PubMed Health⌕ Search

PubMed · 16813983

Antimicrobial stewardship.

Abstract

Antimicrobial stewardship is a key component of a multifaceted approach to preventing emergence of antimicrobial resistance. Good antimicrobial stewardship involves selecting an appropriate drug and optimizing its dose and duration to cure an infection while minimizing toxicity and conditions for selection of resistant bacterial strains. Studies conducted over the years indicate that antibiotic use is unnecessary or inappropriate in as many as 50% of cases in the United States, and this creates unnecessary pressure for the selection of resistant species. Because the pharmaceutical industry pipeline for new antibiotics has been curtailed in recent years, and it may be > or = 10 years before important new antibiotics to treat certain resistant bacteria find their way to market, a premium has been set on maintaining the effectiveness of currently available agents. Several strategies, including prescriber education, formulary restriction, prior approval, streamlining, antibiotic cycling, and computer-assisted programs have been proposed to improve antibiotic use. Although rigorous clinical data in support of these strategies are lacking, the most effective means of improving antimicrobial stewardship will most likely involve a comprehensive program that incorporates multiple strategies and collaboration among various specialties within a given healthcare institution. Computer-assisted software programs may be especially useful in implementing these comprehensive programs. The antimicrobial stewardship program at the Hospital of the University of Pennsylvania, which has been shown to improve appropriateness of antibiotic use and cure rates, decrease failure rates, and reduce healthcare-related costs, is used as an example in support of this multifaceted, multidisciplinary approach. At this time, data from well-controlled studies examining the effect of antibacterial stewardship on emergence of resistance are limited, but available data suggest that good antibiotic stewardship reduces rates of Clostridium difficile-associated diarrhea, resistant gram-negative bacilli, and vancomycin-resistant enterococci.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Neil Fishman. 2006. Antimicrobial stewardship.. https://doi.org/10.1016/j.ajic.2006.05.237

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Chemical composition and antimicrobial activity of volatile compounds of Tamarix boveana (Tamaricaceae).

The chemical composition of the Tamarix boveana volatile oils obtained from the whole aerial part, flowers, leaves and stems by steam distillation was analysed using gas chromatograph (GC)-flame ionization detectors (FID) and GC-MS. Sixty-two components were identified. Hexadecanoic acid (18.14%), docosane (13.34%), germacrene D (7.68%), fenchyl acetate (7.34%), Benzyl benzoate (4.11%) were found to be the major components in the whole aerial parts. This composition differed according to the tested part: 2.4 Nonadienal was the main compound in the flowers (12.13%) while germacrene D was the major component in leaves (31.43%) and hexadecanoic acid in the stems (13.94%). To evaluate in vitro antimicrobial activity, all volatile oils were tested against six Gram-positive and Gram-negative bacteria and four fungi. The T. boveana volatile oils exhibited an interesting antibacterial activity against all strains tested except Pseudomonas aeruginosa but no antifungal activity was detected.

Anti-Infective Agents↗

Role of human neutrophil peptides in the initial interaction between lung epithelial cells and CD4+ lymphocytes.

Human neutrophil peptides (HNP) exert immune-modulating effects. We hypothesized that HNP link innate and adaptive immunity through activation of costimulatory molecules. Human lung epithelial cells and CD4+ lymphocytes were treated with HNP separately or in coculture. Stimulation with HNP induced an increase in cell surface expression of CD54 (ICAM-1), CD80, and CD86 on lung epithelial cells and the corresponding major ligands, CD11a (LFA-1), CD152 (CTLA-4), and CD28 on CD4+ lymphocytes. There was an increased nuclear expression of the transcription factor p53 in human alveolar A549 cells and an elevated NF-kappaB (p50) and a degradation of I-kappaB protein in CD4+ lymphocytes following HNP stimulation. HNP enhanced the interaction between A549 cells and CD4+ lymphocytes by increasing cell adhesion and release of IFN-gamma, IL-2, and IL-8. This was attenuated by using an alpha1-proteinase inhibitor to neutralize HNP. We conclude that HNP play an important role in linking innate to acquired immunity by activation of costimulatory molecules in lung epithelial cells and CD4+ lymphocytes.

Anti-Infective Agents↗