Molecular epidemiology of a clonal outbreak of multidrug-resistant Acinetobacter baumannii in a university hospital in Italy
This study investigated the molecular epidemiology of a clonal outbreak of multidrug-resistant Acinetobacter baumannii that occurred between June 2003 and June 2004 in a tertiary-care hospital in Naples, Italy. A. baumannii was isolated from 74 patients, of whom 38 were infected and 36 were colonise...
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| Veröffentlicht in: | Clinical microbiology and infection 2007-05, Vol.13 (5), p.481-489 |
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| creator | Zarrilli, R. Casillo, R. Di Popolo, A. Tripodi, M.-F. Bagattini, M. Cuccurullo, S. Crivaro, V. Ragone, E. Mattei, A. Galdieri, N. Triassi, M. Utili, R. |
| description | This study investigated the molecular epidemiology of a clonal outbreak of multidrug-resistant Acinetobacter baumannii that occurred between June 2003 and June 2004 in a tertiary-care hospital in Naples, Italy. A. baumannii was isolated from 74 patients, of whom 38 were infected and 36 were colonised. Thirty-three patients had ventilator-associated pneumonia, three had hospital-acquired pneumonia, and two had sepsis. Genotypic analysis of 45 available A. baumannii isolates revealed two distinct pulsed-field gel electrophoresis (PFGE) patterns. Of these, PFGE pattern 1 was represented by isolates from 44 patients and was identical to that of an epidemic A. baumannii clone isolated in another hospital of Naples during 2002. All A. baumannii isolates of PFGE type 1 showed identical multiresistant antibiotypes, characterised by resistance to all antimicrobial agents tested, including carbapenems, with the exception of colistin. In these isolates, inhibition of OXA enzymes by 200 mM NaCl reduced the imipenem MIC by up to four-fold. Molecular analysis of antimicrobial resistance genes showed that all A. baumannii isolates of PFGE type 1 harboured a class 1 integron containing the aacA4, orfX and blaOXA-20 gene cassettes, an ampC gene and a blaOXA-51-like allele. Moreover, a blaOXA-58-like gene surrounded by the regulatory elements ISAba2 and ISAba3 was identified in a 30-kb plasmid from A. baumannii isolates of PFGE type 1, but not PFGE type 2. Thus, selection of a single A. baumannii clone producing an OXA-58-type carbapenem-hydrolysing oxacillinase was responsible for the increase in the number of A. baumannii infections that occurred in this hospital. |
| doi_str_mv | 10.1111/j.1469-0691.2006.01675.x |
| format | Article |
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A. baumannii was isolated from 74 patients, of whom 38 were infected and 36 were colonised. Thirty-three patients had ventilator-associated pneumonia, three had hospital-acquired pneumonia, and two had sepsis. Genotypic analysis of 45 available A. baumannii isolates revealed two distinct pulsed-field gel electrophoresis (PFGE) patterns. Of these, PFGE pattern 1 was represented by isolates from 44 patients and was identical to that of an epidemic A. baumannii clone isolated in another hospital of Naples during 2002. All A. baumannii isolates of PFGE type 1 showed identical multiresistant antibiotypes, characterised by resistance to all antimicrobial agents tested, including carbapenems, with the exception of colistin. In these isolates, inhibition of OXA enzymes by 200 mM NaCl reduced the imipenem MIC by up to four-fold. Molecular analysis of antimicrobial resistance genes showed that all A. baumannii isolates of PFGE type 1 harboured a class 1 integron containing the aacA4, orfX and blaOXA-20 gene cassettes, an ampC gene and a blaOXA-51-like allele. Moreover, a blaOXA-58-like gene surrounded by the regulatory elements ISAba2 and ISAba3 was identified in a 30-kb plasmid from A. baumannii isolates of PFGE type 1, but not PFGE type 2. Thus, selection of a single A. baumannii clone producing an OXA-58-type carbapenem-hydrolysing oxacillinase was responsible for the increase in the number of A. baumannii infections that occurred in this hospital.</description><identifier>ISSN: 1198-743X</identifier><identifier>EISSN: 1469-0691</identifier><identifier>DOI: 10.1111/j.1469-0691.2006.01675.x</identifier><identifier>PMID: 17430339</identifier><language>eng</language><publisher>Oxford, UK: Elsevier Ltd</publisher><subject>Acinetobacter baumannii ; Acinetobacter baumannii - drug effects ; Acinetobacter baumannii - genetics ; Acinetobacter baumannii - pathogenicity ; Acinetobacter Infections - drug therapy ; Acinetobacter Infections - epidemiology ; Acinetobacter Infections - genetics ; Aged ; Antibacterial agents ; Antibiotics. Antiinfectious agents. Antiparasitic agents ; beta-Lactamases - classification ; beta-Lactamases - genetics ; Biological and medical sciences ; carbapenem resistance ; Carbapenems - pharmacology ; Community-Acquired Infections - drug therapy ; Community-Acquired Infections - genetics ; Community-Acquired Infections - microbiology ; Cross Infection - microbiology ; Cross Infection - mortality ; Disease Outbreaks ; Drug Resistance, Multiple, Bacterial ; Electrophoresis, Gel, Pulsed-Field ; Female ; General aspects ; Hospitals, University ; Human infectious diseases. Experimental studies and models ; Humans ; Infectious diseases ; Intensive Care Units ; Italy - epidemiology ; Male ; Medical sciences ; Microbial Sensitivity Tests ; molecular epidemiology ; nosocomial infection ; outbreak ; OXA-58 ; Pharmacology. 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A. baumannii was isolated from 74 patients, of whom 38 were infected and 36 were colonised. Thirty-three patients had ventilator-associated pneumonia, three had hospital-acquired pneumonia, and two had sepsis. Genotypic analysis of 45 available A. baumannii isolates revealed two distinct pulsed-field gel electrophoresis (PFGE) patterns. Of these, PFGE pattern 1 was represented by isolates from 44 patients and was identical to that of an epidemic A. baumannii clone isolated in another hospital of Naples during 2002. All A. baumannii isolates of PFGE type 1 showed identical multiresistant antibiotypes, characterised by resistance to all antimicrobial agents tested, including carbapenems, with the exception of colistin. In these isolates, inhibition of OXA enzymes by 200 mM NaCl reduced the imipenem MIC by up to four-fold. Molecular analysis of antimicrobial resistance genes showed that all A. baumannii isolates of PFGE type 1 harboured a class 1 integron containing the aacA4, orfX and blaOXA-20 gene cassettes, an ampC gene and a blaOXA-51-like allele. Moreover, a blaOXA-58-like gene surrounded by the regulatory elements ISAba2 and ISAba3 was identified in a 30-kb plasmid from A. baumannii isolates of PFGE type 1, but not PFGE type 2. Thus, selection of a single A. baumannii clone producing an OXA-58-type carbapenem-hydrolysing oxacillinase was responsible for the increase in the number of A. baumannii infections that occurred in this hospital.</description><subject>Acinetobacter baumannii</subject><subject>Acinetobacter baumannii - drug effects</subject><subject>Acinetobacter baumannii - genetics</subject><subject>Acinetobacter baumannii - pathogenicity</subject><subject>Acinetobacter Infections - drug therapy</subject><subject>Acinetobacter Infections - epidemiology</subject><subject>Acinetobacter Infections - genetics</subject><subject>Aged</subject><subject>Antibacterial agents</subject><subject>Antibiotics. Antiinfectious agents. Antiparasitic agents</subject><subject>beta-Lactamases - classification</subject><subject>beta-Lactamases - genetics</subject><subject>Biological and medical sciences</subject><subject>carbapenem resistance</subject><subject>Carbapenems - pharmacology</subject><subject>Community-Acquired Infections - drug therapy</subject><subject>Community-Acquired Infections - genetics</subject><subject>Community-Acquired Infections - microbiology</subject><subject>Cross Infection - microbiology</subject><subject>Cross Infection - mortality</subject><subject>Disease Outbreaks</subject><subject>Drug Resistance, Multiple, Bacterial</subject><subject>Electrophoresis, Gel, Pulsed-Field</subject><subject>Female</subject><subject>General aspects</subject><subject>Hospitals, University</subject><subject>Human infectious diseases. Experimental studies and models</subject><subject>Humans</subject><subject>Infectious diseases</subject><subject>Intensive Care Units</subject><subject>Italy - epidemiology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Microbial Sensitivity Tests</subject><subject>molecular epidemiology</subject><subject>nosocomial infection</subject><subject>outbreak</subject><subject>OXA-58</subject><subject>Pharmacology. 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Antiinfectious agents. Antiparasitic agents</topic><topic>beta-Lactamases - classification</topic><topic>beta-Lactamases - genetics</topic><topic>Biological and medical sciences</topic><topic>carbapenem resistance</topic><topic>Carbapenems - pharmacology</topic><topic>Community-Acquired Infections - drug therapy</topic><topic>Community-Acquired Infections - genetics</topic><topic>Community-Acquired Infections - microbiology</topic><topic>Cross Infection - microbiology</topic><topic>Cross Infection - mortality</topic><topic>Disease Outbreaks</topic><topic>Drug Resistance, Multiple, Bacterial</topic><topic>Electrophoresis, Gel, Pulsed-Field</topic><topic>Female</topic><topic>General aspects</topic><topic>Hospitals, University</topic><topic>Human infectious diseases. 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A. baumannii was isolated from 74 patients, of whom 38 were infected and 36 were colonised. Thirty-three patients had ventilator-associated pneumonia, three had hospital-acquired pneumonia, and two had sepsis. Genotypic analysis of 45 available A. baumannii isolates revealed two distinct pulsed-field gel electrophoresis (PFGE) patterns. Of these, PFGE pattern 1 was represented by isolates from 44 patients and was identical to that of an epidemic A. baumannii clone isolated in another hospital of Naples during 2002. All A. baumannii isolates of PFGE type 1 showed identical multiresistant antibiotypes, characterised by resistance to all antimicrobial agents tested, including carbapenems, with the exception of colistin. In these isolates, inhibition of OXA enzymes by 200 mM NaCl reduced the imipenem MIC by up to four-fold. Molecular analysis of antimicrobial resistance genes showed that all A. baumannii isolates of PFGE type 1 harboured a class 1 integron containing the aacA4, orfX and blaOXA-20 gene cassettes, an ampC gene and a blaOXA-51-like allele. Moreover, a blaOXA-58-like gene surrounded by the regulatory elements ISAba2 and ISAba3 was identified in a 30-kb plasmid from A. baumannii isolates of PFGE type 1, but not PFGE type 2. Thus, selection of a single A. baumannii clone producing an OXA-58-type carbapenem-hydrolysing oxacillinase was responsible for the increase in the number of A. baumannii infections that occurred in this hospital.</abstract><cop>Oxford, UK</cop><pub>Elsevier Ltd</pub><pmid>17430339</pmid><doi>10.1111/j.1469-0691.2006.01675.x</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Clinical microbiology and infection, 2007-05, Vol.13 (5), p.481-489 |
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| subjects | Acinetobacter baumannii Acinetobacter baumannii - drug effects Acinetobacter baumannii - genetics Acinetobacter baumannii - pathogenicity Acinetobacter Infections - drug therapy Acinetobacter Infections - epidemiology Acinetobacter Infections - genetics Aged Antibacterial agents Antibiotics. Antiinfectious agents. Antiparasitic agents beta-Lactamases - classification beta-Lactamases - genetics Biological and medical sciences carbapenem resistance Carbapenems - pharmacology Community-Acquired Infections - drug therapy Community-Acquired Infections - genetics Community-Acquired Infections - microbiology Cross Infection - microbiology Cross Infection - mortality Disease Outbreaks Drug Resistance, Multiple, Bacterial Electrophoresis, Gel, Pulsed-Field Female General aspects Hospitals, University Human infectious diseases. Experimental studies and models Humans Infectious diseases Intensive Care Units Italy - epidemiology Male Medical sciences Microbial Sensitivity Tests molecular epidemiology nosocomial infection outbreak OXA-58 Pharmacology. Drug treatments |
| title | Molecular epidemiology of a clonal outbreak of multidrug-resistant Acinetobacter baumannii in a university hospital in Italy |
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