Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q29983 (MIC)
 21,138 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Consecutive isolates of quinolone-resistant campylobacter isolated over a 5 year period (1990-1995) from the faeces of patients with enteritis in Plymouth, UK, were examined for the epidemiology of mutations in gyrA (n = 127). In addition, clinical isolates and poultry isolates from Germany, The Netherlands and other regions of the UK collected before 1995 were examined for mutations in the quinolone resistance-determining region of gyrA by single-stranded conformational polymorphism analysis and direct sequencing of a 270 bp fragment of PCR-generated DNA. The majority of isolates (173/208) carried a mutation at codon 86 in gyrA resulting in substitution of Ile for Thr; all of these were resistant to ciprofloxacin (MIC > or = 2 mg/L). One isolate of Campylobacter jejuni had a mutation at Asp-90, and another had a double mutation at Thr-86 and Pro-104. Only two resistant isolates showed no mutation in gyrA. A novel gyrA sequence was amplified from two Campylobacter lari and one C. jejuni, which exhibited a valine at codon 86. Only 8/192 isolates had changes in gyrB; all were shown to relate to silent mutations in gyrB and presumably reflect natural polymorphisms in the gene.
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PMID:Fluoroquinolone resistance in Campylobacter species from man and animals: detection of mutations in topoisomerase genes. 1249 83

A fluorogenic polymerase chain reaction assay for the gyrA gene was used to determine the frequency of a Thr-86 mutation in Campylobacter jejuni isolates from food animals and humans in northern Thailand and to investigate the correlation between this mutation and bacterial resistance to fluoroquinolones. Eighty-four isolates of C. jejuni were used: 65 from healthy chickens on farms, 16 from chickens at the slaughterhouse, 1 from chicken meat at the market, and 1 from a healthy farm worker. The microbroth dilution technique was used for in vitro susceptibility testing. MIC breakpoints established by the National Antimicrobial Resistance Monitoring System were used to categorize the resistance of C. jejuni to ciprofloxacin and nalidixic acid. Sixty of the 84 C. jejuni isolates tested carried the Thr-86 mutation in the gyrA gene. All isolates with ciprofloxacin MICs of > or = 2 mg/liter carried the mutation, and no isolates with nalidixic acid MICs of < or = 16 mg/liter carried the Thr-86-to-Ile mutation. There was a very strong association between ciprofloxacin resistance and the presence of the mutation (kappa = 0.971, P < 0.01). The association between the presence of the Thr-86-to-Ile mutation and nalidixic acid resistance was weaker (kappa 0.859: P < or = 0.01).
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PMID:Determination of ciprofloxacin and nalidixic acid resistance in Campylobacter jejuni with a fluorogenic polymerase chain reaction assay. 1259 95

Seventeen clinical isolates of Streptococcus pneumoniae showing reduced susceptibility to ciprofloxacin (MIC >/= 4 micro g/ml) collected from eight different Asian countries were analyzed by antimicrobial susceptibility, serotyping, pulsed-field gel electrophoresis (PFGE), and DNA sequencing of the quinolone resistance-determining regions (QRDRs) in gyrA, gyrB, parC, and parE. All isolates but one showed more than one amino acid alteration in QRDRs of four responsible genes. Ile460 --> Val in parE was the most common mutation. Data suggest that Lys137 --> Asn in parC may be a primary step in the development of high-level and multiple FQ resistance. An additional mutation of Ser81 --> Phe in gyrA resulted in high-level resistance to ciprofloxacin, levofloxacin, and gatifloxacin, whereas Ser79 --> Phe in parC may exert an important role in the development of moxifloxacin resistance. Two novel amino acid changes in gyrB, Ala390 --> Val and Asn423 --> Thr, were found. Data from PFGE suggest an introduction and local spread of multiple resistant Spain(23F)-1 clone in Hong Kong, but isolates from other Asian countries were not related to this clone.
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PMID:Fluoroquinolone resistance in clinical isolates of Streptococcus pneumoniae from Asian countries: ANSORP study. 1514 Mar 92

Two new secondary metabolites designated as Sch 419558 (1) and Sch 419559 (2), were isolated from the fermentation broth of Pseudomonas fluorescens. Structure elucidation of 1 and 2 was accomplished by spectroscopic data analyses including MS and NMR experiments. Both compounds were identified as lipopeptides containing valine and threonine linked with 1-amino-1-hydroxy-heptadec-9-en-2-one or 1-amino-1-hydroxy-pentadecan-2-one carbon chains, respectively. Characterization of the amino acids was further confirmed by amino acid analysis. Compounds 1 and 2 exhibited antibacterial activity against a sensitized E. coli strain with minimum inhibitory concentration of 0.3 and 0.6 microg/mL, respectively. Overexpression of RpoE in the E. coli strain increased the MIC over 60-fold for compounds 1 and 2.
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PMID:Two novel antibiotics, Sch 419558 and Sch 419559, produced by Pseudomonas fluorescens: effect on activity by overexpression of RpoE. 1515 1

Of 203 human clinical isolates of Campylobacter jejuni from Alberta, Canada (1999 to 2002), 101 isolates (50%) were resistant to at least 64 microg of tetracycline/ml, with four isolates exhibiting higher levels of tetracycline resistance (512 microg/ml). In total, the MICs for 37% of tetracycline-resistant isolates (256 to 512 microg/ml) were higher than those previously reported in C. jejuni (64 to 128 microg/ml). In the tetracycline-resistant clinical isolates, 67% contained plasmids and all contained the tet(O) gene. Four isolates resistant to high levels of tetracycline (MIC = 512 microg/ml) contained plasmids carrying the tet(O) gene, which could be transferred to other isolates of C. jejuni. The tetracycline MICs for transconjugants were comparable to those of the donors. Cloning of tet(O) from the four high-level tetracycline-resistant isolates conferred an MIC of 32 microg/ml for Escherichia coli DH5alpha. In contrast, transfer to a strain of C. jejuni by using mobilization conferred an MIC of 128 microg/ml. DNA sequence analysis determined that the tet(O) genes encoding lower MICs (64 to 128 microg/ml) were identical to one other, although the tet(O) genes encoding a 512-microg/ml MIC demonstrated several nucleotide substitutions. The quinolone resistance determining region of four ciprofloxacin-resistant isolates (2%) was analyzed, and resistance was associated with a chromosomal mutation in the gyrA gene resulting in a Thr-86-Ile substitution. In addition, six kanamycin-resistant isolates contained large plasmids that carry the aphA-3 marker coding for 3'-aminoglycoside phosphotransferase. Resistance to erythromycin was not detected in 203 isolates. In general, resistance to most antibiotics in C. jejuni remains low, except for resistance to tetracycline, which has increased from about 8 to 50% over the past 20 years.
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PMID:Incidence of antibiotic resistance in Campylobacter jejuni isolated in Alberta, Canada, from 1999 to 2002, with special reference to tet(O)-mediated tetracycline resistance. 1532 9

The presence of fluoroquinolone resistance-associated alterations in topoisomerase II and IV were investigated for 103 nfxC-like type Pseudomonas aeruginosa isolates. The most nfxC-like type isolates (98.1%) possessed the substitution of Ile for Thr-83 in GyrA. A single alteration in GyrA (Thr-83-->Ile) was the most frequently detected and the next common alteration was two alterations with Thr-83-->Ile in GyrA and Ser-87-->Leu in ParC. A novel alteration at position Glin-106 of GyrA, which was suggested to be responsible for fluoroquinolone resistance, was identified. Our study revealed that the alterations in GyrB (Glu-468-->Asp) and in ParE (Asp-419-->Asn or Glu-459-->Asp) play a complementary role in the acquisition of resistance to fluoroquinolone. There was a correlation between the ciprofloxacin MIC and the number of resistance-associated alterations in GyrA, GyrB, ParC and ParE of P. aeruginosa isolates.
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PMID:Alterations in the GyrA and GyrB subunits of topoisomerase II and the ParC and ParE subunits of topoisomerase IV in ciprofloxacin-resistant clinical isolates of Pseudomonas aeruginosa. 1578 7

We examined the potential for the development of fluoroquinolone resistance in Neisseria meningitidis by cultivating two clinical isolates of meningococci in the presence of concentrations of ciprofloxacin at and about the predetermined MIC. The quinolone resistance determining regions (QRDRs) of gyrA and parC of 50 stable quinolone-resistant mutants derived in vitro were sequenced and compared with QRDR alterations reported in clinical isolates of quinolone-resistant meningococci and gonococci. MICs to ciprofloxacin and trovafloxacin were determined and sequence changes were correlated with quinolone MICs. Ciprofloxacin and trovafloxacin MICs of the in vitro-derived quinolone-resistant mutants ranged up to 16 mg/liter. Single GyrA alterations were the first change detected and were accompanied by raised MICs, followed by double GyrA changes and still higher MICs. MICs increased further as single ParC substitutions appeared and these were always in the presence of a single or double GyrA change. GyrA changes occurred at positions 91 and 95 with substitutions of Asp-95-->Asn and Thr-91-->Ala and Ile. Changes in the parC QRDR occurred at positions 85, 86, and 91 with four substitutions, Gly-85-->Asp, Asp-86-->Asn, Glu-91-->Gly, and Glu-91-->Lys, detected. The nature of the individual QRDR substitution appeared to influence the level of quinolone resistance expressed, and this varied with the quinolone agent examined. Close similarities occurred between the sequence and nature of QRDR changes in clinical and in vitro-generated quinolone-resistant mutants and with those previously reported for clinical and in vitro-generated quinolone-resistant gonococci. This suggests that quinolone resistance in meningococci may arise in the same manner and reach similar levels in vivo to those seen in quinolone-resistant Neisseria gonorrhoeae.
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PMID:In vitro assessment of the further potential for development of fluoroquinolone resistance in Neisseria meningitidis. 1585 92

Hassallidin A (1), a new antifungal glycosylated lipopeptide, was isolated from an epilithic cyanobacterium collected in Bellano, Italy, identified as Tolypothrix (basionym Hassallia) species. Chemical, mass spectrometric, and spectroscopic analyses, including one- and two-dimensional NMR, were performed to determine an esterified eight-residue cyclic peptide linked with a carbohydrate and a fatty acid residue. Chiral GC-MS analysis revealed the occurrence of the nonproteinogenic amino acids D-allo-Thr, D-Thr, D-Tyr, D-Gln, and dehydroaminobutyric acid (Dhb) within the peptide moiety. The additional components of hassallidin A could be identified as alpha,beta-dihydroxytetradecanoic acid (Dht) and mannose. This is the first report on a cyclic peptide of cyanobacterial origin that contains both a fatty acid and a carbohydrate moiety. Compound 1 exhibits antifungal activity against Aspergillus fumigatus and Candida albicans with MIC values of 4.8 microg/mL for both test organisms.
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PMID:Hassallidin A, a glycosylated lipopeptide with antifungal activity from the cyanobacterium Hassallia sp. 1592 12

Campylobacter spp. are an important cause of diarrhea in Kuwait. Because susceptibility data for ciprofloxacin and erythromycin, the two recommended drugs for treatment, are not available for this part of the world, 64 Campylobacter spp. isolates obtained from human diarrheal stools in Kuwait during 2000--2003 were studied for susceptibility to these antimicrobials by E-test. The utility of a simple mismatch amplification mutation assay (MAMA) PCR to detect base substitution in the gyrA gene mediating resistance to ciprofloxacin was also explored. Approximately, 53% (34/64) of the isolates were resistant to ciprofloxacin (MIC, 4-64 microg/ml) and 5% (3/64) to erythromycin (MIC>256 microg/ml). MAMA PCR showed a Thr-86-to-Ile mutation in gyrA gene of 23/26 ciprofloxacin-resistant C. jejuni, and in all resistant C. coli. Sequencing of PCR product showed that two resistant strains of C. coli studied had Thr-86-to-Ile (ACT--> ATT) gyrA mutation and three resistant strains of C. jejuni studied had Thr-86-to-Ile (ACA--> ATA) gyrA mutation. In addition, all the three C. jejuni strains had silent mutations. Thus, ciprofloxacin is of limited use for treatment in Kuwait and MAMA PCR is a useful assay to study gyrA mutation. Because Kuwait has a large expatriate population of workers, it can be a focus of spread of antimicrobial resistance.
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PMID:Ciprofloxacin resistance and its molecular mechanism in Campylobacter spp. isolated in Kuwait. 1620 30

Norepinephrine-stimulated skin secretions were obtained from male specimens of the South American bullfrog, Leptodactylus pentadactylus and shown to contain two peptides that inhibited the growth of microorganisms. The primary structure of a previously undescribed peptide, termed pentadactylin, was established as Gly-Leu-Leu-Asp-Thr-Leu-Lys-Gly-Ala-Ala-Lys-Asn-Val-Val-Gly-Ser-Leu-Ala-Ser-Lys-Val-Met-Glu-Lys-Leu.NH2. The second peptide, which differs from pentadactylin by eight amino acid residues, is identical to fallaxin previously isolated from skin secretions of the Caribbean mountain chicken frog L. fallax. Pentadactylin inhibited the growth of reference strains of both Gram-negative bacteria (Escherichia coli, Enterobacter cloacae, Klebsiella pneumoniae, Pseudomonas aeruginosa) and Gram-positive bacteria (Staphylococcus aureus, Staphylococcus epidermidis, Enterococcus faecalis, Streptococcus group B) but potencies were relatively low (MIC values in the range 25-200 microM). The peptide showed very low hemolytic activity against human erythrocytes (LD50>400 microM).
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PMID:Pentadactylin: an antimicrobial peptide from the skin secretions of the South American bullfrog Leptodactylus pentadactylus. 1623 55


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