Increasing frequency of gram-positive cocci and gram-negative multidrug-resistant bacteria in spontaneous bacterial peritonitis.

BACKGROUND

Spontaneous bacterial peritonitis (SBP) is historically caused by Gram-negative bacteria (GNB) almost exclusively Enterobacteriaceae. Recently, an increasing rate of infections with Gram-positive cocci (GPC) and multidrug-resistant (MDR) microorganisms was demonstrated.

AIMS

To assess possible recent changes of the bacteria causing SBP in cirrhotic patients.

METHODS

We retrospectively recorded 47 cases (66% males) during a 4-year-period (2008-2011).

RESULTS

Twenty-eight (60%) patients had healthcare-associated infections while 15 (32%) received prophylactic quinolone treatment. GPC were found to be the most frequent cause (55%). The most prevalent organisms in a descending order were Streptococcus spp (n = 10), Enterococcus spp (n = 9), Escherichia coli (n = 8), Klebsiella pneumonia (n = 5), methicillin-sensitive Staphylococcus aureus (n = 4) and coagulase-negative Staphylococcus spp (n = 3). Nine of the isolated bacteria (19%) were MDR, including carbapenemase-producing K. pneumonia (n = 4), followed by extended-spectrum beta-lactamase-producing E. coli (n = 3) and Pseudomonas aeruginosa (n = 2). MDR bacteria were more frequently isolated in healthcare-associated than in community-acquired infections (100% vs 50%, P = 0.006), in patients receiving long-term quinolone prophylaxis (67% vs 24%, P = 0.013) and in those with advanced liver disease as suggested by higher MELD score (28 vs 19, P = 0.012). More infections with GNB than GPC were healthcare-associated (81% vs 42%, P = 0.007). Third-generation cephalosporin resistance was observed in 49% and quinolone resistance in 47%.

CONCLUSIONS

GPC were the most frequent bacteria in culture-positive SBP and a variety of drug-resistant microorganisms have emerged. As a result of high rates of resistance in currently recommended therapy and prophylaxis, the choice of optimal antibiotic therapy is vital in the individual patient.