Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases
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Clin. Microbiol. Infect. · Jun 2008
Clusters of imipenem-resistant Acinetobacter baumannii clones producing different carbapenemases in an intensive care unit.
During a 2-year period (April 2005-March 2007), 31 intensive care unit (ICU) patients in a Greek hospital were infected or colonised with imipenem-resistant isolates of Acinetobacter baumannii. Twelve patients died, with imipenem-resistant A. baumannii infection contributing to the death of seven patients. ⋯ PCR, curing and hybridisation experiments indicated that the bla(VIM) alleles were chromosomally located, whereas the bla(OXA-58) alleles were plasmid-located. This study provides the first description of the clonal spread of multidrug-resistant A. baumannii isolates carrying bla(VIM-1) and bla(VIM-4) metallo-beta-lactamase genes, and revealed that distinct carbapenem-resistant A. baumannii clusters bearing different carbapenemase genes may emerge and cause severe infections, even in a well-defined regional hospital setting.
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Clin. Microbiol. Infect. · Jun 2008
Efficacy of amoxycillin-clavulanate in an experimental model of murine pneumonia caused by AmpC-non-hyperproducing clinical isolates of Escherichia coli resistant to cefoxitin.
The algorithms included in most automated systems used for antimicrobial susceptibility testing (e.g., Vitek 2) consider that Escherichia coli isolates resistant to cefoxitin are AmpC-hyperproducers and, consequently, resistant also to amoxycillin-clavulanate. However, a recent study revealed that 30% of E. coli clinical isolates resistant to cefoxitin remained susceptible in vitro to amoxycillin-clavulanate. The aim of the present study was to evaluate the in-vivo efficacy of amoxycillin-clavulanate in the treatment of an experimental model of pneumonia, using two clonally related isolates (with identical repetitive extragenic palindromic sequence (REP)-PCR patterns) of AmpC-non-hyperproducing and OmpF-lacking E. coli (Ec985 and Ec571) that were resistant to cefoxitin and susceptible to cefotaxime and amoxycillin-clavulanate. ⋯ Amoxycillin, amoxycillin-clavulanate and cefotaxime were bactericidal for Ec985, and amoxycillin-clavulanate and cefotaxime were bactericidal for Ec571 at different concentrations and time-points, as determined using time-kill assays. Treatment with amoxycillin, amoxycillin-clavulanate and cefotaxime reduced the bacterial lung concentration of Ec985 compared with non-treated controls (p <0.05), whereas amoxycillin-clavulanate and cefotaxime showed efficacy against Ec571 when compared with the control and amoxycillin groups (p <0.05). Regardless of the exact underlying mechanism(s) of resistance, amoxycillin-clavulanate was effective in the experimental murine model in the treatment of pneumonia caused by AmpC-non-hyperproducing strains of E. coli resistant to cefoxitin.
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Clin. Microbiol. Infect. · May 2008
ReviewInfection control measures to limit the spread of Clostridium difficile.
Clostridium difficile-associated diarrhoea (CDAD) presents mainly as a nosocomial infection, usually after antimicrobial therapy. Many outbreaks have been attributed to C. difficile, some due to a new hyper-virulent strain that may cause more severe disease and a worse patient outcome. As a result of CDAD, large numbers of C. difficile spores may be excreted by affected patients. ⋯ This article provides a review of the literature that can be used for evidence-based guidelines to limit the spread of C. difficile. These include early diagnosis of CDAD, surveillance of CDAD cases, education of staff, appropriate use of isolation precautions, hand hygiene, protective clothing, environmental cleaning and cleaning of medical equipment, good antibiotic stewardship, and specific measures during outbreaks. Existing local protocols and practices for the control of C. difficile should be carefully reviewed and modified if necessary.
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Clin. Microbiol. Infect. · May 2008
ReviewNew options for treatment of candidaemia in critically ill patients.
Bloodstream infections caused by Candida spp. are increasingly recognised in critically ill adult and paediatric individuals, with significant associated morbidity and mortality. Candida albicans is the single most common fungal species to cause nosocomial infections. ⋯ Until the 1980s, the therapeutic possibilities for invasive candidosis were limited to amphotericin B, but with the advent of new antifungal agents, such as azoles and echinocandins, less toxic therapeutic options have become available and there are now possibilities for prevention and optimised therapy for documented Candida infections. In this review, the currently available options for the treatment of candidaemia and invasive candidosis are discussed with regard to the role of liposomal amphotericin B in comparison with the echinocandins and azoles.
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Species of Candida and Aspergillus remain the most common causes of invasive fungal infections, but other yeasts and filamentous fungi are emerging as significant pathogens. Opportunistic yeast-like fungi and moulds such as Zygomycetes, Fusarium spp. and Scedosporium spp. are increasingly being recognised in patient groups such as those with leukaemia and in bone marrow transplant recipients. Recognition of these epidemiological changes is critical to patient care. The key elements in selecting an appropriate antifungal agent are the type of patient (solid-organ or stem-cell transplant), severity of immunosuppression, history of prolonged exposure to antifungal drugs, and knowledge of the genera and species of the infecting pathogen and its typical susceptibility pattern.