The Genetic Differences among Colistin-Resistant Enterobacterales, Acinetobacter spp. and Pseudomonas aeruginosa

A special issue of Antibiotics (ISSN 2079-6382). This special issue belongs to the section "Mechanism and Evolution of Antibiotic Resistance".

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 4306

Special Issue Editors


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Guest Editor
Clinical Microbiology Laboratory, Attikon General University Hospital of Athens, Athens, Greece
Interests: antibiotic resistance; carbapenems; carbapenemases; hospital infections; Acinetobacter; Klebsiella; molecular epidemiology; infection control; antibiotic stewardship; medical microbiology

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Guest Editor
Department of Public Health, University of Naples Federico II, Naples, Italy
Interests: genotyping; horizontal gene transfer of antimicrobial resistance; MDR Acinetobacter baumannii; MDR Klebsiella pneumoniae; molecular epidemiology of healthcare-associated infections
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Department of Bacteriology, University Hospital of Besançon, Besançon, France
Interests: antibiotic resistance mechanisms; Pseudomonas aeruginosa; Acinetobacter baumannii; cystic fibrosis

Special Issue Information

Dear Colleagues,

Colistin is one of the few remaining antimicrobials able to be used as last resort against severe infections caused by Enterobacterales, Acinetobacter spp. and Pseudomonas aeruginosa. This Special Issue will focus on colistin resistance in Enterobacterales, Acinetobacter spp. and Pseudomonas aeruginosa. The aim is to present original research or review manuscripts dealing with different aspects of colistin resistance: molecular epidemiology and dissemination of colistin-resistant pathogens; molecular mechanisms of resistance and genetic acquisition; diagnostics; antimicrobial regimen–antimicrobial therapy. Particular consideration will be given to transdisciplinary research focused on the development of molecular, cellular, microbiological, computational and epidemiological approaches to addressing pathogen drug resistance. Studies assessing interactions among multi- and pan-drug resistance phenotypes and their genetic basis are encouraged, along with those examining the genomic and evolutionary context of mobilized, amplified or rearranged drug resistance genes. Lastly, papers bridging molecular diagnostics and surveillance of genetic elements associated with drug resistance would be appreciated.

Dr. Spyros Pournaras
Prof. Dr. Raffaele Zarrilli
Prof. Dr. Katy Jeannot
Guest Editors

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Published Papers (2 papers)

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Research

8 pages, 9477 KiB  
Article
Emergence of Colistin-Resistant Acinetobacter junii in China
by Zhiren Wang, Xuanyang Fan, Shuyi Wang, Shuguang Li, Yue Gao, Hui Wang and Henan Li
Antibiotics 2022, 11(12), 1693; https://doi.org/10.3390/antibiotics11121693 - 24 Nov 2022
Cited by 2 | Viewed by 1758
Abstract
The increasing number of multidrug-resistant Gram-negative bacteria presents a serious threat to global health. However, colistin-resistant Acinetobacter junii has rarely been reported. We identified a colistin-resistant A. junii clinical isolate, AJ6079, in blood. The colony of AJ6079 presented a dry phenotype, and it [...] Read more.
The increasing number of multidrug-resistant Gram-negative bacteria presents a serious threat to global health. However, colistin-resistant Acinetobacter junii has rarely been reported. We identified a colistin-resistant A. junii clinical isolate, AJ6079, in blood. The colony of AJ6079 presented a dry phenotype, and it was difficult to form a bacterial suspension, whilst transmission electron microscopy revealed that AJ6079 possessed a thick outer membrane. The phenotypic and genomic comparisons were conducted with one colistin-susceptible A. junii, which had the same antibiotic susceptibility profile except for colistin, and had the same KL25 capsule biosynthesis locus. The AJ6079 exhibited a slower growth rate, indicating that colistin-resistant A. junii possesses a higher fitness cost. The genome of AJ6079 had a G+C content of 38.7% and contained one 3,362,966 bp circular chromosome with no plasmid or mobile colistin resistance (mcr) gene. Comparative genomic analysis revealed that the AJ6079 contained several previously unreported point mutations in colistin-resistance-related genes involving amino acid substitutions in PmrB (N5K, G147C), LpxA (I107F, H131Y), and LpxD (F20I, K263R), which might be correlated with colistin resistance in A. junii. Further research is needed for verification as the genetic background was not exactly the same between the two isolates. Full article
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12 pages, 1091 KiB  
Article
Colistin Resistance Mechanisms in Human and Veterinary Klebsiella pneumoniae Isolates
by Manuela Tietgen, Lisa Sedlaczek, Paul G. Higgins, Heike Kaspar, Christa Ewers and Stephan Göttig
Antibiotics 2022, 11(11), 1672; https://doi.org/10.3390/antibiotics11111672 - 21 Nov 2022
Cited by 5 | Viewed by 1962
Abstract
Colistin (polymyxin E) is increasingly used as a last-resort antibiotic for the treatment of severe infections with multidrug-resistant Gram-negative bacteria. In contrast to human medicine, colistin is also used in veterinary medicine for metaphylaxis. Our objective was to decipher common colistin resistance mechanisms [...] Read more.
Colistin (polymyxin E) is increasingly used as a last-resort antibiotic for the treatment of severe infections with multidrug-resistant Gram-negative bacteria. In contrast to human medicine, colistin is also used in veterinary medicine for metaphylaxis. Our objective was to decipher common colistin resistance mechanisms in Klebsiella pneumoniae isolates from animals. In total, 276 veterinary K. pneumoniae isolates, derived from companion animals or livestock, and 12 isolates from human patients were included for comparison. Six out of 276 veterinary isolates were colistin resistant (2.2%). Human isolates belonging to high-risk clonal lineages (e.g., ST15, ST101, ST258), displayed multidrug-resistant phenotypes and harboured many resistance genes compared to the veterinary isolates. However, the common colistin resistance mechanism in both human and animal K. pneumoniae isolates were diverse alterations of MgrB, a critical regulator of lipid A modification. Additionally, deleterious variations of lipopolysaccharide (LPS)-associated proteins (e.g., PmrB P95L, PmrE P89L, LpxB A152T) were identified. Phylogenetic analysis and mutation patterns in genes encoding LPS-associated proteins indicated that colistin resistance mechanisms developed independently in human and animal isolates. Since only very few antibiotics remain to treat infections with MDR bacteria, it is important to further analyse resistance mechanisms and the dissemination within different isolates and sources. Full article
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