Baumannii Complex Isolates Research Articles

Treatment outcomes of patients with non-bacteremic pneumonia caused by extensively drug-resistant Acinetobacter calcoaceticus-Acinetobacter baumannii complex isolates

Few therapeutic options exist for various infections caused by extensively drug-resistant Acinetobacter calcoaceticus-Acinetobacter baumannii (XDR-Acb) complex isolates, including pneumonia. This study investigated the clinical efficacy between aerosolized colistimethate sodium (AS-CMS, 2 million units thrice a day) treatment alone or in combination with standard-dose tigecycline (TGC) in patients with non-bacteremic pneumonia due to XDR-Acb, and explored the factors influencing patients’ 30-day mortality.A 1:1 case (n = 106; receiving TGC plus AS-CMS) control (receiving AS-CMS alone with matching scores) observational study was conducted among adult patients with non-bacteremic XDR-Acb complex pneumonia in a Taiwanese medical center from January 2014 through December 2016. The clinically relevant data were retrospectively recorded. The primary endpoint was 30-day case fatality. Secondary endpoints investigated that if the co-morbidities, XDR-A. baumannii as a pneumonic pathogen, therapy-related factors, or airway colonization with colistin-resistant Acb negatively influenced the 14-day clinical condition of enrolled patients.A higher 30-day mortality rate was noted among the group receiving combination therapy (34.0% vs 22.6%; P = .17). The ≥7-day AS-CMS therapy successfully eradicated > 90% of airway XDR-Acb isolates. Nevertheless, follow-up sputum specimens from 10 (6.4% [10/156]) patients were colonized with colistin-resistant Acb isolates. After the conditional factors were adjusted by multivariate logistic analysis, the only factor independently predicting the 30-day case-fatality was the failure of treating XDR-Acb pneumonia at 14 days (adjusted odds ratio [aOR] = 38.2; 95% confidence interval [CI] = 9.96–142.29; P < .001). Cox proportional regression analysis found that chronic obstructive pulmonary disease (COPD) (adjusted hazard ratio [aHR] = 2.08; 95% CI = 1.05–4.10; P = .035), chronic renal failure (aHR = 3.00; 95% CI = 1.52–5.90; P = .002), non-invasive ventilation use (aHR = 2.68; 95% CI = 1.37–5.25; P = .004), and lack of TGC therapy (aHR = 0.52; 95% CI = 0.27–1.00; P = .049) adversely influenced the 14-day clinical outcomes. Conversely, the emergence of colistin-resistant Acb isolates in the follow-up sputum samples was not statistically significantly associated with curing or improving XDR-Acb pneumonia.In conclusion, aggressive pulmonary hygiene care, the addition of TGC, and corticosteroid dose tapering were beneficial in improving the 14-day patients’ outcomes.

Seasonal and Temperature-Associated Increase in Community-Onset Acinetobacter baumannii Complex Colonization or Infection.

Identifying the trends in community-onset Acinetobacter baumannii complex isolation and diversity according to temperature could help provide insight into the behavior of the A. baumannii complex. We performed a retrospective analysis of A. baumannii complex (Acinetobacter baumannii, Acinetobacter nosocomialis, Acinetobacter pittii, and Acinetobacter calcoaceticus) isolates obtained from patients at a Korean community hospital from 2006 to 2015 with reference to seasonal temperatures. The incidence rates were compared between warm (June–September) and cold (November–March) months, defined as an average mean temperature ≥20℃ and ≤5℃, respectively. Incidence rate was calculated as the number of cases per month, converted to cases/105 admissions for healthcare-acquired isolates and cases/103 outpatients for community-onset isolates. Approximately 3,500 A. baumannii complex cases were identified, and 26.2% of them were community-onset cases. The median (interquartile range) number of community-onset A. baumannii complex cases was significantly higher (P=0.0002) in warm months at 13.8 (9.5–17.6) than in cold months at 10.1 (6.3–13.2). There was a strong correlation between community-onset A. baumannii complex cases and temperature (Pearson's r=0.6805, P=0.0149). Thus, we identified a seasonality pattern for community-onset A. baumannii complex colonization or infection, but not for healthcare-acquired cases.

MOLECULAR CHARACTERIZATION OF GENES ENCODING ACQUIRED CARBAPENEMASE OF CARBAPENEMRESISTANT ACINETOBACTER BAUMANNII ISOLATES

Background: Today carbapenem-resistant A. baumannii isolates are rising in several parts of the world including Vietnam, they are recognized to be among the most difficult resistant bacteria to treat and control. Carbapenem resistance is most commonly caused by the production of OXA-type carbapenemases and metallo-β-lactamases (MBLs). Objectives: Determine the rate and detect the genes encoding acquired carbapenemase of carbapenem-resistant A. baumannii isolates. Materials and methods: Study design is cross-sectional descriptive study. Carbapenem-resistant A. baumannii isolates in 90 A. baumannii (ACB) complex isolates were collected from Hue Central Hospital (HCH) and Hue University Hospital (HUP). Susceptibility to carbapenem of A. baumannii strains were performed by MicroScan method. Multiplex PCRs were performed to detect the genes encoding acquired carbapenemase. Results: Carbapenem resistance rates in A. baumannii were 88.5% and 87.5% in HCH and HHUMP, respectively. All of genes blaOXA-51, blaOXA-23, blaOXA-58, blaIMP, blaNDM as well as coexistence of two genes (blaIMP, blaNDM) or three genes ((blaOXA-51, blaOXA-23, blaOXA-58) or (blaIMP, blaNDM, blaOXA-58)) were detected in carbapenem resistant A. baumannii isolates. Conclusions: Carbapenem resistance rate in A. baumannii was relatively high. The emergence of carbapenem resistance in A. baumannii is associated with the production of OXA-type carbapenemases and metallo-β-lactamases (MBLs). Key words: Acinetobacter baumannii; carbapenem resistance; carbapenemase

Effects of biocide exposure on P. Aeruginosa, E. coli and A. Baumannii complex isolates from hospital and household environments

Background: Bacterial responses to biocide exposure and its effects on survival and persistence remain to be studied in greater detail.Aim: To analyse the viability and survival of environmental isolates from household and hospital settings after biocide exposure.Methods: The minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) of chlorhexidine (CHxG), benzalkonium chloride (BAC) and triclosan (TC) were determined in isolates of Pseudomonas aeruginosa, Acinetobacter baumannii complex and Escherichia coli collected from hospital and households environments. Viability was monitored after exposure and removal of biocides using agar cultures and flow cytometry.Findings: P. aeruginosa isolates showed greater tolerance for all biocides tested whereas A. baumannii complex and E. coli were less tolerant.When compared with reference strains, biocide tolerance was up to 8 to 13-fold higher for TC and BAC respectively. Flow cytometry showed that biocide exposure may induce viable but non-growing states in P. aeruginosa and E. coli isolates before becoming fully replicative. Changes in the susceptibility profile in one isolate of A. baumannii complex were observed after biocide exposure.Discussion: Bacteria isolates from hospital and households were able to recover after biocide exposure at bactericidal concentrations favouring persistence and spread of biocide-tolerant strains. This study reinforces that cleaning compliance should be monitored by non-culture based tests. Novel formulations in cleaning and disinfection protocols should be revisited in hospitals harbouring P. aeruginosa and A. baumannii multidrug resistant isolates.

Distinct Genetic Diversity of Carbapenem-Resistant Acinetobacter baumannii from Colombian Hospitals.

The global success of multidrug-resistant Acinetobacter baumannii has been associated with the dissemination of a high-risk clone designated clonal complex (CC) 92B (Bartual scheme)/CC2P (Pasteur scheme), which is the most frequent genetic lineage in European, Asian, and North American carbapenem-resistant Acinetobacter isolates. In these isolates, carbapenem resistance is mainly mediated by β-lactamases encoded by blaOXA-23-like, blaOXA-24-like, blaOXA-51-like, and/or blaOXA-58-like genes. In this study, we characterized the population genetics of 121 carbapenem-resistant A. baumannii complex isolates recovered from 14 hospitals in seven cities in Colombia (2008-2010). Multiplex PCR was used to detect blaOXA-23-like, blaOXA-24-like, blaOXA-51-like, and blaOXA-58-like genes. Molecular typing was performed using pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST). PCR showed that 118 (97.5%) of the isolates were positive for both blaOXA-23-like and blaOXA-51-like genes, and three other isolates were only positive for blaOXA-51-like. PFGE identified 18 different pulsotypes, while MLST identified 11 different sequence types (STs), seven of which had not been previously described in Acinetobacter. None of the STs found in this study was associated with CC92B/CC2P. The most widespread STs in our isolates belonged to ST636 and their single-locus variants ST121/ST124/ST634 (CC636B) followed by STs belonging to CC110B. Our observations suggest a wide distribution of diverse A. baumannii complex clones containing blaOXA-23-like in Colombian hospitals (especially CC636B and CC110B) that differ from the high-risk clones commonly found in other regions of the world, indicating a distinct molecular epidemiology of carbapenem-resistant Acinetobacter spp. in Colombia.

Molecular Epidemiology of Carbapenem-Resistant Acinetobacter Baumannii Complex Isolates from Patients that were Injured During the Eastern Ukrainian Conflict.

This study addressed carbapenem-resistant Acinetobacter baumannii complex (ABC) isolates from patients that were injured during the military conflict in the Eastern Ukraine and treated at German Armed Forces Hospitals in 2014 and 2015. Clonal diversity of the strains and potential ways of transmission were analyzed.Patients with one or several isolation events of carbapenem-resistant ABC were included. Isolates were characterized by VITEK II-based identification and resistance testing, molecular screening for frequent carbapenemase genes, and DiversiLab rep-PCR-based typing. Available clinical information of the patients was assessed.From 21 young male Ukrainian patients with battle injuries, 32 carbapenem- and fluoroquinolone-resistant ABC strains were isolated. Four major clonal clusters were detected. From four patients (19%), ABC isolates from more than one clonal cluster were isolated. The composition of the clusters suggested transmission events prior to the admission to the German hospitals.The infection and colonization pressure in the conflict regions of the Eastern Ukraine with ABC of low clonal diversity is considerable. Respective infection risks have to be considered in case of battle-related injuries in these regions. The low number of local clones makes any molecular exclusion of transmission events difficult.

In Vivo and In Vitro Efficacy of Minocycline-Based Combination Therapy for Minocycline-Resistant Acinetobacter baumannii

Minocycline-based combination therapy has been suggested to be a possible choice for the treatment of infections caused by minocycline-susceptible Acinetobacter baumannii, but its use for the treatment of infections caused by minocycline-resistant A. baumannii is not well established. In this study, we compared the efficacy of minocycline-based combination therapy (with colistin, cefoperazone-sulbactam, or meropenem) to that of colistin in combination with meropenem for the treatment of minocycline-resistant A. baumannii infection. From 2006 to 2010, 191 (17.6%) of 1,083 A. baumannii complex isolates not susceptible to minocycline from the Taiwan Surveillance of Antimicrobial Resistance program were collected. Four representative A. baumannii isolates resistant to minocycline, amikacin, ampicillin-sulbactam, ceftazidime, ciprofloxacin, cefepime, gentamicin, imipenem, levofloxacin, meropenem, and piperacillin-tazobactam were selected on the basis of the diversity of their pulsotypes, collection years, health care setting origins, and geographic areas of origination. All four isolates had tetB and overexpressed adeABC, as revealed by quantitative reverse transcription-PCR. Among all minocycline-based regimens, only the combination with colistin produced a fractional inhibitory concentration index comparable to that achieved with meropenem combined with colistin. Minocycline (4 or 16 μg/ml) in combination with colistin (0.5 μg/ml) also synergistically killed minocycline-resistant isolates in time-kill studies. Minocycline (50 mg/kg of body weight) in combination with colistin (10 mg/kg) significantly improved the survival of mice and reduced the number of bacteria present in the lungs of mice compared to the results of monotherapy. However, minocycline (16 μg/ml)-based therapy was not effective at reducing biofilm-associated bacteria at 24 or 48 h when its effectiveness was compared to that of colistin (0.5 μg/ml) and meropenem (8 μg/ml). The clinical use of minocycline in combination with colistin for the treatment of minocycline-resistant A. baumannii may warrant further investigation.

Comparison of the Virulence-Associated Phenotypes of Five Species of Acinetobacter baumannii Complex

In this study, we compared the virulence-associated factors of Acinetobacter baumannii complex species. Sixty-three isolates of five A. baumannii complex species, including 19 A. baumannii, 15 A. nosocomialis, 13 A. seifertii, 13 A. pittii, and 3 A. calcoaceticus isolates, were included in this study. For all isolates, biofilm formation, A549 cell adherence, resistance to normal human serum, and motility were evaluated. A. baumannii complex isolates showed diversity in biofilm formation, A549 cell adherence, and serum resistance, and no strong positive relationships among these virulence characteristics. However, A. seifertii showed relatively consistent virulence-associated phenotypes. In addition, A. baumannii clone ST110 exhibited consistently high virulence-associated phenotypes. Motility was observed in seven isolates, and all four A. baumannii ST110 isolates showed twitching motility. Although some inconsistencies in virulence-associated phenotypes were seen, high virulence characteristics were observed in A. seifertii, which has been mainly reported in Korea and shows high rates of colistin resistance.

A distinct alleles and genetic recombination of pmrCAB operon in species of Acinetobacter baumannii complex isolates

To investigate pmrCAB sequence divergence in 5 species of Acinetobacter baumannii complex, a total of 80 isolates from a Korean hospital were explored. We evaluated nucleotide and amino acid polymorphisms of pmrCAB operon, and phylogenetic trees were constructed for each gene of prmCAB operon. Colistin and polymyxin B susceptibility was determined for all isolates, and multilocus sequence typing was also performed for A. baumannii isolates. Our results showed that each species of A. baumannii complex has divergent pmrCAB operon sequences. We identified a distinct pmrCAB allele allied with Acinetobacter nosocomialis in gene trees. Different grouping in each gene tree suggests sporadic recombination or emergence of pmrCAB genes among Acinetobacter species. Sequence polymorphisms among Acinetobacter species might not be associated with colistin resistance. We revealed that a distinct pmrCAB allele may be widespread across the continents such as North America and Asia and that sporadic genetic recombination or emergence of pmrCAB genes might occur.

Substitutions of Ser83Leu in GyrA and Ser80Leu in ParC Associated with Quinolone Resistance in Acinetobacter pittii.

To investigate the prevalence and the mechanism of quinolone-resistant Acinetobacter pittii, 634 Acinetobacter calcoaceticus-Acinetobacter baumannii complex isolates were collected throughout Zhejiang Province. Identification of isolates was conducted by matrix-assisted laser desorption ionization/time of flight mass spectrometry (MALDI-TOF MS), blaOXA-51-like gene, and partial RNA polymerase β-subunit (rpoB) amplification. Twenty-seven isolates of A. pittii were identified. Among the 634 isolates, A. baumannii, A. pittii, Acinetobacter nosocomialis, and A. calcoaceticus counted for 87.22%, 4.26%, 8.20%, and 0.32%, respectively. Antimicrobial susceptibility of nalidixic acid, ofloxacin, enoxacin, ciprofloxacin, lomefloxacin, levofloxacin, sparfloxacin, moxifloxacin, and gatifloxacin for 27 A. pittii were determined by the agar dilution method. Detection of quinolone-resistant determining regions of gyrA, gyrB, parC, and parE was performed for the A. pittii isolates. In addition, plasmid-mediated quinolone resistance (PMQR) determinants (qnrA, qnrB, qnrS, qnrC, qnrD, aac(6')-Ib-cr, qepA, oqxA, and oqxB) were investigated. All the 27 isolates demonstrated a higher minimum inhibitory concentration (MIC) to old quinolones than the new fluoroquinolones. No mutation in gyrA, gyrB, parC, or parE was detected in 20 ciprofloxacin-susceptible isolates. Seven ciprofloxacin-resistant A. pittii were identified with a Ser83Leu mutation in GyrA. Among them, six isolates with simultaneous Ser83Leu amino acid substitution in GyrA and Ser80Leu in ParC displayed higher MIC values against ciprofloxacin. Additionally, three were identified with a Met370Ile substitution in ParE, and two were detected with a Tyr317His mutation in ParE, which were reported for the first time. No PMQR determinants were identified in the 27 A. pittii isolates. In conclusion, mutations in chromosome play a major role in quinolone resistance in A. pittii, while resistance mechanisms mediated by plasmid have not been found. Ser83Leu substitution in GyrA and Ser80Leu substitution in ParC are associated with quinolone resistance in A. pittii. Whether Met370Ile and Tyr317His substitutions in ParE play a minor role requires further investigation.

Antibiotic susceptibility and molecular epidemiology of Acinetobacter calcoaceticus-baumannii complex strains isolated from a referral hospital in northern Vietnam.

Acinetobacter calcoaceticus–baumannii complex is a common cause of hospital-acquired infections (HAIs) globally, remarkable for its high rate of antibiotic resistance, including to carbapenems. There are few data on the resistance of A. baumannii in Vietnam, which are essential for developing evidence-based treatment guidelines for HAIs. Antibiotic susceptibility testing was conducted by VITEK®2, and pulsed-field gel electrophoresis (PFGE) was performed on 66 clinical A. baumannii complex isolates recovered during 2009 at the National Hospital of Tropical Diseases (NHTD), a referral hospital in Hanoi, Vietnam. Basic demographic and clinical data were collected and analysed using descriptive statistics. Most isolates came from lower respiratory tract specimens (59; 89.4%) from intensive care unit (ICU) patients [64/65 (98.5%) with available data] who had been admitted to NHTD for ≥2 days [42/46 (91.3%) with available data]. More than 90% of the isolates were resistant to the tested β-lactamase/β-lactamase inhibitors, cephalosporins, carbapenems, fluoroquinolones and trimethoprim/sulfamethoxazole. Moreover, 25.4% (16/63) were resistant to all tested β-lactams, quinolones and aminoglycosides. All isolates remained sensitive to colistin and 58.7% were susceptible to tigecycline. Of the 66 isolates, 49 could be classified into eight PFGE types (A–H). Every PFGE type, except D, had cluster(s) of three or more isolates with a temporal relationship. In conclusion, these data suggest a significant rise in A. baumannii antibiotic resistance in Vietnam. Clustering within PFGE types supports cross-transmission of A. baumannii within the ICU at NHTD. Increased research and resources in optimising treatment, infection control and antibiotic stewardship are needed.

Clinical outcomes of hospital-acquired infection with Acinetobacter nosocomialis and Acinetobacter pittii.

The role of Acinetobacter nosocomialis and Acinetobacter pittii, which belong to the A. calcoaceticus-A. baumannii complex, in hospital-acquired infections is increasingly recognized. Here we describe a retrospective cohort study of hospital-acquired A. calcoaceticus-A. baumannii complex infections at a university hospital in Thailand. A total of 222 unique cases were identified between January 2010 and December 2011. The genomospecies of the A. calcoaceticus-A. baumannii complex isolates were classified as follows: A. baumannii, 197 (89%); A. nosocomialis, 18 (8%); and A. pittii, 7 (3%). All A. nosocomialis and A. pittii isolates were susceptible to imipenem and meropenem. The patients infected with A. nosocomialis and A. pittii had lower 30-day mortality than those infected with carbapenem-susceptible A. baumannii (P = 0.025) and carbapenem-resistant A. baumannii (P = 0.013). The factors influencing 30-day mortality were infection with non-baumannii A. calcoaceticus-A. baumannii complex (hazard ratio [HR], 0.12; 95% confidence interval [CI], 0.03 to 0.51; P = 0.004), infection with carbapenem-resistant A. baumannii (HR, 1.57; 95% CI, 0.89 to 2.79; P = 0.105), appropriate empirical antimicrobial therapy (HR, 0.38; 95% CI, 0.23 to 0.61; P < 0.001), and higher acute physiology and chronic health evaluation II (APACHE II) score (HR, 1.15; 95% CI, 1.10 to 1.19; P < 0.001). In Galleria mellonella assays, the survival rates were significantly higher for the larvae infected with A. nosocomialis or A. pittii than for those infected with either carbapenem-susceptible A. baumannii or carbapenem-resistant A. baumannii, but no differences in survival rates were observed between carbapenem-susceptible A. baumannii and carbapenem-resistant A. baumannii. These findings suggest intrinsic differences in virulence between non-baumannii A. calcoaceticus-A. baumannii complex species and A. baumannii but not between carbapenem-susceptible and resistant A. baumannii.

Emergence of NDM-producing non-baumannii Acinetobacter spp. isolated from China

One hundred and thirty-six bla OXA-51-negative strains were identified from 1,067 Acinetobacter calcoaceticus-A. baumannii complex (ACB complex) isolates, which were collected during October 2010 to March 2013 from 15 general hospitals in 10 cities throughout Zhejiang Province, China. Seven of the 136 bla OXA-51-negative ACB complex isolates were New Delhi metallo-β-lactamase-1 (NDM-1)-positive, among which three were identified as A. nosocomialis and four were identified as A. pittii strains using 16S-23S rRNA gene intergenic spacer (ITS) sequencing and partial RNA polymerase β-subunit (rpoB) sequencing. Pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST) analysis showed that the seven NDM-positive isolates belonged to three clonal strains with three novel sequence types (STs). Polymerase chain reaction (PCR) assays and DNA sequence analysis of the carbapenemase and other β-lactamase genes indicated that all the isolates harbored the bla NDM-1 gene, and that only one strain of A. nosocomialis isolates harbored both bla NDM-1 and bla OXA-23. All of them were positive for bla ADC, from which three novel bla ADC genes (designated as bla ADC-69, bla ADC-70, and bla ADC-71) were detected for the first time. The presence of ISAba125 upstream of bla NDM-1 was identified through genetic environment analysis. Carbapenem resistance can be transferred from A. nosocomialis and A. pittii to Escherichia coli EC600 by the conjugation experiment. Plasmid analysis, DNA hybridization, and extraction experiments indicated that bla NDM-1 was located on a plasmid of approximately 50 kb. In conclusion, we characterized the dissemination of NDM-1-positive A. pittii strains in Zhejiang Province, China, and reported the NDM-producing A. nosocomialis for the first time.

Prevalence of blaPER-1 and Integrons in Ceftazidime-Resistant Gram-Negative Bacteria at a University Hospital in Turkey

In this study, we examined the prevalence of the PER-1 enzyme and the presence of clinically important integron classes in ceftazidime-resistant Gram-negative bacteria isolated at a university hospital. The blaPER-1 gene was detected by PCR in 33 (19.5%) of the total 169 Gram-negative bacteria, including 17 (23.3%) of the 73 Pseudomonas aeruginosa isolates and 16 (25%) of the 64 Acinetobacter baumannii complex isolates. Molecular fingerprinting revealed that blaPER-1 prevalence was mostly due to the dissemination of clonally related P. aeruginosa and A. baumannii complex strains. Class 1 integron (intI1) was detected in 52.7% of the 169 bacteria examined in this study. Its detection rates were estimated at 49.3% and 57.8% of the P. aeruginosa and A. baumannii complex strains isolated, respectively. It was also detected in 11 of the 16 Escherichia coli isolates and 5 of the 10 Klebsiella pneumoniae isolates. A single E. coli isolate and another K. pneumoniae isolate contained both class 1 and class 2 integrase genes. The results of this study revealed that clonally related blaPER-1-positive P. aeruginosa and A. baumannii complex strains, mostly harboring intI1, had disseminated at our hospital.

Lack of Seasonality in the Occurrence of Multidrug-Resistant Acinectobacter baumannii Complex

Lack of Seasonality in the Occurrence of Multidrug-Resistant <i>Acinectobacter baumannii</i> Complex

Diversity of Acinetobacter baumannii in Four French Military Hospitals, as Assessed by Multiple Locus Variable Number of Tandem Repeats Analysis

BackgroundInfections by A. calcoaceticus-A. baumannii (ACB) complex isolates represent a serious threat for wounded and burn patients. Three international multidrug-resistant (MDR) clones (EU clone I-III) are responsible for a large proportion of nosocomial infections with A. baumannii but other emerging strains with high epidemic potential also occur.Methodology/Principal FindingsWe automatized a Multiple locus variable number of tandem repeats (VNTR) analysis (MLVA) protocol and used it to investigate the genetic diversity of 136 ACB isolates from four military hospitals and one childrens hospital. Acinetobacter sp other than baumannii isolates represented 22.6% (31/137) with a majority being A. pittii. The genotyping protocol designed for A.baumannii was also efficient to cluster A. pittii isolates. Fifty-five percent of A. baumannii isolates belonged to the two international clones I and II, and we identified new clones which members were found in the different hospitals. Analysis of two CRISPR-cas systems helped define two clonal complexes and provided phylogenetic information to help trace back their emergence.Conclusions/SignificanceThe increasing occurrence of A. baumannii infections in the hospital calls for measures to rapidly characterize the isolates and identify emerging clones. The automatized MLVA protocol can be the instrument for such surveys. In addition, the investigation of CRISPR/cas systems may give important keys to understand the evolution of some highly successful clonal complexes.

Changes in antimicrobial susceptibility and major clones of Acinetobacter calcoaceticus–baumannii complex isolates from a single hospital in Korea over 7 years

Acinetobacter species have emerged as opportunistic nosocomial pathogens in intensive care units. Epidemic spread and outbreaks of multidrug-resistant or carbapenem-resistant Acinetobacter baumannii infections have been described worldwide. Species distribution, antimicrobial resistance and genotypes were investigated for Acinetobacter species isolates collected from a single institution in Korea over 7 years. Two hundred and eighty-seven Acinetobacter species isolates were collected from patients with bloodstream infections in one Korean hospital from 2003 to 2010. Most of them belonged to the Acinetobacter calcoaceticus-baumannii complex (94.4 %). The most frequently isolated species was A. baumannii (44.2 %), followed by Acinetobacter nosocomialis (formerly Acinetobacter genomic species 13TU) (34.1 %). The proportion of A. baumannii increased significantly from 2008 to 2010 (40.4 to 50.0 %). From 2008, imipenem and meropenem resistance rates increased significantly compared with 2003-2007 (12.9 % and 20.5 %, respectively, to 41.4 % and 41.5 %, respectively). An increased carbapenem resistance rate between the two periods was identified more clearly amongst A. baumannii isolates. Polymyxin-resistant A. baumannii isolates emerged in 2008-2010, despite the availability of few isolates. The increase of carbapenem resistance in A. baumannii might be due to the substitution of main clones. Although ST92 and ST69 were the most prevalent clones amongst A. baumannii in 2003-2007 (47.8 % and 15.9 %, respectively), ST75 and ST138 had increased in 2008-2010 (39.7 % and 25.9 %, respectively). Although ST92 showed moderate resistance to carbapenems, most ST75 and ST138 isolates were resistant to carbapenems. All ST75 and ST138 isolates, but only one ST92 isolate, contained the bla(OXA-23-like) gene. Increased carbapenem resistance in Acinetobacter species and A. baumannii isolates might be due to the expansion of specific carbapenem-resistant clones.

臨床分離 &lt;i&gt;Acinetobacter baumannii &lt;/i&gt;complex の各種抗菌薬に対する感受性および多剤耐性 &lt;i&gt;Acinetobacter&lt;/i&gt;（MDRA）の性状

The antimicrobial susceptibility of 93 Acinetobacter baumannii complex isolates from clinical specimens collected nationwide between May and October 2009 were measured by microdilution antimicrobial susceptibility testing based on CLSI M100-S20. Beta-lactamase genes, including classes B and D and ISAbal in meropenem nonsusceptible, including intermediate or resistant isolates, were detected using PCR. Rates of isolates nonsusceptible to meropenem were 18%, to ciprofloxacin 41% and to amikacin 14%. L7-L8: The rate of multidrug-resistant Acinetobacter (MDRA) isolates which were resistant to all 3 antimicrobial agents was 4.3%. MDRA isolates were classified into ST92 by multilocus sequence typing. No metallo-beta-lactamase producer was seen among the 17 meropenem nonsusceptible isolates. The blaoxa-51-like carbapenemase gene and ISAbal were detected in all 17 isolates. ISAba1 upstream presence of the blaOXA-51-like gene was observed in 7 of 17 isolates and the blaOXA-23 like gene in 5 of 17. Consistent with overseas reports, our results confirm the existence of MDRA isolates and isolates harboring OXA carbapenemase genes in Japan. While resistance rates were lower than reports elsewhere, it is clear that resistance trends must be carefully monitored.

Increasing imipenem resistance and dissemination of the ISAba1-associated bla OXA-23 gene among Acinetobacter baumannii isolates in an intensive care unit

The antibiotic susceptibility of Acinetobacter calcoaceticus-Acinetobacter baumannii complex strains recovered from the intensive care unit (ICU) of West China Hospital, Sichuan, PR China, from 2006 to 2009 was investigated. The identification of A. baumannii and analysis of carbapenemase-encoding genes and their relationship with ISAba1 were performed by PCR. Furthermore, a DiversiLab repetitive extragenic palindromic sequence-based PCR (rep-PCR) microbial typing system and a multilocus sequence typing (MLST) scheme were applied to assess the genetic relationship of the isolates. The results showed that the antibiotic susceptibility of the A. calcoaceticus-A. baumannii complex isolates changed and imipenem resistance increased rapidly between 2006 and 2009. The blaOXA-51-like and ISAba1-associated blaOXA-23 genes were prevalent in the imipenem-resistant A. baumannii isolates. However, the blaOXA-58-like gene was found in only one isolate and no metallo-β-lactamase genes were detected. The representative multidrug-resistant A. baumannii isolates were identified as one cluster by rep-PCR fingerprinting and belonged to the clonal complex 92 (CC92) according to MLST. These findings indicate a situation of increasing resistance and wide distribution of class D β-lactamase genes, especially the acquired ISAba1-associated blaOXA-23 gene, in A. baumannii isolates in the ICU of West China Hospital, probably caused by expansion of the CC92 clone.