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Biomedical subjects

N Woodford

Publications and source records attributed to N Woodford.

At least 19 recordsLinked to original sources
PubMed1996

Detection of the mec-A gene and phenotypic detection of resistance in Staphylococcus aureus isolates with borderline or low-level methicillinresistance.

Eighty-three isolates of Staphylococcus aureus for which MICs of methicillin of 4-16 mg/L had previously been recorded were tested for the presence of the mecA gene with a DNA probe and a PCR assay. There was complete agreement between the results obtained by these methods; 39 isolates were mecA-positive and 44 were mecA-negative. Using the presence of mecA as the defining standard, several phenotypic methods for determining resistance to methicillin were evaluated and a high-inoculum, agar-incorporation breakpoint test was found to offer the best combination of high sensitivity and high specificity. However twenty-seven of the 44 mecA-negative strains were methicillin-resistant according to agar dilution MICs (MIC > 4 mg/L on at least one of the four media used) but none had MICs exceeding 32 mg/L. One of the mecA-positive strains had a methicillin MIC of only 8 mg/L and did not appear to be heteroresistant. The clinical significance of these two groups of 'atypical' isolates may need further investigation. This study highlights the problems of detecting reliably S. aureus with low level methicillin resistance by phenotype methods and the usefulness of direct detection of the mecA gene.

Bacterial Proteins↗
PubMed1995

Urinary isolates of apramycin-resistant Escherichia coli and Klebsiella pneumoniae from Dublin.

Twenty-two gentamicin-resistant urinary isolates of Escherichia coli and five gentamicin-resistant urinary isolates of Klebsiella pneumoniae from a Dublin hospital were examined for resistance to the veterinary aminoglycoside antibiotic apramycin. Five isolates of E. coli and one isolate of K. pneumoniae were found to be resistant. The apramycin-resistant isolates, which were also resistant to the veterinary anthelmintic agent hygromycin B, hybridized with a DNA probe for the gene encoding the enzyme 3-N-aminoglycoside acetyltransferase type IV (AAC(3)IV). Resistance to apramycin and hygromycin B was co-transferable in four of the five isolates of E. coli and the isolate of K. pneumoniae. In one isolate of E. coli apramycin resistance was not transferable. On the basis of their restriction enzyme digestion profiles and the antimicrobial resistance traits encoded, the transferable plasmids encoding resistance to apramycin and hygromycin B comprised three distinct types. Genetic linkage between the gene encoding AAC(3)IV and genes encoding resistance to ampicillin and either tetracycline or trimethoprim, means that the relatively widespread use of these antimicrobial agents provides a selective pressure for the persistence of resistance to apramycin and gentamicin even in the absence of bacterial exposure to aminoglycosides.

Conjugation, Genetic↗
PubMed1995

Linkage of vancomycin and high-level gentamicin resistance genes on the same plasmid in a clinical isolate of Enterococcus faecalis.

A transferable 55-MDa plasmid which encoded resistance to both vancomycin and high concentrations of gentamicin was identified in a clinical isolate of Enterococcus faecalis. The plasmid hybridized with probes for the vanB and aac6'aph2" resistance genes. This is the first report of linkage of glycopeptide and high-level aminoglycoside resistance genes in an Enterococcus sp.

Base Sequence↗
PubMed1995

Current perspectives on glycopeptide resistance.

In the last 5 years, clinical isolates of gram-positive bacteria with intrinsic or acquired resistance to glycopeptide antibiotics have been encountered increasingly. In many of these isolates, resistance arises from an alteration of the antibiotic target site, with the terminal D-alanyl-D-alanine moiety of peptidoglycan precursors being replaced by groups that do not bind glycopeptides. Although the criteria for defining resistance have been revised frequently, the reliable detection of low-level glycopeptide resistance remains problematic and is influenced by the method chosen. Glycopeptide-resistant enterococci have emerged as a particular problem in hospitals, where in addition to sporadic cases, clusters of infections with evidence of interpatient spread have occurred. Studies using molecular typing methods have implicated colonization of patients, staff carriage, and environmental contamination in the dissemination of these bacteria. Choice of antimicrobial therapy for infections caused by glycopeptide-resistant bacteria may be complicated by resistance to other antibiotics. Severe therapeutic difficulties are being encountered among patients infected with enterococci, with some infections being untreatable with currently available antibiotics.

Anti-Bacterial Agents↗
PubMed1994

Gentamicin resistance in clinical isolates of Escherichia coli encoded by genes of veterinary origin.

Seven (27%) of 26 gentamicin-resistant human clinical isolates of Escherichia coli were resistant to the veterinary aminoglycoside antibiotic apramycin. A gentamicin-resistant Klebsiella pneumoniae isolate from a patient infected with gentamicin/apramycin-resistant E. coli was also resistant to apramycin. DNA hybridisation studies showed that all gentamicin/apramycin-resistant isolates contained a gene encoding the enzyme 3-N-aminoglycoside acetyltransferase type IV (AAC[3]IV) that mediates resistance to gentamicin and apramycin in bacteria isolated from animals. Seven of the eight gentamicin/apramycin-resistant isolates were also resistant to the veterinary antihelminthic agent hygromycin B, a phenomenon observed previously in gentamicin/apramycin-resistant Enterobacteriaceae isolated from animals. Resistance to gentamicin/apramycin and hygromycin B was co-transferable in six of the isolates. Restriction enzyme analysis of plasmids in apramycin-resistant transconjugants derived from E. coli and K. pneumoniae isolates from the same patient were virtually identical, suggesting that inter-generic transfer of plasmids encoding apramycin resistance had occurred in vivo. These findings support the view that resistance to gentamicin and apramycin in clinical isolates of E. coli results from the spread of resistant organisms from animals to man, with subsequent inter-strain or inter-species spread, or both, of resistance genes on transferable plasmids.

Acetyltransferases↗
PubMed1993

Nosocomial spread of Staphylococcus aureus showing intermediate resistance to methicillin.

A nosocomial outbreak of infection and colonization involving six patients and caused by a strain of Staphylococcus aureus showing intermediate resistance to methicillin (MIC = 4-8 mg l-1) is described. The outbreak was associated with skin-carriage of the epidemic strain by a nurse suffering from severe eczema. The reduced susceptibility of the outbreak strain to methicillin was associated with beta-lactamase production. Elimination or inhibition of beta-lactamase activity produced a two-fold decrease in methicillin MIC. There was no evidence for the presence of either penicillin-binding protein 2a or the corresponding mec gene, which mediate resistance in fully methicillin-resistant strains.

Carrier State↗
PubMed1993

Comparison of high-level gentamicin-resistant Enterococcus faecium isolates from different continents.

Eight clinical isolates of Enterococcus faecium highly resistant to gentamicin (MIC, > 1,000 mg/liter) from patients in six hospitals on three continents were investigated for evidence of spread of either a clone of high-level gentamicin-resistant (HLGR) E. faecium or wide dissemination of a gentamicin resistance (Gmr) plasmid. A combination of ribotypes, plasmid profiles, and extended antimicrobial susceptibilities enabled us to distinguish all but two of the isolates and did not suggest clonal dissemination of a single strain. Two isolates from hospitals situated close together appeared identical by these methods. All of the isolates carried Gmr plasmids which appeared to be closely related following digestion with restriction endonucleases. Cross-hybridization studies confirmed extensive DNA homology between these plasmids. The fragments of these plasmids which hybridized with a probe specific for the aac6'aph2" resistance gene did not resemble those seen in the Gmr transposon Tn5281, which was characterized previously in E. faecalis HH22. This study suggests that there has been widespread dissemination of a single Gmr plasmid and its derivatives amongst isolates of HLGR E. faecium, although a Gmr plasmid from an HLGR E. faecium isolated in the United States showed little homology with the other Gmr plasmids studied.

Conjugation, Genetic↗
PubMed1993

Application of DNA probes for rRNA and vanA genes to investigation of a nosocomial cluster of vancomycin-resistant enterococci.

DNA probes specific for genes encoding rRNA and the glycopeptide resistance gene vanA were used to investigate a cluster of vancomycin-resistant (MICs, > 512 mg/liter) Enterococcus faecalis and Enterococcus faecium isolated from separate patients in a renal unit in a London hospital. When digested with BamHI, 12 of 13 vancomycin-resistant E. faecalis isolates exhibited a common restriction fragment length polymorphism pattern of rRNA genes (ribotype). A vanA probe hybridized with chromosomal DNA in these 12 isolates. The other isolate of vancomycin-resistant E. faecalis had a different ribotype and the vanA gene was located on plasmid DNA. These data suggest that cross-infection with a single strain of vancomycin-resistant E. faecalis occurred in most instances. In contrast, 23 vancomycin-resistant E. faecium isolates showed greater heterogeneity, comprising 8 ribotypes, suggesting that multiple strains were present in the unit. Twenty-one of these 23 isolates harbored a 24-MDa plasmid which hybridized with the vanA probe, implying that interstrain dissemination of a vancomycin resistance plasmid may have occurred among E. faecium isolates in the renal unit.

Bacterial Proteins↗
PubMed1992

High-level resistance to gentamicin in Enterococcus faecium.

During a six-month period in a hospital in Ireland, four patients were infected (isolation from blood cultures) and two were colonized (isolation from rectal swabs) with strains of Enterococcus faecium highly resistant to gentamicin. MICs of gentamicin were greater than 1000 mg/L for all six strains, and each possessed a plasmid of approximately 50 MDa. Resistance to gentamicin was transferable by conjugation from two of the six strains, and was associated with transfer of the 50 MDa plasmid. This plasmid hybridized with a DNA probe specific for the bifunctional AAC(6')-APH(2") aminoglycoside-modifying enzyme. The mechanism of high-level gentamicin resistance in these strains appeared therefore, to be identical to that encountered in Enterococcus faecalis strains worldwide and reported in E. faecium strains in the USA.

Conjugation, Genetic↗