Emerging serotype III sequence type 17 group B streptococcus invasive infection in infants: the clinical characteristics and impacts on outcomes.
Bacteremia
Drug resistance
Epidemiology
Group B streptococcus
Invasive streptococcal infection
Journal
BMC infectious diseases
ISSN: 1471-2334
Titre abrégé: BMC Infect Dis
Pays: England
ID NLM: 100968551
Informations de publication
Date de publication:
19 Jun 2019
19 Jun 2019
Historique:
received:
30
01
2019
accepted:
10
06
2019
entrez:
21
6
2019
pubmed:
21
6
2019
medline:
28
8
2019
Statut:
epublish
Résumé
Group B Streptococcus (GBS) is an important pathogen that causes high mortality and morbidity in young infants. However, data on clinical manifestations between different GBS serotypes and correlation with molecular epidemiology are largely incomplete. The aim of this study was to determine the serotype distribution, antimicrobial resistance, clinical features and molecular characteristics of invasive GBS isolates recovered from Taiwanese infants. From 2003 to 2017, 182 non-duplicate GBS isolates that caused invasive disease in infants less than one year of age underwent serotyping, multilocus sequence typing (MLST) and antibiotic susceptibility testing. The clinical features of these infants with GBS disease were also reviewed. Of the 182 patients with invasive GBS disease, 41 (22.5%) were early-onset disease, 121 (66.5%) were late-onset disease and 20 (11.0%) were late late-onset disease (> 90 days of age). All these patients were treated with effective antibiotics on time. Among them, 51 (28.0%) had meningitis, 29 (16.0%) had neurological complications, 12 (6.6%) died during hospitalization, and 15 (8.8%) out of 170 patients who survived had long-term neurological sequelae at discharge. Serotype III GBS strains accounted for 64.8%, followed by serotype Ia (18.1%) and Ib (8.2%). MLST analysis revealed 11 different sequence types among the 182 isolates and ST-17 was the most dominant sequence type (56.6%). The correlation between serotype III and ST17 was evident, as ST17 accounted for 87.3% of all serotype III isolates. There was an obvious increasing trend of type III/ST-17 GBS that caused invasive disease in infants. All isolates were susceptible to penicillin, cefotaxime, and vancomycin, while 68.1 and 65.9% were resistant to erythromycin and clindamycin, respectively. Despite timely and appropriate antibiotic treatment, a significant proportion of invasive GBS disease still inevitably causes adverse outcomes. Further study to explore preventive strategies and development of serotype-based vaccines will be necessary in the future.
Sections du résumé
BACKGROUND
BACKGROUND
Group B Streptococcus (GBS) is an important pathogen that causes high mortality and morbidity in young infants. However, data on clinical manifestations between different GBS serotypes and correlation with molecular epidemiology are largely incomplete. The aim of this study was to determine the serotype distribution, antimicrobial resistance, clinical features and molecular characteristics of invasive GBS isolates recovered from Taiwanese infants.
METHODS
METHODS
From 2003 to 2017, 182 non-duplicate GBS isolates that caused invasive disease in infants less than one year of age underwent serotyping, multilocus sequence typing (MLST) and antibiotic susceptibility testing. The clinical features of these infants with GBS disease were also reviewed.
RESULTS
RESULTS
Of the 182 patients with invasive GBS disease, 41 (22.5%) were early-onset disease, 121 (66.5%) were late-onset disease and 20 (11.0%) were late late-onset disease (> 90 days of age). All these patients were treated with effective antibiotics on time. Among them, 51 (28.0%) had meningitis, 29 (16.0%) had neurological complications, 12 (6.6%) died during hospitalization, and 15 (8.8%) out of 170 patients who survived had long-term neurological sequelae at discharge. Serotype III GBS strains accounted for 64.8%, followed by serotype Ia (18.1%) and Ib (8.2%). MLST analysis revealed 11 different sequence types among the 182 isolates and ST-17 was the most dominant sequence type (56.6%). The correlation between serotype III and ST17 was evident, as ST17 accounted for 87.3% of all serotype III isolates. There was an obvious increasing trend of type III/ST-17 GBS that caused invasive disease in infants. All isolates were susceptible to penicillin, cefotaxime, and vancomycin, while 68.1 and 65.9% were resistant to erythromycin and clindamycin, respectively.
CONCLUSIONS
CONCLUSIONS
Despite timely and appropriate antibiotic treatment, a significant proportion of invasive GBS disease still inevitably causes adverse outcomes. Further study to explore preventive strategies and development of serotype-based vaccines will be necessary in the future.
Identifiants
pubmed: 31216993
doi: 10.1186/s12879-019-4177-y
pii: 10.1186/s12879-019-4177-y
pmc: PMC6585028
doi:
Substances chimiques
Anti-Bacterial Agents
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
538Subventions
Organisme : Chang Gung Memorial Hospital, Linkou
ID : CMRPG3H0190
Références
J Clin Microbiol. 2009 Apr;47(4):1143-8
pubmed: 19158264
J Clin Microbiol. 2010 Jul;48(7):2571-4
pubmed: 20444969
Pediatr Int. 2011 Apr;53(2):236-9
pubmed: 20487368
Clin Microbiol Infect. 2011 Sep;17(9):1294-303
pubmed: 21672083
J Microbiol Immunol Infect. 2011 Dec;44(6):430-4
pubmed: 21697020
Neurology. 2012 Nov 20;79(21):2133-9
pubmed: 23136260
Int J Infect Dis. 2013 Jun;17(6):e379-84
pubmed: 23305911
Clin Infect Dis. 2013 Sep;57(5):682-8
pubmed: 23845950
Clin Microbiol Infect. 2014 Jul;20(7):629-35
pubmed: 24118384
Clin Microbiol Infect. 2014 Jun;20(6):O370-3
pubmed: 24118553
Pediatrics. 2014 Feb;133(2):196-203
pubmed: 24446442
N Engl J Med. 2014 Feb 27;370(9):885-6
pubmed: 24571775
Pediatr Infect Dis J. 2014 Oct;33(10):1091-2
pubmed: 24776515
Euro Surveill. 2014 Jun 12;19(23):null
pubmed: 24957747
Pediatr Infect Dis J. 2014 Dec;33(12):1211-5
pubmed: 25037035
Nat Commun. 2014 Aug 04;5:4544
pubmed: 25088811
Lancet. 2015 May 2;385(9979):1767-1776
pubmed: 25842221
J Pediatr. 2015 May;166(5):1187-1192.e1
pubmed: 25919727
Clin Microbiol Infect. 2015 Oct;21(10):910-6
pubmed: 26055414
Antimicrob Agents Chemother. 2016 Jan 04;60(3):1702-7
pubmed: 26729498
Clin Microbiol Infect. 2016 May;22 Suppl 3:S37-62
pubmed: 27062097
J Clin Microbiol. 2016 Jul;54(7):1774-1781
pubmed: 27098960
JAMA Pediatr. 2016 Oct 1;170(10):954-963
pubmed: 27479919
Vaccine. 2016 Dec 1;34(49):6038-6046
pubmed: 27491687
Front Microbiol. 2016 Aug 15;7:1265
pubmed: 27574519
Front Microbiol. 2016 Aug 30;7:1308
pubmed: 27625635
J Clin Microbiol. 2017 Feb;55(2):412-422
pubmed: 27852675
Pediatr Infect Dis J. 2017 Mar;36(3):256-262
pubmed: 27870810
Pediatr Infect Dis J. 2017 Oct;36(10):e242-e247
pubmed: 28060047
Clin Microbiol Infect. 2017 Aug;23(8):574.e7-574.e14
pubmed: 28257899
Clin Microbiol Infect. 2017 Sep;23(9):673.e9-673.e16
pubmed: 28274774
J Antimicrob Chemother. 2017 Jul 1;72(7):1886-1892
pubmed: 28333320
Front Microbiol. 2017 Mar 28;8:499
pubmed: 28400757
Clin Microbiol Infect. 2017 Dec;23(12):974-979
pubmed: 28478240
Clin Microbiol Infect. 2017 Dec;23(12):948-951
pubmed: 28487166
Pediatrics. 2017 Jul;140(1):null
pubmed: 28600447
Clin Microbiol Infect. 2018 May;24(5):514-521
pubmed: 28870726
Clin Infect Dis. 2017 Nov 6;65(suppl_2):S160-S172
pubmed: 29117326
Clin Infect Dis. 2017 Nov 6;65(suppl_2):S100-S111
pubmed: 29117327
Clin Microbiol Infect. 2018 Aug;24(8):865-870
pubmed: 29221995
Am J Infect Control. 2018 Mar;46(3):e19-e24
pubmed: 29305279
BMC Infect Dis. 2018 Jan 8;18(1):14
pubmed: 29310577
Vaccine. 2018 Apr 5;36(15):1941-1948
pubmed: 29519594
Front Microbiol. 2018 Mar 14;9:437
pubmed: 29593684
Pediatr Infect Dis J. 2018 Dec;37(12):e306-e314
pubmed: 29601454
J Infect. 2019 Jan;78(1):54-57
pubmed: 30063913
Pediatr Infect Dis J. 2018 Nov;37(11):1145-1153
pubmed: 30312265
Front Neurol. 2018 Oct 24;9:903
pubmed: 30405525
Front Microbiol. 2019 Feb 18;10:264
pubmed: 30833941
Pediatr Infect Dis J. 2019 Jul;38(7):731-734
pubmed: 31192978