Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Increasing reports of Acinetobacter infections that cause pneumonia, meningitis, endocarditis, and bacteriaemia underline the clinical importance of this pathogen. Members of the genus Acinetobacter, particularly Acinetobacter baumannii, are now recognized as significant nosocomial pathogens, particularly for the subset of critically-ill patients requiring mechanical ventilation in hospital intensive care units. A. baumannii has itself a quite high level of naturally-occurring antibiotic resistance. The organism can survive for long periods in the hospital environment including dry and humid areas. One of the most worrying antibiotic resistance problems in A. baumannii is the increasing trend of carbapenem resistance, present also in few Croatian hospitals. Infections caused by this Gram-negative bacillus are common in the intensive care units anticipated by colonized patients. The increasing trend of carbapenem resistance in A. baumannii could be mediated from metallo-beta-lactamases (VIM, IMP, and SIM), carbapenem-hydrolyzing oxacillinases (OXA), porin modifications for influx of carbapenems (33-kDa CarO protein) and/or often combined mechanisms of resistance. The investigation of the background of carbapenem resistance in relevant clinical isolates of A. baumannii from Split University Hospital confirmed present of carbapenem-hydrolyzing oxacillinases OXA-107 representing a more recent evolutionary adaptation OXA-51-like enzyme to antibiotic challenge with carbapenems.
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PMID:[The review of carbapenem resistance in clinical isolates of Acinetobacter baumannii]. 2003 29

Acinetobacter baumannii is a common cause of serious nosocomial infections. Although community-acquired infections are observed, the vast majority occur in people with preexisting comorbidities. A. baumannii emerged as a problematic pathogen in the 1980s when an increase in virulence, difficulty in treatment due to drug resistance, and opportunities for infection turned it into one of the most important threats to human health. Some of the clinical manifestations of A. baumannii nosocomial infection are pneumonia; bloodstream infections; lower respiratory tract, urinary tract, and wound infections; burn infections; skin and soft tissue infections (including necrotizing fasciitis); meningitis; osteomyelitis; and endocarditis. A. baumannii has an extraordinary genetic plasticity that results in a high capacity to acquire antimicrobial resistance traits. In particular, acquisition of resistance to carbapenems, which are among the antimicrobials of last resort for treatment of multidrug infections, is increasing among A. baumannii strains compounding the problem of nosocomial infections caused by this pathogen. It is not uncommon to find multidrug-resistant (MDR, resistance to at least three classes of antimicrobials), extensively drug-resistant (XDR, MDR plus resistance to carbapenems), and pan-drug-resistant (PDR, XDR plus resistance to polymyxins) nosocomial isolates that are hard to treat with the currently available drugs. In this article we review the acquired resistance to carbapenems by A. baumannii. We describe the enzymes within the OXA, NDM, VIM, IMP, and KPC groups of carbapenemases and the coding genes found in A. baumannii clinical isolates.
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PMID:Carbapenemases: Transforming Acinetobacter baumannii into a Yet More Dangerous Menace. 3238 24