In this large, prospective, multinational cohort, more than one half of all cases of non-HACEK gram-negative bacillus endocarditis were associated with health care contact. Non-HACEK gram-negative bacillus endocarditis is not primarily a disease of injection drug users.

Objective: To document the types of, and mortality from, Staphylococcus aureus bacteraemia in Australia and New Zealand, and determine factors associated with mortality. Design and setting: Prospective observational study in 27 independent or hospital pathology laboratories in Australia (24) and New Zealand (3), employing a web‐based database to prospectively record demographic features, selected risk factors, principal antibiotic treatment and mortality data on all patients with positive blood cultures for S. aureus from June 2007 to May 2008. Main outcome measure: 30‐day all‐cause mortality. Results: 1994 episodes of S. aureus bacteraemia were identified, and complete 30‐day follow‐up data were available for 1865. Most episodes had their onset in the community (60.8%; 95% CI, 58.7%–63.0%). Methicillin‐resistant S. aureus (MRSA) caused 450 episodes (24.1%; 95% CI, 22.2%–25.9%), and 123 of these (27.3%) had a susceptibility profile consistent with community‐associated MRSA. All‐cause mortality at 30 days was 20.6% (95% CI, 18.8%–22.5%). On univariate analysis, increased mortality was significantly associated with older age, European ethnicity, MRSA infection, infections not originating from a medical device, sepsis syndrome, pneumonia/empyema, and treatment with a glycopeptide or other non‐β‐lactam antibiotic. On multivariable analysis, independent predictors of mortality were age, sepsis syndrome, pneumonia/empyema, device‐associated infection with a secondary focus, left‐sided endocarditis, and treatment with a glycopeptide such as vancomycin, but not MRSA infection. Conclusions: S. aureus bacteraemia is a common infection in both the community and hospitals in Australia and New Zealand, and is associated with appreciable mortality. Invasive MRSA infection may be more life‐threatening, partly because of the inferior efficacy of the standard treatment, vancomycin. National web‐based surveillance of S. aureus bacteraemia and its outcomes is not only important but also easily achievable.

Alcohol-based disinfectants and particularly hand rubs are a key way to control hospital infections worldwide. Such disinfectants restrict transmission of pathogens, such as multidrug-resistant and Despite this success, health care infections caused by are increasing. We tested alcohol tolerance of 139 hospital isolates of obtained between 1997 and 2015 and found that isolates after 2010 were 10-fold more tolerant to killing by alcohol than were older isolates. Using a mouse gut colonization model of transmission, we showed that alcohol-tolerant resisted standard 70% isopropanol surface disinfection, resulting in greater mouse gut colonization compared to alcohol-sensitive We next looked for bacterial genomic signatures of adaptation. Alcohol-tolerant accumulated mutations in genes involved in carbohydrate uptake and metabolism. Mutagenesis confirmed the roles of these genes in the tolerance of to isopropanol. These findings suggest that bacterial adaptation is complicating infection control recommendations, necessitating additional procedures to prevent from spreading in hospital settings.

Nosocomial infections are increasingly being recognised as a major patient safety issue. The modern hospital environment and associated health care practices have provided a niche for the rapid evolution of microbial pathogens that are well adapted to surviving and proliferating in this setting, after which they can infect susceptible patients. This is clearly the case for bacterial pathogens such as Methicillin Resistant Staphylococcus aureus (MRSA) and Vancomycin Resistant Enterococcus (VRE) species, both of which have acquired resistance to antimicrobial agents as well as enhanced survival and virulence properties that present serious therapeutic dilemmas for treating physicians. It has recently become apparent that the spore-forming bacterium Clostridium difficile also falls within this category. Since 2000, there has been a striking increase in C. difficile nosocomial infections worldwide, predominantly due to the emergence of epidemic or hypervirulent isolates that appear to possess extended antibiotic resistance and virulence properties. Various hypotheses have been proposed for the emergence of these strains, and for their persistence and increased virulence, but supportive experimental data are lacking. Here we describe a genetic approach using isogenic strains to identify a factor linked to the development of hypervirulence in C. difficile. This study provides evidence that a naturally occurring mutation in a negative regulator of toxin production, the anti-sigma factor TcdC, is an important factor in the development of hypervirulence in epidemic C. difficile isolates, presumably because the mutation leads to significantly increased toxin production, a contentious hypothesis until now. These results have important implications for C. difficile pathogenesis and virulence since they suggest that strains carrying a similar mutation have the inherent potential to develop a hypervirulent phenotype.

PIVC-associated SAB is an under-recognised complication. The high incidences of SAB associated with PIVCs inserted in emergency locations and with prolonged dwell times support recommendations in clinical guidelines for routine removal of PIVCs.