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PubMed2005

Characterization of the naturally occurring oxacillinase of Acinetobacter baumannii.

A chromosomally encoded oxacillinase, OXA-69, was characterized from Acinetobacter baumannii AYE. beta-Lactamase OXA-69 shared 97% amino acid identity with the recently described OXA-51 enzyme of A. baumannii and 62 and 56% amino acid identity with the carbapenem-hydrolyzing oxacillinases OXA-24 and OXA-23, respectively. Biochemical characterization of the purified OXA-69 revealed a narrow-spectrum hydrolysis profile but including, at a low level, imipenem and meropenem. By PCR and sequencing bla(OXA-69)-like genes were identified in all A. baumannii strains tested (n = 12), suggesting that this oxacillinase is naturally occurring in that species.

Acinetobacter baumannii↗

PubMed2006

Sequence and organization of pMAC, an Acinetobacter baumannii plasmid harboring genes involved in organic peroxide resistance.

Acinetobacter baumannii 19606 harbors pMAC, a 9540-bp plasmid that contains 11 predicted open-reading frames (ORFs). Cloning and transformation experiments using Acinetobacter calcoaceticus BD413 mapped replication functions within a region containing four 21-bp direct repeats (ori) and ORF 1, which codes for a predicted replication protein. Subcloning and tri-parental mating experiments mapped mobilization functions to the product of ORF 11 and an adjacent predicted oriT. Three ORFs code for proteins that share similarity to hypothetical proteins encoded by plasmid genes found in other bacteria, while the predicted products of three others do not match any known sequence. The product of ORF 8 is similar to Ohr, a hydroperoxide reductase responsible for organic peroxide detoxification and resistance in bacteria. This ORF is immediately upstream of a coding region whose product is related to the MarR family of transcriptional regulators. Disk diffusion assays showed that A. baumannii 19606 is resistant to the organic peroxide-generating compounds cumene hydroperoxide (CHP) and tert-butyl hydroperoxide (t-BHP), although to levels lower than those detected in Pseudomonas aeruginosa PAO1. Cloning and introduction of the ohr and marR ORFs into Escherichia coli was associated with an increase in resistance to CHP and t-BHP. This appears to be the first case in which the genetic determinants involved in organic peroxide resistance are located in an extrachromosomal element, a situation that can facilitate the horizontal transfer of genetic elements coding for a function that protects bacterial cells from oxidative damage.

Acinetobacter baumannii↗

PubMed2006

Genotypic diversity and antibiotic susceptibility of Acinetobacter baumannii isolates in a Bulgarian hospital.

A set of 18 Acinetobacter baumannii isolates, collected prospectively in a Bulgarian hospital during episodes of increased A. baumannii occurrence during 2000-2002, was investigated for genotypic diversity and antibiotic susceptibility. Four genotypes were identified by amplified fragment length polymorphism genomic fingerprinting, one of which (type 1) accounted for 13 isolates, indicating that a specific strain was predominant. The single isolate allocated to type 2 was identified to European clone I. All isolates were resistant to multiple antibiotics, but most retained susceptibility to tobramycin and colistin, and all except one were susceptible to imipenem.

Acinetobacter Infections↗

PubMed2003

Attachment to and biofilm formation on abiotic surfaces by Acinetobacter baumannii: involvement of a novel chaperone-usher pili assembly system.

Acinetobacter baumannii causes severe infections in compromised patients, survives on abiotic surfaces in hospital environments and colonizes different medical devices. In this study the analysis of the processes involved in surface attachment and biofilm formation by the prototype strain 19606 was initiated. This strain attaches to and forms biofilm structures on plastic and glass surfaces, particularly at the liquid-air interface of cultures incubated stagnantly. The cell aggregates, which contain cell stacks separated by water channels, formed under different culture conditions and were significantly enhanced under iron limitation. Electron and fluorescence microscopy showed that pili and exopolysaccharides are part of the cell aggregates formed by this strain. Electron microscopy of two insertion derivatives deficient in attachment and biofilm formation revealed the disappearance of pili-like structures and DNA sequencing analysis showed that the transposon insertions interrupted genes with the highest similarity to hypothetical genes found in Pseudomonas aeruginosa, Pseudomonas putida and Vibrio parahaemolyticus. Although the products of these genes, which have been named csuC and csuE, have no known functions, they are located within a polycistronic operon that includes four other genes, two of which encode proteins related to chaperones and ushers involved in pili assembly in other bacteria. Introduction of a copy of the csuE parental gene restored the adherence phenotype and the presence of pili on the cell surface of the csuE mutant, but not that of the csuC derivative. These results demonstrate that the expression of a chaperone-usher secretion system, some of whose components appear to be acquired from unrelated sources, is required for pili formation and the concomitant attachment to plastic surfaces and the ensuing formation of biofilms by A. baumannii cells.

Acinetobacter baumannii↗

PubMed2003

[Antibiotic resistance of Acinetobacter baumannii isolates: data from Ibni Sina Hospital for the year 2002].

Acinetobacter spp. have a special role in nosocomial infections. They usually colonize intensive care units and cause infections. Multiple antibiotic resistance is observed to be an important problem in Acinetobacter isolates in recent years. The aim of this study was to evaluate the susceptibilities of 277 Acinetobacter baumannii strains (99 blood, 71 abscess, 26 urine, 81 lower respiratory tract isolates) isolated from adult patients hospitalized in Ankara University Ibni Sina Hospital during one year period in 2002. The resistance rates of the strains against studied antibiotics were found as follows; 31.2% for netilmicin, 44.6% for sulbactam-cefoperazone, 53.6% for imipenem, 59.8% for amikacin, 59.9% for tobramycin, 74% for ciprofloxacin, 78% for gentamicin, 78.3% for ticarcillinclavulanate. 79.5% sulbactam-ampicillin, 82.3% for cotrimoxazole, 84.8% for ticarcillin, 87.3% for piperacillin-tazobactam, 88.1% for ceftazidime and 92.1% for piperacillin. When the isolates obtained from the reanimation unit were compared with the isolates obtained from the other hospital units, a significantly high level of resistance was found from the isolates obtained from the reanimation unit except netilmicin and sulbactam/cefoperazone. The high rate of in-vitro antibiotic resistance of the A. baumannii strains indicated the importance of controlled antibiotic usage and appliance of hospital infection control measures.

Acinetobacter Infections↗

PubMed2005

[Severe community-acquired Acinetobacter baumannii bacteremia with unknown foci].

We report an unusual case of Acinetobacter baumannii (A. baumannii) bacteremia in a man without significant comorbidities. A 50-year-old man who noticed a sudden onset of high fever was admitted to Kobe Nishi City Hospital. After the admission, his condition deteriorated rapidly with development of shock, anuria and agitation. Antibiotic therapy with meropenem and amikacin was begun for suspected septic shock along with the mechanical ventilation and continuous hemodialysis. Venous blood cultures yielded A. baumannii. No definite source of bacteremia was detected. Intensive medical management was effective, and he was discharged on the 27th day. While the most common source of infection that leads to A. baumannii bacteremia is in the respiratory tract, community-acquired bacteremia with unknown foci is considered rare.

Acinetobacter Infections↗

PubMed2006

Rifampicin/imipenem combination in the treatment of carbapenem-resistant Acinetobacter baumannii infections.

BACKGROUND: In the setting of a large endemic of Acinetobacter baumannii infections, treatment of those due to carbapenem-resistant strains, susceptible only to colistin, has become a major problem in our hospital during the past years. Successful results have been reported using colistin, but clinical experience with this antibiotic is limited. In our experimental studies using these strains in a mouse pneumonia model, the best results were observed with a combination of rifampicin and imipenem. METHODS: From July 2000 to September 2001, we performed a pilot study with patients suffering from serious infections due to carbapenem-resistant A. baumannii. Patients were treated with a rifampicin/imipenem combination and followed up prospectively. Cultures were repeated during and after treatment, and in vitro activity of rifampicin was monitored. Genotyping of these strains was performed by means of PFGE. RESULTS: Ten patients were selected: four with ventilator-associated pneumonia, and six with other infections (one catheter-related bacteraemia, five surgical infections). Three patients died, two of whom were considered therapeutic failures. In five of the seven patients who were cured, other procedures were also performed such as surgical drainage or catheter removal. In vitro development of high resistance to rifampicin was shown in seven (70%). PFGE demonstrated that initial isolates and high-resistant strains belonged to the same clones. CONCLUSIONS: The results of our study argue against the use of a rifampicin/imipenem combination for the treatment of carbapenem-resistant A. baumannii infections. However, combinations of rifampicin with other antibiotics merit further studies.

Acinetobacter Infections↗

PubMed2005

Outer membrane protein 38 of Acinetobacter baumannii localizes to the mitochondria and induces apoptosis of epithelial cells.

Acinetobacter baumannii is an important opportunistic pathogen responsible for nosocomial infection. Despite considerable clinical and epidemiological data regarding the role of A. baumannii in nosocomial infection, the specific virulence factor or pathogenic mechanism of this organism has yet to be elucidated. This study investigated the molecular mechanism of apoptosis on the infection of human laryngeal epithelial HEp-2 cells with A. baumannii and examined the contribution of outer membrane protein 38 (Omp38) on the ability of A. baumannii to induce apoptosis of epithelial cells. A. baumannii induced apoptosis of HEp-2 cells through cell surface death receptors and mitochondrial disintegration. The Omp38-deficient mutant was not as able to induce apoptosis as the wild-type A. baumannii strain. Purified Omp38 entered the cells and was localized to the mitochondria, which led to a release of proapoptotic molecules such as cytochrome c and apoptosis-inducing factor (AIF). The activation of caspase-3, which is activated by caspase-9, degraded DNA approximately 180 bp in size, which resulted in the appearance of a characteristic DNA ladder. AIF degraded chromosomal DNA approximately 50 kb in size, which resulted in large-scale DNA fragmentation. These results demonstrate that Omp38 may act as a potential virulence factor to induce apoptosis of epithelial cells in the early stage of A. baumannii infection.

Acinetobacter baumannii↗

PubMed2004

Nosocomial transmission of CTX-M-2 beta-lactamase-producing Acinetobacter baumannii in a neurosurgery ward.

Three strains of cefotaxime (CTX)-resistant Acinetobacter baumannii, FM0209680, FM0300106, and FM0301433, were isolated from transtracheal aspirate cultures of three patients with probable nosocomial infections in a neurosurgery ward in Japan. The CTX MICs for these isolates were greater than 128 microg/ml but were drastically reduced in the presence of 4 microg of clavulanic acid per ml. These strains were also resistant to ceftriaxone, cefpodoxime, and aztreonam but were susceptible to ceftazidime and imipenem. The profile of resistance to various broad-spectrum beta-lactams was transferred by conjugation. Strain FM0209680 was not eradicated from case patient 1 by administration of imipenem, ceftazidime, and levofloxacin, even after a 6-month hospitalization period. Strains FM0300106 and FM0301433 were isolated from case patients 2 and 3 during the sixth week following admission, respectively, and then each patient was colonized for 3 weeks. Eradication of FM0300106 was successfully obtained from case patient 2 by imipenem treatment, while administration of imipenem was continued to prevent pneumonia. Prophylactic antimicrobial therapy was discontinued in case patient 3 because of the lack of pneumonic symptoms, and FM0301433 disappeared after the discontinuation of antimicrobial chemotherapy. All three strains carried the bla(CTX-M-2) gene, and the appearance of colonies in the growth-inhibitory zones around disks of CTX and aztreonam in double-disk synergy tests suggested inducible beta-lactamase production in these A. baumannii strains. The ribotyping investigation suggested that all these strains belong to the same clonal lineage. The plasmids harbored by A. baumannii had the same restriction profile as those harbored by Proteus mirabilis strains previously isolated in a urology ward of the Funabashi Medical Center.

Acinetobacter Infections↗

PubMed2006

Carbapenem resistance in Acinetobacter baumannii: mechanisms and epidemiology.

The increasing trend of carbapenem resistance in Acinetobacter baumannii worldwide is a concern since it limits drastically the range of therapeutic alternatives. Metallo-beta-lactamases (VIM, IMP, SIM) have been reported worldwide, especially in Asia and western Europe, and confer resistance to all beta-lactams except aztreonam. The most widespread beta-lactamases with carbapenemase activity in A. baumannii are carbapenem-hydrolysing class D beta-lactamases (CHDLs) that are mostly specific for this species. These enzymes belong to three unrelated groups of clavulanic acid-resistant beta-lactamases, represented by OXA-23, OXA-24 and OXA-58, that can be either plasmid- or chromosomally-encoded. A. baumannii also possesses an intrinsic carbapenem-hydrolysing oxacillinase, the expression of which may vary, that may play a role in carbapenem resistance. In addition to beta-lactamases, carbapenem resistance in A. baumannii may also result from porin or penicillin-binding protein modifications. Several porins, including the 33-kDa CarO protein, that constitute a pore channel for influx of carbapenems, might be involved in carbapenem resistance.

Acinetobacter Infections↗

PubMed1999

PCR detection of aminoglycoside resistance genes: a rapid molecular typing method for Acinetobacter baumannii.

Aminoglycoside resistance is common among strains of Acinetobacter baumannii responsible for nosocomial infections, and inactivation of these antibiotics by enzymatic modification is the main mechanism. Different types of aminoglycoside acetyltransferases (AAC), nucleotidyltransferases (ANT), and phosphotransferases (APH) are synthesized by clinical isolates, and several enzymes can be produced by a single strain. Using a multiplex PCR procedure carried out on bacterial thermolysates, we analyzed the aminoglycoside resistance gene content of strains belonging to eight clusters identified by pulsed-field gel electrophoresis. In a single reaction were combined three primer pairs in order to amplify the genes coding for AAC(6')-Ih, AAC(3)-I, and AAC(3)-II, three primer pairs for the genes coding for ANT(2'')-I, APH(3')-VI, and rRNA 16S as internal control, and finally two primer pairs for the genes coding for AAC(6')-Ib and APH(3')-I. According to the aminoglycoside resistance gene patterns, the strains of the eight clusters were distributed into seven classes. This simple and rapid (< 8 h) fingerprinting technique could be a useful tool for the epidemiological investigation of A. baumannii nosocomial infections.

Acetyltransferases↗

PubMed2004

Outbreak of nosocomial meningitis caused by Acinetobacter baumannii in neurosurgical patients.

An outbreak of nosocomial meningitis caused by Acinetobacter baumannii, which developed postoperatively in seven neurosurgical patients is described. The clinical isolates of A. baumannii were typed by biochemical profiles and antibiogram patterns, and by random amplified polymorphic DNA polymerase chain reaction (RAPD-PCR) and amplified fragment length polymorphism (AFLP) fingerprinting. The implicated strain was multi-drug resistant, however, susceptibility to imipenem and netilmicin was detected. An extensive search for the environmental source of the epidemic strain was carried out. Two of several isolates from hospital environment, corresponded to the A. baumannii outbreak strain, one being cultured from the suctioning equipment used in the care of these patients. The introduction of multiresistant epidemic A. baumannii into a neurosurgical unit is a severe risk factor for patients undergoing neurosurgical procedures. Genotypic typing methods are important for definitive identification of these strains in patients and their environment.

Acinetobacter Infections↗

PubMed2003

[Community-acquired Acinetobacter baumannii pneumonia].

OBJECTIVES: Description of two cases of community-acquired Acinetobacter baumannii pneumonia. PATIENTS AND METHODS: Two patients, one with a history of diabetes mellitus type 2 and pulmonary thromboembolism 2 years earlier and the second without known risk factors except for the age, were admitted to hospital because of community-acquired A. baumannii pneumonia with cavitation and with favorable final evolution. CONCLUSION: A. baumannii is an infrequent cause of community-acquired pneumonia, although it should be suspected in patients with debilitating illness and in patients who do not evolve favorably on the first days of the admission with conventional treatment.

Acinetobacter Infections↗

PubMed2003

Considerations in control and treatment of nosocomial infections due to multidrug-resistant Acinetobacter baumannii.

We sought to control infection due to multidrug-resistant Acinetobacter baumannii (MDR-Ab) by identifying isolates as clonally related, leading to enhanced infection-control measures, including cohorting, surveillance, contact precaution, initial therapy with ampicillin/sulbactam and local polymyxin B, and, more recently, therapy with synergistic antibiotic combinations. Class restriction of cephalosporins has been associated with a reduction in cephalosporins-cephamycin-carbapenem resistance among nosocomial Klebsiella isolates. This has been supplemented by restriction of carbapenem use after an initial 24-h period in an effort to reduce the selection of porin-deficient, carbapenem-resistant A. baumannii and Pseudomonas aeruginosa. Evidence is reviewed suggesting that eradication of MDR-Ab nosocomial colonization may prevent subsequent infection. Relatively few standard antibacterial drugs remain active against MDR-Ab. Published clinical results of therapy with these agents are reviewed, and in vitro evidence of synergy between them is presented that suggests that combination therapy should be studied for enhanced clinical activity.

Acinetobacter Infections↗

PubMed2003

Identification of an epidemic carbapenem-resistant Acinetobacter baumannii strain at hospitals in Buenos Aires City.

To identify epidemic Acinetobacter baumannii (AB) clones, 38 carbapenem-resistant AB isolates from 5 hospitals were analyzed. Macrorestriction classified 24 isolates as clone IV, susceptibility pattern clustering analysis grouped almost all of them together, and they were uniformly biotype 8. Clone IV was present at all 5 hospitals, so that it represents a carbapenem-resistant AB strain with epidemic behavior.

Acinetobacter Infections↗

PubMed2006

Outbreak of infection by carbapenem-resistant Acinetobacter baumannii producing the carbapenemase OXA-58 in Belgium.

Carbapenem-resistant Acinetobacter baumannii isolates were obtained from 17 patients between September 2004 and August 2005 at the Academisch Ziekenhuis Vrije Universiteit Brussel, Brussels, Belgium. These multidrug-resistant isolates, which belonged to a single clone, remained susceptible to colistin and tigecycline only and produced the carbapenem-hydrolyzing oxacillinase OXA-58. This study highlights the importance of the intercountry spread of this beta-lactamase-mediated resistance mechanism and its epidemic evolution.

Acinetobacter Infections↗

PubMed2006

VEB-1 Extended-spectrum beta-lactamase-producing Acinetobacter baumannii, France.

VEB-1 extended-spectrum beta-lactamase-producing Acinetobacter baumannii was responsible for an outbreak in hospitals in France. A national alert was triggered in September 2003 when 4 hospitals reported clusters of A. baumannii infection with similar susceptibility profiles. Case definitions and laboratory guidelines were disseminated, and prospective surveillance was implemented; strains were sent to a single laboratory for characterization and typing. From April 2003 through June 2004, 53 hospitals reported 290 cases of A. baumannii infection or colonization; 275 isolates were bla(VEB-1)-positive and clonally related. Cases were first reported in 5 districts of northern France, then in 10 other districts in 4 regions. Within a region, interhospital spread was associated with patient transfer. In northern France, investigation and control measures led to a reduction of reported cases after January 2004. The national alert enabled early control of new clusters, demonstrating the usefulness of early warning about antimicrobial drug resist.

Acinetobacter Infections↗

PubMed2005

Concurrent outbreak of multidrug-resistant and susceptible subclones of Acinetobacter baumannii affecting different wards of a single hospital.

BACKGROUND AND OBJECTIVE: Acinetobacter baumannii has emerged as an opportunistic pathogen among acutely ill patients, especially those with thermal injury. A prospective 8-month study was conducted to describe the clinical and molecular epidemiology of multidrug-resistant A. baumannii affecting a single hospital. METHODS: Univariate analysis comparing SmaI macrorestriction patterns of A. baumannii generated by pulsed-field gel electrophoresis (PFGE) versus clinical and demographic risk factors. RESULTS: A total of 200 isolates from 76 patients were collected, of which 185 isolates from 76 patients were analyzed by PFGE. A total of 17 distinct PFGE clonal types were identified. One clonal type (strain A) represented 129 isolates from 49 patients. A group of related clonal types (strain A variants) were identified as 40 isolates from 20 patients. The only risk factor other than geographic location associated with the presence of strain A was prior treatment with antibiotics active against gram-negative bacteria (P = .0015). The two clonal types differed in antibiotic resistance profiles: 25% of strain A isolates, the dominant strain in the burn unit, were susceptible to at least one antibiotic tested. In contrast, approximately 80% of the other strain types were susceptible to at least one antibiotic and were cultured from patients admitted elsewhere in the hospital. No combination of antibiotics was observed to yield additive or synergistic activity. CONCLUSION: Clonally related strains of Acinetobacter that differ in susceptibility patterns may coexist within a single hospital, dependent on the selective pressure related to antibiotic exposure.

Acinetobacter Infections↗