A Fatal Bacteremia Caused by Hypermucousviscous KPC-2 Producing Extensively Drug-Resistant K64-ST11 Klebsiella pneumoniae in Brazil

Campos, Tatiana Amabile de; Gonçalves, Laura Fernandes; Magalhães, Kelly Grace; Martins, Vívian T.; Júnior, Georgios Joannis Pappas; Peirano, Gisele; Pitout, Johann; Gonçalves, Guilherme Bartolomeu; Furlan, João Pedro Rueda; Stehling, Eliana Guedes; Pitondo-Silva, André

doi:10.3389/fmed.2018.00265

Cited by 28 publications

(24 citation statements)

References 30 publications

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“…pneumoniae presented higher virulence than CC11/258 isolates in the Galleria mellonella pathogenicity model ( Andrey et al, 2019 ). Although we had the limitation of not performing any pathogenicity animal model, in our study, the isolates of outbreak A (ST11/KPC-2) presented a higher average number of virulence genes when compared with the isolates from the other outbreaks (outbreak A: average = 35, range = 27–36; outbreak D: average = 20, range = 20–20; outbreak C: average = 19, range = 19–19; outbreak B: average = 6, range = 6–6), a fact that may enable ST11/KPC-2 isolates to be responsible for a high rate of invasive infections, as observed here and worldwide ( Lee et al, 2016 ; de Campos et al, 2018 ). The colibactin cluster genes were only observed in outbreak A, being present in all the isolates of this group, but were disrupted in 17.0%.…”

Section: Resultssupporting

confidence: 55%

Carbapenemase-Producing Klebsiella pneumoniae From Transplanted Patients in Brazil: Phylogeny, Resistome, Virulome and Mobile Genetic Elements Harboring blaKPC–2 or blaNDM–1

et al. 2020

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Objectives Carbapenemase-producing Klebsiella pneumoniae (CP-Kp) is a major cause of infections in transplanted patients and has been associated with high mortality rates in this group. There is a lack of information about the Brazilian structure population of CP-Kp isolated from transplanted patients. By whole-genome sequencing (WGS), we analyzed phylogeny, resistome, virulome of CP-Kp isolates, and the structure of plasmids encoding bla KPC– 2 and bla NDM– 1 genes. Methods One K. pneumoniae isolated from each selected transplanted patient colonized or infected by CP-Kp over a 16-month period in a hospital complex in Porto Alegre (Brazil) was submitted for WGS. The total number of strains sequenced was 80. The hospital complex in Porto Alegre comprised seven different hospitals. High-resolution SNP typing, core genome multilocus sequence typing (cgMLST), resistance and virulence genes inference, and plasmid reconstruction were performed in 80 CP-Kp. Results The mortality rate of CP-Kp colonized or infected transplanted inpatients was 21.3% (17/80). Four CP-Kp epidemic clones were described: ST11/KPC-2, ST16/KPC-2, and ST15/NDM-1, all responsible for interhospital outbreaks; and ST437/KPC-2 affecting a single hospital. The average number of acquired resistance and virulence genes was 9 (range = 2–14) and 27 (range = 6–36), respectively. Two plasmids carrying the bla KPC – 2 were constructed and belonged to IncN and IncM types. Additionally, an IncFIB plasmid carrying the bla NDM– 1 was described. Conclusion We detected intrahospital and interhospital spread of mobile structures and international K . pneumoniae clones as ST11, ST16, and ST15 among transplanted patients, which carry a significant range of acquired resistance and virulence genes and keep spreading across the world.

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Section: Resultssupporting

confidence: 55%

Carbapenemase-Producing Klebsiella pneumoniae From Transplanted Patients in Brazil: Phylogeny, Resistome, Virulome and Mobile Genetic Elements Harboring blaKPC–2 or blaNDM–1

et al. 2020

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“…However, a subsequent retrospective multicenter study showed that ST11-K64 must have been spreading in China for several years and represents the most common type of CR-hvKP ( Zhang et al, 2020 ). Indeed, de Campos et al (2018) reported a hypermucoviscous CRKP strain that caused a fatal bacteremia in a patient in Brazil in 2018. Our report of an interhospital outbreak of ST11-K64 provided further evidence that ST11-K64 K. pneumoniae may be a competent host strain for a hypervirulent plasmid, leading to CR-hvKP, and control measures should be urgently implemented.…”

Section: Discussionmentioning

confidence: 99%

Co-occurrence of Rapid Gene Gain and Loss in an Interhospital Outbreak of Carbapenem-Resistant Hypervirulent ST11-K64 Klebsiella pneumoniae

Xiaotuan

Ouyang

et al. 2020

Front. Microbiol.

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We report an outbreak of carbapenemase-producing hypervirulent Klebsiella pneumoniae in two hospitals that undergo frequent patient transfers. Analysis of 11 completely assembled genomes showed that the bacteria were ST11-K64 strains. Moreover, 12 single nucleotide polymorphisms (SNPs) identified the strains as having originated from the same cluster, and were also indicative of the interhospital transmission of infection. Five plasmids were assembled in each of the strains. One plasmid carried several virulence genes, including the capsular polysaccharide regulators rmpA and rmpA2 . Two others carried antimicrobial-resistance genes, including one for carbapenem resistance, bla KPC–2 . Comparative genomic analysis indicated the occurrence of frequent and rapid gain and loss of genomic content along transmissions and the co-existence of progeny strains in the same ward. A 10-kbp fragment harboring antimicrobial resistance-conferring genes flanked by insert sequences was missing in a plasmid from strain KP20194c in patient 3, and this strain also likely subsequently infected patient 4. However, strains containing the 10-kbp fragment were also isolated from the ward environment at approximately the same time, and harbored different chromosome indels. Tn 1721 and multiple additional insert sequence-mediated transpositions were also seen. These results indicated that there is a rapid reshaping and diversification of the genomic pool of K. pneumoniae facilitated by mobile genetic elements, even a short time after outbreak onset. ST11-K64 CR-hvKP strains have the potential to become new significant superbugs and a threat to public health.

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“…K64 has emerged in a large-scale study in China. 41 We screened several virulence-associated genes through PCR. Both ST11 CRKP95 and ST1764 hvKP were positive for rmpA, rmpA2, and iroN genes, whereas ST11 CRKP95 was non-hypervirulent KP (non-hvKP) (negative for the string test).…”

mentioning

confidence: 99%

Emergence of NDM-5-Producing Carbapenem-Resistant Klebsiella pneumoniae and SIM-Producing Hypervirulent Klebsiella pneumoniae Isolated from Aseptic Body Fluid in a Large Tertiary Hospital, 2017–2018: Genetic Traits of blaNDM-Like and blaSIM-Like Genes as Determined by NGS

Zhu

Kang

et al. 2020

IDR

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To characterize the clinical, resistance, and virulence features of carbapenemresistant Klebsiella pneumonaie (CRKP) and hypervirulent Klebsiella pneumoniae (hvKP) and also provide an effective selection of drug in CRKP and hvKP treatment. Materials and Methods: Twelve strains were collected and investigated these isolates for their antimicrobial susceptibility and molecular features. Resistance mechanisms, virulence-associated genes, multilocus sequence typing (MLST), and serotypes were detected by PCR and sequencing. Next general sequencing (NGS) was carried out to determine the features of carbapenem resistance and virulence. The synergistic activity of tigecycline-imipenem (TGC+IPM), tigecycline-meropenem (TGC+MEM), and tigecycline-aztreonam (TGC+ATM) combinations were performed by microdilution checkerboard method. Results: Eleven CRKP and one hvKP strains were collected. All strains showed highly sensitive rates to tigecycline (TGC) and amikacin (AMK). NDM (33.3%, 4/12) was the main resistance mechanism and MLST assigned 3 of them to ST11. CTX-M-producing (n = 1) and KPC-2-producing (n = 1) isolates belonged to ST147 and ST11, respectively. The MICs of ATM and quinolones in NDM-1 CRKP and NDM-5 CRKP strains were different. The serotype of the majority strains was KL22KL137 (58.3%, 7/12), hvKP stain belonged to K64. CRKP strains harbored plasmid-mediated quinolone resistance genes (oqxA, oqxB, qnrS, qnrB), β-lactams (bla CTX-M-3), aminoglycosides, type I and type III fimbriae genes, siderophore genes, and transporter and pumps. SIM-producing ST1764 K64 showed typical features of hvKP, showing hypermucoviscosity phenotype. The virulence genes, including rmpA2, alls and aerobactin genes, linked to hvKP, were found in ST1764 hvKP. hvKP was sensitive to quinolone; also, oqxA gene was detected. All TGC combinations showed highly synergistic effects and TGC+IPM was more effective treatment. Conclusion: We first identified the NDM-5-producing ST690 CRKP and SIM-producing ST1764 hvKP strains in Shanxi province. Tigecycline-carbapenem combinations were available treatments for CRKP.

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A Fatal Bacteremia Caused by Hypermucousviscous KPC-2 Producing Extensively Drug-Resistant K64-ST11 Klebsiella pneumoniae in Brazil

Cited by 28 publications

References 30 publications

Carbapenemase-Producing Klebsiella pneumoniae From Transplanted Patients in Brazil: Phylogeny, Resistome, Virulome and Mobile Genetic Elements Harboring blaKPC–2 or blaNDM–1

Carbapenemase-Producing Klebsiella pneumoniae From Transplanted Patients in Brazil: Phylogeny, Resistome, Virulome and Mobile Genetic Elements Harboring blaKPC–2 or blaNDM–1

Co-occurrence of Rapid Gene Gain and Loss in an Interhospital Outbreak of Carbapenem-Resistant Hypervirulent ST11-K64 Klebsiella pneumoniae

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