Fluoroquinolonas en aves, huevos, alimentos avícolas y su impacto en la microbiota intestinal de aves / Fluoroquinolone in birds, eggs, poultry feeds and their impact on the intestinal microbiota

Se detectó la presencia de fluoroquinolonas en varios alimentos (huevos, alimentos para aves y pechuga de pollo), así como determinar el perfil de susceptibilidad de ácido nalidíxico y ciprofloxacina de las enterobacterias aisladas del contenido intestinal de pollos de Cumaná. Se estudiaron alimentos iniciadores y de engorde (de cinco marcas comerciales) y uno para gallinas ponedoras, así como pechugas de pollos nacionales y de Brasil. I-2 y E-1 fueron los que tuvieron las concentraciones más altas de enrofloxacina. El alimento para las gallinas ponedoras (AP 2,35 µg/mg) tuvo más enrofloxacina que los de los pollos. En los huevos, la mayor acumulación se vio en las yemas. Los pollos nacionales (0,43-0,56 µg/mg) acumularon más ciprofloxacina que los pollos de Brasil (0,14 µg/mg). De los hisopados rectales de los pollos, E. coli fue la principal especie aislada. Por antibiograma, 48% de las cepas fueron resistentes a las quinolonas probadas (ácido nalidíxico y ciprofloxacina). Cuando se determinó la concentración mínima inhibitoria a ciprofloxacina, todas las cepas fueron resistentes (8-128 µg/ml). Todos los alimentos muestreados exceden los límites máximos de fluoroquinolonas permitidos en humanos, lo cual ejerce una presión selectiva importante en las bacterias de la microbiota intestinal de los pollos

To detect the presence of fluoroquinolones in several foods (eggs, poultry food and chicken breast), as well as to determine the susceptibility profile of nalidixic acid and ciprofloxacin of strains of enterobacterias from chicken's intestinal content from Cumaná. Starter and fattening foods (of five commercial marks), and one for laying hens, were studied, as well as domestic chicken's breast (and Brazil. I-2 and E-1 were the ones with the highest concentrations of enrofloxacin. The food for laying hens (AP 2,35 µg/mg) had more enrofloxacin than those for chickens. In eggs, greatest accumulation was seen in the yolks. Domestic chickens (0,43-0,56 µg/mg) accumulated more ciprofloxacin than Brazilian ones (0,14 µg/mg). E. coli was the main specie from chicken rectal swabs. By antimicrobial susceptibility testing, 48% were resistant to both quinolones (nalidixic acid and ciprofloxacin). When the minimum inhibitory concentration of ciprofloxacin was determined, all strains were resistant (8-128 µg/ml). All sampled foods exceeded the maximum limits of fluoroquinolones allowed in humans, which puts significant selective pressure on the bacteria in the chicken gut microbiota

Mismatch amplification mutation assay-polymerase chain reaction: A method of detecting fluoroquinolone resistance mechanism in bacterial pathogens

The mismatch amplification assay is a modified version of polymerase chain reaction (PCR) that permits specific amplification of gene sequences with single base pair change. The basis of the technique relies on primer designing. The single nucleotide mismatch at the 3' proximity of the reverse oligonucleotide primer makes Taq DNA polymerase unable to carry out extension process. Thus, the primers produce a PCR fragment in the wild type, whereas it is not possible to yield a product with a mutation at the site covered by the mismatch positions on the mismatch amplification mutation assay (MAMA) primer from any gene. The technique offers several advantages over other molecular methods, such as PCR-restriction fragment length polymorphism (RFLP) and oligonucleotide hybridization, which is routinely used in the detection of known point mutations. Since multiple point mutations in the quinolone resistance determining region play a major role in high-level fluoroquinolone resistance in Gram-negative bacteria, the MAMA-PCR technique is preferred for detecting these mutations over PCR-RFLP and sequencing technology.

Antibiotic Resistance Pattern among common Bacterial Uropathogens Isolated in A Tertiary Care Hospital

Introduction: Urinary tract infections (UTI’s) are one of the most common bacterial infections in community and hospital settings and it is important to know the etiology and susceptibility pattern of uropathogens for optimum management of UTI’s.Aim & Objectives:This study was conducted to know the etiologyof UTI and to determine the antibiotic resistance pattern of these isolates.Materials & Methods: A prospective cross sectional study was done on 537 and 486 consecutive urine samples from January to May 2015 and 2016. Isolates obtained were identified by conventional biochemical methods and antimicrobial susceptibility testing was done by Kirby Bauer disk diffusion method as per CLSI guidelines.Results: The prevalence of UTI was 41.71% and 51.85% in 2015 and 2016 respectively. 129 (57.59%) and 148 (58.73%) females and 95(42.41%) and 104(41.27%) males were infected in 2015 and 2016 respectively.Escherichia coli (55.25%) was the predominant organism isolated. An increased resistance to norfloxacin ,ampicillin and cefotaxime were shown in 2016 compared to the antimicrobial resistance pattern obtained in 2015. All the gram negative bacilli studied were sensitive to Imipenem and Piperacillin- Tazobactam. Conclusion:Constant surveillance of resistance rate of uropathogens is necessary to formulate local antibiotic policy and to assist clinicians in the rational choice of antibiotic therapy. KEYWORDS:Urinary Tract Infection, E.coliAntibiogram ,Fluoroquinolone resistance.

Correlation between virulence genotype and fluoroquinolone drugs resistance in Pseudomonas aeruginosa of lower respiratory tract infection / 中国人兽共患病学报

We investigated the correlation between toxin gene exoS,exoU and fluoroquinolone resistance in lower respiratory tract infection with P.aeruginosa so as to provide guidance for reasonable treatment of clinical infections.We collected P.aeruginosa of sputum samples in hospitalized patients from October 2015 to March 2016.The antimicrobial susceptibility was tested by liquid dilution method.The exoS and exoU genes were detected by PCR technique.Results showed that forty-six P.aeruginosa strains were identified from sputum.The exoS and exoU gene positive rate were 86.96 ％ (40/46) and 69.57 ％ (32/ 46) respectively,and the highest proportion of genotype was exoS+/exoU+ (60.87％,28/46).Among them,36.96％ (17/ 46) were multiple drug-resistant bacteria(MDR).Fluoroquinolone non-sensitive (FQ-NS) strain were 78.95％ (15/19) for MDR and 89.47 ％ (17/19) exoU gene were positive,which was significantly higher than the fluoroquinolone sensitive strains (FQ-S).Compared with the FQ-S strain,FQ-NS strains were serious drug resistance.The drug resistant rate of eefepime and aztreonam were more than 70％,and then meropenem and imipenem were more than 50％.The drugs of lower resistance rate in FQ-NS strain had polymyxin B(10.53％,2/19),amikacin(10.53％,2/19),ceftazidime (15.79％,3/19) and gentamicin (21.05％,4/19).P.aeruginosa of lower respiratory infection carried toxin genes exoS and exoU were higher,the main genetpy was exoS+/exoU+.FQ-NS strains were higher drug resistance rate and a higher proportion of exoU+ strains than FQ-S strains.We should strengthen virulence genes test and drug resistance monitoring in clinical practice.

The role of gyrA and parC mutations in fluoroquinolones-resistant Pseudomonas aeruginosa isolates from Iran

Abstract The aim of this study was to examine mutations in the quinolone-resistance-determining region (QRDR) of gyrA and parC genes in Pseudomonas aeruginosa isolates. A total of 100 clinical P. aeruginosa isolates were collected from different university-affiliated hospitals in Tabriz, Iran. Minimum inhibitory concentrations (MICs) of ciprofloxacin and levofloxacin were evaluated by agar dilution assay. DNA sequences of the QRDR of gyrA and parC were determined by the dideoxy chain termination method. Of the total 100 isolates, 64 were resistant to ciprofloxacin. No amino acid alterations were detected in gyrA or parC genes of the ciprofloxacin susceptible or ciprofloxacin intermediate isolates. Thr-83 → Ile substitution in gyrA was found in all 64 ciprofloxacin resistant isolates. Forty-four (68.75%) of them had additional substitution in parC. A correlation was found between the number of the amino acid alterations in the QRDR of gyrA and parC and the level of ciprofloxacin and levofloxacin resistance of the P. aeruginosa isolates. Ala-88 → Pro alteration in parC was generally found in high level ciprofloxacin resistant isolates, which were suggested to be responsible for fluoroquinolone resistance. These findings showed that in P. aeruginosa, gyrA was the primary target for fluoroquinolone and additional mutation in parC led to highly resistant isolates.

Distribution of virulence determinants among antimicrobial‑resistant and antimicrobial-susceptible Escherichia coli implicated in urinary tract infections.

Introduction: Uropathogenic Escherichia coli (UPEC) rely on the correlation of virulence expression with antimicrobial resistance to persist and cause severe urinary tract infections (UTIs). Objectives: We assessed the virulence pattern and prevalence among UPEC strains susceptible and resistant to multiple antimicrobial classes. Methods: A total of 174 non‑duplicate UPEC strains from patients with clinically significant UTIs were analysed for susceptibility to aminoglycoside, antifolate, cephalosporin, nitrofuran and quinolone antibiotics for the production of extended‑spectrum β‑lactamases and for the presence of six virulence determinants encoding adhesins (afimbrial, Type 1 fimbriae, P and S‑fimbriae) and toxins (cytotoxic necrotising factor and haemolysin). Results: Relatively high resistance rates to nalidixic acid, ciprofloxacin, cephalothin and trimethoprim‑sulfamethoxazole (82%, 78%, 62% and 59%, respectively) were observed. Fourteen distinct patterns were identified for the virulence determinants such as afaBC, cnfI, fimH, hylA, papEF and sfaDE. The toxin gene, cnfI (75.3%), was the second most prevalent marker to the adhesin, fimH (97.1%). The significant association of sfaDE/hylA (P < 0.01) among antimicrobial resistant and susceptible strains was also observed notwithstanding an overall greater occurrence of virulence factors among the latter. Conclusions: This study provides a snapshot of UPEC complexity in Jamaica and highlights the significant clonal heterogeneity among strains. Such outcomes emphasise the need for evidence‑based strategies in the effective management and control of UTIs.

Susceptibility to β-lactams and quinolones of Enterobacteriaceae isolated from urinary tract infections in outpatients

Abstract The antibiotic susceptibility profile was evaluated in 71 Enterobacteriaceae isolates obtained from outpatient urine cultures in July 2010 from two health institutions in Santa Fe, Argentina. The highest rates of antibiotic resistance were observed for ampicillin (AMP) (69%), trimethoprim/sulfamethoxazole (TMS) (33%), and ciprofloxacin (CIP) (25%). Meanwhile, 21% of the isolates were resistant to three or more tested antibiotics families. Thirty integron-containing bacteria (42.3%) were detected, and a strong association with TMS resistance was found. Third generation cephalosporin resistance was detected in only one Escherichia coli isolate, and it was characterized as a blaCMY-2 carrier. No plasmid-mediated quinolone resistance (PMQR) was found. Resistance to fluoroquinolone in the isolates was due to alterations in QRDR regions. Two mutations in GyrA (S83L, D87N) and one in ParC (S80I) were observed in all CIP-resistant E. coli. It was determined to be the main phylogenetic groups in E. coli isolates. Minimum Inhibitory Concentration (MIC) values against nalidixic acid (NAL), levofloxacin (LEV), and CIP were determined for 63 uropathogenic E. coli isolates as MIC50 of 4 μg/mL, 0.03125 μg/mL, and 0.03125 μg/mL, respectively, while the MIC90 values of the antibiotics were determined as 1024 μg/mL, 64 μg/mL, and 16 μg/mL, respectively. An association between the phylogenetic groups, A and B1 with fluoroquinolone resistance was observed. These results point to the importance of awareness of the potential risk associated with empirical treatment with both the families of antibiotics.

Enhanced resistance to fluoroquinolones in laboratory-grown mutants & clinical isolates of Shigella due to synergism between efflux pump expression & mutations in quinolone resistance determining region.

Background & objectives: There is a worldwide emergence of fluoroquinolone resistance in Shigella species. To understand the molecular mechanisms associated with fluoroquinolone resistance, naturally occurring fluoroquinolone-resistant strains and laboratory-induced spontaneous mutants of Shigella spp. were used and the relative contributions of acrAB-tolC efflux pumps, gyrase and topoisomerase target gene mutations towards fluoroquinolone resistance were determined. Methods: Eight Shigella flexneri and six S. dysenteriae clinical isolates were studied. Three consecutive mutants resistant to ciprofloxacin for S. flexneri SFM1 (≥0.25 μg/ml), SFM2 (≥4 μg/ml) and SFM3 (≥32 μg/ml) were selected in 15 steps from susceptible isolates by serial exposure to increasing concentrations of nalidixic acid and ciprofloxacin. Similarly, two mutants for S. dysenteriae SDM1 (≥0.25 μg/ml) and SDM2 (≥4 μg/ml) were selected in eight steps. After PCR amplification sequence analyses of gyrase and topoisomerase target genes were performed. Expression of efflux genes acrA, acrB, acrR and tolC was measured using real-time PCR. Results: Mutations were observed in gyrA Ser83→Leu, Asp87→Asn/Gly, Val196→Ala and in parC Phe93→Val, Ser80→Ile, Asp101→Glu and Asp110→Glu. Overall, acrA and acrB overexpression was associated with fluoroquinolone resistance (p<0.05); while tolC and acrR expression levels did not. Interpretation & conclusions: Fluoroquinolone resistance in Shigella spp. is the end product of either a single or a combination of mutations in QRDRs and/ or efflux activity. Novel polymorphisms were observed at Val196→Ala in gyrA in clinical isolates and Phe93→Val, Asp101→Glu, Asp110→Glu and in parC in majority of laboratory-grown mutants.

Genetic diversity and antimicrobial resistance in Streptococcus agalactiae strains recovered from female carriers in the Bucharest area

For the first time, we used multilocus sequence typing (MLST) to understand how Romanian group B streptococcus (GBS) strains fit into the global GBS population structure. Colonising isolates recovered from adult human females were tested for antibiotic resistance, were molecularly serotyped based on the capsular polysaccharide synthesis (cps) gene cluster and further characterised using a set of molecular markers (surface protein genes, pilus-encoded islands and mobile genetic elements inserted in the scpB-lmb intergenic region). Pulsed-field gel electrophoresis was used to complement the MLST clonal distribution pattern of selected strains. Among the 55 strains assigned to six cps types (Ia, Ib, II-V), 18 sequence types (STs) were identified by MLST. Five STs represented new entries to the MLST database. The prevalent STs were ST-1, ST-17, ST-19 and ST-28. Twenty molecular marker profiles were identified. The most common profiles (rib+GBSi1+PI-1, rib+GBSi1+PI-1, PI-2b and alp2/3+PI-1, PI-2a) were associated with the cps III/ST-17 and cps V/ST-1 strains. A cluster of fluoroquinolone-resistant strains was detected among the cps V/ST-19 members; these strains shared alp1 and IS1548 and carried PI-1, PI-2a or both. Our results support the usefulness of implementing an integrated genotyping system at the reference laboratory level to obtain the reliable data required to make comparisons between countries.

Correlation Between Virulence Genotype and Fluoroquinolone Resistance in Carbapenem-Resistant Pseudomonas aeruginosa

BACKGROUND: Pseudomonas aeruginosa is a clinically important pathogen that causes opportunistic infections and nosocomial outbreaks. Recently, the type III secretion system (TTSS) has been shown to play an important role in the virulence of P. aeruginosa. ExoU, in particular, has the greatest impact on disease severity. We examined the relationship among the TTSS effector genotype (exoS and exoU), fluoroquinolone resistance, and target site mutations in 66 carbapenem-resistant P. aeruginosa strains. METHODS: Sixty-six carbapenem-resistant P. aeruginosa strains were collected from patients in a university hospital in Daejeon, Korea, from January 2008 to May 2012. Minimum inhibitory concentrations (MICs) of fluoroquinolones (ciprofloxacin and levofloxacin) were determined by using the agar dilution method. We used PCR and sequencing to determine the TTSS effector genotype and quinolone resistance-determining regions (QRDRs) of the respective target genes gyrA, gyrB, parC, and parE. RESULTS: A higher proportion of exoU+ strains were fluoroquinolone-resistant than exoS+ strains (93.2%, 41/44 vs. 45.0%, 9/20; P< or =0.0001). Additionally, exoU+ strains were more likely to carry combined mutations than exoS+ strains (97.6%, 40/41 vs. 70%, 7/10; P=0.021), and MIC increased as the number of active mutations increased. CONCLUSIONS: The recent overuse of fluoroquinolone has led to both increased resistance and enhanced virulence of carbapenem-resistant P. aeruginosa. These data indicate a specific relationship among exoU genotype, fluoroquinolone resistance, and resistance-conferring mutations.

Contribution of different mechanisms to the resistance to fluoroquinolones in clinical isolates of Salmonella enterica

OBJECTIVES: To study the potential factors include gene mutation, efflux pump and alteration of permeability associated with quinolone-resistance of Salmonella enterica strains isolated from patients with acute gastroenteritis and to evaluate the degree of synergistic activity of efflux pump inhibitors when combined with ciprofloxacin against resistant isolates. METHODS: Antimicrobial resistance patterns of fifty-eight Salmonella isolates were tested. Five isolates were selected to study the mechanism of resistance associated with quinolone group, including mutation in topoisomerase-encoding gene, altered cell permeability, and expression of an active efflux system. In addition, the combination between antibiotics and efflux pump inhibitors to overcome the microbial resistance was evaluated. RESULTS: Five Salmonella isolates totally resistant to all quinolones were studied. All isolates showed alterations in outer membrane proteins including disappearance of some or all of these proteins (Omp-A, Omp-C, Omp-D and Omp-F). Minimum inhibitory concentration values of ciprofloxacin were determined in the presence/absence of the efflux pump inhibitors: carbonyl cyanide m-chlorophenylhydrazone, norepinephrin and trimethoprim. Minimum inhibitory concentration values for two of the isolates were 2-4 fold lower with the addition of efflux pump inhibitors. All five Salmonella isolates were amplified for gyrA and parC genes and only two isolates were sequenced. S. Enteritidis 22 had double mutations at codon 83 and 87 in addition to three mutations at parC at codons 67, 76 and 80 whereas S. Typhimurium 57 had three mutations at codons 83, 87 and 119, but no mutations at parC. CONCLUSIONS: Efflux pump inhibitors may inhibit the major AcrAB-TolC in Salmonella efflux systems which are the major efflux pumps responsible for multidrug resistance in Gramnegative clinical isolates.

An Overview of Fluoroquinolones.

The fluoroquinolones are broad-spectrum bactericidal agents inhibiting DNA synthesis. They are active against gram positive and gram negative organisms like P. aeruginosa, Mycoplasma, Chlamydia, Staphylococci and a few of the Streptococci. They are useful in the treatment of pneumonia, urinary tract infections, bacterial diarrhea, and skin and soft tissue infections. The use of quinolones began with its first generation that consisted of nalidixic acid. From that time, a large number of newer fluoroquinolones having a variety of structures and a broader spectrum of activity have been developed forming the five generations. The more number of fluoroquinolones developed and its widespread usage is attributed to its high bioavailability and tissue penetration. Moreover, the development of resistance to the most commonly used antibiotics has led to the need for alternatives. The various derivatives of fluoroquinolone have varying levels of activity depending on the various groups attached at different positions. Generating a derivative with increased activity will help to reduce the Minimum Inhibitory Concentration (MIC), thereby reducing the possibility of developing resistance to it. This paper gives an overview of fluoroquinolones, their mechanism of action, their uses, resistance development and their adverse effects.

Further Increases in Carbapenem-, Amikacin-, and Fluoroquinolone-Resistant Isolates of Acinetobacter spp. and P. aeruginosa in Korea: KONSAR Study 2009

PURPOSE: The increasing prevalence of antimicrobial resistant bacteria has become a serious worldwide problem. The aim of this study was to analyze antimicrobial resistance data generated in 2009 by hospitals and commercial laboratories participating in the Korean Nationwide Surveillance of Antimicrobial Resistance program. MATERIALS AND METHODS: Susceptibility data were collected from 24 hospitals and two commercial laboratories. In the analysis, resistance did not include intermediate susceptibility. Duplicate isolates were excluded from the analysis of hospital isolates, but not from the commercial laboratory isolates. RESULTS: Among the hospital isolates, methicillin-resistant Staphylococcus aureus, penicillin G-non-susceptible Streptococcus pneumoniae based on meningitis breakpoint, and ampicillin-resistant Enterococcus faecium remained highly prevalent. The proportion of vancomycin-resistant E. faecium gradually increased to 29%. Ceftazidime-resistant Escherichia coli and Klebsiella pneumoniae increased to 17% and 33%, respectively, and fluoroquinolone-resistant K. pneumoniae, Acinetobacter spp. and Pseudomonas aeruginosa increased to 33%, 67% and 39%, respectively. Amikacin-resistant Acinetobacter spp. increased to 48%. Imipenem-resistant Acinetobacter spp. and P. aeruginosa increased to 51% and 26%, respectively. Higher resistance rates were observed in intensive care unit (ICU) isolates than in non-ICU isolates among the isolates from hospitals. Resistance rates were higher in hospital isolates than in clinic isolates among the isolates from commercial laboratories. CONCLUSION: Among the hospital isolates, ceftazidime-resistant K. pneumoniae and fluoroquinolone-resistant K. pneumoniae, Acinetobacter spp., and P. aeruginosa further increased. The increase in imipenem resistance was slight in P. aeruginosa, but drastic in Acinetobacter spp. The problematic antimicrobial-organism combinations were much more prevalent among ICU isolates.

Prevalence and Mechanisms of Low Level Quinolone Resistance among Non-Typhoidal Salmonella Isolates from Human and poultry/Livestock in Korea: Usefulness of Nalidixic Acid Resistance Test / 감염과화학요법

BACKGROUND: Non-typhoidal Salmonella (NTS) are important commensal microorganisms. We intended to investigate the prevalence and mechanisms of nalidixic acid resistance among NTS isolated from human and poultry/livestock. METHODS: A total of 151 Salmonella isolates (36 human and 115 livestock isolates, respectively) was tested for the Minimum inhibitory concentrations (MICs) of nalidixic acid, together with serotyping. As for the nalidixic acid resistant isolates, further studies were taken: MICs of ciprofloxacin, mutation analysis of gyrA and parC genes, and organic solvent tolerance test. RESULTS: Eighty-four isolates of 151 human and livestock isolates were resistant to nalidixic acid. The prevalence of nalidixic acid resistance and was 13.9% (5 of 36 isolates) in human isolates and 68.7% (79 of 151 isolates), in the livestock isolates respectively. Among 84 nalidixic acid-resistant isolates, the The prevalence of ciprofloxacin resistance in livestock isolates was 24.1% (1 resistant and 18 intermediate of 79 strains), but no ciprofloxacin resistance was found in 5 human isolates. Among 65 nalidixic acid resistant, ciprofloxacin-susceptible isolates, 3 (60%, of 5 human isolates) and 60 (100%, all livestock isolates) showed low level fluoroquinolone resistance (ciprofloxacin MIC, 0.125-1.0 microgram/microliter). Six types of point mutations were found in the analysis of DNA sequencing of the gyrA gene in the 84 isolates; 75 isolates showed point mutations on amino acid Ser 83 and/or Asp 87. On the other hand, no point mutation was found from the parC genes. Forty-seven nalidixic acid resistant isolates showed tolerance to organic solvents. CONCLUSIONS: Nalidixic acid resistance was a good marker of low level fluoroquinolone resistance. As for the severe NTS infection, MIC test for nalidixic acid would be required.

Increase of Ceftazidime- and Fluoroquinolone-Resistant Klebsiella pneumoniae and Imipenem-Resistant Acinetobacter spp. in Korea: Analysis of KONSAR Study Data from 2005 and 2007

PURPOSE: Antimicrobial resistance monitoring could be a useful source of information for treating and controlling nosocomial infections. We analyzed antimicrobial resistance data generated by Korean Hospitals and by a commercial laboratory in 2005 and 2007. MATERIALS AND METHODS: Susceptibility data for 2005 and 2007 were collected from 37 and 41 hospitals, respectively, and from one commercial laboratory. Intermediate susceptibility was not included in the calculation of resistance rates. RESULTS: Methicillin-resistant Staphylococcus aureus (MRSA) (64%), third-generation cephalosporin-resistant Klebsiella pneumoniae (29%), fluoroquinolone-resistant Escherichia coli (27%), Pseudomonas aeruginosa (33%), and Acinetobacter spp. (48%), and amikacin-resistant P. aeruginosa (19%) and Acinetobacter spp. (37%) were prevalent in hospitals in 2007. A gradual increase of vancomycin-resistant Enterococcus faecium and imipenem-resistant Acinetobacter spp. was observed. Higher incidences of third-generation cephalosporin-resistant E. coli and K. pneumoniae and imipenem-resistant P. aeruginosa were found in the commercial laboratory than in the hospitals. CONCLUSION: Methicillin-resistant S. aureus, third-generation cephalosporin-resistant K. pneumoniae, and fluoroquinolone-resistant E. coli, P. aeruginosa and Acinetobacter spp. remain prevalent in Korea, while the incidence of vancomycin-resistant E. faecium and imipenem-resistant Acinetobacter spp. has increased gradually. The higher prevalences of third-generation cephalosporin-resistant E. coli and K. pneumoniae, and imipenem-resistant P. aeruginosa in the commercial laboratory are a new concern.

Further Increase of Vancomycin-Resistant Enterococcus faecium, Amikacin- and Fluoroquinolone-Resistant Klebsiella pneumoniae, and Imipenem-Resistant Acinetobacter spp. in Korea: 2003 KONSAR Surveillance

Monitoring temporal trends of antimicrobial resistance can provide useful information for the empirical selection of antimicrobial agents to treat infected patients and for the control of nosocomial infections. In this study, we analyzed antimicrobial resistance of clinically relevant bacteria in 2003 at Korean hospitals and at a commercial laboratory. The following organism-antimicrobial agent resistance combinations were very prevalent: oxacillin-resistant Staphylococcus aureus (68%), expanded-spectrum cephalosporin-resistant Klebsiella pneumoniae (25%), and fluoroquinolone-resistant Escherichia coli (33%), Acinetobacter spp. (58%), and Pseudomonas aeruginosa (40%). Moreover, gradual increases in vancomycin-resistant Enterococcus faecium (20%), cefoxitin-resistant E. coli (10%) and K. pneumoniae (23%), and imipenem-resistant P. aeruginosa (20%) and Acinetobacter spp. (13%) were also observed. The resistance rates of Acinetobacter spp. to most antimicrobial agents at hospitals and at the commercial laboratory were similar. Among the Acinetobacter spp. isolated at a tertiary-care hospital, 46.2% were multidrug-resistant to 9-12 of 13 antimicrobial agents, and 18.3% were panresistant. The exclusion of duplicate isolates at a tertiary-care hospital significantly lowered the proportion of oxacillin-resistant S. aureus, vancomycin-resistant E. faecium, and fluoroquinolone-resistant E. coli.

A mutation in QRDR in the ParC subunit of topoisomerase IV was responsible for fluoroquinolone resistance in clinical isolates of Streptococcus pneumoniae

Forty-one strains of Streptococcus pneumoniae were isolated at Seoul National University Children's Hospital from 1991 to 1997. Isolates were divided into six groups based on MICs of three quinolones, ciprofloxacin, ofloxacin and norfloxacin. Sequencing showed that the isolates which were intermediately resistant to three quinolones or resistant to at least one kind of quinolone had one missense mutation, Lys137-->Asn(AAG-->AAT) substitution in the ParC subunit of topoisomerase IV without additional mutation in QRDR of the GyrA subunit of DNA gyrase. In conclusion, the ParC subunit of DNA topoisomerase IV is the primary target site for fluoroquinolone in S. pneumoniae and Lys137-->Asn substitution renders the quinolone resistance in S. pneumoniae.