OBJECTIVES: The objective of the study was to examine the characteristics of spontaneous bacterial peritonitis (SBP) caused by streptococci, in particular viridans group streptococci (VGS), and to investigate a potential association between the long-term administration of norfloxacin and high-level resistance to fluoroquinolones in these organisms. METHODS: We reviewed 84 episodes of SBP and bacterascites caused by streptococci that occurred in 75 patients over a 6-year period. Isolates were tested for antibiotic susceptibility by the determination of minimum inhibitory concentrations. RESULTS: Of the 84 isolates, 46 (54.8%) were associated with SBP, 12 (14.3%) were associated with symptomatic bacterascites, and 26 (31%) were associated with asymptomatic bacterascites. VGS were responsible for 39 of the 58 episodes of SBP and symptomatic bacterascites, largely preceding group B streptococci (n=7), Streptococcus pneumoniae (n=6) and Streptococcus bovis (n=5). Most of the episodes were community acquired. An extraperitoneal site of infection was found in three patients only. Positive blood cultures were less frequent in patients with VGS infection than in those with SBP caused by other streptococci (12.8 versus 52.6%, P<0.001). The rates of susceptibility to penicillin, amoxicillin and cefotaxime were 84.5, 87.9 and 91.4%, respectively. All isolates, including those from patients receiving norfloxacin, were susceptible to levofloxacin and moxifloxacin. CONCLUSIONS: VGS are an underestimated cause of SBP in patients with cirrhosis. Most isolates are susceptible to beta-lactam agents and new fluoroquinolones.
OBJECTIVES: The objective of the study was to examine the characteristics of spontaneous bacterial peritonitis (SBP) caused by streptococci, in particular viridans group streptococci (VGS), and to investigate a potential association between the long-term administration of norfloxacin and high-level resistance to fluoroquinolones in these organisms. METHODS: We reviewed 84 episodes of SBP and bacterascites caused by streptococci that occurred in 75 patients over a 6-year period. Isolates were tested for antibiotic susceptibility by the determination of minimum inhibitory concentrations. RESULTS: Of the 84 isolates, 46 (54.8%) were associated with SBP, 12 (14.3%) were associated with symptomatic bacterascites, and 26 (31%) were associated with asymptomatic bacterascites. VGS were responsible for 39 of the 58 episodes of SBP and symptomatic bacterascites, largely preceding group B streptococci (n=7), Streptococcus pneumoniae (n=6) and Streptococcus bovis (n=5). Most of the episodes were community acquired. An extraperitoneal site of infection was found in three patients only. Positive blood cultures were less frequent in patients with VGS infection than in those with SBP caused by other streptococci (12.8 versus 52.6%, P<0.001). The rates of susceptibility to penicillin, amoxicillin and cefotaxime were 84.5, 87.9 and 91.4%, respectively. All isolates, including those from patients receiving norfloxacin, were susceptible to levofloxacin and moxifloxacin. CONCLUSIONS: VGS are an underestimated cause of SBP in patients with cirrhosis. Most isolates are susceptible to beta-lactam agents and new fluoroquinolones.