Diseases of the Ear: Pathophysiology

By | 2013-07-19

Otitis extema describes any inflammatory condition of the external ear canal. The estimated incidence of otitis in dogs and cats ranges from 4% to 20% and 2% to 6.6%, respectively. Clinical signs associated with the condition vary, depending on the cause of the otitis General signs consist of head shaking, scratching, otic pain, and a variable accumulation of cerumen or exudate. The external canal responds to chronic inflammation of the dermis and epidermis with epithelial hyperplasia and hyperkeratosis, sebaceous gland hyperplasia, and ceruminous gland hyperplasia and dilation. These changes are associated with increased cerumen production; however, increased humidity, increased pH, and decreased lipid content of the cerumen predispose the animal to secondary infection. Apocrine gland rupture, sebaceous gland degeneration, ear canal stenosis, and fibrosis or ossification of the canal (or both) usually occur with the end stages of otitis. Because permanent changes of the ear canal can occur with any cause of otitis extema, primary, predisposing, and perpetuating factors should be investigated in all cases of otitis.

Primary Factors

Primary factors are capable of causing otitis in normal ears. Primary factors may not be cured but often are controlled with appropriate therapy.


Atopy and food hypersensitivity Otitis externa is a clinical sign in 50% to 80% of atopic or food-sensitive dogs and may be the sole clinical sign associated with atopy. Erythematous ceruminous otitis is most commonly associated with allergic skin disease. Early clinical signs of bilateral pruritus, concave pinnal erythema, and mild erythematous and ceruminous otitis of the proximal ear canal may progress to significant otitis externa and pinnal hyperpigmentation. The pet can develop end-stage otitis if the primary cause is not identified and treated. Aural pruritus is common to atopy and food hypersensitivity; however, steroid responsiveness is usually only seen with atopy. Atopic dogs also tend to have a slower progression of disease than food-sensitive dogs. Secondary infection with either Mcdassezia packydermatis or bacterial cocci is common. A definitive diagnosis is based on biopsy, intradermal skin testing, serologic testing, or dietary restriction and subsequent diet trials.

Contact hypersensitivity and irritant reaction Topical otic preparations may cause a delayed hypersensitivity or irritant reaction to the ear canal. A response to initial therapy is followed by progression of disease or change in the character of the otitis with continued therapy. Worsening of clinical signs can occur if the medication is discontinued then readminis-tered. Neomycin, propylene glycol, and dimethyl sulfoxide have been associated with irritant otitis. Reactions are occasionally noted with alcohol, glycerin, povidone-iodine, and concentrations of acetic acid greater than 2%. Contact hypersensitivity or an irritant reaction should be suspected any time otitis externa is exacerbated by therapy or upon changes in the gross or cytologic appearance of the otitis. Both contact hypersensitivity and irritant reaction act as perpetuating factors of otitis externa despite control of the primary factor.


Otodectes cynotis is the cause of otitis externa (otocariasis) in up to 50% of cats and 10% of dogs with otitis externa. The infestation in cats may be classified as one of the following: (1) otitis externa, (2) ectopic infestation, or (3) asymptomatic carrier. Signs of otitis include significant pruritus, pinnal erythema and crusting, and accumulation of cerumen in the external ear canal. Gross character of the cerumen is not correlated to the microscopic findings, but is usually dark brown to black in color. Mites may be observed on otoscopic examination; however, mineral oil cytology is recommended, because few mites are required to cause clinical signs. Mites may concurrently inhabit the skin of the head and neck in animals with otitis. True ectoparasite infestation usually results in miliary dermatitis and patchy alopecia in cats. Treatment can include any of the following: carbamates, pyrethrins, rotenone, ivermectin, thiabendazole, or fipronyl. Selamectin has recently been proven safe and effective for treating otocariasis in both dogs and cats. The 3-week cycle of the parasite should be considered in treatment planning.

Demodex canis has been associated with mild otitis and excessive cerumen production in dogs with the generalized form of demodicosis. The diagnosis is made with mineral oil cytology; other diagnostics (e.g. biopsy) are less often required. Other parasites such as harvest mites (Neotrombicula autumnahs and Euotrombicula alfredugesi) and ticks (Otobius megnini) may cause otitis externa. Reinfestation is a common problem due to environmental exposure to these parasites.

Foreign Bodies

Younger dogs, especially hunting or working breeds, are predisposed to otic foreign bodies. The most common foreign body associated with otitis is the grass awn; however, other foreign bodies include dirt, sand, cerumen, exudate mixed with hair, and conglomerates of dried ear medication. All can incite inflammation. Dogs are usually acutely painful, bilateral foreign bodies are possible, and approximately 20% of otic foreign bodies penetrate the tympanic membrane, leading to otitis media.

Keratinization Defects

Hypothyroidism, male feminizing syndrome, Sertoli cell tumor, hyperestrogenism, and idiopathic seborrhea may be associated with mild otitis externa. Idiopathic seborrhea in cocker spaniels and hereditary defects in cats leading to seborrhea may cause erythematous ceruminous otitis. Changes in the microenviron-ment of the ear canal lead to secondary purulent otitis.

Idiopathic Inflammatory or Hyperplastic Otitis

Cocker spaniels may be affected by severe, proliferative otitis externa at a young age. Concurrent dermatologic conditions are not necessarily present but should be ruled out for proper management. The cause of the condition is unknown but may be due to a primary glandular disorder.

Other Primary Factors

Immune-mediated disorders such as pemphigus complex may be associated with both pinnal lesions and otitis extema. Pemphigus foliaceus may involve only the ears in some cases, but lesions on other parts of the body are usually present. Drug eruption from systemically administered drugs may also cause both pinnal lesions and otitis extema. Older animals with chronic or recurrent otitis should be evaluated for benign or malignant neoplasia of the skin or adenexal structures of the ear.

Predisposing Factors Predisposing factors make otitis more likely by altering the environment of the external ear canal, thereby making the ear more susceptible to inflammation and secondary infection.

Anatomic Changes

Increased soft tissue within the ear canal, increased compound hair follicles in the canal, and stenotic canals (e.g. Shar Pei, bulldog, chow chow) or chronic changes associated with previous bouts of otitis may be predisposing factors for otitis externa. Dogs with pendulous ears are predisposed to otitis, and otitis is common in breeds of dogs exhibiting increased ceruminous compared with sebaceous gland area (e.g. cocker spaniel, Labrador retriever, springer spaniel). Hair is normally present in the ear canal, and increased numbers of hairs or presence of compound hair follicles have not been correlated to the incidence of otitis in dogs. Routine hair plucking is therefore not recommended and may incite an inflammatory response within the epithelium, perpetuating otitis extema.

External Environment

Increases in temperature and humidity in the environment may be reflected in the ear canal. The incidence of otitis extema is seasonally related to temperature, humidity, and rainfall. A lag period of 1 to 2 months is associated with cases of canine otitis and may vary with geographic location. Positive cultures of the ear canal are more likely during times of increased environmental temperature and humidity.

Perpetuating Factors Perpetuating factors exacerbate the inflammatory process and can maintain the disease after the primary factor has been eliminated. They can induce permanent pathologic changes to the ear canal and are the main reason for treatment failure in otitis externa.

Secondary Bacterial Colonization and Infection

Normal bacterial flora exist in the ear canal of dogs and cats. Staphylococcus species and Streptococcus species are often cultured, Pseudomonas is rarely cultured, and Proteus was not cultured from the normal canine ear canal. Malassezia has also been identified on cytologic examination in normal dogs and cats, and its numbers are significandy increased in erythema-tous ceruminous otitis. Bacteria and yeast are opportunistic pathogens but can cause significant secondary changes of the ear canal with chronic infection. Increased numbers of bacteria without an inflammatory response may represent colonization, which often responds to topical therapy. The presence of inflammatory cells suggests true infection, and culture and susceptibility is recommended due to resistance patterns of many bacteria. In colonization and infection, cleaning the external ear canal removes exudate, debris, toxins, free fatty acids, and bacteria that perpetuate inflammation and secondary changes of the ear canal.

Staphylococcus species are common in dogs with otitis as are Pseudomonas aeruginosa, Proteus species, Escherichia coli, Corynebacterium species, and Streptococcus species. Acute purulent otitis externa is less common than chronic, but with chronicity and repeated treatment, gram-negative bacteria, such as Pseudomonas and Proteus, predominate. The associated otitis may have surface erosions or ulcers and copious exudate. Cats may be secondarily infected with PasteureWa multocida and less often Pseudomonas aeruginosa, Proteus species, or E. coli.

Malassezia Pachydermatis Budding yeast has been identified on ear cytology of normal dogs (up to 50%) and cats (up to 17.6%). Malassezia are considered part of the normal flora and an opportunist in cases of otitis externa, particularly in cases of erythematous ceruminous otitis. Malassezia are lipid-dependent yeast that overgrow in conditions of increased moisture, increased surface lipids, and compromised barrier function of the stratum corneum. Enzymes produced by the yeast may allow depolymerization of the interstitial matrix (e.g. hyaluronidase, chondroitin-sulphatase) and cell membranes (e.g. proteinase, phospholipase), increasing tissue invasion and penetration. Cytologic examination is more valuable than culture, because some species of Malassezia require specific media supplemented with long-chain fatty acids.

Chronic Anatomic Changes

Increased soft tissue volume within the ear canal associated with chronic otic inflammation leads to ear canal stenosis and alters the otic microenvironment. Chronic changes of the epidermis, adenexa, dermis, and cartilage are described in the previous pathophysiology section. The microenviron-mental alterations associated with chronic ear canal stenosis and inflammation favor bacterial and yeast proliferation and the retention of exudate. The changes also hinder proper cleaning and medication of the deeper portions of the external ear canal.

Otitis Media

Untreated infection of the middle ear serves as a source for perpetuating otitis externa. Failure to identify the bacteria, yeast, or byproducts of inflammation in the middle ear may result in recurrent otitis externa and chronic pathologic changes of the middle and external ear.

Treatment Errors, Undertreatment, and Over-treatment

Incorrect treatment of otitis allows bacterial or yeast overgrowth or infection and denies treatment of the primary factor causing otitis. Overapplication of medication or use of occlusive medications increases the humidity of the ear canal, leading to epithelial maceration and inflammation, perpetuating otitis; accumulation of dried medication acts as a foreign body within the ear canal. Undertreatment allows progression of the disease and the development of resistance in the bacteria causing secondary infection.