Insights into <i>Acinetobacter baumannii</i> pathogenicity

Cerqueira, Gustavo M.; Peleg, Anton Y.

doi:10.1002/iub.533

Cited by 160 publications

(134 citation statements)

References 43 publications

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“…The bacterium can survive on solid and dry surfaces up to 5 months, which is attributed to: simplicity of its nutritional requirements, ability to grow in the wide range of temperatures and pH values, high degree of resistance to disinfectants and antiseptics, ability to form biofilm on abiotic substrata (environmental surfaces or medical devices, such as catheters or respiratory equipment) as well as biotic surfaces [1][2][3][4][5]. These features are likely to be a major contributing factor to nosocomial spread of the A. baumannii [5].…”

Section: Introductionmentioning

confidence: 99%

Acinetobacter baumannii: biology and drug resistance — role of carbapenemases

Nowak

Paluchowska

2015

Folia Histochem Cytobiol.

107

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Acinetobacter baumannii is a Gram-negative, glucose-non-fermenting, oxidase-negative coccobacillus, most commonly associated with the hospital settings. The ability to survive in adverse environmental conditions as well as high level of natural and acquired antimicrobial resistance make A. baumannii one of the most important nosocomial pathogens. While carbapenems have long been considered as antimicrobials of last-resort, the rates of clinical A. baumannii strains resistant to these antibiotics are increasing worldwide. Carbapenem resistance among A. baumannii is conferred by coexisting mechanisms including: decrease in permeability of the outer membrane, efflux pumps, production of beta-lactamases, and modification of penicillin-binding proteins. The most prevalent mechanism of carbapenem resistance among A. baumannii is associated with carbapenem-hydrolysing enzymes that belong to Ambler class D and B beta-lactamases. In addition, there have also been reports of resistance mediated by selected Ambler class A carbapenemases among A. baumannii strains. Resistance determinants in A. baumannii are located on chromosome and plasmids, while acquisition of new mechanisms can be mediated by insertion sequences, integrons, transposons, and plasmids. Clinical relevance of carbapenem resistance among strains isolated from infected patients, carriers and hospital environment underlines the need for carbapenemase screening. Currently available methods vary in principle, accuracy and efficiency. The techniques that deserve particular attention belong to both easily accessible unsophisticated methods as well as advanced techniques based on mass spectrometry or molecular biology. While carbapenemases limit the therapeutic options in A. baumannii infections, studies concerning novel beta-lactamase inhibitors offer a new insight into effective therapy.

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Section: Introductionmentioning

confidence: 99%

Acinetobacter baumannii: biology and drug resistance — role of carbapenemases

Nowak

Paluchowska

2015

Folia Histochem Cytobiol.

107

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“…A. baumannii infection can cause pneumonia, bacteremia, endocarditis, skin and soft-tissue infections, urinary tract infections, and meningitis (2). Mortality rates from A. baumannii infections range from 20 to 70% (3).…”

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confidence: 99%

The Nod1, Nod2, and Rip2 Axis Contributes to Host Immune Defense against Intracellular Acinetobacter baumannii Infection

et al. 2014

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Acinetobacter baumannii is a major extensively drug-resistant lethal human nosocomial bacterium. However, the host innate immune mechanisms controlling A. baumannii are not well understood. Although viewed as an extracellular pathogen, A. baumannii can also invade and survive intracellularly. However, whether host innate immune pathways sensing intracellular bacteria contribute to immunity against A. baumannii is not known. Here, we provide evidence for the first time that intracellular antibacterial innate immune receptors Nod1 and Nod2, and their adaptor Rip2, play critical roles in the sensing and clearance of A. baumannii by human airway epithelial cells in vitro. A. baumannii infection upregulated Rip2 expression. Silencing of Nod1, Nod2, and Rip2 expression profoundly increased intracellular invasion and prolonged the multiplication and survival of A. baumannii in lung epithelial cells. Notably, the Nod1/2-Rip2 axis did not contribute to the control of A. baumannii infection of human macrophages, indicating that they play cell type-specific roles. The Nod1/2-Rip2 axis was needed for A. baumannii infection-induced activation of NF-B but not mitogen-activated protein kinases. Moreover, the Nod1/2-Rip2 axis was critical to induce optimal cytokine and chemokine responses to A. baumannii infection. Mechanistic studies showed that the Nod1/2 pathway contributed to the innate control of A. baumannii infection through the production of ␤-defensin 2 by airway epithelial cells. This study revealed new insights into the immune control of A. baumannii and may contribute to the development of effective immune therapeutics and vaccines against A. baumannii.

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“…It has become alarmingly clear that A. baumannii clinical isolates have developed mechanisms of resistance to currently available antimicrobial chemotherapies, making treatment of serious infections caused by this pathogen a significant challenge in human medicine (2)(3)(4)(5). Although much is known about antibiotic resistance and the epidemiology of infections caused by A. baumannii, the virulence properties and the pathobiology of this emerging pathogen are still poorly understood.…”

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confidence: 99%

Functional Features of TonB Energy Transduction Systems of Acinetobacter baumannii

et al. 2013

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Acinetobacter baumannii is an opportunistic pathogen that causes severe nosocomial infections. Strain ATCC 19606 T utilizes the siderophore acinetobactin to acquire iron under iron-limiting conditions encountered in the host. Accordingly, the genome of this strain has three tonB genes encoding proteins for energy transduction functions needed for the active transport of nutrients, including iron, through the outer membrane. Phylogenetic analysis indicates that these tonB genes, which are present in the genomes of all sequenced A. baumannii strains, were acquired from different sources. Two of these genes occur as components of tonB-exbB-exbD operons and one as a monocistronic copy; all are actively transcribed in ATCC 19606T . The abilities of components of these TonB systems to complement the growth defect of Escherichia coli W3110 mutants KP1344 (tonB) and RA1051 (exbBD) under iron-chelated conditions further support the roles of these TonB systems in iron acquisition. Mutagenesis analysis of ATCC 19606 T tonB 1 (subscripted numbers represent different copies of genes or proteins) and tonB 2 supports this hypothesis: their inactivation results in growth defects in iron-chelated media, without affecting acinetobactin biosynthesis or the production of the acinetobactin outer membrane receptor protein BauA. In vivo assays using Galleria mellonella show that each TonB protein is involved in, but not essential for, bacterial virulence in this infection model. Furthermore, we observed that TonB 2 plays a role in the ability of bacteria to bind to fibronectin and to adhere to A549 cells by uncharacterized mechanisms. Taken together, these results indicate that A. baumannii ATCC 19606 T produces three independent TonB proteins, which appear to provide the energy-transducing functions needed for iron acquisition and cellular processes that play a role in the virulence of this pathogen.

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Insights into Acinetobacter baumannii pathogenicity

Cited by 160 publications

References 43 publications

Acinetobacter baumannii: biology and drug resistance — role of carbapenemases

Acinetobacter baumannii: biology and drug resistance — role of carbapenemases

The Nod1, Nod2, and Rip2 Axis Contributes to Host Immune Defense against Intracellular Acinetobacter baumannii Infection

Functional Features of TonB Energy Transduction Systems of Acinetobacter baumannii

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