Biomedical subjects

Geoffrey W Coombs

Publications and source records attributed to Geoffrey W Coombs.

4 recordsLinked to original sources

PubMed2003

Alterations in phage-typing patterns in vancomycin-intermediate Staphylococcus aureus.

The ability of phage-typing and SmaI chromosomal RFLPs to conclude appropriate strain relatedness between a collection of 12 well-characterized in vitro-selected vancomycin-intermediate Staphylococcus aureus (VISA) strains and their seven vancomycin-susceptible parent strains is reported. Generally, no SmaI RFLP alterations were observed in VISA strains when they were compared with their respective parent strains, and clonal relationships between isogenic strains were clearly evident. Unlike the SmaI RFLP results, parent strains and VISA derivatives generally did not share similar phage-typing profiles. Depending on the phage set investigated, some VISA strains even became untypable by this method. Loss of phage infectivity is probably due to cell wall (phage receptor) alterations that are expressed by the VISA strains investigated. Collectively, these findings indicate that inappropriate relationships between VISA and vancomycin-susceptible parents might be drawn if only phage-typing and antibiotic susceptibility are utilized to determine epidemiological relationships.

Anti-Bacterial Agents↗

PubMed2002

Proteome analysis of highly immunoreactive proteins of Helicobacter pylori.

BACKGROUND: Identification of the immunoreactive proteins of Helicobacter pylori is important for the development of both diagnostic tests and vaccines relating to the organism. Our aim was to determine whether there are significant differences between human IgG and IgA reactivities to individual H. pylori proteins, and whether patterns of immunoreactivity are sustained across different strains of H. pylori. METHOD: The total complement of protein from seven strains of H. pylori was resolved by two-dimensional polyacrylamide gel electrophoresis (2D-PAGE). Proteins were transferred electrophoretically onto polyvinylene difluoride (PVDF) membranes, which were probed with sera pooled either from H. pylori-infected patients, or noninfected (control) patients. Highly immunoreactive proteins were detected using chromogenic enzyme-antibody conjugates recognising either serum IgG or IgA. These proteins were then characterised by tryptic peptide-mass fingerprinting using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS). RESULTS: Highly immunoreactive proteins were detected which were common to all seven strains, and recognised by both immunoglobulin subclasses. The proteins appear to be localised in five groups. Protein analysis established that these groups encompass multiple isoforms of chaperonin HspB (two subgroups); urease beta-subunit UreB; elongation factor EF-Tu; and flagellin FlaA. The pattern of highly immunoreactive proteins was strongly conserved across the seven strains. CONCLUSION: These results suggest that within a tightly defined region on the H. pylori proteome map there are five groups of proteins that are highly reactive to both IgG and IgA. Our analysis suggests it is unlikely that the highly immunoreactive clusters harbour any significant proteins other than isoforms of HspB, UreB, EF-Tu and FlaA, and that, with the partial exception of FlaA, these clusters are strongly conserved across all seven strains.

Bacterial Proteins↗

PubMed2002

Genetic organization of mecA and mecA-regulatory genes in epidemic methicillin-resistant Staphylococcus aureus from Australia and England.

The mecA gene that encodes methicillin resistance in Staphylococcus aureus may be regulated by the mecR1 and mecI genes, and this region has been referred to as the mec complex. An analysis of these regulatory genes in 35 epidemic methicillin-resistant S. aureus (MRSA) isolated in England and Australia has found that they contain three classes of mec complex. Firstly, the Class A mec complex with complete mecR1 and mecI genes. Secondly, a new variant of Class A, the Class A1 mec complex, with a 166 bp deletion in the membrane-spanning domain of mecR1 and a complete mecI gene. Thirdly, the Class B mec complex, in which the penicillin-binding domain of mecR1 and the whole mecI gene are deleted by the insertion of a partial sequence of IS1272. Seven MRSA isolated in England and Australia over different time periods had the Class A mec complex. However, the isolates did not have closely related pulsed-field gel electrophoresis (PFGE) patterns. The Class A1 mec complex was found in 12 Australian isolates and the English epidemic MRSA, EMRSA-1. All these organisms were isolated in the early 1980s and had closely related PFGE patterns. The Class B mec complex region was found in nine EMRSA and seven Australian MRSA isolated over the period from the 1970s to 2000. These isolates had related PFGE patterns. The mecA region was also compared in the isolates and all but two of the isolates had an XbaI restriction site. These results support the global spread of epidemic clones and confirm the close relationship between the Australian and English MRSA strains.

Australia↗

PubMed2002

Dissemination of new methicillin-resistant Staphylococcus aureus clones in the community.

Multiple methicillin-resistant Staphylococcus aureus (MRSA) clones carrying type IV staphylococcal cassette chromosome mec were identified in the community-acquired MRSA strains of both the United States and Australia. They multiplied much faster than health-care-associated MRSA and were resistant to fewer non-beta-lactam antibiotics. They seem to have been derived from more diverse S. aureus populations than health-care-associated MRSA strains.

Anti-Bacterial Agents↗