Predicting the Impact of Typhoid Conjugate Vaccines on Antimicrobial Resistance.
Anti-Bacterial Agents
/ pharmacology
Carrier State
/ microbiology
Drug Resistance, Multiple, Bacterial
Humans
Microbial Sensitivity Tests
Models, Biological
Predictive Value of Tests
Prevalence
Salmonella typhi
/ drug effects
Typhoid Fever
/ epidemiology
Typhoid-Paratyphoid Vaccines
/ administration & dosage
Vaccination Coverage
/ statistics & numerical data
Vaccines, Conjugate
/ administration & dosage
Salmonella Typhi
multidrug resistance
transmission dynamics
treatment
vaccination
Journal
Clinical infectious diseases : an official publication of the Infectious Diseases Society of America
ISSN: 1537-6591
Titre abrégé: Clin Infect Dis
Pays: United States
ID NLM: 9203213
Informations de publication
Date de publication:
07 03 2019
07 03 2019
Historique:
entrez:
8
3
2019
pubmed:
8
3
2019
medline:
29
5
2020
Statut:
ppublish
Résumé
Empiric prescribing of antimicrobials in typhoid-endemic settings has increased selective pressure on the development of antimicrobial-resistant Salmonella enterica serovar Typhi. The introduction of typhoid conjugate vaccines (TCVs) in these settings may relieve this selective pressure, thereby reducing resistant infections and improving health outcomes. A deterministic transmission dynamic model was developed to simulate the impact of TCVs on the number and proportion of antimicrobial-resistant typhoid infections and chronic carriers. One-way sensitivity analyses were performed to ascertain particularly impactful model parameters influencing the proportion of antimicrobial-resistant infections and the proportion of cases averted over 10 years. The model simulations suggested that increasing vaccination coverage would decrease the total number of antimicrobial-resistant typhoid infections but not affect the proportion of cases that were antimicrobial resistant. In the base-case scenario with 80% vaccination coverage, 35% of all typhoid infections were antimicrobial resistant, and 44% of the total cases were averted over 10 years by vaccination. Vaccination also decreased both the total number and proportion of chronic carriers of antimicrobial-resistant infections. The prevalence of chronic carriers, recovery rates from infection, and relative fitness of resistant strains were identified as crucially important parameters. Model predictions for the proportion of antimicrobial resistant infections and number of cases averted depended strongly on the relative fitness of the resistant strain(s), prevalence of chronic carriers, and rates of recovery without treatment. Further elucidation of these parameter values in real-world typhoid-endemic settings will improve model predictions and assist in targeting future vaccination campaigns and treatment strategies.
Sections du résumé
BACKGROUND
Empiric prescribing of antimicrobials in typhoid-endemic settings has increased selective pressure on the development of antimicrobial-resistant Salmonella enterica serovar Typhi. The introduction of typhoid conjugate vaccines (TCVs) in these settings may relieve this selective pressure, thereby reducing resistant infections and improving health outcomes.
METHODS
A deterministic transmission dynamic model was developed to simulate the impact of TCVs on the number and proportion of antimicrobial-resistant typhoid infections and chronic carriers. One-way sensitivity analyses were performed to ascertain particularly impactful model parameters influencing the proportion of antimicrobial-resistant infections and the proportion of cases averted over 10 years.
RESULTS
The model simulations suggested that increasing vaccination coverage would decrease the total number of antimicrobial-resistant typhoid infections but not affect the proportion of cases that were antimicrobial resistant. In the base-case scenario with 80% vaccination coverage, 35% of all typhoid infections were antimicrobial resistant, and 44% of the total cases were averted over 10 years by vaccination. Vaccination also decreased both the total number and proportion of chronic carriers of antimicrobial-resistant infections. The prevalence of chronic carriers, recovery rates from infection, and relative fitness of resistant strains were identified as crucially important parameters.
CONCLUSIONS
Model predictions for the proportion of antimicrobial resistant infections and number of cases averted depended strongly on the relative fitness of the resistant strain(s), prevalence of chronic carriers, and rates of recovery without treatment. Further elucidation of these parameter values in real-world typhoid-endemic settings will improve model predictions and assist in targeting future vaccination campaigns and treatment strategies.
Identifiants
pubmed: 30845324
pii: 5371224
doi: 10.1093/cid/ciy1108
pmc: PMC6405272
doi:
Substances chimiques
Anti-Bacterial Agents
0
Typhoid-Paratyphoid Vaccines
0
Vaccines, Conjugate
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
S96-S104Subventions
Organisme : NIAID NIH HHS
ID : K01 AI119603
Pays : United States
Organisme : Wellcome Trust
ID : 106158/Z/14/Z
Pays : United Kingdom
Informations de copyright
© The Author(s) 2019. Published by Oxford University Press for the Infectious Diseases Society of America.
Références
Clin Infect Dis. 2016 Mar 15;62 Suppl 1:S56-68
pubmed: 26933023
Clin Infect Dis. 2018 Aug 1;67(4):628-638
pubmed: 29522159
PLoS Negl Trop Dis. 2014 Jan 09;8(1):e2642
pubmed: 24416466
PLoS Negl Trop Dis. 2017 Feb 27;11(2):e0005376
pubmed: 28241011
MBio. 2018 Feb 20;9(1):
pubmed: 29463654
Lancet Infect Dis. 2019 Jan;19(1):e26-e30
pubmed: 30170987
Clin Infect Dis. 2018 Jun 18;67(1):18-24
pubmed: 29351594
Vaccine. 2017 Jun 14;35(27):3506-3514
pubmed: 28527687
Clin Infect Dis. 2019 Apr 8;68(8):1265-1273
pubmed: 30252031
Lancet. 1987 Apr 25;1(8539):976
pubmed: 2882361
J Infect Dis. 2018 Nov 10;218(suppl_4):S232-S242
pubmed: 29444257
N Engl J Med. 1970 Sep 24;283(13):686-91
pubmed: 4916913
Antimicrob Agents Chemother. 2005 Jun;49(6):2561-4
pubmed: 15917574
Bull World Health Organ. 2004 May;82(5):346-53
pubmed: 15298225
Lancet. 2017 Dec 2;390(10111):2472-2480
pubmed: 28965718
PLoS Negl Trop Dis. 2016 Apr 15;10(4):e0004616
pubmed: 27082958
J Infect Dis. 2012 Feb 1;205(3):401-11
pubmed: 22158567
Annu Rev Microbiol. 2014;68:317-36
pubmed: 25208300
Elife. 2013 Dec 10;2:e01229
pubmed: 24327559
Am J Public Health Nations Health. 1943 Mar;33(3):221-30
pubmed: 18015749
Clin Infect Dis. 2016 May 1;62(9):1119-25
pubmed: 26908787
N Engl J Med. 2001 Apr 26;344(17):1263-9
pubmed: 11320385
Lancet Glob Health. 2014 Oct;2(10):e570-80
pubmed: 25304633
PLoS One. 2012;7(10):e47342
pubmed: 23077595
Trends Microbiol. 2014 Nov;22(11):648-55
pubmed: 25065707
Nat Med. 2018 Jan 9;24(1):10-19
pubmed: 29315295
Lancet. 2016 Jan 9;387(10014):168-75
pubmed: 26603918
PLoS Negl Trop Dis. 2011 Jul;5(7):e1245
pubmed: 21811646
Clin Infect Dis. 2015 Nov 1;61 Suppl 4:S251-8
pubmed: 26449939
Nat Genet. 2015 Jun;47(6):632-9
pubmed: 25961941
Bull World Health Organ. 2008 Apr;86(4):260-8
pubmed: 18438514
BMJ. 1996 Jan 20;312(7024):160-1
pubmed: 8563536
PLoS Negl Trop Dis. 2015 Apr 24;9(4):e0003748
pubmed: 25909750
Lancet Respir Med. 2016 May;4(5):399-406
pubmed: 26987984
J Infect Dis. 2018 Nov 10;218(suppl_4):S214-S221
pubmed: 28961918
J Infect Dis. 1988 Jun;157(6):1235-9
pubmed: 3373023
N Engl J Med. 1970 Oct 1;283(14):739-46
pubmed: 4916916
Arch Dis Child. 1996 Sep;75(3):214-7
pubmed: 8976660
Clin Infect Dis. 2015 Aug 1;61(3):393-402
pubmed: 25870324