Molecular Epidemiology of Erythromycin Resistance in Streptococcus pneumoniae Isolates from Blood and Noninvasive Sites

Abstract

Erythromycin-resistant isolates of Streptococcus pneumoniae from blood cultures and noninvasive sites were studied over a 3-year period. The prevalence of erythromycin resistance was 11.9% (19 of 160) in blood culture isolates but 4.2% (60 of 1,435) in noninvasive-site isolates. Sixty-two of the 79 resistant isolates were available for study. The M phenotype was responsible for 76% (47 of 62) of resistance, largely due to a serotype 14 clone, characterized by multilocus sequence typing as ST9, which accounted for 79% (37 of 47) of M phenotype resistance. The ST9 clone was 4.8 times more common in blood than in noninvasive sites. All M phenotype isolates were PCR positive for mef(A), but sequencing revealed that the ST9 clone possessed the mef(A) sequence commonly associated with Streptococcus pyogenes. All M phenotype isolates with this mef(A) sequence also had sequences consistent with the presence of the Tn1207.1 genetic element inserted in the celB gene. In contrast, isolates with the mef(E) sequence normally associated with S. pneumoniae contained sequences consistent with the presence of the mega insertion element. All MLS B isolates carried erm(B), and two isolates carried both erm(B) and mef(E). Fourteen of the 15 MLS B isolates were tetracycline resistant and contained tet(M). However, six M phenotype isolates of serotypes 19 (two isolates) and 23 (four isolates) were also tetracycline resistant and contained tet(M). MICs for isolates with the mef(A) sequence were significantly higher than MICs for isolates with the mef(E) sequence (P < 0.001). Thus, the ST9 clone of S. pneumoniae is a significant cause of invasive pneumococcal disease in northeast Scotland and is the single most important contributor to M phenotype erythromycin resistance.

Prevalence and Molecular Analysis of Macrolide and Fluoroquinolone Resistance among Isolates of Streptococcus pneumoniae Collected during the 2000-2001 PROTEKT US Study

“…This phenomenon may occur because erm(B) and mef(A) are associated with different conjugative transposons (Tn1545 and Tn916, respectively) (25,34,36). It is possible that the insertion of erm(B) into transposon Tn1545 already associated with tet(M) and other resistance genes has evolved over a long time period, whereas the association of mef(A) and tet(M) on Tn916 has occurred more recently (1,25,35). It will be interesting to see if any further evolutionary changes are observed as the PROTEKT US surveillance study continues.…”

Molecular Epidemiology of Multiresistant Streptococcus pneumoniae with Both erm (B)- and mef (A)-Mediated Macrolide Resistance

“…Detection of tet(M), msr(A), Tn1207.1, and mega was done as previously described (1). Discrimination between mef(A) and mef(A) subclass mef(E) was performed by amplifying a segment of the mef(A) gene and then comparing the sequence to the sequences with GenBank accession numbers U70055 [mef(A)] and U83667 [mef(A) subclass mef(E)].…”

Molecular Epidemiology of Macrolide-Resistant Isolates of Streptococcus pneumoniae Collected from Blood and Respiratory Specimens in Norway

“…The ST9 clone has been identified as an important cause of meningitis throughout the United Kingdom (19) and is recognized as a cause of invasive disease in several other countries (http://www.mlst .net). Dissemination of invasive ST9 isolates has also been reported for Canada, Scotland, and, most recently, Greece (2,17,18). The mechanisms behind the impressive global spread of England 14 -9 remain unknown.…”