Heteroresistance to colistin in oxacillinase-producing carbapenem-resistant Acinetobacter baumannii clinical isolates from Gorgan, Northern Iran

Ezadi, Fereshteh; Jamali, Ailar; Heidari, Ahmad; Javid, Naeme; Ardebili, Abdollah

doi:10.1016/j.jgar.2019.11.010

Cited by 20 publications

(15 citation statements)

References 30 publications

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“…In this study, most of the CRAB isolates harbored one or two OXA carbapenemase genes, bla OXA-23-like and/ or bla OXA-58-like , similar to previous studies from Thailand (Lertsrisatit et al 2017;Leungtongkam et al 2018). In agreement with other reports, bla OXA-23-like was the major resistance determinant (40-100%) among the CRAB isolates, indicating that carbapenem monotherapy is now no longer used as a therapeutic option against the MDR A. baumannii infections (Ezadi et al 2019;Salehi et al 2018).…”

Section: Discussionsupporting

confidence: 91%

“…These isolates were from blood and respiratory tract, and susceptible to colistin with MICs of ≤ 0.25 to 0.5 µg/mL but grew on MHA containing 4 µg/ mL of colistin. Recently, 9 of 44 (20.5%) colistin-susceptible CRAB isolates from northern Iran have been identified as colistin-heteroresistant with subpopulations growing in the presence of 6-8 µg/mL of colistin (Ezadi et al 2019). The colistin heteroresistance rates may be different due to inoculum size applied (10-100 μL) and cut-off for identifying heteroresistant subpopulations (4 or ≥ 8 μg/mL) (Hawley et al 2008;Li et al 2006;Srinivas et al 2018).…”

Section: Discussionmentioning

confidence: 99%

“…The fingerprints were verified by BioNumerics software (version 7.6, Applied Maths, Belgium) using the Dice coefficient and the unweighted pair group method of averages (UPGMA) with 1% optimization and 1% position tolerance. Isolates showing ≥ 80% similarity were considered clonally related (Ezadi et al 2019).…”

Section: Strain Typingmentioning

confidence: 99%

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Colistin heteroresistance in carbapenem-resistant Acinetobacter baumannii clinical isolates from a Thai university hospital

Thet

Lunha

Srisrattakarn

et al. 2020

World J Microbiol Biotechnol

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Colistin is the last resort for the treatment of infections with carbapenem-resistant (CR) Gram-negative bacteria particularly Acinetobacter baumannii (CRAB). Currently, both colistin-resistant and-heteroresistant A. baumannii isolates have been reported globally. We therefore investigated the colistin heteroresistance rate in 75 non-duplicate colistin-susceptible CRAB clinical isolates from a Thai university collected in 2016. Minimum inhibitory concentrations (MICs) of colistin for all isolates were determined by broth microdilution method and carbapenemase genes were detected by PCR methods. All isolates were genotyped by ERIC-PCR method and screened for colistin heteroresistance by modified population analysis profile (PAP) method. The colistin MIC range for the 75 isolates was 0.5-2 µg/mL, with MIC 50 and MIC 90 of 1 and 2 µg/mL, respectively. Thirty-three isolates (44%) were considered colistin-heteroresistant with subpopulations growing at 3-8 μg/mL of colistin. After three daily passages of the subpopulations on antibiotic-free medium, their colistin MICs ranged from 4 to > 32 µg/mL, with MIC 50 and MIC 90 of 32 and > 32 µg/mL, respectively. Eight different ERIC-PCR profiles were obtained among the 33 isolates and all carried bla OXA-23-like. The high rate of colistin heteroresistance in the CRAB isolates highlights the possibility of treatment failure of CRAB infections by colistin due to the selection of colistin-resistant subpopulations.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 99%

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Colistin heteroresistance in carbapenem-resistant Acinetobacter baumannii clinical isolates from a Thai university hospital

Thet

Lunha

Srisrattakarn

et al. 2020

World J Microbiol Biotechnol

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“…A similar phenotype has also been described in clinical isolates of Stenotrophomonas maltophilia [29] and carbapenem-resistant A. baumannii [30]. Curiously, this phenomenon has enhanced colistin resistance in A. baumannii [31], an issue that is now of great interest, since colistin is the drug of choice for A. baumannii therapy [32][33][34] To answer the question of whether this phenotypic manifestation has a genetic basis, further investigation is required, including genomic sequencing. Choi and Ko stated that the two-component gene system PmrA/B is associated with the emergence of colistin heteroresistance in A.baumannii [35].…”

Section: Discussionmentioning

confidence: 63%

“…Moreover, several researchers showed increased incidence of heteroresistant A. baumannii isolates, e.g., Ezadi et al, who characterized 20.45% of isolates as colistin-heteroresistant [32], Li et al, who found 93.8% resistance in 16 clinical isolates [1], Hawley et al, who showed 100% resistance in 19 isolates [33], and Charretier and co-workers, who described half of their A. baumannii isolates as heteroresistant [36]. This makes it necessary to evaluate the appearance of heteroresistance in A. baumannii during colistin treatment.…”

Section: Discussionmentioning

confidence: 99%

Acquisition of Colistin Resistance Links Cell Membrane Thickness Alteration with a Point Mutation in the lpxD Gene in Acinetobacter baumannii

et al. 2020

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Acinetobacter baumannii is one of the most common causes of nosocomial infections in intensive care units. Its ability to acquire diverse mechanisms of resistance limits the therapeutic choices for its treatment. This especially concerns colistin, which has been reused recently as a last-resort drug against A. baumannii. Here, we explored the impact of gaining colistin resistance on the susceptibility of A. baumannii to other antibiotics and linked colistin resistance acquisition to a gene mutation in A. baumannii. The susceptibility of 95 A. baumannii isolates revealed that 89 isolates were multi-drug resistance (MDR), and nine isolates were resistant to colistin. Subsequently, three isolates, i.e., MS48, MS50, and MS64, exhibited different resistance patterns when colistin resistance was induced and gained resistance to almost all tested antibiotics. Upon TEM examination, morphological alterations were reported for all induced isolates and a colistin-resistant clinical isolate (MS34Col-R) compared to the parental sensitive strains. Finally, genetic alterations in PmrB and LpxACD were assessed, and a point mutation in LpxD was identified in the MS64Col-R and MS34Col-R mutants, corresponding to Lys117Glu substitution in the lipid-binding domain. Our findings shed light on the implications of using colistin in the treatment of A. baumannii, especially at sub-minimum inhibitory concentrations concentrations, since cross-resistance to other classes of antibiotics may emerge, beside the rapid acquisition of resistance against colistin itself due to distinct genetic events.

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Whole-Genome Sequence Analysis of Carbapenem-Heteroresistant Klebsiella pneumoniae and Escherichia coli Isolates

Sancak

Arı²,

Durmaz³

2022

Curr Microbiol

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Heteroresistance to colistin in oxacillinase-producing carbapenem-resistant Acinetobacter baumannii clinical isolates from Gorgan, Northern Iran

Cited by 20 publications

References 30 publications

Colistin heteroresistance in carbapenem-resistant Acinetobacter baumannii clinical isolates from a Thai university hospital

Colistin heteroresistance in carbapenem-resistant Acinetobacter baumannii clinical isolates from a Thai university hospital

Acquisition of Colistin Resistance Links Cell Membrane Thickness Alteration with a Point Mutation in the lpxD Gene in Acinetobacter baumannii

Whole-Genome Sequence Analysis of Carbapenem-Heteroresistant Klebsiella pneumoniae and Escherichia coli Isolates

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