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PubMed2006

Activity of cecropin A-melittin hybrid peptides against colistin-resistant clinical strains of Acinetobacter baumannii: molecular basis for the differential mechanisms of action.

Acinetobacter baumannii has successfully developed resistance against all common antibiotics, including colistin (polymyxin E), the last universally active drug against this pathogen. The possible widespread distribution of colistin-resistant A. baumannii strains may create an alarming clinical situation. In a previous work, we reported differences in lethal mechanisms between polymyxin B (PXB) and the cecropin A-melittin (CA-M) hybrid peptide CA(1-8)M(1-18) (KWKLFKKIGIGAVLKVLTTGLPALIS-NH2) on colistin-susceptible strains (J. M. Saugar, T. Alarcón, S. López-Hernández, M. López-Brea, D. Andreu, and L. Rivas, Antimicrob. Agents Chemother. 46:875-878, 2002). We now demonstrate that CA(1-8)M(1-18) and three short analogues, namely CA(1-7)M(2-9) (KWKLFKKIGAVLKVL-NH2), its Nalpha-octanoyl derivative (Oct-KWKLFKKIGAVLKVL-NH2), and CA(1-7)M(5-9) (KWKLLKKIGAVLKVL-NH2) are active against two colistin-resistant clinical strains. In vitro, resistance to colistin sulfate was targeted to the outer membrane, as spheroplasts were equally lysed by a given peptide, regardless of their respective level of colistin resistance. The CA-M hybrids were more efficient than colistin in displacing lipopolysaccharide-bound dansyl-polymyxin B from colistin-resistant but not from colistin-susceptible strains. Similar improved performance of the CA-M hybrids in permeation of the inner membrane was observed, regardless of the resistance pattern of the strain. These results argue in favor of a possible use of CA-M peptides, and by extension other antimicrobial peptides with similar features, as alternative chemotherapy in colistin-resistant Acinetobacter infections.

Acinetobacter baumannii↗

PubMed2006

Fulminant community-acquired Acinetobacter baumannii pneumonia as a distinct clinical syndrome.

STUDY OBJECTIVES: Acinetobacter baumannii (AB) is an important cause of hospital-acquired pneumonia (HAP), and an uncommon but important cause of community-acquired pneumonia (CAP) with high mortality. To better characterize CAP-AB, we compared its clinical features and outcomes with a control group of HAP-AB patients. METHODS: This is a retrospective case-control study comparing CAP-AB and HAP-AB patients, which was performed at United Christian Hospital between July 2000 and December 2003. RESULTS: There were 19 cases of CAP-AB and 74 cases of HAP-AB. When compared with the HAP-AB group, the CAP-AB group had more ever-smokers (84.3% vs 55.4%, respectively; p = 0.031), more COPD patients (63.2% vs 29.7%, respectively; p = 0.014), and fewer median days of hospitalization (HAP-AB group, median, 0 days; CAP-AB group, 0 days [range, 0 to 30 days]; p = 0.049) in the previous year. The CAP-AB group had more patients with positive blood culture findings (31.6% vs 0%, respectively; p < 0.001), a higher frequency of ARDS (84.2% vs 17.6%, respectively; p < 0.001), and disseminated intravascular coagulation (DIC) (57.9% vs 8.1%, respectively; p < 0.001). The median survival time was only 8 days in the CAP-AB group, vs 103 days in the HAP-AB group (p = 0.003). Factors associated with the higher mortality in the CAP-AB group included the presence of AB bacteremia (p = 0.040), platelet count of < 120 x 10(9) cells/L (p = 0.026), pH < 7.35 on presentation (p = 0.047), and the presence of DIC (p = 0.004). CONCLUSIONS: CAP-AB appears to be a unique clinical entity with a high incidence of bacteremia, ARDS, DIC, and death, when compared to HAP-AB. Further studies are needed to investigate the mechanism of the fulminant nature of CAP-AB.

Acinetobacter Infections↗

PubMed2025

A novel genus of virulent phage targeting Acinetobacter baumannii: Efficacy and safety in a murine model of pulmonary infection.

Acinetobacter baumannii is a notable opportunistic pathogen responsible for severe hospital-acquired infections, with multidrug-resistant strains posing significant treatment challenges. Phage therapy, which employs bacteriophages as natural bacterial antagonists, has gained renewed attention as a promising solution to combat antibiotic-resistant infections. In this study, we isolated and characterized a novel virulent phage, vB_AbaS_qsb1, which specifically lyses A.baumannii. Phylogenetic and genomic analyses indicate that vB_AbaS_qsb1 is the founding member of a previously unreported genus, which we propose to name Acinibactriovirus, with Acinibactriovirus lysinus as the type species. vB_AbaS_qsb1 demonstrated robust stability across diverse temperature and pH ranges, a short latent period, and no known virulence or antibiotic resistance genes within its 54,713 bp dsDNA genome. Safety assessments showed that high-dose vB_AbaS_qsb1 induced no adverse effects in mice, with histopathology confirming its safety profile. Therapeutic experiments further indicated that vB_AbaS_qsb1 provided at least 50% protection against A.baumannii-induced pneumonia, significantly reducing bacterial loads and inflammation markers, while maintaining high phage titers in lung tissue.This study introduces vB_AbaS_qsb1 as a promising candidate for phage therapy against A.baumannii, offering both innovative insights and a valuable framework for future isolation, genomic characterization, and efficacy evaluation of phages targeting antibiotic-resistant bacteria.

Animals↗

PubMed2005

Early prosthetic valve endocarditis due to Acinetobacter baumannii: a case report and brief review of the literature.

Acinetobacter is a highly resistant microorganism, commonly isolated in intensive and post-operative care units. Although rarely reported, it may constitute 1 of the several causes of early prosthetic valve endocarditis. A diffuse, red maculopapular rash may be encountered in patients with Acinetobacter endocarditis. Here we present a case of early prosthetic valve endocarditis due to Acinetobacter baumannii and accompanied by a cutaneous eruption.

Acinetobacter Infections↗

PubMed2005

Cloning and functional analysis of the gene encoding the 33- to 36-kilodalton outer membrane protein associated with carbapenem resistance in Acinetobacter baumannii.

We investigated a multiresistant strain of Acinetobacter baumannii isolated in our hospital. Analysis of the N-terminal peptide sequence of the outer membrane proteins (OMPs) purified from the strain allowed us to clone and sequence the nucleotides of the gene encoding the 33- to 36-kDa OMP associated with carbapenem resistance in A. baumannii.

Acinetobacter↗

PubMed2005

Development of a multilocus sequence typing scheme for characterization of clinical isolates of Acinetobacter baumannii.

In this study a multilocus sequence typing (MLST) scheme for Acinetobacter baumannii was developed and evaluated by using 40 clinical A. baumannii isolates recovered from outbreaks in Spanish and German hospitals during the years 1990 to 2001, as well as isolates from other European hospitals and two DSMZ reference strains of A. baumannii. For comparison, two isolates of Acinetobacter species 13 (sensu Tjernberg and Ursing), two clinical isolates, and three DSMZ strains of A. calcoaceticus (both belonging to the A. calcoaceticus-A. baumannii complex) were also investigated. Primers were designed for conserved regions of housekeeping genes, and 305- to 513-bp internal fragments of seven such genes-gltA, gyrB, gdhB, recA, cpn60, gpi, and rpoD-were sequenced for all strains. The number of alleles at individual loci ranged from 6 to 12, and a total of 20 allelic profiles or sequence types were distinguished among the investigated A. baumannii strains. The MLST data were in high concordance with the epidemiologic typing results generated by pulsed-field gel electrophoresis and amplified fragment length polymorphism fingerprinting. The MLST scheme provides a high level of resolution and an excellent tool for studying the population structure and long-term epidemiology of A. baumannii.

Acinetobacter Infections↗

PubMed2003

[In vitro activity of azithromycin against clinical isolates of Acinetobacter baumannii].

The activity of azithromycin against 225 clinical strains of Acinetobacter baumannii isolated consecutively from 26 Spanish hospitals in November 2000 was studied. The MICs of azithromycin were determined by microdilution, according to the NCCLS guidelines. The bactericidal activity of azithromycin against 15 clonally unrelated A. baumannii strains with different antimicrobial susceptibility patterns was tested using the subculture method. The killing-curves method was also performed against five strains with different susceptibility to azithromycin. The MIC(50) and MIC(90) of azithromycin were 32 and 64 mg/l, respectively. Moderate bactericidal activity was observed in 14 out of the 15 strains evaluated by the subculture method (MBCs from 1 to 4 dilution steps higher than the MICs) and by the killing-curve method. For three strains the number of CFU/ml was reduced 1 to 1.4 log by concentrations of azithromycin equivalent to 1 and 4 times their MICs. lt is concluded that azithromycin has moderate bactericidal activity against the strains of A. baumannii evaluated.

Acinetobacter Infections↗

PubMed2025

Genomic and phenotypic insights into ST164 blaNDM-1-positive Acinetobacter baumannii from intestinal colonization in China.

BACKGROUND: Carbapenem-resistant Acinetobacter baumannii (CRAB) poses a critical global threat, especially in ICUs. Yet, reports on ST164 CRAB harboring blaNDM-1 remain scarce. This study investigates two clinical CRAB isolates, L4773hy and L4796hy, derived from intestinal colonization in Hangzhou, China, focusing on their phenotypic and genomic characteristics as well as the broader transmission of ST164 A. baumannii. METHODS: Bacterial identification was performed using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF) mass spectrometry. Antimicrobial susceptibility was assessed via agar and broth microdilution. Whole-genome sequencing employed Illumina NovaSeq 6000 and Oxford Nanopore platforms. Resistance genes, insertion elements, transposons, and integrons were detected using ResFinder, PlasmidFinder, VFDB, ISFinder, pdifFinder, and IntegronFinder. Strains were typed by MLST, and a phylogenetic tree was constructed with kSNP3.0. Genetic environment diagrams were generated using Easyfig 2.2.5. RESULTS: Two blaNDM-1-carrying A. baumannii isolates exhibiting extensive resistance to carbapenems, cephalosporins, and fluoroquinolones. Whole-genome sequencing and genetic environment analysis revealed the presence of a conserved structural sequence (ISAba14-ISAba14-aphA-ISAba125-blaNDM-1-bleMBL) on their chromosomes. Phylogenetic and clonal dissemination analysis showed that ST164 CRAB is primarily distributed in China and exhibits clonal spread. Pathogenicity studies indicated that blaNDM-1-positive ST164 strains have enhanced survival under immune pressure but do not display increased virulence in infection models. CONCLUSION: This study provides the genomic and phenotypic characterization of intestinally colonized ST164 blaNDM-1 positive CRAB in Hangzhou, China. The elucidation of the genetic environment of blaNDM-1 further confirms the clonal dissemination of ST164 isolates, highlighting the importance of enhanced surveillance and infection control measures to mitigate the spread of these multidrug-resistant pathogens.

Acinetobacter baumannii↗

PubMed1992

Characterization of a high-affinity iron transport system in Acinetobacter baumannii.

Analysis of a clinical isolate of Acinetobacter baumannii showed that this bacterium was able to grow under iron-limiting conditions, using chemically defined growth media containing different iron chelators such as human transferrin, ethylenediaminedi-(o-hydroxyphenyl)acetic acid, nitrilotriacetic acid, and 2,2'-bipyridyl. This iron uptake-proficient phenotype was due to the synthesis and secretion of a catechol-type siderophore compound. Utilization bioassays using the Salmonella typhimurium iron uptake mutants enb-1 and enb-7 proved that this siderophore is different from enterobactin. This catechol siderophore was partially purified from culture supernatants by adsorption chromatography using an XAD-7 resin. The purified component exhibited a chromatographic behavior and a UV-visible light absorption spectrum different from those of 2,3-dihydroxybenzoic acid and other bacterial catechol siderophores. Furthermore, the siderophore activity of this extracellular catechol was confirmed by its ability to stimulate energy-dependent uptake of 55Fe(III) as well as to promote the growth of A. baumannii bacterial cells under iron-deficient conditions imposed by 60 microM human transferrin. Polyacrylamide gel electrophoresis analysis showed the presence of iron-regulated proteins in both inner and outer membranes of this clinical isolate of A. baumannii. Some of these membrane proteins may be involved in the recognition and internalization of the iron-siderophore complexes.

Acinetobacter calcoaceticus↗

PubMed1997

Molecular typing of Acinetobacter baumannii from ten different intensive care units of a university hospital.

Thirty-one isolates of Acinetobacter baumannii were collected from ten intensive care units of an Austrian university hospital. All isolates were typed by enterobacterial repetitive intergenic consensus polymerase chain reaction (ERIC-PCR). Two strains colonizing 13 infants in the neonatal intensive care unit were identified by ERIC-PCR. All other Acinetobacter baumannii isolates had highly divergent ERIC-PCR patterns, despite having the same antibiogram. Thus, a hospital-wide clonal distribution, as suggested by identical antibiogram patterns, was excluded by ERIC-PCR.

Acinetobacter↗

PubMed2002

Molecular epidemiology of nosocomial infection associated with multi-resistant Acinetobacter baumannii by infrequent-restriction-site PCR.

Acinetobacter baumannii was considered endemic in a university-affiliated tertiary hospital. A significant increase was noted in the proportion of nosocomial infections associated with this micro-organism from 1996 to 1999, although no apparent clusters could be found. Between July 1998 and February 2000, 58 nosocomial isolates of A. baumannii were collected and characterized by antibiotyping and a genotyping method, infrequent-restriction-site PCR (IRS-PCR). High resistance to the 14 antimicrobial agents examined was observed among the isolates. Of the 13 antibiograms detected, eight were multi-resistant to gentamicin and almost all of the traditional and extended-spectrum beta-lactams. These multi-resistant strains consisted of 41 isolates (71%), distributed amongst different wards and intensive care units (ICUs). By IRS-PCR, 23 types were obtained, with one major type found among 28 (48%) isolates. All of these 28 isolates were collected from surgical ICUs. It appears that a single strain of multi-resistant A. baumannii was responsible for the prevalence of nosocomial infection amongst surgical patients, clearly differentiating this outbreak from the previous endemic situation. An efficient molecular typing method played a vital role in making this discrimination.

Acinetobacter↗

PubMed1998

Outbreak of nosocomial Acinetobacter baumannii bacteremia in a high risk ward.

Acinetobacter baumannii is emerging as a major cause of nosocomial infections particularly in high risk patients. Being resistant to adverse environmental conditions, it can stay for prolonged periods in the hospital environment. We report an outbreak in the medical oncology ward where nine patients suspected of bacteraemia were blood culture positive for A. baumannii from the two samples each, one collected through the i.v. cannula and another through the peripheral veneous puncture. The bacteria was also isolated from the environmental sources from the various samples collected. The biotype, antibiogram, cellular protein profiles on SDS-PAGE and the restriction enzyme analysis patterns of the patient isolates and the environmental isolates were similar. This points to the environment as a source of infection. With reinforcement of proper barrier nursing and use of disposable heparine ampoules it was possible to control the outbreak.

Acinetobacter Infections↗

PubMed2005

Multidrug-resistant Acinetobacter baumannii.

To understand the epidemiology of multidrug-resistant (MDR) Acinetobacter baumannii and define individual risk factors for multidrug resistance, we used epidemiologic methods, performed organism typing by pulsed-field gel electrophoresis (PFGE), and conducted a matched case-control retrospective study. We investigated 118 patients, on 27 wards in Israel, in whom MDR A. baumannii was isolated from clinical cultures. Each case-patient had a control without MDR A. baumannii and was matched for hospital length of stay, ward, and calendar time. The epidemiologic investigation found small clusters of up to 6 patients each with no common identified source. Ten different PFGE clones were found, of which 2 dominated. The PFGE pattern differed within temporospatial clusters, and antimicrobial drug susceptibility patterns varied within and between clones. Multivariate analysis identified the following significant risk factors: male sex, cardiovascular disease, having undergone mechanical ventilation, and having been treated with antimicrobial drugs (particularly metronidazole). Penicillins were protective. The complex epidemiology may explain why the emergence of MDR A. baumannii is difficult to control.

Acinetobacter Infections↗

PubMed1999

Alterations in surface hydrophobicity of Acinetobacter baumannii induced by meropenem.

Six strains of Acinetobacter baumannii out of eleven strains tested revealed a strong hydrophobic character. This was demonstrated by adherence of bacteria to xylene in the range of 90-94%. Changes in surface hydrophobicity of these strains were studied after treatment with meropenem at subinhibitory concentrations (sub-MICs) (1/4, 1/8, 1/16 or 1/32 of the MICs). All strains showed a reduced adherence to xylene after the action of meropenem at 1/4 or 1/16 of the MICs. Hydrophobicity of the treated bacteria was decreased to 1.3-70% (1/16 of the MICs) or to 12-86% (1/4 of the MICs), depending on the strain. A decrease in surface hydrophobicity of three strains was also observed after their exposure to meropenem at 1/8 of the MICs (to 18-71% of the control values). Meropenem at 1/32 of the MICs practically did not affect bacterial hydrophobic properties, with the exception of one strain.

Acinetobacter↗

PubMed2005

Role of environmental cleaning in controlling an outbreak of Acinetobacter baumannii on a neurosurgical intensive care unit.

An outbreak of Acinetobacter baumannii colonization and infection occurred in 19 patients over a 14-month period during 1998-1999 on a neurosurgical intensive care unit. During efforts to control the outbreak a significant correlation was observed between the number of environmental isolates of A. baumannii obtained during each monthly screening and the number of patients with A. baumannii colonization/infection in the same calendar month (P=0.004). Use of 1000 ppm hypochlorite solution and the introduction of new cleaning protocols reduced the number of environmental isolates. Failure to maintain low levels of environmental contamination with A. baumannii resulted in increases in patient colonization. This study showed that high standards of cleaning play an integral role in controlling outbreaks of A. baumannii in the intensive care unit setting.

Acinetobacter Infections↗

PubMed2004

Role of environmental cleaning in controlling an outbreak of Acinetobacter baumannii on a neurosurgical intensive care unit.

An outbreak of Acinetobacter baumannii colonization and infection occurred in 19 patients over a 14-month period during 1998-1999 on a neurosurgical intensive care unit. During efforts to control the outbreak a significant correlation was observed between the number of environmental isolates of A. baumannii obtained during each monthly screening and the number of patients with A. baumannii colonization/infection in the same calendar month (P < 0.004). Use of 1000 ppm hypochlorite solution and the introduction of new cleaning protocols reduced the number of environmental isolates. Failure to maintain low levels of environmental contamination with A. baumannii resulted in increases in patient colonization. This study showed that high standards of cleaning play an integral role in controlling outbreaks of A. baumannii in the intensive care unit setting.

Acinetobacter Infections↗

PubMed1995

[Sensitivity of Acinetobacter baumannii to antibiotics and disinfectants used in a Tunisian hospital milieu].

Seventy-nine strains of Acinetobacter baumannii isolated from pathologic products obtained mainly from surgical and intensive care units at the Rabta Hospital in Tunisia were studied. The sensitivity of these bacteria to the antibiotics used singly or in combination was tested in order to determine the most effective agents. Sensitivity to the disinfectants routinely used in our hospital was also studied using the "dilution-neutralisation" method according to "AFNOR" norms in order to identify the product with the most powerful preventive effect for Acinetobacter baumannii infection. The bacteria tested were resistant to all antibiotics except imipernem, colistin, and some aminoglycosides. A combination of imipenem-amikacin was effective against all strains. Best disinfection was obtained after 5 minutes of bacterial contact with aldehyde, phenol and amphotere.

Acinetobacter Infections↗

PubMed2001

Resistance-nodulation-cell division-type efflux pump involved in aminoglycoside resistance in Acinetobacter baumannii strain BM4454.

Multidrug-resistant strain Acinetobacter baumannii BM4454 was isolated from a patient with a urinary tract infection. The adeB gene, which encodes a resistance-nodulation-cell division (RND) protein, was detected in this strain by PCR with two degenerate oligodeoxynucleotides. Insertional inactivation of adeB in BM4454, which generated BM4454-1, showed that the corresponding protein was responsible for aminoglycoside resistance and was involved in the level of susceptibility to other drugs including fluoroquinolones, tetracyclines, chloramphenicol, erythromycin, trimethoprim, and ethidium bromide. Study of ethidium bromide accumulation in BM4454 and BM4454-1, in the presence or in the absence of carbonyl cyanide m-chlorophenylhydrazone, demonstrated that AdeB was responsible for the decrease in intracellular ethidium bromide levels in a proton motive force-dependent manner. The adeB gene was part of a cluster that included adeA and adeC which encodes proteins homologous to membrane fusion and outer membrane proteins of RND-type three-component efflux systems, respectively. The products of two upstream open reading frames encoding a putative two-component regulatory system might be involved in the regulation of expression of the adeABC gene cluster.

Acinetobacter↗