Frontiers in Genetics (Jun 2019)

Age-Dependent Dissimilarity of the Nasopharyngeal and Middle Ear Microbiota in Children With Acute Otitis Media

  • Silvio D. Brugger,
  • Silvio D. Brugger,
  • Silvio D. Brugger,
  • Julia G. Kraemer,
  • Julia G. Kraemer,
  • Weihong Qi,
  • Lindsey Bomar,
  • Lindsey Bomar,
  • Anne Oppliger,
  • Markus Hilty

DOI
https://doi.org/10.3389/fgene.2019.00555
Journal volume & issue
Vol. 10

Abstract

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Acute bacterial otitis media is usually caused by otopathogens ascending to the middle ear from the nasopharynx (NP). However, it is unknown if the nasopharyngeal microbiota of children with acute otitis media (AOM) can serve as an age-dependent or independent proxy for the microbial communities of the middle ear fluid (MEF) as there is a lack of 16S rRNA amplicon sequencing studies simultaneously analyzing the microbial communities of the two sites. Within this study, we performed 16S rRNA next generation sequencing on a total of 286 nasopharyngeal swabs (NPSs) collected between 2004 and 2013 within a Swiss national AOM surveillance program from children (0–6 years) with AOM. In addition, 42/286 children had spontaneous tympanic membrane perforation and, therefore, those MEF could also be analyzed. We found that alpha [Richness, Shannon diversity index (SDI) and Evenness] and beta diversity measurements of the nasopharyngeal bacterial microbiota showed a clear dependency of the increasing age of the children. In more detail, bacterial richness and personalized profiles (measured by beta dispersion) were higher and more frequent in older children, respectively. Dissimilarity values based on the binary distance matrix of the microbiota patterns of the NP and the MEF also correlated with increasing age. In general, positive (PPV) and negative predictive values (NPV) of the most abundant operational taxonomic units (OTUs) in the NP were moderately and well predictive for their presence in the MEF, respectively. This data is crucial to better understand polymicrobial infections and therefore AOM pathogenesis.

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