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Multiresistant Acinetobacter baumannii isolates in intensive care units in Greece

2003; Elsevier BV; Volume: 9; Issue: 6 Linguagem: Inglês

10.1046/j.1469-0691.2003.00558.x

1469-0691

Antonios N. Maniatis, Spyros Pournaras, S. Orkopoulou, Panayotis T. Tassios, N.J. Legakis,

Vibrio bacteria research studies

One hundred and twenty-one clinical isolates of Acinetobacter baumannii recovered from the intensive care units (ICUs) of nine tertiary-care hospitals in Athens, Greece were studied in order to determine whether the increasing appearance of resistant acinetobacters is due to the spread of epidemic strains. The majority of the isolates exhibited resistance to ampicillin–sulbactam, and the most common antibiotic resistance profiles comprised resistance to nine and eight of the 11 potentially active antibiotics tested, respectively. Pulsed-field gel electrophoresis showed that 68% of the isolates, recovered from all ICUs, belonged to two clonal groups, indicating inter-hospital dissemination of multiresistant A. baumannii in our region. One hundred and twenty-one clinical isolates of Acinetobacter baumannii recovered from the intensive care units (ICUs) of nine tertiary-care hospitals in Athens, Greece were studied in order to determine whether the increasing appearance of resistant acinetobacters is due to the spread of epidemic strains. The majority of the isolates exhibited resistance to ampicillin–sulbactam, and the most common antibiotic resistance profiles comprised resistance to nine and eight of the 11 potentially active antibiotics tested, respectively. Pulsed-field gel electrophoresis showed that 68% of the isolates, recovered from all ICUs, belonged to two clonal groups, indicating inter-hospital dissemination of multiresistant A. baumannii in our region. Acinetobacter baumannii is increasingly recognized as an important cause of nosocomial infection. It plays a substantial role in the colonization and infection of patients admitted to hospitals, and is one of the predominant etiologic agents of nosocomial pneumonia, particularly among intensive care unit (ICU) patients suffering from ventilator-associated pneumonia [1Beck-Sague CM Jarvis WR Brook JH et al.Epidemic bacteremia due to Acinetobacter baumannii in five intensive care units.Am J Epidemiol. 1990; 132: 723-733PubMed Google Scholar, 2Bergogne-Berezin E Towner KJ Acinetobacter spp. as nosocomial pathogens: microbiological, clinical and epidemiological features.Clin Microbiol Rev. 1996; 9: 148-165PubMed Google Scholar, 3Biendo M Laurans G Lefebvre JF Daoudi F Eb F Epidemiological study of an Acinetobacter baumannii outbreak by using a combination of antibiotyping and ribotyping.J Clin Microbiol. 1999; 37: 2170-2175PubMed Google Scholar]. The resistance of A. baumannii isolates to the major groups of antibiotics seems to be increasing [2Bergogne-Berezin E Towner KJ Acinetobacter spp. as nosocomial pathogens: microbiological, clinical and epidemiological features.Clin Microbiol Rev. 1996; 9: 148-165PubMed Google Scholar], causing significant difficulties in the treatment of severe hospital infections. Such isolates have an enhanced potential to survive for prolonged periods in the hospital environment and contaminate medical equipment and devices. A. baumannii can thus easily spread and persist, once it is introduced into the hospital environment. Numerous outbreaks of hospital infection with acinetobacters have been reported, and they are often associated with the spread of multiresistant strains [1Beck-Sague CM Jarvis WR Brook JH et al.Epidemic bacteremia due to Acinetobacter baumannii in five intensive care units.Am J Epidemiol. 1990; 132: 723-733PubMed Google Scholar,3Biendo M Laurans G Lefebvre JF Daoudi F Eb F Epidemiological study of an Acinetobacter baumannii outbreak by using a combination of antibiotyping and ribotyping.J Clin Microbiol. 1999; 37: 2170-2175PubMed Google Scholar, 4Bou G Cervero G Angeles Dominguez M Quereda C Martinez-Beltran J Characterization of a nosocomial outbreak caused by a multiresistant Acinetobacter baumannii: high-level carbapenem resistance in A. baumannii is not due solely to the presence of β-lactamases.J Clin Microbiol. 2000; 38: 3299-3305PubMed Google Scholar, 5Struelens MJ Carlier E Maes N Serruys E Quint WGV van Belkum A Nosocomial colonization and infection with multi-resistant Acinetobacter baumannii: outbreak delineation using DNA macrorestriction and PCR-fingerprinting.J Hosp Infect. 1993; 25: 15-32Abstract Full Text PDF PubMed Scopus (127) Google Scholar]. Several genotypic methods have been used for the epidemiologic typing of A. baumannii; among them, pulsed-field gel electrophoresis (PFGE) has exhibited reproducibility and excellent discriminatory power [6Seifert H Schulze A Baginski R Pulverer G Comparison of four different methods for epidemiologic typing of Acinetobacter baumannii.J Clin Microbiol. 1994; 32: 1816-1819PubMed Google Scholar,7Dijkshoorn L Aucken H Gerner-Schmidt P et al.Comparison of outbreak and nonoutbreak Acinetobacter baumannii strains by genotypic and phenotypic methods.J Clin Microbiol. 1996; 34: 1519-1525PubMed Google Scholar]. A. baumannii is frequently encountered in Greek hospitals, and many isolates exhibit resistance to the antimicrobials commonly used against such bacterial infections [8Legakis NJ Tzouvelekis LS Tsakris A Legakis JN Vatopoulos AC On the incidence of antibiotic resistance among aerobic gram-negative rods isolated in Greek hospitals.J Hosp Infect. 1993; 24: 233-237Abstract Full Text PDF PubMed Scopus (30) Google Scholar, 9Douboyas J Tzouvelekis LS Tsakris A In-vitro activity of ampicillin/sulbactam against multiresistant Acinetobacter calcoaceticus var. anitratus clinical isolates.J Antimicrob Chemother. 1994; 34: 298-300Crossref PubMed Scopus (11) Google Scholar, 10Tsakris A Pantazi A Pournaras S Maniatis A Polyzou A Sofianou D Pseudo-outbreak of imipenem-resistant Acinetobacter baumannii resulting from false susceptibility testing by a rapid automated system.J Clin Microbiol. 2000; 38: 3505-3507PubMed Google Scholar]. The main objectives of this study were to obtain data on the diversity of clinical isolates of A. baumannii collected from ICUs of Greek hospitals, and to determine whether the increasing appearance of resistant acinetobacters is due to the spread of epidemic strains. One hundred and twenty-one non-replicate A. baumannii isolates were collected prospectively during a 4-month period from January to April 1998, from patients hospitalized in ICUs of nine tertiary-care hospitals in Athens, Greece. Isolates were recovered from bronchial secretions, wound exudates, blood, and catheter swabs. All isolates were identified as belonging to the genus Acinetobacter on the basis of the following properties: presence of non-motile coccobacilli that were Gram-negative, strictly aerobic, catalase positive, and oxidase negative. The isolates were provisionally identified by the API 20NE system (bioMerieux API, Marcy 1′ Etoile, France) according to the manufacturer's instructions. The identification of A. baumannii was performed by the simplified identification scheme described by Bouvet and Grimont [11Bouvet PJM Grimont PAD Taxonomy of the genus Acinetobacter with the recognition of Acinetobacter baumannii sp. nov., Acinetobacter haemolyticus sp. nov., Acinetobacter johnsoni sp. nov. & Acinetobacter junii sp. nov., emended description of Acinetobacter calcoaceticus and Acinetobacter lwoffii.Int J Syst Bacteriol. 1986; 36: 228-240Crossref Scopus (493) Google Scholar]. Susceptibility testing was performed by a broth microdilution method, according to the guidelines established by the National Committee for Clinical Laboratory Standards (NCCLS) [12National Committee for Clinical Laboratory Standards Methods for dilution antimicrobial susceptibility tests for bacteria that grow aerobically, 4th edn. Approved Standard M7-A4. NCCLS, Wayne, PA1997Google Scholar]. The antimicrobial agents tested were amikacin, ampicillin–sulbactam, aztreonam, ceftazidime, ciprofloxacin, gentamicin, imipenem, netilmicin, piperacillin, ticarcillin–clavulanate, and tobramycin. Control strains of Pseudomonas aeruginosa (ATCC 27853) and Escherichia coli (ATCC 25922) were included in each assay. Susceptibility categories were assigned according to NCCLS interpretative criteria [12National Committee for Clinical Laboratory Standards Methods for dilution antimicrobial susceptibility tests for bacteria that grow aerobically, 4th edn. Approved Standard M7-A4. NCCLS, Wayne, PA1997Google Scholar]. Sixty-nine of the isolates were randomly selected for pulsed-field gel electrophoresis (PFGE), following ApaI macrorestriction. The isolates were typed in a central laboratory (Department of Microbiology, Medical School, University of Athens), as results from different laboratories are often difficult to compare, due to variations in the protocols used. The preparation of agarose plugs and the restriction of genomic DNA were done as described previously [6Seifert H Schulze A Baginski R Pulverer G Comparison of four different methods for epidemiologic typing of Acinetobacter baumannii.J Clin Microbiol. 1994; 32: 1816-1819PubMed Google Scholar]. DNA fragments were separated by PFGE in a 1.2% agarose gel for 24 h at 6 V/cm, using a CHEF-DRIII apparatus (Bio-Rad, Hemel Hempstead, UK). The pulse times ranged from 5 to 20 s. Banding patterns were analyzed with the aid of GelCompar software (Applied Maths, Kortrijk, Belgium). The Dice correlation coefficient was applied; the strains were clustered at the 80% level of genetic similarity by the method of unweighted pair-group matching by arithmetic averages algorithm, and a dendrogram of percentage similarity was produced. The major restriction types were defined with the use of capital letters. The majority of isolates (74, 61.2%) were recovered from bronchial cultures. All isolates were sensitive to imipenem. Amikacin and netilmicin were the most active of the remaining antimicrobials, with 36 (29.8%) and 68 (56.2%) of the A. baumannii isolates being resistant to the above drugs, respectively. An unexpectedly high proportion of the isolates (71, 58.7%) was resistant to ampicillin–sulbactam, while even higher proportions of isolates exhibited resistance to the remaining antibiotics (Table 1). The most common phenotype comprised resistance to ampicillin–sulbactam, aztreonam, ceftazidime, ciprofloxacin, gentamicin, netilmicin, piperacillin, ticarcillin–clavulanate, and tobramycin, and was noticed in as many as 25 (20.7%) of the isolates, while 21 (17.4%) further isolates exhibited resistance to the same antimicrobials except for ampicillin–sulbactam.Table 1In vitro activity of 11 antimicrobial agents against 121 A. baumannii isolatesAntimicrobial agentMIC50 (mg/L)MIC90 (mg/L)RangePercentage of resistant isolatesAmikacin8641–6429.8Ampicillin–sulbactam161284–12858.7Aztreonam1281281–12893.4Ceftazidime32324–12895.9Ciprofloxacin440.5–12892.6Gentamicin16161–3287.6Imipenem241–40Netilmicin16321–12856.2Piperacillin1281288–25697.5Ticarcillin–clavulanate1281282–12895.9Tobramycin16161–3272.7 Open table in a new tab The dendrogram constructed from the PFGE patterns of the 69 isolates tested is shown in Figure 1. The PFGE profiles, dates, departments, clinical sources of isolation and resistance phenotypes of the 69 A. baumannii isolates tested in this study are shown in Table 2. The majority of the A. baumannii isolates (57, 82.6%) were clustered into four clonal groups (PFGE profiles designated as B, F, H, J; Table 2, Figure 1); two of them (profiles F and H) accounted for 47 (68.1%) of the examined isolates, while profiles B and J accounted for nine (13.0%) of them. The remaining acinetobacters belonged to nine additional groups that contained one to three isolates. A variety of resistance phenotypes was detected among the major clonal groups.Table 2Departments, dates, clinical sources of isolation, resistance phenotypes and PFGE profiles of 69 multiresistant A. baumannii isolates tested in this studyIsolateWardDate of isolation (day/month/yearSite of isolationResistance pattern of clinical isolatesaAbbreviations: Ak, amikacin; As, ampicillin–sulbactam; Az, aztreonam; Cp, ciprofloxacin; Cz, ceftazidime; Gm, gentamicin; Im, imipenem; Nt, netilmicin; Pi, piperacillin; Tc, ticarcillin–clavulanate; To, tobramycin.PFGE type4332ICU-108/02/98BronchialAs, Az, Cp, Cz, Gm, Nt, Pi, Tc, ToA4263ICU-419/01/98BronchialAs, Az, Cp, Cz, Gm, Nt, Pi, Tc, ToB4129ICU-626/01/98BloodAs, Az, Cp, Cz, Pi, Tc, ToB4128ICU-625/01/98BronchialCp, Cz, Nt, Pi, TcB4264ICU-421/01/98BronchialAs, Az, Cp, Cz, Gm, Pi, Tc, ToB4161ICU-311/01/98BloodAs, Az, Cp, Cz, Gm, Nt, Pi, Tc, ToB4228ICU-528/02/98BronchialAs, Az, Cp, Cz, Gm, Pi, Tc, ToC771ICU-912/04/98BronchialAz, Cz, Gm, Pi, Tc, ToC165ICU-922/01/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToD4222ICU-521/02/98BronchialAs, Az, Cp, Cz, Gm, Pi, Tc, ToE4236ICU-718/02/98Intravascular catheterAz, Cp, Cz, Gm, Pi, Tc, ToE562ICU-926/03/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToF347ICU-916/02/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToF4276ICU-229/01/98SputumAs, Cp, Cz, Pi, TcF536ICU-907/01/98BronchialAz, Cz, Gm, Pi, Tc, ToF583ICU-929/03/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToF4388ICU-711/04/98PusAz, Cp, Cz, Gm, Pi, Tc, ToF581ICU-928/03/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToF4233ICU-713/02/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToF4054ICU-815/01/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToF4235ICU-715/02/98BronchialAz, Cp, Cz, Pi, Tc, ToF4265ICU-125/01/98BloodAz, Cp, Cz, Gm, Nt, Pi, Tc, ToF4213ICU-513/02/98BronchialAs, Az, Cp, Cz, Gm, Pi, Tc, ToF4226ICU-524/02/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToF4231ICU-712/02/98BronchialAz, Cp, Cz, Gm, Nt, Pi, Tc, ToF4210ICU-510/02/98SputumAs, Az, Cp, Cz, Gm, Pi, Tc, ToF4411ICU-824/04/98Intravascular catheterAz, Cp, Cz, Gm, Pi, TcF4061ICU-816/01/98BronchialAz, Cp, Cz, Gm, Pi, TcF4169ICU-314/01/98BronchialAz, Cp, Cz, Pi, TcF4396ICU-312/02/98BronchialAk, As, Az, Cp, Gm, Nt, Pi, TcF4217ICU-517/02/98BronchialPi, TcF4221ICU-520/02/98BronchialAs, Az, Cp, Cz, Gm, Pi, Tc, ToF4277ICU-220/01/98Intravascular catheterAs, Az, Cp, Cz, Pi, TcF41ICU-903/01/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToF922ICU-929/04/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToF2ICU-611/03/98BronchialAs, Az, Cp, Gm, Pi, TcF4099ICU-806/02/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToF4409ICU-823/04/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToF4042ICU-806/01/98BronchialAz, Cp, Cz, Gm, Nt, Pi, Tc, ToG4412ICU-824/04/98Intravascular catheterAz, Cp, Cz, Gm, Pi, TcH4413ICU-825/04/98SputumAz, Cp, Cz, Gm, Pi, TcH4279ICU-227/01/98PusAk, As, Az, Cp, Cz, Pi, TcH4280ICU-225/02/98Intravascular catheterAs, Az, Cp, Cz, Gm, Pi, TcH167ICU-922/01/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToH37ICU-902/01/98BronchialAz, Cp, Cz, Gm, Nt, Pi, Tc, ToH504ICU-920/03/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToH290ICU-914/02/98BronchialCp, Cz, Pi, Tc, ToH310ICU-918/02/98BronchialAz, Cp, Cz, Gm, Nt, Pi, Tc, ToH4281ICU-231/03/98PusAk, Az, Cp, Gm, Nt, Pi, TcH4288ICU-230/04/98BronchialAs, Az, Cz, Gm, Pi, Tc, ToH4395ICU-326/02/98BronchialAs, Az, Cp, Cz, Gm, Nt, Pi, Tc, ToH4212ICU-513/02/98BronchialAs, Az, Cp, Cz, Gm, Pi, Tc, ToH4335ICU-115/02/98BronchialAs, Az, Cp, Cz, Gm, Nt, Pi, Tc, ToH4275ICU-227/01/98SputumAs, Az, Cp, Cz, Pi, TcH4214ICU-514/02/98BronchialAs, Az, Cp, Cz, Gm, Pi, Tc, ToH4234ICU-714/02/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToH4232ICU-712/02/98BloodAz, Cp, Cz, Gm, Pi, Tc, ToH826ICU-921/04/98BronchialAz, Cp, Cz, Gm, Pi, Tc, ToH4052ICU-815/01/98BronchialAz, Cp, Cz, Gm, Nt, Pi, Tc, ToH4278ICU-226/03/98SputumAs, Az, Cp, Cz, Pi, TcI4097ICU-805/02/98PusAz, Cp, Cz, Gm, Nt, Pi, Tc, ToI4175ICU-409/01/98UrineAz, Cp, Cz, Nt, Pi, Tc, ToJ4176ICU-410/01/98BronchialAz, Cp, Cz, Pi, Tc, ToJ4177ICU-410/01/98BronchialAz, Cz, Gm, Pi, TcJ4387ICU-710/04/98PusAz, Cp, Cz, Pi, Tc, ToJ4219ICU-519/02/98BronchialPiK4043ICU-807/01/98BronchialAz, Cp, Cz, Gm, Nt, Pi, Tc, ToK4390ICU-326/01/98BloodAk, Az, Cz, Pi, TcL4397ICU-329/03/98PusAk, As, Az, Cp, Gm, Nt, Pi, TcMa Abbreviations: Ak, amikacin; As, ampicillin–sulbactam; Az, aztreonam; Cp, ciprofloxacin; Cz, ceftazidime; Gm, gentamicin; Im, imipenem; Nt, netilmicin; Pi, piperacillin; Tc, ticarcillin–clavulanate; To, tobramycin. Open table in a new tab A. baumannii is an important cause of hospital-acquired infections, particularly among immunocompromised patients, in whom such infections are associated with high rates of mortality. In our region, Acinetobacter species are among the most frequent pathogens, and the majority of them are multiresistant [9Douboyas J Tzouvelekis LS Tsakris A In-vitro activity of ampicillin/sulbactam against multiresistant Acinetobacter calcoaceticus var. anitratus clinical isolates.J Antimicrob Chemother. 1994; 34: 298-300Crossref PubMed Scopus (11) Google Scholar]. Several recent studies reported increasing frequencies of A. baumannii strains exhibiting multiresistance [4Bou G Cervero G Angeles Dominguez M Quereda C Martinez-Beltran J Characterization of a nosocomial outbreak caused by a multiresistant Acinetobacter baumannii: high-level carbapenem resistance in A. baumannii is not due solely to the presence of β-lactamases.J Clin Microbiol. 2000; 38: 3299-3305PubMed Google Scholar,2Bergogne-Berezin E Towner KJ Acinetobacter spp. as nosocomial pathogens: microbiological, clinical and epidemiological features.Clin Microbiol Rev. 1996; 9: 148-165PubMed Google Scholar,13Vila J Ruiz J Navia M et al.Spread of amikacin resistance in Acinetobacter baumannii strains due to an epidemic strain.J Clin Microbiol. 1999; 37: 758-761PubMed Google Scholar], a characteristic that is considered to be a risk factor for epidemic behavior [14Koeleman JG van der Bijl MW Stoof J Vanden-broucke-Grauls CM Savelkoul PH Antibiotic resistance is a major risk factor for epidemic behavior of Acinetobacter baumannii.Infect Control Hosp Epidemiol. 2001; 22: 284-288Crossref PubMed Scopus (40) Google Scholar]. In our study, 92.6% of the isolates were resistant to ciprofloxacin, and similar rates of resistance have been observed in other European countries [. 15Seifert H Baginski R Schulze A Pulverer G Antimicrobial susceptibility of Acinetobacter species.Antimicrob Agents Chemother. 1993; 37: 750-753Crossref PubMed Scopus (153) Google Scholar,16Cisneros JM Reyes MJ Pachon J et al.Bacteremia due to Acinetobacter baumannii: epidemiology, clinical findings, and prognostic features.Clin Infect Dis. 1996; 22: 1026-1032Crossref PubMed Scopus (291) Google Scholar]. However, studies from other regions have reported much lower proportions of resistant isolates [17Chang SC Chen YC Luh KT Hsieh WC In vitro activities of antimicrobial agents, alone or in combination, against Acinetobacter baumannii isolated from blood.Diagn Microbiol Infect Dis. 1995; 23: 105-110Abstract Full Text PDF PubMed Scopus (46) Google Scholar,18Wisplinghoff H Edmond MB Pfaller MA Jones RN Wenzel RP Seifert H Nosocomial bloodstream infections caused by Acinetobacter species in United States hospitals: clinical features, molecular epidemiology and antimicrobial susceptibility.Clin Infect Dis. 2000; 31: 690-697Crossref PubMed Scopus (183) Google Scholar]. Resistance to aminoglycosides was common, with 87.6% and 56.2% of isolates being resistant to gentamicin and netilmicin, respectively, while amikacin retained activity against 70.2% of isolates. We also detected high rates of resistance to β-lactam antibiotics, such as aztreonam and ceftazidime. The majority of isolates exhibited resistance to at least four different classes of antibiotics. The most common phenotypes comprised resistance to nine and eight of the 11 potentially active antibiotics tested, respectively. Imipenem-resistant acinetobacters have not been isolated in our study, or in others done in our country [9Douboyas J Tzouvelekis LS Tsakris A In-vitro activity of ampicillin/sulbactam against multiresistant Acinetobacter calcoaceticus var. anitratus clinical isolates.J Antimicrob Chemother. 1994; 34: 298-300Crossref PubMed Scopus (11) Google Scholar,2Bergogne-Berezin E Towner KJ Acinetobacter spp. as nosocomial pathogens: microbiological, clinical and epidemiological features.Clin Microbiol Rev. 1996; 9: 148-165PubMed Google Scholar]. However, after the study period, a few imipenem-resistant acinetobacters have emerged in a large Greek hospital that participated in the study (H. Malamou-Lada, personal communication). The emergence of imipenem resistance is alarming, as these strains may spread rapidly in the hospital environment [19Corbella X Montero A Pujol M et al.Emergence and rapid spread of carbapenem resistance during a large and sustained hospital outbreak of multiresistant Acinetobacter baumannii.J Clin Microbiol. 2000; 38: 4086-4095PubMed Google Scholar]. It should be noted that imipenem-resistant isolates from other regions usually exhibit resistance to all clinically available antibiotics [20Brown S Bantar C Young HK Amyes SG Limitation of Acinetobacter baumannii treatment by plasmid-mediated carbapenemase ARI-2.Lancet. 1998; 351: 186-187Abstract Full Text Full Text PDF PubMed Scopus (50) Google Scholar]. In this report, the diversity of the multiresistant A. baumannii isolates from ICUs of Greek hospitals was also studied. Although an outbreak due to a resistant A. baumannii strain may be initially recognized on the basis of the antibiotic resistance profiles, discrimination between strains with similar multiresistance phenotypes may be difficult. Therefore, genotypic methods, such as plasmid typing, ribotyping, PCR fingerprinting, and macrorestriction analysis, have been applied to the study of nosocomial outbreaks due to A. baumannii [6Seifert H Schulze A Baginski R Pulverer G Comparison of four different methods for epidemiologic typing of Acinetobacter baumannii.J Clin Microbiol. 1994; 32: 1816-1819PubMed Google Scholar]. Of these methods, PFGE has been shown to allow precise strain identification, and has been used to investigate nosocomial A. baumannii outbreaks [5Struelens MJ Carlier E Maes N Serruys E Quint WGV van Belkum A Nosocomial colonization and infection with multi-resistant Acinetobacter baumannii: outbreak delineation using DNA macrorestriction and PCR-fingerprinting.J Hosp Infect. 1993; 25: 15-32Abstract Full Text PDF PubMed Scopus (127) Google Scholar,2Bergogne-Berezin E Towner KJ Acinetobacter spp. as nosocomial pathogens: microbiological, clinical and epidemiological features.Clin Microbiol Rev. 1996; 9: 148-165PubMed Google Scholar]. The genomic macrorestriction results showed that two prevalent clonal groups of A. baumannii accounted for 68% of the isolations, exhibiting very similar fingerprinting profiles, indicating that a common clonal origin of the isolates is a possible explanation. Isolates exhibiting the most common macrorestriction profile were recovered in eight of the nine ICUs that participated in the study, while the second most common profile was detected in seven of the ICUs, suggesting inter-hospital dissemination of multiresistant A. baumannii strains. Several studies have also supported the inter-hospital spread of clonal A. baumannii strains [13Vila J Ruiz J Navia M et al.Spread of amikacin resistance in Acinetobacter baumannii strains due to an epidemic strain.J Clin Microbiol. 1999; 37: 758-761PubMed Google Scholar,21Nemec A Janda L Melter O Dijckshoorn L Genotypic and phenotypic similarity of multiresistant Acinetobacter baumannii isolates in the Czech Republic.J Med Microbiol. 1999; 48: 287-296Crossref PubMed Scopus (50) Google Scholar]. It seems that, in our ICUs, early recognition, epidemiologic surveillance and the possible implementation of appropriate infection control measures may prevent their intra- and inter-hospital dissemination. A. Avlami (Laikon), A. Katrahoura (Metaxa), S. Kitsou (A. Olga), C. Koutsia (Voula), C. Oikono-mopoulou (Tzanneio), O. Paniara (Evangelismos), H. Malamou-Lada (GHA), E. Papoutsaki (KAT), A. Stylianea (GHN).