Factors influencing activity of com
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Chronic otitis media
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Factors Influencing Activity of Chronic Otitis Media (COM)
Source: Scott-Brown's Otorhinolaryngology Head & Neck Surgery, Vol. 2, Chapter 83
COM can be active (discharging/progressive) or inactive. The factors that drive or sustain activity are broadly grouped below.
1. Infection
The mucopus from active COM is rarely sterile. Cultures yield multiple organisms that vary with climate, patient population, and prior antibiotic use. In patients who had no antibiotics for 4 weeks, aerobic isolates included:
| Organism | % of ears |
|---|---|
| Proteus spp. | 95% |
| Staphylococcus aureus | 40% |
| Pseudomonas spp. | 30% |
| Coagulase-negative staphylococci | 30% |
| 'Coliform' bacilli | 25% |
64% of cultures yielded only aerobes, 32% both aerobes and anaerobes. An important caveat: cultures from almost 50% of patients with inactive COM yield an identical flora to that in active COM - meaning bacteria alone do not determine activity. Pseudomonas likely acts as an opportunistic secondary invader via adherence to already-damaged epithelium ("opportunistic adherence"), rather than being a primary initiating cause.
2. Biofilms
Bacteria preferentially form biofilms - complex, surface-attached multicellular communities with far greater antimicrobial resistance and resistance to host defences. Studies show:
- 60% biofilm incidence in active COM vs. 10% in uninfected controls
- Biofilms are more abundant in squamous COM: 82% of cholesteatoma ears had biofilms vs. 42% in mucosal COM vs. 9% in normal middle ears
Biofilms explain the persistence of infection despite antimicrobials and the self-perpetuating inflammatory cycle.
3. Upper Respiratory Tract Infections (URTIs)
Many patients clinically report flare-ups of COM with URTIs. The proposed mechanism is that URTIs cause transient Eustachian tube dysfunction even in healthy individuals. Since the respiratory mucosa of the Eustachian tube is continuous with the middle ear, it can become primarily infected or secondarily superinfected with bacteria, triggering mucosal activity.
4. Eustachian Tube Dysfunction
Eustachian tube dysfunction is more common in patients with COM than in middle-ear-disease-free individuals. Whether it is the initiating factor for COM or a consequence of chronic middle ear disease remains unresolved. In cholesteatoma formation, Eustachian tube dysfunction causes persistent negative middle ear pressure, driving retraction pockets in the pars flaccida or posterosuperior pars tensa - the most likely pathway to squamous COM.
5. Environmental and Socioeconomic Factors
COM prevalence is greater in lower socioeconomic groups. In a large cohort of 12,000 children, significant risk factors for ear discharge included:
- Poor general health scores
- Maternal smoking (household smokers: HR = 4.56 in Koch's prospective study)
- Day-care attendance (HR = 3.18)
- Breastfeeding had a weak and non-significant protective effect
Improvements in housing and health care in New Zealand Maori children reduced COM prevalence from 9% (1978) to 3% (1987), supporting the role of hygiene and living conditions in activity. Nutritional and environmental factors are thought to predispose individuals to COM, explaining higher rates in deprived communities.
6. Immune Deficiency
AIDS/HIV is strongly associated with active COM. A case-control study in Sub-Saharan African children found:
- Active COM rate of 26% in HIV-positive children vs. <4% in HIV-negative children
- Antiretroviral treatment was associated with lower COM prevalence
Diabetes and other immunocompromised states also impair the ability to resolve infection and may drive persistent activity.
7. Genetic and Racial Factors
There is a high incidence of COM in American Indians (varying by tribe, suggesting genetic basis) and Inuit populations (Inuit descent had an HR of 5.56 for COM in a Greenlandic cohort). Genetic factors are difficult to disentangle from socioeconomic confounders, but the tribal variation among American Indians argues for a genuine genetic contribution.
8. Craniofacial Abnormalities
Cleft palate is associated with ~20% incidence of COM by age 10, with 2% developing cholesteatoma. The tensor veli palatini muscle is hypoplastic in cleft palate, predisposing to Eustachian tube dysfunction as the key mechanism.
9. Gastro-oesophageal Reflux Disease (GORD)
Evidence is currently anecdotal. A systematic review found a possibly higher prevalence of GORD in children with OME and recurrent AOM, and pepsin/pepsinogen has been detected in the middle ear (suggesting reflux reaches the Eustachian tube ostium). A cause-and-effect relationship with COM remains unproven.
10. Autoimmune Disease
COM was present in 29% of consecutive patients with ankylosing spondylitis in one study, but whether autoimmune disease directly predisposes to COM is still uncertain.
11. Continuing Activity - Consequences that Perpetuate Disease
Once COM is active, the inflammatory reaction with granulation tissue drives osteoclastic bone resorption of the ossicular chain - particularly the long process of the incus and stapes superstructure - creating a self-perpetuating cycle of structural damage. Otorrhoea with multiple infecting organisms is associated with more rapid ossicular deterioration.
Summary Table
| Factor | Mechanism |
|---|---|
| Infection (Pseudomonas, Proteus, S. aureus) | Secondary mucosal invasion and sustained inflammation |
| Biofilms | Antibiotic resistance, persistent colonization |
| URTIs | Eustachian tube dysfunction → mucosal activation |
| Eustachian tube dysfunction | Negative middle ear pressure → retraction → cholesteatoma |
| Low socioeconomic status / poor hygiene | Nutritional, environmental, overcrowding factors |
| Passive smoking | HR 4.56 for active COM |
| Day-care attendance | HR 3.18 (increased exposure to pathogens) |
| Immune deficiency (HIV, diabetes) | Impaired pathogen clearance |
| Genetic/racial factors | Inuit, American Indian predisposition |
| Cleft palate | Hypoplastic tensor veli palatini → ET dysfunction |
| GORD | Pepsin reflux to middle ear (weak evidence) |
Scott-Brown's Otorhinolaryngology Head & Neck Surgery, Vol. 2, Chapter 83 (Browning, Weir, Kelly, Swan)
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