Staphylococcus aureus is a highly virulent pathogen and is implicated in approximately 50% of cases of septic arthritis. Studies investigating other S. aureus-related infections have suggested that alpha (Hla), beta (Hlb) and gamma (Hlg) toxins are key virulence factors. In particular, the ‘pore-forming’ alpha toxin is believed to be most potent. In this study, we have assessed the influence of alpha toxin on in situ chondrocyte viability. Osteochondral explants were harvested from the metacarpophalangeal joints of 3-year-old cows and placed into flasks containing Dulbecco's Modified Eagle's Medium. The flasks were then inoculated with the following isogenic ‘knockout’ strains of S. aureus: DU5946 (Hla+Hlb-Hlg-) or DU1090 (Hla-Hlb+Hlg+). The explants were incubated (37°C) and stained after 18, 24 and 40hrs with chloromethylfluorescein di-acetate and propidium iodide, labelling living chondrocytes green and dead cells red, respectively. Axial sections were imaged by confocal microscopy and the percentage cell death obtained using Volocity 4 software. The alpha toxin-producing S. aureus caused rapid cell death, with 24.8+/−3.7% at 18hrs and 44.6+/−7.2% at 24hrs. At 40hrs, there was significantly more chondrocyte death (87.4+/−3.6%; p<0.001) compared to the alpha toxin knockout strain (4.1+/−1.7%; means +/− SEM; n=4). In situ chondrocyte viability was significantly compromised by alpha toxin, with beta and gamma toxins having minimal effect. Further work will clarify the exact mechanism through which this important toxin induces chondrocyte death. Thereafter, it is hoped that targeted treatments can be developed to reduce the extent of cartilage destruction during, and after, an episode of septic arthritis

We performed a retrospective study of a departmental database to assess the efficacy of a new model of orthopaedic care on the outcome of patients with a fracture of the proximal femur. All 1578 patients admitted to a university teaching hospital with a fracture of the proximal femur between December 2007 and December 2009 were included. The allocation of Foundation doctors years 1 and 2 was restructured from individual teams covering several wards to pairs covering individual wards. No alterations were made in the numbers of doctors, their hours, out-of-hours cover, or any other aspect of standard patient care. Outcome measures comprised 30-day mortality and cause, complications and length of stay. Mortality was reduced from 11.7% to 7.6% (p = 0.007, Cox’s regression analysis); adjusted odds ratio was 1.559 (95% confidence interval 1.128 to 2.156). Reductions were seen in Clostridium difficile colitis (p = 0.017), deep wound infection (p = 0.043) and gastrointestinal haemorrhage (p = 0.033). There were no differences in any patient risk factors (except the prevalence of chronic obstructive pulmonary disease), cause of death and length of stay before and after intervention. The underlying mechanisms are unclear, but may include improved efficiency and medical contact time.

These findings may have implications for all specialties caring for patients on several wards, and we believe they justify a prospective trial to further assess this effect.