INVASIVE PNEUMOCOCCAL DISEASE;
VIRIDANS GROUP STREPTOCOCCI;
DNA TOPOISOMERASE-IV;
IN-VITRO;
PARC;
MUTATIONS;
SUSCEPTIBILITY;
GYRASE;
CIPROFLOXACIN;
EPIDEMIOLOGY;
D O I:
10.3201/eid1506.080684
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
Among 4,215 Streptococcus pneumoniae isolates obtained in Spain during 2006, 98 (2.3%) were ciprofloxacin resistant (3.6% from adults and 0.14% from children). In comparison with findings from a 2002 study, global resistance remained stable. Low-level resistance (30 isolates with MIC 4-8 mu g/mL) was caused by a reserpine-sensitive efflux phenotype (n = 4) or single topoisomerase IV (parC [n = 24] or parE [n = 1]) changes. One isolate did not show reserpine-sensitive efflux or mutations. High-level resistance (68 isolates with MIC >= 16 mu g/mL) was caused by changes in gyrase (gyrA) and parC or parE. New changes in parC (S80P) and gyrA (S81V, E85G) were shown to be involved in resistance by genetic transformation. Although 49 genotypes were observed, clones Spain(9v)-ST156 and Sweden(15A)-ST63 accounted for 34.7% of drug-resistant isolates. In comparison with findings from the 2002 study, clones Spain(14)-ST17, Spain(23F)-ST81, and ST88(19F) decreased and 4 new genotypes (ST97(10A), ST570(16), ST433(22), and ST717(33)) appeared in 2006.