Abstract
resistant strains to erythromycin (56%), penicillin (40%), ampicillin (56%), cefotaxime (50%), tetracycline (10%), trimethoprim-sulfamethoxazole (48%), nalidixic acid (16%), clarithromycin (48%), azithromycin (44%) and levofloxacin (4%). All strains were susceptible to chloramphenicol, amikacin, streptomycin and gentamicin. Gene analysis showed that 29 strains (58%) had mef(A) gene, and 24 strains (48%) had the erm(B) gene. Out of all the penicillin resistance and intermediate strains, 6 (20%) and 1 (3.33%) strains harbor mutations in pbp1a and pbp2x genes, respectively, but pbp2b was not identified in any sample. Resistance to penicillin, trimethoprim-sulfamethoxazole, clarithromycin and azithromycin in S. pneumoniae is a serious problem in this area and the local pattern of resistance/susceptibility must be considered for therapeutic regimens. The mef(A) gene was a predominant mechanism of macrolide resistance in this area. With regards to low frequency of pbps resistance genes, monitoring of other kinds of mechanisms is recommended.
Highlights
As a major bacterial pathogen, Streptococcus pneumonia infection starts from colonization of the human upper respiratory tract, causing respiratory tract diseases such as pneumonia, bronchitis, otitis media and sinusitis
The aim of this study was to survey drug resistance and genetic characteristics of macrolide and penicillin resistance in S. pneumoniae. This is a cross-sectional study, which was carried out on 70 samples suspected to be S. pneumoniae isolated from patients who were admitted in Intensive Care Unit (ICU) of southwest of Iran, in 2010 and 2011
The aim of this study was to determine the genetic mechanisms and the phenotypic expression of macrolide and penicillin resistance in S. pneumoniae strains collected at Intensive Care Unit (ICU) of the University Hospitals of Shiraz, Iran
Summary
As a major bacterial pathogen, Streptococcus pneumonia infection starts from colonization of the human upper respiratory tract, causing respiratory tract diseases such as pneumonia, bronchitis, otitis media and sinusitis. Many factors that contribute to the colonization and/or invasion of host epithelial cells have been characterized in S. pneumoniae. The target site of macrolides in 50S ribosomal subunit can be modified by methylation of the 23S rRNA adenine residue A2058 resulting in resistance to macrolide, lincosamides and streptogramin B (MLSB phenotype). This mechanism is mediated by erythromycin ribosome methyltransferase encoded by erm(B) and to a lesser extent by erm(A) genes. Macrolide resistance in S. pneumoniae may result from an efflux system leading to the selective efflux of 14- and 15membered macrolides (M phenotype) encoded by the mef(A) gene (Li, 2010; Weber, 2010)
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