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Pneumococcal Colonization and the Nasopharyngeal Microbiota of Children in Botswana

Kelly, Matthew S., MD, MPH*,†; Surette, Michael G., PhD; Smieja, Marek, MD, PhD‡,§,¶,‖; Rossi, Laura, BSc; Luinstra, Kathy, BSc; Steenhoff, Andrew P., MBBCh, FCPaed*,**,††; Goldfarb, David M., MD*,‡‡; Pernica, Jeffrey M., MD; Arscott-Mills, Tonya, MD, MPH*,**; Boiditswe, Sefelani, BNSc*; Mazhani, Tiny, MD§§; Rawls, John F., PhD¶¶; Cunningham, Coleen K., MD; Shah, Samir S., MD, MSCE‖‖,***; Feemster, Kristen A., MD, MPH, MSHPR**,††; Seed, Patrick C., MD, PhD†††,‡‡‡

The Pediatric Infectious Disease Journal: November 2018 - Volume 37 - Issue 11 - p 1176–1183
doi: 10.1097/INF.0000000000002174
Translational Medicine Reports
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Background: Nasopharyngeal colonization precedes infections caused by Streptococcus pneumoniae. A more detailed understanding of interactions between S. pneumoniae and the nasopharyngeal microbiota of children could inform strategies to prevent pneumococcal infections.

Methods: We collected nasopharyngeal swabs from children 1 to 23 months of age in Botswana between August 2012 and June 2016. We tested samples for S. pneumoniae and common respiratory viruses using polymerase chain reaction. We sequenced the V3 region of the bacterial 16S ribosomal RNA gene and used random forest models to identify clinical variables and bacterial genera that were associated with pneumococcal colonization.

Results: Mean age of the 170 children included in this study was 8.3 months. Ninety-six (56%) children were colonized with S. pneumoniae. Pneumococcal colonization was associated with older age (P = 0.0001), a lack of electricity in the home (P = 0.02) and household use of wood as a cooking fuel (P = 0.002). Upper respiratory symptoms were more frequent in children with S. pneumoniae colonization (60% vs. 32%; P = 0.001). Adjusting for age, nasopharyngeal microbiota composition differed in colonized and noncolonized children (P = 0.001). S. pneumoniae colonization was associated with a higher relative abundance of Moraxella (P = 0.001) and lower relative abundances of Corynebacterium (P = 0.001) and Staphylococcus (P = 0.03). A decision tree model containing the relative abundances of bacterial genera had 81% sensitivity and 85% specificity for the determination of S. pneumoniae colonization status.

Conclusions: S. pneumoniae colonization is associated with characteristic alterations of the nasopharyngeal microbiota of children. Prospective studies should determine if nasopharyngeal microbial composition alters the risk of pneumococcal colonization and thus could be modified as a novel pneumonia prevention strategy.

From the *Botswana-UPenn Partnership, Gaborone, Botswana

Division of Pediatric Infectious Diseases, Duke University Medical Center, Durham, NC

Department of Medicine

§Department of Pathology and Molecular Medicine

Department of Pediatrics, McMaster University, Hamilton, Ontario, Canada

St. Joseph’s Healthcare, Hamilton, Ontario, Canada

**Global Health Center

††Division of Pediatric Infectious Diseases, Children’s Hospital of Philadelphia, Philadelphia, PA

‡‡Department of Pathology and Laboratory Medicine, BC Children’s Hospital, Vancouver, British Columbia, Canada

§§University of Botswana School of Medicine, Gaborone, Botswana

¶¶Duke Microbiome Center, Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC

‖‖Divisions of Hospital Medicine and Infectious Diseases, Cincinnati Children’s Hospital Medical Center, Cincinnati, OH

***University of Cincinnati College of Medicine, Cincinnati, OH

†††Division of Pediatric Infectious Diseases, Ann and Robert Lurie Children’s Hospital, Chicago, IL

‡‡‡Department of Pediatrics, Feinberg School of Medicine, Northwestern University, Chicago, IL.

Accepted for publication August 2, 2018.

The authors have no conflicts of interest to declare. This research was supported by an Early Career Award from the Thrasher Research Fund (to M.S.K.), a Burroughs Wellcome / American Society of Tropical Medicine and Hygiene Postdoctoral Fellowship in Tropical Infectious Diseases (to M.S.K.), by Children’s Hospital of Philadelphia (to A.P.S., K.A.F.) and Pincus Family Foundation, and through core services from the Penn Center for AIDS Research, a National Institutes of Health (NIH)-funded program (P30-AI045008). Funding for this project was also made possible in part by a CIPHER grant (to M.S.K.) from the International AIDS Society, supported by ViiV Healthcare. The views expressed in this publication do not necessarily reflect the official policies of the International AIDS Society or ViiV Healthcare. M.S.K. and C.K.C. received financial support from the NIH through the Duke Center for AIDS Research (P30-AI064518). M.S.K. was supported by an NIH Career Development Award (K23-AI135090) and a research grant from the Society for Pediatric Research (2018-2). J.M.P. was supported by a Hamilton Health Sciences Early Career Award. P.C.S. received funding from the NIH through a Research Project Grant (7R01-GM108494).

Drs. Feemster and Seed contributed equally to this work.

Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal’s website (www.pidj.com).

Address for correspondence: Matthew S. Kelly, MD, MPH, Box 3499, Duke University Medical Center, Durham, NC 27710. E-mail: matthew.kelly@duke.edu.

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