Dechra Pharmaceuticals

New Treatment of Malassezia Otitis Externa In Dogs

Louis N. Gotthelf, DVM and Steven E. Young, DVM

Veterinary Forum, August 25, 1997

Though not a life-threatening ailment, otitis externa can be a frustrating disease for canine patients and their owners. An estimated 15-20 percent of canine patients and as many as seven percent of feline patients have ear disease.1,2 Clinicians and patients could benefit from a ready treatment for otitis externa.

In addition to treating the ear, clinicians must consider that most ear diseases have an underlying mechanism responsible for inciting the disease. Dermatologists frequently refer to primary causes and predisposing and perpetuating factors when considering diagnostics and therapies for ear disease.1,2 Primary causes of otitis include parasites, hypersensitivity, keratinization disorders, foreign bodies, ear gland disorders, and autoimmune diseases. These conditions are responsible for altering the ear canal to allow for abnormal colonization of microorganisms. Treatment of these underlying conditions cannot be overlooked in the eventual resolution of otitis.3 Predisposing factors include such conditions as pendulous pinnae, stenosis, neoplasms, hair in the ears, excessive cerumen production, trauma, and high humidity.

Perpetuating factors include bacteria (primarily Staphylococcus spp. and Pseudomonas spp.); yeasts (primarily Malassezia spp.); and pathologic changes, such as glandular hyperplasia, epithelial folds, neoplasia, edema, mineralization, and fibrosis. Secondary otitis media often perpetuates otitis externa. These conditions are frequently seen as the cause of the ear infection, when in actuality they are sequelae to an underlying primary cause.

Malassezia pachydermatis (syn. Pityrosporum canis) is a common commensal organism of the anal sacs, anus, auditory canal, and skin of dogs. The lipophilic, oval, budding yeast is a common etiologic agent in canine otitis externa and may be found in as many as 36 percent of normal canine ear canals. Factors favoring its growth include abnormal levels of ceruminous lipids, high humidity, and abnormal cell-mediated immunity. Alterations in normal microflora in the ear and skin from prior or concurrent antibiotic therapy may play a role as predisposing factors in allowing the overgrowth of Malassezia organisms.4

Treatment of Malassezia otitis externa involves careful cleaning of the external auditory canal and removal of lipid substrates necessary for the organisms' growth and reproduction.3 Numerous ear cleaners commercially available to veterinarians contain a variety of ingredients, such as alcohols, organic acids, propylene glycol, various peroxides, and detergents. The authors were unable to find published data to demonstrate that ear cleaners alone can effectively treat symptomatic Malassezia otitis externa in dogs.

Searching for an underlying cause of otitis, such as atopy, food allergy, or keratinization disorders, may prove beneficial in identifying primary causes. Therapies for these underlying causes may require long periods of time to be effective. Topical agents are useful to shorten the course of Malassezia otitis externa, but no preparation has become widely accepted for such therapy. Empiric use of various ear cleaners has always been recommended in the treatment of otitis externa to remove otic exudates and allow topical medications to contact the diseased epithelium.

Chronic Malassezia otitis externa frequently involves a number of pathologic conditions that result in hyperplastic cerumen glands, cerumen gland rumors, polyps, chronic fibrosis, otitis media, and ear canal anatomical variations, all of which preclude effective ear canal hygiene (Figures 1-4).

Figure 1

Malassezia otitis externa in a six-month-old Cocker Spaniel. The ceruminous exudate predisposes this dog to yeasts in the ears.

Figure 2

The same Cocker Spaniel as in Figure 1 after ear cleaning. The cerumen glands are numerous and are actively producing cerumen.

Figure 3

Cobblestone appearance in the horizontal canal of a five-year-old Cocker Spaniel with Malassezia otitis externa. Note absence of tympanum. Specimen aspirated from the bulla also revealed Malassezia.

Figure 4

Multiple abnormal growths in the horizontal ear canal of this hypothyroid nine-year-old Golden Retriever with chronic Malassezia otitis externa.

Human studies investigating treatment of otomycosis and vaginal yeast infections have revealed the usefulness of boric acid. One study reported that after three weeks of a four percent boric acid treatment for otomycosis, there was a 100 percent cure rate.5 Another study reported a 95 percent cure rate for vaginal yeast infection through the use of boric acid vaginal suppositories.6 To date, no studies in the veterinary literature show that boric acid can reduce or eliminate Malassezia in dogs' ears.

Recently published veterinary reports have, however, noted the usefulness of acetic acid in the treatment of both Pseudomonas and Malassezia otitis externa and as a rinse for Cutaneous Malassezia.2,3,7,8

Clinical trial

Since boric acid has been documented to be useful against numerous human fungal organisms5,6 and acetic acid has been determined to be useful against canine Cutaneous Malassezia,2,3,7,5 this study was undertaken to demonstrate the usefulness of an ear-cleaning solution containing both acetic acid and boric acid in the treatment of Malassezia otitis externa in the dog.

Seventeen dogs from Alabama (Gotthelf) and Rhode Island (Young) meeting certain criteria completed this study (Table 1). cases presented to either veterinarian over a two-month period (August and September 1996) for the primary complaint of symptomatic ear disease of at least two weeks' duration. Each clinician confirmed the presence of otitis externa by otoscopic exam. To be included in the study, the dog had to be exhibiting clinical signs, such as pruritus, head shaking, erythema, exudate, or ulceration. It also had to have intact tympanic membranes to confirm that the disease was limited to the external ear canal. Six of the 17 dogs in this study had been treated for Malassezia otitis externa by the investigators or by other veterinarians within the previous six months.


Table 1

Patient Age Sex Breed Duration
Ear Disease
Pruritus Erythema Head
1B 9 yr F Poodle 5 mo X X X
1D 9 yr M Lhasa
2 yr X X X
1E 5 mo M Labrador
6 wk X X O
1G 3 yr M Mixed
3 wk X X X
1H 6 yr M Cocker 3 mo X X X
1I 4 mo M Cocker 2 wk X O O
1J 12 yr F Mixed
1 mo X X X
1K 6 yr F Yorkshire
2 wk X X X
1L 8 yr M Poodle 3 mo X X X
1M 2 yr F Pointer 4 wk X X X
1N 3 yr F Beagle 3 wk X X X
2A 6 mo F Am. Water
1 mo X X X
2B 3 yr F Rottweiler 1 yr X X X
2D 1.5 yr F Bull
2 mo X X X
2E 1.5 yr M Pug 2 mo X X X
2F 4 yr F Basset
2 yr X X X
2G 6 yr F Beagle 1 yr X X X
        Total 17/17 16/17 15/17

In addition, there had to be a confirmed high population of Malassezia (>15 organisms per high-power field [HPF]) by ear-roll swab cytologic evaluation. To determine which patients had only Malassezia, roll swabs were prepared by inserting a small-tip cotton swab into each ear canal and removing some exudate. The swab was then rolled along the length of a precleaned, frosted microscope slide. The case number, sequence number (initial, seven-day, 14-day), and the left ear or right ear swab rolls were labeled on the slide. The slides were dried and stained with Wright's stain. After the stained slide was dried, a coverslip was applied over liquid slide-mounting medium. The roll smear was examined under high power, particularly for clusters of budding Malassezia yeasts on the surface of keratinocytes, indicating active growth and reproduction. An average of the number of Malassezia organisms [HPF] for 10 HPFs was determined (Table 2).


Table 2








1B 9 yr F Poodle T 0 0
1D 9 yr M Lhasa Apso M F 0
1E 5 mo M Labrador Retriever T M 0
1G 3 yr M Mixed Doberman T 0 0
1H 6 yr M Cocker T 0 0
1I 4 mo M Cocker T 0 0
1J 12 yr F Mixed Breed T M 0
1K 6 yr F Yorkshire Terrier M 0 0
1L 8 yr M Poodle M 0 0
1M 2 yr F Pointer T 0 0
1N 3 yr F Beagle T 0 0
2A 6 mo F Am. Water Spaniel M 0 0
2B 3 yr F Rottweiler M 0 0
2D 1.5 yr F Bull Terrier T 0 0
2E 1.5 yr M Pug T F 0
2F 4 yr F Basset Hound T F F
2G 6 yr F Beagle M 0 0
T=teeming (>30/HPF); M=moderate (16-30/HPF);
F-few (5-15/HPF); 0=none seen

Each patient was treated initially by the diagnosing clinician. The procedure for treatment was to fill the ear canal to overflowing with a two percent acetic acid/two percent boric acid solution (DermaPet Ear/Skin Cleaner); massage the ear canals; and after five minutes, wipe out any over-flow with a cotton ball. The pet owners were then sent home with the acetic acid/boric acid solution and instructed to repeat the same procedure for six additional days and then return to the veterinarian for a follow-up ear cytology. For the next seven days, there was no treatment to the ears. After the seven-day period with no treatment, the owners were instructed to return to the clinic for a 14-day ear exam and cytology. During the 14-day trial, no other skin or ear treatments were used.

At initial presentation, seven days, and 14 days, clinicians filled out observation reports that evaluated clinical disease progression/resolution for each patient. Observations of pain on otoscopic exam; pruritus; erythema (canal erythema vs. pinnal erythema); ulceration along the canals; quantity, color, and character of the exudate; and the areas of the canal that were affected were noted on the forms. Ear cytology forms were also completed at initial presentation, seven days, and 14 days to assess the amount of bacteria, yeast, neutrophils, and red blood cells.

Owners were asked about initial symptoms of their dog's ear disease, including their observations of the severity of odor, scratching, excessive discharge, head shaking, ear pain, and head tilt. At the end of the 14-day period, owners were asked for their posttreatment observations.


A total of 17 dogs completed the two-week protocol (Tables 2 and 3). On initial presentation, all canine subjects showed significant discomfort, evidenced by pruritus, erythema, or head shaking. All ear cytology slides showed significant Malassezia infestation (>15 organisms/HPF).

After the seven-day treatment with once-daily acetic acid/boric acid ear rinses, only two dogs showed any evidence of pruritus, and one dog still showed mild erythema. None of the dogs exhibited head shaking. Cytology for Malassezia was negative in 12 dogs. Three dogs had a few Malassezia (five to 15 organisms/HPF), and two dogs had moderate numbers of Malassezia (16-30 organisms/HPF).

After an additional seven-day period, in which no treatment was given, two dogs still showed pruritus, none had erythematous canals, and none exhibited head shaking. At this time, only one dog out of the 17 cases treated (a Bassett Hound that also had Cutaneous Malassezia) showed a few Malassezia.

The majority of pet owners identified itchy ears as the primary presenting complaint. Most clients reported good to excellent results at two weeks, compared with the start of the protocol. Many reported difficulty in manipulating the ears at the start of the protocol but, at the end, ease of manipulating the head. The one consistent objection by the owners was that there was a vinegar smell to the dog during the treatment period.

This protocol for treating clinical cases of Malassezia otitis externa using acetic acid/boric acid ear washes for seven days proved effective in removing the yeast organisms from the external ear canal. In addition, reduction in clinical signs associated with removal of the yeast organisms occurred rapidly (most within seven days).

At the end of the first week, five dogs had a few or moderate numbers of Malassezia organisms remaining when the cytology was done. These lingering organisms can be explained by the fact that many of these patients also had cerumen remaining in the ears at day 7. Although occasional Malassezia yeasts were present on day 7, we did not consider them significant because they were not found in the actively reproducing colonies of budding yeasts on epithelial cells. Instead, they were present in the debris that was stained and examined. We surmise that by day 14, the yeast organisms had disintegrated, since no additional cleaning or medicating was done and only one dog showed any presence of Malassezia organisms.


The mechanism by which boric acid and acetic acid eliminate Malassezia is unknown. Recent reports in the human dermatology literature may offer some clues.

Table 3

Changes in clinical signs in the 17 subjects

Surface lipid composition may play a role in Malassezia infection. Human patients with acquired immunodeficiency syndrome along with DermaBenSs dermatitis often develop Cutaneous Malassezia infections. When the composition of skin-surface lipid was studied both in symptomatic human immunodeficiency virus-positive and in unaffected subjects, it was discovered that low levels of free fatty acids in surface lipids, coupled with increased levels of surface triglycerides, were conducive to Malassezia infections.9

The cleansing and desquamating effect of the acetic acid/boric acid solution essentially removes all the substrates necessary for the metabolism and reproduction of Malassezia. Other types of ear cleaners may also perform the same cleansing function.

In human psoriatic patients, it was demonstrated that Malassezia produces a chemotactic factor for polymorphonuclear leukocytes. This factor was characterized as hydrophilic, acidlabile, and protein in nature,10 and its presence may help explain why only a few Malassezia organisms can cause such profound erythema and pruritus. At pH 4.9, the acetic acid/boric acid solution may inactivate the chemoattractant and account for the rapid reduction in inflammation and pruritus. Boric acid, being hydroscopic, dries out the humid ear canal and may also interfere with the function of this hydrophilic chemoattractant cytokine by removing the moisture necessary for it to function.

It is interesting that during the week of no treatment, the Malassezia organisms remained absent from the ear cytology. Malassezia organisms must colonize keratinocytes, and we assume that the acetic acid/boric acid solution changed the epithelial layer of the external ear canal in some way that inhibited the binding mechanism.

The acetic acid/boric acid treatment protocol used in this study differs from conventional methods of treatment. Most drug treatments for otitis externa are composed of antifungal drugs in an oily vehicle that is placed into the ear canal and left there. Twice-daily treatments often fail to eliminate Malassezia. These medications do not effectively change the lipid environment within the epithelial layer of the external ear canal.

The most common therapies used in the treatment of Malassezia involve use of combination antifungal pharmaceutical products. While these medications frequently provide resolution of symptoms, treatment failures that do occur are presumably related to the initial diminution of inflammation, attributable to the corticosteroid used in the ear medications,11 and when the steroid treatment stops, the pruritus will return.

This effect could be explained by allergic disease. A report of dogs with pruritic skin disease revealed that 55 percent of the dogs that had shown elevated Cutaneous Malassezia populations were atopic.12 It has also been demonstrated that human atopic dermatitis (AD) patients who develop Malassezia have high serum levels of Malassezia-specific IgE antibody not found in noninfected AD patients or controls.13,14 Interestingly, when the disease was treated and resolved, the Malassezia specific IgE levels fell.15

Although an exact mechanism has not been determined, this study demonstrated that a solution of two percent boric acid and two percent acetic acid used daily for seven days without any other treatment successfully eliminated Malassezia yeasts in the ears of dogs with otitis externa and resolved symptomatic ear disease in the patients treated.

It is our hope that this demonstration of how effective one ear-cleaning solution can be in the treatment of Malassezia will stimulate other investigators to conduct controlled studies focusing on ear hygiene as a treatment for Malassezia otitis externa in the dog.


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  • Ostlere LS, Taylor CR, Harris UW, et al. Skin surface lipids in HIV-positive patients with and without DermaBenSs dermatitis. Int J Dermatol. 1996;35:276-279.
  • Bunse T, Mahrle 0. Soluble Pityrosporum-derived chemoattractant for polymotphonuclear leukocytes of psoriatic patients. Acta Derm Venereal. 1996;76:l0-12.
  • Merchant S. Pathogenesis and clinical management of otitis externa in the dog. 19th Annual Waltham Ohio State University Symposium for the Treatment of Small Animal Diseases, October 14-15, 1995:Proceedings: 83.
  • Bond R, Ferguston EA, Curtis CF, et al. Factors associated with elevated Cutaneous Malassezia pachydermatis populations in dogs with pruritic skin disease. J Sm Anim Pract. 1996;37:103-1C7.
  • 13. Ito K, Sakamoto T, Kikuchi S, et 551. Detection of IgE antibody to Pityrosporum orbiculare in patients with atopic dermatitis. Arerugi. 1995;44:481-490.
  • Kroger S, Neuber K, Gruseck E, et. al. Pityrosporum ovale extracts increase inter-leukin-4, interleukin-10, and IgE synthesis in patients with atopic eczema. Acta Derm Venereal. 1995;75:357-360.
  • Back O, Scheynius A, Johansson SO. Ketoconatole in atopic dermatitis: therapeutic response is correlated with decrease in serum IgE. Arch Dermatol Res. 1995;287:448-451.




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