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PubMed2006

Cure of multiresistant Acinetobacter baumannii central nervous system infections with intraventricular or intrathecal colistin: case series and literature review.

OBJECTIVES: CNS infections due to multiresistant Acinetobacter baumannii (MRAB) are an emerging problem in neurosurgical patients. Colistin remains one of the few remaining treatment options for MRAB but has poor CNS penetration. We describe our experience with intraventricular or intrathecal colistin for this infection. METHODS: Cases known to have received intraventricular or intrathecal colistin for CNS infections due to MRAB were retrospectively reviewed regarding colistin treatment, colistin efficacy and adverse events. RESULTS: Five patients were identified. All were admissions to the neurosurgical ICU and all were cured of their CNS infections. Three cases were complicated by drug-induced aseptic meningitis or ventriculitis. CONCLUSIONS: This largest case series to date shows that direct instillation of colistin into the CNS may cause chemical meningitis or ventriculitis but it is an effective treatment option for MRAB CNS infection. Further study of dosing regimens is needed.

Acinetobacter Infections↗
PubMed1996

Biotypes, serovars and antimicrobial resistance patterns of Acinetobacter baumannii clinical isolates.

255 Acinetobacter strains, from clinical specimens of inpatients and outpatients, were identified phenotypically according to the new taxonomy proposed by Bouvet and Grimont. A. baumannii was the most frequent species (80.8%). This species underwent biotyping and serotyping according to the scheme of Bouvet and Grimont, and that of Traub, respectively, 81.2% of samples belonged to biotypes 2, 6 and 9 with a predominance of biotype 2. 86.6% of the strains could be serotyped; 2 new serotypes were encountered. The new serotype 29, being the most frequently isolated, was related to biotype 2 (86.6%), whereas serotype 13 was related to biotype 6 (84.8%). These clones presented marked multiple resistance patterns and were widespread in different wards. No outbreak was reported during the period studied. These phenotypical methods proved to be useful in differentiating strains of A. baumannii and, if used together, they showed a high discriminatory power.

Acinetobacter↗
PubMed2004

In vitro and in vivo activity of meropenem and sulbactam against a multidrug-resistant Acinetobacter baumannii strain.

OBJECTIVES: The potential therapeutic role of meropenem combined with sulbactam against a clinical endemic isolate of multidrug-resistant Acinetobacter baumannii, Ab-153, was investigated. METHODS: The antimicrobial susceptibility of Ab-153 to various drugs was studied by the agar dilution method and Etest strips. The antibacterial activity of meropenem and sulbactam were investigated by a time-kill study in vitro and further examined for therapeutic efficacy in vivo in a murine model. RESULTS: In the time-kill study, at a concentration of 0.5 x MIC (4 mg/L) of meropenem, 1 x MIC (8 mg/L) of sulbactam and both in combination, only the combination demonstrated bactericidal effects and there was at least a 5 log(10) reduction in bacterial colony counts after 48 h, compared with either drug alone. BALB/c mice infected with 2.1-2.6 x 10(7) cfu of Ab-153 were treated with 20 mg/kg meropenem every 8 h, 40 mg/kg sulbactam every 8 h or both in combination. The survival rate of mice in the combination group was significantly higher than that in the meropenem-treated or sulbactam-treated group (87% versus 35%, P = 0.0004; 87% versus 30%, P = 0.0002). CONCLUSIONS: Meropenem in conjunction with sulbactam can exhibit more potent antimicrobial activity against Ab-153 than meropenem or sulbactam alone.

Acinetobacter Infections↗
PubMed2026

Molecular epidemiology and genomic characteristics of clinical Acinetobacter baumannii isolates from patients with hospital-acquired pneumonia in China, 2019-2020: a multicentre retrospective study.

BACKGROUND: Carbapenem-resistant Acinetobacter baumannii (CRAB) is a leading cause of hospital-acquired pneumonia (HAP) with high mortality. However, large-scale nationwide data of HAP-causing CRAB in China remain limited. METHODS: Here, we performed a nationwide multicentre retrospective study to characterise the molecular epidemiology and genomic features of 802 A. baumannii isolates from patients with HAP across 33 tertiary hospitals in China during 2019-2020. Antimicrobial susceptibility testing (AST), whole-genome sequencing (WGS), phylogenetic and comparative genomic analysis were used to investigate molecular epidemiology of HAP-causing CRAB strain. Clinical comparative analyses were carried out on data from 500 patients with HAP stratified by distinct antimicrobial susceptibility and genomic profiles, and a Galleria mellonella infection model was utilised for in vivo virulence assessment. FINDINGS: The overall carbapenem resistance rate of A. baumannii was 82.0% (658/802), with marked regional variations. CRAB exhibited high resistance to conventional agents but remained largely susceptible to polymyxin, tigecycline, cefiderocol and sulbactam-durlobactam. Among enrolled patients, CRAB infection was linked to substantially higher mortality (39.0% vs. 17.5%), and multivariate analysis confirmed ICU admission and advanced age as independent risk factors for patients with CRAB infection. Molecular typing revealed STPas2 (96.2%) as the absolutely predominant type; STOxf208, STOxf195, STOxf540, and STOxf369 were the most prevalent Oxford sequence types with obvious geographic stratification and divergent comorbidity profiles among corresponding patients. A total of 654 CRAB isolates harboured carbapenemase genes, with blaOXA-23 dominating at 98.8%. Genomic analysis revealed lineage-specific features: STOxf208 carried more virulence genes, while STOxf540 harboured a broader antimicrobial resistance genes (ARGs). The STOxf208 clone mainly belonged to KL2 (62.1%) and KL7 (36.8%) serotypes, with KL2 strains possessing richer ARGs and virulence factors, and in vivo virulence assays further validated that KL2 strains possessed higher pathogenicity than KL7 strains. INTERPRETATION: This study demonstrates the extremely high prevalence and clonal dominance of CRAB in Chinese patients with HAP, providing critical evidence for clinical treatment, antimicrobial stewardship, and targeted infection control. FUNDING: National Key Research and Development Program of China (2024YFE0106200), National Natural Science Foundation of China (U22A20338, 82502763, W2621007), Zhejiang Provincial Natural Science Foundation of China (LQN25H190006), Zhejiang Provincial Postdoctoral Science Foundation (ZJ2025058).

Acinetobacter baumannii↗
PubMed2006

Predictive biomarkers for drug-resistant Acinetobacter baumannii isolates with bla(TEM-1), AmpC-type bla and integrase 1 genotypes.

BACKGROUND AND PURPOSE: We tested whether antibiotic susceptibilities of drug-resistant Acinetobacter baumannii isolates could be used to predict the clinically important genotypes bla(TEM-1), AmpC-type bla, and integrase 1 gene (IntI1). METHODS: We analyzed 401 A. baumannii isolates obtained at Changhua Christian Hospital between April 2001 and March 2002. The isolates were all from blood cultures, and identification of A. baumannii was confirmed by API-20NE. Antibiotic susceptibility testing (phenotype) was performed by disk diffusion method. Polymerase chain reaction was used to detect the genes bla(TEM-1), AmpC-type bla and IntI1. RESULTS: Of 32 A. baumannii isolates, 10 possessed bla(TEM-1), 21 AmpC-type bla, and 26 IntI1. Resistance to ceftazidime (CAZ) predicted bla(TEM-1) genotype with 63.6% sensitivity, 100% specificity, 55.6% positive predictive value (PPV) and 0% negative predictive value (NPV). Trimethoprim-sulfamethoxazole (SXT) and gentamicin (GM) resistance predicted IntI1 genotype with 83.3% sensitivity, 71.4% specificity, 95.2% PPV and 45.4% NPV. No resistance phenotype could predict the AmpC-type bla genotype. CONCLUSIONS: CAZ resistance predicted the bla(TEM-1) genotype with 100% specificity, and SXT and GM resistance predicted the IntI1 genotype with 92.5% PPV. Therefore, antibiotic susceptibilities to CAZ, SXT, and GM can be utilized clinically to detect critical genotypes in A. baumannii.

Acinetobacter Infections↗
PubMed2004

[Aminoglycoside resistance of Acinetobacter baumannii hospital strains in the Czech Republic].

OBJECTIVE: To investigate the nature of aminoglycoside resistance of clinically important multidrug-resistant (MDR) Acinetobacter baumannii strains from the Czech Republic. MATERIAL AND METHODS: Seventy MDR hospital strains from 1991-2001 classified into pan-European clones I (n = 41) and II (n = 21) and a group of other MDR strains (n = 8) were studied. Fifteen other strains wild-type susceptible to aminoglycosides were used as controls. Susceptibility to aminoglycosides was determined by the disk diffusion and agar dilution tests. The presence of six genes encoding different aminoglycoside-modifying enzymes (AME) and of the adeB gene encoding a component of the AdeABC efflux pump was detected using PCR. RESULTS: MDR strains showed the following pattern of resistance to aminoglycosides: kanamycin (93 %; inhibition zone diameters < or =13 mm), gentamicin (87 %; MICs > or =16 mg/l), amikacin (47 %; MICs > or =64 mg/l), tobramycin (31 %; MICs > or = 16 mg/l) and netilmicin (17 %; MICs ? 32 mg/l). Forty-six (66 %) MDR strains had netilmicin MICs of 8-16 mg/l in contrast to 0.5-1.0 mg/l found for control susceptible strains. The presence of at least one of the following AME genes was detected in 66 (94 %) MDR strains: aphA1 (n = 56), aacC1 (n = 52), aphA6 (n = 39) and aadB (n = 20). The presence of these genes and phenotypes of resistance to kanamycin, gentamicin, tobramycin and amikacin were in good agreement. The genes encoding netilmicin-modifying enzymes (aacC2, aacA4) were not detected in any strain. Fifty-six (80 %) MDR strains comprised two to four different AME genes in eight combinations. Clones I and II shared all of the genes studied (with the exception of aadB not detected in clone I). The gene adeB was found in all MDR strains and eight of 15 control susceptible strains. CONCLUSION: Clinically relevant aminoglycoside resistance of Czech A. baumannii strains is significantly associated with the genes encoding enzymatic modification of kanamycin, gentamicin, amikacin and tobramycin. These genes can spread horizontally and emerge in different combinations leading to high-level resistance to multiple aminoglycosides. The AdeABC pump is likely to play a role in the intermediate susceptibility to netilmicin but further study is needed in this regard.

Acinetobacter baumannii↗
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↗
PubMed2026

Phenylacetic acid mediates Acinetobacter baumannii entry into a viable but non-culturable state.

Desiccation tolerance is central to the pathogenic success of the opportunistic pathogen Acinetobacter baumannii, allowing its survival on hospital surfaces in the absence of water and nutrients for months at a time, compromising surface decontamination and aiding cross-contamination between staff and patients. Despite the importance of desiccation tolerance, the regulation underpinning this behaviour remains largely elusive. In this work, transcriptomic analyses of desiccated cells revealed phenylacetic acid (PAA) catabolism as an essential mediator of desiccation tolerance. We subsequently demonstrate that deletion of the paa operon abolished the clonogenicity of desiccated cells. Strikingly, these A. baumannii cells remained viable by entering the viable but non-culturable (VBNC) state, a means to survive extreme stressors like antibiotic exposure. Furthermore, we uncover that PAA catabolism is necessary to mediate PAA-driven biofilm regulation. These findings highlight PAA catabolism as a modulator of biofilm formation and a key pathway for entry into the VBNC state in response to desiccation. This reveals PAA catabolism as a target for novel infection prevention strategies.

Phenylacetates↗
PubMedDate not supplied

A multi-resistant Acinetobacter baumannii outbreak in a general intensive care unit.

In an Intensive Care Unit, three patients were found infected and two colonized with multiresistant Acinetobacter baumannii within a period of one week. To identify the outbreak source, two surveillance studies were performed concerning patients and the environment. Genotyping of isolates was performed by random amplification of polymorphic DNA analysis (RAPD). Environmental sampling failed to yield A. baumannii, with the exception of a single sample from a trunking. RAPD-fingerprinting yielded identical patterns for all patient isolates including the trunking isolate, thus confirming the suspected cluster. Since the strain from the trunking had a susceptibility pattern and a RAPD pattern identical to that of the strains isolated from the patients, we believe that this was the likely source of the outbreak. In conclusion, A. baumannii outbreaks may be quickly controlled by appropriate action of the hospital infection staff. RAPD-fingerprinting may provide a useful and rapid identification technique for the epidemiological investigation of a hospital outbreak.

Acinetobacter Infections↗
PubMed2006

[Susceptibility pattern of Acinetobacter baumannii clinical isolates in Madrid vs. Hong Kong].

The objective of this study was to compare the susceptibility to seven antimicrobials of Acinetobacter baumannii clinical isolates from H. U. de La Princesa of Madrid vs. A. baumannii clinical isolates from Hospital Queen Mary of Hong Kong from January 2004 to March 2005. A total of 74 strains isolated from our hospital and 30 strains attended to Hospital Queen Mary were studied. The MIC (minimal inhibitory concentration) was determined by agar dilution method. NCCLS recommended breakpoints were used against imipenem, tobramycin, amikacin, ofloxacin and ceftazidime. For sulbactam the break point for ampicillin/sulbactam was used. BSAC breakpoint was considered against colistin. Colistin showed the highest susceptibility percentage in Spanish strains (98.64%), followed by imipenem (94.59%) and tobramycin (78.37%). About 50% of the clinical isolates were susceptible to sulbactam (54.05%) and amikacin (51.35%). The majority of the strains were resistant to ofloxacin (2.7% of susceptible strains) and ceftazidime (1.35% of susceptible strains). In the Hong Kong clinical isolates, high susceptibility percentages were shown for most antimicrobials: 96.66% to colistin, sulbactam, tobramycin and amikacin; lower for imipenem (93.33%) and ofloxacin (90%). Ceftazidime presented the lowest susceptibility percentage (10%). In conclusion, higher resistant percentages in Spanish strains than Chinese strains were obtained for most antimicrobials tested. To ofloxacin, 90% of Hong Kong isolates were susceptible while 93% of Madrid isolates were resistant. Geographically remote populations (such as Madrid and Hong Kong) showed important differences according to the susceptibility patterns.

Acinetobacter Infections↗
PubMed2006

Successful treatment of septic shock due to pan-resistant Acinetobacter baumannii using combined antimicrobial therapy including tigecycline.

Reported here is the case of a patient with septic shock due to multidrug-resistant Acinetobacter baumannii, which developed after complicated acute pancreatitis with intra-abdominal abscess. Treatment with colistin methanesulphonate and high doses of meropenem were initiated, but since shock persisted, tigecycline was added to the regimen, resulting in successful resolution of the infection.

Acinetobacter Infections↗
PubMed2006

Outbreak of multiple clones of imipenem-resistant Acinetobacter baumannii isolates expressing OXA-58 carbapenemase in an intensive care unit.

OBJECTIVES: To investigate the resistance mechanisms and the genetic relationship of imipenem-resistant Acinetobacter baumannii isolates recovered in the intensive care unit (ICU) of a tertiary care hospital. METHODS: Imipenem-resistant A. baumannii clinical and environmental isolates were collected in the ICU of the Red Cross General Hospital, Athens, Greece between March and October 2002. The isolates were tested by Etest MBL, PCR, RT-PCR and sequencing for carbapenemase-encoding genes, PFGE and synergy experiments using meropenem and the efflux pump inhibitor carbonyl cyanide chlorophenylhydrazone. RESULTS: During the study period, 15 clinical and two environmental imipenem-resistant (MIC 8 to >128 mg/L) A. baumannii isolates were recovered. PFGE showed six different clones that included both clinical and environmental isolates. All 17 isolates were negative by Etest MBL and PCR for genes bla(IMP), bla(VIM), bla(SPM), bla(OXA-23-like) and bla(OXA-24-like). Genes bla(OXA-51-like) and bla(OXA-58-like) were amplified from 15 and 14 isolates, respectively. Sequencing of bla(OXA-51-like) amplicons identified bla(OXA-66) (nine cases) and bla(OXA-69) (six cases), whereas bla(OXA-58-like) sequences were classical bla(OXA-58). Reverse transcriptase-PCR showed that bla(OXA-51-like) genes were expressed in 12 and bla(OXA-58) in 10 isolates; in these isolates, inhibition of OXA enzymes by 200 mM of NaCl reduced carbapenem MICs by up to 4-fold. Overexpression of proton-gradient dependent efflux pumps did not contribute to carbapenem resistance in any isolate. Similarly, although AmpC expression was demonstrated in eight isolates, inhibition of AmpC with cloxacillin did not reduce the MICs of carbapenems significantly. CONCLUSIONS: These findings indicate wide dissemination of OXA-58 carbapenemase, which contributes, at least partially, to the imipenem resistance of unrelated A. baumannii isolates in our ICU.

Acinetobacter Infections↗
PubMed2000

Outer-membrane proteins pattern and detection of beta-lactamases in clinical isolates of imipenem-resistant Acinetobacter baumannii from Brazil.

In order to compare imipenem-sensitive and -resistant Acinetobacter baumannii strains isolated from three patients, ribotyping, plasmid, beta-lactamase detection and outer-membrane analysis were performed. Ribotyping and the use of a beta-lactam during the period when the strains were isolated suggested that they had a common origin and that resistance occurred in vivo. Outer membrane analysis showed no difference between susceptible and resistant strains with the exception of an A2 imipenem-resistant strain that lost a protein band of 31-36 kDa. Beta-lactamases were detected using isoelectric focusing in all strains (pI of 7.4). In addition, two beta-lactamases (pI of 5.9 and 6.7) were found in imipenem-resistant isolates. The double-disc technique demonstrated the presence of a beta-lactamase capable of imipenem inactivation in resistant strains. Plasmid analysis showed that all susceptible strains had the same pattern, one resistant strain did not have any plasmid, one had the same plasmid pattern of its susceptible pair and only one had a different pattern when compared with its susceptible pair.

Acinetobacter↗
PubMed2006

Colistin, meropenem and rifampin in a combination therapy for multi-drug-resistant Acinetobacter baumannii multifocal infection. A case report.

A 16 year-old girl underwent a multifocal (lungs, skin, soft tissues) infection due to multiresistant Acinetobacter baumannii after a car crash. To treat such a severe disease we used a combination therapy of colistin (2 millions Units twice/day), rifampicin (600 mg/day), meropenem (1 g 3 times a day) after a synergistic activity test was performed (checkerboard method on Mueller-Hinton broth and 5x10(5) cfu/mL inoculum). After 24 days, when a significant clinical improvement was gained, the 3-drugs combination therapy was replaced with i.v. levofloxacin 500 mg twice/day but, after 10 days of quinolones therapy, fever started again and the same multidrug resistant (MDR) A. baumannii was isolated from the skin grafts, central venous catheter tip and bronchial alveolar lavage. A combination therapy with colistin and meropenem was therefore started and definitive defervescence was obtained after 10 days. This therapy was continued for 70 days even if the patient was apyretic because A. baumannii was still present in the skin secretions. After 109 days of hospitalization in our intensive care unit, the patient was transferred to a rehabilitative unit. This case shows how useful is, in selected cases, rediscovering old antibiotic drugs, specially when they are adopted as a combination therapy, and highlights the importance of the clinical microbiological laboratory as it may help clinicians in choosing the best drugs combination.

Accidents, Traffic↗
PubMed2006

Comparison of mortality of patients with Acinetobacter baumannii bacteraemia receiving appropriate and inappropriate empirical therapy.

OBJECTIVES: To evaluate the effect of inappropriate empirical antimicrobial treatment on the mortality of patients with Acinetobacter baumannii bacteraemia. METHODS: Retrospective cohort study of patients with A. baumannii bacteraemia hospitalized at the Henry Dunant hospital from January 2002 to December 2004. RESULTS: Among 40 patients with A. baumannii bacteraemia, 22 (55%) and 18 (45%) received inappropriate and appropriate antibiotic therapy, respectively, during the 3 day period after obtaining the blood culture(s) from which the pathogen was isolated. Failure to cure the infection was more common in the first group [16/22 patients (72.7%) versus 5/18 (27.8%), P = 0.005]. Although without statistical significance, probably due to the small number of studied patients, considerably increased mortality was noted in the first group compared with the second group [13/22 patients (59.1%) versus 6/18 (33.3%), P = 0.10]. CONCLUSIONS: A. baumannii bacteraemia was associated with worse outcome regarding the cure of infection in patients who received inappropriate empirical antimicrobial treatment compared with those who received appropriate treatment.

Acinetobacter Infections↗