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Acinetobacter lwoffi was isolated from the lungs of two hens. The isolate was sensitive to chloramphenicol, ampicillin, erythromycin, oxytetracycline but resistant to penicillin and nitrofurantoin.
BACKGROUND: Acinetobacter baumannii is one of the most important nosocomial pathogens, and its multiple antibiotic resistance has emerged as an obstacle in the treatment of these infections worldwide. AIMS: To identify risk factors of mortality for A. baumannii bacteraemia. METHODS: A retrospective cohort study of 72 patients with significant A. baumannii bacteraemia was conducted to evaluate risk factors for mortality. RESULTS: The median age of the 72 enrolled patients was 48 years, 96% of the cases were hospital-acquired, and the bacteraemia-related mortality rate was 29% (21 of 72 patients). Univariate analysis revealed that the risk factors for mortality included: an elevated acute physiology and chronic health evaluation (APACHE II) score, receipt of in vitro ineffective definitive antimicrobial therapy, in vitro A. baumannii resistance to cefoperazone/ sulbactam, neutropenia, and presentation with septic shock. Multivariate analysis reveals that the independent risk factors for mortality are neutropenia and elevated APACHE II scores. CONCLUSION: Risk factors such as neutropenia and elevated APACHE II scores are found to be associated with higher mortality rates of A. baumannii bacteraemia. Further study is necessary for the determination of optimal strategies for both the prevention and treatment of these infections.
The in-vivo activity of colistin was evaluated in an experimental rabbit model of Acinetobacter baumannii endocarditis with a strain susceptible to colistin and intermediate to imipenem. Compared to a control group, colistin was effective (p < 0.05) in bacterial clearance from blood and in the sterilisation of blood cultures, but was not effective in clearing A. baumannii from vegetations. Thus, although colistin may be effective in treating bacteraemia caused by susceptible strains of A. baumannii, it may not be a suitable treatment for endocarditis, perhaps because of poor penetration into vegetations and a low C(max)/MIC ratio in tissue.
Acinetobacter baumannii is now one of the most frequently encountered nosocomial pathogens in intensive therapy units, and is renowned for being difficult to treat because of resistance to most antibiotics. Carbapenems are the remaining drugs of choice in many centres, but carbapenem resistance is now emerging in strains worldwide. Two subgroups of carbapenem-hydrolysing beta-lactamases, which differ in their amino-acid homology, have been found in some resistant strains. This report describes the emergence and characterisation of a novel carbapenemase (OXA-51) in genetically distinct carbapenem-resistant A. baumannii strains from Argentina. Enzyme kinetics and inhibitor studies were performed spectrophotometrically with purified beta-lactamase. Amplification of the gene was achieved with a two-step PCR method employing arbitrary partially degenerate and gene-specific primers. Transfer of imipenem resistance was attempted with the use of broth and membrane filter methods. Attempts to produce plasmid-cured variants were made in ethidium bromide curing experiments. OXA-51 was identified in two clones of A. baumannii, and was found to have < 63% amino-acid identity with subgroups 1 and 2. Enzyme kinetic studies confirmed that OXA-51 was a molecular class D enzyme with carbapenemase activity, and that it displayed the highest affinity for imipenem (Km value 11 microM). Sequence analysis of the gene identified distinct differences within conserved class D motifs when compared with subgroups 1 and 2. Attempts to transfer imipenem resistance and to determine a plasmid location for the gene failed. OXA-51 is the first of a new subgroup of carbapenemases to emerge in multiresistant clinical isolates of A. baumannii.
A guinea-pig pneumonia model involving imipenem-susceptible and imipenem-resistant strains of Acinetobacter baumannii was developed to assess the in-vitro and in-vivo activities of imipenem, alone or in combination with amikacin, and the pharmacokinetic and pharmacodynamic parameters. Serum levels were measured by bioassay (imipenem) or immunoassay (amikacin), followed by calculation of pharmacokinetic and pharmacodynamic parameters (Cmax, AUC, t1/2, Cmax/MIC, AUC/MIC, and Deltat/MIC). In-vivo efficacy was evaluated by comparing bacterial counts in the lungs of treatment groups with end-of-therapy controls by anova and post-hoc tests. Decreases in the Cmax (13.4%), AUC (13%), t1/2 (25%) and Deltat/MIC (11.8-32.2%) of imipenem were observed when it was administered with amikacin, compared with administration of imipenem alone. Similarly, decreases in the Cmax (34.5%), AUC (11.6%), Cmax/MIC (34.5%) and AUC/MIC (11.7%) of amikacin were observed when it was administered with imipenem. Bacterial counts in lungs were reduced by imipenem (p 0.004) with the imipenem-susceptible strain, and by amikacin (p 0.001) with the imipenem-resistant strain. The combination of imipenem plus amikacin was inferior to imipenem alone with the imipenem-susceptible strain (p 0.01), despite their in-vitro synergy, and was inferior to amikacin alone with the imipenem-resistant strain (p < 0.0001). In summary, combined use of imipenem with amikacin was less efficacious than monotherapy, probably because of a drug-drug interaction that resulted in decreased pharmacokinetic and pharmacodynamic parameters for both antimicrobial agents.
Between October 2001 and August 2002, 30 hospital patients became infected or colonised by a multiresistant (including to carbapenems) epidemic strain of Acinetobacter baumannii (AbMR) in a hospital outbreak. This study analysed the risk-factors associated with acquisition of this epidemic strain and investigated the prognosis of patients infected by AbMR, with the aim of elucidating factors which lead to mortality. A case-control study of the acquisition of AbMR in patients infected or colonised in the hospital outbreak was performed. Independent risk-factors leading to death were studied by logistic regression analysis. Multivariate analysis of the risk-factors for colonisation/infection with AbMR revealed an independent association with the presence of an arterial catheter (OR, 1.13; 95% CI, 1.03-1.25) and administration of imipenem as monotherapy (OR, 11.12; 95% CI, 2.33-53.09). Multivariate analysis of the prognostic features leading to mortality revealed a significant association with hypotension or shock (OR, 24.63; 95% CI, 1.56-387.56) at the time of bacterial isolation.
Potential risk-factors for the acquisition of imipenem-resistant Acinetobacter baumannii were investigated in a cohort study in 25 Spanish hospitals. The clonal relationship among isolates was determined by pulsed-field gel electrophoresis (PFGE). In total, A. baumannii was isolated from 203 patients, with imipenem-resistant (MIC(90) 128 mg/L) isolates being obtained from 88 patients (43%), and imipenem-susceptible isolates from 115 patients (57%). A wide clonal distribution was observed among the imipenem-resistant isolates, but spread of the same clone among centres was not demonstrated. The results indicated that imipenem-resistant A. baumannii is a widely distributed nosocomial pathogen in Spain and reaches an alarming frequency in some centres. Independent risk-factors for the acquisition of imipenem-resistant A. baumannii were a hospital size of >500 beds (multivariate OR, 6.5; 95% CI, 1.8--23), previous antimicrobial treatment (multivariate OR, 4.3; 95% CI, 1.6--11), a urinary catheter (multivariate OR, 2.7; 95% CI, 1.1--6.7) and surgery (multivariate OR, 2; 95% CI, 1.07--3.8).
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.
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.
Twelve non-repetitive Acinetobacter baumannii isolates producing the carbapenem-hydrolysing oxacillinase OXA-58 were recovered from patients in the same paediatric hospital in Athens, Greece, between November 2003 and May 2005. All isolates were clonally related, but the bla(OXA-58) gene was not always plasmid-located and there were variations in the DNA sequences surrounding the OXA-58 gene in different isolates. This study emphasises the importance of the bla(OXA-58) carbapenemase gene in conferring carbapenem resistance among A. baumannii isolates in Greece.
Acinetobacter baumannii 65FFC, an imipenem-resistant clinical strain, isolated from the urine of a patient at the Coimbra University Hospital, Portugal, in 1998, produced a metallo-beta-lactamase with a calculated pI 9.3. The isolate was highly resistant to penicillins, broad-spectrum cephalosporins, including ceftazidime, ceftriaxone, cefepime, cefpirome, and to aztreonam, but it remained susceptible to ampicillin/sulbactam, aminoglycosides and quinolones. Nucleotide sequence revealed a new allelic variant of other bla(IMP) genes, named bla(IMP-5). IMP-5 beta-lactamase showed a greater homology with IMP-1, IMP-3 and IMP-4 (identified in Southeast Asia), than with IMP-2, found in Italy (93%, 92%, 91% and 87% of amino acid identity, respectively). bla(IMP-5) was the only gene cassette inserted into a class 1 integron, named In76. This is the first IMP-enzyme reported in Portugal and the second in Europe, indicating a wider dissemination in the environment of bla(IMP) alleles.
328 clinical isolates of Acinetobacter calcoaceticus from hospitalized patients and persons attending general practitioners were characterized according to biotype and resistance-pattern. 117 strains of biotype (b.) anitratus, 200 of b.lwoffi, 11 of b. haemolyticus and no strains of b. alcaligenes were found. B. anitratus was more frequently isolated from patients in hospitals than b.lwoffi; b.lwoffi was more often found in general practice. Strains of b. anitratus had more resistance traits than b.lwoffi. Strains of b. anitratus obtained in hospitals were more resistant than strains from general practice. No such difference was found with b.lwoffi.
A collection of Acinetobacter strains consisting of 168 consecutive clinical strains and 30 type and reference strains was studied by DNA-DNA hybridization and a few phenotypic tests. The field strains could be allotted to 13 DNA groups. By means of reference strains ten of these could be identified with groups described by Bouvet & Grimont (1986), while three groups were new; they were given the numbers 13-15. The type strain of A. radioresistens--recently described by Nishimura et al. (1988)--was shown to be a member of DNA group 12, which comprised 31 clinical isolates. Of the 19 strains of A. junii, eight showed hemolytic activity on sheep and human blood agar and an additional four strains on human blood agar only. Strains of this species have previously been regarded as non-hemolytic. Reciprocal DNA pairing data for the reference strains of the DNA groups were treated by UPGMA clustering. The reference strains for A. calcoaceticus, A. baumannii and for DNA groups 3 and 13 formed a cluster with about 70% relatedness within the cluster. Other DNA groups joined at levels below 60%.
One hundred and twelve clinical strains of Acinetobacter were collected during a 7-month period in 1990-1991 from Danish clinical microbiology departments. According to the old notation, 37 strains were biovar anitratus and 75 b.lwoffii. Using the newest terminology, 35 strains were unambiguously identified as the species A. haemolyticus, A. johnsonii, A. radioresistens, and as the unnamed phenons 6, 10, and 14, by a numerical approach using a simplified phenotypical identification scheme. Most of the remaining strains were identified to the genotypically heterogeneous A. calcoaceticus-A. baumannii complex and the A. lwoffii phenotype. Sixteen strains (14%) were left unidentified. Eight A. lwoffii strains were glucose-oxidizing and were thus classified as b. anitratus using the old terminology. The strains were tested for susceptibility to ampicillin, piperacillin, ticarcillin, cefotaxime, ceftazidime, imipenem, gentamicin, tetracycline, sulphonamide, and nalidixic acid. All strains were susceptible to imipenem. The susceptibility to the remaining beta-lactams was variable, the A. lwoffii isolates being the most and the A. calcoaceticus-A. baumannii complex strains the least susceptible. All non-A. calcoaceticus-A. baumannii complex strains were susceptible to all other antibiotics tested, except for one A. lwoffii strain that was sulphonamide resistant. Twenty-two percent of the strains in the A. calcoaceticus-A. baumannii complex showed reduced susceptibility or resistance to gentamicin, but only sporadic resistance to sulphonamides, tetracyclines, and nalidixic acid. Eight infections were recorded: three cases of septicaemia, three cases of peritonitis related to continuous ambulatory peritoneal dialysis, and two cases of recurrent urinary tract infection. No epidemics were detected.
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.
Multidrug-resistant Acinetobacter baumannii has emerged as a significant clinical problem worldwide and colistin is being used increasingly as "salvage" therapy. MICs of colistin against A. baumannii indicate its significant activity. However, resistance to colistin in A. baumannii has been reported recently. Clonotypes of 16 clinical A. baumannii isolates and ATCC 19606 were determined by pulsed-field gel electrophoresis (PFGE), and colistin MICs were measured. The time-kill kinetics of colistin against A. baumannii ATCC 19606 and clinical isolate 6 were investigated, and population analysis profiles (PAPs) were conducted. Resistance development was investigated by serial passaging with or without exposure to colistin. Five different PFGE banding patterns were found in the clinical isolates. MICs of colistin against all isolates were within 0.25 to 2 microg/ml. Colistin showed early concentration-dependent killing, but bacterial regrowth was observed at 24 h. PAPs revealed that heteroresistance to colistin occurred in 15 of the 16 clinical isolates. Subpopulations (<0.1% from inocula of 10(8) to 10(9) CFU/ml) of ATCC 19606, and most clinical isolates grew in the presence of colistin 3 to 10 microg/ml. Four successive passages of ATCC 19606 in broth containing colistin (up to 200 microg/ml) substantially increased the proportion of the resistant subpopulations able to grow in the presence of colistin at 10 microg/ml from 0.000023 to 100%; even after 16 passages in colistin-free broth, the proportion only decreased to 2.1%. This represents the first demonstration of heterogeneous colistin-resistant A. baumannii in "colistin-susceptible" clinical isolates. Our findings give a strong warning that colistin-resistant A. baumannii may be observed more frequently due to potential suboptimal dosage regimens recommended in the product information of some products of colistin methanesulfonate.
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.
The aim of this study was to investigate imipenem distribution in muscle and lung interstitial fluids of rats with Acinetobacter baumannii pulmonary infection. By combining microdialysis in blood and tissues, it was possible to demonstrate that free imipenem concentrations were virtually identical in blood, muscle, and lung.