Sunday, June 29, 2008

Treatment of infective endocarditis caused by methicillin-resistant Staphylococcus aureus: Teicoplanin versus vancomycin in a retrospective study.

Treatment of infective endocarditis caused by methicillin-resistant Staphylococcus aureus: Teicoplanin versus vancomycin in a retrospective study.

Scand J Infect Dis. 2008

Huang JH, Hsu RB.
From the Department of Surgery, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, ROC, Taiwan.

Infective endocarditis caused by methicillin-resistant Staphylococcus aureus (MRSA) is increasing. Vancomycin and teicoplanin are 2 intravenous glycopeptides appropriate for its treatment. There is no human study comparing teicoplanin and vancomycin for the treatment of MRSA endocarditis. Between 1996 and 2006, 51 MRSA endocarditis patients were treated at the authors' hospital. There were 29 patients with nosocomial infection; 15 were treated with teicoplanin. Teicoplanin was used as the first therapeutic agent in 3 patients because of renal insufficiency. Vancomycin was used as the first therapeutic agent in 12 patients. Treatment was changed to teicoplanin because of adverse reactions in 10 and persistent bacteremia in 2 patients. Early operation was performed in 2 patients because of persistent MRSA bacteremia. Overall, 7 patients died in hospital. There was no statistically significant difference in hospital mortality rate (42% vs 47%) and bacteriologic failure rate (34% vs 40%) between 36 patients treated with vancomycin and 15 patients treated with teicoplanin. Teicoplanin can be an alternative therapy of MRSA infective endocarditis.

Informaworld

Friday, June 27, 2008

A computational model of antibiotic-resistance mechanisms in Methicillin-Resistant Staphylococcus aureus (MRSA

A computational model of antibiotic-resistance mechanisms in Methicillin-Resistant Staphylococcus aureus (MRSA
J Theor Biol. 2008 Jun 4

Murphy JT, Walshe R, Devocelle M.
Modelling and Scientific Computing Group, School of Computing, Faculty of Engineering and Computing, Dublin City University, Glasnevin, Dublin 9, Ireland; Centre for Synthesis and Chemical Biology, Department of Pharmaceutical and Medicinal Chemistry, Royal College of Surgeons in Ireland, 123 St. Stephen's Green, Dublin 2, Ireland.

An agent-based model of bacteria-antibiotic interactions has been developed that incorporates the antibiotic-resistance mechanisms of Methicillin-Resistant Staphylococcus aureus (MRSA). The model, called the Micro-Gen Bacterial Simulator, uses information about the cell biology of bacteria to produce global information about population growth in different environmental conditions. It facilitates a detailed systems-level investigation of the dynamics involved in bacteria-antibiotic interactions and a means to relate this information to traditional high-level properties such as the Minimum Inhibitory Concentration (MIC) of an antibiotic. The two main resistance strategies against beta-lactam antibiotics employed by MRSA were incorporated into the model: beta-lactamase enzymes, which hydrolytically cleave antibiotic molecules, and penicillin-binding proteins (PBP2a) with reduced binding affinities for antibiotics. Initial tests with three common antibiotics (penicillin, ampicillin and cephalothin) indicate that the model can be used to generate quantitatively accurate predictions of MICs for antibiotics against different strains of MRSA from basic cellular and biochemical information. Furthermore, by varying key parameters in the model, the relative impact of different kinetic parameters associated with the two resistance mechanisms to beta-lactam antibiotics on cell survival in the presence of antibiotics was investigated.

Elsevier Science Direct

Tuesday, June 10, 2008

Risk of Infection and Death due to Methicillin-Resistant Staphylococcus aureus in Long-term Carriers.

Risk of Infection and Death due to Methicillin-Resistant Staphylococcus aureus in Long-term Carriers.

Clin Infect Dis. 2008 Jun

Datta R, Huang SS.
1Department of Ambulatory Care and Prevention, Harvard Medical School and Harvard Pilgrim Health Care, and 2Channing Laboratory, Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts; 3Division of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, Connecticut; and 4Division of Infectious Diseases, University of California Irvine School of Medicine, Irvine.

Background: Patients with newly acquired methicillin-resistant Staphylococcus aureus (MRSA) have significant risks of short-term morbidity and mortality due to this pathogen. We were interested in assessing whether long-term carriers have persistent risks of disease and whether all carriers, regardless of the duration of carriage, should be considered to be reasonable candidates for interventions to reduce the risk of infection. Methods. We conducted a single-center retrospective cohort study to evaluate the risk of subsequent MRSA infection and death among patients known to have harbored MRSA for at least 1 year (i.e., prevalent carriers).

Results: Among 281 prevalent carriers, 65 (23%) developed a total of 96 discrete and unrelated MRSA infections in the year after their identification as prevalent carriers. The most common infections were pneumonia (accounting for 39% of MRSA infections), soft-tissue infection (14%), and central venous catheter infection (14%). Twenty-four percent of all infections involved bacteremia. Thirty-eight MRSA infections occurred during a new hospitalization, and 32 (84%) of these infections were the reason for admission to the hospital. MRSA contributed to 14 deaths, with 6 of these deaths deemed to be attributable to MRSA. Harboring MRSA for less then 2 and MRSA colonization at the time of detection as a prevalent carrier were predictive of subsequent infection with MRSA.

Conclusions: Individuals who are known to have harbored MRSA for greater 1 year are at high risk for subsequent MRSA morbidity and mortality and should be considered to be targets for intervention, in addition to individuals who have newly acquired this pathogen.

PMID: 18532892 [PubMed - as supplied by publisher]