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      Imipenem Resistance in Clostridium difficile Ribotype 017, Portugal

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          Abstract

          We describe imipenem-resistant and imipenem-susceptible clinical isolates of Clostridium difficile ribotype 017 in Portugal. All ribotype 017 isolates carried an extra penicillin-binding protein gene, pbp5, and the imipenem-resistant isolates had additional substitutions near the transpeptidase active sites of pbp1 and pbp3. These clones could disseminate and contribute to imipenem resistance.

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          Most cited references10

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          Clostridium difficile infection

          Infection of the colon with the Gram-positive bacterium Clostridium difficile is potentially life threatening, especially in elderly people and in patients who have dysbiosis of the gut microbiota following antimicrobial drug exposure. C. difficile is the leading cause of health-care-associated infective diarrhoea. The life cycle of C. difficile is influenced by antimicrobial agents, the host immune system, and the host microbiota and its associated metabolites. The primary mediators of inflammation in C. difficile infection (CDI) are large clostridial toxins, toxin A (TcdA) and toxin B (TcdB), and, in some bacterial strains, the binary toxin CDT. The toxins trigger a complex cascade of host cellular responses to cause diarrhoea, inflammation and tissue necrosis - the major symptoms of CDI. The factors responsible for the epidemic of some C. difficile strains are poorly understood. Recurrent infections are common and can be debilitating. Toxin detection for diagnosis is important for accurate epidemiological study, and for optimal management and prevention strategies. Infections are commonly treated with specific antimicrobial agents, but faecal microbiota transplants have shown promise for recurrent infections. Future biotherapies for C. difficile infections are likely to involve defined combinations of key gut microbiota.
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            The changing epidemiology of Clostridium difficile infections.

            The epidemiology of Clostridium difficile infection (CDI) has changed dramatically during this millennium. Infection rates have increased markedly in most countries with detailed surveillance data. There have been clear changes in the clinical presentation, response to treatment, and outcome of CDI. These changes have been driven to a major degree by the emergence and epidemic spread of a novel strain, known as PCR ribotype 027 (sometimes referred to as BI/NAP1/027). We review the evidence for the changing epidemiology, clinical virulence and outcome of treatment of CDI, and the similarities and differences between data from various countries and continents. Community-acquired CDI has also emerged, although the evidence for this as a distinct new entity is less clear. There are new data on the etiology of and potential risk factors for CDI; controversial issues include specific antimicrobial agents, gastric acid suppressants, potential animal and food sources of C. difficile, and the effect of the use of alcohol-based hand hygiene agents.
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              Penicillin-binding proteins and beta-lactam resistance.

              A number of ways and means have evolved to provide resistance to eubacteria challenged by beta-lactams. This review is focused on pathogens that resist by expressing low-affinity targets for these antibiotics, the penicillin-binding proteins (PBPs). Even within this narrow focus, a great variety of strategies have been uncovered such as the acquisition of an additional low-affinity PBP, the overexpression of an endogenous low-affinity PBP, the alteration of endogenous PBPs by point mutations or homologous recombination or a combination of the above.
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                Author and article information

                Journal
                Emerg Infect Dis
                Emerging Infect. Dis
                EID
                Emerging Infectious Diseases
                Centers for Disease Control and Prevention
                1080-6040
                1080-6059
                April 2018
                : 24
                : 4
                : 741-745
                Affiliations
                [1]National Institute of Health, Lisbon, Portugal (J. Isidro, A. Santos, A. Nunes, V. Borges, C. Silva, L. Vieira, J.P. Gomes, M. Oleastro);
                [2]Instituto de Tecnologia Química e Biológica António Xavier, Oeiras, Portugal (A.L. Mendes, M. Serrano, A.O. Henriques)
                Author notes
                Address for correspondence: Mónica Oleastro, National Institute of Health Dr. Ricardo Jorge, National Reference Laboratory for Gastrointestinal Infections, Department of Infectious Diseases, Av Padre Cruz, 1649-016 Lisbon, Portugal; email: monica.oleastro@ 123456insa.min-saude.pt
                Article
                17-0095
                10.3201/eid2404.170095
                5875251
                29553322
                78376161-47ed-4694-b711-a32c355b7037
                History
                Categories
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                Dispatch
                Imipenem Resistance in Clostridium difficile Ribotype 017, Portugal

                Infectious disease & Microbiology
                clostridium difficile infection,cdi,imipenem resistance,clostridium difficile,penicillin-binding proteins,ribotype 017,multidrug resistance,bacteria,antimicrobial resistance,portugal

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