The incidence of OM decreases steadily as the age of a child increases. Epidemiologic studies reveal the peak rate of infections occurring in patients between 6 and 18 months [4]. This is likely reflective of increased maturity of the immune system and completion of childhood vaccinations. A decrease is also observed as the anatomy of the eustachian tube changes with craniofacial maturation, which will be further discussed in another section .

Risk factors for OM propensity include host, environmental, and pathogen-related factors. As such, OM is a multifactorial condition. Risk factors for OM susceptibility will be discussed in detail in a separate chapter.

Studies of patients born with craniofacial abnormalities provide evidence to the role of Eustachian Tube (ET) maturation in the pathogenesis of OM. Histologic studies of ET tissue from children born with cleft lip or palate show evidence of immaturity of the cartilaginous tissue of the tube, which may explain the higher propensity toward infection in those children. Similarly, imaging studies demonstrate a more horizontal orientation of the tube, allowing for more direct entry of bacteria into the middle ear.

Children < 2 years of age in regular contact with large groups of other children , especially in daycare settings, or who recently have received antimicrobial treatment are at largest risk for harboring resistant bacteria in the nasopharynx and middle-ear space. Many strains of each of the abovementioned pathogenic bacteria that commonly cause AOM are resistant to commonly used antimicrobial drugs.

Although antimicrobial resistance rates vary across the globe, in the USA approximately 40 % of strains of NTHi and a great majority of M. catarrhalis strains are resistant to aminopenicillins (e.g., ampicillin and amoxicillin) . For these organisms, the resistance is attributable to production of β-lactamase against the penicillin molecule, which may be overcome by combining amoxicillin with a β-lactamase inhibitor (clavulanate) or by using a β-lactamase-stable antibiotic. It is worth noting that bacterial resistance rates in northern European countries where antibiotic usage is less are comparatively exceedingly lower (β -lactamase resistance in 6–10 % of isolates) than in the US.

In the USA, approximately 50 % of strains of S. pneumoniae are penicillin-nonsusceptible, divided approximately equally between penicillin-intermediate and, even more difficult to treat, penicillin-resistant strains. As opposed to NTHi and M. catarrhalis, resistance by S. pneumoniae to the penicillins and other β-lactam antibiotics is mediated not by β-lactamase production, but almost exclusively due to alterations in penicillin-binding proteins, which are overcome not by adding β-lactamase inhibitors, but by increasing the dosage of the penicillin-based antibiotic and increasing the local concentration of the drug in the middle-ear space. In general, as penicillin resistance increases, so also does resistance to other antimicrobial classes. Resistance to macrolides, including azithromycin and clarithromycin, by S. pneumoniae has increased rapidly, rendering theses antimicrobials minimally effective in AOM.