Otitis externa causes

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Causes

The two factors that are required for external otitis to develop are (1) the presence of germs that can infect the skin and (2) impairments in the integrity of the skin of the ear canal that allow infection to occur. If the skin is healthy and uninjured, only exposure to a high concentration of pathogens, such as submersion in a pond contaminated by sewage, is likely to set off an episode. However, if there are chronic skin conditions that affect the ear canal skin, such as atopic dermatitis, seborrheic dermatitis, psoriasis or abnormalities of keratin production, or if there has been a break in the skin from trauma, even the normal bacteria found in the ear canal may cause infection and full-blown symptoms of external otitis.

The most common bacterial pathogens causing otitis externa are Pseudomonas aeruginosa and Staphylococcus aureus, followed by a great number of other gram-positive and gram-negative species.[1] Candida albicans and Aspergillus species are the most common fungal pathogens responsible for the condition.

Fungal ear canal infections, also known as otomycosis, range from inconsequential to very severe. Fungus can be saprophytic, in which there are no symptoms and the fungus simply co-exists in the ear canal in a harmless parasitic relationship with the host, in which case the only physical finding is presence of the fungus. If for any reason the fungus begins active reproduction, the ear canal can fill with dense fungal debris, causing pressure and ever-increasing pain that is unrelenting until the fungus is removed from the canal and anti-fungal medication is used. Most antibacterial ear drops also contain a steroid to hasten resolution of canal edema and pain. Unfortunately such drops make fungal infection worse. Prolonged use of them promotes growth of fungus in the ear canal.

References

  1. Roland P, Stroman D (2002). "Microbiology of acute otitis externa". Laryngoscope. 112 (7 Pt 1): 1166–77. PMID 12169893.

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