Antimicrobial Susceptibility Patterns and Macrolide Resistance Genes of β-Hemolytic Streptococci in Korea

Abstract

In 540 beta-hemolytic streptococci, the rates of resistance to tetracycline, chloramphenicol, erythromycin, and clindamycin were 80.0, 22.8, 20.2, and 19.1%, respectively. Of the erythromycin-resistant isolates, 63.3% had the constitutive macrolide-lincosamide-streptogramin B (MLS B ) resistance phenotype, 23.9% had the M phenotype, and 12.8% had the inducible MLS B resistance phenotype. The constitutive MLS B resistance phenotype with the erm(B) gene was dominant in Korea.Current practice guidelines for the management of pharyngitis caused by Streptococcus pyogenes include the use of erythromycin as an alternative to penicillin when indicated and clindamycin for persons with multiple recurrent episodes (5). Macrolide or lincosamide therapy is also a recommended treatment option for S. agalactiae infection or for prophylaxis when streptococcal colonization among pregnant women is suspected (16). However, recent studies have shown that changes in the susceptibility of beta-hemolytic streptococci (BHS) to erythromycin and clindamycin have been substantial, although differences in rates of resistance to these agents have existed according to geographical location and investigators. The objectives of the present study were to investigate the incidence and possible trends in susceptibility among the BHS isolated from clinical specimens in a Korean hospital and to clarify the phenotypes and genotypes of erythromycin-resistant isolates.A total of 540 strains of BHS were collected from clinical specimens between January 1990 and December 2000 at Wonju Christian Hospital, a 1,000-bed teaching hospital in South Korea. Multiple isolates from the same patient were avoided. The isolates were identified by standard methods. Beta-hemolytic strains with group F antigens were excluded. Susceptibility to penicillin G, erythromycin, clindamycin, tetracycline, ceftriaxone (Sigma Chemical Co., St. Louis, Mo.), vancomycin (Daewoong Lilly, Seoul, Korea), and chloramphenicol (Chongkundang, Seoul, Korea) was tested by the agar dilution method (14). The resistance phenotypes of erythromycin-resistant (intermediate and resistant) isolates were determined by the double-disk test with erythromycin (15 g) and clindamycin (2 g) disks (17). The presence of erm and mef class genes was determined by PCR amplification with previously described primers (11,18) specific for erm(A) subclasses erm(TR), erm(B), erm(C), and mef(A).The overall resistance rates of BHS were found to be 80.0% for tetracycline, 22.8% for chloramphenicol, 20.2% for erythromycin, and 19.1% for clindamycin, whereas all isolates were susceptible to penicillin G, ceftriaxone, and vancomycin (Table 1). The rates of resistance to erythromycin found in this study were as follows, in order of decreasing rank: S. agalactiae, 25.3%; S. pyogenes, 16.1%; group C streptococci, 9.1%; group G streptococci, 9.0%. S. agalactiae had the highest rate of clindamycin resistance (28.2%), followed by S. pyogenes (9.8%), group C streptococci (4.5%), and group G streptococci (1.5%

Heterogeneity of Genotype-Phenotype Correlation among Macrolide-Resistant Streptococcus agalactiae Isolates

“…The M phenotype (P4) could be detected in 15 isolates (20%) strongly associated with the mefA gene (Table 1). All three phenotypes (P1, P3, and P4) correspond well to the ones previously described by different authors (10,19) while P2, in contrast, has not been described so far. The most prevalent serotypes (ST) among all erythromycin-resistant GBS isolates were ST V (37%) and III (27%) ( Table 2).…”

Resistance to Erythromycin and Telithromycin in Streptococcus pyogenes Isolates Obtained between 1999 and 2002 from Greek Children with Tonsillopharyngitis: Phenotypic and Genotypic Analysis

“…Since the late 1990s, resistance to erythromycin and other 14-and 15-membered ring macrolides has been increasingly detected in S. pyogenes in several European countries (1,10,16) and other parts of the world, such as Korea (24). The main known mechanisms of macrolide resistance in S. pyogenes are a 14-and 15-membered ring macrolide-specific efflux mechanism (M phenotype) (21), encoded by the mef(A) gene (6), as well as the modification of the ribosomal target by a methylase encoded by the erm(B) (26) or the erm(TR) gene (18); the latter is currently referred to as erm(A) or erm(A), subclass erm(TR) gene (17).…”

Epidemiology and Erythromycin Resistance ofStreptococcus pyogenesin the Last 20 Years

“…In that report, erythromycin resistance was first observed in 1994. Although the number of isolates tested was low (23 strains), phenotypic distribution showed 9, 6, and 8 strains each for the cMLSB, iMLSB, and M phenotypes, respectively [19]. Erythromycin resistance was observed in 23% of clinical isolates collected between 1997 and 2003 in Seoul [20].…”

“…The erythromycin resistance rate of GAS strains collected between 1980 and 1992 was 2% [18]. GAS strains isolated between 1990 and 2000 showed resistance rates of 16.1% and 9.8% to erythromycin and clindamycin, respectively in Wonju, Korea [19]. In that report, erythromycin resistance was first observed in 1994.…”