In a retrospective cohort study, investigators found the addition of a β-lactam antibiotic to daptomycin led to less clinical failure (60-day all-cause mortality and/or 60-day recurrence) in patients with methicillin-resistant Staphylococcus aureus bacteremia.
In a retrospective cohort study, empiric anti-methicillin-resistant Staphylococcus aureus treatment was not associated with a reduction in mortality in any subgroup of patients studied and appeared to cause harm in many.
The key change from the 2009 vancomycin guidelines is the switch from trough-based to area under the curve (AUC)-based dosing and monitoring. This article will highlight key differences between the 2009 and 2020 guidelines, limitations of the new guidelines, and implementation issues.
In a retrospective cohort study, 88,605 patients in the Veterans Administration system who were hospitalized with pneumonia were examined. Thirty-eight percent received empiric anti-methicillin-resistant Staphylococcus aureus (MRSA) treatment. Empiric anti-MRSA treatment was not associated with a reduction in mortality in any subgroup of patients studied and appeared to cause harm in many patients.
In a randomized clinical trial conducted at 27 hospitals in four countries, researchers found that the addition of an antistaphylococcal beta-lactam to vancomycin or daptomycin (99% received vancomycin) did not lead to improved outcomes in MRSA bacteremia. The trial was stopped early because of safety concerns, including a higher risk of acute kidney injury in the combination group.
Using a population-based database, investigators found that the rate of readmission within 30 days following hospitalization for S. aureus bacteremia was high (22%) and resulted in high cost to the healthcare system.
One can quibble over a number of the guideline recommendations, but they provide a valuable touchstone for clinical management of patients with community-acquired pneumonia, despite the fact that so many of the recommendations are based on low- or very low-quality evidence.
In an experimental study, investigators found cigarette smoke increases the virulence of Staphylococcus aureus strains through several mechanisms, including augmented biofilm formation, increased invasion ability, and persistence within bronchial alveolar cells.