How Mastoiditis Develops
Mastoiditis occurs when bacterial infection from acute otitis media (middle ear infection) spreads directly into the mastoid air cells—the honeycomb-like bone structures behind the ear—causing inflammation and potentially bone destruction. 1
The Pathophysiologic Sequence
The development of mastoiditis follows a predictable anatomical pathway:
Initial bacterial colonization: The process begins with dense bacterial colonization of the nasopharynx, where common otopathogens (Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis) reside. 1, 2
Viral infection facilitates bacterial ascent: During upper respiratory infections or "colds," viruses ascend through the Eustachian tube to the middle ear, creating an environment that allows bacterial otopathogens to follow and establish infection. 1
Middle ear effusion develops: Bacteria multiply in the middle ear cavity, producing middle ear effusion (MEE) with signs of acute infection—the hallmark of acute otitis media. 1
Extension into mastoid air cells: The infection then extends posteriorly from the middle ear cavity into the mastoid air cells, which are directly connected to the middle ear space. This represents the transition from simple otitis media to mastoid involvement. 2, 3
Progressive inflammation and bone destruction: As bacteria colonize the mastoid air cells, inflammation intensifies. In more severe cases, coalescence of the air cells occurs with potential erosion of bony structures (osteomastoiditis). 4, 5
Key Bacterial Pathogens
The microbiology mirrors that of acute otitis media:
Streptococcus pneumoniae remains the most common pathogen, isolated in approximately 28-33% of cases despite pneumococcal vaccination. 1, 5, 6
Haemophilus influenzae (predominantly nontypable strains) accounts for 20-30% of cases, with 20-30% producing β-lactamase. 1, 7
Moraxella catarrhalis is found in 7-20% of cases, with the majority producing β-lactamase. 1, 7
Staphylococcus aureus has emerged as an increasingly important pathogen, with some series reporting rates as high as 16%. 5, 6
Important caveat: Cultures from mastoid infections may be negative in 33-53% of cases, likely due to prior antibiotic exposure or sampling issues. 4, 5
Critical Clinical Context
Several important nuances affect how mastoiditis develops:
Prior antibiotic treatment does NOT reliably prevent mastoiditis: Studies show that 48-81% of mastoiditis cases had received antibiotics for otitis media before developing mastoiditis, even in the absence of penicillin-resistant pathogens. 5, 8, 6 This challenges the assumption that adequate antibiotic treatment invariably prevents progression.
Age vulnerability: Mastoiditis disproportionately affects very young children (67% under 3 years old), who may present with mastoiditis as the first clinical sign of middle ear infection without preceding recognized otitis media. 5, 8, 6
Socioeconomic factors: Limited access to healthcare significantly increases risk, as delayed recognition and treatment of initial otitis media allows progression to mastoid involvement. 3
Increasing incidence and severity: Multiple studies document a concerning trend of increasing mastoiditis incidence and complications over the past two decades, with surgical intervention rates rising from 4% to 33-70% in some centers. 5
Common Pitfalls in Understanding Mastoiditis Development
Mastoiditis is not simply "untreated otitis media": The relationship is more complex—adequate antibiotic therapy for AOM does not guarantee prevention of mastoiditis, suggesting host factors and bacterial virulence play important roles beyond simple treatment adequacy. 8
The mastoid is not a separate compartment: The mastoid air cells are anatomically continuous with the middle ear cavity, making extension of infection a direct anatomical consequence rather than a distant complication. 1, 2
Antibiotic resistance is not the sole driver: While resistance patterns matter, even penicillin-sensitive S. pneumoniae can cause mastoiditis in adequately treated patients, indicating that factors beyond antimicrobial susceptibility influence disease progression. 8