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Colistin heteroresistance in Enterobacter cloacae is regualted by PhoPQ-dependent 4-amino-4-deoxy-L arabinose addition to lipid A

ABSTRACT: We report the transcriptional expression from wild type, ΔphoPQ, and ΔpmrAB to understand their contribution to colistin resistance.

ORGANISM(S): Enterobacter cloacae subsp. cloacae ATCC 13047

PROVIDER: GSE127802 | GEO | 2019/06/20

REPOSITORIES: GEO

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Colistin heteroresistance in Enterobacter cloacae is regulated by PhoPQ-dependent 4-amino-4-deoxy-l-arabinose addition to lipid A.

Project description:The Enterobacter cloacae complex (ECC) consists of closely related bacteria commonly associated with the human microbiota. ECC are increasingly isolated from healthcare-associated infections, demonstrating that these Enterobacteriaceae are emerging nosocomial pathogens. ECC can rapidly acquire multidrug resistance to conventional antibiotics. Cationic antimicrobial peptides (CAMPs) have served as therapeutic alternatives because they target the highly conserved lipid A component of the Gram-negative outer membrane. Many Enterobacteriaceae fortify their outer membrane with cationic amine-containing moieties to prevent CAMP binding, which can lead to cell lysis. The PmrAB two-component system (TCS) directly activates 4-amino-4-deoxy-l-arabinose (l-Ara4N) biosynthesis to result in cationic amine moiety addition to lipid A in many Enterobacteriaceae such as E. coli and Salmonella. In contrast, PmrAB is dispensable for CAMP resistance in E. cloacae. Interestingly, some ECC clusters exhibit colistin heteroresistance, where a subpopulation of cells exhibit clinically significant resistance levels compared to the majority population. We demonstrate that E. cloacae lipid A is modified with l-Ara4N to induce CAMP heteroresistance and the regulatory mechanism is independent of the PmrABEcl TCS. Instead, PhoPEcl binds to the arnBEcl promoter to induce l-Ara4N biosynthesis and PmrAB-independent addition to the lipid A disaccharolipid. Therefore, PhoPQEcl contributes to regulation of CAMP heteroresistance in some ECC clusters.

| S-EPMC6561824 | biostudies-literature

Colistin heteroresistance in Enterobacter cloacae is regualted by PhoPQ-dependent 4-amino-4-deoxy-L arabinose addition to lipid A

Project description:Colistin heteroresistance in Enterobacter cloacae is regualted by PhoPQ-dependent 4-amino-4-deoxy-L arabinose addition to lipid A

| PRJNA525427 | ENA

Colistin-resistance in Enterobacter cloacae

Project description:Colistin-resistance mediated by amino acid alterations in PhoQ sensor kinase in clinical Enterobacter cloacae ST-335 strain

| PRJEB22680 | ENA

Carbapenem- and Colistin-Resistant Enterobacter cloacae from Delta, Colorado, in 2015.

Project description:Resistance to carbapenems in Enterobacteriaceae is a clinical problem of growing significance. Difficulty in treating multidrug-resistant Gram-negative organisms with conventional antibiotics has led to a renewed and increasing use of polymyxin compounds, such as colistin. Here, we report the isolation of carbapenem- and colistin-resistant Enterobacter cloacae from a polymicrobial lower extremity wound in an ambulatory patient. Whole-genome sequencing demonstrated the presence of chromosomal blaIMI-1 and blaAmpC, as well as numerous efflux pump genes.

| S-EPMC4862446 | biostudies-literature

Colistin resistant A. baumannii: genomic and transcriptomic traits acquired under colistin therapy

Project description:Comparative Genomic and Transcriptomic Characterization of Colistin-Resistant Acinetobacter baumannii

2019-01-23 | GSE109951 | GEO

Aminocandin versus Aminocandin plus Colistin

Project description:We found that the antibiotic colistin acts synergistically with antifungals of the echinocandin class (e.g. aminocandin) on C. albicans cells. In order to elucidate the mode of action of colistin in fungi we performed microarray analysis of samples treated with only aminocandin (0.00125µg/ml) or treated with aminocandin (0.00125µg/ml) and colistin (5µg/ml). We compared: (A). untreated cells to cells treated with aminocandin only; (B). cells treated with aminocandin to cells treated with aminocandin and colistin (which is the focus of this experiment). By comparing those datasets it should be possible to identify genes differentially expressed in response to aminocandin and in response to both drugs. And subsequently to be able to interpret where in the cell colistin acts. (See related experiment in ArrayExpress: E-MEXP-3437 for comparison between untreated cells vs cells treated with aminocandin only.)

2012-03-03 | E-MEXP-3438 | biostudies-arrayexpress

Absence of mgrB Alleviates Negative Growth Effects of Colistin Resistance in Enterobacter cloacae.

Project description:Colistin is an important last-line antibiotic to treat highly resistant Enterobacter infections. Resistance to colistin has emerged among clinical isolates but has been associated with a significant growth defect. Here, we describe a clinical Enterobacter isolate with a deletion of mgrB, a regulator of colistin resistance, leading to high-level resistance in the absence of a growth defect. The identification of a path to resistance unrestrained by growth defects suggests colistin resistance could become more common in Enterobacter.

| S-EPMC7699182 | biostudies-literature

Colistin heteroresistance in Enterobacter cloacae is associated with cross-resistance to the host antimicrobial lysozyme.

Project description:Here, we describe the first identification of colistin-heteroresistant Enterobacter cloacae in the United States. Treatment of this isolate with colistin increased the frequency of the resistant subpopulation and induced cross-resistance to the host antimicrobial lysozyme. This is the first description of heteroresistance conferring cross-resistance to a host antimicrobial and suggests that clinical treatment with colistin may inadvertently select for bacteria that are resistant to components of the host innate immune system.

| S-EPMC4135841 | biostudies-other

First identification of an IMI-1 carbapenemase-producing colistin-resistant Enterobacter cloacae in China.

Project description:BackgroundCarbapenem resistance among the Enterobacteriaceae is a serious healthcare challenge. bla IMI is a carbapenemase gene mediating resistance to carbapenems but has not been commonly found. A bla IMI-carrying Enterobacter cloacae, which was also resistant to colistin, is reported here.FindingsE. cloacae strain WCHECl-1060 was recovered from a blood sample of a leukemia patient, who was not previously exposed to colistin. Strain WCHECl-1060 belongs to a new sequence type, ST410, and was resistant to carbapenems and colistin but was susceptible to third-generation cephalosporins. A new allelic variant of bla IMI-1, which has two silent mutations compared to the original bla IMI-1 variant, was found in strain WCHECl-1060. Conjugation and transformation experiments failed to transfer bla IMI-1, suggesting a likely chromosome origin.ConclusionsTo our knowledge, this is the first report of an IMI-1 carbapenemase-producing colistin-resistant E. cloacae in China. Microbiological laboratories should be aware of the unusual carbapenem-resistant but third-generation cephalosporin-susceptible profiles of these IMI-producing isolates. The trend of colistin resistance among the Enterobacteriaceae should be also monitored.

| S-EPMC4658791 | biostudies-literature

Characterization of resistance mechanisms of Enterobacter cloacae Complex co-resistant to carbapenem and colistin.

Project description:BackgroundThe emergence of carbapenem-resistant and colistin-resistant ECC pose a huge challenge to infection control. The purpose of this study was to clarify the mechanism of the carbapenems and colistin co-resistance in Enterobacter cloacae Complex (ECC) strains.ResultsThis study showed that the mechanisms of carbapenem resistance in this study are: 1. Generating carbapenemase (7 of 19); 2. The production of AmpC or ESBLs combined with decreased expression of out membrane protein (12 of 19). hsp60 sequence analysis suggested 10 of 19 the strains belong to colistin hetero-resistant clusters and the mechanism of colistin resistance is increasing expression of acrA in the efflux pump AcrAB-TolC alone (18 of 19) or accompanied by a decrease of affinity between colistin and outer membrane caused by the modification of lipid A (14 of 19). Moreover, an ECC strain co-harboring plasmid-mediated mcr-4.3 and blaNDM-1 has been found.ConclusionsThis study suggested that there is no overlap between the resistance mechanism of co-resistant ECC strains to carbapenem and colistin. However, the emergence of strain co-harboring plasmid-mediated resistance genes indicated that ECC is a potential carrier for the horizontal spread of carbapenems and colistin resistance.

| S-EPMC8268410 | biostudies-literature

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