Epidemiology and molecular characteristics of the type VI secretion system in Klebsiella pneumoniae isolated from bloodstream infections.
Klebsiella pneumoniae
T6SS
bloodstream infections
hypervirulent
virulence factor
Journal
Journal of clinical laboratory analysis
ISSN: 1098-2825
Titre abrégé: J Clin Lab Anal
Pays: United States
ID NLM: 8801384
Informations de publication
Date de publication:
Nov 2020
Nov 2020
Historique:
received:
19
05
2020
revised:
30
05
2020
accepted:
12
06
2020
pubmed:
14
7
2020
medline:
8
9
2021
entrez:
14
7
2020
Statut:
ppublish
Résumé
The type VI secretion system (T6SS) has been identified as a novel virulence factor. This study aimed to investigate the prevalence of the T6SS genes in Klebsiella pneumoniae-induced bloodstream infections (BSIs). We also evaluated clinical and molecular characteristics of T6SS-positive K pneumoniae. A total of 344 non-repetitive K. pneumoniae bloodstream isolates and relevant clinical data were collected from January 2016 to January 2019. For all isolates, T6SS genes, capsular serotypes, and virulence genes were detected by polymerase chain reaction, and antimicrobial susceptibility was tested by VITEK® 2 Compact. MLST was being conducted for hypervirulent K. pneumoniae (HVKP). 69 (20.1%) were identified as T6SS-positive K. pneumoniae among 344 isolates recovered from patients with BSIs. The rate of K1 capsular serotypes and ten virulence genes in T6SS-positive strains was higher than T6SS-negative strains (P = .000). The T6SS-positive rate was significantly higher than T6SS-negative rate among HVKP isolates. (P = .000). The T6SS-positive K. pneumoniae isolates were significantly more susceptible to cefoperazone-sulbactam, ampicillin-sulbactam, cefazolin, ceftriaxone, cefotan, aztreonam, ertapenem, amikacin, gentamicin, levofloxacin, and ciprofloxacin (P < 0.05). More strains isolated from the community and liver abscess were T6SS-positive K. pneumoniae (P < .05). Multivariate regression analysis indicated that community-acquired BSIs (OR 2.986), the carriage of wcaG (OR 10.579), iucA (OR 2.441), and p-rmpA (OR 7.438) virulence genes, and biliary diseases (OR 5.361) were independent risk factors for T6SS-positive K. pneumoniae-induced BSIs. The T6SS-positive K. pneumoniae was prevalent in individuals with BSIs. T6SS-positive K. pneumoniae strains seemed to be hypervirulent which revealed the potential pathogenicity of this emerging gene cluster.
Sections du résumé
BACKGROUND
BACKGROUND
The type VI secretion system (T6SS) has been identified as a novel virulence factor. This study aimed to investigate the prevalence of the T6SS genes in Klebsiella pneumoniae-induced bloodstream infections (BSIs). We also evaluated clinical and molecular characteristics of T6SS-positive K pneumoniae.
METHODS
METHODS
A total of 344 non-repetitive K. pneumoniae bloodstream isolates and relevant clinical data were collected from January 2016 to January 2019. For all isolates, T6SS genes, capsular serotypes, and virulence genes were detected by polymerase chain reaction, and antimicrobial susceptibility was tested by VITEK® 2 Compact. MLST was being conducted for hypervirulent K. pneumoniae (HVKP).
RESULTS
RESULTS
69 (20.1%) were identified as T6SS-positive K. pneumoniae among 344 isolates recovered from patients with BSIs. The rate of K1 capsular serotypes and ten virulence genes in T6SS-positive strains was higher than T6SS-negative strains (P = .000). The T6SS-positive rate was significantly higher than T6SS-negative rate among HVKP isolates. (P = .000). The T6SS-positive K. pneumoniae isolates were significantly more susceptible to cefoperazone-sulbactam, ampicillin-sulbactam, cefazolin, ceftriaxone, cefotan, aztreonam, ertapenem, amikacin, gentamicin, levofloxacin, and ciprofloxacin (P < 0.05). More strains isolated from the community and liver abscess were T6SS-positive K. pneumoniae (P < .05). Multivariate regression analysis indicated that community-acquired BSIs (OR 2.986), the carriage of wcaG (OR 10.579), iucA (OR 2.441), and p-rmpA (OR 7.438) virulence genes, and biliary diseases (OR 5.361) were independent risk factors for T6SS-positive K. pneumoniae-induced BSIs.
CONCLUSION
CONCLUSIONS
The T6SS-positive K. pneumoniae was prevalent in individuals with BSIs. T6SS-positive K. pneumoniae strains seemed to be hypervirulent which revealed the potential pathogenicity of this emerging gene cluster.
Identifiants
pubmed: 32656871
doi: 10.1002/jcla.23459
pmc: PMC7676210
doi:
Substances chimiques
Type VI Secretion Systems
0
Virulence Factors
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
e23459Subventions
Organisme : National Natural Science Foundation of China
ID : 81672066
Informations de copyright
© 2020 The Authors. Journal of Clinical Laboratory Analysis Published by Wiley Periodicals LLC.
Références
Future Microbiol. 2012 Jun;7(6):669-71
pubmed: 22702521
Ann Lab Med. 2019 Mar;39(2):167-175
pubmed: 30430779
PLoS Genet. 2019 Apr 15;15(4):e1008114
pubmed: 30986243
Clin Microbiol Infect. 2016 Feb;22(2):154-160
pubmed: 26454059
Infect Immun. 2014 Jun;82(6):2356-67
pubmed: 24664504
Nature. 2011 Jul 20;475(7356):343-7
pubmed: 21776080
J Clin Microbiol. 2011 Nov;49(11):3761-5
pubmed: 21900521
Clin Microbiol Infect. 2014 Nov;20(11):O818-24
pubmed: 24804560
Front Cell Infect Microbiol. 2017 Feb 01;7:24
pubmed: 28203549
BMC Microbiol. 2019 Sep 18;19(1):219
pubmed: 31533609
Eur J Clin Microbiol Infect Dis. 2018 Apr;37(4):679-689
pubmed: 29238932
Antimicrob Agents Chemother. 2014 Sep;58(9):5379-85
pubmed: 24982067
BMC Infect Dis. 2019 Mar 7;19(1):237
pubmed: 30845966
Front Cell Infect Microbiol. 2018 Feb 23;8:21
pubmed: 29527517
J Infect Dis. 2019 Jan 29;219(4):637-647
pubmed: 30202982
Infect Immun. 2012 Mar;80(3):1243-51
pubmed: 22184413
J Clin Microbiol. 2014 Dec;52(12):4377-80
pubmed: 25275000
PLoS One. 2012;7(4):e34639
pubmed: 22514651
Lancet Infect Dis. 2012 Nov;12(11):881-7
pubmed: 23099082
J Med Microbiol. 2007 May;56(Pt 5):593-597
pubmed: 17446279
J Bacteriol. 2004 Mar;186(5):1518-30
pubmed: 14973027
Microbiol Spectr. 2019 Mar;7(2):
pubmed: 30825301
Front Cell Infect Microbiol. 2017 Nov 21;7:483
pubmed: 29209595
Infect Chemother. 2018 Sep;50(3):210-218
pubmed: 30270580
J Biol Chem. 2011 Apr 8;286(14):12317-27
pubmed: 21325275
PLoS One. 2012;7(8):e42842
pubmed: 22952616
Infect Immun. 2004 Oct;72(10):5983-92
pubmed: 15385502
J Clin Lab Anal. 2020 Nov;34(11):e23459
pubmed: 32656871
J Mol Biol. 2018 Sep 14;430(18 Pt B):3143-3156
pubmed: 30031895
J Infect. 2015 Nov;71(5):553-60
pubmed: 26304687
J Bacteriol. 2010 Jun;192(12):3144-58
pubmed: 20382770
Clin Infect Dis. 1998 Jun;26(6):1434-8
pubmed: 9636876
Lancet Infect Dis. 2018 Jan;18(1):37-46
pubmed: 28864030
Virulence. 2017 Oct 3;8(7):1111-1123
pubmed: 28402698
Open Forum Infect Dis. 2014 Jun 02;1(1):ofu028
pubmed: 25734101
BMC Genomics. 2019 Jun 18;20(1):506
pubmed: 31215404
Front Microbiol. 2019 Jun 07;10:1100
pubmed: 31231316
Front Microbiol. 2019 Jan 22;9:3198
pubmed: 30723463
J Clin Microbiol. 2008 Dec;46(12):4061-3
pubmed: 18971367
Microbiol Mol Biol Rev. 2016 Jun 15;80(3):629-61
pubmed: 27307579
Clin Infect Dis. 2007 Aug 1;45(3):284-93
pubmed: 17599305
Microb Pathog. 2017 Mar;104:254-262
pubmed: 28132768
J Clin Lab Anal. 2019 May;33(4):e22838
pubmed: 30737883
Nat Rev Microbiol. 2014 Feb;12(2):137-48
pubmed: 24384601
Virulence. 2013 Feb 15;4(2):107-18
pubmed: 23302790
BMC Infect Dis. 2017 Jan 17;17(1):82
pubmed: 28095785
Eur J Clin Microbiol Infect Dis. 2016 Mar;35(3):387-96
pubmed: 26753990
Trends Microbiol. 2014 Sep;22(9):498-507
pubmed: 25042941