Abstract

BackgroundStreptococcus pneumoniae causes serious infections worldwide. The aim of this study was to determine the molecular characteristic, antibiotic resistance pattern and capsular types of invasive S. pneumoniae in Tehran, Iran.ResultsOf the 44 pneumococcal invasive isolates, 39 (89%) were isolated from children and 5 (11%) from adults. The results show that all pneumococcal isolates were susceptible to linezolid but had varying resistance to trimethoprim-sulfamethoxazole (86%), erythromycin (73%), tetracycline (66%), clindamycin (43%), penicillin (16%), chloramphenicol (14%) and levofloxacin (2%). The range of erythromycin, tetracycline and penicillin MICs were 2 - ≥ 256 μg/mL, 4 - ≥ 48 μg/mL, and 0.047 - ≥ 256 respectively. All of the penicillin resistant isolates were multidrug resistant (MDR) and in addition to penicillin were resistant to tetracycline, erythromycin and trimethoprim-sulfamethoxazole. The most common capsular types detected in 64% of the pneumococcal isolates was 6A/B, 19A, 15A, 23F. The multilocus sequence typing (MLST) of 10 pneumococcal isolates revealed 9 different sequence types (STs), including ST 15139 (capsular type 19A) and ST 15140 (capsular type 23F), which have not previously been reported.ConclusionsThe study revealed that the S. pneumoniae isolates belonged to diverse capsular types and clones with high rate of resistance to erythromycin, tetracycline, and penicillin.

Highlights

  • The results show that all isolates were susceptible to linezolid but had varying resistance to trimethoprim-sulfamethoxazole (86%), erythromycin (73%), tetracycline (66%), clindamycin (43%), penicillin (16%), chloramphenicol (14%) and levofloxacin (2%)

  • As to macrolide resistant genes, the most prevalent gene was ermB found in 52% (23/44) of the isolates, followed by mefA/E found in 50% (22/44) of the isolates

  • Our result showed that all of the penicillin resistant isolates were multidrug resistant (MDR) and in addition to penicillin were resistant to tetracycline, erythromycin and trimethoprim-sulfamethoxazole

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Summary

Introduction

The incredible capacity of S. pneumoniae to uptake genes has facilitated the spread of resistance in the Beheshti et al BMC Microbiology (2020) 20:167 pneumococcal population to penicillin and other antibiotics such as macrolides that used routinely to treat the disease [6,7,8,9]. The major resistant determinant is acquisition of the ermB gene that encodes a methylase [9, 11, 12]. The majority of isolates that encode ermB exhibit the MLSB (Macrolide, lincosamide and streptogramin B) phenotype. The most common mechanism of resistance to tetracycline in S. pneumoniae is acquisition one of the two genes, tetM and less frequently the tetO genes [12, 14, 15] both of which located in mobile genetic elements such as transposons and encode ribosomal protection proteins [14, 15]. The main source of the tetM gene is Tn916 family [14]

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