The prevailing theory of the development of middle ear inflammation and effusion has been that eustachian tube inflammation leads to the build-up of bacteria and a resultant secondary bacterial infection of the middle ear space.
URTIs caused by rhinovirus, respiratory syncytial virus, influenza virus, and adenovirus have been implicated in the pathophysiology of eustachian tube inflammation and middle ear inflammation.
Most studies agree that viruses directly damage eustachian tube lining and can result in decreased mucociliary clearance.
Studies also suggest a more direct role of viruses in the development of middle ear inflammation. Research has demonstrated direct viral invasion of middle ear mucosa without evidence of bacterial secondary infection. Animal studies have concluded that the immune response to middle ear and eustachian tube viral infection continues to propagate the resultant inflammation long after clearance of viral antigen. Purely immune-mediated cases of otitis media (OM) have been developed in animal studies.
Multiple cytokines have been investigated as contributing to otitis media (OM) and have been started in middle ear effusions. These cytokines include interleukin-1beta, tumor necrosis factor-alpha, and gamma-interferon. Other cytokines and cell surface markers have been described in animal studies, including interleukin-1alpha and intracellular adhesion molecule (ICAM). This theory of a persistent sterile effusion following viral URTI gives credence to the expectant management of nonsevere otitis media (OM) as practiced in the Netherlands and elsewhere in Europe.
Other theories include reflux of nasopharyngeal bacteria through the eustachian tube causing infection of the middle ear cleft.
Streptococcus pneumoniae, nontypeable Haemophilus influenzae, and Moraxella catarrhalis are the most commonly isolated bacteria of middle ear infections. Less frequent isolates include group A streptococci, Staphylococcus aureus, and enteric bacteria found in newborns such as Escherichia coli, species of Klebsiella, Enterobacter, and Pseudomonas aeruginosa.
A study by Martin et al looking at AOM cases between 1999 and 2014 in children aged 6-23 months found that, while nasopharyngeal colonization with S pneumoniae has reportedly decreased since pneumococcal conjugate vaccines (PCVs) were introduced, colonization with H influenzae in the study subjects initially increased before dropping back to levels seen prior to routine administration of 7-valent PCV (PCV7). The investigators obtained nasopharyngeal cultures from four cohorts of children with AOM. The first cohort was cultured in 1999-2000, before routine PCV7 use, while in the second (2003-2005) and third (2006-2009) cohorts, two or more doses of PCV7 were administered to 93% and 100% of children, respectively, and in the fourth cohort (2012-2014), 100% of the children received two or more doses of 13-valent PCV (PCV13). Nasopharyngeal colonization with H influenzae in cohorts 1, 2, 3, and 4 occurred in 26%, 41%, 33%, and 29% of children, respectively. [14]
Historically, allergy has been associated with the development of eustachian tube and middle ear inflammation; however, clear evidence has not been elucidated.
Anatomic abnormalities, such as those observed in patients with cleft palate or other cranial facial abnormalities, may lead to middle ear and eustachian tube inflammation by a direct effect on eustachian tube function. Moreover,a study by Paltura et al suggested that smaller eustachian tube diameter is a factor in the development of chronic otitis media (COM). The study, which included 154 patients with unilateral chronic otitis media (COM), found that the mean diameter of the eustachian tube in diseased ears was 1788 mm, compared with 1947 mm in the healthy ears. [15]
Environmental factors, such as daycare attendance, passive smoke exposure, and pacifier usage, may contribute to nasopharyngeal and middle ear inflammation. [16]
The method of feeding infants may contribute to middle ear infection. Maternal immunoglobulin G (IgG) in breast milk may be protective against the development of middle ear infection. With breastfeeding, any detrimental effects of bottle feeding may be avoided, although conclusive data regarding these effects are unavailable.
Gastroesophageal reflux has also been implicated as an etiological agent in the development of middle ear and eustachian tube inflammation. [17] Nasopharyngeal pH has been noted to be lower in a subset of patients with adenoiditis and otalgia, although the degree of decreased pH required for pathology has not been standardized.
