Nasopharyngeal Carriage of Streptococcus pneumoniae in Children in Coastal Kenya

Claire J. Heath Division of Pediatric Infectious Diseases, Stanford University School of Medicine, Palo Alto, California;

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Monica Nayakwadi-Singer Division of Pediatric Infectious Diseases, UCSF Benioff Children’s Hospital Oakland and Children’s Hospital Oakland Research Institute, Oakland, California;

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Charles H. King Center for Global Health and Diseases, Case Western Reserve University, Cleveland, Ohio;

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Indu Malhotra Center for Global Health and Diseases, Case Western Reserve University, Cleveland, Ohio;

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Francis Mutuku Technical University of Mombasa, Mombasa, Kenya;

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Dunstan Mukoko Vector Borne Disease Control Unit, Nairobi, Kenya

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A. Desiree LaBeaud Division of Pediatric Infectious Diseases, Stanford University School of Medicine, Palo Alto, California;

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Streptococcus pneumoniae (SP) is a leading cause of child mortality globally, killing around half a million children aged 5 years and less per year. Nasopharyngeal carriage of SP is a prerequisite to disease, and the prevalence of colonization reaches 100% within the first few years of life. Serotype prevalence varies geographically, impacting the serotype coverage of pneumococcal vaccines, and serotype prevalence data are limited from large regions of the world, including sub-Saharan Africa. We enrolled 323 unvaccinated children, aged 4–7 years from coastal Kenya and obtained nasopharyngeal swab samples before and after vaccination with the 10-valent pneumococcal vaccine. Vaccination did not reduce the overall prevalence of pneumococcal carriage in our cohort, with 65 (20%) children colonized before vaccination and 63 (19.4%) colonized postvaccination. However, the prevalence of vaccine-included serotypes (vaccine strains) declined from 43% to 19% of positive swabs, whereas non-vaccine serotypes increased from 46% to 73%. This study contributes to the few data available regarding pneumococcal carriage and serotype prevalence in Kenya and is in concordance with reports of dynamic serotype replacement, driven by vaccine pressure.

Author Notes

Address correspondence to Claire J. Heath, Stanford University School of Medicine, 300 Pasteur Drive, Palo Alto, CA 94305. E-mail: claire.j.heath@gmail.com

Financial support: This work was supported by a grant awarded to the principal investigator C. H. K. by the Bill & Melinda Gates Foundation (grant number: OPP1066865).

Authors’ addresses: Claire J. Heath and A. Desiree LaBeaud, Division of Pediatric Infectious Diseases, Stanford University School of Medicine, Palo Alto, CA, E-mails: cjheath@stanford.edu and dlabeaud@stanford.edu. Monica Nayakwadi-Singer, Division of Pediatric Infectious Diseases, UCSF Benioff Children’s Hospital Oakland, Children’s Hospital Oakland Research Institute, Oakland, CA, E-mail: msinger@mail.cho.org. Charles H. King and Indu Malhotra, Center for Global Health and Diseases, Case Western Reserve University, Cleveland, OH, E-mails: chk@case.edu and indu.malhotra@case.edu. Francis Mutuku, Technical University of Mombasa, Mombasa, Kenya, E-mail: fmutuku73@gmail.com. Dunstan Mukoko, Vector Borne Disease Control Unit, Nairobi, Kenya, E-mail: dunstan.mukoko29@gmail.com.

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