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PubMedDate not supplied

[Intrahospital septicemia due to Acinetobacter calcoaceticus var. anitratus in a neonatal intensive care unit].

Twenty-one cases of sepsis by Acinetobacter calcoaceticus biovar anitratus occurred, ten in 1989 and eleven in 1990 (January-April). In this last year, there were nine cases with characteristics of an epidemic outbreak. It was noted that sepsis was predominant in males, babies of less than 2,500 g and less than 37 weeks of gestation. They were hospitalized in our Intensive Care Unit for different problems, but almost all had mechanical ventilation, parenteral nutrition and received antibiotics previously, being these risk factors the most important. Clinical and laboratory features were not different from sepsis produced by other microorganisms. It is important to remark the increased frequency of Acinetobacter calcoaceticus biovar anitratus as a nosocomial agent, but also his greater aggressivity and antibiotic resistance, all factors that produced an elevated mortality, eight of eleven cases. Finally, due to the adoption of several measures the epidemic outbreak was stopped.

Acinetobacter Infections↗
PubMed1990

[Acinetobacter as a problem pathogen in patients with long-term tocolysis].

A hospital outbreak of Acinetobacter Calcoaceticus in a ward with patients with intravenous tokolysis is reported. Within 2 months 9 pregnant women who had tokolysis for premature labour developed septic fever that only subsisted after the administration of tokolysis was stopped. In 7 cases blood culture was positive for Acinetobacter Calcoaceticus. This endemic outbreak was responsible for premature deliveries in four cases, leading top post partum death of two infants. Source identification was inconclusive, no further outbreaks have occurred since the reported endemic occurrence. Dangers of nosocomial infections in patients with intravenous tokolysis are discussed.

Acinetobacter↗
PubMedDate not supplied

Outbreak of a multiply resistant Acinetobacter in a surgical intensive care unit: epidemiology and control.

During January, 1976 seven patients in an SICU became colonized or infected with Acinetobacter calcoaceticus (variation, anitratum) at an attack rate of 12.5 per cent. The organism showed a marked reduction in antimicrobial sensitivity from previous experience. Comparison with 34 uninfected control patients indicated that intubation and continuous ventilatory assistance were significantly associated with acquiring the organism (p = 0.0154). Acinetobacter was cultured from nurses' hands, AMBU adaptors, respirator apparatus, respirometers, and unlabeled bottles of saline used for tracheal irrigation. Control measures were designed to interrupt transmission. The investigation identified the nursing techniques and reservoirs that allowed this outbreak to occur, and we emphasize the need for close surveillance of patient care procedures in an intensive care unit.

Acinetobacter↗
PubMedDate not supplied

[Acinetobacter calcoaceticus as a cause of infection in wounds and burns].

Over the period from January 1985 to July 1986 2038 samples of the patients with open wounds and burns, treated in the Military Medical Academy in Belgrade, were tested. Acinetobacter calcoaceticus was found in 152 samples (7.45%). The sensitivity to standard hemotherapeutics for Gram-negative bacteria was assessed. Results indicated that Acinetobacter calcoaceticus showed a high resistance to all hemotherapeutics used in this investigation. Even if it was a opportunistic pathogen bacterium its clinical importance was great because in some conditions this bacterium could cause long-lasting and hard infectious treatment.

Acinetobacter↗
PubMed1977

Community-acquired Acinetobacter calcoaceticus var anitratus pneumonia.

Two patients had community-acquired Acinetobacter calcoaceticus var anitratus pneumonia. Both patients were alcoholic and one was cirrhotic. One patient died and the other received two weeks of gentamicin therapy and survived. Misinterpretation of the sputum Gram stain delayed diagnosis and institution of proper therapy in both cases. In addition to organisms sensitive to penicillins such as Neisseria or Haemophilus, Acinetobacter must be considered in the differential diagnosis of community-acquired Gram-negative coccobacillary pneumonia.

Acinetobacter↗
PubMed1982

[Antibiotic sensitivity of Acinetobacter calcoaceticus in patients with infected burns].

Sensitivity of Acinetobacter calcoaceticus var. anitratum isolated from infected burn wounds was studied with respect to 24 antibiotics. It was found that the isolates were multiple drug resistant. Sensitivity was observed at least to 8 out of 24 antibiotics. The majority of the isolates were resistant to 10--15 drugs. Many strains were resistant to 16--17 antibiotics. 11 antibacterial drugs, i. e. tobramycin, sisomicin, gentamicin, amicacin, neomycin, carbenicillin, polymyxin M, erythromycin, tetracycline, rifampicin and dioxidine proved to be most active against Acinetobacter calcoaceticus. The strains were resistant to 6 antibiotics, i. e. penicillin, oxacillin, lincomycin, ceporin, fusidin and ristomycin. The activity of streptomycin, ampicillin and levomycetin was negligible.

Acinetobacter↗
PubMed1994

Emergence of multidrug-resistant isolates of Acinetobacter baumannii.

Patterns of antimicrobial resistance during an outbreak of nosocomial infections caused by Acinetobacter baumannii were studied. The medical records of all patients admitted to the hospital between February 1993 and February 1994 from whom A. baumannii was cultured were reviewed for demographic data, confirmation of the isolation report, admission date, date of first isolation of the organism, and antimicrobial use before and after the culture and susceptibility test results were obtained. The culture and susceptibility test data were reviewed for all specimens submitted to the laboratory during the review period. A total of 87 patients (mean +/- S.D. age, 37.9 +/- 8.7 years) with nosocomial infection or colonization with A. baumannii were identified. All the patients were surgical intensive care unit residents and had predisposing factors for acinetobacter infection. A total of 107 isolates of the organism were cultured from various sites; sputum was the most common source. The number of isolates per month increased steadily beginning in September 1993 and then declined over the winter. The median time between admission and first isolation of resistant A. baumannii was 11 days. Infections were manifested clinically as pneumonia (36 patients), bacteremia (8), wound infection (6), and urinary-tract infection (2). Of the 107 isolates, all were resistant to formulary cephalosporins, extended-spectrum penicillins, quinolones, and aztreonam. Only nine isolates were susceptible to one or more aminoglycosides. All the isolates were susceptible to imipenem-cilastatin. During an outbreak of nosocomial infections with A. baumannii, all or nearly all of the 107 isolates were resistant to a broad range of antimicrobials with the exception of imipenem-cilastatin, to which all the isolates were susceptible.

Acinetobacter↗
PubMed1977

The clinical significance of Acinetobacter species.

Of 50 consecutive patients from whom Acinetobacter species were isolated, only one had an infection due to the organism which required antibiotic therapy. Fourteen of the isolates were associated with minor body surface infections and the remainder occurred as the result of either colonization without infection or culture contamination. The taxonomy, natural occurrence and antibiotic sensitivity of Acinetobacter species and their differentiation from more pathogenic organisms are reviewed.

Acinetobacter↗
PubMed1995

Epidemiological analysis of Acinetobacter baumannii strains isolated from a surgical intensive care unit.

A serious epidemic of Acinetobacter baumannii resistant to imipenem occurred in the surgical intensive care unit of the hospital Charles-Nicolle in Tunis during February 1994, causing two deaths among three patients. The Acinetobacter strains were isolated from various samples of the intensive care unit. The techniques used for typing were biotyping, antibiogram, plasmid profiles and chromosomal DNA by random amplified polymorphic DNA (RAPD). The A baumannii strains isolated from patients exhibited an identical pattern with all the epidemiological markers utilized; the strains from the surrounding areas showed four and six different patterns respectively for phenotypic and genotypic characters. The strain isolated from a care table had the same phenotypic and genotypic pattern as that of the patients' strains.

Acinetobacter↗
PubMed1997

Epidemiological study of Acinetobacter species isolated from an intensive care unit.

An epidemiological survey of the increase in Acinetobacter species isolates occurring in the intensive care unit of a Spanish teaching hospital during 1993 and 1994 was carried out. Different laboratory methods were used to find out, whether there was a genetic linkage. The isolates were divided into three main groups according to the resistance patterns to 11 drugs. Using API 20NE biotyping, eight different types were found. The two most common contained 20 and 11 isolates, respectively. Five different plasmid profile types were observed, although plasmids were only demonstrated in 40% of the isolates. Ribotyping with EcoRI, SalI and ClaI enzymes revealed 10, 9, and 8 different patterns, respectively. In total, 15 different ribotypes were identified using these three enzymes. Twenty-one isolates belonged to exactly the same ribotype, and 13 were associated with two highly related ribotypes. In the first ribotype, only five isolates harboured plasmids. The ribotyping method produced 100% typability and ribotypes were easy to compare; it also had taxonomic value. Ribotyping allowed us to determine the genetic linkage between Acinetobacter isolates recovered from ICU patients.

Acinetobacter↗
PubMed1997

[Selection of resistance mutants and bacteriostatic and bactericidal activity of meropenem and imipenem against Acinetobacter spp].

BACKGROUND: To evaluate the inhibitory and bactericidal activity of meropenem and imipenem against multiresistant isolates of Acinetobacter spp and to compare the frequency of mutation for both antibiotics. METHODS: Minimum inhibitory concentrations were determined by the agar dilution method. Bactericidal activities were evaluated by killing curves method employing 8 times the MIC. One-step resistant mutant selection was performed by spreading more than 5 x 10(8) ufc/ml on agar Mueller Hinton plates containing 2, 4 and 8 times the MIC of meropenem or imipenem. RESULTS: In the group of sensitive strains (MIC < 4 mg/l for imipenem and meropenem) we detected lower MIC for imipenem than meropenem (61.5% of the strains). Strains with reduced susceptibility to imipenem (MIC = 4 mg/l) were more sensitive to meropenem with MICs equivalents to the sensitive group. Bactericidal activity was detected in 6 hs for imipenem and in 24 hs for meropenem. Meropenem was bactericidal in 4 clinical isolates with MICs = 4 mg/l for imipenem and imipenem was bactericidal in laboratory mutants resistant to meropenem. It was no possible to select mutants resistant to imipenem but for meropenem the rate of mutation was 1.4 x 10(-9) to 1.0 x 10(-8). Mutants resistant to meropenem were susceptible to imipenem and 57% of them were stable. CONCLUSIONS: From the laboratory point of view we consider that imipenem is more active than meropenem because it presents lower MICs, better bactericidal activity, and no risk to select resistance. However meropenem could be useful in some strains resistant to imipenem (MIC = 4 mg/l). Cross-resistance was no detected so we consider that both antibiotics should be tested against Acinetobacter spp. because they are not equivalents.

Acinetobacter↗
PubMed2006

Proteomic analysis of a fraction enriched in cell envelope proteins of Acinetobacter baumannii.

Acinetobacter baumannii is a multiresistant opportunistic nosocomial pathogen. A protein fraction was purified and analyzed by 2-DE. Twenty-nine major protein spots were selected for protein identification using trypsin digestion and MS analysis. As the A. baumannii genome has not yet been described, protein identification was performed by homology with other Acinetobacter species in the NCBi database. We identified ribosomal proteins, chaperones, elongation factors and outer membrane proteins (Omp), such as OmpA and the 33-36-kDa OMP. Proteomic analysis of A. baumannii provides a platform for further studies in antimicrobial resistance.

Acinetobacter baumannii↗
PubMed2000

Engineering of heterologous cytochrome P450 in Acinetobacter sp.: application for pollutant degradation.

Many organisms do not contain the necessary biochemical armoury to carry out the initial oxidative attack of many pollutant chemicals. In the present study, Acinetobacter sp. strain BD413 has been genetically engineered to express the cytochrome P450 xenobiotic-metabolising enzyme CYP105D1 from Streptomyces griseus that has in its repertoire a diverse array of organic pollutants. Further, it is shown that the transformed Acinetobacter calcoaceticus strain BD413 can grow on pollutants unlike control bacteria not expressing cytochrome P450 and that was reflected in release of radiolabel with growth on radiolabelled chlortoluron. We show that cytochrome P450 can enhance the biodegrading repertoire of A. calcoaceticus and discuss the application of such results to bioremediation strategies.

Acinetobacter calcoaceticus↗
PubMed2001

Complete nucleotide sequence and overexpression of cat1 gene cluster, and roles of the putative transcriptional activator CatR1 in Acinetobacter lwoffii K24 capable of aniline degradation.

The aniline-assimilating bacterium Acinetobacter lwoffii K24 has two cat gene clusters (cat1 and cat2). In this study, we completely sequenced 10-kb DNA fragment of cat1 genes of A. lwoffii K24, which had been cloned in plasmid pCD1-1. Sequence analysis revealed that the order of genes in the cat1 operon-containing gene cluster was ORF porin, catR1, catB1C1A1D, ORF1, and ORF2. Two ORFs located immediately downstream catD were most similar with two ORFs in cat gene cluster of Acinetobacter calcoaceticus ADP1 but the gene structure of catR1B1C1A1 was closest to that found in Frateurua sp. ANA-18 or Pseudomonas putida PRS2000. CatA1 gene product was significantly overexpressed and detected in SDS-PAGE when four cat1 genes (catB1C1A1D) were placed under the control of a lac promoter in pUC118 while overexpressions of other cat genes were accomplished under the control of a lac promoter in pET vector system. All gene products were verified by N-terminal amino acid sequencing. Gel retardation assay revealed that the putative regulatory gene activator CatR1 for the catB1C1A1 operon could bind the promoter region of catB2 as well as catB1, suggesting that transcription of catB1 or catB2 might be controlled by the putative gene activator CatR1. However, the promoter regions of catA1 and catA2 were found to have no affinity with catR1.

Acinetobacter↗
PubMed1998

Functional characterization of the low-molecular-mass phosphotyrosine-protein phosphatase of Acinetobacter johnsonii.

The ptp gene of Acinetobacter johnsonii was previously reported to encode a low-molecular-mass protein, Ptp, whose amino acid sequence, predicted from the theoretical analysis of the nucleotide sequence of the gene, exhibits a high degree of similarity with those of different eukaryotic and prokaryotic phosphotyrosine-protein phophatases. We have now overexpressed the ptp gene in Escherichia coli cells, purified the Ptp protein to homogeneity by a single-step chromatographic procedure, and analysed its functional properties. We have shown that Ptp can catalyse the dephosphorylation of p-nitrophenyl phosphate and phosphotyrosine, but has no effect on phosphoserine or phosphothreonine. Its activity is blocked by ammonium molybdate and sodium orthovanadate, which are strong inhibitors of phosphotyrosine-protein phosphatases, as well as by N-ethylmaleimide and iodoacetic acid. Such specificity of Ptp for phosphotyrosine has been confirmed by the observation that it can dephosphorylate endogenous proteins phosphorylated on tyrosine, but not proteins modified on either serine or threonine. In addition, Ptp has been shown to quantitatively dephosphorylate two exogenous peptides, derived respectively from leech hirudin and human gastrin, previously phosphorylated on tyrosine. Moreover, site-directed mutagenesis experiments performed on Cys11 and Arg16, which are both present in the sequence motif (H/V)C(X5)R(S/T) typical of eukaryotic phosphotyrosine-protein phosphatases, have demonstrated that each amino acid residue is essential for the catalytic activity of Ptp. Taken together, these data provide evidence that Ptp is a member of the phosphotyrosine-protein phosphatase family. Furthermore, in search for the biological function of Ptp, we have found that it can specifically dephosphorylate an endogenous protein kinase, termed Ptk, which is known to autophosphorylate at multiple tyrosine residues in the inner membrane of Acinetobacter johnsonii cells. This represents the first identification of a protein substrate for a bacterial phosphotyrosine-protein phosphatase, and therefore constitutes a possible model for analysing the role of reversible phosphorylation on tyrosine in the regulation of microbial physiology.

Acinetobacter↗
PubMed1993

Metal resistance in Acinetobacter and its relation to beta-lactamase production.

Thirty nine clinical isolates of Acinetobacter belonging to six species were tested for resistance to 20 metal ions and their ability to produce beta-lactamase. Fifty two percent of the strains produced beta-lactamase. beta-Lactamase producers and non-producers were almost equally distributed in the different species. A. baumannii was the predominant biotype and was found to be most resistant to metals. Resistance to mercury was prevalent in beta-lactamase-producing A. baumannii only. Silver resistant strains of A. baumannii produced beta-lactamase. Sensitivity and resistance to copper and cadium was equally distributed between beta-lactamase producers and non-producers. beta-Lactamase-producer and -non-producer strains were uniformly sensitive to cadmium except Acinetobacter genospecies 1.

Acinetobacter↗
PubMed1995

The glucose dehydrogenase-mediated energization of Acinetobacter calcoaceticus as a tool for evaluating its susceptibility to, and defence against, hazardous chemicals.

Cells of Acinetobacter calcoaceticus 69-V could be energized by glucose oxidation after the growth on acetate, ethanol, hexanol and benzoate. The velocities of glucose oxidation-driven ATP syntheses were relatively constant in the range from pH 5.4 to 7.5. With decreasing pH values (7.0, 6.0, 5.4) ATP synthesis was inhibited more strongly by the action of 2,4-dinitrophenol and at the same pH value glucose oxidation was nearly unimpaired or inhibited more weakly. This finding is expressed by a decrease of the P/O ratios, indicating the uncoupling of the electron-transport phosphorylation by 2,4-dinitrophenol. The sensitivity towards this uncoupling effect was higher in ethanol-grown cells of Acinetobacter calcoaceticus 69-V than in hexanol- or acetate-grown cells. This increase in sensitivity was accompanied by a decrease of the ratio of saturated (mainly C16:0) to unsaturated (C16:1, C18:1) fatty acids in ethanol-grown cells compared with hexanol-grown ones. The knowledge of such differences in the susceptibility and its molecular background, e.g. possible substrate-induced changes of the fatty acid composition of the cytoplasmic membranes, should help elucidate mechanisms of poisoning by membrane-active hazardous chemicals and develop defence strategies.

2,4-Dinitrophenol↗
PubMed1995

Acinetobacter calcoaceticus liberates chromosomal DNA during induction of competence by cell lysis.

A transformation assay was used to assay the amount of DNA present in the extracellular medium of a growing culture of Acinetobacter calcoaceticus. It was observed that small amounts of DNA were liberated during the entire exponential growth phase in a batch culture. Release of DNA could be fully accounted for by lysis of cells. Lysis was quantified via simultaneous measurement of beta-galactosidase activity of cells and supernatant, with a strain that contained a plasmid (pAPA100) with lacZ under control of a constitutive beta-lactamase promoter. In conclusion, no evidence could be obtained indicating that Acinetobacter calcoaceticus actively excretes DNA, to be used for DNA exchange.

Acinetobacter calcoaceticus↗