Summary Objectives Staphylococcus aureus bacteraemia is a common, often fatal infection. Our aim was to describe how its clinical presentation varies between populations and to identify common determinants of outcome. Methods We conducted a pooled analysis on 3395 consecutive adult patients with S. aureus bacteraemia. Patients were enrolled between 2006 and 2011 in five prospective studies in 20 tertiary care centres in Germany, Spain, United Kingdom, and United States. Results The median age of participants was 64 years (interquartile range 50–75 years) and 63.8% were male. 25.4% of infections were associated with diabetes mellitus, 40.7% were nosocomial, 20.6% were caused by methicillin-resistant S. aureus (MRSA), although these proportions varied significantly across studies. Intravenous catheters were the commonest identified infective focus (27.7%); 8.3% had endocarditis. Crude 14 and 90-day mortality was 14.6% and 29.2%, respectively. Age, MRSA bacteraemia, nosocomial acquisition, endocarditis, and pneumonia were independently associated with death, but a strong association was with an unidentified infective focus (adjusted hazard ratio for 90-day mortality 2.92; 95% confidence interval 2.33 to 3.67, p < 0.0001). Conclusion The baseline demographic and clinical features of S. aureus bacteraemia vary significantly between populations. Mortality could be reduced by assiduous MRSA control and early identification of the infective focus.

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Morbidity and mortality attributable to third-generation-cephalosporin-resistant E. coli BSI is significant. If prevailing resistance trends continue, high societal and economic costs can be expected. Better management of infections caused by resistant E. coli is becoming essential.

A simple criteria set for patients with nosocomial SAB can identify patients at low risk of IE. Patients who meet these criteria may not routinely require TEE.

. Their excess LOS was 9.2 days. MSSA patients also had higher 30-day (aOR ‫؍‬ 2.4) and hospital (aHR ‫؍‬ 3.1) mortality and an excess LOS of 8.6 days. When the outcomes from the two cohorts were compared, an effect attributable to methicillin resistance was found for 30-day mortality (OR ‫؍‬ 1.8; P ‫؍‬ 0.04), but not for hospital mortality (HR ‫؍‬ 1.1; P ‫؍‬ 0.63) or LOS (difference ‫؍‬ 0.6 days; P ‫؍‬ 0.96). Irrespective of methicillin susceptibility, S. aureus BSI has a significant impact on morbidity and mortality. In addition, MRSA BSI leads to a fatal outcome more frequently than MSSA BSI. Infection control efforts in hospitals should aim to contain infections caused by both resistant and susceptible S. aureus.The emergence of resistant bacteria is a natural consequence of antibiotic use and complicates the treatment of infected patients. Staphylococcus aureus resistant to isoxazolyl penicillins (methicillin-resistant S. aureus [MRSA]) is one of the most frequent pathogens causing resistant infections in hospitals worldwide (14,21,33). The questions are whether and to what extent resistance affects survival and the duration of hospital admission in patients with bacterial infections. Previous studies compared patients with MRSA infections to those infected by methicillin-susceptible S. aureus (MSSA), using mortality as one of the main endpoints. New insights challenge this approach for a number of reasons.Several studies have shown that patients with MRSA bloodstream infection (BSI) differ in many ways from those with MSSA BSI; they are older, have more comorbidities, and experience longer hospital admissions before the onset of infection (6,22,37). If these two groups of patients are compared directly, bias is introduced, compromising the validity of the results. Of all hospitalized patients at risk of acquiring MRSA BSI, the younger, relatively more healthy MSSA patients are selected as the control group, magnifying the possible impact of resistance (20). Moreover, time-dependent distortions are introduced, as patients staying in the hospital for a shorter period, like MSSA patients, have a smaller chance of acquiring MRSA BSI than patients hospitalized for longer periods, who for many reasons are more likely to die, thus leading to overestimation of the clinical impact of resistance (36).

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Female patients with CA-SAB experienced increased 30-day mortality compared with male patients. Gender should be considered in the triage and risk stratification of CA-SAB patients.

The intracellular protozoan Toxoplasma gondii is auxotrophic for low-density lipoprotein (LDL)-derived cholesterol (C). We previously showed that T. gondii scavenges this essential lipid from host endolysosomal compartments and that C delivery to the parasitophorous vacuole (PV) does not require transit through host Golgi or endoplasmic reticulum. In this study, we explore the itinerary of C from the host endolysosomes to the PV. Labeled C incorporated into LDL is rapidly detected in intravacuolar parasites and partially esterified by the parasites. In contrast to diverse mammalian organelles, the post-endolysosomal transfer of C to the PV does not involve the host plasma membrane as an intermediate. Nevertheless, the PV membrane is accessible to extracellular sterol acceptors, suggesting C trafficking from intracellular parasites to host plasma membrane. C movement to the PV requires temperatures permissive for vesicular transport, metabolic energy and functional microtubules. Host caveolae vesicles and the sterol carrier protein-2 do not participate in this process. Proteolytic treatment of purified PV or free parasites abolishes C acquisition by the parasites. Altogether, these results support a vesicular transport system from host endolysosomes to the PV, and a requirement for PV membrane and parasite plasma membrane proteins in C delivery to T. gondii.