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PubMed2004

Morphological changes induced by imipenem and meropenem at sub-inhibitory concentrations in Acinetobacter baumannii.

Abstract Sub-inhibitory concentrations of imipenem and meropenem were evaluated for their ability to induce morphological changes with six strains of Acinetobacter baumannii isolated from patients with nosocomial pneumonia. Three strains were susceptible and three were resistant to carbapenems. The strains were grown in the presence of 0 (controls), 0.25x, 0.5x and 1x the MIC of both carbapenems for 4 h, and then examined after Gram's stain. Cells > or = 3 microm in size (spheroplasts) were considered to be altered. Both carbapenems induced significant numbers of spheroplasts compared to controls. Imipenem had more effect against susceptible strains, while meropenem had a greater effect against resistant strains.

Acinetobacter baumannii↗

PubMed2006

Multicity outbreak of carbapenem-resistant Acinetobacter baumannii isolates producing the carbapenemase OXA-40.

During 2005 we detected a multicity outbreak of infections or colonization due to high-level imipenem-resistant Acinetobacter baumannii (MIC, 64 microg/ml). One hundred isolates from diverse sources were obtained from seven acute-care hospitals and two extended-care facilities; 97% of the isolates belonged to one clone. Susceptibility testing of the first 42 isolates (January to April 2005) revealed broad resistance profiles. Half of the isolates were susceptible to ceftazidime, with many isolates susceptible only to colistin. The level of AmpC beta-lactamase expression was stronger in isolates resistant to ceftazidime. PCR and subsequent nucleotide sequencing analysis identified bla(OXA-40). The presence of an OXA-40 beta-lactamase in these isolates correlated with the carbapenem resistance. By Southern blot analysis, a bla(OXA-40)-specific probe revealed that the gene was both plasmid and chromosomally located. This is the first time in the United States that such carbapenem resistance in A. baumannii has been attributable to a carbapenemase.

Acinetobacter Infections↗

PubMed2006

[Factors predicting metallo-beta-lactamase-producing Acinetobacter baumannii in Iwate Medical University Hospital].

We conducted a decision tree analysis in which 6 isolates of metallo-beta-lactamase (MBL) -producing Acinetobacter baumannii detected by a sodium mercaptoacetic acid disk method and 38 isolates of MBL nonproducing A. baumannii were investigated from January 2003 to December 2003 in Iwate Medical University Hospital. Factors predicting MBL-producing A. baumannii were analyzed from the clinical backgrounds such as laboratory data, therapeutic histories and bacterial circumstances. In the decision tree analysis, seven significant rules were found for predicting MBL-producing A. baumannii; previous isolation of P. aeruginosa, administration period of 3rd generation cephem antibiotics > 11 days, both TP < or = 6.9 g/dl and Hb < or = 6.3 g/dl, both administration of anticancer drugs and a use of respirator, TP > 6.9 g/dl, CRP > 22.7 mg/dl, both CRP 8.7 mg/dl and body temperature > 36.6 degrees C. Two cases, which were matched with the rule of TP > 6.9 g/dl, were hospitalized in the same division, and their pulsed-field gel electrophoresis patterns were identical. In comparison with conventional statistical analysis, the decision tree analysis has advantages in explaining the tendencies and the relationships of the data. It is possible that, based on the rules extracted in this study, we could issue precautions in preventing nosocomial MBL-producing strains even in the earlier stages when the number of these isolates are still small.

Acinetobacter baumannii↗

PubMed2002

An outbreak due to multiresistant Acinetobacter baumannii in a burn unit: risk factors for acquisition and management.

OBJECTIVES: To describe the investigation and management of an outbreak due to multiresistant Acinetobacter baumannii and to determine risk factors for acquisition of the organism. SETTING: A 14-bed regional burn unit in a Canadian tertiary-care teaching hospital. DESIGN: Case-control study with multivariate analysis of potential risk factors using logistic regression analysis. Surveillance cultures were obtained from the hospital environment, from noninfected patients, and from healthcare providers. RESULTS: A total of 31 (13%) of 247 patients with acute burn injuries acquired multiresistant A. baumannii between December 1998 and March 2000; 18 (58%) of the patients were infected. The organism was recovered from the hospital environment and the hands of healthcare providers. Significant risk factors for acquisition of multiresistant A. baumannii were receipt of blood products (odds ratio [OR], 10.8; 95% confidence interval [CI95], 3.4 to 34.4; P < .001); procedures performed in the hydrotherapy room (OR, 4.1; CI95, 1.3 to 13.1; P = .02); and increased duration of mechanical ventilation (OR, 1.1 per day; CI95, 1.0 to 1.1; P= .02). INTERVENTIONS: Improved compliance with hand hygiene, strict patient isolation, meticulous environmental cleaning, and temporary closure of the unit to new admissions. CONCLUSIONS: Acquisition of multiresistant A. baumannii was likely multifactorial, related to environmental contamination and contact with transiently colonized healthcare providers. Control measures addressing these potential sources of multiresistant A. baumannii were successful in terminating the outbreak. Ongoing surveillance and continued attention to hand hygiene and adequate environmental cleaning are essential to prevent recurrent outbreaks due to antibiotic-resistant bacteria in burn units.

Acinetobacter Infections↗

PubMed2005

An outbreak of Acinetobacter baumannii septicemia in a neonatal intensive care unit of a university hospital in Brazil.

We studied an outbreak of two multi-drug resistant clones of Acinetobacter baumannii in the Neonatal Intensive Care Unit of the Uberlândia Federal University Hospital in Minas Gerais state, Brazil, and we analyzed the contribution of cross-transmission in the rise in infection rates. Eleven neonates who developed multi-drug resistant A. baumannii nosocomial infection were matched to 22 neonates who were admitted to the same unit and did not develop an infection during the outbreak period, in order to identify risk factors for infection. Three out of the 11 neonates died. Epidemiological investigation included molecular typing, using pulsed field gel electrophoresis. Prior to the outbreak, from December 2001 to March 2002, no case of infection by this microorganism was diagnosed. Environmental and healthcare worker hand cultures were negative. Nine isolates had similar pulsed field gel electrophoresis patterns and two had another clone. The first clone was brought into the unit by an infected patient who was transferred from another hospital without a history of antibiotic use. The second clone did have its origin clearly defined. Both infected groups led us to conclude that several factors contributed to infection with A. baumannii. These factors were: exposure to antibiotics and invasive devices, birth weight < 1500 g, age < or = 7 days and duration of hospitalization > or = 7 days. Based on logistic regression, infected neonates were more exposed to carbapenem and mechanical ventilation than the control group. Cross transmission between infants contributed to the rise in the rates of multi-drug resistant A. baumannii infection.

Acinetobacter Infections↗

PubMed2005

Mutations in the gyrA and parC genes in ciprofloxacin-resistant clinical isolates of Acinetobacter baumannii in Korea.

Mutation with Ser-83-->Leu in gyrA gene was associated with the principal mutation for ciprofloxacin resistance in clinical isolates of Acinetobacter baumannii. Double mutation, Ser-83-->Leu in gyrA gene and Ser-80-->Leu in parC gene, was the most frequently detected among ciprofloxacin-resistant isolates. A novel mutation with Ser-80-->Trp in parC gene, in addition to mutation in gyrA gene, was associated with a high-level ciprofloxacin resistance. These results suggested that the presence of an additional mutation in the parC gene contributed to a higher-level of ciprofloxacin resistance than a single mutation in the gyrA gene (geometric mean MICs of ciprofloxacin, 44.1 versus 16 microg/ml, P < 0.05).

Acinetobacter baumannii↗

PubMed2006

Attributable mortality of Acinetobacter baumannii infections in critically ill patients: a systematic review of matched cohort and case-control studies.

INTRODUCTION: There has been a continuing controversy about whether infection with Acinetobacter baumannii increases morbidity and mortality independently of the effect of other confounding factors. METHODS: We performed a systematic review of matched case-control and cohort studies examining the mortality attributable to infection with or acquisition of A. baumannii (infection or colonization). We included in our review studies that compared mortality and/or morbidity of patients with acquisition of or infection with A. baumannii (cases) with the outcomes of matched patients without A. baumannii isolation from clinical specimens (controls). The relevant studies were identified from searches of the PubMed and the Cochrane Library databases. Two independent reviewers performed the literature search, study selection, and data extraction from nine identified relevant studies. RESULTS: The attributable mortalities, in the hospital and in the intensive care unit, of patients with A. baumannii infection in six matched case-control studies included in our review ranged from 7.8% to 23% and from 10% to 43%, respectively. In addition, a statistically significantly higher mortality was reported for patients with A. baumannii acquisition; that is, colonization or infection (cases) compared with controls without such an acquisition in all four reviewed studies that reported data on this comparison. CONCLUSION: Although definitive statements about the mortality attributable to the acquisition of A. baumannii cannot be made from the available studies because of their methodological heterogeneity, the reviewed data suggest that infection with or acquisition of A. baumannii seems to be associated with increased mortality.

Acinetobacter Infections↗

PubMed1999

Risk factors for nosocomial bloodstream infections due to Acinetobacter baumannii: a case-control study of adult burn patients.

Risk factors for Acinetobacter baumannii bloodstream infection (BSI) were studied in patients with severe thermal injury in a burn intensive care unit where A. baumannii was endemic. Of 367 patients hospitalized for severe thermal injury during the study period, 29 patients with nosocomial A. baumannii BSI were identified (attack rate, 7.9%). Cases were compared with 58 matched controls without A. baumannii BSI. The overall mortality rate was 31% among cases and 14% among controls; only two deaths (7%) were considered directly related to A. baumannii BSI. Molecular typing of A. baumannii blood isolates by means of randomly amplified polymorphic DNA analysis and pulsed-field gel electrophoresis revealed the presence of three different strain types. Multivariate analysis showed that female gender (P = .027), total body surface area burn of > 50% (P = .016), prior nosocomial colonization with A. baumannii at a distant site (P = .0002), and use of hydrotherapy (P = .037) were independently associated with the acquisition of A. baumannii BSI in burn patients. These data underscore the need for effective infection control measures for this emerging nosocomial problem.

Acinetobacter↗

PubMed2005

Amikacin and colistin for treatment of Acinetobacter baumannii meningitis.

We report a case of a 52-year-old man with post-surgical meningitis due to a multi-drug resistant Acinetobacter baumannii. Despite therapy with intravenous amikacin and imipenem the meningitis progressed. Upon institution of combination therapy with amikacin by the intravenous and intrathecal (IT) routes, and intravenous colistin the patient experienced successful clinical and microbiological outcomes.

Acinetobacter Infections↗

PubMed2005

Novel acquired metallo-beta-lactamase gene, bla(SIM-1), in a class 1 integron from Acinetobacter baumannii clinical isolates from Korea.

Carbapenem resistance mediated by acquired carbapenemase genes has been increasingly reported, particularly for clinical isolates of Pseudomonas aeruginosa and Acinetobacter spp. Of 1,234 non-duplicate isolates of carbapenem-resistant Pseudomonas spp. and Acinetobacter spp. isolated at a tertiary-care hospital in Seoul, Korea, 211 (17%) were positive for metallo-beta-lactamase (MBL). Of these, 204 (96%) had either the bla(IMP-1) or bla(VIM-2) allele. In addition, seven Acinetobacter baumannii isolates were found to have a novel MBL gene, which was designated bla(SIM-1). The SIM-1 protein has a pI of 7.2, is a new member of subclass B1, and exhibits 64 to 69% identity with the IMP-type MBLs, which are its closest relatives. All SIM-1-producing isolates exhibited relatively low imipenem and meropenem MICs (8 to 16 microg/ml) and had a multidrug resistance phenotype. Expression of the cloned bla(SIM-1) gene in Escherichia coli revealed that the encoded enzyme is capable of hydrolyzing a broad array of beta-lactams, including penicillins, narrow- to expanded-spectrum cephalosporins, and carbapenems. The bla(SIM-1) gene was carried on a gene cassette inserted into a class 1 integron, which included three additional cassettes (arr-3, catB3, and aadA1). The strains were isolated from sputum and urine specimens from patients with pneumonia and urinary tract infections, respectively. All patients had various underlying diseases. Pulsed-field gel electrophoresis of SmaI-digested genomic DNAs showed that the strains belonged to two different clonal lineages, indicating that horizontal transfer of this gene had occurred and suggesting the possibility of further spread of resistance in the future.

Acinetobacter baumannii↗

PubMed2004

Distribution of tetracycline resistance genes in genotypically related and unrelated multiresistant Acinetobacter baumannii strains from different European hospitals.

The presence of tetracycline (TET) resistance genes was investigated in 49 genotypically related and unrelated multidrug-resistant Acinetobacter baumannii (MDRAB) strains from European hospitals including representatives of pan-European clones I and II. Except for one strain, all MDRAB strains displayed resistance to tetracycline (MIC range of 16 to > 512 microg/ml) but were susceptible (MIC < 4 microg/ml) or exhibited intermediate resistance (MIC of 4-8 microg/ml) to minocycline (MIN). In 37 strains, either tet(A) or tet(B) was detected and one of these strains possessed both tet(A) and tet(M). In addition, all MDRAB strains contained the aspecific efflux gene adeB irrespectively of whether they harbored tet genes or not. Repetitive DNA element (rep)-PCR fingerprinting using the (GTG)5 primer [(GTG)5-PCR] revealed that strains previously assigned to pan-European clones I and II were grouped into two separate clusters. In addition, these clusters also contained strains that had not been typed previously, indicating that (GTG)5-PCR is a valuable method for recognizing putative new members of MDRAB clones. Most, but not all, members of clones I and II were linked to the presence of either tet(A) or tet(B) and displayed different levels of TET resistance with MIC values of 32 to > 512 microg/ml and > 512 microg/ml, respectively. Of these two genes only tet(B) encodes an efflux of both TET and MIN, which was reflected by the relatively high MIC values for MIN (4 microg/ml) shown by the majority of the tet(B)-carrying clone II strains as opposed to the low MIC values for MIN (< 1 microg/ml) displayed by most tet(A)-containing clone I strains. Collectively, our phenotypic and genotypic resistance data support the therapeutic evaluation of second-generation tetracyclines like MIN as promising agents for treating MDRAB infections.

Acinetobacter Infections↗

PubMed2001

Apoptotic cell death induced by Acinetobacter baumannii in epithelial cells through caspase-3 activation.

Epithelial cell death induced by Acinetobacter baumannii infection was investigated using in vitro assays. Eight hours after live A. baumannii infection, HeLa cells exhibited detachment from the dish, rounding morphologies, high proportions of trypan blue-positive cells and extensive DNA breakdown with faint apoptotic banding, which is indicative of cells undergoing apoptosis. The enzymatic activity of caspase-3 was increased in cells as early as 2 h after infection. In addition, apoptosis of HeLa cells was induced by treatment with bacterial culture filtrates but not with formalin-killed bacteria. These results indicate that A. baumannii infection triggers apoptosis in HeLa cells through caspase-3 activation.

Acinetobacter↗

PubMedDate not supplied

Bacteremia due to Acinetobacter species other than Acinetobacter baumannii.

The objective of this study was to describe the clinical features, possible predisposing factors and treatment outcomes associated with bacteremia du to Acinetobacter species other than Acinetobacter baumannii. A review of laboratory and medical charts over a period of 18 months revealed 61 cases of bacteremia due to Acinetobacter species other than A. baumannii occurring in 59 patients. Six of these were considered not significant. Fifty cases represented catheter-related bacteremia, one case was associated with meningitis following brain surgery, and four cases could not be classified. Clinical courses wre usually benign: all but four patients were cured, but death was not related to Acinetobacter bacteremia in any case. Therapy included catheter removal alone (32.8%), appropriate antimicrobials alone (12.7%), or both (49.1%). Plasmid analysis showed distinct patterns in all strains isolated from different patients and did not reveal any epidemiological relationship among cases. Acinetobacter species other than A. baumannii are clinically significant organisms with limited pathogenic potential. They are almost exclusively involved in devise-related bacteremia. Clinical and epidemiological features of infections due to these organisms are clearly distinct from infections due to A. baumannii.

Acinetobacter↗

PubMed2006

Prevention of rifampicin resistance in Acinetobacter baumannii in an experimental pneumonia murine model, using rifampicin associated with imipenem or sulbactam.

OBJECTIVES: To examine the development of rifampicin resistance in multidrug-resistant Acinetobacter baumannii exposed to rifampicin and the prevention of the appearance of rifampicin-resistant mutants when rifampicin is used in association with imipenem or sulbactam. METHODS: A clinical strain of multidrug-resistant A. baumannii was used to examine the frequency of resistance to rifampicin in vivo, in a pneumonia model in immunocompetent C57BL/6 mice. The in vitro and in vivo prevention of the development of resistance to rifampicin was analysed using rifampicin alone or in association with imipenem or sulbactam, in time-kill studies and in the experimental murine pneumonia, respectively. RESULTS: Rifampicin-resistant mutants were found at 48 and 72 h, both in vitro and in vivo, when rifampicin was used alone, with the MIC increasing from 4 to > or =128 mg/L. The in vivo frequency of rifampicin-resistant mutants was 3 x 10(-6). On the contrary, no resistant mutants appeared after 72 h, in vitro or in vivo, when rifampicin was employed in association with imipenem or sulbactam. After six daily passages in rifampicin-free agar plates the resistant mutants maintained the high resistance to rifampicin (> or =128 mg/L). CONCLUSIONS: These results suggest that rifampicin must not be used alone in the treatment of infections caused by multidrug-resistant A. baumannii. In these cases, rifampicin may be used in combination with imipenem or sulbactam, which prevent the development of resistance to rifampicin.

Acinetobacter Infections↗

PubMed2003

The epidemiology of multidrug-resistant Acinetobacter baumannii: does the community represent a reservoir?

OBJECTIVE: To explore the role of the community as a potential reservoir for Acinetobacter baumannii. DESIGN: Antimicrobial resistance patterns and genotypes of A. baumannii isolates from patients in two Manhattan hospitals were compared with those of A. baumannii isolates from the hands of community members. RESULTS: A total of 103 isolates from two hospitals (hospital A, 81; hospital B, 22) and 23 isolates from community residents were studied. Of the hospital isolates, 36.6% were multidrug resistant (hospital A, 68.2%; hospital B, 27.8%). In contrast, there were no multidrug-resistant isolates from the community (P < .005 between hospital and community). The prevalence of A. baumannii on the hands of community residents was 10.4% (23 of 222). By molecular typing, 42 strains of A. baumannii were identified. Of the isolates from hospital A and hospital B, 55.6% (45 of 81) and 68.2% (15 of 22), respectively, were indistinguishable or closely related. In contrast, most community (83.3%) isolates were unrelated (P = .001 between hospital and community). CONCLUSION: Acinetobacter isolates from the community, characterized by a large variety of unrelated strains (83.3%), were distinct from the hospital isolates, of which 58.3% were closely related. The absence of multidrug-resistant strains in the community compared with 36.8% prevalence among hospital isolates suggests that the reservoir for epidemic strains resides in the hospital environment itself. To our knowledge, this is the first study to examine the community as a potential reservoir for hospital strains of A. baumannii.

Acinetobacter Infections↗

PubMed2002

Efficacy of colistin versus beta-lactams, aminoglycosides, and rifampin as monotherapy in a mouse model of pneumonia caused by multiresistant Acinetobacter baumannii.

The treatment of life-threatening infections due to carbapenem-resistant Acinetobacter baumannii has become a serious challenge for physicians worldwide. Often, only colistin shows in general good in vitro activity against these carbapenem-resistant strains, but its antibacterial efficacy in comparison with the antibiotics most used in clinical practice is not well known. We studied the efficacy of colistin versus those of imipenem, sulbactam, tobramycin, and rifampin in an experimental pneumonia model with immunocompetent mice. We used three strains of A. baumannii corresponding to the main clones (A, D, and E) involved in the outbreaks of our hospital, with different grades of resistance to imipenem (imipenem MICs of 1, 8, and 512 microg/ml, respectively) and to the other antibiotics. The MIC of colistin was 0.5 microg/ml for the three strains. Reduction of log(10) CFU/g in lung bacterial counts, clearance of bacteremia, and survival versus results with controls were used as parameters of efficacy. Imipenem and sulbactam (Deltalung counts: -5.38 and -4.64 log(10) CFU/ml) showed the highest level of bactericidal efficacy in infections by susceptible and even intermediate strains. Tobramycin and rifampin (-4.16 and -5.15 log(10) CFU/ml) provided good results against intermediate or moderately resistant strains, in agreement with killing curves and pharmacodynamics. On the contrary, colistin showed the weakest antibacterial effect among the antibiotics tested, both in killing curves and in the in vivo model (-2.39 log(10) CFU/ml; P < 0.05). We conclude that colistin did not appear as a good option for treatment of patients with pneumonia due to carbapenem-resistant A. baumannii strains. Other alternatives, including combinations with rifampin, may offer better therapeutic profiles and thus should be studied.

Acinetobacter↗

PubMed1996

Differentiation of Acinetobacter baumannii biotypes by amplification of 16S-23S rRNA intergenic spacer sequences.

Isolates of Acinetobacter baumannii (32 strains) from blood samples obtained from patients in five Chilean hospitals were identified and biotyped according to their phenotypic properties. They were also submitted to random amplified polymorphic DNA (RAPD) using eight randomly designed 10-mers and the core sequence of M13 phage (15-mers) as well as amplification of the spacer regions between 16S and 23S genes in the prokaryotic rRNA genetic loci. With some primers, RAPD discriminated between biotypes, whereas with others each isolate showed a particular profile. When amplification of spacer regions was performed, a clear correlation between patterns and biotypes was found. This last technique allowed correct biotyping of clinical isolates. Both genetic methods might be used for the identification of A. baumannii biotypes.

Acinetobacter↗

PubMed2004

Pharmacodynamics of meropenem and imipenem against Enterobacteriaceae, Acinetobacter baumannii, and Pseudomonas aeruginosa.

STUDY OBJECTIVE: To compare the pharmacodynamics of meropenem and imipenem, both administered as 500 mg every 6 hours, against populations of Enterobacteriaceae, Acinetobacter baumannii, and Pseudomonas aeruginosa. DESIGN: Ten thousand-subject Monte Carlo simulation. INTERVENTION: Variability in total body clearance (ClT), volume of distribution as calculated by the terminal elimination rate (Vdbeta), and minimum inhibitory concentration (MIC) distributions (Escherichia coli, Klebsiella pneumoniae, Enterobacter cloacae, Serratia marcescens, A. baumannii, P. aeruginosa) were derived from the literature for both meropenem and imipenem. For the free drug concentrations, the percentage of the dosing interval that the drug concentrations remain above the MIC (%T>MIC) for each carbapenem-bacteria combination was calculated for 10,000 iterations, substituting a different ClT, Vdbeta, fraction of unbound drug, and MIC into the equation each time based on the probability distribution for each parameter. Probabilities of attaining targets of 30%, 50%, and 100% T>MIC were calculated. MEASUREMENTS AND MAIN RESULTS: Meropenem free drug %T>MIC exposure was significantly greater than that of imipenem against Enterobacteriaceae and P. aeruginosa, whereas imipenem exposure was greater for A. baumannii. For both agents, free drug %T>MIC exposure was greatest against Enterobacteriaceae and less for A. baumannii and P. aeruginosa. Probabilities of target attainment for 30% and 50% T>MIC were similar between drugs for most bacteria. At 100% T>MIC, meropenem target attainments were greater than those of imipenem against Enterobacteriaceae and P. aeruginosa, and imipenem attainment was higher for A. baumannii. CONCLUSION: The probability of attaining lower pharmacodynamic targets for most gram-negative bacteria is similar for these carbapenems; however, differences become apparent as the pharmacodynamic requirement increases. Further study of the benefits of achieving this pharmacodynamic breakpoint with a higher probability of attaining targets is necessary.

Acinetobacter baumannii↗