Abstract
BackgroundEvolving gonococcal antimicrobial resistance (AMR) poses a serious threat to public health. The aim of this study was to: update antimicrobial susceptibility data of Neisseria gonorrhoeae recently isolated in Nanjing, China and identify specific deteminants of antimicrobial resistance and gentoypes of isolates with decreased sensitivity to ceftriaxone.Methods334 N. gonorrhoeae isolates were collected consecutively from symptomatic men attending the Nanjing STD Clinic between April 2011 and December 2012. The minimum inhibitory concentrations (MICs) for penicillin, tetracycline, ciprofloxacin, spectinomycin and ceftriaxone were determined by agar plate dilution for each isolate. Penicillinase-producing N. gonorrhoeae (PPNG) and tetracycline-resistant N. gonorrhoeae (TRNG) were examined and typed for β-lactamase and tetM encoding plasmids respectively. Isolates that displayed elevated MICs to ceftriaxone (MIC ≥0.125 mg/L) were also tested for mutations in penA, mtrR, porB1b, ponA and pilQ genes and characterized by Neisseria gonorrhoeae multi-antigen sequence typing (NG-MAST).Results98.8% (330/334) of N. gonorrhoeae isolates were resistant to ciprofloxacin; 97.9% (327/334) to tetracycline and 67.7% (226/334) to penicillin. All isolates were susceptible to ceftriaxone (MIC ≤0.25 mg/L) and spectinomycin (MIC ≤32 mg/L). Plasmid mediated resistance was exhibited by 175/334 (52%) of isolates: 120/334 (36%) of isolates were PPNG and 104/334 (31%) were TRNG. 90.0% (108/120) of PPNG isolates carried the Asia type β-lactamase encoding plasmid and 96% (100/104) of TRNG isolates carried the Dutch type tetM containing plasmid. Elevated MICs for ceftriaxone were present in 15 (4.5%) isolates; multiple mutations were found in penA, mtrR, porB1b and ponA genes. The 15 isolates were distributed into diverse NG-MAST sequence types; four different non-mosaic penA alleles were identified, including one new type.ConclusionsN. gonorrhoeae isolates in Nanjing generally retained similar antimicrobial resistance patterns to isolates obtained five years ago. Fluctuations in resistance plasmid profiles imply that genetic exchange among gonococcal strains is ongoing and is frequent. Ceftriaxone and spectinomycin remain treatments of choice of gonorrhea in Nanjing, however, decreased susceptibility to ceftriaxone and rising MICs for spectinomycin of N. gonorrhoeae isolates underscore the importance of maintaining surveillance for AMR (both phenotypic and genotypic).Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-014-0622-0) contains supplementary material, which is available to authorized users.
Highlights
Evolving gonococcal antimicrobial resistance (AMR) poses a serious threat to public health
Antimicrobial susceptibilities Among 652 consecutively enrolled male subjects with urethritis, 340 (52.1%) were infected with N. gonorrhoeae; antimicrobial susceptibility testing of 334 successfully retrieved isolatesis is summarized in Table 1
Resistance rates to antibiotics formerly or recommended for treatment of gonorrhea in China were: ciprofloxacin 98.8%, tetracycline 97.9%, penicillin 67.7%, all isolates were susceptible to spectinomycin and ceftriaxone
Summary
Evolving gonococcal antimicrobial resistance (AMR) poses a serious threat to public health. The aim of this study was to: update antimicrobial susceptibility data of Neisseria gonorrhoeae recently isolated in Nanjing, China and identify specific deteminants of antimicrobial resistance and gentoypes of isolates with decreased sensitivity to ceftriaxone. Effective treatment is key in preventing complications and controlling transmission of N. gonorrhoeae. This bacterium has developed resistance to antimicrobials (AMR) including sulfonamides, penicillins, tetracyclines and quinolones [3,4]. In recent years treatment failures have occurred when extended-spectrum cephalosporins (ESCs), the most widely used agents for treatment of gonorrhea, were used, and associated increases in AMR to ESCs have been reported in several countries [5,6,7,8,9,10,11]. The molecular mechanisms associated with reduced susceptibility or resistance to ESCs include mutations in several gene loci; penA [12,13,14,15,16], mtrR [17,18], penB [17,19], ponA [6,20] and pilQ [21,22] and their multifaceted interactions [6,23]
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