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PubMed1989

Glucose dehydrogenase activity in Acinetobacter species.

A study of D-glucose oxidation by Acinetobacter species was carried out. Glucose-oxidizing strains were found distributed among almost all Acinetobacter species. 14C-glucose oxidation kinetics by non-proliferating cells with separation of oxidation products (14C-gluconate) by DEAE-cellulose paper chromatography was studied. Inhibition of glucose dehydrogenase (GDH) activity by 11 carbohydrates (mono- and disaccharides) and determination of the kinetic parameters showed that glucose oxidation was due to the action of membrane-bound GDH (inactive in vivo on disaccharides). On the basis of GDH inhibition patterns obtained, two groups were individualized. The first group of strains (identified as A. calcoaceticus, A. baumannii, A. lwoffii, A. johnsonii and Acinetobacter species 3, 9, 10 and 11) showed a greater affinity for glucose than the second group (A. haemolyticus, A. junii and Acinetobacter species 6 and 12). Restoration of GDH activity after addition of pyrroloquinoline quinone (PQQ) was studied in 187 strains previously found unable to oxidize glucose. GDH activity of 150 out of 166 strains identified as A. baumannii, A. johnsonii, A. lwoffii and Acinetobacter species 11 and 12 was restored. Eighteen of 21 strains identified as A. haemolyticus and Acinetobacter species 6 were unable to produce acid from glucose after addition of PQQ. Our results confirm that the former taxonomic scheme for the genus Acinetobacter (2 species differing only by glucose oxidation) is untenable and that, accordingly, identification of Acinetobacter strains at the species level must be performed using more modern methods, i.e. carbon source utilization tests.

Acinetobacter↗
PubMed1999

Phylogenetic analysis of proteolytic Acinetobacter strains based on the sequence of genes encoding aminoglycoside 6'-N-acetyltransferases.

The sequence of seven aac(6')-I genes encoding aminoglycoside 6'-N-acetyltransferases from proteolytic Acinetobacter strains including genomic species 14, 15, 16, and 17 and from ungrouped proteolytic strains 631, 640, and BM2722 was determined. Pulsed-field gel electrophoresis of genomic DNA of these strains and of Acinetobacter sp. 6 CIP A165 digested with SfiI followed by hybridization with rRNA and aac(6')-I specific probes indicated that these genes were located in the chromosome. Phylogenetic analysis of the genes indicated that aac(6')-I of A. baumannii, Acinetobacter ungrouped strain 631, and Acinetobacter sp. 16 formed a cluster (91.5 to 92.3% identity) whereas aac(6')-I of Acinetobacter sp. 15, sp. 17, and Acinetobacter ungrouped strain BM2722 formed another cluster (90.7 to 94.6% identity). A third cluster was constituted by A. haemolyticus and Acinetobacter sp. 6 (83.6% identity). The phylogeny drawn from aac(6')-I sequences was consistent with that based on DNA-DNA hybridization and phenotype comparison. The aac(6')-I genes were all species specific except for aac(6')-Ih located in a 13.7-kb non conjugative plasmid from A. baumannii BM2686. We conclude that aac(6')-I genes may be suitable for identification at the species level and for analysis of the phylogenetic relationships of Acinetobacter.

Acetyltransferases↗
PubMed2001

RAPD-PCR typing of Acinetobacter isolates from activated sludge systems designed to remove phosphorus microbiologically.

AIMS: This study investigated whether there were differences in RAPD fingerprints between already described genomic species of Acinetobacter and those from activated sludge systems. Whether plant-specific populations of acinetobacters exist was also examined. METHODS AND RESULTS: Fifty-two isolates of Acinetobacter from four biological phosphorus removal (EBPR) systems of different configurations, and the known genomic species, were characterized using RAPD-PCR, and fragments separated on agarose gels. Patterns were analysed using Gel Pro software and data analysed numerically. RAPD-PCR produced patterns suggesting that many environmental isolates differ from known genomic species. In two cases, strains from individual plants clustered closely enough together to imply that there may be plant-specific populations of acinetobacters. CONCLUSION: The data suggest that current understanding of the taxonomic status of Acinetobacter may need modifying to accommodate non-clinical isolates, as many of the clusters emerging after numerical analysis of RAPD-PCR fragments from activated sludge isolates were quite separate from the clusters containing the already described genomic species. Some evidence was also obtained from the clusters generated to support a view that particular populations of Acinetobacter may occur in individual activated sludge plants. SIGNIFICANCE AND IMPACT OF THE STUDY: These data suggest that the current understanding of the systematics of Acinetobacter, based as it is almost exclusively on clinical isolates, may need drastic revision to accommodate environmental strains. They also suggest that a re-examination of the importance and role of Acinetobacter in the activated sludge process may be appropriate.

Acinetobacter↗
PubMed2006

The Acinetobacter outer membrane protein A (OmpA) is a secreted emulsifier.

Acinetobacter strains use hydrophobic carbon sources and most of them are efficient oil degraders. They secrete a variety of emulsifiers which are efficient in producing and stabilizing oil-in-water emulsions. The bioemulsifier of Acinetobacter radioresistens KA53 (Alasan) is a high-mass complex of proteins and polysaccharides. The major emulsification activity of this complex is associated with a 45 kDa protein (AlnA), which is homologous to the outer membrane protein OmpA. The emulsification ability of AlnA depends on the presence of hydrophobic residues in the four loops spanning the transmembrane domains. The finding of a secreted OmpA was unexpected, in view of the fact that this protein is essential in all Gram-negative bacteria, has four trans-membrane domains and is considered to be an integral structural component of the outer membrane. However, secretion of an OmpA with emulsifying ability could be of physiological importance in the utilization of hydrophobic substrates as carbon sources. Here we examined the possibility that secretion of OmpA with emulsifying activity is a general property of the oil-degrading Acinetobacter strains. The results indicate that OmpA is secreted in five strains of Acinetobacter, including strain Acinetobacter sp. ADP1 whose genome has been sequenced. The ompA genes of ADP1 and an additional strain, Acinetobacter sp. V-26 were cloned and sequenced. Structure analysis of the sequence of the two proteins indicated the existence of the hydrophobic regions, previously shown to be responsible for the emulsification activity of AlnA. Further examination of the recombinant OmpA proteins indicated that they are, indeed, strong emulsifiers, even when produced in Escherichia coli. The finding that Acinetobacter OmpA has emulsifying activity and that it is secreted in five strains of Acinetobacter may be physiologically significant and suggests the involvement of this protein in biodegradation of hydrophobic substrates, including hydrocarbons.

Acinetobacter↗
PubMed1997

Activities of beta-lactams against Acinetobacter genospecies as determined by agar dilution and E-test MIC methods.

The agar dilution MIC method was used to test activities of ticarcillin, ticarcillin-clavulanate, amoxicillin, amoxicillin-clavulanate, ampicillin, ampicillin-sulbactam, piperacillin, piperacillin-tazobactam, inhibitors alone, ceftazidime, and imipenem against 237 Acinetobacter genospecies. A total of 93.2% of strains were beta-lactamase positive by the chromogenic cephalosporin method. Overall, ampicillin-sulbactam was the most active combination against all strains (MIC at which 50% of the isolates are inhibited [MIC50] and MIC90, 4.0 and 32.0 microg/ml; 86.9% susceptible at < or = 16 microg/ml), followed by ticarcillin-clavulanate (16.0 and 128.0 microg/ml; 85.7% susceptible at < or = 64 microg/ml), piperacillin-tazobactam (16.0 and 128.0 microg/ml; 84.8% susceptible at < or = 64 microg/ml), and amoxicillin-clavulanate (16.0 and 64.0 microg/ml; 54.4% susceptible at < or =16 microg/ml). Ceftazidime and imipenem yielded MIC50s and MIC90s of 8.0 and 64.0 microg/ml (ceftazidime) and 0.5 and 1.0 microg/ml (imipenem), respectively; 71.3% of strains were susceptible to ceftazidime at < or = 16 microg/ml, and 99.2% were susceptible to imipenem at < or = 8 microg/ml. Sulbactam was the most active beta-lactamase inhibitor alone (MIC50 and MIC90, 2.0 and 16.0 microg/ml); clavulanate and tazobactam were less active (16.0 and 32.0 microg/ml for both compounds). Enhancement of beta-lactams by beta-lactamase inhibitors was not always seen in beta-lactamase-positive strains, and activity of combinations such as ampicillin-sulbactam was due to the inhibitor alone. Acinetobacter baumannii was the most resistant genospecies. By contrast, Acinetobacter haemolyticus, Acinetobacter calcoaceticus, Acinetobacter johnsonii, Acinetobacter junii, Acinetobacter radioresistens, and other non-Acinetobacter baumannii strains were more susceptible to all compounds tested. E-test MICs were within 1 dilution of agar dilution MICs in 38.4 to 89.6% of cases and within 2 dilutions in 61.6 to 98.6% of cases.

Acinetobacter↗
PubMed2005

Identification of a new allelic variant of the Acinetobacter baumannii cephalosporinase, ADC-7 beta-lactamase: defining a unique family of class C enzymes.

Acinetobacter spp. are emerging as opportunistic hospital pathogens that demonstrate resistance to many classes of antibiotics. In a metropolitan hospital in Cleveland, a clinical isolate of Acinetobacter baumannii that tested resistant to cefepime and ceftazidime (MIC = 32 microg/ml) was identified. Herein, we sought to determine the molecular basis for the extended-spectrum-cephalosporin resistance. Using analytical isoelectric focusing, a beta-lactamase with a pI of > or = 9.2 was detected. PCR amplification with specific A. baumannii cephalosporinase primers yielded a 1,152-bp product which, when sequenced, identified a novel 383-amino-acid class C enzyme. Expressed in Escherichia coli DH10B, this beta-lactamase demonstrated greater resistance against ceftazidime and cefotaxime than cefepime (4.0 microg/ml versus 0.06 microg/ml). The kinetic characteristics of this beta-lactamase were similar to other cephalosporinases found in Acinetobacter spp. In addition, this cephalosporinase was inhibited by meropenem, imipenem, ertapenem, and sulopenem (K(i) < 40 microM). The amino acid compositions of this novel enzyme and other class C beta-lactamases thus far described for A. baumannii, Acinetobacter genomic species 3, and Oligella urethralis in Europe and South Africa suggest that this cephalosporinase defines a unique family of class C enzymes. We propose a uniform designation for this family of cephalosporinases (Acinetobacter-derived cephalosporinases [ADC]) found in Acinetobacter spp. and identify this enzyme as ADC-7 beta-lactamase. The coalescence of Acinetobacter ampC beta-lactamases into a single common ancestor and the substantial phylogenetic distance separating them from other ampC genes support the logical value of developing a system of nomenclature for these Acinetobacter cephalosporinase genes.

Acinetobacter baumannii↗
PubMed2005

Relationship between antimicrobial resistance and aminoglycoside-modifying enzyme gene expressions in Acinetobacter baumannii.

BACKGROUND: Acinetobacter baumannii is one of the main gram-negative bacilli in clinical practice. Nosocomial infections caused by multi-drug resistance Acinetobacter baumannii is very difficult to treat. This study was designed to investigate the antimicrobial resistance characteristics and four resistant gene expressions of aminoglycoside-modifying enzymes including N-acetyltransferases and O-phosphotransferases in Acinetobacter baumannii. METHODS: Bacterial identification and antimicrobial susceptibility test were performed by Phoenix system in 247 strains of Acinetobacter baumannii. Minimal inhibitory concentrations (MICs) of seven aminoglycosides including gentamicin, amikacin, kanamycin, tobramycin, netilmicin, neomycin and streptomycin in 15 strains of multi-drug resistant Acinetobacter baumannii were detected by agar dilution. Four aminoglycoside-modifying enzyme genes were amplified by polymerase chain reaction (PCR) and verified by DNA sequencer. RESULTS: The resistance rates of 247 strains of Acinetobacter baumannii against cefotaxime, levofloxacin, piperacillin, aztreonam, tetracycline, ciprofloxacin and chloramphenicol were more than 50%. Imipenem and meropenem showed high antibacterial activities with resistance rates of 3.2% and 4.1%. MIC50 and MIC90 of gentamicin, amikacin, streptomycin and kanamycin in 15 strains of multi-drug resistant Acinetobacter baumanii were all more than 1024 mg/L, and the resistance rates were 100%, 100%, 100% and 93.3%, respectively. But their resistance rates to tobramycin, netilmicin and neomycin were 86.7%, 93.3% and 46.7%, respectively. Three modifying enzyme genes, including aacC1, aacC2 and aacA4 genes, were found in 15 strains, but aphA6 had not been detected. Their positive rates were 93.3%, 20.0% and 20.0%, respectively. These three genes existed simultaneously in No.19 strain. Nucleotide sequences of aacC1, aacC2 and aacA4 genes shared 100%, 97.9% and 99.7% identities with GenBank genes (AY307113, S68058 and AY307114). CONCLUSION: Multi-drug resistant Acinetobacter baumannii strains are rapidly spreading in our hospital, and their resistance to aminoglycosides may be associated with aminoglycoside-modifying enzyme gene expressions.

Acinetobacter baumannii↗
PubMed2005

Genomic species identification of Acinetobacter of clinical isolates by 16S rDNA sequencing.

INTRODUCTION: This study aims to identify Acinetobacter of clinical isolates from the University of Malaya Medical Centre (UMMC), Kuala Lumpur, to the species level by 16S rDNA sequencing. METHODS: 12 representative Acinetobacter isolates of the UMMC inpatients were randomly picked and used for the study. The 16S rDNA sequences were determined and phylogenetic relationships to all known Acinetobacter species were established. RESULTS: Based on the 16S rDNA sequences, all the UMMC isolates were identified as Acinetobacter baumannii. The isolates shared a common ancestral lineage with the prototypes Acinetobacter baumannii DSM30007 and DSM30008 with 99-100 percent sequence similarities. The isolates could be differentiated into two groups by a single nucleotide difference (thymine-cytosine) within the 16S rRNA sequence. Three different genotypes, 1, 3 and 4, were recognised using REP-PCR. CONCLUSION: The previously uncharacterised Acinetobacter isolates from the UMMC were identified by their 16S rDNA sequences as Acinetobacter baumannii. The isolates were distinguished into at least three different genotypes by REP-PCR genotyping. These findings confirmed for the first time the presence of Acinetobacter baumannii of different genotypes among patients at UMMC.

Acinetobacter baumannii↗
PubMed1997

Treatment of Acinetobacter infections.

Gram-negative non-fermentative aerobic bacilli are becoming increasingly more involved in nosocomial infections. It has generally been recognised that the members of the Acinetobacter genus are among the most common agents responsible for severe hospital infections; their clinical importance has increased due to the development of antibacterial resistance mechanisms by these organisms. Over the last two decades the antibacterial armamentarium has progressed significantly and newer broad spectrum antibiotics have been used during therapy of hospital infections due to drug-resistant Acinetobacter spp. Despite various mechanisms of resistance to beta-lactams, aminoglycosides, fluoroquinolones developed by these organisms, the control of Acinetobacter infections can be effected by the use of several antibiotic combinations in 'conventional' antibiotic therapy. Recent surveys have pointed out the importance of using combinations of 2-amino-5-thiazolyl cephalosporins, or imipenem with aminoglycosides, or alpha-carboxy- penicillins (ticarcillin) combined with beta-lactamase inhibitors. Amongst the latter drugs, the place of sulbactam should be redefined thanks to its intrinsic activity against the Acinetobacter species, associated with its inhibitory power against beta-lactamases. The fluoroquinolones were initially very active against Acinetobacter infections, but resistance to this major class of drugs has occurred very rapidly. However, newer compounds of this class with increased anti-Acinetobacter activities can be used in combinations with beta-lactams or aminoglycosides. The potential role of rifampicin is still underestimated for the treatment of Acinetobacter infections despite promising in vitro activity. Novel derivatives of cephalosporins, carbapenems, fluoroquinolones, or completely new antibiotic classes, of which several investigational drugs seem promising, may constitute the future of antibiotic therapy and hence the treatment of Acinetobacter infections.

Journal Article↗
PubMed1995

The increasing significance of outbreaks of Acinetobacter spp.: the need for control and new agents.

Acinetobacter spp. are Gram-negative non-fermentative bacteria which may be isolated as commensals from human skin, throat and intestine but are also increasingly responsible for hospital infections. Owing to frequent changes in their taxonomy, their pathogenic role in humans has not been clear but today acinetobacter is considered to be a significant nosocomial pathogen in outbreaks of hospital infections predominantly in intensive care units. Nosocomial infections due to acinetobacter include urinary tract infections, bacteraemia, wound and burn infections, but also they are frequently isolated from ventilator-associated nosocomial pneumonia. The frequency of hospital outbreaks of acinetobacter infections has required the development of reliable typing methods. As well as conventional 'phenotypic' methods (serology, biotyping, phage typing), 'genotypic' systems (ribotyping, plasmid profiles, pulsed-field gel electrophoresis) have been utilized for strain identification. These typing systems should allow a better understanding of the epidemiology of acinetobacter in the hospital environment, e.g. sources, modes of transmission, and result in more efficient preventive measures. Acinetobacter infections are difficult to treat owing to their frequent multiple resistance to the antibiotics currently available for the treatment of nosocomial infections; various mechanisms of resistance to beta-lactams and amino-glycosides have been identified in the genus. Combination therapy is usually recommended for treatment of acinetobacter nosocomial infections and active antibacterials include imipenem, ceftazidime, amikacin and the newer fluoroquinolones. Careful in vitro testing of the activity of combinations of these drugs is recommended prior to their use.

Acinetobacter↗
PubMed2004

Resistance trends of Acinetobacter spp. in Latin America and characterization of international dissemination of multi-drug resistant strains: five-year report of the SENTRY Antimicrobial Surveillance Program.

OBJECTIVES: To analyze the antimicrobial susceptibility of Acinetobacter spp. isolates collected from Latin American medical centers as part of the SENTRY Antimicrobial Surveillance Program and also to evaluate the dissemination of multi-drug resistant Acinetobacter spp. strains in the region. METHODS: A total of 826 isolates of Acinetobacter spp. from multiple infection sites were collected from January 1997 to December 2001 in ten medical centers and susceptibility tested to >25 selected agents by broth microdilution. Multi-drug resistant Acinetobacter spp. isolates were molecular typed. RESULTS: Resistance rates to carbapenems varied significantly among countries. A continued annual increase occurred in the Argentinean medical centers. In contrast, carbapenem resistance was rare in Chilean centers, and decreased significantly in the Brazilian institutions. Acinetobacter spp. isolates recovered from lower respiratory tract and bloodstream infections were associated with lower antimicrobial susceptibility rates. Resistance rates to imipenem were higher among isolates collected from intensive care units (13.5%) than among isolates from other units. A major ribogroup pattern (521-1) was detected among eight Acinetobacter spp. strains isolated from three distinct Latin American countries. CONCLUSIONS: This study found that antimicrobial resistance is still a major issue among Acinetobacter spp. isolates collected from some Latin American countries. The dissemination of a major bacterial cluster in different regions reinforces the importance of longitudinal surveillance programs, such as SENTRY, as valuable tools for monitoring antimicrobial susceptibility rates and guiding local interventions.

Acinetobacter↗
PubMed1995

Acinetobacter species as a cause of catheter-related infections.

In recent years, Acinetobacter species have emerged as clinically important pathogens. Though these organisms are widely prevalent in nature, most human infections are hospital-acquired. Acinetobacter baumannii is the predominant species. Nosocomial Acinetobacter baumannii infections such as respiratory tract infections, urinary tract infections, meningitis following neurosurgical procedures, and bacteremia mainly affect patients with severe underlying disease in the ICU and often, in the setting of nosocomial outbreak. The occurrence of multiresistant strains often limits therapeutic options. A substantial part of Acinetobacter baumannii bacteremia cases represent catheter-related infections that usually carry a favorable prognosis. Acinetobacter species other than Acinetobacter baumannii are less frequently reported as a cause of infection in humans. Bacteremia due to these organisms is mostly sporadic and almost exclusively related to intravascular devices. The underlying diseases are often less severe than those of patients affected by Acinetobacter baumannii infections. The clinical course is usually benign and the infection responds readily to catheter removal irrespective of the appropriateness of antimicrobial therapy.

Acinetobacter↗
PubMed2001

Emerging importance of multidrug-resistant Acinetobacter species and Stenotrophomonas maltophilia as pathogens in seriously ill patients: geographic patterns, epidemiological features, and trends in the SENTRY Antimicrobial Surveillance Program (1997-1999).

As part of the SENTRY Antimicrobial Surveillance Program, a total of 1078 Acinetobacter species and 842 Stenotrophomonas maltophilia isolates were collected between January 1997 and December 1999 from 5 geographic regions (Canada, the United States, Latin America, Europe, and the Asia-Pacific). The frequency of infections (by geographic region and body site), including those due to imipenem-resistant Acinetobacter species and trimethoprim-sulfamethoxazole (TMP-SMZ)-resistant S. maltophilia, was evaluated. The possibility of seasonal variations in bloodstream infections caused by Acinetobacter species was studied, as was the activity of several therapeutic antimicrobials against all strains. Acinetobacter species and S. maltophilia were most frequently associated with pulmonary infections, independent of the region evaluated. In contrast, patterns of antimicrobial resistance markedly varied among distinct geographic regions, especially for nosocomial isolates. Although the carbapenems were the most active antimicrobials against Acinetobacter species, nearly 11.0% of the nosocomial isolates were resistant to this drug group in both regions. TMP-SMZ, ticarcillin-clavulanic acid, gatifloxacin, and trovafloxacin were the only agents with consistent therapeutic activity against S. maltophilia isolates. Rates of resistance to TMP-SMZ ranged from 2% in Canada and Latin America to 10% in Europe. The geographic differences in resistance patterns among Acinetobacter species and S. maltophilia isolates observed in this study emphasize the importance of local surveillance in determining the most adequate therapy for acinetobacter and S. maltophilia infections and the possible clonal, epidemic nature of occurrence.

Acinetobacter↗
PubMed1997

Distribution of Acinetobacter species on human skin: comparison of phenotypic and genotypic identification methods.

At least 19 genomic species are recognized as constituting the genus Acinetobacter. However, little is known about the natural reservoirs of the various members of the genus. An epidemiological study was therefore performed to investigate the colonization with Acinetobacter spp. of the skin and mucous membranes of 40 patients hospitalized in a cardiology ward and 40 healthy controls. Single samples were obtained once from each of nine different body sites, i.e., forehead, ear, nose, throat, axilla, hand, groin, perineum, and toe web. Identification of Acinetobacter isolates was achieved by using phenotypic properties and was compared to identification by amplified ribosomal DNA restriction analysis. Selected isolates were further investigated with sodium dodecyl sulfate-polyacrylamide gel electrophoresis, ribotyping, and DNA-DNA hybridization. Plasmid profile analysis was used for epidemiological typing. Thirty patients (75%) and 17 controls (42.5%) were found to be colonized with Acinetobacter spp., and the colonization rates of patients increased during their hospital stay. The most frequently isolated species were Acinetobacter lwoffii (47%), A. johnsonii (21%), A. radioresistens (12%), and DNA group 3 (11%). In contrast, A. baumannii and DNA group 13TU, the most important nosocomial Acinetobacter spp., were found only rarely on human skin (0.5 and 1%, respectively) and their natural habitat remains to be defined. A good correlation between phenotypic and genotypic methods for identification of Acinetobacter spp. was observed, and only two isolates could not be assigned to any of the known DNA groups.

Acinetobacter↗
PubMed2006

Nosocomial infections due to Acinetobacter species: Clinical findings, risk and prognostic factors.

PURPOSE: Nosocomial infections caused by Acinetobacter species is of increasing concern in critically ill patients, and the risk factors for this infection are not well established. The present investigation was done to determine incidence of nosocomial Acinetobacter infections. Our study retrospectively attempts to find risk and prognostic factors for the nosocomial acquisition of Acinetobacter infection. METHODS: The medical records of 43 patients with Acinetobacter infection during two-year period (Oct1998-Oct2000) were reviewed to find the factors involved in the nosocomial acquisition of Acinetobacter. Acinetobacter isolates that were obtained from these patients were phenotypically typed using carbon assimilation tests. Antimicrobial susceptibility testing results were noted from the microbiology records. RESULTS: Acinetobacter baumannii accounted for 41.8% (n=18) of all the infections. By multivariate logistic regression analysis, only resistant antibiotype {(Ceftazidime- OR, 7.13 [95% CI, 1 to 46];p= 0.044); (Cefotaxime- OR, 6.09 [CI, 0.87 to 30];p = 0.045)} and mechanical ventilation (OR, 5.84 [CI, 0.83 to 31];p = 0.05) were found to be potential independent risk factors for mortality. Overall mortality rate was 33%. CONCLUSIONS: Most of A. baumannii isolates were multidrug resistant in our set up and infections due to them were associated with high mortality. Prevention of Multiple drug resistant (MDR) A. baumannii infections was achieved after discontinuation of cefotaxime in ICU. Infection with resistant clones and mechanical ventilation were found to be potential independent risk factors for mortality.

Acinetobacter↗
PubMed2002

Identification of Acinetobacter species isolated from clinical specimens by amplified ribosomal DNA restriction analysis.

BACKGROUND & OBJECTIVES: Taxonomy of Acinetobacter has been changing ever since it was recognized to be associated with human infections. Many biochemical schemes and molecular methods have been used for the species identification of this bacterium. Recently a simple molecular method called amplified ribosomal DNA restriction analysis (ARDRA) has been used to determine the genomospecies of ACINETOBACTER: An attempt is made in the present study to identify the Acinetobacter genomospecies isolated from clinical specimens using ARDRA and to see whether the environmental isolates are similar to those obtained from clinical specimens. METHODS: A total of 142 consecutive isolates of Acinetobacter sp. obtained from different clinical specimens (125) and environmental samples (17) of postoperative neurosurgery-intensive care unit were studied using ARDRA. Amplification was done using primers of 16S rRNA gene followed by restriction with Alu I, Cfo I and Mbo I enzymes separately to obtain a profile of patterns specific for a species. RESULTS: Of the 125 clinical isolates, 107 were Acinetobacter baumannii (genomospecies 2) and 18 were A. calcoaceticus (genomospecies 1); while 11 of the 17 environmental isolates were A. baumannii and 6 had unidentifiable patterns which were not found in the clinical isolates. INTERPRETATION & CONCLUSION: We found that ARDRA was a simple and reproducible method to be used in a clinical laboratory for identification of Acinetobacter species. A. baumannii was found to be the commonest species isolated from the patients and environment in our hospital. The presence of the same species of Acinetobacter in the environment suggests the role of environment as a source of infection to the patients in high risk units.

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↗
PubMed2005

Epidemiological investigation of nosocomial Acinetobacter infections using arbitrarily primed PCR & pulse field gel electrophoresis.

BACKGROUND & OBJECTIVE: Nosocomial infections caused by Acinetobacter spp. are a significant problem worldwide. Information on epidemiological investigation of outbreaks caused by Acinetobacter species in India is lacking. The present investigation was carried out to elucidate molecular epidemiology of Acinetobacter species isolated from nosocomial infections in a tertiary care hospital in south India using two DNA-based typing methods. METHODS: The medical records of 43 patients with Acinetobacter infection during a period of 24 months were reviewed and Acinetobacter isolates obtained from these patients were characterized phenotypically by assimilation tests and genotypically by arbitrarily primed PCR (AP-PCR) and pulse field gel electrophoresis (PFGE). Susceptibility testing results of the Acinetobacter isolates were also analysed. RESULTS: Most of the infections were nosocomial, and the majority of these were acquired in intensive care units (ICUs). A. baumannii accounted for 41.8 per cent (n=18) of all pneumonia acquired in the ICU. AP-PCR with M13 primer distinguished 8 different PCR patterns comprising of 2 to 6 DNA fragments of 0.1 to 1.0 kb. PFGE identified 9 distinct profiles with five subvarients. By APPCR, epidemiologically unrelated strains could not be differentiated and often differences within biotypes of A. baumannii were not detectable. ApaI macrorestriction (PFGE) identified at least 4 outbreaks caused by 3 clones of A. baumannii and one clone of DNA group 13TU, one replacing the other in a well-defined temporal order. INTERPRETATION & CONCLUSION: Most of A. baumannii isolates were multidrug resistant. PFGE was more discriminatory [Discriminatory Index (DI)=0.96 than AP-PCR fingerprinting (DI=0.88)] in the present study. However, AP-PCR fingerprinting is more useful as a simple and rapid identification technique for epidemiological investigation of nosocomial Acinetobacter infections.

Acinetobacter↗