scholarly journals Development of fluoroquinolone resistance in Enterococcus faecalis and role of mutations in the DNA gyrase gyrA gene.

1996 ◽  
Vol 40 (11) ◽  
pp. 2558-2561 ◽  
Author(s):  
J Tankovic ◽  
F Mahjoubi ◽  
P Courvalin ◽  
J Duval ◽  
R Leclerco
Keyword(s):  
Enterococcus Faecalis ◽  
Resistant Isolate ◽  
Fluoroquinolone Resistance ◽  
Gyra Gene ◽  
Single Clone ◽  
Total Dna ◽  
Resistant Strains ◽  
French Hospital ◽  
High Level

We have analyzed the development of fluoroquinolone resistance between 1986 and 1993 among clinical isolates of Enterococcus faecalis from a French hospital. One hundred randomly selected isolates per year were screened for resistance to ciprofloxacin (MIC > 2 micrograms/ml) and for high-level resistance to gentamicin (MIC > 1,000 micrograms/ml). The percentages of ciprofloxacin-resistant strains for these years were as follows: 1986, 0; 1987, 1; 1988 to 1989, 2; 1990, 6; 1991, 16; 1992, 24; and 1993, 14. Eighty-three percent of the ciprofloxacin-resistant isolates were coresistant to high levels of gentamicin. Forty-eight high-level gentamicin-resistant E. faecalis strains, which were resistant (24 strains) or susceptible (24 strains) to ciprofloxacin, were examined by pulsed-field gel electrophoresis (PFGE) of SmaI-digested total DNA. Numerous PFGE types were observed among the ciprofloxacin-susceptible isolates, whereas one type was largely predominant among the ciprofloxacin-resistant strains, which suggests that the increase in fluoroquinolone resistance was due to the spread of a single clone. A 241-bp fragment of gyrA, corresponding to the quinolone resistance-determining region, was amplified and sequenced for seven ciprofloxacin-resistant isolates. Six strains had high levels of resistance (MICs, 32 to 64 micrograms/ml) and had a mutation at position 83 (Escherichia coli coordinates) from Ser to Arg (three strains) or to Ile (two strains) or at position 87 from Glu to Gly (one strain), whereas the low-level-resistant isolate (MIC, 8 micrograms/ml) had no mutations.

scholarly journals Genetic evidence for a role of parC mutations in development of high-level fluoroquinolone resistance in Escherichia coli.

1996 ◽  
Vol 40 (4) ◽  
pp. 879-885 ◽  
Author(s):  
P Heisig
Keyword(s):  
Escherichia Coli ◽  
Fluoroquinolone Resistance ◽  
Gyra Gene ◽  
Topoisomerase Iv ◽  
E Coli ◽  
Resistant Strains ◽  
Gyra Mutation ◽  
High Level ◽  
Moderately Resistant

Fifteen strains of Escherichia coli with MICs of ciprofloxacin (CIP) between 0.015 and 256 micrograms/ml were examined for the presence of mutations in the quinolone resistance-determining region of the gyrA gene and in an analogous region of the parC gene. No mutation was found in a susceptible isolate (MIC of CIP, 0.015 microgram/ml). Four moderately resistant strains (MIC of CIP 0.06 to 4 micrograms/ml) carried one gyrA mutation affecting serine 83, but in only one strain was an additional parC mutation (Gly-78 to Asp) detected. All ten highly resistant strains examined (MIC of CIP, > 4 micrograms/ml) carried two gyrA mutations affecting residues serine 83 and aspartate 87, and at least one parC mutation. These parC mutations included alterations of serine 80 to arginine or isoleucine and glutamate 84 to glycine or lysine. The parC+ and two mutant alleles (parCI-80 and parCI-80,G-84) were inserted into the mobilizable vector pBP507. Transfer of a plasmid-coded parC+ allele into parC+ strains did not alter the susceptibilities towards ciprofloxacin or nalidixic acid, while a significant increase in susceptibility was detectable for parC mutants. This increase, however, did not restore wild-type susceptibility, whereas transfer of a plasmid-coded gyrA+ allele alone or in combination with parC+ did. These data are in agreement with the view that topoisomerase IV is a secondary, less sensitive target for quinolone action in Escherichia coli and that the development of high-level fluoroquinolone resistance in E. coli requires at least one parC mutation in addition to the gyrA mutation(s).

scholarly journals Alterations in GyrA and ParC Associated with Fluoroquinolone Resistance in Enterococcus faecium

1999 ◽  
Vol 43 (4) ◽  
pp. 947-949 ◽  
Author(s):  
Nagwa el Amin ◽  
Shah Jalal ◽  
Bengt Wretlind
Keyword(s):  
Enterococcus Faecalis ◽  
Resistant Strain ◽  
Enterococcus Faecium ◽  
The Other ◽  
Fluoroquinolone Resistance ◽  
Topoisomerase Iv ◽  
Gram Positive Bacteria ◽  
Efflux Mechanism ◽  
Resistant Strains ◽  
High Level

ABSTRACT High-level quinolone resistance in Enterococcus faeciumwas associated with mutations in both gyrA andparC genes in 10 of 11 resistant strains. One low-level resistant strain without such mutations may instead possess an efflux mechanism or alterations in the other subunits of the gyrase or topoisomerase IV genes. These findings are similar to those for other gram-positive bacteria, such as Enterococcus faecalis.

scholarly journals Role of embB in natural and acquired resistance to ethambutol in mycobacteria.

1997 ◽  
Vol 41 (10) ◽  
pp. 2270-2273 ◽  
Author(s):  
F Alcaide ◽  
G E Pfyffer ◽  
A Telenti
Keyword(s):  
Nontuberculous Mycobacteria ◽  
Practical Implication ◽  
Acquired Resistance ◽  
Fold Increase ◽  
Drug Susceptibility ◽  
Natural Resistance ◽  
Intrinsic Resistance ◽  
Resistant Strains ◽  
High Level

The mycobacterial embCAB operon encodes arabinosyl transferases, putative targets of the antimycobacterial agent ethambutol (EMB). Mutations in embB lead to resistance to EMB in Mycobacterium tuberculosis. The basis for natural, intrinsic resistance to EMB in nontuberculous mycobacteria (NTM) is not known; neither is the practical implication of resistance to EMB in the absence of embB mutations in M. tuberculosis well understood. The conserved embB resistance-determining region (ERDR) of a collection of 13 strains of NTM and 12 EMB-resistant strains of M. tuberculosis was investigated. Genotypes were correlated with drug susceptibility phenotypes. High-level natural resistance to EMB (MIC, . or =64 microg/ml) was associated with a variant amino acid motif in the ERDR of M. abscessus, M. chelonae, and M. leprae. Transfer of the M. abscessus emb allele to M. smegmatis resulted in a 500-fold increase in the MICs. In M. tuberculosis, embB mutations were associated with MICs of > or =20 microg/ml while resistance not associated with an ERDR mutation generally resulted in MICs of < or =10 microg/ml. These data further support the notion that the emb region determines intrinsic and acquired resistance to EMB and might help in the reassessment of the current recommendations for the screening and treatment of infections with EMB-resistant M. tuberculosis and NTM.

scholarly journals Role of Hypermutability in the Evolution of the Genus Oenococcus

2007 ◽  
Vol 190 (2) ◽  
pp. 564-570 ◽  
Author(s):  
Angela M. Marcobal ◽  
David A. Sela ◽  
Yuri I. Wolf ◽  
Kira S. Makarova ◽  
David A. Mills
Keyword(s):  
Lactic Acid ◽  
Leuconostoc Mesenteroides ◽  
Genomic Analysis ◽  
Oenococcus Oeni ◽  
Mutation Rates ◽  
Comparative Genomic ◽  
Allelic Polymorphism ◽  
Resistant Strains ◽  
High Level

ABSTRACT Oenococcus oeni is an alcohol-tolerant, acidophilic lactic acid bacterium primarily responsible for malolactic fermentation in wine. A recent comparative genomic analysis of O. oeni PSU-1 with other sequenced lactic acid bacteria indicates that PSU-1 lacks the mismatch repair (MMR) genes mutS and mutL. Consistent with the lack of MMR, mutation rates for O. oeni PSU-1 and a second oenococcal species, O. kitaharae, were higher than those observed for neighboring taxa, Pediococcus pentosaceus and Leuconostoc mesenteroides. Sequence analysis of the rpoB mutations in rifampin-resistant strains from both oenococcal species revealed a high percentage of transition mutations, a result indicative of the lack of MMR. An analysis of common alleles in the two sequenced O. oeni strains, PSU-1 and BAA-1163, also revealed a significantly higher level of transition substitutions than were observed in other Lactobacillales species. These results suggest that the genus Oenococcus is hypermutable due to the loss of mutS and mutL, which occurred with the divergence away from the neighboring Leuconostoc branch. The hypermutable status of the genus Oenococcus explains the observed high level of allelic polymorphism among known O. oeni isolates and likely contributed to the unique adaptation of this genus to acidic and alcoholic environments.

scholarly journals Single and Double Mutations in gyrA but Not in gyrB Are Associated with Low- and High-Level Fluoroquinolone Resistance in Helicobacter pylori

2003 ◽  
Vol 47 (12) ◽  
pp. 3942-3944 ◽  
Author(s):  
Jacques Tankovic ◽  
Christine Lascols ◽  
Quentin Sculo ◽  
Jean-Claude Petit ◽  
Claude-James Soussy
Keyword(s):  
Helicobacter Pylori ◽  
Single Step ◽  
Fluoroquinolone Resistance ◽  
Clinical Strains ◽  
French Hospital ◽  
High Level ◽  
High Mics

ABSTRACT In one French hospital the rate of resistance to ciprofloxacin in Helicobacter pylori was 3.3% (2 of 60 strains) in 1999. The six resistant clinical strains (four from 1996 and two from 1999) and three ciprofloxacin-selected single-step mutants studied carried one gyrA mutation but none in gyrB. Clinafloxacin and garenoxacin were the most active fluoroquinolones against these mutants. Occurrence of a second gyrA mutation was associated with high MICs of all fluoroquinolones tested.

Salmonella enterica serovar Typhi in Japan, 2001–2006: emergence of high-level fluoroquinolone-resistant strains

2009 ◽  
Vol 138 (3) ◽  
pp. 318-321 ◽  
Author(s):  
M. MORITA ◽  
K. HIROSE ◽  
N. TAKAI ◽  
J. TERAJIMA ◽  
H. WATANABE ◽  
...  
Keyword(s):  
Salmonella Enterica ◽  
Multidrug Resistant ◽  
Fluoroquinolone Resistance ◽  
South East Asia ◽  
Asian Countries ◽  
Salmonella Enterica Serovar Typhi ◽  
Phage Types ◽  
Imported Cases ◽  
Resistant Strains ◽  
High Level

SUMMARYThe phage types and antimicrobial susceptibilities of 226 isolates of Salmonella enterica serovar Typhi from imported cases in Japan between 2001 and 2006 were investigated. Most (93·8%) had travelled to Asian countries, particularly South East Asia. Twenty-one phage types were identified with E1 (30·5%), UVS (15·9%) and B1 (9·3%) being the most common. The frequency of multidrug-resistant strains reached 37·0% in 2006 with phage types E1 and E9 predominating. Almost half (48·2%) of the isolates were resistant to nalidixic acid and two isolates displayed high-level fluoroquinolone resistance. Three mutations, two in gyrA and one in parC, were identified in both isolates.

scholarly journals Identification of chromosomal location of mupA gene, encoding low-level mupirocin resistance in staphylococcal isolates.

1996 ◽  
Vol 40 (12) ◽  
pp. 2820-2823 ◽  
Author(s):  
M A Ramsey ◽  
S F Bradley ◽  
C A Kauffman ◽  
T M Morton
Keyword(s):  
Genomic Dna ◽  
Southern Blot Analysis ◽  
Chromosomal Location ◽  
Pcr Amplification ◽  
Resistant Isolate ◽  
Gene Encoding ◽  
Low Level ◽  
Resistant Strains ◽  
Mupirocin Resistance ◽  
High Level

Low- and high-level mupirocin resistance have been reported in Staphylococcus aureus. The expression of plasmid-encoded mupA is responsible for high-level mupirocin resistance. Low-level mupirocin-resistant strains do not contain plasmid-encoded mupA, and a chromosomal location for this gene has not previously been reported. We examined high- and low-level mupirocin-resistant S. aureus strains to determine if mupA was present on the chromosome of low-level-resistant isolates. Southern blot analysis of DNA from four mupirocin-resistant strains identified mupA in both high- and low-level mupirocin-resistant strains. Low-level mupirocin-resistant strains contained a copy of mupA on the chromosome, while the high-level mupirocin-resistant isolate contained a copy of the gene on the plasmid. PCR amplification of genomic DNA from each mupirocin-resistant strain resulted in a 1.65-kb fragment, the predicted product from the intragenic mupA primers. This is the first report of a chromosomal location for the mupA gene conferring low-level mupirocin resistance.

Outbreak of Infections in a Greek University Hospital Involving a Single Clone of High-Level Aminoglycoside-ResistantEnterococcus faecalis

2000 ◽  
Vol 21 (12) ◽  
pp. 786-789 ◽  
Author(s):  
Spyros Pournaras ◽  
Athanassios Tsakris ◽  
Mary E. Kaufmann ◽  
John Douboyas ◽  
Antonios Antoniadis
Keyword(s):  
Enterococcus Faecalis ◽  
Resistance Genes ◽  
University Hospital ◽  
Aminoglycoside Resistance ◽  
Single Clone ◽  
Aminoglycoside Resistance Genes ◽  
High Level ◽  
Level Resistance

Among 145Enterococcus faecalisisolates recovered during a 15-month period (April 1997-June 1998) in AHEPA University Hospital, Thessaloniki, Greece, 94 (65%) exhibited high-level resistance to gentamicin or streptomycin and 61 (42%) to both aminoglycosides; 73% of the high-level aminoglycoside-resistantE faecalisisolates belonged to a single clone carrying the geneaac(6')-Ie-aph(2”)-Ia. These findings differ from those of other regions, where high-level aminoglycoside-resistance genes are dispersed into genetically unrelated strains.

scholarly journals Genetic Basis of Antibiotic Resistance in Streptococcus agalactiae Strains Isolated in a French Hospital

2003 ◽  
Vol 47 (2) ◽  
pp. 794-797 ◽  
Author(s):  
Claire Poyart ◽  
Laurence Jardy ◽  
Gilles Quesne ◽  
Patrick Berche ◽  
Patrick Trieu-Cuot
Keyword(s):  
Antibiotic Resistance ◽  
Streptococcus Agalactiae ◽  
Genetic Basis ◽  
Group B Streptococci ◽  
Resistant Strains ◽  
French Hospital ◽  
Group B ◽  
High Level ◽  
Level Resistance

ABSTRACT The genetic basis of antibiotic resistance in 113 unrelated group B streptococci was studied by PCR. Ninety-four strains were resistant to tetracycline-minocycline, and tet(M) was detected in 85% of these isolates. Seventeen erythromycin-resistant strains contained the erm(B), erm(TR), or mef(A) gene. Eleven strains exhibited high-level resistance to kanamycin due to the presence of the aphA3 gene; eight of these strains were also highly resistant to streptomycin; aad-6-related sequences were detected in seven strains.

scholarly journals Native Microbial Colonization of Drosophila melanogaster and Its Use as a Model of Enterococcus faecalis Pathogenesis

2007 ◽  
Vol 75 (4) ◽  
pp. 1565-1576 ◽  
Author(s):  
Christopher R. Cox ◽  
Michael S. Gilmore
Keyword(s):  
Drosophila Melanogaster ◽  
Enterococcus Faecalis ◽  
Immunohistochemical Staining ◽  
Microbial Colonization ◽  
Gi Tract ◽  
Thin Sections ◽  
Anatomical Distribution ◽  
Bacterial Phyla ◽  
High Level

ABSTRACT Enterococci are commensal organisms of the gastrointestinal (GI) tracts of a broad range of mammalian and insect hosts, but they are also leading causes of nosocomial infection. Little is known about the ecological role of enterococci in the GI tract consortia. To develop a tractable model for studying the roles of these organisms as commensals and pathogens, we characterized the Drosophila melanogaster microflora and examined the occurrence of enterococci in the gastrointestinal consortium of Drosophila. In a survey of laboratory-reared Drosophila and wild-captured flies, we found that Drosophila was naturally colonized by representatives of five bacterial phyla. Among these organisms were several species of enterococci, including Enterococcus faecalis, Enterococcus faecium, Enterococcus gallinaraum, and Enterococcus durans, as well as a previously detected but uncultured Enterococcus species. Drosophila could be cured of enterococcal carriage by antibiotic treatment and could be reassociated with laboratory strains. High-level colonization by a well-characterized strain expressing the enterococcal cytolysin was found to be detrimental to Drosophila compared to the effect of an isogenic, noncytolytic control. The anatomical distribution of enterococci in the Drosophila GI tract was determined by immunohistochemical staining of thin sections of naturally colonized and reassociated flies.

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