2254. Correlation of Antibody Levels to Pneumococcal Proteins with Protection from Acute Otitis Media but not Nasopharyngeal Colonization in Young Children
Session: Poster Abstract Session: New Antibiotics in Development
Saturday, October 29, 2016
Room: Poster Hall
Background:  We previously found that nasopharyngeal (NP) colonization byStreptococcus pneumonia (Spn) elicits mucosal antibody responses to three protein vaccine candidates: pneumococcal histidine triad protein D (PhtD), pneumococcal choline binding protein A (PcpA), and pneumolysin (Ply). Here we sought to determine if mucosal antibody levels to these three proteins correlated with protection from acute otitis media (AOM) and NP colonization.

Methods:  Healthy infants had NP samples prospectively collected at 6-24 months of age. Whenever a child was diagnosed with AOM, tympanocentesis was performed and middle ear fluid samples collected to confirm the diagnosis by microbiologic culture. NP mucosal IgG and IgA titers to PhtD, PcpA and Ply were quantified by ELISA. The correlation of antibody levels with protection from AOM and NP colonization were analyzed using a generalized estimating equation model.

Results:  Higher levels of naturally acquired mucosal antibody to PhtD, PcpA and Ply induced by NP colonization correlated with protection from subsequent AOM infections by Spn but did not correlate with subsequent NP colonization events. Children who experienced 1-3 episodes of AOM caused by Spn had 2-5-fold lower mucosal IgG levels to PcpA , 6-8-fold lower IgA to PhtD; 2-3-folder lower IgA to PcpA, and 2-3-fold lower GM of IgA to Ply. NP mucosal antibody IgG to PcpA, and IgA levels to all three proteins were negatively associated with possibility of future episodes of AOM caused by Spn(P<0.0001). Mucosal antibody levels to the three proteins did not correlate with protection from subsequent NP colonization with Spn.

Conclusion:  NP mucosal IgG levels to PcpA, IgA to PhtD, PcpA and Ply, and IgG to PcpA correlate with protection against pneumococcal AOM in young children but not with protection against NP colonization. This study was supported by an investigator-initiated grant from Sanofi pasteur and NIH NIDCD RO1 08671

Qingfu Xu, PhD1, Janet Casey, MD2, Anthony Almudevar, PhD3 and Michael Pichichero, MD1, (1)Rochester General Hospital Research Institute, Rochester, NY, (2)Legacy Pediatrics, Rochester, NY, (3)Biostatistics and Computational Biology, University of Rochester Medical Center, Rochester, NY

Disclosures:

Q. Xu, Sanofi Pasteur: Grant Investigator , Research support

J. Casey, Sanofi Pasteur: Grant Investigator , Research support

A. Almudevar, None

M. Pichichero, Sanofi Pasteur: Consultant and Grant Investigator , Research support

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