深圳市人民医院沙门菌对抗菌药物敏感性分析

目的监测我院2002—2007年临床分离沙门菌对各类抗菌药物敏感性，指导临床合理使用抗菌药物。方法采用琼脂稀释法检测各类抗菌药物对95株沙门菌MIC，数据分析采用WHONET5．3软件。结果伤寒沙门菌和甲型副伤寒沙门菌对氨苄西林、氯霉素、复方磺胺甲噁唑敏感率仍分别高达96％～100％和97％～100％，未发现多重耐药株（MDR）；52％（13／25）伤寒沙门菌和94％（62／66）甲型副伤寒沙门菌对萘啶酸耐药，对环丙沙星敏感性降低（MIC=0．125～1mg／L）伤寒和甲型副伤寒沙门菌分别占24．0％（6／25）和92．4％（61／66）；1株乙型副伤寒沙门菌和1株鼠伤寒沙门菌对环丙沙星等氟喹诺酮类药物高耐药（MIC≥16mg／L），且对氨苄西林、氯霉素和复方磺胺甲口恶唑多重耐药。结论我院环丙沙星敏感性降低伤寒和甲型副伤寒沙门菌较常见，出现高耐氟喹诺酮类药物且多重耐药的乙型副伤寒沙门菌和鼠伤寒沙门菌，应加强对沙门菌耐药性监测。     

浙江省温州地区志贺菌流行菌株的血清分型及耐药性分析

目的调查志贺菌在浙江省温州地区流行的主要血清型和耐药性。方法收集临床分离的志贺菌株进行生化鉴定、血清学分型和抗生素敏感性试验。结果116株志贺菌中28 株为宋内志贺菌,占24.1%;80 株为福氏志贺菌,占68.9%(包括4 株福氏变异株,占总数的3.5%),痢疾志贺菌7株占6.0%,鲍氏志贺菌1株占0.9%。宋内志贺菌对抗菌药物的敏感率依次为氟喹诺酮类（萘啶酸为14.4%）100%、第三、四代头孢为92.9%,对复方新诺明、萘啶酸、氨苄西林呈高耐药性。福氏志贺菌对诺氟沙星、环丙沙星、莫西沙星、洛美沙星、左氟沙星的敏感率为80%左右;对三、四代头孢的敏感率为97%,但头孢噻肟的敏感率仅为22.3%。鲍氏志贺菌出现严重耐药,只有亚胺培南和美洛匹宁敏感,其他均耐药。结论温州地区志贺菌感染以福氏志贺菌和宋内志贺菌为主,福氏志贺菌中以福氏4c型为主, 其次为血清2a 型和2b型。福氏志贺菌对各种抗生素耐药性有增高趋势;并出现严重耐药菌株,必须引起临床重视。     

岳阳地区266株淋球菌药敏结果分析

[目的]了解岳阳地区淋球菌对青霉素、环丙沙星、头孢曲松钠、壮观霉素的敏感性,指导临床用药.[方法]以琼脂稀释法测定266株淋球菌对青霉素、环丙沙星、头孢曲松钠、壮观霉素的最小抑菌浓度(MIC),以监测淋球菌对临床常用的抗生素的耐药状况.[结果]4种抗生素的MIC范围依次为0.06～64 mg/L、0.03～64 mg/L、0.00～0.5 mg/L及2～64 mg/L .266株淋球菌中分别有263株、262株对头孢曲松钠敏感、壮观霉素敏感,敏感率分别为98.5%和98.1%.266株淋球菌分别有251株、241株对青霉素和环丙沙星耐药,耐药率分别为94.3%、90.4%.[结论]头孢曲松钠及壮观霉素作为治疗淋病的一线药物对淋球菌临床分离株仍相当有效,青霉素及氟喹诺酮类药物因高耐药率已不再适宜作为治疗淋球菌感染常规药物.     

解脲脲原体对喹诺酮类药物耐药性的研究

目的通过研究解脲脲原体(Uu)对目前临床使用的主要喹诺酮类药物的耐药性与敏感性,分析临床分离Uu的耐药表型和长时间低浓度喹诺酮类药物刺激对Uu耐药性产生的影响,为指导临床合理应用抗生素及经验性选择有效抗生素提供理论依据,并为后续耐药机制研究提供基础条件。方法 (1)检测就诊患者标本1123例,并收集阳性菌株,采用微量肉汤稀释法检测对喹诺酮类药物中敏的Uu株的最小抑菌浓度,分析临床分离Uu的耐药表型。(2)选10株对左氧氟沙星(LEV)敏感的Uu进行抗生素耐药诱导试验,用亚抑菌浓度(1/2MIC)左氧氟沙星持续4代刺激。结果(1)1123例样本中,筛选出Uu阳性共319株,检出率达28.4%。检出的319例Uu标本对喹诺酮类药物耐药率均比较高,以环丙沙星(CIP)及诺氟沙星(NFX)最高,达75.9%与73%;氧氟沙星(OFL)耐药率居中,达37.9%;司帕沙星(SPA)与LEV较低,分别为29.7%和27.9%。(2)对Uu喹诺酮类药物中敏的Uu菌株中,SPA与LEV活性最强,OFL次之,CIP及NFX活性最差。(3)对喹诺酮类抗菌药物中敏Uu株的第一代诱导中第9管出现亚抑菌(浓度0.5mg/L),第2代与第3代诱导后,亚抑菌管均为第7管(2mg/L),第4代诱导后,亚抑菌管为第5管(8mg/L)。结论 Uu对目前临床常用的喹诺酮类药物耐药性居高不下,加大剂量或长时间使用易产生耐药,药物敏感性测定对临床合理用药、减少耐药率具有指导意义。     

韶关地区淋球菌耐药性调查分析

目的 监测韶关地区2009年度分离的淋球菌对青霉素、四环素、大观霉素、头孢曲松和环丙沙星5种抗生素的敏感性,分析研究淋球菌的耐药性特点,为临床用药提供参考依据.方法 采用琼脂稀释法测定菌株对5种抗生素的最小抑菌浓度（MIC）,判断标准按世界卫生组织（WHO）西太区淋球菌耐药性监测统一标准.用纸片碘量法检测产β-内酰胺酶淋球菌（PPNG）菌株.结果 200株淋球菌中检出154株对青霉素耐药（77.0%）,PPNG菌株36株（占18.0%）;四环素耐药率为79.5%,其中质粒介导高度耐四环素淋球菌（TRNG）29株,占14.5%;环丙沙星耐药率为70.0%;未发现对大观霉素和头孢曲松耐药菌株.青霉素、四环素和环丙沙星的50%菌株抑菌浓度（MIC50）及90%菌株抑菌浓度（MIC90）均已超过耐药标准.结论 淋球菌对大观霉素和头孢曲松的敏感性较高,可作为治疗的首选药物,对青霉素、四环素和环丙沙星耐药率较高,提示对淋病的治疗效果差.     

空肠弯曲菌耐药谱特征分析

目的 分析十几年间我国空肠弯曲菌临床分离株对10种抗生素耐药谱特征,了解我国空肠弯曲菌耐药的变迁趋势。 方法 采用世界卫生组织(WHO)全球食源性病原菌感染网络(GFN)推荐的弯曲菌琼脂稀释法,测定1995年至今分离的116株空肠弯曲菌对6类10种抗生素的最小抑菌浓度(MIC)。 结果 经对实验结果整体分析,甲硝唑的总体耐药率最高为97.4%(113/116),四环素为82.8%(96/116),环丙沙星为80.2%(93/116),萘啶酸为79.3%(92/116),左氧氟沙星和氨苄西林耐药率相同,为40.5%(47/116),氯霉素为18.1%(21/116),庆大霉素为8.6%(10/116),链霉素为4.3%(5/116),最低为红霉素0(0/116)。随着时间的推进,萘啶酸、环丙沙星、左氧氟沙星和氨苄西林的MIC有明显增高趋势;四环素、红霉素、庆大霉素、氯霉素和甲硝唑的MIC值变化不明显;链霉素的MIC值变化有下降的趋势。6.1%的菌株出现了8种抗生素多重耐药的结果,且菌株均出现在2010年后。经统计学分析,萘啶酸、环丙沙星、链霉素、庆大霉素、氯霉素和氨苄西林6种抗生素在2001年前、2001-2005年、2006-2010年和2010年后4个时间段中耐药率差异有统计学意义。 结论 空肠弯曲菌对红霉素、庆大霉素以及链霉素3种抗生素依旧保持了较高的敏感性,对萘啶酸、环丙沙星、左氧氟沙星、四环素、甲硝唑以及氨苄西林6种抗生素产生了较大程度的耐药。     

80株大肠埃希菌靶位基因突变对喹诺酮类药物耐药的影响

目的：探讨大肠埃希菌靶位基因突变对喹诺酮类药物耐药的影响。方法：本研究分别用琼脂稀释法和K-B纸片扩散法药敏试验检测了80株致泌尿系感染的大肠埃希菌环丙沙星MIC的分布和对四种喹诺酮类药物的敏感性；PCR扩增大肠埃希菌的gyrA基因的QRDR区，并进行限制性内切酶酶切分析以检测药物靶位基因可能存在的突变。结果：80株致泌尿系感染的大肠埃希菌中有47株对环丙沙星耐药，耐药率达58．75％，20株对环丙沙星敏感的菌株gyrA基因QRDR区未发生改变，而13株敏感株和47株耐药株gyrA247bp处均存在突变，且这13株对环丙沙星敏感的菌株均对萘啶酸耐药。结论：①80株致泌尿感染的大肠埃希菌对环丙沙星的敏感性和对萘啶酸的敏感性存在明显差异。②gyrA基因是大肠埃希菌喹诺酮类药物的主要作用靶位，在某些菌株中，其247位核苷酸位点的改变仅使细菌对环丙沙星的敏感性下降，其它靶位基因的突变促进细菌的耐药程度增加。     

2018-2021年湖南省人源非O1/非O139群霍乱弧菌药物敏感性及基因组特征

目的 了解2018—2021年间湖南省从病例分离到的非O1/非O139群霍乱弧菌的药物敏感性及基因组特征。方法 选取2018—2021年间湖南省腹泻病例肠道标本分离的非O1/非O139群霍乱弧菌分离株4株和非腹泻病例血液标本分离的非O1/非O139群霍乱弧菌分离株3株,进行药物敏感性测试以及基因组序列测定,分析其药物敏感性及基因组特征。结果 3株血液样品分离株对氨苄西林、诺氟沙星、头孢曲松、美罗培南、米诺环素、复方磺胺甲恶唑、庆大霉素、头孢噻肟、萘啶酸、环丙沙星全部敏感,1株对四环素中介,1株对氯霉素耐药;4株粪便样品分离株对诺氟沙星、头孢曲松、美罗培南、米诺环素、复方磺胺甲恶唑、庆大霉素、头孢噻肟全部敏感,1株对四环素、氯霉素中介,1株对氯霉素耐药,2株对氨苄西林、环丙沙星、萘啶酸耐药;其中1株对氨苄西林、萘啶酸、环丙沙星二重耐药;1株对氨苄西林、萘啶酸、环丙沙星、氯霉素多重耐药。7株非O1/非O139群霍乱弧菌的基因组序列表现出明显的多样性,但是部分菌株在核心基因组和泛基因组都高度相似。基因组序列中均未检出ctxAB基因、VPI-1和VSPII基因组岛。分离自粪便的菌株携带耐药基因...     

深圳社区感染沙门菌耐药基因调查与同源性分析

目的 调查深圳社区感染沙门菌耐药特点和分子机制,并进行同源性分析.方法 收集深圳市人民医院2002——2007年临床分离沙门菌共93株,PCR和DNA测序分析沙门菌gyrA、gyrB、parC和parE基因QRDR的突变,PCR检测质粒介导喹诺酮耐药基因qnr和aac(6')-Ib-cr,β内酰胺酶基因blaTEM、blaSHV、blaOXA和blaCTX-M基因,以及Ⅰ类整合子,PFGE对沙门菌进行分子分型.结果 伤寒沙门菌和甲型副伤寒沙门菌对氨苄西林、氯霉素、复方磺胺甲噁唑、头孢曲松和环丙沙尾敏感率为96%～100%;52%(13/25)伤寒沙门菌和95%(61/64)甲型副伤寒沙门菌对萘啶酸耐药.24%(6/25)萘啶酸耐药伤寒沙门菌和94%(60/64)萘啶酸耐药甲型副伤寒沙门菌对环丙沙星敏感性降低(MIC 0.125～μg/ml).75株萘啶酸耐药环丙沙星敏感沙门菌仅GyrA的QRDR均存在第83位或87位单个氨基酸替代,其中Ser83Phe突变占91%(68/75).2株环丙沙星耐药沙门菌在QRDR中均携带GyrA上2个点突变和parC上1个点突变.93株沙门菌均未发现质粒介导的qnr和aac(6')-Ib-cr 基因.1株头孢曲松耐药甲型副伤寒沙门菌检测到blaCTX-M-14基因,且该基因上游存在插入序列ISEcpl.3株多重耐药沙门菌均存在一个1 900 bp的Ⅰ类整合子,其基因盒均为dhfrⅫ-orfF-aadA2,同时携带blaTEM-1或blaOXA-30基因.25株伤寒沙门菌共有22种不同的PFGE带型,64株甲型副伤寒沙门菌的PFGE带型平均相似性为91%.90例患者均系社区感染,6例甲型副伤寒患者发病前30天内曾前往外地旅行.结论 深圳社区感染伤寒和甲型副伤寒沙门菌对萘啶酸耐药率较高,沙门菌GyrA的QRDR点突变是萘啶酸耐药的重要机制,甲型副伤寒沙门菌菌株间遗传同源性极高,来自同一克隆.

Abstract：

Objective To investigate the antimicrobial resistance mechanisms and genetic homogeny of Salmonella from community acquired infections in Shenzhen,China.Methods Ninety-three of Salmonella were isolated from 2002 to 2007 at Shenzhen People's Hospital,China.PCR and DNA sequencing were used to investigate the mutation in QRDR of the gyrA,gyrB,parC and parE.Plasmid mediated quinolone resistance genes including qnr and aac(6')-Ib-cr,β-lactamase genes including blaTEM,blaSHV,blaOXA, blaCTX-M, and class 1 integron were detected. All isolates were typed by PFGE. Results S. enterica typhi and S. enterica paratyphi A were susceptible to ampicillin, chloramphenicol, trimethoprim/sulfamethoxazole, ceftriaxone and ciprofloxacin, with the susceptible rate of 96%-100%. Fifty-two percent (13/25) of S. enterica typhi and 95% (61/64) of S. enterica paratyphi A were resistant to nalidixic acid. Twenty-four percent (6/25) of nalidixic acid-resistant S. enterica typhi and 94% (60/64) of nalidixic acid-resistant S. enterica paratyphi A showed decreased susceptibility to ciprofloxacin (MIC of 0. 125-1 μg/ml).All nalidixic acid-resistant (susceptible to ciprofloxacin ) Salmonella (NARS) isolates had a single substitution in the QRDR of GyrA, and 91% (68/75) of these isolates carried the substitution Ser83Phe in GyrA. Two mutations in the QRDR of GyrA were detected in both of two ciprnfloxacin-resistant Salmonella,with the additional one mutation in the QRDR of parC. Plasmid mediated quinolone resistance genes including qnr and aac(6')-lb-cr were not detected in any isolate. The blaCTX-M-14 gene was detected in a ceftriaxoneresistant isolate of S. enterica paratyphi A, with ISEcpl located on the upstream of it. Three muhidrugresistant strains of Salmonella all carried one 1 900 bp classⅠ integron gene cassette dhfrⅫ-orfF-aadA2,with the additional one β-lactamase gene of blaTEM-1, or blaOXA-30. Twenty-two distinct PFGE patterns were observed among twenty-five S. enterica typhi. The PFGE patterns of sixty-four S. enterica paratyphi A showed limited genetic diversity (average similarity of 91% ). Ninety investigated inpatients were infected in the community. Six patients infected by S. enterica paratyphi A had a travel history before infection. Conclusions Nalidixic acid-resistant S. enterica typhi and S. enterica paratyphi A are highly prevalent in Shenzhen,China. The mutation in the QRDR of GyrA is the prevalent mechanism responsible for the resistance to nalidixic acid in Slmonella. The great genetic similarity among S. enterica paratyphi A isolates indicates endemic disease from the presence of a single clone over 6-year period.     

2014-2017年上海市闵行区副溶血弧菌的耐药性分析及预测

目的 探讨副溶血弧菌对11种抗生素的耐药谱,敏感株的敏感性变化趋势并进行耐药预测。方法 收集2014-2017年上海市闵行区腹泻病监测点分离的副溶血弧菌,用K-B法测定其对头孢噻肟（CTX）、头孢呋辛（CXM）、头孢西丁（FOX）、环丙沙星（CIP）、诺氟沙星（NOR）、左氧氟沙星（LEV）、四环素（TE）、庆大霉素（CN）、萘啶酸（NA）、氯霉素（C）、复方新诺明（SXT）的敏感性。用单因素方差分析比较不同年份的抑菌圈直径差异,并分析其耐药趋势。结果 副溶血弧菌对CTX、CXM、FOX的耐药率分别为1.89%、19.40%和1.60%,中度耐药率分别为8.94%、39.24%和11.55%,对其他8种抗生素的敏感率均>94.00%。CTX、NA的敏感株抑菌圈直径有明显逐年减小趋势。预测副溶血弧菌可能分别在2021、2023年对CTX、NA中度耐药;2024、2027年耐药。结论 副溶血弧菌敏感株对抗生素的敏感性有逐年降低趋势,预计未来可能3~10年内敏感株逐渐耐药。     

Relationships among ciprofloxacin, gatifloxacin, levofloxacin, and norfloxacin MICs for fluoroquinolone-resistant Escherichia coli clinical isolates

Fluoroquinolones are some of the most prescribed antibiotics in the United States. Previously, we and others showed that the fluoroquinolones exhibit a class effect with regard to the CLSI-established breakpoints for resistance, such that decreased susceptibility (i.e., an increased MIC) to one fluoroquinolone means a simultaneously decreased susceptibility to all. For defined strains, however, clear differences exist in the pharmacodynamic properties of each fluoroquinolone and the extent to which resistance-associated genotypes affect the MICs of each fluoroquinolone. In a pilot study of 920 clinical Escherichia coli isolates, we uncovered tremendous variation in norfloxacin MICs. The MICs for all of the fluoroquinolone-resistant isolates exceeded the resistance breakpoint, reaching 1,000 microg/ml. Approximately 25% of the isolates (n = 214), representing the full range of resistant norfloxacin MICs, were selected for the simultaneous determinations of ciprofloxacin, gatifloxacin, levofloxacin, and norfloxacin MICs. We found that (i) great MIC variation existed for all four fluoroquinolones, (ii) the ciprofloxacin and levofloxacin MICs of >90% of the fluoroquinolone-resistant isolates were higher than the resistance breakpoints, (iii) ciprofloxacin and levofloxacin MICs were distributed into two distinct groups, (iv) the MICs of two drug pairs (ciprofloxacin and norfloxacin by Kendall's Tau-b test and gatifloxacin and levofloxacin by paired t test) were similar with statistical significance but were different from each other, and (v) approximately 2% of isolates had unprecedented fluoroquinolone MIC relationships. Thus, although the fluoroquinolones can be considered equivalent with regard to clinical susceptibility or resistance, fluoroquinolone MICs differ dramatically for fluoroquinolone-resistant clinical isolates, likely because of differences in drug structure.     

Emergence of in vitro resistance to fluoroquinolones in Neisseria gonorrhoeae isolated in Japan.

To investigate emerging fluoroquinolone resistance in Neisseria gonorrhoeae isolated in Japan, we compared the in vitro antimicrobial susceptibilities of 79 gonococcal isolates from 1992 through 1993 to 14 fluoroquinolones and 14 other antibiotics with those of 27 isolates from between 1981 and 1984. The MICs at which 90% of the isolates were inhibited by nine fluroquinolones, including norfloxacin, enoxacin, ofloxacin, ciprofloxacin, tosufloxacin, lomefloxacin, fleroxacin, levofloxacin, and sparfloxacin, for isolates from 1992 to 1993 were 8- or 16-fold higher than those for isolates from 1981 to 1984. Furthermore, the MICs at which 90% of the isolates were inhibited by five fluroquinolones, including OPC-17116, T-3761, DU-6859a, AM-1155, and Q-35, that have recently been synthesized but have not yet been introduced for clinical use in Japan for isolates from 1992 to 1993 were also 2- to 16-fold higher than those for isolates from 1981 to 1984. The gonococcal isolates from 1992 to 1993 showed no significant decreases in susceptibility to beta-lactams, tetracyclines, macrolides, and spectinomycin, compared with those for isolates from 1981 to 1984. Our data indicate that the incidence of gonococcal strains with decreased susceptibilities to fluoroquinolones is increasing in Japan.     

Mupirocin resistance in methicillin-resistant Staphylococcus aureus clinical isolates in a Spanish hospital. Co-application of multiplex PCR assay and conventional microbiology methods

A total of 33 Stenotrophomonas maltophilia clinical isolates were tested for their susceptibility to clinafloxacin in comparison with ciprofloxacin, levofloxacin, moxifloxacin, nalidixic acid, norfloxacin, sparfloxacin and trovafloxacin. The MIC(50) and MIC(90) were as follows: ciprofloxacin 4 and 64 microg/mL; clinafoxacin 0.5 and 4 microg/mL; levofloxacin 2 and 32 microg/mL; moxifloxacin 1 and 8 microg/mL; nalidixic acid 8 and 128 microg/mL; norfloxacin 64 and 256 microg/mL; sparfloxacin 1 and 16 microg/mL; and trovafloxacin 1 and 8 microg/mL. Clinafloxacin was the most active quinolone, with only a 15.1% of strains showing resistance. When the MICs were determined in the presence of 25 microg/ml of reserpine, the MIC(90) of trovafloxacin and moxifloxacin did not change, whereas decreased 2-fold for clinafloxacin, levofloxacin, sparfloxacin and nalidixic acid, and 4- and 8-fold for ciprofloxacin and norfloxacin respectively. No clinafloxacin-resistant strains were observed when the MIC was performed in the presence of reserpine. Therefore, clinafloxacin shows the better "in vitro"activity against these 33 strains of S.maltophilia.     

香港海鸥型菌耐喹诺酮类抗菌药物机制的研究

目的建立香港海鸥型菌生物被膜体外模型,对香港海鸥型菌携带的Ⅰ类整合子相关基因进行分析,探讨香港海鸥型菌耐喹诺酮类抗菌药物的机制。方法吉姆萨染色法形态学角度分析及生结晶紫染色法半定量检测香港海鸥型菌临床分离株生物被膜的形成能力;微量肉汤稀释法测定香港海鸥型菌临床分离株在浮游生长状态与生物被膜状态下对诺氟沙星、氧氟沙星、左氧氟沙星、环丙沙星、洛美沙星的敏感性;PCR法检测耐喹诺酮类香港海鸥型菌菌株携带的Ⅰ类整合子相关基因。结果吉姆萨染色法定性结果显示,在55株香港海鸥型菌临床分离株中,有36株形成生物被膜,生物被膜形成率为65.4%(36/55);结晶紫染色法半定量检测香港海鸥型菌生物被膜的形成能力,其中8株香港海鸥型菌的吸光度OD560≤0.15,16株香港海鸥型菌的吸光值0.15OD560≤0.20,7株香港海鸥型菌的OD5600.20;诺氟沙星、氧氟沙星、左氧氟沙星、环丙沙星、洛美沙星对香港海鸥型菌的最小生物被膜抑菌浓度均高于相应浮游菌的最小抑菌浓度(P0.05);55株香港海鸥菌中共有18株耐喹诺酮类药物,耐药率32.7%,且18株香港海鸥型菌菌Ⅰ类整合子均含有耐药基因,该耐药基因在相应菌株中发挥耐药作用。结论香港海鸥型菌耐喹诺酮类基因的形成和耐药基因的播散可能与Ⅰ类整合子有关。     

Emergence of quinolone resistance among clinical isolates of methicillin-resistant Staphylococcus aureus in Ontario, Canada.

One hundred two isolates of methicillin-resistant Staphylococcus aureus (MRSA) randomly selected from across the Canadian province of Ontario were tested for their susceptibility to ciprofloxacin, norfloxacin, and nalidixic acid by the agar dilution method. Forty-nine percent (50 of 102) had high levels of resistance to these quinolone compounds. For the 50 resistant isolates, ciprofloxacin and norfloxacin had high MICs for 90% of isolates (MIC90s) of 128 micrograms/ml and greater than 128 microgram/ml, respectively; for these isolates, the nalidixic acid MIC90 was greater than 640 micrograms/ml. The majority (98%) of the 50 isolates were also resistant to tobramycin (MIC90, greater than 128 micrograms/ml), while 42% of the isolates were resistant to gentamicin (MIC90, 64 micrograms/ml). Quinolone-resistant MRSA isolates were susceptible to bacteriophages from several groups, indicating independent selection of resistant strains. These results suggest that a reappraisal of the use of fluoroquinolones against MRSA in Canada is necessary.     

Differing activities of quinolones against ciprofloxacin-susceptible and ciprofloxacin-resistant, methicillin-resistant Staphylococcus aureus.

The in vitro activities of nine quinolones (seven fluoroquinolones, nalidixic acid, and acrosoxacin) against methicillin-resistant Staphylococcus aureus (MRSA) were compared with those of the glycopeptides teicoplanin and vancomycin. MICs against 160 strains of ciprofloxacin-susceptible (MIC, less than 2.0 micrograms/ml) MRSA and 40 strains of ciprofloxacin-resistant (MIC, greater than or equal to 2.0 micrograms/ml) MRSA were determined. The following MICs for 50% of the strains tested (in micrograms per milliliter) were obtained for ciprofloxacin-susceptible and -resistant strains, respectively: tosufloxacin, 0.06 and 2.0; ofloxacin, 0.25 and 16; ciprofloxacin, 0.5 and 16; pefloxacin, 0.5 and 32; acrosoxacin, 1.0 and greater than 256; enoxacin, 1.0 and 64; fleroxacin, 1.0 and 32; norfloxacin, 2.0 and 64; nalidixic acid, 64 and 512; teicoplanin, 1.0 and 1.0; vancomycin, 2.0 and 2.0. In mutation rate studies using a range of antibiotic concentrations to reflect those achievable in vivo, resistant mutants grew only on plates containing nalidixic acid (rate of mutation to resistance, 10(-7) to 10(-8) and on plates containing low concentrations of ciprofloxacin, enoxacin, and norfloxacin (rate of mutation to resistance, 10(-8) to 10(-9). In time-kill studies, 99.9% killing was found within 8 h for all of the quinolones tested (norfloxacin and nalidixic acid were not tested). Teicoplanin and vancomycin were less rapidly bactericidal. For the clinical isolates of ciprofloxacin-resistant MRSA, different levels and patterns of quinolone resistance were found. Generally, cross-resistance among the fluoroquinolones was complete; however, incomplete cross-resistance did occur with the nonfluorinated quinolone acrosoxacin.     

Decreased susceptibility to fluoroquinolones and gyrA gene mutation in the Salmonella enterica serovar Typhi and Paratyphi A isolated in Katmandu, Nepal, in 2003

Typhoid fever is the most common clinical diagnosis among febrile patients presenting to hospital in Katmandu. Salmonella enterica serovar Typhi (S. enterica serovar Typhi) and Salmonella enterica serovar Paratyphi A (S. enterica serovar Paratyphi A) with decreased susceptibility to fluoroquinolones and resistance to nalidixic acid are common in recent years. In the present study, we examined the in vitro susceptibility to fluoroquinolones and the presence of gyrA gene mutations in 30 clinical strains of S. Typhi and 39 of S. Paratyphi A, all of which were isolated in Katmandu, Nepal, in 2003. In those strains, we found that 73.3% and 94.9% of S. Typhi and S. Paratyphi A strains contained gyrA gene mutation, and showed the resistance to a quinolone, nalidixic acid, and decreased susceptibility to fluoroquinolones, ciprofloxacin, and levofloxacin. Although fluoroquinolones may still be useful as antibiotics for the treatment of typhoid fever, clinicians should be aware of the possibility of treatment failures of infections with S. Typhi and S. Paratyphi A strains with decreased susceptibility to fluoroquinolones.