Viridans group streptococci: an underestimated cause of spontaneous bacterial peritonitis in cirrhotic patients with ascites.

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.

Comparative activity of beta-lactam agents (carbapenem excepted) against Pseudomonas aeruginosa strains with CARB or OXA beta-lactamases.

BACKGROUND: Ticarcillin resistance in Pseudomonas aeruginosa can be mediated by various beta-lactamases of the CARB and OXA groups. METHODS: We investigated the activity of seven beta-lactam agents and two beta-lactam-beta-lactamase inhibitor combinations against 216 P.aeruginosa strains with genotypically characterized beta-lactamases, including 137 CARB, 31 OXA-35, 25 OXA-10, 13 OXA-1 and 10 OXA-2. MICs were determined by the agar dilution method. RESULTS: The activities of ticarcillin and piperacillin were more affected by CARB than by OXA enzymes. beta-Lactamase inhibitors were poorly effective against OXA-1, OXA-35 and OXA-10. OXA-1 conferred resistance to cefepime and cefpirome but not to cefsulodin and aztreonam. Ceftazidime remained the most active agent against all groups of enzymes. Major differences in the susceptibility rates according to NCCLS and CASFM breakpoints were observed. CONCLUSIONS: Significant differences were found in the resistance profile associated with the various types of CARB and OXA beta-lactamases in P. aeruginosa.

Identification of PSE and OXA beta-lactamase genes in Pseudomonas aeruginosa using PCR-restriction fragment length polymorphism.

OBJECTIVE: A method using PCR-restriction fragment length polymorphism was developed to identify Pseudomonas aeruginosa beta-lactamase genes. METHODS: Two hundred and fifty-nine P. aeruginosa isolates were screened by PCR with 11 primer pairs designed to detect genes encoding PSE, OXA, TEM and SHV enzymes. PSE and OXA gene variants were distinguished by restriction of PCR products with endonucleases recognizing sites involved in point mutations. Nucleotide sequences were verified for a few isolates by sequencing the PCR products. RESULTS: Four isolates produced extended-spectrum beta-lactamases (ESBLs) according to the double disc synergy test. PCR detecting bla(PSE) genes was positive in 162 (62.5%) isolates: 151 carried bla(PSE-1) and 11 carried a variant encoding an enzyme differing from PSE-1 by a single amino acid substitution (Pro102 to Ser). PCR detecting sequences for enzymes of the OXA-10 group was positive in 68 (26.3%) isolates: 31 carried bla(OXA-10), one carried bla(OXA-14) and 36 carried a new variant intermediate between bla(OXA-13) and bla(OXA-19). The bla(OXA-2) gene was identified in 13 (5%) isolates. Two other isolates carried bla(OXA-2) variants encoding ESBLs differing from OXA-2 by a single amino acid substitution (Asp150 to Tyr and Trp159 to Cys, respectively). PCR detecting sequences for enzymes of the OXA-1 group was positive in 12 (4.6%) isolates. A bla(TEM) gene was identified in five (1.9%) isolates (three bla(TEM-1), one bla(TEM-2), one bla(TEM-4)). CONCLUSION: This approach is effective for screening P. aeruginosa for beta-lactamase gene carriage in epidemiological studies and for detecting new variants.

Shigella and enteroinvasive Escherichia coli strains are derived from distinct ancestral strains of E. coli.

The differentiation between Shigella subspecies, and the phylogenetic position of Shigella clones within Escherichia coli clones was determined by analysis of restriction fragment length polymorphisms of rDNA (ribotyping). Seventy-five Shigella strains belonging to the four subspecies and 13 enteroinvasive E. coli (EIEC) strains were compared with the 72 E. coli strains of the ECOR collection, which have been classified into four phylogenetic groups (A, B1, B2 and D). Seventeen Shigella dysenteriae ribotypes, 12 Shigella flexneri ribotypes, 23 Shiegella boydii ribotypes, 12 Shigella sonnei ribotypes and 13 EIEC ribotypes were identified following digestion with HindIII and EcoRI. Correspondence analysis of the data showed that S. boydii serotype 13 strains were distantly related to the other Shigella strains, and that S. sonnei and S. flexneri were distinct from S. boydii and S. dysenteriae. The ribotypes of Shigella and ECOR strains were indistinguishable, and S. sonnei, S. flexneri and most S. dysenteriae strains were closely related to phylogenetic group D, whereas S. dysenteriae serotype 1 strains belonged to phylogenetic group B1, and S. boydii strains were evenly distributed between the two groups. The Shigella strains were distantly related to group B2, which contains E. coli strains frequently implicated in extra-intestinal infections in humans. In contrast, the 13 EIEC strains were more widely distributed between phylogenetic groups B1, A and B2. Thus, there was no primordial Shigella species and Shigella and EIEC strains are derived from different ancestral strains.