streptococcus viridans commonly grows as a contaminant in peritoneal fluid cultures.[48] However, it also has been identified as a pathogen in other studies.[49][50]

Pathophysiology

SBP is believed to develop primarily through haematogenous spread of bacteria with subsequent colonisation of the ascitic fluid. The source of the bacteria can be classified into intestinal (more commonly) and non-intestinal (less commonly).

With intestinal sources, bacterial translocation from the intestinal flora occurs by movement to the mesenteric lymph nodes and from there to the bloodstream. The pathophysiology of cirrhosis predisposes to this colonisation and impairs the ability to resist subsequent infection. The bacterial translocation is believed to involve numerous mechanisms that are found in patients with advanced cirrhosis:[51]

  • Depression of the reticulo-endothelial system function of the liver

  • Intestinal bacterial overgrowth, likely to be caused by intestinal hypomotility

  • Venous stasis, resulting from portal hypertension, which causes increased intestinal permeability to enteric bacteria.

SBP is sometimes caused by organisms that are not part of the intestinal flora. In such cases, the source of bacteria is believed to be an extraintestinal infection or procedure, such as:

  • A respiratory infection

  • A urinary tract infection

  • An invasive procedure (e.g., endoscopic sclerotherapy for oesophageal varices, which is associated with a 5% to 30% rate of bacteraemia;​​​ central venous catheterisation; urinary catheterisation; paracentesis; transjugular intrahepatic portosystemic shunt placement).[51][52]​[53]​​

After haematogenous spread of the bacteria to the ascitic fluid, complement in the fluid can serve to protect from infection. However, many patients with cirrhosis have low ascites protein concentration, which correlates with decreased opsonic activity and predisposes to infection.[54]

Classification

International Ascites Club[1]

  • Spontaneous bacterial peritonitis (SBP)

    • Defined by an absolute neutrophil count (ANC) >250 cells/mm³.

    • Because of the difficulties in culturing the pathogen, the criteria do not require a positive culture, although some manuscript authors have used this as part of their diagnosis of SBP.

  • Culture-negative neutrocytic ascites (CNNA)

    • Defined by an ANC >250 cells/mm³, with no culture growth, this is considered a variant of SBP.

    • Studies have demonstrated similar short- and long-term mortality in patients with CNNA and SBP.[2][3]

  • Bacterascites

    • The patient must fulfil all of the following criteria: positive ascitic fluid culture; ANC <250 cells/mm³; and no evidence of systemic or local infection.

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