To describe NP and AOM otopathogens during the time frame 2007 to 2009, 6 to 8 years after the introduction of 7-valent pneumococcal conjugate (PCV7) in the United States and to compare nasopharyngeal (NP) colonization and acute otitis media (AOM) microbiology in children 6 to 36 months of age having first and second AOM episodes with children who are otitis prone.
Prospectively, the microbiology of NP colonization and AOM episodes was determined in 120 children with absent or infrequent AOM episodes. NP samples were collected at 7 routine visits between 6 and 30 months of age and at the time of AOM. For first and subsequent AOM episodes, middle ear fluid (MEF) was obtained by tympanocentesis. Eighty otitis prone children were comparatively studied. All 200 children received age-appropriate doses of PCV7.
We found PCV7 serotypes were virtually absent: (0.9% isolated from both NP and MEF) in both study groups. However, non-PCV7 serotypes replaced PCV serotypes such that the frequency of isolation of S. pneumoniae (Spn) was nearly equal to that of non-typeable Haemophilus influenzae (NTHi). M. catarrhalis (Mcat) was less common and Staphylococcus aureus infrequent in the NP and MEF from the 2 groups. The proportion of Spn, NTHi and Mcat causing AOM was similar in children with first and second AOM episodes compared to otitis prone children. However, oxacillin-resistant Spn isolated from the NP and MEF was 19% for the absent/infrequent and 58% for the otitis prone groups, P < 0.0001. Beta-lactamase producing NTHi occurred more frequently in the otitis prone group, P = 0.04.
Six to 8 years after widespread use of PCV7, Spn strains expressing vaccine-type serotypes have virtually disappeared from the NP and MEF of vaccinated children. NP colonization and AOM has changed to non-PCV7 strains of Spn. NTHi continues to be a major AOM pathogen. The otopathogens in first and second AOM and in otitis prone children are very similar although Spn and NTHi are more often antibiotic resistant in the otitis prone.
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From the *Department of Pediatrics, University of Rochester, Rochester, NY; and †Center for Infectious Disease and Immunology, Rochester General Research Institute, Rochester, NY.
Accepted for publication September 17, 2009.
Supported by R01DC08671, Thrasher Research Fund, and an investigator-initiated grant from Wyeth Vaccines (to M.E.P.).
Address for correspondence: Michael E. Pichichero, MD, Rochester General Research Institute, Rochester General Hospital, 1425 Portland Ave, Rochester, NY 14621. E-mail: firstname.lastname@example.org.
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