Our findings in normal human middle ears seem to be unique, as evidence of cocci adhering to normal middle ear mucosa was previously only established by Dohar et al.22 Their observations in monkeys are in line with the results of our human study. Although, to our knowledge, such findings have not been reported before, it nevertheless seems unlikely that the presence of bacteria in the tympanic cavity of clinically healthy individuals is an exceptional phenomenon, as this region is connected to the nasopharynx, which is colonized by bacteria in individuals with OM as well as in healthy persons.23 Under certain circumstances, eg, subsequent to negative middle ear pressure, these nasopharyngeal bacteria can enter the tympanic cavity via the eustachian tube.24,25 Negative middle ear pressures often develop after blockage of the eustachian tube as a result not only of allergies, pollutants, and viruses, for example,26 but also of sniffing.27 Equilibration of the pressure differences between the middle ear and the nasopharynx is achieved when the eustachian tube reopens. Because air flows toward the middle ear on opening, colonizing nasopharyngeal pathogens may be insufflated into the tympanic cavity.24 Because negative middle ear pressures may occur in normal individuals as well as in persons with (developing) OM,28 it seems likely that almost all individuals will occasionally have to deal with transitory periods of negative middle ear pressure and subsequent pressure equilibrations. Therefore, transfer of bacteria from the nasopharynx to the tympanic cavity will occur not only in persons with middle ear diseases but also in healthy individuals. Furthermore, a preliminary study by Winther et al29 showed that radiopaque contrast medium introduced into the nasopharynx of healthy adults was displaced from the nasopharynx into the middle ear cavity during yawning and/or swallowing. These observations suggest that displacement of bacteria (present in nasopharyngeal secretions) to the middle ear may be a more frequent occurrence than anticipated from earlier reports. Apparently, in healthy individuals, this displacement does not provoke clinical symptoms because the middle ear is protected against invaders by the mucociliary system, by antimicrobial molecules of the innate immunity, and by the adaptive immune system.19,30 Despite these defense systems, attachment of bacteria on the middle ear mucosa can occur, implying that under certain conditions microorganisms are able to evade the mucociliary system and overcome local immune mechanisms (eg, secretory IgA and antimicrobial molecules). To gain access to the mucosal surface, several microbial strategies, such as paralysis of ciliary movement and inactivation of IgA, have evolved. Furthermore, bacteria deploy an array of adhesive molecules that recognize mucosal host cell receptors and facilitate the interaction with, and adhesion to, the epithelial surface.31 In fact, surface determinants of both bacterium and host are involved in adherence, which may be followed by colonization and/or biofilm formation.