Dr. Alberto Martin Cordero received the degree of Doctor in Veterinary Medicine by the University of Guadalajara. He studied Veterinary Dermatology in the European School for Advanced Veterinary Studies, University of Luxembourg. He is a member of the American Academy of Veterinary Dermatology and a founder member of the Latin American Society of Veterinary Dermatology. Is an assistant professor in University of Guadalajara, Department of Veterinary Medicine. He has been a speaker in numerous conferences in Mexico, Latin America and Eastern Europe; and presented articles and clinical cases in Latin America, USA, and Europe. He has been a coordinator in videotoscopy wetlabs and dermatology workshops. He is the coordinator of the dermatology program in Leon Conference (CVDL), currently the second largest veterinary meeting in the world. Dr. Alberto has published articles and clinical cases national and international. He works in private practice and it is the owner of VETDERM: the first veterinary dermatology referral practice the west of Mexico. He has realized visits in the Animal Dermatology Clinics in Southern California and in the Ludwig Maximilian University in Munich and Colorado State University.

Otitis externa is a common condition in dogs and cats and the incidence rates are between 7 and 10% respectively.

For general practitioners as well for veterinary dermatologist the management of otitis externa specially chronic and repetitive conditions is one the most difficult challenges.

For the understanding of the origin of otitis externa we may separate the different causes as well as perpetuating factors into four different categories that we may separate and name by their initials P, P, S, P.

This classification proposed by Griffin may help us understand and manage most of the cases we may see in our practice, specialty or general.

The predisposing factors of otitis externa include ear conformation, excessive hair in the ear canal, iatrogenic irritation and excessive moisture in the ear. We need to comprehend that if one or several factors before mentioned are present this do not mean the patient will present otitis externa but it gathers several requirements for its development, by that matter we must not think as this factors as primary factors and cause of otitis externa.

The primary factors include allergies, endocrine dermatosis, foreign bodies, parasites, keratinization disorders.

The Challenge of Perpetuating Factors

When we are dealing with primary conditions at an early stage, treating and controlling the primary cause of otitis externa may be sufficient to control the problem, but in some cases, chronic changes and perpetuating factors may be treated in a different approach in order to control the problem and establish therapeutic measures to prevent the recurrence of the condition.

Treatment for the perpetuating factors should be continued until they have resolved which may take months of continuous therapy. This named perpetuating factors may be the major reason for poor response to therapy, regardless of the predisposing factors and primary causes control.

Chronic and progressive pathologic responses occurring from inflammation may affect the epidermis, dermis and subsequently the adnexa and lumen of the ear canal. The epidermis becomes acanthotic and hyperkeratotic which because it is confined to the lumen of the canal and surrounded by a cartilaginous tube results in small epithelial folds. The thickened epidermis and the hyperkeratotic stratum corneum increase the keratin debris that is exfoliated into the canal lumen. The increased secretion and epithelial debris may favor the proliferation of bacteria and yeast. These changes also appear to alter the normal epithelial migration. The abnormal epithelial migration may prevent or impede the removal of the waxes, lipids, and exfoliating corneocytes and associated pathogenic bacteria. Inflammation and stenosis may be responsible for altering and even reversing this migration pattern.

The dermis may become edematous, fibrotic and develop nodular pyogranulomas. Fibrosis is more common in end stage otitis in non-Cocker breeds. The pyogranulomas appear to represent areas of previous folliculitis and where apocrine glands have been destroyed or release foreign material. In some cases calcification will occur but is usually found external to the cartilage. These dermal changes also result in increased thickness, which further aggravates the folding and stenosis of the ear canal. The numerous folds inhibit effective cleaning and application of topical medications. These folds also act as sites for the perpetuation and protection of secondary microorganisms.

The adnexa are also affected. This may partly result from the occlusion of the follicular ostia and apocrine ducts. The apocrine glands dilate and appear constipated and may even become hyperplastic. This glandular hyperplasia response is more common in end stage otitis of Cocker Spaniels being present in 73% of cockers but only 28% of other breeds. An occasional case may have sebaceous hyperplasia.

Chronic inflammation can lead to permanent changes in the microanatomy of the ear canal. Folliculitis and furunculosis may also occur.

These progressive responses cause a thickening of the skin, which eventually ulcerates through and extends to both sides of the auricular cartilage. The swelling leads to stenosis of the canal lumen. This means topical therapy will not effectively treat these areas. Even systemic therapy is complicated as effective tissue levels appear difficult to achieve with some of these fibrosing "walled off" deep pyogranulomas.

Calcification may occur in chronic cases and usually involves the dermal fibrous tissue surrounding the cartilage. With calcification treatment becomes like trying to medically manage a case of osteomyelitis. Long-term, high level antibiotic therapy is indicated.

Tympanic membrane alterations occur in response to the accumulation of inflammatory debris and adjacent infection as well as in response to the buildup of exudate and debris that no longer can migrate out or pass through the occluded lumen. The abnormal tympanic membrane thickens, becomes opaque or slightly colored and loses its transparency. It may appear white, off-white, yellow, brown, or gray. The attachment to the manubrium cannot be seen.

Changes to the tympanic membrane following rupturing and healing may lead to the development of aural cholesteatoma in 11% of cases with chronic otitis media. Aural cholesteatoma is a keratinous filled epidermoid cyst located within the middle ear cavity. This syndrome may also be associated with temporal mandibular joint disease, resulting from extension of the inflammation beyond the middle ear. Little and his group have proposed that cholesteatomas occur as a result of a pocket of tympanic membrane forming within the middle ear cavity. One predisposing factor may be spontaneous occlusion of the external ear canal from chronic proliferative changes leading to external ear canal stenosis.

Otitis media is inflammation of the middle ear. When otitis media is present, the ventral tympanic bulla acts as a reservoir to trap the debris and toxins. This portion also has the poorest access and even with a ruptured tympanum cannot be adequately examined by otoscopy. The presence of exudate within the tympanic cavity is difficult to treat with topical therapy and often remains as a source for infections and pro-inflammatory toxins and debris to reach the external ear canal. In more advanced cases, the author has found keratin plugs developing within the tympanic cavity. The keratin may serve as a reservoir for bacteria and source for inflammation.

Eventually, calcification may occur which may be observed radiographically. In some cases osteomyelitis of the bony wall or within the newly proliferated bone will occur. Osteomyelitis is difficult to treat medically and often requires surgery to alleviate. Otitis media occurs commonly with chronic otitis externa. Histologic changes in the middle ear may be present, even with an intact tympanic membrane. The presence of adnexa in some of these cases also supports that previous tympanic membrane rupture was present but the tympanic membranes have since healed - possible even while otitis externa/media is present. The true incidence of otitis media is unknown due to the difficulty in establishing a diagnosis and the criteria utilized.

Dealing with Resistant Bacteria

MRSP has been reported in ears and the number of cases reported in Latin America has been increased. However, until today we are lack of serious research studies that may show us the incidence of MRSP in Latin America in skin and ears of dogs and cats.

Pseudomonas sp. and its control is one of the biggest challenge we may find as dealing with ear conditions. Pseudomonas resistance may be present as well. However the capability of Pseudomonas to form biofilm protect the bacteria from topical and systemic treatments even if resistance is not present according to culture and sensitivity. Cocci has been reported to form biofilm.

Cleaning the ear canal is one of the most successful therapeutic measures when dealing with resistant or chronic infections. By cleaning and flushing the ear canal, biofilm can be wiped out and even if resistance is reported topical treatment combined with ear flushing may result in a faster and effective control of secondary infections.

References

1.  August J. Diseases of the ear canal. In: Complete Manuel of Ear Care. Princeton Junction, NJ: Veterinary Learning Systems; 1986:37–51.

2.  Griffin C. Otitis externa and media. In: Griffin C, Kwochka K, MacDonald JM, eds. Current Veterinary Dermatology: The Science and Art of Therapy. St. Louis, MO: Mosby Year Book; 1993.

3.  Stout-Graham M, et al. Morphologic measurements of the external horizontal ear canal of dogs. Am J Vet Res. 1990;51(7):990–994.

4.  Johnson A, Hawke M. An ink impregnation study of the migratory skin in the external auditory canal of the guinea-pig. Acta Otolaryngol. 1986;101(3–4):269–277.

5.  Saridomichelakis MN, et al. Aetiology of canine otitis externa: a retrospective study of 100 cases. Vet Dermatol. 2007;18(5):341–347.

6.  Scott DW. Observations on canine atopy. J Am Anim Hosp Assoc. 1981;17:91–100.

7.  Griffin C. Canine atopic disease. In: Griffin C, Kwochka K, MacDonald JM, eds. Current Veterinary Dermatology: The Science and Art of Therapy. St. Louis, MO: Mosby Year Book;1993:99–120.

8.  Willemse T, Van den Brom W. Investigations of the symptomatology and the significance of immediate skin test reactivity in canine atopic dermatitis. Res Vet Sci. 1983;34:261–265.

9.  Muse R, Griffin C, Rosenkrantz WS. The prevalence of otic manifestations and otitis externa in allergic dogs. In: Proceeding from AAVD and ACVD; Las Vegas; 1996.

10. Rosser E. Diagnosis of food allergy in dogs. J Am Vet Med Assoc. 1993;203:259–262.