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Front. Microbiol. | doi: 10.3389/fmicb.2018.02670

A population-based descriptive atlas of invasive pneumococcal strains recovered within the U.S. during 2015-2016.

 Bernard Beall1*, Sopio Chochua1,  Robert E. Gertz, Jr.1, Yuan Li1, Zhongya Li1, Lesley McGee1, Benjamin J. Metcalf1, Ricaldi Ricaldi1, Theresa Tran1, Hollis Walker1 and Tamara Pilishvili1
  • 1National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention (CDC), United States

Invasive pneumococcal disease (IPD) has greatly decreased since implementation in the U.S. of the 7 valent conjugate vaccine (PCV7) in 2000 and 13 valent conjugate vaccine (PCV13) in 2010. We used whole genome sequencing (WGS) to predict phenotypic traits (serotypes, antimicrobial phenotypes, and pilus determinants) and determine multilocus genotypes from 5334 isolates (~90% of cases) recovered during 2015-2016 through Active Bacterial Core surveillance. We identified 44 serotypes; 26 accounted for 98% of the isolates. PCV13 serotypes (inclusive of serotype 6C) accounted for 1503 (28.2%) isolates, with serotype 3 most common (657/5334, 12.3%), while serotypes 1 and 5 were undetected. Of 305 isolates from children <5yrs, 60 (19.7%) were of PCV13 serotypes 19A, 19F, 3, 6B, and 23F (58/60 were 19A, 19F, or 3). We quantitated MLST-based lineages first detected during the post-PCV era (since 2002) that potentially arose through serotype-switching. The 7 predominant emergent post-PCV strain complexes included 23B/CC338, 15BC/CC3280, 19A/CC244, 4/CC439, 15A/CC156, 35B/CC156, and 15BC/CC156. These strains accounted for 332 isolates (6.2% of total) and were more frequently observed in children <5yrs (17.7%; 54/305). Fifty-seven categories of recently emerged (in the post PCV7 period) putative serotype-switch variants were identified, accounting for 402 isolates. Many of these putative switch variants represented newly emerged resistant strains. Penicillin-nonsusceptibility (MICs >0.12µg/ml) was found among 22.4% (1193/5334) isolates, with higher penicillin MICs (2-8 µg/ml) found in 8.0% (425/5334) of isolates that were primarily (372/425, 87.5%) serotypes 35B and 19A. Most (792/1193, 66.4%) penicillin-nonsusceptible isolates were macrolide-resistant, 410 (34.4%) of which were erm gene positive and clindamycin-resistant. The proportion of macrolide-resistant isolates increased with increasing penicillin MICs; even isolates with reduced penicillin susceptibility (MIC = 0.06µg/ml) were much more likely to be macrolide-resistant than basally penicillin-susceptible isolates (MIC < 0.03µg/ml). The contribution of recombination to strain diversification was assessed through quantitating 35B/CC558-specific bioinformatic pipeline features among non-CC558 CCs and determining the sizes of gene replacements. Although IPD has decreased greatly and stabilized in the post-PCV13 era, the species continually generates recombinants that adapt to selective pressures exerted by vaccines and antimicrobials. These data serve as a baseline for monitoring future changes within each invasive serotype.

Keywords: Conjugate vaccine, pneumococcal, Clonal complex (CC), serotype diversity, serotype distributions, antibiotic resistance

Received: 03 Aug 2018; Accepted: 19 Oct 2018.

Edited by:

Awdhesh Kalia, University of Texas MD Anderson Cancer Center, United States

Reviewed by:

Anthony Flores, McGovern Medical School, University of Texas, United States
Casey Schroeder, University of Texas MD Anderson Cancer Center, United States  

Copyright: © 2018 Beall, Chochua, Gertz, Jr., Li, Li, McGee, Metcalf, Ricaldi, Tran, Walker and Pilishvili. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Bernard Beall, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, 30329, Georgia, United States, bbeall@cdc.gov