Detection and characterization of NDM-1-producing <i>Klebsiella pneumoniae</i> in Iran: an incursion crisis

Hasani, Alka; Soltani, Elghar; Rezaee, Mohammad Ahangharzadeh; Hasani, Akbar; Gholizadeh, Pourya; Oskouie, Arezoo Noie

doi:10.1080/23744235.2019.1705997

Cited by 7 publications

(5 citation statements)

References 8 publications

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“…Biofilm formation mechanisms in clinical K. pneumoniae is reported to be mediated by a series of genes, including allantoin (allS), aerobactin (iutA), type I (fimA and fimH) and type III fimbriae (mrkA and mrkD), polysaccharides and adhesins (pgaA, pgaB, pgaC, and bcsA), capsular polysaccharide (CPS) (wzc, cpsD, treC, wcaG, wabG, rmpA/A2, magA, k2a, and wzyk2), quorum sensing (QS) (luxS) and colonic acid (wcaJ) (Wu et al, 2011;Alcántar-Curiel et al, 2013;Zheng et al, 2018;Pal et al, 2019;Chen et al, 2020;Hasani et al, 2020). Though these genetic factors were individually studied, a collective approach on their analysis in a set of clinical isolates is still lacking.…”

Section: Introductionmentioning

confidence: 99%

The Influence of Biofilms on Carbapenem Susceptibility and Patient Outcome in Device Associated K. pneumoniae Infections: Insights Into Phenotype vs Genome-Wide Analysis and Correlation

et al. 2020

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Klebsiella pneumoniae is one of the leading causes of nosocomial infections. Carbapenem-resistant K. pneumoniae are on the rise globally. The biofilm forming ability of K. pneumoniae further complicates patient management. There is still a knowledge gap on the association of biofilm formation with patient outcome and carbapenem susceptibility, which is investigated in present study. K. pneumoniae isolates from patients admitted in critical care units with catheters and ventilators were included. K. pneumoniae (n = 72) were subjected to 96-well plate biofilm formation assay followed by MBEC assay for subset of strong biofilm formers. Whole genome sequencing and a core genome phylogenetic analysis in comparison with global isolates were performed. Phenotypic analyses showed a positive correlation between biofilm formation and carbapenem resistance. Planktonic cells observed to be susceptible in vitro exhibited higher MICs in biofilm structure, hence MICs cannot be extrapolated for treatment. The biofilm forming ability had a significant association with morbidity/mortality. Infections by stronger biofilm forming pathogens significantly (p < 0.05) resulted in fewer “average days alive” for the patient (3.33 days) in comparison to those negative for biofilms (11.33 days). Phylogenetic analysis including global isolates revealed clear association of sequence types with genes for biofilm formation and carbapenem resistance. Known hypervirulent clone-ST23 with wcaG, magA, rmpA, rmpA2, and wzc with lack of mutation for hyper-capsulation might be poor biofilm formers. ST15, ST16, ST307, and ST258 (reported global high-risk clones) were wcaJ negative indicating the high potential of biofilm forming capacity. Genes wabG and treC for CPS, bcsA and pgaC for adhesins, luxS for quorum sensing were common in all clades in addition to genes for aerobactin (iutA), allantoin (allS), type I and III fimbriae (fimA, fimH, and mrkD) and pili (pilQ and ecpA). This study is the first of its kind to compare genetic features of antimicrobial resistance with a spectrum covering most of the genetic factors for K. pneumoniae biofilm. These results highlight the importance of biofilm screening to effectively manage nosocomial infections by K. pneumoniae. Further, data obtained on epidemiology and associations of biofilm and resistance genetic factors will serve to enhance our understanding on biofilm mechanisms in K. pneumoniae.

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Section: Introductionmentioning

confidence: 99%

The Influence of Biofilms on Carbapenem Susceptibility and Patient Outcome in Device Associated K. pneumoniae Infections: Insights Into Phenotype vs Genome-Wide Analysis and Correlation

et al. 2020

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“…Furthermore, factors well known for hypervirulence, such as allS, iutA, rmpA/A2, magA, K2A, wabG, wcaG were also reported for their role in biofilm formation [10,11] and magA, K2a, rmpA/A2, wabG and wcaG were shown to regulate CPS synthesis. In fact, wcaG was proven to be an independent risk factor for biofilm formation and highly associated with ST23 [10] .…”

Section: Discussionmentioning

confidence: 98%

“…Biofilm formation mechanisms in clinical K. pneumoniae is reported to be mediated by a series of genetic factors, including allantoin (allS), aerobactin (iutA), type I (fimA and fimH) and type III fimbriae (mrkA and mrkD), polysaccharides and adhesins (pgaA, pgaB, pgaC, bcsA), capsular polysaccharide (CPS) (wzc, cpsD, treC, wcaG, wabG, rmpA/A2, magA, k2a, wzyk2), quorum sensing (QS) (luxS) and colonic acid (wcaJ) [6][7][8][9][10][11] . Though these genetic factors were individually studied, a collective approach on their analysis in a set of clinical isolates is still lacking.…”

Section: Introductionmentioning

confidence: 99%

The influence of biofilm formation on carbapenem resistance in clinicalKlebsiella pneumoniaeinfections: phenotype vs genome-wide analysis

Ragupathi

Sethuvel

Dwarakanathan

et al. 2020

Preprint

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AbstractKlebsiella pneumoniae is one of the leading causes of nosocomial infections. Carbapenem-resistant (CR) K. pneumoniae are on the rise in India. The biofilm forming ability of K. pneumoniae further complicates patient management. There is still a knowledge gap on the association of biofilm formation with patient outcome and carbapenem susceptibility, which is investigated in the present study.K. pneumoniae isolates from patients admitted in critical care units with catheters and ventilators were included. K. pneumoniae (n = 72) were tested for antimicrobial susceptibility as recommended by CLSI 2019 and subjected to 96-well microtitre plate biofilm formation assay. Based on optical density at 570 nm isolates were graded as strong, moderate and weak biofilm formers. Subset of strong biofilm formers were subjected to whole genome sequencing and a core genome phylogenetic analysis in comparison with global isolates were performed. Biofilm formation was compared for an association with the carbapenem susceptibility and with patient outcome. Statistical significance, correlations and graphical representation were performed using SPSS v23.0.Phenotypic analyses showed a positive correlation between biofilm formation and carbapenem resistance. Planktonic cells observed to be susceptible in vitro exhibited higher MICs in biofilm structure. The biofilm forming ability had a significant association with the morbidity/mortality. Infections by stronger biofilm forming pathogens significantly (P<0.05) resulted in fewer ‘average days alive’ for the patient (3.33) in comparison to those negative for biofilms (11.33). Phylogenetic analysis including global isolates revealed the clear association of sequence types with genes for biofilm mechanism and carbapenem resistance. Carbapenemase genes were found specific to each clade. The known hypervirulent clone-ST23 with wcaG, magA, rmpA, rmpA2 and wzc with a lack of mutation for hyper-capsulation might be poor biofilm formers. Interestingly, ST15, ST16, ST307 and ST258 – reported global high-risk clones were wcaJ negative indicating the high potential of biofilm forming capacity. Genes wabG and treC for CPS, bcsA and pgaC for adhesins, luxS for quorum sensing were common in all clades in addition to genes for aerobactin (iutA), allantoin (allS), type I and III fimbriae (fimA, fimH, mrkD) and pili (pilQ, ecpA).This study is the first of its kind to compare genetic features of antimicrobial resistance with a spectrum covering most of the genetic factors for K. pneumoniae biofilm. These results highlight the importance of biofilm screening to effectively manage nosocomial infections by K. pneumoniae. Further, data obtained on epidemiology and associations of biofilm and antimicrobial resistance genetic factors will serve to enhance our understanding on biofilm mechanisms in K. pneumoniae.

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“…However, the epidemiology of each of these carbapenemases among Enterobacterales is heterogeneous. NDMs are endemic in India and China, predominately in Escherichia coli and also in K. pneumoniae ( 2 , 3 ), albeit many clinical cases involving NDM- Enterobacterales are regularly reported from other parts of the world such as South Korea, Iran, and Italy ( 4 – 6 ). OXA-48-like enzymes are predominant in Europe, northern Africa, the Middle East, and increasingly in India ( 7 , 8 ).…”

Section: Introductionmentioning

confidence: 99%

In Vitro Activity of Two Cefepime-Based Novel Combinations, Cefepime/Taniborbactam and Cefepime/Zidebactam, against Carbapenemase-Expressing Enterobacterales Collected in India

Bakthavatchalam

Elangovan²,

Jaganathan

et al. 2023

Microbiol Spectr

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The study revealed the differential ability of cefepime/taniborbactam and cefepime/zidebactam in tackling carbapenemase-producing Indian clinical isolates that also harbored additional mechanisms of resistance. NDM-expressing E. coli with 4-amino-acid insert in PBP3 are predominately resistant to cefepime/taniborbactam, while the β-lactam enhancer mechanism-based cefepime/zidebactam showed consistent activity against single- or dual-carbapenemase-producing isolates including E. coli with PBP3 inserts.

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Detection and characterization of NDM-1-producing Klebsiella pneumoniae in Iran: an incursion crisis

Cited by 7 publications

References 8 publications

The Influence of Biofilms on Carbapenem Susceptibility and Patient Outcome in Device Associated K. pneumoniae Infections: Insights Into Phenotype vs Genome-Wide Analysis and Correlation

The Influence of Biofilms on Carbapenem Susceptibility and Patient Outcome in Device Associated K. pneumoniae Infections: Insights Into Phenotype vs Genome-Wide Analysis and Correlation

The influence of biofilm formation on carbapenem resistance in clinicalKlebsiella pneumoniaeinfections: phenotype vs genome-wide analysis

In Vitro Activity of Two Cefepime-Based Novel Combinations, Cefepime/Taniborbactam and Cefepime/Zidebactam, against Carbapenemase-Expressing Enterobacterales Collected in India

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