Guidelines for the prophylaxis and treatment of methicillin-resistant Staphylococcus aureus (MRSA) infections in the UK.

These evidence-based guidelines have been produced after a literature review of the treatment and prophylaxis of methicillin-resistant Staphylococcus aureus (MRSA) infection. The guidelines were further informed by antibiotic susceptibility data on MRSA from the UK. Recommendations are given for the treatment of common infections caused by MRSA, elimination of MRSA from carriage sites and prophylaxis of surgical site infection. There are several antibiotics currently available that are suitable for use in the management of this problem and potentially useful new agents are continuing to emerge.

Guidelines for the laboratory diagnosis and susceptibility testing of methicillin-resistant Staphylococcus aureus (MRSA).

These evidence-based guidelines have been produced after a literature review of the laboratory diagnosis and susceptibility testing of methicillin-resistant Staphylococcus aureus (MRSA). We have considered the detection of MRSA in screening samples and the detection of reduced susceptibility to glycopeptides in S. aureus. Recommendations are given for the identification of S. aureus and for suitable methods of susceptibility testing and screening for MRSA and for S. aureus with reduced susceptibility to glycopeptides. These guidelines indicate what tests should be used but not when the tests are applicable, as aspects of this are dealt with in guidelines on control of MRSA. There are currently several developments in screening media and molecular methods. It is likely that some of our recommendations will require modification as the new methods become available.

Metronidazole resistance in Helicobacter pylori.

Modern triple drug regimens are highly effective for treating Helicobacter pylori infection, but bacterial resistance to one of the most effective antibiotics, metronidazole, is a serious and increasing problem. The activity of metronidazole in H. pylori is dependent on reduction of its nitro moiety to highly reactive compounds that cause DNA strand breakage. The acquisition of resistance is highly associated with mutational inactivation of the rdxA gene, which encodes an oxygen-insensitive NADPH nitroreductase. Recent evidence has suggested that inactivation of frxA (NADPH flavin oxidoreductase), fdxB (ferredoxin-like protein) and possibly other reductase-encoding genes may also contribute to the resistant phenotype. Improved understanding of the mechanisms of metronidazole resistance in H. pylori is essential for the development and validation of biopsy-based tests for detection of resistance in clinical practice.