肺炎链球菌大环内酯类抗生素的耐药性分析

目的 本研究通过对肺炎链球菌耐药表型检测分析,掌握本地区肺炎链球菌耐药的现状和趋势.方法 本文用E试验和K-B纸片扩散法检测84株肺炎链球菌临床分离株对9种抗生素的敏感性;用双纸片法确定大环内酯类耐药表型.结果 84株肺炎链球菌红霉素耐药占85.7%(72/84),对青霉素不敏感率达57.1%(48/84).左氧氟沙星、阿莫西林/克拉维酸对该组细菌有较好的体外活性,敏感率分别为83.3%(70/84)和88.1%(74/84).结论 肺炎链球菌对大环内酯耐药严重,且表现对四环素、复方磺胺甲噁唑、青霉素等多重耐药;南昌地区大环内酯类耐药表型主要以cMLSB为主.     

肺炎链球菌大环内酯类耐药表型与相关基因的关系

目的了解肺炎链球菌临床分离株红霉素耐药基因的流行情况和耐药表型的关系。方法对42株肺炎链球菌用E-试验和K-B纸片扩散法检测其对10种抗生素的敏感性;用红霉素和克林霉素双纸片协同试验确定其耐药表型;用PCR扩增这些菌株的耐药基因ermB、mefA和mefE。结果 42株肺炎链球菌中耐药基因ermB总检出率为95.2%(40/42),mefE总检出率为26.1%(11/42),未检出mefA基因。耐药基因组合ermB(+)mefE(-)和ermB(+)mefE(+)占95.2%,两者均呈cMLSB耐药表型。ermB(-)mefE(+)占4.8%(2/42),耐药表型为M型。结论耐药基因ermB导致的cMLSB耐药是大环内酯类耐药的主要原因。大环内酯类抗生素已不是治疗肺炎链球菌的有效药物。     

乐清地区儿童肺炎链球菌耐药性及大环内酯类耐药表型和耐药基因型

目的：了解乐清地区儿童患者分离的肺炎链球菌耐药性及大环内酯类耐药表型和耐药基因型分布情况。方法对2014年乐清地区儿童患者分离的124株肺炎链球菌采用细菌鉴定分析仪进行9种抗菌药物的最低抑菌浓度（MIC）检测,同时对大环内酯类耐药肺炎链球菌用红霉素和克林霉素双纸片协同试验确定其耐药表型,用聚合酶链反应（PCR）扩增这些菌株的耐药基因ermB和mefE。结果124株肺炎链球菌中,红霉素、克林霉素、四环素和复方新诺明的耐药率依次为96.77％、93.55％、84.68％和81.45％;青霉素、氯霉素和左旋氧氟沙星的耐药率较低,分别为20.16％、5.65％和0.81％,未发现对阿莫西林/克拉维酸和万古霉素耐药的菌株。120株大环内酯类耐药肺炎链球菌中,大环内酯类耐药表型cMLS占96.67％、iMLS占0.83％、M型占2.50％;耐药基因ermB检出率为97.50％,mefE的检出率为6.67％。结论乐清地区儿童肺炎链球菌对大环内酯类抗生素的耐药性严重,ermB基因介导的cMLS型耐药是大环内酯类耐药的主要原因,大环内酯类抗生素已不是治疗乐清地区儿童肺炎链球菌感染的有效药物。     

青霉素Etest法评价肺炎链球菌苯唑西林的纸片筛选试验

目的 青霉素Etest法评价肺炎链球菌苯唑西林的纸片筛选试验。方法 对临床分离的96株肺炎链球菌非脑膜炎株,用Etest作为测定青霉素敏感性的标准方法,评价苯唑西林的纸片筛选试验的灵敏度和特异性。结果 96株肺炎链球菌非脑膜炎株,用Etest测定青霉素敏感株(PSSP)为96.9%(93/96),青霉素中度敏感株(PISP)为3.1%(3/96),未发现青霉素耐药株(PRSP)。苯唑西林纸片法初筛出16株PSSP,灵敏度为17.2%,特异性为100.0%。苯唑西林纸片法与Etest方法比较,差异有统计学意义(χ2=77,P<0.01)。结论 苯唑西林纸片法作为肺炎链球菌非脑膜炎株青霉素注射剂敏感性的初筛方法灵敏度低,大部分肺炎链球菌必须用Etest等MIC方法检测。     

52株肺炎链球菌耐药性分析

目的调查分析临床标本分离到肺炎链球菌对青霉素等17种抗生素的体外抗菌活性,为临床治疗肺炎链球菌感染提供参考.方法对我院从2003年1月至2005年7月临床标本分离到的52株肺炎链球菌,用美国DADE-BEHRING公司的MICro STREP Plus链球菌药敏测定板检测肺炎链球菌对17种不同抗菌药物的MIC值.结果52株肺炎链球菌对红霉素、四环素的耐药率最高达71.2%,5株对青霉素耐药(9.6%),18株对青霉素低度耐药(34.6%),29株对青霉素敏感(55.8%),对阿奇霉素、克林霉素的耐药率为63.5%,对万古霉素、阿莫西林/棒酸、加替沙星的耐药率为0.00%.青霉素不敏感菌株对红霉素、阿奇霉素、克林霉素、氯霉素、头孢克洛、头孢呋辛的耐药率显著高于敏感株.结论肺炎链球菌对大环内酯类和四环素耐药率高,对青霉素以低度耐药为主,喹喏酮类药物和阿莫西林/棒酸刘肺炎链球菌抗菌活性较高,可作为首选药物.     

肺炎链球菌对抗菌药物的耐药性调查及对大环内酯类抗生素耐药机制研究

目的：调查成都地区肺炎链球菌对抗菌药物的敏感性，研究成都地区肺炎链球菌对大环内酯类抗生素耐药机制。方法：收集2001年9月-2002年9月成都地区临床分离的肺炎链球菌，测定其对13种抗菌药物的耐药性及对大环内酯类抗生素的耐药表型；用聚合酶链反应(PCR)扩增耐药基因ermB和mefA，并对ermB和mefA进行基因序列分析。结果：82株肺炎链球菌中13株对青霉素低度耐药(占15．9％),肺炎链球菌对大环内酯类抗生素和克林霉素表现出较高的耐药率，对红霉素和克林霉素耐药率分别为80．5％(66／82)和68．3％(56／82)。耐大环内酯类肺炎链球菌中,96．4％菌株表现为内在型耐药。标准菌株ATCC49619及16株红霉素敏感菌株均未检测到ermB基因及mefA基因；ermB基因和；mefA基因分别在62和11株耐红霉素肺炎链球菌中检测到，其中7株菌同时检测到ermB基因和mefA基因。所测ermB和mefA基因序列与基因库收录序列高度一致。结论：成都地区临床分离的肺炎链球菌对青霉素耐药率较低，但对大环内酯类抗生素和克林霉素耐药却非常普遍。ermB基因介导的靶位改变是成都地区肺炎链球菌对大环内酯类抗生素的主要耐药机制。     

A群β溶血性链球菌药敏试验及大环内酯抗生素耐药基因检测

目的 研究我国儿科A群β溶血性链球菌(GAS)临床分离株抗菌药物敏感性情况.方法 收集5所儿童医院2005-2006年222株GAS感染的临床菌株,采用琼脂稀释法测定11种抗菌药物的MIC值;诱导试验分析大环内酯类抗生素耐药表型;PCR检测大环内酯类抗生素耐药基因ermB、ermTR和mefA.结果 分离株对大环内酯类抗生素和克林霉素耐药率在93.69%～98.65%,MIC90＞512 rag/L;对四环素的耐药率为94.14%;对青霉素、头孢他啶的敏感率高达100%.分离株大环内酯类抗生索耐药以耐大环内酯类、林可酰胺类和链阳性菌素B表型(cMLS)为主,占99.04%.iMLS表型仅2株,未检测到M型;ermB、ermTR和mef似阳性率分别为94.71%、2.89%和0.结论 所测儿科GAS感染流行菌株对大环内酯类抗生素和克林霉素耐药率高.主要耐药机制为ermB编码的23SrRNA甲基化酶导致靶位改变,青霉素类和头孢菌素类抗生素是治疗我国GAS感染首选药物.     

肺炎链球菌对大环内酯类抗生素耐药及传播机制研究

目的 研究上海3所医院临床分离肺炎链球菌对大环内酯类抗生素的耐药机制及传播方式。方法收集上海市3所医院临床分离的红霉素耐药肺炎链球菌共118株，用E试验和K-B纸片扩散法检测对12种抗菌药的敏感度；用双纸片法（D试验）确定大环内酯类耐药表型；用PCR扩增检测耐药基因ermB、mefA、mefE、msrD及Tn1545-Tn916家族转座子整合酶基因intTn；用转化试验证实耐药传播方式。结果①118株肺炎链球菌对红霉素的MIC范围为4-256mg／L，其中5．9％对克林霉素敏感，对青霉素不敏感率达72．7％。左氧氟沙星、阿莫西林-克拉维酸对红霉素耐药的肺炎链球菌仍有较好的体外活性；②该组细菌耐药基因ermB检出率为88．1％，mefE、msrD检出率各为50％，未检出，mefA基因，转座子整合酶基因intTn检出率达97．5％。耐药基因组合模式以ermB（＋）reefE（＋）msrD（＋）intTn（＋）和ermB（＋）mefE（-）msrD（-）intTn（＋）为主，两者均为cMLSB型耐药。ermB（-）mefE（＋）msrD（＋）intTn（＋）模式占5．9％，耐药表型为M型。③cMLSB型耐药代表菌株ET37和M型耐药代表菌株RJ324基因组DNA均成功转化敏感株，使之表现红霉素耐药性并可传代。结论上海地区肺炎链球菌对大环内酯抗生素耐药以ermB介导的cMLSB耐药表型为主；大环内酯外排基因有流行趋势，但仅限于起源于肺炎链球菌的，mefE。耐药基因可以转化方式进行传播，转座子可能在本地区肺炎链球菌耐药基因的传播中起重要作用。     

肺炎链球菌对大环内酯-林可酰胺-链阳菌素的耐药监测及耐药机制研究

目的研究肺炎链球菌对大环内酯-林可酰胺-链阳菌素类抗菌素的耐药机制。方法K-B纸片法测定肺炎链球菌对红霉素、克林霉素、泰利霉素和喹奴普汀/达福普汀的耐药性。对全部红霉素耐药菌株和部分红霉素敏感菌株用聚合酶链反应(PCR)检测ermB和mefA基因。结果97株肺炎链球菌对红霉素、克林霉素、泰利霉素和喹奴普汀/达福普汀的耐药率分别为60.8%、58.8%、0和0。59株红霉素耐药菌株均检出ermB和/或mefA基因,其中34株(57.6%)ermB阳性,18株(30.5%)ermB和mefA同时阳性,7株(11.8%)mefA阳性。5株敏感菌株ermB和mefA基因均为阴性。结论本研究显示肺炎链球菌对泰利霉素和喹奴普汀/达福普汀高度敏感,而对红霉素和林可霉素则表现出较高的耐药性。肺炎链球菌对大环内酯-林可酰胺-链阳菌素的耐药机制以ermB基因介导的靶位改变为主。     

泌尿生殖道分离无乳链球菌药物敏感性分析

目的了解泌尿生殖道无乳链球菌感染及耐药状况,为临床用药提供依据。方法对临床送检的泌尿生殖道标本常规培养鉴定,并对分离出的无乳链球菌进行纸片扩散法药敏试验,对红霉素耐药、克林霉素敏感的菌株做D试验检测。结果144株无乳链球菌(尿77株,前列腺液36株,阴道分泌物31株)药敏结果显示,对万古霉素、利奈唑胺、青霉素和头孢曲松的耐药率最低,全部144株无乳链球菌中未发现耐药株;左氧氟沙星的耐药率较低,为16.2%;红霉素和克林霉素耐药率较高,分别为56.2%和53.5%。D试验阳性率为26.7%。结论从泌尿生殖道分离的无乳链球菌对青霉素、氨苄西林和头孢菌素类抗菌药物的敏感性较高,但对大环内酯类和克林霉素已有一定的耐药。     

Antimicrobial susceptibility patterns and macrolide resistance genes of viridans group streptococci from blood cultures in Korea

OBJECTIVES: Our aim was to study the antimicrobial susceptibilities and macrolide resistance mechanisms of viridans group streptococci (VGS) in a Korean tertiary hospital. METHODS: MICs of five antimicrobials were determined for 106 VGS isolated from blood cultures. The macrolide resistance mechanisms of erythromycin non-susceptible isolates were studied by the double-disc test and PCR. RESULTS: In all, 42.4% of the isolates were susceptible to penicillin. Nine of 61 penicillin non-susceptible isolates were fully resistant (MIC >/= 4 mg/L). Rates of non-susceptibility to erythromycin, clindamycin and ceftriaxone were 33.9%, 17.9% and 9.4%, respectively. Twenty-two (61.1%) of 36 erythromycin non-susceptible isolates expressed constitutive resistance to macrolide-lincosamide-streptogramin B antibiotics (a constitutive MLS(B) phenotype); 13 isolates (36.1%) expressed an M phenotype; and one isolate, a Streptococcus bovis isolate, had an inducible MLS(B) resistance phenotype. erm(B) was found in isolates with constitutive/inducible MLS(B) phenotypes, and mef(A) in isolates with the M phenotype. In three isolates (two isolates with a constitutive MLS(B) phenotype and in one isolate with the M phenotype), none of erm(A), erm(B), erm(C) or mef(A) was detected by PCR. CONCLUSIONS: Penicillin non-susceptible VGS were more resistant to erythromycin, clindamycin and ceftriaxone than were penicillin-susceptible isolates. A constitutive MLS(B) phenotype associated with erm(B) was the predominant mechanism of macrolide resistance among erythromycin non-susceptible isolates from this Korean hospital.     

Phenotypes of macrolide resistance of group A streptococci isolated from outpatients in Bavaria and susceptibility to 16 antibiotics

The purpose of the present study was to determine the antimicrobial resistance among Streptococcus pyogenes in Bavaria, Germany. Five hundred and forty isolates of S. pyogenes were collected from patients with tonsillopharyngitis. Of these, 425 isolates were obtained from children and 115 from adult patients. All isolates were tested for susceptibility to macrolides, clindamycin, penicillin and 10 other commonly prescribed antimicrobial agents, using broth microdilution tests. All isolates were fully susceptible to penicillin, amoxicillin and cephalosporins; 16.1% of the isolates were resistant to tetracycline. MIC(90) values of erythromycin, clarithromycin, azithromycin and josamycin were 16, 4, 16 and 0.5 mg/L. The overall resistance rate of S. pyogenes to erythromycin, clarithromycin and azithromycin was 13.3%. All isolates resistant to erythromycin were also resistant to clarithromycin and azithromycin, and vice versa. Erythromycin resistance rates were higher in adult patients (19.1%) than in children (11.8%). The resistance rate to josamycin was only 1.5%, a value similar to that of clindamycin (1.1%). Among the 72 erythromycin-resistant isolates the M phenotype of macrolide resistance predominated (78%), while percentages of cMLS(B) (8%) and iMLS(B) (14%) phenotypes were low. Of the iMLS(B) strains (n = 10), the majority were of the subtype C (n = 8). The M phenotype was associated with a low, and the iMLS(B)-C phenotype with a high, rate of resistance to tetracycline. Conclusively, present data point to rising macrolide resistance among S. pyogenes in Bavaria.     

Antibiotic resistance patterns of aerobic coryneforms and furazolidone-resistant Gram-positive cocci from the skin surface of the human axilla and fourth toe cleft

Samples of skin surface bacteria from 28 healthy subjects plated directly on to selective and non-selective media revealed that the proportion of aerobic coryneforms and furazolidone-resistant Gram-positive cocci (FURECs) resistant to erythromycin was significantly greater in the fourth toe cleft than in the axilla (P < 0.05). There were more erythromycin-resistant bacteria than tetracycline-resistant bacteria at both sites (P = 0.001 for the toe cleft; P < 0.01 for the axilla). In total, 160 distinct isolates were obtained, of which 42 were FURECs and 118 were aerobic coryneforms. Of these, 153 (96%) were resistant to erythromycin and 66 (41%) to tetracycline. All except seven of the tetracycline-resistant strains were also resistant to erythromycin. The resistant isolates belonged to a variety of species. CDC group ANF corynebacteria were most numerous and composed 31% of all isolates. The majority (76%) of FURECs were identified as Micrococcus luteus. MIC determinations on selected strains revealed that tetracycline-resistant FURECs were sensitive to doxycycline and minocycline, as were most tetracycline-resistant coryneforms. Nine coryneform isolates were cross-resistant to all three tetracyclines. Only a minority of erythromycin-resistant FURECs (21%) demonstrated a macrolide-lincosamide-streptogramin type B (MLS)-resistant phenotype with inducible or constitutive cross-resistance to clindamycin and the type B streptogramin, pristinamycin IA. Twenty-nine erythromycin-resistant FURECs had a novel phenotype distinct from MLS and macrolide-streptogramin type B resistance. In contrast, most coryneforms (79%) were MLS resistant. Among the remainder, two unusual erythromycin resistance phenotypes were apparent, both of which differed from the unusual phenotype in FURECs. This study has revealed that the non-staphylococcal aerobic flora of skin contains a considerable reservoir of tetracycline and erythromycin resistance determinants. The three unusual macrolide resistance phenotypes may be associated with novel resistance mechanisms.     

肺炎链球菌对大环内酯类抗生素耐药机制研究

目的了解肺炎链球菌对大环内酯类抗生素的耐药机制和转座子整合酶的流行情况。方法188株红霉素耐药肺炎链球菌，用E试验和K—B纸片扩散法检测其对11种抗菌药物的敏感性；用双纸片法（红霉素和克林霉素）确定其耐药表型；用PCR扩增这些菌株的耐药基因ermB、mefa、mefE、tetM及转座子整合酶基因intTn。结果188株红霉素耐药株中耐药基因ermB总检出率为91．5％（172／188），mefE总检出率为38．3％，未检出mefA基因。97．9Yoo的红霉素耐药株中存在转座子整合酶intTn。耐药基因组合ermB（＋）mefE（-）和ermB（＋）mef（＋），占91．5％，两者均呈cMLSB耐药表型。ermB（-）mefE（＋）占8．5％，耐药表型为M型。结论我院分离的肺炎链球菌大环内酯耐药以errnB介导的cMLS。耐药表型为主。转座子可能在本地区肺炎链球菌耐药基因的水平转移和克隆播散中起重要作用。     

Macrolide resistance determinants of group A streptococci in Ankara,Turkey

OBJECTIVES: Macrolide-lincosamide-streptogramin B (MLSB) resistance determinants of group A streptococci (GAS) in Ankara, Turkey, were defined for the first time. ISOLATES AND METHODS: A total of 1355 GAS isolates, collected from three different regions of Ankara, were screened for erythromycin resistance. Resistance phenotypes were determined by a triple-disc test, and the gene determinants responsible were determined by PCR. MICs of erythromycin, clindamycin and spiramycin were measured for the resistant isolates, and susceptibility rates to some further antibiotics were determined. RESULTS: Thirty-six isolates (2.6%) were resistant to erythromycin. Of these, 17 (47.2%) expressed macrolide-restricted resistance (M phenotype), while the remainder expressed inducible (16 isolates, 44.4%) or constitutive (three isolates, 8.3%) MLSB resistance. All isolates of the M phenotype harboured the mef(A) gene. Of non-M isolates, 14 harboured erm(A) subclass erm(TR) and five had erm(B) genes. There was a significant relationship between tetracycline resistance and the inducible phenotype (P < 0.05). Macrolide resistance was significantly higher in adults (P < 0.05), and increased more than two-fold in 2002 compared with 2001 (P < 0.05). CONCLUSION: The prevalence of macrolide resistance in GAS is low in Ankara; therefore, routine antimicrobial susceptibility testing against these agents seems unwarranted.     

Phenotypes and Genotypes of Erythromycin-Resistant Streptococcus pyogenes Strains in Italy and Heterogeneity of Inducibly Resistant Strains

A total of 387 clinical strains of erythromycin-resistant (MIC, >/=1 microg/ml) Streptococcus pyogenes, all isolated in Italian laboratories from 1995 to 1998, were examined. By the erythromycin-clindamycin double-disk test, 203 (52.5%) strains were assigned to the recently described M phenotype, 120 (31.0%) were assigned to the inducible macrolide, lincosamide, and streptogramin B resistance (iMLS) phenotype, and 64 (16.5%) were assigned to the constitutive MLS resistance (cMLS) phenotype. The inducible character of the resistance of the iMLS strains was confirmed by comparing the clindamycin MICs determined under normal testing conditions and those determined after induction by pregrowth in 0.05 microg of erythromycin per ml. The MICs of erythromycin, clarithromycin, azithromycin, josamycin, spiramycin, and the ketolide HMR3004 were then determined and compared. Homogeneous susceptibility patterns were observed for the isolates of the cMLS phenotype (for all but one of the strains, HMR3004 MICs were 0.5 to 8 microg/ml and the MICs of the other drugs were >128 microg/ml) and those of the M phenotype (resistance only to the 14- and 15-membered macrolides was recorded, with MICs of 2 to 32 microg/ml). Conversely, heterogeneous susceptibility patterns were observed in the isolates of the iMLS phenotype, which were subdivided into three distinct subtypes designated iMLS-A, iMLS-B, and iMLS-C. The iMLS-A strains (n = 84) were highly resistant to the 14-, 15-, and 16-membered macrolides and demonstrated reduced susceptibility to low-level resistance to HMR3004. The iMLS-B strains (n = 12) were highly resistant to the 14- and 15-membered macrolides, susceptible to the 16-membered macrolides (but highly resistant to josamycin after induction), and susceptible to HMR3004 (but intermediate or resistant after induction). The iMLS-C strains (n = 24) had lower levels of resistance to the 14- and 15-membered macrolides (with erythromycin MICs increasing two to four times after induction), were susceptible to the 16-membered macrolides (but resistant to josamycin after induction), and remained susceptible to HMR3004, also after induction. The erythromycin resistance genes in 100 isolates of the different groups were investigated by PCR. All cMLS and iMLS-A isolates tested had the ermAM (ermB) gene, whereas all iMLS-B and iMLS-C isolates had the ermTR gene (neither methylase gene was found in isolates of other groups). The M isolates had only the macrolide efflux (mefA) gene, which was also found in variable proportions of cMLS, iMLS-A, iMLS-B, and iMLS-C isolates. The three iMLS subtypes were easily differentiated by a triple-disk test set up by adding a josamycin disk to the erythromycin and clindamycin disks of the conventional double-disk test. Tetracycline resistance was not detected in any isolate of the iMLS-A subtype, whereas it was observed in over 90% of both iMLS-B and iMLS-C isolates.     

High prevalence of erythromycin-resistant, clindamycin/miocamycin-susceptible (M phenotype) Streptococcus pyogenes: results of a Spanish multicentre study in 1998. Spanish Group for the Study of Infection in the Primary Health Care Setting

Using the standard agar dilution method we studied the prevalence of susceptibility to 14-, 15- and 16-membered ring macrolides and clindamycin in Streptococcus pyogenes isolated in 1998 from 21 laboratories in Spain. The number of strains admitted to the study was proportional to the numbers of inhabitants in each geographical area. We also determined the susceptibility phenotypes and the genetic basis for the antibiotic resistance. A total of 486 unduplicated isolates of S. pyogenes were used. Throat swab samples provided 359 (73.9%) isolates, and the remaining 127 isolates were from other sources. One hundred and fourteen (23.5%) isolates were resistant to erythromycin, a 14-membered ring macrolide, and azithromycin, a 15-membered macrolide, whereas only 1% of isolates were resistant to miocamycin, a 16-membered macrolide and 0.8% were resistant to clindamycin. Of the 114 erythromycin-resistant strains, 109 (95.6%) were susceptible to clindamycin and miocamycin. Since induction with erythromycin did not modify susceptibility to the latter antibiotics, these 109 strains were considered to have the M phenotype. Twenty strains with the M phenotype, one per laboratory, were assayed by PCR and showed the presence of the mef gene, which is responsible for antibiotic resistance by an efflux system. Among comparable studies covering entire countries, ours demonstrates one of the highest rates of S. pyogenes erythromycin resistance and clindamycin and miocamycin susceptibility in the world. Strains with the M phenotype account for the great majority of these isolates.     

葡萄球菌属对抗菌药物的耐药性分析

目的了解葡萄球菌属临床分离株的耐药性及对大环内酯类、林可霉素类及链阳霉素类（MLS）的耐药表型。方法用Kirby-Bauer法测定葡萄球菌属对14种抗菌药的敏感性，进行D试验测定MLS耐药表型。结果在230株葡萄球菌属中，耐甲氧西林金葡菌（MRSA）和耐甲氧西林凝固酶阴性葡萄球菌（MRSCN）分别为9．9％和79．8％。对青霉素都呈现高度耐药。未发现万古霉素及替考拉宁耐药菌株，126株葡萄球菌属对红霉素耐药，54．8％（23／42）株金葡菌为结构型耐药；在凝固酶阴性葡萄球菌中（CNS），44．0％（37／84）为结构型耐药，41．7％（35／84）为外排型耐药。对红霉素耐药但对克林霉素敏感的葡萄球菌中，17株为诱导型克林霉素耐药。结论应加强对葡萄球菌的耐药性监测，临床微生物实验室应进行D试验。指导临床合理使用抗生素。     

Reemergence of macrolide resistance in pharyngeal isolates of group a streptococci in southwestern Pennsylvania

We previously reported on the emergence of macrolide-resistant pharyngeal isolates of group A streptococci (GAS) in our community. The purpose of the present study was to track longitudinal trends in macrolide resistance in these isolates in southwestern Pennsylvania. Testing for susceptibility to erythromycin and clindamycin was performed for all pharyngeal GAS isolates recovered at the Children's Hospital of Pittsburgh and a local pediatric practice between September 2001 and May 2002. Macrolide resistance phenotypes and genotypes were determined by double-disk diffusion and PCR, respectively. Strain relatedness was determined by field inversion gel electrophoresis and emm gene sequence typing. A total of 708 isolates of GAS were recovered during the study period; 68 (9.6%) were macrolide resistant, while all isolates were sensitive to clindamycin. The monthly prevalence of macrolide resistance ranged from 0 to 41%. Only 21 of 573 (3.7%) strains recovered from September 2001 through March 2002 were macrolide resistant. A sudden increase in the rate of macrolide resistance (47 of 135 isolates [35%]) was seen in April and May 2002. Sixty-two isolates demonstrated the M phenotype (resistance to macrolide antibiotics), and six isolates demonstrated the MLS(B) phenotype (resistance to most macrolide, lincosamide, and streptogramin B antibiotics); these isolates were confirmed to be mef(A) and erm(A), respectively. Three unique mef(A) clones and four unique erm(A) clones were identified among the resistant isolates. The MIC at which 50% of isolates are inhibited (MIC(50)) for the mef(A) strains was 16 micro g/ml, while the MIC(50) for erm(A) strains was 8 micro g/ml. The finding of high levels of macrolide resistance among pharyngeal isolates of GAS for a second successive year in our community raises the concern that this problem may be more common in the United States than was previously appreciated. Longitudinal surveillance of isolates from multiple centers is needed to define the prevalence of antimicrobial agent-resistant GAS in the United States.     

Antimicrobial susceptibility patterns and macrolide resistance genes of viridans group streptococci from normal flora

OBJECTIVES: Our aim was to study the antimicrobial susceptibilities and macrolide resistance mechanisms of viridans group streptococci isolated from the normal flora. METHODS: In vitro susceptibilities of 16 antimicrobials were studied for 161 viridans streptococci (on average 5.8 isolates per person) from the normal flora of 28 elderly persons. Resistance mechanisms of erythromycin-resistant isolates were studied by the double disc test and PCR. RESULTS: In all, 16.8% of the isolates were non-susceptible (MIC > or =0.25 mg/L) to penicillin, but none showed high-level resistance (MIC > or =4 mg/L). Resistance to erythromycin, tetracycline, quinupristin/dalfopristin, levofloxacin and moxifloxacin was found in 22.4, 27.3, 13.0, 1.9 and 1.9% of the isolates, respectively. Combined resistance to erythromycin and tetracycline was found in 13.0% of the isolates. Erythromycin-resistant isolates were isolated from 57% of the study persons. Of the erythromycin-resistant isolates 80.6% were of the M phenotype and 19.4% were of the macrolide-lincosamide-streptogramin B (MLSB) phenotype (one isolate with constitutive and six with inducible expression). Isolates with the M phenotype were the least susceptible to telithromycin, a new ketolide. The mef(A) gene was found in the isolates with the M phenotype and the erm(B) gene in the isolates with the MLSB phenotype. CONCLUSIONS: The distribution of phenotypes among the viridans streptococci resembles that found in Streptococcus pyogenes, with predominance of the M phenotype. However, the coding gene for the MLSB phenotype, erm(B), is the same in viridans streptococci as in Streptococcus pneumoniae. Viridans group streptococci carrying different resistance traits provide a pool of resistant bacteria that may transfer resistance determinants to more pathogenic organisms.