Summary The ability of Staphylococcus aureus cells to induce platelet aggregation has long been recognized. However, despite several attempts to identify the mechanisms involved in this interaction, the nature of the bacterial receptors required remains poorly understood. Using genetic manipulation, this study for the first time provides clear evidence that several S. aureus surface proteins participate in the inter‐action with platelets. Mutants of S. aureus strain Newman lacking one or more surface proteins were tested for their ability to stimulate platelet aggre‐gation. This approach was complemented by the expression of a number of candidate proteins in the non‐aggregating Gram‐positive bacterium Lacto‐coccus lactis. S. aureus‐induced aggregation was monophasic and was dependent on the platelet receptor GPIIb/IIIa. The fibrinogen‐binding proteins, clumping factors A and B and the serine‐aspartate repeat protein SdrE could each induce aggregation when expressed in L. lactis. Although protein A expressed in L. lactis was not capable of inducing aggregation independently, it enhanced the aggregation response when expressed on the surface of S. aureus. Thus, S. aureus has multiple mechanisms for stimulating platelet aggregation. Such functional redundancy suggests that this phenomenon may be important in the pathogenesis of invasive diseases such as infective endocarditis.

The importance of the fibrinogen-binding adhesin clumping factor A (ClfA) in the pathogenesis of Staphylococcus aureus septic arthritis was examined in an animal model. The protective effect of active and passive immunization with ClfA also was investigated in S. aureus infection models. The severity of arthritis was markedly reduced in mice challenged intravenously with a clfA mutant, compared with mice infected with the wild-type strain. Mice immunized with recombinant ClfA and challenged with S. aureus developed less-severe arthritis than did mice immunized with a control antigen. Passive immunization of mice with rat and rabbit anti-ClfA antibodies protected against S. aureus arthritis and sepsis-induced death, indicating that the protection by active immunization is antibody mediated. Taken together, these data strongly suggest that ClfA is a crucial virulence determinant for septic arthritis and an excellent target for the generation of immune therapies directed against S. aureus.

SummaryStaphylococcus aureus is an important cause of sepsis in both community and hospital settings, a major risk factor for which is nasal carriage of the bacterium. Eradication of carriage by topical antibiotics reduces sepsis rates in high-risk individuals, an important strategy for the reduction of nosocomial infection in targeted patient populations. Understanding the mechanisms by which S. aureus adheres to nasal epithelial cells in vivo may lead to alternative methods of decolonization that do not rely on sustained antimicrobial susceptibility. Here, we demonstrate for the first time that the S. aureus surfaceexpressed protein, clumping factor B (ClfB), promotes adherence to immobilized epidermal cytokeratins in vitro . By expressing a range of S. aureus adhesins on the surface of the heterologous host Lactococcus lactis , we demonstrated that adherence to epidermal cytokeratins was conferred by ClfB. Adherence of wild-type S. aureus was inhibited by recombinant ClfB protein or anti-ClfB antibodies, and S. aureus mutants defective in ClfB adhered poorly to epidermal cytokeratins. Expression of ClfB promoted adherence of L. lactis to human desquamated nasal epithelial cells, and a mutant of S. aureus defective in ClfB had reduced adherence compared with wild type. ClfB also promoted adherence of L. lactis cells to a human keratinocyte cell line. Cytokeratin 10 molecules were shown by flow cytometry to be exposed on the surface of both desquamated nasal epithelial cells and keratinocytes. Cytokeratin 10 was also detected on the surface of desquamated human nasal cells using immunofluorescence, and recombinant ClfB protein was shown to bind to cytokeratin K10 extracted from these cells. We also showed that ClfB is transcribed by S. aureus in the human nares. We propose that ClfB is a major determinant in S. aureus nasal colonization.

There is substantial evidence supporting the need for effective intervention for children and families living with parental mental illness. However, translation of this knowledge into mental health workforce practice remains variable, with a range of clinical practices and models of care evident. Nurses, who constitute the majority of the mental health workforce, are in prime positions to support children and families and provide preventative measures, identify those at risk, and intervene early. In this paper, we provide a framework for practice for nurses working with consumer parents. We contend that traditional models of nursing practice concentrating on the consumer are insufficient in meeting the needs of children and families living with parental mental illness. A focus on families needs to be core business for mental health nurses. A family-focused approach can be used to prevent problems for children and their families, and identify their strengths as well as vulnerabilities. Family-focused care is a useful framework from which to support families and address the challenges that might arise from parental mental illness, and to build individual and family resilience.

The primary habitat of Staphylococcus aureus in humans is the moist squamous epithelium of the anterior nares. We showed previously that S. aureus adheres to desquamated epithelial cells and that clumping factor B (ClfB), a surface-located MSCRAMM (microbial surface components recognizing adhesive matrix molecules) known for its ability to bind to the ␣-chain of fibrinogen, is partly responsible ( We provide an explanation for the molecular basis for S. aureus adherence to the squamous epithelium and suggest that nasal colonization might be prevented by reagents that inhibit this interaction.

This paper reports the findings of a qualitative study that used a hermeneutic phenomenological methodology to develop insights into the experience of parents of young people who engage in self-harming behaviour. Six mothers (and one father who accompanied his wife) participated in the study. Findings reveal that mothers experienced guilt and shame, and that these feelings shaped their reactions and responses. These mothers described experiencing emotional dilemmas, such as the degree to which they could be responsible, uncertainty about how to understand self harm, and the best course of action to take with their child. They also encountered difficulties in combating the negative emotional effects for themselves and other family members. Findings provide insights that can help nurses and family health workers to understand and assist parents with greater effectiveness; by maintaining a non-judgemental stance, acknowledging the difficulties of their experiences, encouraging confidence in their parenting abilities, and promoting effective stress management strategies.

A Staphylococcus aureus norA disruption mutant was created by allelic replacement. Exposure of this mutant to norfloxacin produced SA K1748, a derivative with raised fluoroquinolone MICs, found to be the result of a grlA mutation, and raised organic cation MICs. Ethidium and enoxacin uptake was identical in SA K1748 and its parent, but pre-exposure of SA K1748 to organic cations caused a reduction in ethidium uptake as a result of increased efflux. Altered ethidium uptake and efflux, as well as increased MICs of other organic cations, suggest that SA K1748 possesses a non-NorA multidrug efflux transporter that is inducible by its substrates.

Working shifts for nurses is a reality that comes with the profession. While there is a significant body of research on shiftwork, little of this has been specifically applied to nursing, and the implications for individual nurses needing to care for their own health have not been drawn.