Biofilm Producing Methicillin-Resistant Staphylococcus aureus (MRSA) Infections in Humans: Clinical Implications and Management.

Since its initial description in the 1960s, methicillin-resistant Staphylococcus aureus (MRSA) has developed multiple mechanisms for antimicrobial resistance and evading the immune system, including biofilm production. MRSA is now a widespread pathogen, causing a spectrum of infections ranging from superficial skin issues to severe conditions like osteoarticular infections and endocarditis, leading to high morbidity and mortality. Biofilm production is a key aspect of MRSA's ability to invade, spread, and resist antimicrobial treatments. Environmental factors, such as suboptimal antibiotics, pH, temperature, and tissue oxygen levels, enhance biofilm formation. Biofilms are intricate bacterial structures with dense organisms embedded in polysaccharides, promoting their resilience. The process involves stages of attachment, expansion, maturation, and eventually disassembly or dispersion. MRSA's biofilm formation has a complex molecular foundation, involving genes like icaADBC, fnbA, fnbB, clfA, clfB, atl, agr, sarA, sarZ, sigB, sarX, psm, icaR, and srtA. Recognizing pivotal genes for biofilm formation has led to potential therapeutic strategies targeting elemental and enzymatic properties to combat MRSA biofilms. This review provides a practical approach for healthcare practitioners, addressing biofilm pathogenesis, disease spectrum, and management guidelines, including advances in treatment. Effective management involves appropriate antimicrobial therapy, surgical interventions, foreign body removal, and robust infection control practices to curtail spread within healthcare environments.

Trends in antibiotic use before and during the coronavirus disease 2019 (COVID-19) pandemic across an integrated health system with different antimicrobial stewardship program models trends in antibiotic use by ASP model.

Changes in antimicrobial use during the pandemic in relation to long-term trends in utilization among different antimicrobial stewardship program models have not been fully characterized. We analyzed data from an integrated health system using joinpoint regression and found temporal fluctuations in prescribing as well as continuation of existing trends.

Comparative evaluation of six extended-interval gentamicin dosing regimens in premature and full-term neonates.

PURPOSE: Six extended-interval gentamicin dosing regimens were comparatively evaluated in premature and full-term neonates. METHODS: Data regarding six physician-ordered dosing regimens of gentamicin for neonates in a hospital neonatal intensive care unit were collected and analyzed. Neonates of gestational age (GA) 29 weeks or younger received 4.5 mg/kg every 48 hours. Neonates of GA 30-34 weeks received one of three dosing regimens: 3.5, 4, or 4.5 mg/kg every 36 hours. Neonates of GA 35 weeks or older received either 3.5 or 4 mg/kg every 24 hours. Blood samples were collected 30 minutes before and 30 minutes after the third dose was infused for binary trough and peak level determinations, respectively. RESULTS: Peak gentamicin concentrations in the target range were attained most often in neonates of GA 29 weeks or younger who received gentamicin 4.5 mg/kg every 48 hours, in neonates of GA 30-34 weeks treated with gentamicin 3.5 mg/kg every 36 hours, and in neonates of GA 35 weeks or older treated with gentamicin 3.5 mg/kg every 24 hours. CONCLUSION: For neonates of GA 30-34 weeks, gentamicin 3.5 mg/kg every 36 hours resulted in the highest percentage of peaks in the target range compared with 4 and 4.5 mg/kg every 36 hours. For neonates of GA 35 weeks or older, gentamicin 3.5 mg/kg every 24 hours provided the highest percentage of peaks in the target range compared with 4 mg/kg every 24 hours. The differences between the percentages of trough values in the target range of 0.5-2 µg/mL were not significant among dosing subgroups within each age group.