Penicillin-binding proteins, porins and outer-membrane permeability of carbenicillin-resistant and -susceptible strains of Pseudomonas aeruginosa

Reduced cell permeability and target penicillin-binding protein modification were investigated as mechanisms of intrinsic resistance in strains of Pseudomonas aeruginosa resistant to carbenicillin (MIC greater than 128 mg/L) independently of beta-lactamase production. The carbenicillin-resistant strains were also remarkably resistant to other beta-lactams, quinolones, tetracyline and chloramphenicol, whereas carbenicillin-hypersusceptible strains (MIC less than 2 mg/L) were very sensitive to these antimicrobial compounds. These observations suggested a non-specific mechanism of resistance involving reduced permeability of the outer layers of the bacterial cell. However, carbenicillin-resistant and carbenicillin-sensitive strains had identical porin levels and the target penicillin-binding proteins of carbenicillin-resistant (MIC 256-2048 mg/L), carbenicillin-sensitive (MIC 64 mg/L) and carbenicillin-hypersusceptible (MIC 0.015 mg/L) strains were equally sensitive to beta-lactams. Thus, subtle changes in porin function or additional outer-membrane barriers regulating permeability may be involved in intrinsic resistance.     

Antibacterial activity of enoxacin in vitro and in urine

Minimal inhibitory concentrations (MIC) of enoxacin (ENO) were evaluated by agar dilution, in comparison with MIC of nalidixic acid (NAL), pipemidic acid (PIP), oxolinic acid (OXO), pefloxacin (PEF), norfloxacin (NOR), ofloxacin (OFL) and ciprofloxacin (CIP), for eleven Enterobacteriaceae reference strains chosen as a function of sensitivity and level of resistance to NAL. In the four strains susceptible to NAL, MIC of ENO (0.06 to 0.25 micrograms/ml) were similar to those for PEF and NOR, 2 to 4 times inferior to those for OXO, 16 to those for PIP and 32 to those for NAL; this ratio of activity was also seen in the majority of strains resistant to NAL. Measurement of MIC of ENO for 397 recent clinical isolates confirmed efficacy of this substance against Enterobacteriaceae and showed its activity against Pseudomonas aeruginosa (mode MIC: 0.5-1 micrograms/ml), and Gram positive cocci, essentially Staphylococcus aureus (mode MIC: 0.5-1). Antibacterial activity in the urine was measured by the Heilman test in 5 male adults after two doses of 200 mg of ENO administered at 12 hours intervals, two doses of 400 mg of ENO and, in comparison two of 400 mg of PIP administered under the same conditions. Maximal inhibitory dilutions obtained with ENO reached (mean for 5 subjects): 1/64 to 1/128 after 200 mg and 1/128 to 1/512 after 400 mg for a sensitive Providencia strain (MIC ENO: 0.25); 1/32 to 1/128 and 1/64 to 1/256 for an E. coli strain of low level of resistance to NAL (MIC ENO: 2); activity was very low on a Serratia strain highly resistant to NAL (MIC ENO: 16).(ABSTRACT TRUNCATED AT 250 WORDS)     

Susceptibility of strains of the Mycobacterium tuberculosis complex to fusidic acid.

The activity of fusidic acid was studied in 40 strains of M. tuberculosis (of which 20 strains were mono- or multiresistant to standard antituberculosis drugs) and 10 strains of M. bovis. Minimum inhibitory concentration (MIC) was determined by the radiometric (BACTEC) broth method. The MIC for the 50 strains varied between 8 and 32 mg/l, with a MIC90 of 16 mg/l for M. tuberculosis and a MIC90 of 32 mg/l for M. bovis. Minimal bactericidal concentration (MBC, defined as the lowest concentration of fusidic acid which killed 99% or more of the population) varied between 32 mg/l and 500 mg/l, with a MBC90 of 250 mg/l for M. tuberculosis and 500 mg/l for M. bovis. No cross-resistance to other antituberculosis drugs (ethambutol, isoniazid, rifampicin, streptomycin, pyrazinamide, ofloxacin, ciprofloxacin) was observed as strains resistant to one or more standard antituberculosis drugs were as susceptible to fusidin as sensitive strains of M. tuberculosis. No synergism or antagonism could be demonstrated when fusidic acid was combined with either ethambutol, isoniazid, rifampicin or streptomycin against strains of M. tuberculosis resistant to one or more standard antituberculosis drugs. Addition of pooled human serum to the medium increased both MIC and MBC by factors of 4 and 8 at serum concentrations of 10% and 50%, respectively. Single-step mutation to high-level resistance to fusidic acid at a frequency of less than 1.7 x 10(-8) could be readily selected at four times the MIC. These fusidic acid-resistant organisms had a generation time 2.0-2.7 x longer than their parent organisms.     

Drug resistance in Campylobacter jejuni, C coli, and C lari isolated from humans in north west England and Wales, 1997

AIMS: To test the sensitivity of strains of Campylobacter species isolated from humans in England and Wales against a range of antimicrobial agents for the purpose of monitoring therapeutic efficacy and as an epidemiological marker. METHODS: An agar dilution breakpoint technique was used to screen isolates against ampicillin, chloramphenicol, gentamicin, kanamycin, neomycin, tetracycline, nalidixic acid, ciprofloxacin, and erythromycin. Minimal inhibitory concentrations (MIC) were also determined for a sample of quinolone resistant strains. RESULTS: Approximately 50% of strains tested were resistant to at least one drug. Strains which were resistant to four or more of the drugs tested were classified as multiresistant; this occurred in 11.3% of C jejuni, 19.9% of C coli, and 63.6% of C lari. Resistance to erythromycin occurred in 1.0% of C jejuni and 12.8% of C coli. Resistance to quinolones occurred in 12% of strains, with a ciprofloxacin MIC of > 8 mg/l and a nalidixic acid MIC of > 256 mg/l; a further 4% of strains had intermediate resistance with a ciprofloxacin MIC of between 0.5 and 2 mg/l (fully sensitive strains, 0.25 mg/l or less) and a nalidixic acid MIC of between 32 and 64 mg/l (fully sensitive strains, 8 mg/l or less). CONCLUSIONS: Resistance to quinolones in campylobacters from human infection may relate to clinical overuse or use of fluoroquinolones in animal husbandry. Both veterinary and clinical use should be reconsidered and fluoroquinolone drugs used only as a treatment for serious infections requiring hospital admission. Erythromycin resistance is still rare in C jejuni but much more common in C coli.     

Rapid identification of fluconazole resistance using Chromagar Candida

Although extremely rare 10 years ago, antifungal drug resistance is becoming a major problem in certain populations, especially in those infected with HIV. This study was undertaken to study the resistance of Candida species isolated in our hospital to Fluconazole using Chrom agar Candida. The Candida strains which were routinely isolated from clinical specimens like blood, urine, sputum, pus, fluid and homograft isolates were included in the study. 142 Candida isolates were tested by using Chrom agar Candida incorporated with fluconazole. 16 strains were found to be resistant to Fluconazole and 126 strains sensitive to Fluconazole. Nine were C tropicalis, 3 C krusei, 2 C guillermondii, 1 Geotrichum candidum and one was an unidentified strain of Candida. The MIC of the 16 strains were done using RPMI 1640 medium by macro broth dilution method. MIC of 9 strains was 64 & > 64 micrograms/ml of 6 strains 32 micrograms/ml and 1 strain 16 micrograms/ml.     

粉防己碱抑制耐氟康唑热带念珠菌外排泵机制的研究

目的探讨粉防己碱抑制耐氟康唑热带念珠菌外排泵的机制。方法通过MTT法确定24h粉防己碱对耐氟康唑热带念珠菌的无细胞毒性剂量,并以此剂量处理5株耐氟康唑热带念珠菌。粉防己碱组（20mg／L）及对照组（PBS）加入不同浓度的氟康唑（10～50mg/L）处理48h以测定MIC值。半定量PCR分析粉防己碱（20mg/L）作用24h前后,耐氟康唑热带念珠菌外排泵基因CDR1和MDR1转录水平的变化;流式细胞术检测粉防己碱（20mg／L）作用24h后对耐氟康唑热带念珠菌罗丹明123的蓄积能力的影响。结果粉防己碱对耐氟康唑热带念珠菌的最大无细胞毒性剂量为20mg／L。以此浓度处理5株耐氟康唑热带念珠菌,与对照组相比,MIC的范围由64（64～128）mg/L减少到32（24-64）mg/L（P〈0．05）。粉防己碱可以将耐氟康唑热带念珠菌CDR1和MDR1基因mRNA水平的表达由0．905±0．026及b．649±0．028分别下调至0．715±0．131和0．342±0．068（均P〈0．05）。粉防己碱作用后的耐氟康唑热带念珠菌对罗丹明123的蓄积量提升至（37．7±3．5）％,高于对照组的（16．3±2．2）％（P〈0．05）。结论粉防己碱可以减少耐氟康唑热带念珠菌外排蛋白的表达,增加细胞内药物的蓄积,从而抑制氟康唑的耐药作用。     

Antimicrobial resistance in invasive and colonising Streptococcus pneumoniae in North India

The present study was done to detect the antibiotic resistance in S. pneumoniae. One hundred twenty S. pneumoniae isolates from clinical specimens and 50 from nasopharyngeal sites were subjected to antimicrobial susceptibility testing by Kirby Bauer disk diffusion method and minimum inhibitory concentration (MIC) determination for penicillin and cefotaxime non-susceptible isolates. A total of 22 isolates (18.3%) from clinical sites and eight (16%) from nasopharyngeal sites showed decreased susceptibility to penicillin by oxacillin disk diffusion test. MICs of 26 of these resistant strains ranged from 0.12-1 microg/mL (intermediate resistance) by broth dilution and E test. Only four isolates, two from sputum and two from nasopharyngeal swabs, showed MIC of 2 microg/mL (complete resistance). However, MIC of two cefotaxime resistant isolates (by disk diffusion) was in the susceptible range (0.5 microg/mL). Highest antimicrobial resistance was seen to cotrimoxazole (55.2%) and tetracycline (61.2%). Antimicrobial resistance to cotrimoxazole and tetracycline was much more in clinical isolates than colonizing isolates. Multi-drug resistant phenotype was detected in 76.9% (20 of 26) of isolates that were intermediately sensitive to penicillin and 50% (2 of 4) of penicillin resistant isolates (co-resistant to tetracycline and cotrimoxazole). Routine screening for antibiotic susceptibility is recommended for clinical isolates of pneumococci. Strains with reduced susceptibility to penicillin should be subjected to MIC determination to detect relative resistance or true resistance as such strains are associated with increased virulence.The choice of antibiotics should be guided by the prevalence of local resistance patterns of pneumococci.     

Ceftriaxone resistant Shigella flexneri, an emerging problem

Shigellosis is a disease of public health importance in developing countries. It may cause self-limited diarrhea to severe dysentery. Emergence of multi drug resistant (MDR) strains is a growing concern globally. Ceftriaxone and ciprofloxacin are the drugs of choice for MDR cases. Here, we report a case of MDR Shigella flexneri from an immunocompromised patient. The strain was resistant to ceftriaxone [minimum inhibitory concentration (MIC) ≥ 64 μg/ml], limiting the treatment option. Simultaneously, the strain was also found to be resistant to ciprofloxacin (MIC ≥ 4 μg/ml). However, it was susceptible to ceftazidime (MIC 4 μg/ml). This is the first case of ceftriaxone resistant Shigella spp. reported from our hospital.     

Distribution and transferability of plasmids encoding trimethoprim resistance in urinary pathogens from Greece

Of 505 strains of Enterobacteriaceae responsible for significant bacteriuria and isolated from hospital patients in two Greek cities in 1989, 151 strains (30%) were resistant to trimethoprim (MIC greater than or equal to 4 mg/L) and 220 (44%) were resistant to sulphamethoxazole (MIC greater than or equal to 64 mg/L); 127 (84%) of the trimethoprim-resistant strains exhibited high-level resistance (MIC greater than 1024 mg/L) and 121 (80%) were additionally resistant to four or more other antibiotics. Plasmids were detected in 141 (93%) of the trimethoprim-resistant strains. Trimethoprim resistance was encoded on self-transmissible plasmids in 79 (52%) of the resistant strains, and in a further seven strains (5%), plasmids coding for trimethoprim resistance could be mobilised by X+ factor. Co-transfer of various other antimicrobial resistances with trimethoprim resistance was observed, tetracycline resistance being the most common. The low degree of linkage observed between trimethoprim resistance and resistance to streptomycin and spectinomycin suggests that Tn7 is relatively uncommon in Greece. Classification of trimethoprim-resistance plasmids on the basis of their antimicrobial-resistance patterns and molecular mass revealed 39 different profiles. Overall, these findings differ from those from other European countries where the prevalence of transferable high-level trimethoprim resistance is low and where chromosomal Tn7-encoded trimethoprim resistance is common.     

In vitro activity of 4 fluoroquinolones against Klebsiella pneumoniae. Distribution according to phenotype resistance to aminoglycosides or beta-lactams

Minimal inhibitory concentrations (MIC) of pefloxacin (PEF), norfloxacin (NOR), ofloxacin (OFL) and ciprofloxacin (CIP) are evaluated by agar dilution against 100 Klebsiella pneumoniae strains isolated in hospital. MIC 50 and 90%, micrograms/ml, are respectively: CIP (0.25/8), OFL (1/16), NOR (1/32), PEF (2/64). We determined the phenotypes PEF/NOR/OFL/CIP by taking into account the critic concentrations of the French Committee for Antibiogram. The results are: SSSS = 45%, RI/RI/RI/RI = 20%, RI/SSS = 19%, RI/RI/RI/S = 8%, RI/RI/SS = 7%. When a strain is resistant to pefloxacin alone, the MICs of the other fluoroquinolones are higher than those of the sensitive strains. The resistance to fluoroquinolones is most frequent in strains that have acquired resistance to aminoglycosides or betalactams, but exists also in strains that have no acquired resistance to these antibiotics.     

Rapid identification of fluconazole resistance using Chrom agar Candida

All though extremely rare 10 years ago, antifungal drug resistance is becoming a major problem in certain populations, especially in those infected with HIV. This study was undertaken to study the resistance of Candida species isolated in our hospital to Fluconazole using Chrom agar Candida. The Candida strains which were routinely isolated from clinical specimens like blood, urine, sputum, pus, fluid and homograft isolates were included in the study. 142 Candida isolates were tested by using Chrom agar Candida incorporated with Fluconazole. 16 strains were found to be resistant to Fluconazole and 126 strains sensitive to Fluconazole. Nine were C. tropicalis, 3 C. krusei, 2 C. guillermondii, 1 Geotrichum candidum and one was an unidentified strain of Candida. The MIC of the 16 strains were done using RPMI 1640 medium by macro broth dilution method. MIC of 9 strains was 64 & > 64 ug/ml of 6 strains 32 ug/ml and 1 strain 16 ug/ml.     

氟喹诺酮体外诱导肺炎克雷伯菌外排蛋白表达差异的研究

目的 探讨氟喹诺酮体外诱导肺炎克雷伯菌外排蛋白表达的差异。方法 取临床分离对喹诺酮敏感的肺炎克雷伯菌20株，分2组，每组10株，1组作对照组，观察组将应用不同浓度梯度环丙沙星逐级诱导，最后成为耐药株，观察2组细菌在不同浓度抗生素应用后的差异，并比较观察组的10株敏感菌和诱导后耐药菌在应用外排泵抑制剂前后最低抑菌浓度（MIC）及SDS-PAGE电泳外排泵膜蛋白表达的差异。结果 环丙沙星从小至大剂量体外诱导出高度耐药株的出现，其53KDa外膜蛋白TolC表达增多。应用外排泵抑制剂利血平后，70％诱导耐药菌MIc有明显下降。结论 喹诺酮体外诱导可使肺炎克雷伯菌的耐药性出现，TolC表达增多表明外排泵在肺炎克雷伯菌耐药机制中起重要作用。外排泵抑制剂的应用对肺炎克雷伯菌耐药有一定的遏制作用。     

In vitro antibacterial activity of a new macrolide, miokamycin. Results of a multicenter study

Minimal inhibitory concentration (MIC) of miokamycin (M) were evaluated by agar dilution for 1,024 bacterial strains isolated in 6 hospitals and classed as a function of susceptibility and resistance to macrolides, lincosamides, streptogramins group (MLS). MIC of M ranged from 0.25 to 4 micrograms/ml (mode MIC 1-2) on Staphylococcus susceptible to MLS and on MLSB inducible strains; M was inactive on MLSB constitutive strains. MIC of M ranged from 0.016 to 4 micrograms/ml (mode MIC 0.12 to 0.5) for Streptococci and Pneumococci susceptible to erythromycin (E) and from 0.12 to greater than 128 for strains resistant to E. Enterococci susceptible to E were inhibited by 0.5 to 2 micrograms/ml (mode MIC 1) and strains resistant to E by 4 to greater than 128. Haemophilus were inhibited by 2 to 64 micrograms/ml (mode MIC 32), Neisseria by 0.12 to 4 (mode MIC 0.5-1) and B. catarrhalis by 0.12 to 8 (mode MIC 1). L. pneumophila was very susceptible to M: MIC 0.016 to 0.12 (mode MIC 0.06). MIC of M ranged generally from 0.5 to 2 micrograms/ml (mode MIC 1) for C. perfringens and from 0.03 to 2 (mode MIC 1) for B. fragilis. Thus, M was shown to be among macrolide antibiotics of resistance non-inducing type on MLSB inducible resistance strains. Its activity was similar to that of spiramycin slightly superior on Staphylococci, slightly inferior on Streptococci and Enterococci, similar on Pneumococci, very superior on Neisseria, Legionella and anaerobes. M had a good activity on Branhamella and, as others macrolides, was poorly active on Haemophilus.     

Emergence of low level vancomycin resistance in MRSA

One hundred and twenty methicillin resistant Staphylococcus aureus (MRSA) strains were checked for minimum inhibitory concenteration (MIC) of vancomycin. The results showed that 98 strains (81.7 %) had MIC < 4microg/mL, 18 strains (15 %) had MIC 8 microg/mL, and 4 (03.3%) had MIC 16 microg/mL which being borderline between sensitive (< 4microg/mL) and resistant (>32 microg/mL) values points towards possible emergence of low level vancomycin resistance in the organisms and may explain the reasons of delayed therapeutic success of vancomycin in S. aureus bacteraemia in some situations.     

Acquisition of antibiotic resistance by Staphylococcus aureus in skin patients.

Acquisition of resistance to neomycin, gentamicin, fusidic acid, or clindamycin has been observed in three strains of Staphylococcus aureus and data from three patients infected with these strains are presented in detail. Clindamycin resistance followed the expected pattern by appearing in a strain of Staph. aureus with dissociated resistance to erythromycin after treatment with erythromycin and clindamycin. Low-level resistance to fusidic acid appeared in two strains in the apparent absence of exposure to that antibiotic. Labile neomycin resistance was encountered in a previously sensitive strain after topical neomycin therapy. Gentamicin resistance appeared in all three strains after topical therapy. In all three strains, a labile resistance (presumably plasmid-mediated) occurred with minimum inhibitory concentrations (MICs) of 64-128 microgram/ml but in one strain a stable resistance with MIC over 3000 microgram/ml appeared.     

Multicenter study of ofloxacin activity on bacteria isolated from a hospital environment

Minimal inhibitory concentrations (MICs) of ofloxacin were evaluated by agar dilution for 1508 bacterial strains isolated in five hospitals. For Enterobacteriaceae sensitive to nalidixic acid, MICs ranged from 0.008 to 1 microgram/ml (mode MIC: 0.12); the different species of Enterobacteriaceae exhibited similar mode MICs (0.12) with the exception of E. coli (0.06-0.12), P. mirabilis (0.5) and Providencia (0.25). Among strains intermediate and resistant to nalidixic acid, most of which were Serratia, Providencia and Citrobacter, 41% had a MIC within the susceptibility range, while the others had a MIC of 2 to 8 micrograms/ml, or even 64 micrograms/ml in a few instances. Ofloxacin also exhibited satisfactory activity against P. aeruginosa, with MICs ranging from 0.25 to 16 micrograms/ml (mode MIC: 2) for 87% of strains, and A. calcoaceticus, with MICs from 0.25 to 2 micrograms/ml (mode MIC: 1). Haemophilus sp. (MIC: 0.008 to 0.06 microgram/ml; mode MIC: 0.03), Gonococci (mode MIC: 0.008), and Meningococci (mode MIC: 0.016) were very sensitive to ofloxacin. The spectrum of ofloxacin included Gram positive cocci: MICs of Staphylococci were 0.06 to 2 micrograms/ml (mode MIC: 0.5); Enterococci, other Streptococci and Pneumococci were less sensitive, with MICs of 2 to 4 micrograms/ml for the majority of strains. As for anaerobic bacteria, ofloxacin proved more active against Clostridium (0.5 to 2 micrograms/ml) than Bacteroides (0.5 to 16 micrograms/ml).     

Spread in hospital units of a Pseudomonas aeruginosa phenotype producing a beta-lactamase highly inducible by clavulanic acid in vitro]

Pseudomonas aeruginosa strains belonging to the serogroup O:11 exhibiting susceptibility to ticarcillin (TIC) and resistance to the ticarcillin-clavulanic acid (CA) combination were found in 19 inpatients over a 14 month period. Mean inhibition diameters obtained using the agar diffusion method were 21.75 mm around the TIC disks (75 micrograms) and 15.96 mm around the TIC+CA disks (75 + 10 micrograms). With control PaO:11 strains, these diameters were 25.27 and 25 mm, respectively. MIC for ticarcillin determined using the checkerboard method rose to 64 mg with CA levels of 16 mg/l or more. CA exhibited dose-dependent antagonism on TIC killing curves when TIC levels approximated the MIC; this effect was no longer present with higher TIC levels. In the crude bacterial extract, a betalactamase of the cephalosporinase type was detected in the absence of induction and increased threefold after exposure to cefoxitin (100 mg/l) and fourfold after exposure to CA (5 mg/l). All these PaO:11 strains exhibited the same antimicrobial resistance phenotype with decreased susceptibility to ureidopenicillins and resistance to aminoglycosides and fluoroquinolones. The induction of a chromosome-encoded cephalosporinase by CA proved useful as an epidemiologic marker. Nosocomial spread of this phenotype was likely the result of selection due to use of antimicrobials.     

环丙沙星诱导耐药肺炎克雷伯菌对其他抗菌药物的耐药性研究

探讨环丙沙星诱导耐药肺炎克雷伯菌(KPn)对几类常见的抗生素的耐药性。方法 琼脂二倍稀释法测定环丙沙星对20株临床分离KPn敏感株的最低抑菌浓度(MIC),用环丙沙星对其进行体外多步诱导成耐药株。诱导前和诱导后K-B纸片扩散法进行药敏试验检测其对头孢他啶、头孢西丁、氨曲南、亚胺培南、莫西沙星、阿米卡星的敏感性。诱导后进行产超广谱β-内酰胺酶(ESBL)初筛和确证实验。结果 20株KPn有17株成功诱导成环丙沙星高度耐药株,ESBL筛选和确证实验显示17株诱导耐药株无一产ESBL。诱导耐药株对莫西沙星全部耐药,对头孢他啶、亚胺培南、氨曲南全部敏感,对阿米卡星的敏感率为88.2％(15/17),而对头孢西丁耐药率达88.2％ (15/17)、中介率12.8％(2/17)。结论 KPn在长期低剂量接触环丙沙星后可产生耐药性,且对莫西沙星和头孢西丁有交叉耐药。环丙沙星诱导耐药的KPn对头孢西丁交叉耐药的机制可能相似。     

Detection of clindamycin susceptibility in macrolide resistant phenotypes of Staphylococcus aureus

The present study aimed at in vitro detection of macrolide resistant phenotypes of methicillin resistant Staphylococcus aureus (MRSA) and interpretation of susceptibility tests to guide therapy. The study included 25 MRSA strains that were resistant to erythromycin and clindamycin, 25 MRSA strains that were sensitive to both erythromycin and clindamycin and 100 MRSA isolates which displayed erythromycin resistant but clindamycin susceptible phenotype. Erythromycin and clindamycin double disc susceptibility testing was done to detect inducible clindamycin resistance. Dilution susceptibility testing for clindamycin and erythromycin alone and in combination was performed for all 150 strains. Seventy-six strains showed blunting around clindamycin disc (inducible resistance). After induction with erythromycin, minimum inhibitory concentration (MIC) of clindamycin was noticed to rise from at least 16 to 256 g/mL in iMLSB phenotypes indicating inducible resistance. The detailed result analysis suggests the possible role of clindamycin in treatment of some of the erythromycin resistant isolates (non inducible), as there are multiplicity of resistance mechanisms and diversity of phenotypic expressions.     

CTX-M型超广谱β-内酰胺酶基因在头孢他啶诱导的阴沟肠杆菌中的表达

目的 对比临床耐药株与经头孢他啶诱导形成的耐药株(诱导耐药株)CTX-M型超广谱β-内酰胺酶(ESBL)基因在阴沟肠杆菌中的表达情况.方法 取临床分离的对头孢他啶敏感的10株阴沟肠杆菌,应用不同浓度梯度头孢他啶[1/2×最小抑菌浓度(MIC)、1× MIC、2×MIC、4×MIC并呈倍数到128 mg/L]逐级诱导并使其成为耐药株.分别培养诱导耐药株及临床敏感株、临床耐药株各10株,并提取其DNA.采用PCR检测诱导耐药株及临床敏感株、临床耐药株CTX-M型ESBL基因的表达情况.结果 成功诱导出对头孢他啶耐药的阴沟肠杆菌形成诱导耐药株.PCR结果显示在10株诱导耐药株中,有5株表达CTX-M型ESBL基因,可见约900 bp的条带形成;在10株临床耐药株中,则有4株可见约900 bp的条带形成;在10株临床敏感株中则未见此条带形成.结论 头孢他啶可以诱导CTX-M型ESBL基因的表达,临床头孢他啶的不合理使用可能是诱导其产生的重要原因之一.