Nicole L. Pershing (United States of America)
University of Utah
Pediatric Infectious Disease
Nicole Pershing is a Pediatric Infectious Disease physician scientist at the University of Utah. She completed her pediatric infectious disease fellowship at the University of Utah in 2021, working with Dr. Anne Blaschke studying the genomic evolution of pneumococci causing invasive disease among Utah children. She is currently conducting postdoctoral research in Dr. June Round’s lab studying the influence of bacterial prophage on mucosal response to bacterial pathobionts. She is interested in the complex interplay between bacteria, their lysogenic phage, and mammalian immune responses governing pathophysiology of bacterial colonization versus invasive disease. Nicole completed a BS in biology at MIT, and MD/PhD at Duke University. She lives in Salt Lake City, Utah where she enjoys exploring the great outdoors with her family.

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O073 - PHYLOGENETIC PATTERNS OF PEDIATRIC INVASIVE PNEUMOCOCCAL SEROTYPE DECLINE, PERSISTENCE, AND EMERGENCE IN UTAH FOLLOWING PNEUMOCOCCAL VACCINE INTRODUCTION (ID 598)

Session Name
0740 - Parallel Session 09: Vaccine Impact (ID 63)
Session Type
Parallel Session
Date
Wed, 22.06.2022
Session Time
15:05 - 16:35
Room
Birchwood Ballroom
Presenter
Lecture Time
15:30 - 15:40

Abstract

Background

Streptococcus pneumoniae is a common cause of pediatric invasive bacterial infections. Incidence of invasive pneumococcal disease (IPD) has decreased following pneumococcal conjugate vaccine (PCV) introduction. However, limited efficacy against some serotypes and emergence of new serotypes threatens vaccine durability.

Methods

We performed Illumina sequencing, de novo genome assembly/annotation, serotyping, pan-genome assembly and global pneumococcal sequence cluster (GPSC) assignment of clinical sterile site pneumococcal isolates from pediatric patients at Primary Children’s Hospital (Salt Lake City, UT) isolated between 1996-2018. Antimicrobial resistance was determined phenotypically and genomically. Core genome SNP alignment was used for maximum likelihood phylogeny.

Results

366 pneumococcal isolates from 39 serotypes (ST) were analyzed. Some GPSC with predominantly vaccine serotypes declined during the study period, including GPSC31 (ST1), GPSC1 (ST19A/F), and GPSC15 (ST7F); GPSC12 (ST3) and GPSC119 (ST19F) increased, comprising 24% of post-PCV13 strains. Two GPSC appeared to undergo serotype switching following PCV introduction: GPSC4 and 6, from ST19A and ST9V to ST15B/C and ST35B, respectively. Notably, many GPSC6 isolates retained multiple drug resistance despite the switch. Predominantly non-vaccine serotype GPSC emerged representing 33% of post-PCV13 isolates, including GPSC3 (ST11A and 33F), GPSC5 (ST23A/B1), GPSC7 (ST23A/B/B1), GPSC19 (ST22F), GPSC98 (ST8), and GPSC140 (ST15A).

Conclusions

While some PCV serotypes are now infrequently isolated from IPD patients, others including ST3 and ST19F have remained common and phylogenetically similar despite vaccine pressure. Additionally, phylogenetic diversification promotes continual emergence of new pneumococcal serotypes, and novel vaccine approaches are needed.

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