Abstract
Otitis media is very common in children. A subpopulation of children, representing 5–10% of the general population, are otitis prone and they experience 4 or more episodes of acute otitis media (AOM) in the first year of life. Nasopharyngeal colonization with the three major middle ear pathogens, S. pneumoniae, nontypeable H. influenzae and M. catarrhalis is frequent in otitis prone children and is directly related to the frequency of AOM. Colonization stimulates the production of mucosal as well as serum antibodies to the pathogens. Specific IgA mucosal antibody limits the duration and frequency of colonization. Serum IgG antibody protects children against the development of otitis media but does not affect colonization. Antibody detected in the middle ear often reflects passive transfer from serum rather than local production. Antibody responses to the three pathogens following AOM are generally reduced in the first 2 years of life and rise rapidly thereafter. There are many different strains of Streptococcus pneumoniae, Haemophilus influenzae and Moraxella catarrhalis. Among the different strains, there are heterologous surface antigens and some conserved antigens. Conserved antigens induce broadly protective antibodies while strain specific antigens induce limited protection. Although otitis prone children may display strain specific immunity, they often fail to develop a broadly protective antibody response. This subtle immunologic defect makes them susceptible to recurrent and persistent otitis media.
Conclusions Otitis media is common. Otitis prone children appear to display a subtle immunologic abnormality that predisposes them to recurrent infections. Recent advances in vaccine development may reduce the frequency of otitis media in the general population but the impact on otitis prone children remains unknown.
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Received: 18 September 2000 and in revised form: 25 January 2001 / Accepted: 30 January 2001
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Faden, H. The microbiologic and immunologic basis for recurrent otitis media in children. Eur J Pediatr 160, 407–413 (2001). https://doi.org/10.1007/s004310100754
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DOI: https://doi.org/10.1007/s004310100754