Superantigen gene profile, emm type and antibiotic resistance genes among group A streptococcal isolates from Barcelona, Spain

Abstract

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...

Distribution of Phage-Associated Virulence Genes in Pharyngeal Group A Streptococcal Strains Isolated in Italy

“…The incidence of the other vir genes ranged between 3.7 and 14.4%. In the particular case of speA, its low prevalence contrasts with the significantly higher values (30 to 50%) reported in other works (13,15,20,21). The most prevalent resistance gene was mef(A) (73%) (Fig.…”

“…1). These latter genes were also frequently detected in previous works (13,20,21). The incidence of the other vir genes ranged between 3.7 and 14.4%.…”

Epidemiological and molecular characteristics of clinical isolates of Streptococcus pyogenes collected between 2005 and 2008 from Chinese children

“…For instance, in Taiwan, isolates with the genotypes emm1.0, emm4.0 and emm12.0 were the leading causes of noninvasive diseases, whereas a few isolates with the genotype emm1.0 contained speC and speH genes, and a few isolates with the genotype emm12.0 contained speJ and smeZ (Lin et al, 2008). In Spain, S. pyogenes isolates with the genotype emm1.0, associated with pharyngitis, possessed speA, speG and speJ genes but not speC, speH, speI or ssa genes (Rivera et al, 2006). Furthermore, the distribution of emm genotypes and their superantigen gene profiles varied in a timedependent manner.…”

Clinical and molecular epidemiology of beta-hemolytic streptococcal infections in India

“…Exotoxin genes, including speA, speB, speC, speF, smeZ, ssa, speG, speH, speJ, speL, speM, and speI were detected by PCR using published primers [10,11]. Amplification of all the genes was performed with an initial five-minute denaturation at 94°C, followed by 30 cycles of denaturation at 94°C for 30 seconds, 30 seconds of annealing at temperatures standardized in the laboratory for each gene, and 60 seconds of extension at 72°C, with a final extension step at 72°C for seven minutes.…”