Pathogenisis of Otitis Externa: Understanding Primary Causes

John C. Angus, DVM, Diplomate American College of Veterinary Dermatology
Southern Arizona Veterinary Specialists
Tucson, AZ, USA

Introduction

Otitis externa is a common disease in small animal veterinary practice, affecting 10-20% of all canine patients and 2-6% of all feline patients. Poor response to therapy and recurrent disease frequently results in ongoing pain, inflammation, and infection, eventually progressing to chronic, end-stage otitis. Chronic recurrence, progression and treatment failure are sources of frustration for the client and veterinarian, as well as causes of obvious discomfort and diminished quality of life for the patient. Many different conditions can contribute to the development of a patient's first episode of otitis; additional factors result in progression of severity and development of chronic otitis externa. The key to success in the long term is aggressive pursuit of all contributing factors during the early phases of ear disease. Failure to identify and treat relevant etiologic factors during initial management may result in poor response and worsening otitis. Therefore, the clinical approach to ear disease requires more than selection of the right topical or oral medication; it requires a detailed understanding of the multifactorial pathogenesis of otitis. Appropriate application of this knowledge will improve the outcome of "simple" cases, decrease recurrence, decrease progression of disease, and enhance your ability to manage difficult, chronic cases.

A key point in understanding the complex pathogenesis of ear disease is that "otitis externa" is not a final diagnosis; rather "otitis externa" is a clinical sign of underlying disease. To illustrate, think of a patient with a clinical presentation of polyuria, polydipsea, and urine specific gravity of 1.009. You would never consider making a final diagnosis of "isosthenuria" without pursuing the primary disease that is causing isosthenuria. You would make a list of differential diagnoses and perform the appropriate diagnostics necessary to identify the primary cause (renal disease, hepatic disease, endocrine disorders, etc. etc.). Similarly, many different primary diseases result in otitis externa, and yet veterinarians frequently choose to treat the clinical sign rather than the underlying cause.

Another important point to remember is that bacteria or yeast are not primary causes of otitis externa. Rather bacteria and yeast are the result otitis externa. Certainly, microorganisms contribute to the severity and progression of otitis externa and infection require attention during the management of the case, but they are not the primary cause. The majority of cases of otitis externa are associated with overgrowth or infection by a normal resident organism or opportunistic pathogen; rarely if ever can bacteria or yeast cause disease in a normal, healthy ear canal.

Multifactorial Pathogenisis

In 1988, John August published an article outlining a conceptual approach to the complex pathogenesis otitis externa. In this approach, all etiologic factors are divided into three categories: predisposing, primary and perpetuating (Table 1). Predisposing factors are conditions that increase the risk of developing otitis, but do not directly cause disease. Etiologic factors in this category include conditions that decreased ventilation, increased moisture, prevent normal clearance of debris, damage normal barrier function, or suppress immunity. Primary causes are conditions that can directly cause clinical disease in the absence of other factors. These primary diseases should be the focus of diagnostic and therapeutic intervention in long term management of otitis externa. Perpetuating factors are changes in the microenvironment or anatomy resulting from acute or chronic otitis that then go on to maintain disease and prevent resolution, even if the primary cause is identified and managed. Examples of perpetuating factors include bacteria, yeast, secondary changes (e.g. hyperkeratosis, hyperplasia, edema, glandular hypertrophy, loss of epithelial migration, ceruminoliths, stenosis, fibrosis, mineralization, cholesteatoma formation), and otitis media. While perpetuating factors are very important in the management of otitis externa details of these conditions are not discussed in detail here.

Hypersensitvity Reactions

The most common primary disease resulting in otitis externa is atopic dermatitis. Although the precise incidence of atopy is unknown, an estimated 10% of dogs have clinically significant atopy. Of these up to 80% exhibit otitis externa as part of their disease. Atopy is a complex disease that involves both genetic susceptibility and environmental factors that lead to hypersensitivity reactions to otherwise harmless antigens. A variety of abnormal immunologic events occur, resulting in inflammation, vasodilation, edema, erythema, and pruritus. In the ear canal, early pathologic changes include alteration of epidermal barrier, changes in cerumen composition, dermal edema, and glandular hyperplasia. Narrowing of the canal coupled with accumulation of ceruminous debris provides a better environment for microorganism overgrowth. Microorganisms exacerbate local inflammation as exotoxins and antigens penetrate the altered epidermal barrier. The combination of allergic reaction and secondary infection amplifies inflammation resulting in progressive deterioration of clinical signs. Even if the initial allergen trigger abates due to seasonal change, secondary infections perpetuate signs year-round. In severe cases, chronic allergen, bacteria, and yeast stimulation causes severe proliferative changes, fibrosis, and ossification, ultimately leading to permanent stenosis of the canal lumen. Cocker Spaniels are especially prone to developing profound ceruminous gland hyperplasia.

Adverse reaction to dietary antigen can produce nearly identical clinical signs to those seen in atopics reacting to environmental allergens. Although the immunologic mechanism of food allergy is not clearly understood, ingestion of offending proteins results in similar changes in barrier function, cerumen composition, edema, and glandular hyperplasia. Food allergies tend to be expressed year-round and are reported to be less responsive to corticosteroid therapy; however, clinical presentation is typically indistinguishable from atopy. For this reason, an elimination diet trial is an essential diagnostic test for all patients with chronic or recurrent otitis.

An uncommon cause for otitis externa is contact allergies. Contact reactions results from Type-IV (delayed) hypersensitivity to topically applied substances. Reactions are most commonly in response to medications used to treat otitis externa associated with other disease. A typical history is a good initial response to therapy followed by progressive worsening of signs, or resolution of a previous episode followed by treatment failure when the same medication is used on subsequent episodes. Neomycin, silver sulfadiazine, propylene glycol, botanical extracts, topical anesthetics, and topical insecticides have all been implicated.

Table 1 : Summary of factors contributing to clinical signs of otitis externa. Common factors are in bold

Parasite

Otodectes cynotis is the most common cause for otitis externa in cats; however, this highly contagious, non-species specific parasite is frequently and inappropriately overlooked as cause of otitis in dogs. O. cynotis can induce Type-I hypersensitivity reactions resulting in local mast cell degranulation, release of vasoactive peptides, edema, and inflammation of the external ear canal. Additionally, Type-III, or Arthus-type, reactions occur when mite antigen and host antibody form immune complexes along the epidermal-dermal junction or in dermal vessels of the ear canal. Immune complex deposition triggers activation of the complement cascade followed by cell-mediated immune response. This type of reaction causes intense local inflammation, pruritus, and pain. As few as 2 or 3 mites can trigger these reactions; therefore, adult dogs with very low mite burdens can have severe otitis externa. Because of the severity of inflammation and the low number of mites, the diagnosis can easily be missed. Always keep parasite hypersensitivity on the list of differential diagnoses for primary cause of otitis, unless the patient is currently receiving specific, effective therapy for O. cynotis. Other parasites implicated in otitis externa include Otobius megnini (spinous ear tick) and Demodex spp.

Nasal Pharygeal Polyp

Nasopharyngeal polyps are fleshy benign masses of fibrous connective tissue that arise from the respiratory epithelium of the nasopharynx, Eustachian tube, or tympanic cavity of cats. Young cats are more frequently affected than older cats. Most commonly cats present with clinical signs of upper respiratory disease, including nasal discharge, sneezing, and stertorous respirations. Other signs include dysphagia and recurrent bouts of gagging. If the polyp invades the tympanic cavity or ruptures the tympanic membrane patients may present for unilateral otitis externa, purulent or hemorrhagic otic discharge, frequent head shaking, nystagmus, head-tilt, ataxia, or even Horner's syndrome. Cats can occasional develop bilateral disease.

Neoplasia

Any obstructive mass, benign or malignant, can result in overgrowth of bacteria or yeast and subsequent clinical otitis. The most common malignancy in either dogs or cats is ceruminous gland adenocarcinoma. Tumors may occur in animals with a history of chronic otitis externa from other causes, suggesting that chronic inflammation and cerumen gland hyperplasia is a risk factor for malignant transformation. On otoscopic examination adenocarcinoma is seen as an irregular, friable, ulcerative mass, attached to the wall of either the vertical or horizontal canal. However, malignant tumors can also appear as smooth nodules similar to benign masses such as polyps or ceruminous gland adenomas. Management decisions should always be based on a histopathologic diagnosis and not gross appearance. Prognosis for ceruminous gland adenocarcinoma is mixed. The tumor tends to be locally invasive rather than metastatic. If caught early, the auricular cartilage acts as a physical barrier to invasion, permitting surgical intervention and complete excision. However, the tumor will eventually breach the auricular cartilage and extend into the parotid region. Extension of the mass beyond the cartilage carries a worse prognosis, since complete surgical excision is now unlikely. Early diagnosis and aggressive surgical management is the best course for any mass in the ear canal.

Hypothyroidism

Hypothyroidism may be a primary cause of otitis externa or may contribute to severity of disease when coupled with other primary diseases, such as atopy or food allergy. Patients with hypothyroidism exhibit impaired immune response, increased cerumen production, and alteration of epidermal barrier function. These changes can contribute to overgrowth of Malassezia and bacteria resulting in clinical disease. Thorough evaluation for concurrent primary diseases should continue even in patients diagnosed with hypothyroidism

Uncommon Causes

Less common causes of otitis externa in dogs or cats include immune-mediated dermatitis, such as pemphigus, lupus, or juvenile cellulitis; adverse drug reactions, erythema multiforme, canine distemper virus, seborrheic dermatoses, and traumatic injury to cartilage. Typically uncommon primary causes have other clinical signs or involve other areas of the body, leading the veterinarian to suspect these diseases.

Application of Knowledge

Successful management of otitis requires accurate identification and management of concurrent infection, inflammation, and of course the primary disease. For each patient, practitioners should generate an appropriate list of differential diagnoses of primary causes. Physical examination and history help order the likely causes, but very few differentials can be ruled in or out based on these findings alone. Each patient should have careful otoscopic examination for foreign objects or obstructive masses, cytology, mineral oil preparation for ear mites, a parasite treatment trial with a systemic avermectin, an 8-week elimination diet trial, and thyroid profile. If history and clinical signs are consistent with atopy and other common causes (food, parasite) have been ruled-out, then specific antigen testing by intradermal allergy test or serology should be considered. Antigen testing for environmental allergens is not a diagnostic test for atopy; rather it is a method for identifying which allergens should be included in a desensitization treatment set for a patient with the clinical diagnosis of atopy. Failure to identify and treat the primary cause of otitis externa will consistently result in poor response to therapy, recurrence, and progression of disease.

Recommended Reading

1. Gotthelf LN Small Animal Ear Diseases: An Illustrated Guide. 2nd Ed, 2005.
2. Matousek JL (ed) Ear Disease. Vet Clin North Amer Sm Anim Pract March 2004

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