RESUMO
Objective To retrospectively analyze the drug resistance evolution of Staphylococcus aureus and MRSA,to provide the basis for prevention and control measures.Methods 576 strains of clinical isolated Staphylococcus aureus from 2009 to 2012 were analyzed.The bacteria identification and drug sensitivity test were detected by VITEK 2 Compact automatic bacteria identification instrument.Results The separation rate of MRSA from 2009 to 2012 was 59.5％,but the separation rate was gradually decreased per year.The antibacterial activity of MRSA was better to vancomycin,linezolid,quinupristin/Dalfopristin,teicoplanin,nitrofurantoin (resistance rate ＜ 2.4％).The resistance rate and sensitive rate of MRSA to tigecycline was 0.0％,intermediary rate was 100.0％.The resistance of MRSA to gentamicin,ciprofloxacin,moxifloxacin,clindamycin,tetracycline and erythromycin was gradually decreased.From 2010 to 2012,The resistance of MRSA to cotrimoxazole decreased significantly,from 65.3％ in 2010 to 28.2％ in 2011 and 4.7％ in 2012 (P ＜ 0.05).Conclusion Separation of MRSA and drug resistance is reduced year by year,we should continue to strengthen the administration of antimicrobial agents,scientific and reasonable application of antibacterial drugs,reduce the incidence of multiresistant bacteria and drug resistance.
RESUMO
Human Immunodeficiency Virus Type 1 exists in vivo as quasispecies, and one of the genome's characteristics is its diversity. During the antiretroviral therapy, drug resistance is the main obstacle to effective viral prevention. Understanding the molecular evolution process is fundamental to analyze the mechanism of drug resistance and develop a strategy to minimize resistance. Objective: The molecular evolution of drug resistance of one patient who had received reverse transcriptase inhibitors for a long time and had treatment which replaced Nevirapine with Indinavir was analyzed, with the aim of observing the drug resistance evolution pathway. Methods: The patient, XLF, was followed-up for six successive times. The viral populations were amplified and sequenced by single-genome amplification. All the sequences were submitted to the Stanford HIV Drug Resistance Database for the analysis of genotypic drug resistance. Results: 149 entire protease and 171 entire reverse transcriptase sequences were obtained from these samples, and all sequences were identified as subtype B. Before the patient received Indinavir, the viral population only had some polymorphisms in the protease sequences. After the patient began Indinavir treatment, the variants carrying polymorphisms declined while variants carrying the secondary mutation G73S gained the advantage. As therapy was prolonged, G73S was combined with M46I/L90M to form a resistance pattern M46I/G73S/L90M, which then became the dominant population. 97.9% of variants had the M46I/G73S/L90M pattern at XLF6. During the emergence of protease inhibitors resistance, reverse transcriptase inhibitors resistance maintained high levels. Conclusion: Indinavir- resistance evolution was observed by single-genome amplification. During the course of changing the regimen to incorporate Indinavir, the G73S mutation occurred and was combined with M46I/L90M.