Otomycosis; clinical features, predisposing factors and treatment impl…

Abstract

DISCUSSION

Otomycosis is a superficial mycotic infection of the outer ear canal frequently encountered by otolaryngologist and can usually be diagnosed by clinical examination. However the correct diagnosis requires a high index of suspicion. The infection may be either sub acute or acute and is characterized by inflammation, pruritis, scaling and severe discomfort. The mycosis results in inflammation, superficial epithelial masses of debris containing hyphae, suppuration and pain. In addition, symptoms of hearing loss and aural fullness are as a result of accumulation of fungal debris in the canal. Pruritis has been frequently cited as one of the hallmark symptoms up to 93% in one study.^8.9 It was reported among the chief complaints in 108 (77%) of the current study population.

Aspergillus and Candida species are the most commonly identified fungal pathogens in otomycosis.^10.11

=> Infections with Candida can be more difficult to detect clinically because of its lack of a characteristic appearance like aspergillus and can present as otorrhoea not responding to aural antimicrobial.¹² Otomycosis attributed to Candida is often identified by culture data. Although multiple in vitro studies have examined the efficacy of various antifungal agents, there is no consensus on the most effective agent.¹³ Various agents have also been used clinically with variable rate of success.^14.15 Nevertheless, application of appropriate topical antifungal agents coupled with frequent mechanical debridement usually results in prompt resolution of symptoms, although recurrent or residual disease can be common.

 In this series more than 70% of the patients had resolution of the infection with initial treatment, often in less than two weeks. Topical clotrimazole is our preferred antifungal agents for its efficacy against both aspergillus and Candida species. There were only 4 (2.2%) cases of local sensitivity to clotrimazole and the infections seem to resolve faster and display a lower recurrence rate.

TM perforation and serous otitis media are not uncommon with otomycosis and tend to resolve with treatment. The pathophysiology of the TM perforation may be attributed to avascular necrosis of the TM as a result of mycotic thrombosis in the adjacent blood vessels. The rate of 20% (8 patients) of TM perforation in this series is similar to that observed by Pradhan et al.⁹ There were no clinical features predictive of TM perforation. TM involvement is likely a consequence of fungal inoculation in most medial aspects of the external canal or direct extension of the disease from adjacent skin.

There appear to be little consensus with respect to the predisposing factors for otomycosis. For instance the presence of cerumen has been speculated to be supportive of fungal growth by some, yet inhibitory by others.^1,8,15 There have also been reports of autoinoculation of ear canal that result in otomycosis by patient with untreated dermatomycosis.

More recently there has been increasing concern with respect to increasing incidence of otomycosis from wide spread use of fluoroquinolone otic drops.¹⁶

In this series neomycin-polymyxin B noted in 8% of the patients in the study appears to increase the risk for developing otomycosis. This is higher than that reported in other series such as that by Pradhan et al,⁹ where 4.6% of the subjects were post mastoidectomy patients. The data appear to support prior otologic procedures particularly that result in a mastoid cavity, as a potential risk factor for otomycosis. Several factors may contribute to the development of otomycosis in the previously operated ear. First recurrent drainage or subsequent antibiotic / antiseptic application may alter the local environment of the external canal and allow super infection of nosocomial fungi. Second alteration of the anatomy by canal wall down procedures may also produce changes in cerumen production or relative humidity that favor fungal growth. This suggests that eradication of disease is more difficult in the presence of mastoid cavity.

 The addition of oral antifungals is reserved for cases with severe disease and poor response to topical therapy. We believe oral antifungals are unlikely to succeed in the absence of adequate local care. The limitation of this study is the increase heat and humidity in our geographical region which may limit the applicability of these findings in regions with a more temperate climate. Future research may include better characterization of the effective treatment dose and duration of the various available antifungal agents.