ABSTRACT
We investigated the molecular epidemiology of gentamicin-resistant, extended-spectrum beta-lactamase (ESBL)-producing Klebsiella pneumoniae and Serratia marcescens, and risk factors associated with their acquisition in a neonatal intensive care unit (NICU) of a university hospital in Italy. During the study period (April-November 2004), S. marcescens was responsible for six infections and 31 colonisations, while K. pneumoniae was responsible for six infections and 103 colonisations. Concurrent isolation of both organisms occurred in 24 neonates. Molecular typing identified one major pulsed-field gel electrophoresis pattern each for S. marcescens and K. pneumoniae strains isolated during the study period. An 80 kb plasmid containing bla(SHV-12), bla(TEM-1) and aac(6')-Ib genes, isolated from both S. marcescens and K. pneumoniae strains, and showing identical restriction profiles, transferred resistance to third-generation cephalosporins to a previously susceptible Escherichia coli host. Birthweight, gestational age and use of invasive devices were significantly associated with S. marcescens and K. pneumoniae acquisition on univariate analysis, while empiric antimicrobial treatment with ampicillin and gentamicin, and duration of hospital stay, proved to be the only independent risk factors. In conclusion, conjugal plasmid transfer and empiric antimicrobial therapy with ampicillin and gentamicin might have contributed to the selection and spread of gentamicin-resistant ESBL-producing Enterobacteriaceae in the NICU.
Subject(s)
Klebsiella Infections/microbiology , Klebsiella pneumoniae/enzymology , Serratia Infections/microbiology , Serratia marcescens/enzymology , beta-Lactamases/genetics , Acetyltransferases/genetics , Ampicillin/therapeutic use , Anti-Bacterial Agents/pharmacology , Anti-Bacterial Agents/therapeutic use , Bacterial Typing Techniques , Birth Weight , Carrier State/microbiology , Cephalosporins/pharmacology , DNA Fingerprinting , DNA, Bacterial/genetics , Drug Resistance, Bacterial , Electrophoresis, Gel, Pulsed-Field , Genotype , Gentamicins/pharmacology , Gestational Age , Humans , Infant , Infant, Newborn , Intensive Care Units, Neonatal , Italy , Klebsiella Infections/epidemiology , Klebsiella pneumoniae/classification , Klebsiella pneumoniae/drug effects , Klebsiella pneumoniae/isolation & purification , Molecular Epidemiology , Molecular Sequence Data , Plasmids/genetics , Risk Factors , Sequence Analysis, DNA , Serratia Infections/epidemiology , Serratia marcescens/classification , Serratia marcescens/drug effects , Serratia marcescens/isolation & purification , Surgical Procedures, OperativeABSTRACT
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 bla(OXA-20) gene cassettes, an ampC gene and a bla(OXA-51)-like allele. Moreover, a bla(OXA-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.
Subject(s)
Acinetobacter Infections/epidemiology , Acinetobacter baumannii/genetics , Carbapenems/pharmacology , Cross Infection/microbiology , Disease Outbreaks , beta-Lactamases/genetics , Acinetobacter Infections/drug therapy , Acinetobacter Infections/genetics , Acinetobacter baumannii/drug effects , Acinetobacter baumannii/pathogenicity , Aged , Community-Acquired Infections/drug therapy , Community-Acquired Infections/genetics , Community-Acquired Infections/microbiology , Cross Infection/mortality , Drug Resistance, Multiple, Bacterial , Electrophoresis, Gel, Pulsed-Field , Female , Hospitals, University , Humans , Intensive Care Units , Italy/epidemiology , Male , Microbial Sensitivity Tests , beta-Lactamases/classificationABSTRACT
Treatment of neonatal jaundice is currently recommended for higher bilirubinemia levels than before. Using the Brazelton Neonatal Behavior Assessment Scale, we found that a series of 28 healthy, untreated, term neonates with moderate bilirubinemia scored significantly less than an equal number of appropriately matched controls with low bilirubinemia for visual and auditory items, both inanimate and animate. Also, a greater lability of state, a lower self-quieting ability and more frequent tremors were found in the jaundiced group. We conclude that hyperbilirubinemia per se, even in the concentration range where phototherapy is not currently recommended, can give rise to alterations in neonatal behavior.
