Group A streptococcus (GAS) has been described as an emerging cause of severe invasive infections. A retrospective hospital-based study was conducted, including GAS isolates causing invasive or non-invasive infections from January 1999 to June 2003 in Barcelona. Demographic and clinical information on the invasive cases was obtained from medical files. GAS isolates collected from 27 patients with invasive infections and 99 patients with non-invasive infections were characterized by emm type and subtype, superantigen (SAg) gene profile (speA-C, speF-J, speL, speM, ssa and smeZ), allelic variants of speA and smeZ genes, antibiotic susceptibility and genetic resistance determinants. The most prevalent emm type was emm1 (17?5 %), followed by emm3 (8?7 %), emm4 (8?7 %), emm12 (7?1 %) and emm28 (7?1 %). The smeZ allele and SAg gene profiles were closely associated with the emm type. The speA2, speA3 and speA4 alleles were found in emm1, emm3 and emm6 isolates, respectively. Overall, 27?8, 25?4 and 11?9 % of isolates were resistant to erythromycin, tetracycline or both agents, respectively. Reduced susceptibility to ciprofloxacin and levofloxacin (MIC 2-4 mg ml "1 ) was found in 3?2 % of isolates. mef(A)-positive emm types 4, 12 and 75, and erm(B)-positive emm types 11 and 25 were responsible for up to 80 % of the erythromycin-resistant isolates. No significant differences in emm-type distribution, SAg gene profile or resistance rates were found between invasive and non-invasive isolates. The SAg and antibiotic resistance genes appeared to be associated with the emm type and were independent of the disease type. INTRODUCTIONGroup A streptococcus (GAS) is a human pathogen that is responsible for a wide array of infections, varying in severity from acute pharyngitis and impetigo to severe invasive infections such as necrotizing fasciitis (NF) and streptococcal toxic shock syndrome (STSS) (Cunningham, 2000).The resurgence and persistence of severe forms of GAS diseases reported since the mid 1980s (Hoge et al., 1993;Stevens, 2002) has motivated intensive research on epidemiological, microbiological and clinical aspects of invasive GAS disease. Several factors have been considered to explain differences in disease frequency and severity, including changes in the virulence of the bacterium (Banks et al., 2002;Musser et al., 1993) and the role of host immunity (Å kesson et al., 2004;Basma et al., 1999;Kotb et al., 2002; NorrbyTeglund et al., 2000).Among the many factors involved in the virulence of the pathogen, the M protein and a group of exotoxins known as streptococcal superantigens (SAgs) have received considerable attention. Sequence analysis of the emm gene (encoding the M protein) has become an important surveillance tool for investigating the dynamics of GAS infection and more than 150 emm gene sequence types and several emm subtypes have been documented (Facklam et al., 2002;Li et al., 2003).SAgs are thought to contribute to the pathogenesis of severe GAS infections by virtue of their potent immunostimulatory activ...

Resistance mechanisms and clonal relationships were determined for six Streptococcus pyogenes isolates with low- or high-level ciprofloxacin resistance. Four isolates displayed reduced susceptibility to ciprofloxacin and levofloxacin and had alterations in ParC: Ser80-->Pro (isolate emm3.1); Ser79-->Ala (two isolates emm6.0); and a double substitution Ser79-->Phe and Ala121-->Val (isolate emm12.27). Two isolates (emm12.26) displayed high-level resistance to ciprofloxacin and levofloxacin, as well as to other quinolones. These isolates had the same double substitution in ParC as isolate emm12.27, and an additional substitution (Ser81-->Tyr) in GyrA. Resistance patterns, emm typing and sequencing of the quinolone resistance-determining regions defined two clusters containing three and two isolates, respectively.

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