Article

Methicillin-resistant–Staphylococcus aureus Hospitalizations, United States

Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA.
Emerging infectious diseases (Impact Factor: 7.33). 07/2005; 11(6):868-72. DOI: 10.3201/eid1106.040831
Source: PubMed

ABSTRACT Methicillin-resistant Staphylococcus aureus (MRSA) is increasingly a cause of nosocomial and community-onset infection with unknown national scope and magnitude. We used the National Hospital Discharge Survey to calculate the number of US hospital discharges listing S. aureus-specific diagnoses, defined as those having at least 1 International Classification of Diseases (ICD)-9 code specific for S. aureus infection. The number of hospital discharges listing S. aureus-specific diagnoses was multiplied by the proportion of methicillin resistance for each corresponding infection site to determine the number of MRSA infections. From 1999 to 2000, an estimated 125,969 hospitalizations with a diagnosis of MRSA infection occurred annually, including 31,440 for septicemia, 29,823 for pneumonia, and 64,706 for other infections, accounting for 3.95 per 1,000 hospital discharges. The method used in our analysis may provide a simple way to assess trends of the magnitude of MRSA infection nationally.

Download full-text

Full-text

Available from: Holly Hill, Oct 03, 2014
2 Followers
 · 
148 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Staphylococcus aureus is a versatile pathogen that can cause life-threatening infections. The growing emergence of methicillin-resistant S. aureus strains and a decrease in the discovery of new antibiotics warrant the search for new therapeutic targets to combat infections. Staphylococcus aureus produces many extracellular virulence factors that contribute to its pathogenicity. Therefore, targeting bacterial virulence as an alternative strategy to the development of new antimicrobials has gained great interest. α-Toxin is a 33.2-kDa, water-soluble, pore-forming toxin that is secreted by most S. aureus strains. α-Toxin is essential for the pathogenesis of pneumonia, as strains lacking α-toxin display a profound defect in virulence. In this report, we demonstrate that isoalantolactone (IAL), a naturally occurring compound found in Inula helenium (Compositae), has no anti-S. aureus activity as per MIC evaluation in vitro. However, IAL can markedly inhibit the expression of α-toxin in S. aureus at very low concentrations. Furthermore, the in vivo data indicate that treatment with IAL protects mice from S. aureus pneumonia.
    FEMS Microbiology Letters 11/2011; 324(2):147-55. DOI:10.1111/j.1574-6968.2011.02397.x · 2.72 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Meticillin-resistant Staphylococcus aureus (MRSA) can persist in alveolar macrophages and contribute to clinical failure of intravenous vancomycin to cure pneumonia. In this study, it was shown that vancomycin in standard solution is unable to kill intracellular MRSA within macrophages. The intracellular viability of MRSA inside macrophages treated with two different formulations of encapsulated liposomal vancomycin prepared using a hydration-dehydration method was then determined. In contrast to the observations with standard vancomycin, treatment with conventional non-pegylated liposomal vancomycin (lacking any surface modification) resulted in a sufficient concentration of antibiotic inside the intracellular compartment of the macrophages to exert a marked bactericidal effect against MRSA. On the other hand, treatment of infected macrophages with surface-pegylated liposomes resulted in no impact on MRSA survival, and this lack of an inhibitory effect may likely reflect delayed phagocytosis owing to the 'stealth' effect by pegylation. This study indicates the potential for a novel liposomal delivery system that may improve clinical vancomycin treatment outcomes by targeting intracellular MRSA infection.
    International journal of antimicrobial agents 02/2011; 37(2):140-4. DOI:10.1016/j.ijantimicag.2010.10.011 · 4.26 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Iron is required for bacterial proliferation, and Staphylococcus aureus steals this metal from host hemoglobin during invasive infections. This process involves hemoglobin binding to the cell wall of S. aureus, heme extraction, passage through the cell envelope, and degradation to release free iron. Herein, we demonstrate an enhanced ability of S. aureus to bind hemoglobin derived from humans as compared to other mammals. Increased specificity for human hemoglobin (hHb) translates into an improved ability to acquire iron and is entirely dependent on the staphylococcal hemoglobin receptor IsdB. This feature affects host-pathogen interaction as demonstrated by the increased susceptibility of hHb-expressing mice to systemic staphylococcal infection. Interestingly, enhanced utilization of human hemoglobin is not a uniform property of all bacterial pathogens. These results suggest a step in the evolution of S. aureus to better colonize the human host and establish hHb-expressing mice as a model of S. aureus pathogenesis.
    Cell host & microbe 12/2010; 8(6):544-50. DOI:10.1016/j.chom.2010.11.002 · 12.19 Impact Factor