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Competing Interests: The authors declare no conflicts of interest.

Aims: To describe clinical features and molecular epidemiology of non-multiresistant methicillin-resistant Staphylococcus aureus (MRSA) bacteraemia., Methods: Patients with non-multiresistant MRSA isolated from blood at South Western Area Pathology Service from 1 January 1999 to 31 December 2001 were enrolled. Pulsed field gel electrophoresis, phage typing, and (selected instances) multilocus sequence and staphylococcal cassette chromosome typing was performed. PCR was used to detect Panton-Valentine leukocidin (PVL), toxic shock syndrome toxin-1 (TSST-1), and enterotoxin genes., Results: Sixteen patients were detected: eight with UK EMRSA-15 (ST22-MRSA-IV), three with Oceania (South-West Pacific/Western Samoan phage pattern) (ST30-MRSA-IV), two with WA MRSA-5 (ST8-MRSA-IV), and one each with WA MRSA-1 (ST1-MRSA-IV), Queensland strain (ST93-MRSA-IV), and WA MRSA-15 (ST59-MRSA-IV). Prior hospital admissions occurred with six of the eight patients with UK EMRSA-15, none of the three with Oceania, and three of the five with other strains. Thirteen of 16 patients had underlying disease. Three of the three patients with Oceania strain bacteraemia were Polynesians; 11 of 13 of the others were Caucasians. PVL genes were detected in four of 16 isolates (all Oceania and Queensland strains). entC was detected in two EMRSA-15 strains; entA in one Oceania, two WA MRSA-5 and the WA MRSA-1 strain, with entA and entB in the WA MRSA-15 strain. tst was not detected., Conclusions: Multiple epidemic strains cause non-multiresistant MRSA bacteraemia. Most patients had risk factors. Oceania and Queensland strains possess the PVL gene.

The detection of Helicobacter pylori antigen directly in faecal specimens may offer an alternative non-invasive method for determining the presence of H. pylori infection. This study compared the performance of the Premier Platinum HpSA enzyme immunoassay (HpSA) with histology and CLOtest, a rapid urease test. Of 134 patients undergoing upper gastrointestinal endoscopy, 37 (28%) were H. pylori-positive by histology and CLOtest. Using the HpSA test, H. pylori was detected in 35 H. pylori-positive patients (95% sensitivity) and one H. pylori-negative patient (99% specificity). The positive and negative predictive values for HpSA were 97 and 98%, respectively. HpSA is a rapid, easily performed, non-invasive method for detecting H. pylori.

Proteome analysis involves the simultaneous resolution and display of proteins produced by an organism, followed by the quantitation, characterisation and identification of these proteins. As part of an ongoing study mapping and comparing the proteins expressed by various strains of the pathogenic bacterium Helicobacter pylori, we have resolved and identified 93 of the most abundant proteins expressed by type reference strain NCTC 11637. Proteins were separated by two-dimensional gel electrophoresis and stained with Coomassie G250. Intensely-stained spots were excised and digested with trypsin, and the resulting peptides were characterised by mass spectrometry. Proteins were then identified by correlating actual peptide profiles with theoretical profiles generated from published nucleotide sequences. Ninety-three of the most intensely-stained protein spots were identified as the products of 35 genes, giving a ratio of 2.7 protein gene-products per gene. The products of the tsaA, pfr, ureA and ureB genes were amongst several proteins present in multiple isoforms. Peptide mass fingerprinting data were used to identify probable post-translational protein modifications. These results suggest that H. pylori proteins are subject to a high degree of post-translational modification. Comparative proteomics of H. pylori strains should greatly assist in investigating the pathogenic properties of this bacterium.