SEARCH · PubMed Health

Results for “Acinetobacter baumannii”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources

PubMed2000

Detection of carbapenemase-producing Acinetobacter baumannii in a hospital.

Acinetobacter baumannii strains resistant to both imipenem (IPM) and ceftazidime (CAZ) were isolated from 1994 through 1996 at Gunma University Hospital. Nine isolates from different inpatients were examined for carbapenem-hydrolyzing activity and for the carbapemase gene bla(IMP) by the PCR method. All nine isolates were carbapenemase-producing strains that hydrolyzed IPM and that harbored bla(IMP). The bla(IMP) gene was transmissible by conjugation to an IPM-susceptible recipient strain of A. baumannii and conferred resistance to IPM, CAZ, cefotaxime (CTX), ampicillin (AMP), and piperacillin (PIP). Either intermediate or high-level resistance to amikacin (AMK) was transferred from two and five strains, respectively, concomitantly with bla(IMP), and gentamicin (GEN) resistance was also transferred in one instance of high-level AMK resistance. Comparative examination of clinical isolates for resistance patterns to nine drugs, IPM, CAZ, CTX, aztreonam, AMP, PIP, AMK, GEN, and norfloxacin, in addition to pulsed-field gel electrophoresis patterns with NotI-digested genomic DNA, confirmed nosocomial transmission of infections involving carbapenemase-producing A. baumannii strains.

Acinetobacter↗

PubMed2004

[Study on the molecular epidemiology of SHV type beta-lactamase-encoding genes of multiple-drug-resistant acinetobacter baumannii].

OBJECTIVE: To analyse the plasmid-mediated SHV type beta-lactamases-encoding genes sequence and to identify its subtype of multiple-drug-resistant acinetobacter baumannii isolated from Huzhou district, Zhejiang province, China. METHODS: Sixty strains of acinetobacter baumannii were isolated from hospitalized patients between Jul, 2000 and Dec, 2002. Susceptibility of antimicrobial agents and confirmatory tests for Extended-spectrum beta-lactamases (ESBLs) were tested by microdilute method. SHV type beta-lactamases-encoding genes were tested by polymerase chain reaction (PCR). SHV sequences of acinetobacter baumannii HZ02 and HZ10 strains were detected by ABI automated sequencer and were analysed to compare with SHV genes that had been published in GenBank. RESULTS: Eighteen (30.0%) strains of acinetobacter baumannii isolated between Jun, 2001 and Jan, 2002 were carrying SHV beta-lactamases resistant gene of plasmids. Detected SHV sequences of acinetobacter baumannii HZ02 strain and HZ10 strain had 825 and 833 nucleotides respectively and had the same gene sequence as the gene encoding SHV-12 subtype of ESBLs discovered in Switzerland. CONCLUSIONS: Thirty percentage of the clinically isolated acinetobacter baumannii were carrying SHV type (extended-spectrum) beta-lactamases resistant gene of plasmids and causing an outbreak in hospital and was discovered to have carried the strains of SHV-12 subtype producing ESBLs gene in acinetobacter baumannii which was the first reported case in the world.

Acinetobacter Infections↗

PubMed2003

Multidrug resistant Acinetobacter baumannii isolates from a teaching hospital.

Abstract Acinetobacter baumannii is the most common nosocomial pathogen among all Acinetobacter spp. A. baumannii tend to be resistant to multiple antibiotics, and represent a severe threat in the treatment of hospitalized patients. The purpose of this study was to evaluate the prevalence, biotyping, and antibiotic resistance status of A. baumannii isolates recovered from submitted hospital clinical specimens. The in-vitro activity of 29 currently used antimicrobial agents was studied in 180 isolates of A. baumannii. The prevalence was higher in wound exudates (32%) and urine samples (22%) than in other specimens. Forty-six percent of the isolates were of biotype 9. The evolution of resistance from November 1996 through October 1998 was studied. More than 75% of the isolates were multidrug resistant (MDR) and more than 70% were #-lactamase producers. Amikacin, ampicillin + sulbactam, and imipenem are still effective antimicrobial agents, but a steady rise in the values of the minimum inhibitory concentration at which 50% of the isolates were inhibited (MIC50 )and MIC90 was observed. Resistance to aztreonam (60%), enrofloxacin (60%), imipenem (29%), moxalactam (73%), and sparfloxacin (25%) was noted; enrofloxacin and sparfloxacin are not generally used in this hospital. From the findings of the present study, no single drug appears to be suitable for empirical therapy for this nosocomial pathogen. Abstract Acinetobacter baumannii is the most common nosocomial pathogen among all Acinetobacter spp. A. baumannii tend to be resistant to multiple antibiotics, and represent a severe threat in the treatment of hospitalized patients. The purpose of this study was to evaluate the prevalence, biotyping, and antibiotic resistance status of A. baumannii isolates recovered from submitted hospital clinical specimens. The in-vitro activity of 29 currently used antimicrobial agents was studied in 180 isolates of A. baumannii. The prevalence was higher in wound exudates (32%) and urine samples (22%) than in other specimens. Forty-six percent of the isolates were of biotype 9. The evolution of resistance from November 1996 through October 1998 was studied. More than 75% of the isolates were multidrug resistant (MDR) and more than 70% were #-lactamase producers. Amikacin, ampicillin + sulbactam, and imipenem are still effective antimicrobial agents, but a steady rise in the values of the minimum inhibitory concentration at which 50% of the isolates were inhibited (MIC50) and MIC90 was observed. Resistance to aztreonam (60%), enrofloxacin (60%), imipenem (29%), moxalactam (73%), and sparfloxacin (25%) was noted; enrofloxacin and sparfloxacin are not generally used in this hospital. From the findings of the present study, no single drug appears to be suitable for empirical therapy for this nosocomial pathogen.

Acinetobacter baumannii↗

PubMed1992

The clinical significance of Acinetobacter baumannii in blood cultures.

Acinetobacter baumannii was isolated from blood cultures in 31 patients in 4 intensive care units at a large teaching hospital over a period of 6 months. In 23 of these patients, Acinetobacter was also isolated from tracheal aspirates. Catheter-related infection could be identified as the cause of bacteremia in 14 cases, whereas pneumonia was present in only 6 cases. All patients were seriously ill and 7 (24%) died of their infection.

Acinetobacter↗

PubMed1996

In vitro bactericidal effect of a beta-lactam+aminoglycoside combination against multiresistant Pseudomonas aeruginosa and Acinetobacter baumannii.

Pseudomonas aeruginosa and Acinetobacter baumannii are frequently isolated in hospital outbreaks of nosocomial infections. In our hospital, among 1018 strains isolated one year in an intensive care unit, 84 strains (8.3%) of P. aeruginosa and 155 strains (15.2%) of A. baumannii were considered responsible for infections. The major problem related to these bacteria is their multiresistant characteristic which confers great difficulty in treating infections. We carried out a 24 h time-kill study to assess the bactericidal effect of three beta-lactams [imipenem (IPM), ticarcillin+clavulanic acid (TCC), piperacillin+tazobactam (PTB)] in combination with each other and with sulbactam (SUL) and amikacin (AKN) against 8 P. aeruginosa strains and 8 A. baumannii strains. The initial inoculum was 10(6) cfu/ml. Antibiotics were tested at clinically achievable concentrations: TCC (112 mg/l), PTB (100 mg/l), IPM (25 mg/l) and AKN (15 mg/l). The results showed: IMP + TCC + AKN = PTB + SUL + AKN = PTB + TCC + AKN > > IMP + SUL + AKN against P. aeruginosa; and PTB + SUL + AKN = PTB + TCC + AKN > IMP + SUL + AKN or IMP + TCC + AKN against A. baumannii. When infection due to these multiresistant strains was suspected, PTB + AKN combined with either TCC or SUL was bactericidal against both strains. These combinations appeared to be an alternative therapy in the treatment of undocumented nosocomial infections in intensive care units. These in vitro results are being evaluated in patients and seem to give good results for the moment.

Acinetobacter↗

PubMed2001

Characterization of OXA-25, OXA-26, and OXA-27, molecular class D beta-lactamases associated with carbapenem resistance in clinical isolates of Acinetobacter baumannii.

Carbapenem resistance in Acinetobacter spp. is increasingly being associated with OXA-type beta-lactamases with weak hydrolytic activity against imipenem and meropenem. Such enzymes were characterized from Acinetobacter isolates collected in Belgium, Kuwait, Singapore, and Spain. The isolates from Spain and Belgium had novel class D beta-lactamases that were active against carbapenems. These were designated OXA-25 and OXA-26, respectively, and had >98% amino acid homology with each other and with the OXA-24 enzyme recently described by others from an Acinetobacter isolate collected elsewhere in Spain. The isolate from Singapore had OXA-27 beta-lactamase, another novel class D type with only 60% homology to OXA-24, -25, and -26, but with 99% homology to OXA-23 (ARI-1), described previously from an Acinetobacter baumannii isolate collected in Scotland. Sequence data were not obtained for the carbapenem-hydrolyzing OXA enzyme from the isolate from Kuwait; nevertheless, the enzyme was phenotypically similar to OXA-25 and -26. The enzymes OXA-23, -24, -25, -26, and -27 retained the STFK and SXV motifs typical of class D beta-lactamases, but the YGN motif was altered to FGN. The KTG motif was retained by OXA-27 and -23 but was replaced by KSG in OXA-24, -25, and -26. OXA-25 and -26 enzymes were strongly active against oxacillin, but unusually for an OXA-type beta-lactamase, OXA-27 had apparently weak activity, although measurement was complicated by biphasic kinetics. None of the new enzymes was transmissible to Escherichia coli recipients. Many Acinetobacter isolates are multiresistant to other antibiotics, and the emergence of class D enzymes with carbapenem-hydrolyzing activity is a disturbing development for antimicrobial chemotherapy.

Acinetobacter↗

PubMed2005

OXA-58, a novel class D {beta}-lactamase involved in resistance to carbapenems in Acinetobacter baumannii.

A carbapenem-resistant Acinetobacter baumannii strain was isolated in Toulouse, France, in 2003. Cloning and expression in Escherichia coli identified the carbapenem-hydrolyzing beta-lactamase OXA-58, which is weakly related (less than 50% amino acid identity) to other oxacillinases. It hydrolyzed penicillins, oxacillin, and imipenem but not expanded-spectrum cephalosporins. The bla(OXA-58) gene was located on a ca. 30-kb non-self-transferable plasmid. After electrotransformation in the A. baumannii CIP7010(T) reference strain, it conferred reduced susceptibility to carbapenems. The bla(OXA-58) gene was bracketed by two novel ISAba3-like insertion elements. This study describes a newly characterized beta-lactamase that may contribute to carbapenem resistance in A. baumannii.

Acinetobacter baumannii↗

PubMed2003

Healthcare-associated outbreak due to pan-drug resistant Acinetobacter baumannii in a surgical intensive care unit.

Acinetobacter baumannii is ubiquitous and has recently become one of the most important healthcare-associated (HA) pathogens in hospitals. Infection caused by this organism often leads to significant morbidity and mortality. Outbreaks of pan-drug resistant Acinetobacter baumannii (PDRAB) have rarely been reported. During a two-month period, an outbreak of PDRAB colonization and infection affecting 7 patients occurred in our surgical intensive care unit (SICU). The colonized sites were respiratory tract (N = 7) and central venous catheter (N = 2). One of the patients had a surgical wound infection. Extensive environmental contamination was identified, including sites such as bed rails, bedside tables, surface of ventilators and infusion pump, water for nasogastric feeding and ventilator rinsing and sinks. All of the isolates were analysed by pulsed-field gel electrophoresis (PFGE) and showed an identical pattern. After use of strict cohort nursing, hand hygiene environmental cleaning, and replacement of a dysfunctional high-efficiency particulate air filter (HEPA), the outbreak was controlled.

Acinetobacter Infections↗

PubMed2005

Evaluation of adherence, hemagglutination, and presence of genes codifying for virulence factors of Acinetobacter baumannii causing urinary tract infection.

Acinetobacter baumannii is a strictly aerobic bacterium which causes severe infections, however its pathogenic characteristics are not well defined. Thirteen A. baumannii strains isolated from urine of hospitalized and nonhospitalized patients with different ages were investigated for the presence of virulence factors. The isolates belonged to biotypes 2, 6, and 9 and were sensitive to imipenem. The majority of them showed resistance to amikacin, ceftazidime, ceftriaxone, ciprofloxacin, gentamicin, norfloxacin, and trimethoprim-sulfamethoxazole. None of A. baumannii strains presented genes codifying for 17 different virulence factors previously described in uropathogenic Escherichia coli, when tested by polymerase chain reaction (PCR). Nine isolates agglutinated human group AB erythrocytes, in presence of mannose, but none of them agglutinated group O erythrocytes. Adherence to polystyrene was observed in 7 isolates, and this result did not correlate with that obtained in hemagglutination assay. All the isolates were able to grow in iron-limiting conditions, showing that A. baumannii produces some type of siderophore. However, the genes iutA and fyuA, from iron uptake system of E. coli and Yersinia sp., respectively, were not present in the isolates, suggesting the presence of a different type of siderophore. The fimbriae of A. baumannii strains that mediates the adherence are possibly mannose-resistant, even though the mechanism of adherence to human epithelial cells still remains to be elucidated.

Acinetobacter Infections↗

PubMed2006

The epidemiology and control of Acinetobacter baumannii in health care facilities.

Acinetobacter baumannii is a ubiquitous pathogen capable of causing both community and health care-associated infections (HAIs), although HAIs are the most common form. This organism has emerged recently as a major cause of HAI because of the extent of its antimicrobial resistance and its propensity to cause large, often multifacility, nosocomial outbreaks. The occurrence of outbreak is facilitated by both tolerance to desiccation and multidrug resistance, contributing to the maintenance of these organisms in the hospital environment. In addition, the epidemiology of A. baumannii infection is often complex, with the coexistence of epidemic and endemic infections, the latter of which often is favored by the selection pressure of antimicrobials. The only good news is that potentially severe A. baumannii infection, such as bacteremia or pneumonia in patients in the intensive care unit who are undergoing intubation, do not seem to be associated with a higher attributable mortality rate or an increased length of hospital stay.

Acinetobacter Infections↗

PubMed2005

[Comparison of different phenotypic methods detecting extended spectrum beta-lactamases in Pseudomonas aeruginosa and Acinetobacter baumannii strains].

Pseudomonas aeruginosa and Acinetobacter baumannii which are of great concern as the frequent causative agents of nosocomial infections, frequently exhibit resistance to beta-lactam antibiotics. One of the most common causes of this resistance is the presence of extended spectrum beta-lactamases (ESBL). There is still no standardized method for the detection of ESBLs in P. aeruginosa and A.baumannii strains. The aim of this study was to compare the results of Epsilomer test (E-test), combined disk (CD) and double disk synergy (DDS) methods for the detection of ESBL in a total of 38 P. aeruginosa and 45 A.baumannii strains with ceftazidim or cefotaxime MIC > or = 1 microg/ml, isolated from different clinical samples. Cefepime was included in the group of indicator antibiotics and the distance between clavulanic acid containing disk and indicator antibiotic disks was reduced to increase the sensitivity of DDS test. Of the P. aeruginosa strains, 78.9% was detected as ESBL producers by ceftazidime/ ceftazidime-clavulanic acid and 21.1% detected by cefotaxime/cefotaxime-clavulanic acid ratio. Among this group of strains, 31.5% was positive by DDS test and 84.2% was positive by CD method. Of the A.baumannii strains, 93.3% of them was positive by ceftazidime/ceftazidime-clavulanic acid and 6.6% was positive by cefotaxime/cefotaxime-clavulanic acid ratio. DDS test detected 20% and CD method detected 53.3% of the strains positive by E-test method. The use of cefotaxime together with ceftazidime as an indicator antibiotic increased the sensitivity of detection of ESBL enzymes. Although inclusion of cefepime and reduction of the distance between disks increased the detection of ESBL by DDS method, it was still less effective than E-test. Although, 28.9% of the P. aeruginosa and 13.3% of the A. baumannii strains were susceptible to ceftazidime by in vitro tests, they were ESBL producers. In conclusion, E-test method was found to be the most sensitive phenotypic method for the detection of ESBL in our study collection.

Acinetobacter baumannii↗

PubMed2003

Relationship between beta-lactamase production, outer membrane protein and penicillin-binding protein profiles on the activity of carbapenems against clinical isolates of Acinetobacter baumannii.

Twenty blood isolates of Acinetobacter baumannii were studied, representing eight pulsed-field gel electrophoresis patterns and all different antimicrobial susceptibility patterns observed during 1995-97 at the University Hospital Virgen Macarena, Seville, Spain. The MIC(90)s (mg/L) of imipenem and meropenem decreased from 16 to 0.5 and from 8 to 4, respectively, in the presence of BRL 42715 (BRL) but not clavulanic acid. Hydrolysing activity (nmol/min/mg) of bacterial supernatants against cefaloridine ranged from 8.8 to 552.3 for A. baumannii type I (imipenem MICs < or = 2), which expressed only a beta-lactamase of pI > or = 9, and from 12.3 to 1543.5 for A. baumannii type II (imipenem MICs > or = 4), which expressed a beta-lactamase of pI > or = 9 and two others of pI 6.3 and 7. The hydrolysing activities of A. baumannii type II against imipenem, meropenem and oxacillin were higher than those observed for A. baumannii type I. Ten outer membrane protein (OMP) profiles (A. baumannii types I and II) were visualized on 10% SDS-PAGE gels with 6 M urea, whereas only five OMP profiles (A. baumannii types I and II) were differentiated in 12% SDS-PAGE gels. Five A. baumannii with OMP profile type B, characterized by the absence of a 22.5 kDa OMP, were resistant to meropenem and/or imipenem. Twelve penicillin-binding protein (PBP) patterns were observed. PBP patterns of A. baumannii type II were characterized by the absence of a 73.2 kDa band (PBP 2). We concluded that production of beta-lactamases of pI 6.3 and 7.0 and reduced expression of PBP 2 are the most frequently observed mechanisms of resistance to carbapenems. In some isolates, loss of a 22.5 kDa OMP is also related to resistance to carbapenems.

Acinetobacter baumannii↗

PubMed2002

Molecular characterization of bla(IMP-5), a new integron-borne metallo-beta-lactamase gene from an Acinetobacter baumannii nosocomial isolate in Portugal.

Acinetobacter baumannii 65FFC, an imipenem-resistant clinical strain, isolated from the urine of a patient at the Coimbra University Hospital, Portugal, in 1998, produced a metallo-beta-lactamase with a calculated pI 9.3. The isolate was highly resistant to penicillins, broad-spectrum cephalosporins, including ceftazidime, ceftriaxone, cefepime, cefpirome, and to aztreonam, but it remained susceptible to ampicillin/sulbactam, aminoglycosides and quinolones. Nucleotide sequence revealed a new allelic variant of other bla(IMP) genes, named bla(IMP-5). IMP-5 beta-lactamase showed a greater homology with IMP-1, IMP-3 and IMP-4 (identified in Southeast Asia), than with IMP-2, found in Italy (93%, 92%, 91% and 87% of amino acid identity, respectively). bla(IMP-5) was the only gene cassette inserted into a class 1 integron, named In76. This is the first IMP-enzyme reported in Portugal and the second in Europe, indicating a wider dissemination in the environment of bla(IMP) alleles.

Acinetobacter Infections↗

PubMed2002

Underlying characteristics of patients harboring highly resistant Acinetobacter baumannii.

BACKGROUND: Highly resistant (HR) Acinetobacter baumannii (AB) are frequently hospital-acquired and may be important causes of severe nosocomial infections. OBJECTIVE: Determine risk factors associated with such colonization/infection. METHOD: Retrospective review in 2000 of all AB isolates from sterile (blood, cerebrospinal fluid [CSF]) and nonsterile (respiratory, urine, and miscellaneous) sites. HR was defined as resistance to amikacin and/or imipenem and/or ampicillin-sulbactam. Isolates were analyzed as representing infection or colonization. A database including prior hospitalization, prior antibiotic use, nursing home residency, and procedures undergone was compiled. RESULTS: One hundred twenty-two cases of AB were identified. Eighty-four met the definition of HR; 6 (4.9%) were completely resistant to all antibiotics. Four (4.7%) isolates were from sterile body sites (3 blood, 1 CSF); 43 (51.2%) were from respiratory sites; 20 (23.8%) were from urinary sites; and 17 (20.2%) were from "other" sites. Only 4 (20%) of the urinary, 6 (35.2%) of the miscellaneous, and 23 (53.4%) of the respiratory isolates were deemed true pathogens; all blood/CSF isolates were considered pathogens. Associated risk factors included prior antibiotic usage (71%); prior hospitalization (24%); prior nursing home residency (34%); ventilator use (77%); tracheostomy placement (56%); and Foley catheterization (85%). Twenty-seven (63%) of 43 respiratory, 8 (40%) of 20 urinary, and 6 (35%) of 17 "other" body isolates were treated. Outcome was not statistically significant in treated versus untreated patients. All patients with CSF/blood isolates underwent successful microbiologic eradication with 50% survival. The overall mortality rate was 10%. CONCLUSION: Antibiotics, Foley catheters, and tracheostomy/ventilator usage were strongly associated with AB isolation. Prior hospitalization and nursing home residency were less common risk factors. Outcome was not different in treated versus untreated patients, indicating colonization is a marker of severe illness but is not necessarily causal.

Acinetobacter Infections↗

PubMed2025

Characterization of blaOXA-542-mediated carbapenem resistance in Acinetobacter baumannii.

BACKGROUND: Carbapenem-resistant Acinetobacter baumannii (CRAB) causes multiple anatomical site infections, representing a significant public health threat. AIM: This study reports the isolation and characterization of a carbapenem-resistant A. baumannii harbouring blaOXA-542, followed by a comprehensive investigation of its antimicrobial resistance mechanisms and genomic characteristics. METHODS: Firstly, antimicrobial susceptibility testing was performed using the broth microdilution method. Subsequently, whole-genome sequencing was employed to identify and characterize the resistance and virulence determinants. The functional validation of resistance mechanisms was performed by gene knockdown and construction of expression vectors. The fitness cost of β-lactamase expression was identified by a bacterial growth kinetic test. Molecular docking was utilized to predict potential binding sites of β-lactamase and carbapenems. Finally, the genetic characteristics of the isolates were analysed through comparative genomics analyses and phylogenetic tree construction. RESULTS AND CONCLUSIONS: The results demonstrated that blaOXA-542 confers resistance to carbapenem and penicillin in A. baumannii and Escherichia coli while exhibiting no significant impact on cephalosporins. The ability of blaOXA-542 to hydrolyze meropenem was further confirmed by modified carbapenem inactivation assay (mCIM). Expression of blaOXA-542 in E. coli BL21 showed no significant growth rate alteration. Comparative analysis of the blaOXA-542 genetic environment revealed a close association with Acinetobacter pitti. This study reports the emergence of blaOXA-542-mediated carbapenem and penicillin resistance in a novel A. baumannii lineage (ST2795Pas/ST3464Oxf), highlighting the urgent need for rational antibiotic use against specific pathogens.

Acinetobacter baumannii↗

PubMed1998

Nosocomial Acinetobacter baumannii infections: microbiological and clinical epidemiology.

BACKGROUND: Acinetobacter baumannii is an important opportunistic pathogen that is rapidly evolving toward multidrug resistance and is involved in various nosocomial infections that are often severe. It is difficult to prevent A. baumannii infection because A. baumannii is ubiquitous and the epidemiology of the infections it causes is complex. OBJECTIVE: To study the epidemiology of A. baumannii infections and assess the relation between fluoroquinolone use and the persistence of multidrug-resistant clones. DESIGN: Three case-control studies and a retrospective cohort study. SETTING: A 20-bed medical and surgical intensive care unit. PATIENTS: Acinetobacter baumannii was isolated from 45 patients in urine (31%), the lower respiratory tract (26.7%), wounds (17.8%), blood (11.1%), skin (6.7%), cerebrospinal fluid (4.4%), and sinus specimens (2.2%). One death was due to A. baumannii infection. MEASUREMENTS: Antimicrobial resistance pattern and molecular typing were used to characterize isolates. The incidence of A. baumannii infection and the use of fluoroquinolones were calculated annually. RESULTS: Initially, 28 patients developed A. baumannii infection. Eleven isolates had the same antimicrobial susceptibility profile, genotypic profile, or both (epidemic cases), and 17 were heterogeneous (endemic cases). A surgical procedure done in an emergency operating room was the main risk factor for epidemic cases, whereas previous receipt of a fluoroquinolone was the only risk factor for endemic cases. The opening of a new operating room combined with the restriction of fluoroquinolone use contributed to a transitory reduction in the incidence of infection. When a third epidemiologic study was done, previous receipt of a fluoroquinolone was again an independent risk factor and a parallel was seen between the amount of intravenous fluoroquinolones prescribed and the incidence of endemic infection. CONCLUSION: Epidemic infections coexisted with endemic infections favored by the selection pressure of intravenous fluoroquinolones.

Acinetobacter↗

PubMed2003

The impact of Acinetobacter baumannii in the intensive care unit.

Acinetobacter baumannii is a significant problem in critically ill patients. It is widespread, can colonise patients quickly and causes virulent infections. However, its overall impact on morbidity and mortality in the critically ill remains unmeasured. This study was designed to investigate A. baumannii colonisation and infection rates in a critically ill population over an 18-month period. Twenty-seven patients from a population of 347 were identified as having A. baumannii. Sixteen were colonised, whereas 11 were infected. Eleven of the 27 patients with A. baumannii died (41%). Of these, eight were colonised and three were infected. In the same period, 320 patients did not have A. baumannii and their mortality rate was 20% (n = 64). The mortality rate of patients with A. baumannii was significantly higher than that of patients without infection.

Acinetobacter Infections↗

PubMed2006

Emergence of PER and VEB extended-spectrum beta-lactamases in Acinetobacter baumannii in Belgium.

OBJECTIVES: Strains of Acinetobacter baumannii producing the extended-spectrum beta-lactamase (ESBL) PER-1 are widespread in Turkey and have also been reported from Korea and France. In contrast, A. baumannii producing the ESBL VEB-1 have only been reported from France, where one strain was responsible for a nationwide outbreak in 2003-2004. Here we describe the emergence of strains of A. baumannii producing VEB-1 and PER- 1 in Belgium. METHODS: Belgian hospitals were alerted in December 2003 to the emergence in France of VEB-1-producing A. baumannii susceptible only to meropenem and colistin. Isolates with a compatible susceptibility profile were sent to a single central laboratory for VEB-1 confirmation, molecular characterization and typing. RESULTS: From December 2003 to March 2005, three hospitals located close to the French border and one in the Brussels area reported isolation of eight A. baumannii isolates compatible with the French epidemic clone. Using PCR, six were identified as VEB-1-positive and two as PER-1-positive. All the VEB-1-positive isolates were clonally related by PFGE and by integron analysis to the French epidemic strain. The PER-1-positive strains were indistinguishable by PFGE but not related to the known French isolate or to several Turkish isolates. Both genes were chromosomally encoded. CONCLUSIONS: This work illustrates the inter-country spread of VEB-1-producing A. baumannii isolates as well as the emergence of PER-1-producing A. baumannii strains in Belgium.

Acinetobacter Infections↗