QacE and QacE?1 Genes and Their Correlation to Antibiotics and Biocides Resistance Pseudomonas aeruginosa

Helal, Zeinab H.; Khan, Mazhar I.

doi:10.5099/aj150200052

Cited by 11 publications

(10 citation statements)

References 21 publications

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“…After the laboratory diagnosis, 69 isolates of P. aeruginosa including 24 wounds isolates (35%) and 45 burns isolates (65%). P. aeurginosa is most bacteria causes burn infections because it lives in the humid environment and hospitals and is a major cause of both burns and wound infections [7], the present study is similar to that of the researchers [8,9]. These results was agreed with Kucken et al [8] who determined the prevalence of the gene 81% in P. aeruginosa isolated from different clinical sources which encodes quaternary ammonium compound delta qacE∆1 which responsible for the resistance to disinfectants, that including quaternary ammonium compound and cetramide, as well as with the researcher Helal and Khan [9], who determined the prevalence of the gene 79% in P.aeruginosa, while the agreement with Dabiri et al [10] who showed that 64.4% gene prevalence in P.…”

Section: Resultssupporting

confidence: 87%

DNA Sequences of qacE∆1 Gene in Pseudomonas Aeruginosa Isolated from Wounds and Burns Infections.

Al-Azzawi¹,

Abdullah²

2019

KUJSS

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A total of 69 isolates of Pseudomonas aeruginosa were obtained from different clinical samples including wounds 24 (35%) and burns 67 (65%)، the genes that responsible for Pseudomonas aeruginosa resistance isolates was detected, the results showed that quaternary ammonium compound delta 1 (qacE∆1) gene was 97.1% in Pseudomonas aeruginosa isolation. 24 (35%) in the wounds and 63 (62.31%) in burns, the size of the gene showed 285 bp, the results of the qacE∆1 analysis showed a single mutation of the mutation type. The results of genetic analysis tree were showed after comparing presence of genetic variations of the qacE∆1 gene with their relatives from the nucleotide sequences as containing variations occurring at one distance and equally in Pseudomonas aeruginosa and other bacterial species.

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Section: Resultssupporting

confidence: 87%

DNA Sequences of qacE∆1 Gene in Pseudomonas Aeruginosa Isolated from Wounds and Burns Infections.

Al-Azzawi¹,

Abdullah²

2019

KUJSS

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“…This, alongside the broad range of substrates (QAC compounds, disinfectants, antibiotics, etc.) that SMRs can extrude and their increasing prevalence on plasmids and integrons in clinical and multidrug-resistant strains of bacteria (13,(27)(28)(29)(30)(31)(32)(33)(34)(35), marks these proteins as important therapeutic targets.…”

Section: Discussionmentioning

confidence: 99%

Peptide-Based Efflux Pump Inhibitors of the Small Multidrug Resistance Protein from Pseudomonas aeruginosa

Mitchell

Stone

Deber

2019

Antimicrob Agents Chemother

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Bacteria have acquired multiple mechanisms to evade the lethal effects of current therapeutics, hindering treatment of bacterial infections, such as those caused by the pathogen Pseudomonas aeruginosa, which is responsible for nosocomial and cystic fibrosis lung infections. One resistance mechanism involves membrane-embedded multidrug efflux pumps that can effectively extrude an array of substrates, including common antibiotics, dyes, and biocides. Among these is a small multidrug resistance (SMR) efflux protein, consisting of four transmembrane (TM) helices, that functions as an antiparallel dimer. TM helices 1 to 3 (TM1 to TM3) comprise the substrate binding pocket, while TM4 contains a GG7 heptad sequence motif that mediates the SMR TM4-TM4 dimerization. In the present work, we synthesized a series of peptides containing the residues centered on the TM4-TM4 binding interface found in the P. aeruginosa SMR (PAsmr), typified by Ac-Ala-(Sar)3-LLGIGLIIAGVLV-KKK-NH2 (helix-helix interaction residues are underlined). Here, the acetylated N-terminal sarcosine (N-methyl-Gly) tag [Ac-Ala-(Sar)3] promotes membrane penetration, while the C-terminal Lys tag promotes selectivity for the negatively charged bacterial membranes. This peptide was observed to competitively disrupt PAsmr-mediated efflux, as measured by efflux inhibition of the fluorescent dye ethidium bromide, while having no effect on cell membrane integrity. Alternatively, a corresponding peptide in which the TM4 binding motif is scrambled was inactive in this assay. In addition, when Escherichia coli cells expressing PAsmr were combined with sublethal concentrations of several biocides, growth was significantly inhibited when peptide was added, notably, by up to 95% with the disinfectant benzylalkonium chloride. These results demonstrate promise for an efflux pump inhibitor to address the increasing threat of antibiotic-resistant bacteria.

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“…Moreover, multiple antibiotic, biocide, and metal resistance genes were identified: qacEΔ1 (biocide resistance [24,25]), sulI (sulfonamide resistance [26]), the mphR(A)/mphA/mrx gene cluster (macrolide/erythromycin resistance [27]), and chrA (chromate resistance [28,29]). The qacEΔ1 gene encodes a truncated and less-efficient cation efflux pump version of qacE (24). Additionally, both segments included similarity to the GNAT (acetyltransferase) and sulI3 genes (30).…”

mentioning

confidence: 99%

“…The dfrB4 gene was carried with intI1 (class 1 integron integrase/recombinase) and tnpA (transposase), which are indispensable for integration of mobile genetic elements (23). Moreover, multiple antibiotic, biocide, and metal resistance genes were identified: qacEΔ1 (biocide resistance [24,25]), sulI (sulfonamide resistance [26]), the mphR(A)/mphA/mrx gene cluster (macrolide/erythromycin resistance [27]), and chrA (chromate resistance [28,29]). The qacEΔ1 gene encodes a truncated and less-efficient cation efflux pump version of qacE (24).…”

mentioning

confidence: 99%

Integron-Associated DfrB4, a Previously Uncharacterized Member of the Trimethoprim-Resistant Dihydrofolate Reductase B Family, Is a Clinically Identified Emergent Source of Antibiotic Resistance

Edens²,

Alejaldre

et al. 2017

Antimicrob Agents Chemother

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Whole-genome sequencing of trimethoprim-resistant Escherichia coli clinical isolates identified a member of the trimethoprim-resistant type II dihydrofolate reductase gene family (dfrB). The dfrB4 gene was located within a class I integron flanked by multiple resistance genes. This arrangement was previously reported in a 130.6-kb multiresistance plasmid. The DfrB4 protein conferred a Ͼ2,000-fold increased trimethoprim resistance on overexpression in E. coli. Our results are consistent with the finding that dfrB4 contributes to clinical trimethoprim resistance.KEYWORDS type II dihydrofolate reductase, trimethoprim resistance, E. coli clinical isolates, dfrB4, antibiotic-resistant genes, class I integron, urinary tract infection P ublic health agencies worldwide rank trimethoprim (TMP) a broad-spectrum antibiotic of importance in human medicine (1). Widely used as a result of its low cost and effectiveness, TMP inhibits the activity of many microbial chromosomal dihydrofolate reductases (DHFRs); thus, DHFRs have long served as prioritized targets of antiproliferative drugs (2). Although the majority of living cells harbor a chromosomal member of the type I DHFR family, encoded by a dfrA homolog, the dfrB genes encode a family of plasmid-borne type II DHFRs that are evolutionarily unrelated to type I DHFRs. The dfrB genes have been found in pathogenic bacteria recovered from many food sources, including fish (3), pigs (4, 5), and cows (6), where they confer TMP resistance. Bacteria carrying dfrB genes have also been identified in wastewater samples (7). Over the past decade, dfrB genes have been tracked indirectly in antibiotic resistance studies through identification of integron-related elements (8-10). Therefore, the importance of dfrB genes in TMP resistance in human pathogens may be underappreciated (11,12).To date, only seven members of the dfrB gene family are known, and they are highly homologous (77% to 94% genetic identity, 77% to 99% amino acid identity) ( Table 1). Among these, the DfrB1 protein (also known as R67 DHFR) is the best-studied type II DHFR (13)(14)(15)(16)(17). It is proposed to be recently evolved, and it confers a significant survival advantage under TMP exposure to microbes that harbor it (18). To date, the family of dfrB genes has consistently been reported to be contained within the following mobile

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QacE and QacE?1 Genes and Their Correlation to Antibiotics and Biocides Resistance Pseudomonas aeruginosa

Cited by 11 publications

References 21 publications

DNA Sequences of qacE∆1 Gene in Pseudomonas Aeruginosa Isolated from Wounds and Burns Infections.

DNA Sequences of qacE∆1 Gene in Pseudomonas Aeruginosa Isolated from Wounds and Burns Infections.

Peptide-Based Efflux Pump Inhibitors of the Small Multidrug Resistance Protein from Pseudomonas aeruginosa

Integron-Associated DfrB4, a Previously Uncharacterized Member of the Trimethoprim-Resistant Dihydrofolate Reductase B Family, Is a Clinically Identified Emergent Source of Antibiotic Resistance

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