[Carbapenem resistance and Acinetobacter baumannii].
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Acinetobacter Infections↗
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PER-1 type beta-lactamase production in Acinetobacter baumannii is related to cell adhesion.
BACKGROUND: Recently, the dissemination of ESBL (PER-1) among Acinetobacter isolates was reported in Turkish hospitals. We investigated the presence and the association of various virulence determinants in 20 Acinetobacter baumannii isolates, of which 13 were blaPER-1 positive. MATERIAL/METHODS: Virulence tests were slime and hemolysin production, gelatinase and protease activity, biofilm formation, and Caco2 cell adhesion. RAPD analysis was also performed with ERIC primers. RESULTS: None of the strains was positive for slime or hemolysin production and gelatinase or protease activity. A total of 16 strains, five of which were PER-1 gene negative, formed a biofilm on polymer surfaces. There was no relation between the presence of the PER gene and biofilm formation. On the other hand, nine strains (all PER-1 gene positive) were positive in adhesion experiments to Caco2 cell lines. All PER-negative strains were negative for cell adhesion. CONCLUSIONS: This study indicates the existence of a relation between PER-1 gene and cell adhesion in Acinetobacter strains.
Acinetobacter baumannii↗
Corneal ulcer of the side port after phacoemulsification induced by Acinetobacter baumannii.
A 75-year-old man had clear corneal phacoemulsification using a temporal approach in the left eye. Two months after surgery, a focal corneal epithelial defect developed with infiltration near the lower limbus on the site of the side-port incision. The culture of corneal scrapping grew Acinetobacter baumannii, which is resistant to most ordinary antibiotics in sensitivity tests. After appropriate antibiotic treatment, the ulcer healed gradually with vessel ingrowth. Acinetobacter baumannii is usually found in nosocomial infection of immune-compromised patients in the intensive care unit. It is a rare pathogen of infectious keratitis. Our case, with its unusual infection site, may point to potential risk factors for this pathogen.
Acinetobacter↗
Investigation of a nosocomial outbreak of imipenem-resistant Acinetobacter baumannii producing the OXA-23 beta-lactamase in korea.
We investigated an outbreak of Acinetobacter baumannii in an intensive care unit and in the surgery, medicine, neurology, and urology wards of the Kosin University Gospel Hospital in Busan, Korea. The outbreak involved 36 cases of infection by A. baumannii producing the OXA-23 beta-lactamase over an 8-month period and was caused by a single pulsed-field gel electrophoresis clone. The epidemic isolates were characterized by a modified cloverleaf synergy test. Isoelectric focusing of crude bacterial extracts detected one nitrocefin-positive band with a pI value of 6.65. PCR amplification and characterization of the amplicons by direct sequencing indicated that the epidemic isolates carried a bla(OXA-23) determinant. The epidemic isolates were characterized by a multidrug resistance phenotype that remained unchanged over the outbreak, including penicillins, cephamycins, extended-spectrum cephalosporins, carbapenems, monobactams, and aminoglycosides. This study shows that the bla(OXA-23) resistance determinant may become an emerging therapeutic problem.
Acinetobacter baumannii↗
Genetic structures at the origin of acquisition and expression of the carbapenem-hydrolyzing oxacillinase gene blaOXA-58 in Acinetobacter baumannii.
Genetic structures surrounding the carbapenem-hydrolyzing oxacillinase gene blaOXA-58 were characterized in a series of OXA-58-positive Acinetobacter baumannii strains isolated from different countries. We showed that in most of the cases, acquisitions of the blaOXA-58-containing overall structure, including insertion sequence elements, may be likely the results of recombination events. In type strain A. baumannii MAD, the genetic structure surrounding the blaOXA-58 gene was bracketed by two 27-bp repeated sequences. The isolation of a clonally related OXA-58-negative A. baumannii isolate that possessed the same plasmid backbone as A. baumannii MAD but lacked this genetic structure indicated that the mechanism of acquisition could be reversible. Parts of the structure identified in A. baumannii MAD were conserved in other blaOXA-58-positive isolates from various European countries. Primer extension experiments showed that blaOXA-58 expression was related to promoter sequences brought by different insertion sequence elements, such as an ISAba3-like element, ISAba1, ISAba2, and IS18. This work identified novel structures at the origin of acquisition and expression of a carbapenem-hydrolyzing beta-lactamase identified in non-clonally related A. baumannii isolates.
Acinetobacter baumannii↗
The reductase of p-hydroxyphenylacetate 3-hydroxylase from Acinetobacter baumannii requires p-hydroxyphenylacetate for effective catalysis.
p-Hydroxyphenylacetate (HPA) hydroxylase (HPAH) from Acinetobacter baumannii catalyzes hydroxylation of HPA to form 3,4-dihydroxyphenylacetate. It is a two-protein system consisting of a smaller reductase component (C(1)) and a larger oxygenase component (C(2)). C(1) is a flavoprotein containing FMN, and its function is to provide reduced flavin for C(2) to hydroxylate HPA. We have shown here that HPA plays important roles in the reaction of C(1). The apoenzyme of C(1) binds to oxidized FMN tightly with a K(d) of 0.006 microM at 4 degrees C, but with a K(d) of 0.038 microM in the presence of HPA. Reduction of C(1) by NADH occurs in two phases with rate constants of 11.6 and 3.1 s(-)(1) and K(d) values for NADH binding of 2.1 and 1.5 mM, respectively. This result indicates that C(1) exists as a mixture of isoforms. However, in the presence of HPA, the reduction of C(1) by NADH occurred in a single phase at 300 s(-)(1) with a K(d) of 25 microM for NADH binding at 4 degrees C. Formation of the C(1)-HPA complex prior to binding of NADH was required for this stimulation. The redox potentials indicate that the rate enhancement is not due to thermodynamics (E degrees (m) of the C(1)-HPA complex is -245 mV compared to an E degrees (m) of C(1) of -236 mV). When the C(1)-HPA complex was reduced by 4(S)-NADH, the reduction rate was changed from 300 to 30 s(-)(1), giving a primary isotope effect of 10 and indicating that C(1) is specifically reduced by the pro-(S)-hydride. In the reaction of reduced C(1) with oxygen, the reoxidation reaction is also biphasic, consistent with reduced C(1) being a mixture of fast and slow reacting species. Rate constants for both phases were the same in the absence and presence of HPA, but in the presence of HPA, the equilibrium shifted toward the faster reacting species.
Acinetobacter baumannii↗
The sequences of seven class D beta-lactamases isolated from carbapenem-resistant Acinetobacter baumannii from four continents.
Carbapenem resistance associated with class D beta-lactamases is an increasing problem in Acinetobacter baumannii. Most enzymes of this class reported so far belong to two subgroups, 1 and 2; however, a novel class D carbapenemase (OXA-51) has been reported recently which shares 56% and < 63% amino-acid identity with subgroups 1 and 2, respectively, and which belongs to a third subgroup. This study describes a further seven novel subgroup 3 beta-lactamases in carbapenem-resistant A. baumannii isolates from four continents.
Acinetobacter baumannii↗
Antibiotic-resistant Acinetobacter baumannii can be killed by a combination of bacteriophages and complement.
Infections caused by multidrug-resistant Acinetobacter baumannii are an emerging global health threat. Although phages have shown promising results in treating bacterial infections, the mechanisms of the combined effect of phages and innate immunity on clearing A. baumannii remain unclear. Here, we report a synergistic effect of the complement system and phages on clearing multidrug-resistant A. baumannii. We show that A. baumannii rapidly adapts and becomes resistant to phage or serum complement by modifying the expression of capsule and lipooligosaccharides, which can be regulated through reversible transposon mutagenesis in the K locus. Compared to the encapsulated phenotype, the non-encapsulated, phage-resistant A. baumannii showed a higher level of membrane attack complex deposition and were susceptible to killing by complement. In contrast, the encapsulated phenotype escaped the complement system by shedding the membrane attack complex to the environment. Thus, while the complement system targets the non-encapsulated phenotype, the phage infects and eliminates the encapsulated subpopulation. These results suggest means of combatting antibiotic-resistant A. baumannii by a simultaneous treatment with phages and complement, a combination which can be supplemented further with antibacterial antibodies.
Acinetobacter baumannii↗
bla(OXA-51)-type beta-lactamase genes are ubiquitous and vary within a strain in Acinetobacter baumannii.
We investigated the spread of bla(OXA-51)-type beta-lactamase genes in 200 Acinetobacter spp. clinical strains isolated in Argentina from 1982 to 2005. bla(OXA-51)-type genes were present in all Acinetobacter baumannii isolates tested (n=194), whereas they were not detected in two Acinetobacter haemolyticus, two genomic species 10 or two Acinetobacter lwoffii isolates. The bla(OXA-51)-type alleles varied within a strain and were found in six different A. baumannii pulsed-field gel electrophoresis clones that were susceptible or resistant to imipenem, suggesting a controversial role in imipenem resistance. Our findings agree with previous reports showing that bla(OXA-51)-type genes are naturally harboured by A. baumannii isolates from various geographical origins and support the presence of a direct reservoir of beta-lactam resistance genes within the nosocomial environment.
Acinetobacter baumannii↗
Acinetobacter baumannii: emergence and spread in Israeli hospitals 1997-2002.
The incidence of multi-drug-resistant Acinetobacter baumannii bloodstream infections (BSIs) increased two- to four-fold in three Israeli hospitals between 1997 and 2002, accounting for 3.5-18% of all hospital-acquired BSIs. This was associated with increasing carbapenem resistance reaching 35-54%, and by a dramatic increase in carbapenem consumption. In-hospital fatality rates ranged between 47% and 58% and were significantly higher than those seen with other nosocomial Gram-negative pathogens. A. baumannii was not restricted to intensive care units, but had spread to all hospital wards. Multi-drug-resistant A. baumannii has the potential to reach endemicity in hospitals and warrants more vigorous and innovative efforts to limit its spread.
Acinetobacter Infections↗
Use of macrorestriction analysis to demonstrate interhospital spread of multiresistant Acinetobacter baumannii in São Paulo, Brazil.
We evaluated the spread of Acinetobacter baumannii strains among three hospitals located in São Paulo, Brazil. A total of 46 isolates, which were typed by chromosomal DNA analysis with use of pulsed field gel electrophoresis (PFGE), were tested for susceptibility to the fluoroquinolones, carbapenems, aminoglycosides (amikacin), cephalosporins, polymyxin B, and ampicillin/sulbactam by means of the broth microdilution method, disk diffusion, and the E-test. Isolates with an identical PFGE pattern (pattern B) that were susceptible only to carbapenems, polymyxin B, and ampicillin/ sulbactam were recovered in all three hospitals. In addition, isolates with PFGE pattern A that were susceptible only to polymyxin B and ampicillin/sulbactam were recovered in hospitals 1 and 2. The results of our study strongly suggest the interhospital transmission of multiresistant epidemic strains of A. baumannii in São Paulo. Once in the hospital, these strains can disseminate and cause outbreaks with devastating consequences.
Acinetobacter↗
Comparison of antimicrobial resistance of Acinetobacter baumannii clinical isolates from Shanghai and Hong Kong.
OBJECTIVE: To compare the antimicrobial resistance patterns of Acinetobacter baumannii isolates from Shanghai and Hong Kong. MATERIALS AND METHODS: A total of 212 A. baumannii strains of one isolate per patient were collected from Shanghai and Hong Kong from August 2002 to August 2003 that were tested against 15 commonly used antimicrobial agents by the agar dilution method according to the NCCLS guidelines. RESULTS: Most beta-lactams showed no significant increase in activity after adding beta-lactamase inhibitors. The resistance rates of the isolates against ticarcillin-clavulanate, piperacillin-tazobactam and ampicillin-sulbactam were for Shanghai 74.9, 70.9, 69.1% and Hong Kong 24.3, 18.9, 13.5%, respectively. Only cefoperazone-sulbactam showed a significant increase in activity against both Shanghai and Hong Kong strains, as the resistance rates dropped from 93.7 to 8.6% and 83.8 to 5.4%, respectively. The resistance rates of ceftazidime, cefepime, and gentamicin against Shanghai strains were 69.7, 72.0, 73.7% and Hong Kong strains 69.7, 29.7, 18.9%, respectively. About 65% of Shanghai strains were found to be amikacin-resistant, however, all Hong Kong strains were sensitive. Fluoroquinolones including ciprofloxacin and levofloxacin had resistance rates over 60% against Shanghai strains, but only 13.5% against Hong Kong strains. Shanghai strains had imipenem and meropenem resistance rate of 6.3%. Though 10.8% Hong Kong strains were resistant to meropenem, only 2.7% of them were resistant to imipenem. CONCLUSION: A. baumannii isolated from Shanghai were more resistant to all drugs except meropenem than Hong Kong isolates. The results indicate a need for measures to control the abuse of antibiotic usage in order to prevent the emergence of more multidrug-resistant isolates in both cities.
Acinetobacter baumannii↗
[Acinetobacter baumannii pandrug-resistant: update in epidemiological and antimicrobial managing issues].
In the last two decades Acinetobacter baumannii has emerged as a major relevant world nosocomial pathogen. A. baumannii can be a causal agent of diseases like pneumonia, bacteremia, meningitis, soft tissue and urinary tract infections, associating to high mortality. Several national and foreign communications reveal the isolation of A. baumannii resistant to almost all commercially available antimicrobial agents, drastically limiting the therapeutic options. To optimize the therapy of these infections, the need of development of new antibacterial agents is raised as is the revival of certain forgotten compounds, as the polymyxins. In order to check and evaluate the information on the management of multi-resistant A. baumannii infections, we performed a systematical review of the medical scientific literature, that included Medline and LILACS, identifying and categorizing the clinical relevancy of the sources gathered to the date of this investigation. Clinically relevant epidemiological aspects, microbiological information and clinical studies in patients with pandrug (AB-PDR) or multidrug resistant (AB-MDR) A. baumannii infections were reviewed. The response adapted to the management of AB-PDR infection is complex, its eradication needs adherence to suitable practices of infection control and the prudent and effective use of antimicrobial therapy. Potential options of therapy could be colistin, betalactam associations with sulbactam and tetracyclines, but there are no random and controlled studies in the matter.
Acinetobacter Infections↗
Endemic carbapenem resistance associated with OXA-40 carbapenemase among Acinetobacter baumannii isolates from a hospital in northern Spain.
Eighty-two carbapenem-resistant isolates of Acinetobacter baumannii from a single hospital in Bilbao were typed into two major clusters and several subclusters. Disk synergy tests and PCR indicated the production of a zinc-independent OXA-class carbapenemase. Sequencing identified this enzyme, OXA-40, as a variant of the OXA-24-OXA-25-OXA-26 cluster.
Acinetobacter Infections↗
Emergence of carbapenem resistance in Acinetobacter baumannii recovered from blood cultures in Australia.
We describe the first emergence of carbapenem-resistant Acinetobacter baumannii in Australia. Ninety A. baumannii isolates recovered from cultures of blood specimens from 69 patients were analyzed. Overall, 58 isolates (64%) were resistant to meropenem. The chi 2 test for linear trend revealed that emergence of carbapenem resistance was statistically significant during the 32-month study period. Selected isolates were of the same clonal type, and no genes encoding carbapenemases were identified.
Acinetobacter baumannii↗
Genomic fingerprinting Acinetobacter baumannii: amplification of multiple inter-repetitive extragenic palindromic sequences.
Acinetobacter species are important nosocomial pathogens. A rapid and sensitive identification system, capable of providing strain identity at the genetic level, is required to identify outbreak strains and facilitate the early implementation of infection control procedures. Repetitive extragenic palindromic (REP) elements, have been identified in numerous bacteria and these genomic sequences provide useful targets for DNA amplification. A method for amplifying inter-REP DNA sequences, REP-multiple arbitrary amplicon profiling (REP-MAAP), is described and applied to 29 Acinetobacter baumannii from clinical samples. Amplified polymorphic DNA patterns were demonstrated for all isolates and those displaying identical REP-MAAP patterns were considered identical at the genetic level. In the spring of 1993, 10 intensive care unit patients had endotracheal colonization with A. baumannii (five with REP-MAAP I and five with REP-MAAP II patterns). These findings suggested nosocomial transmission of organisms which was terminated by standard infection control measures. No further A. baumannii were detected until the winter of 1993 when isolates of different REP-MAAP groups emerged, suggesting that factors other than nosocomial transmission were implicated.
Acinetobacter↗
Risk factors for acquisition of imipenem-resistant Acinetobacter baumannii: a case-control study.
Risk factors for the nosocomial occurrence of imipenem-resistant Acinetobacter baumannii (IRAB) were determined. A case-control study design was used for a comparison of two groups of A. baumannii-positive patients with control patients. Nosocomial IRAB was isolated from the first group of A. baumannii-positive patients, and imipenem-susceptible A. baumannii (ISAB) was isolated from the second group. The control patients were randomly selected in a 4:1 ratio from the same medical or surgical services from which the A. baumannii-positive patients were receiving care when the isolation of IRAB occurred. Risk factors analyzed included demographic variables, comorbid conditions, variables related to hospitalization, and the antimicrobials used. IRAB was isolated from 104 patients, and ISAB was isolated from 387 patients between January and December 2000. The risk factors for IRAB were a previous intensive care unit (ICU) stay (odds ratio [OR], 21.54; 95% confidence interval [CI], 10.73 to 43.23) and prior exposure to imipenem (OR, 9.18; 95% CI, 3.99 to 21.13) or third-generation cephalosporins (OR, 2.11; 95% CI, 1.13 to 3.95). Risk factors for ISAB were a previous ICU stay (OR, 8.05; 95% CI, 5.67 to 11.44) and exposure to third-generation cephalosporins (OR, 2.07; 95% CI, 1.47 to 2.91). Our results suggest that the nosocomial occurrence of IRAB or ISAB is strongly related to an ICU stay, and IRAB occurrence may be favored by the selection pressure of imipenem.
Acinetobacter Infections↗
Survival of Acinetobacter baumannii on dry surfaces: comparison of outbreak and sporadic isolates.
Acinetobacter spp. are important nosocomial pathogens reported with increasing frequency in outbreaks of cross-infection during the past 2 decades. The majority of such outbreaks are caused by Acinetobacter baumannii. To investigate whether desiccation tolerance may be involved in the ability of certain strains of A. baumannii to cause hospital outbreaks, a blind study was carried out with 39 epidemiologically well-characterized clinical isolates of A. baumannii for which survival times were determined under simulated hospital conditions. The survival times on glass coverslips of 22 strains isolated from eight well-defined hospital outbreaks in a German metropolitan area were compared with the survival times of 17 sporadic strains not involved in outbreaks but rather isolated from inpatients in the same geographic area. All sporadic isolates have been shown by pulsed-field gel electrophoresis to represent different strain types. There was no statistically significant difference between the survival times of sporadic strains of A. baumannii and outbreak strains (27.2 versus 26.5 days, respectively; P < or = 0.44) by the Wilcoxon-Mann-Whitney test. All investigated A. baumannii strains, irrespective of their areas of endemicity or epidemic occurrence, have the ability to survive for a long time on dry surfaces. Antimicrobial susceptibility testing showed that A. baumannii outbreak strains were significantly more resistant to various broad-spectrum antimicrobial agents than sporadic strains. Both desiccation tolerance and multidrug resistance may contribute to their maintenance in the hospital setting and may explain in part their propensity to cause prolonged outbreaks of nosocomial infection.
Acinetobacter↗