Fluoroquinolone resistance in Neisseria meningitidis in Spain

Enriquez, Rocío; Abad, Raquel; Salcedo, Celia; Pérez, Sonia González; Vázquez, Julio

doi:10.1093/jac/dkm452

Cited by 34 publications

(20 citation statements)

References 11 publications

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“…Bioluminescent signals in mice that were infected with clone AS12lux (ciprofloxacin MIC of 0.125 g/ml) continued to increase, regardless of ciprofloxacin treatment, suggesting that the strain is resistant to ciprofloxacin. Meningococcal resistance to ciprofloxacin remains rare (2,7,(12)(13)(14)(15). Our current data show that alterations of the QRDR are still detected only in the gyrA gene and these alterations are associated with increased ciprofloxacin MICs.…”

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confidence: 55%

Target Gene Sequencing To Define the Susceptibility of Neisseria meningitidis to Ciprofloxacin

Hong

Hedberg

Abad

et al. 2013

Antimicrob Agents Chemother

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e Meningococcal gyrA gene sequence data, MICs, and mouse infection were used to define the ciprofloxacin breakpoint for Neisseria meningitidis. Residue T91 or D95 of GyrA was altered in all meningococcal isolates with MICs of >0.064 g/ml but not among isolates with MICs of <0.032 g/ml. Experimental infection of ciprofloxacin-treated mice showed slower bacterial clearance when GyrA was altered. These data suggest a MIC of >0.064 g/ml as the ciprofloxacin breakpoint for meningococci and argue for the molecular detection of ciprofloxacin resistance. N eisseria meningitidis is a Gram-negative encapsulated bacterium isolated only from humans, where it may provoke severe invasive infections (mainly septicemia and meningitis). Management of meningococcal disease requires prompt treatment of patients, as well as vaccination and/or chemoprophylaxis of contacts. The antibiotics currently recommended for chemoprophylaxis are rifampin, ciprofloxacin, and ceftriaxone (1). The emergence and expansion of meningococcal clones resistant to these antibiotics may jeopardize these recommendations. Ciprofloxacin resistance in meningococci was earlier linked to mutations in the quinolone resistance-determining region (QRDR) of the gyrA gene (encodes subunit A of DNA gyrase) but no mutations in the QRDR of gyrB, parC, and parE (2). Here we correlate gyrA mutations and their in vivo impact on ciprofloxacin MICs for meningococcal clinical isolates.This study examined all of the available meningococcal isolates collected from 1995 to 2011 with ciprofloxacin MICs of Ն0.064 g/ml (n ϭ 19) in four countries (France, Italy, Spain, and Sweden). Representative isolates with ciprofloxacin MICs of Յ0.032 g/ml (n ϭ 177) were also tested, as were two isolates of N. gonorrhoeae and N. cinerea with ciprofloxacin MICs of 0.250 and 0.125 g/ml, respectively. Isolate typing was performed as previously described (3), and all those data are available at the Neisseria

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confidence: 55%

Target Gene Sequencing To Define the Susceptibility of Neisseria meningitidis to Ciprofloxacin

Hong

Hedberg

Abad

et al. 2013

Antimicrob Agents Chemother

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“…The reduced susceptibility to ciprofloxacin in NM has been associated with point mutations in the QRDRs of the target sites for the fluorquinolones and specifically with changes in the GyrA subunit of DNA gyrase [40]. This paper describes twoW135∶2a:P1.5,2:ST-11:ST-11 complex isolates displaying resistance to ciprofloxacin associated with a mutation in the QRDR of gyr A gene Thr91-Ile.…”

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confidence: 99%

Phenotypic and Genotypic Characteristics of Neisseria meningitidis Disease-Causing Strains in Argentina, 2010

et al. 2013

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Phenotypic and genotypic characterization of 133 isolates of Neisseria meningitidis obtained from meningococcal disease cases in Argentina during 2010 were performed by the National Reference Laboratory as part of a project coordinated by the PAHO within the SIREVA II network. Serogroup, serotype, serosubtype and MLST characterization were performed. Minimum Inhibitory Concentration to penicillin, ampicillin, ceftriaxone, rifampin, chloramphenicol, tetracycline and ciprofloxacin were determined and interpreted according to CLSI guidelines. Almost 49% of isolates were W135, and two serotype:serosubtype combinations, W135∶2a:P1.5,2:ST-11 and W135∶2a:P1.2:ST-11 accounted for 78% of all W135 isolates. Serogroup B accounted for 42.1% of isolates, and was both phenotypically and genotypically diverse. Serogroup C isolates represented 5.3% of the dataset, and one isolate belonging to the ST-198 complex was non-groupable. Isolates belonged mainly to the ST-11 complex (48%) and to a lesser extent to the ST-865 (18%), ST-32 (9,8%) and the ST-35 complexes (9%). Intermediate resistance to penicillin and ampicillin was detected in 35.4% and 33.1% of isolates respectively. Two W135∶2a:P1.5,2:ST-11:ST-11 isolates presented resistance to ciprofloxacin associated with a mutation in the QRDR of gyrA gene Thr91-Ile. These data show serogroup W135 was the first cause of disease in Argentina in 2010, and was strongly associated with the W135∶2a:P1.5,2:ST-11 epidemic clone. Serogroup B was the second cause of disease and isolates belonging to this serogroup were phenotypically and genotypically diverse. The presence of isolates with intermediate resistance to penicillin and the presence of fluorquinolone-resistant isolates highlight the necessity and importance of maintaining and strengthening National Surveillance Programs.

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“…In Gram-negative cocci, such as Neisseria gonorrhoeae and N. meningitidis, the mechanism of fluoroquinolone resistance involves amino acid substitutions in the quinolone resistance-determining region (QRDR) of GyrA and ParC and reduced fluoroquinolone accumulation in the cells (7)(8)(9). In a recent study, we showed that T80I substitution in GyrA is involved in low-level fluoroquinolone resistance in M. catarrhalis clinical isolates (10).…”

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Molecular Characterization of Fluoroquinolone-Resistant Moraxella catarrhalis Variants Generated In Vitro by Stepwise Selection

Yamada

Saito

Muto

et al. 2017

Antimicrob Agents Chemother

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Moraxella catarrhalis causes respiratory infections. In this study, fluoroquinolone-resistant strains were selected in vitro to evaluate the mechanism of fluoroquinolone resistance. Strains with reduced fluoroquinolone susceptibility were obtained by stepwise selection in levofloxacin, and fluoroquinolone targets gyr and par were sequenced. Six novel mutations in GyrA (D84Y, T594dup, and A722dup), GyrB (E479K and D439N), and ParE (Q395R) involved in M. catarrhalis resistance to fluoroquinolones were revealed.KEYWORDS Moraxella catarrhalis, fluoroquinolone, gyr, par, quinolone resistancedetermining region M oraxella catarrhalis is a Gram-negative aerobic diplococcus that causes upper and lower respiratory tract infections (1). M. catarrhalis is known to be resistant to penicillin and first-generation cephalosporins, owing to its ability to produce BRO ␤-lactamase; however, it typically remains susceptible to other antibiotics, including fluoroquinolones (2-4). Fluoroquinolones act primarily by inhibiting DNA gyrase and topoisomerase IV. These two enzymes work together during DNA replication, transcription, recombination, and repair, which are essential for bacterial growth. Both DNA gyrase and topoisomerase IV are large, complex enzymes composed of two pairs of subunits. DNA gyrase comprises the GyrA and GyrB subunits, encoded by the gyrA and gyrB genes, respectively, while topoisomerase IV is composed of ParC and ParE, encoded by the parC and parE genes, respectively (5, 6).In Gram-negative cocci, such as Neisseria gonorrhoeae and N. meningitidis, the mechanism of fluoroquinolone resistance involves amino acid substitutions in the quinolone resistance-determining region (QRDR) of GyrA and ParC and reduced fluoroquinolone accumulation in the cells (7-9). In a recent study, we showed that T80I substitution in GyrA is involved in low-level fluoroquinolone resistance in M. catarrhalis clinical isolates (10). However, the molecular mechanism of high-level fluoroquinolone resistance in M. catarrhalis is unknown. Therefore, we selected fluoroquinolone-resistant M. catarrhalis strains in vitro and identified the mechanism of fluoroquinolone resistance.To obtain fluoroquinolone-resistant M. catarrhalis strains, we performed stepwise selection in brain heart infusion (BHI; BD, Tokyo, Japan) agar plates, as previously described, with modifications (11). The ATCC 49143 reference strain was used as the parental strain (P1) and cultured on BHI agar plates containing levofloxacin at half of the previously determined MIC. The agar plates were then incubated at 35°C for 10 h

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Fluoroquinolone resistance in Neisseria meningitidis in Spain

Cited by 34 publications

References 11 publications

Target Gene Sequencing To Define the Susceptibility of Neisseria meningitidis to Ciprofloxacin

Target Gene Sequencing To Define the Susceptibility of Neisseria meningitidis to Ciprofloxacin

Phenotypic and Genotypic Characteristics of Neisseria meningitidis Disease-Causing Strains in Argentina, 2010

Molecular Characterization of Fluoroquinolone-Resistant Moraxella catarrhalis Variants Generated In Vitro by Stepwise Selection

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