Diversity of Class 1 Integrons, and Disruption of carO and dacD by Insertion Sequences Among Acinetobacter baumannii Isolates in Tehran, Iran

Mirshekar, Maryam; Shahcheraghi, Fereshteh; Azizi, Omid; Solgi, Hamid; Badmasti, Farzad

doi:10.1089/mdr.2017.0152

Cited by 28 publications

(11 citation statements)

References 26 publications

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“…[ 10 , 25 ] IS Aba1 has been shown to be associated with bla OXA-23 -like- and bla OXA-51 -like-related CR of A. baumannii . [ 26 , 27 ] Its absence in the upstream of OXA-51-like but presence in that of OXA-23-like revealed that OXA-51-like was not as important as OXA-23-like in contributing to the CR phenotype in our study. This was proofed by the null expression of OXA-66/-69 in the strains.…”

Section: Discussionmentioning

confidence: 50%

bla OXA-23-like and bla TEM rather than bla OXA-51-like contributed to a high level of carbapenem resistance in Acinetobacter baumannii strains from a teaching hospital in Xi’an, China

Han

Lei²,

Xu³

et al. 2017

Medicine

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Acinetobacter baumannii is one of the major threats in clinical infections due to its antibiotic resistance ability. It shows increasing resistance to carbapenems, mainly due to β-lactamase mediated mechanisms. The aim of this study was to investigate carbapenem resistance (CR) profiles and analyze β-lactamases genes composition of clinical A. baumannii strains from a teaching hospital in Xi’an. The resistance patterns to imipenem and meropenem were checked for 51 clinical A. baumannii strains. The existence of 15 β-lactamases genes was detected by polymerase chain reaction (PCR), and the positive genes were sequenced. The correlation between PCR-positive genes and CR phenotype was analyzed using Chi-square test and contingency coefficient. The expressions of PCR-positive genes were investigated. Forty-five out of 51 strains were resistant to imipenem and meropenem. blaTEM, blaOXA-23-like, and blaOXA-51-like were positive among 15 β-lactamases genes, and TEM-1, OXA-23, and OXA-66/69 were their subtypes. TEM and OXA-23-like only showed up in CR isolates, with the occurrence rate of 91.1% and 97.8%, respectively, whereas OXA-51-like appeared in all strains. ISAba1 was present in the upstream of OXA-23-like, but absent from that of OXA-51-like in our strains. OXA-23-like had highest relationship with CR, followed by TEM, but OXA-51-like had no correlation. This was verified by RT-qPCR that the expression was positive for OXA-23 and TEM-1, but negative for OXA-66/-69. A high rate of CR A. baumannii was detected in this study. Coexistence of TEM, OXA-23-like, and OXA-51-like was the primary resistance profile. The expressions of OXA-23-like and TEM genes were closely related with CR, while OXA-51-like had no contribution to the CR phenotype.

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Section: Discussionmentioning

confidence: 50%

bla OXA-23-like and bla TEM rather than bla OXA-51-like contributed to a high level of carbapenem resistance in Acinetobacter baumannii strains from a teaching hospital in Xi’an, China

Han

Lei²,

Xu³

et al. 2017

Medicine

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“…A BLAST search with the first 300 nt of the aadB transcript yields hits to Ͼ100 A. baumannii genomes, with coverage ranging from 73% to 100%. Integrons encoding aminoglycoside modifying enzymes, including aadB, are also widely reported in the A. baumannii literature (45)(46)(47)(48)(49)(50). As the ϳ300-nt sRNA appears to be encoded mostly within the integron promoter region, it is possible that other integrons, even those not harboring aadB, still contain this transcript.…”

Section: Discussionmentioning

confidence: 99%

Copy Number of an Integron-Encoded Antibiotic Resistance Locus Regulates a Virulence and Opacity Switch in Acinetobacter baumannii AB5075

Anderson

Chin

Weiss

et al. 2020

mBio

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We describe a novel genetic mechanism in which tandem amplification of a plasmid-borne integron regulates virulence, opacity variation, and global gene expression by altering levels of a putative small RNA (sRNA) in Acinetobacter baumannii AB5075. Copy number of this amplified locus correlated with the rate of switching between virulent opaque (VIR-O) and avirulent translucent (AV-T) cells. We found that prototypical VIR-O colonies, which exhibit high levels of switching and visible sectoring with AV-T cells by 24 h of growth, harbor two copies of this locus. However, a subset of opaque colonies that did not form AV-T sectors within 24 h were found to harbor only one copy. The colonies with decreased sectoring to AV-T were designated low-switching opaque (LSO) variants and were found to exhibit a 3-log decrease in switching relative to that of the VIR-O. Overexpression studies revealed that the element regulating switching was localized to the 5′ end of the aadB gene within the amplified locus. Northern blotting indicated that an sRNA of approximately 300 nucleotides (nt) is encoded in this region and is likely responsible for regulating switching to AV-T. Copy number of the ∼300-nt sRNA was also found to affect virulence, as the LSO variant exhibited decreased virulence during murine lung infections. Global transcriptional profiling revealed that >100 genes were differentially expressed between VIR-O and LSO variants, suggesting that the ∼300-nt sRNA may act as a global regulator. Several virulence genes exhibited decreased expression in LSO cells, potentially explaining their decreased virulence. IMPORTANCE Acinetobacter baumannii remains a leading cause of hospital-acquired infections. Widespread multidrug resistance in this species has prompted the WHO to name carbapenem-resistant A. baumannii as its top priority for research and development of new antibiotics. Many strains of A. baumannii undergo a high-frequency virulence switch, which is an attractive target for new therapeutics targeting this pathogen. This study reports a novel mechanism controlling the frequency of switching in strain AB5075. The rate of switching from the virulent opaque (VIR-O) to the avirulent translucent (AV-T) variant is positively influenced by the copy number of an antibiotic resistance locus encoded on a plasmid-borne composite integron. Our data suggest that this locus encodes a small RNA that regulates opacity switching. Low-switching opaque variants, which harbor a single copy of this locus, also exhibit decreased virulence. This study increases our understanding of this critical phenotypic switch, while also identifying potential targets for virulence-based A. baumannii treatments.

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“…A recent study from Egypt revealed that ISAba1 has been inserted in carO gene leading to interruption of its expression [173]. A report about an insertion sequence disrupting the gene encoding the penicillin binding protein PBP6b (also known as dacD) was identified in an endemic carbapenem-resistant clone in a Spanish hospital [174]. Additionally, a collective set of changes involving disruptions in carO and dacD, as well as carbapenemase production, developed resistance to carbapenems among clinical isolates of A. baumannii [175].…”

Section: Nonenzymatic β-Lactam Resistance Mechanismsmentioning

confidence: 99%

Insights into Acinetobacter baumannii: A Review of Microbiological, Virulence, and Resistance Traits in a Threatening Nosocomial Pathogen

2020

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Being a multidrug-resistant and an invasive pathogen, Acinetobacter baumannii is one of the major causes of nosocomial infections in the current healthcare system. It has been recognized as an agent of pneumonia, septicemia, meningitis, urinary tract and wound infections, and is associated with high mortality. Pathogenesis in A. baumannii infections is an outcome of multiple virulence factors, including porins, capsules, and cell wall lipopolysaccharide, enzymes, biofilm production, motility, and iron-acquisition systems, among others. Such virulence factors help the organism to resist stressful environmental conditions and enable development of severe infections. Parallel to increased prevalence of infections caused by A. baumannii, challenging and diverse resistance mechanisms in this pathogen are well recognized, with major classes of antibiotics becoming minimally effective. Through a wide array of antibiotic-hydrolyzing enzymes, efflux pump changes, impermeability, and antibiotic target mutations, A. baumannii models a unique ability to maintain a multidrug-resistant phenotype, further complicating treatment. Understanding mechanisms behind diseases, virulence, and resistance acquisition are central to infectious disease knowledge about A. baumannii. The aims of this review are to highlight infections and disease-producing factors in A. baumannii and to touch base on mechanisms of resistance to various antibiotic classes.

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Diversity of Class 1 Integrons, and Disruption of carO and dacD by Insertion Sequences Among Acinetobacter baumannii Isolates in Tehran, Iran

Cited by 28 publications

References 26 publications

bla OXA-23-like and bla TEM rather than bla OXA-51-like contributed to a high level of carbapenem resistance in Acinetobacter baumannii strains from a teaching hospital in Xi’an, China

bla OXA-23-like and bla TEM rather than bla OXA-51-like contributed to a high level of carbapenem resistance in Acinetobacter baumannii strains from a teaching hospital in Xi’an, China

Copy Number of an Integron-Encoded Antibiotic Resistance Locus Regulates a Virulence and Opacity Switch in Acinetobacter baumannii AB5075

Insights into Acinetobacter baumannii: A Review of Microbiological, Virulence, and Resistance Traits in a Threatening Nosocomial Pathogen

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