Bacterial Blepharitis

The most common reason for bacterial blepharitis is infections caused by Staphylococcus spp. Bacterial infection of the eyelids often is secondary to another condition that alters the cutaneous microenvironment and favors bacterial colonization. Hypersensitivity or allergic reactions (e.g., atopic dermatitis or cutaneous adverse food reactions) can cause the animal to self-traumatize the area, which predisposes to secondary infection. Facial-fold pyoderma occurs in certain breeds, particularly those that are brachycephalic. If the folds are close to the eyelids, moisture accumulation and bacterial colonization may occur within the skinfolds and extend to the eyelids. Mucocutaneous pyoderma also can develop secondary to a “drainage board” effect at the medial canthi in dogs with chronic epiphora.

Clinical signs of bacterial blepharitis include erythema, swelling, depigmentation, alopecia, and variable degrees of ulceration and crusting. There may be pruritus, particularly if bacterial blepharitis is secondary to underlying allergic disease. There also may be concurrent mucopurulent ocular discharge. Treatment should include appropriate systemic and topical antibiotics and identification of any underlying predisposing skin or ophthalmic disease. In some dogs, surgical removal of facial skinfolds may be beneficial or curative.

Bacterial infection of the various glands within the eyelid is termed hordeolum. Such infections, usually involving Staphylococcus spp., are thought to originate from the ocular surface flora. Infection of the glands of Zeis or Moll is termed external hordeolum or stye. Similar involvement of the meibomian glands is referred to as internal hordeolum. Both of these conditions are observed more frequently in young dogs and may represent an immunologic incompetency during the juvenile period. The clinical presentation of both conditions is similar, consisting of swollen, inflamed, and painful eyelid margins. The course often is self-limiting but may be shortened with application of hot compresses along with administration of broad-spectrum topical ophthalmic and systemic antibiotics.

A chalazion results when meibomian secretions thicken, obstruct the duct, and cause the buildup of secretory material in the gland. This eventually leads to glandular rupture and lipogranuloma formation. Clinically chalazia present as firm, noninflamed nodules within the eyelid. When viewed through the palpebral conjunctiva, they appear as aggregates of yellow material. Treatment involves incision of the overlying palpebral conjunctiva and curettage of the granulomatous material. Postoperative treatment is topical application of an ophthalmic antibiotic-steroid ointment for 7 to 14 days.

Fungal Blepharitis

The most common fungal organisms identified in the dog or cat with dermatophytosis are Microsporum canis, Microsporum gypseum, and Trichophyton mentagrophytes. These fungal organisms are adapted to colonize hair and cornified layers of the skin, where they digest keratin protein. Most animals must be exposed to a minimum infective dose of dermatophyte spores before an infection can become established. This dose varies, and development of infection is influenced by the individual animal’s overall health and immunologic status.

Dermatophytosis in dogs often results in localized lesions, most commonly affecting the face, feet, or tail. Dogs often are brought in with the classical circular alopecia with scale, crust, and follicular papules. A kerion is a localized inflammatory lesion secondary to a dermatophyte infection and presents clinically as a well-circumscribed nodular lesion of furunculosis, often located on the face or distal extremity. Dermatophyte lesions in cats are more pleomorphic. Classic lesions include one or more areas of partial alopecia, with scaling and crusting most commonly noted on the head or forelimbs. Facial lesions often are asymmetric. Dermatophytosis may result in lesions that resemble miliary dermatitis.

The clinical appearance of skin lesions is unreliable as the sole criterion for diagnosis of dermatophytosis, and additional tests are required (see Chapter 105). A Wood lamp examination can be helpful in some cases, but positive fluorescence occurs in only 50% of M. canis infections, and other dermatophyte species of veterinary significance do not fluoresce at all. Definitive diagnosis of dermatophytosis requires a fungal culture and identification of the organism. Culture samples can be obtained from hairs plucked from suspicious lesions based on clinical appearance or from fluorescence-positive areas identified with a Wood lamp.

Topical therapy long has been advocated for the treatment of dermatophytosis. However, numerous studies have shown that topical therapies alone are less effective than systemic therapy. Lime sulfur and enilconazole are the two most effective antifungal topical therapies. Systemic antifungal therapy has been demonstrated to decrease both the duration and severity of dermatophytosis. Itraconazole (10 mg/kg) is now preferred systemic therapy for treatment of dermatophytosis. Ketoconazole (10 mg/kg), fluconazole (10 mg/kg), griseofulvin, and terbinafine are other antifungal agents with activity against dermatophytes.

Malassezia pachydermatis is a normal commensal inhabitant of the skin and external ear canal in dogs and cats. The organism may cause dermatitis as a result of inflammatory or hypersensitivity reactions to yeast antigens by the host. Most dogs with Malassezia dermatitis have concurrent skin diseases. Dogs with allergic dermatitis often have increased numbers of Malassezia colonizing their skin, and when they are treated appropriately with antifungal therapies, both the overall appearance of the skin and the degree of pruritus improve. About 40% of allergic dogs with Malassezia dermatitis also have concurrent superficial pyoderma. Cats with allergic dermatitis also may be predisposed to Malassezia dermatitis. The diagnosis of generalized Malassezia infection in a cat is reported to be linked strongly to concurrent serious systemic disease: diabetes mellitus, positive retroviral status, and systemic neoplasia. Malassezia dermatitis is diagnosed on the basis of cytologic documentation of increased numbers of the yeast organism. Malassezia organisms are lipophilic, and isolation by fungal culture often requires the addition of olive oil to the medium. The authors have seen localized Malassezia dermatitis in the periocular region in dogs who were being treated with topical ophthalmic medications in a lipid base. Topical treatment (miconazole, ketoconazole) may be effective, but in cases of chronic or generalized infection systemic therapy with 5 mg/kg of ketoconazole, fluconazole, or itraconazole daily may be necessary. Griseofulvin has no activity against Malassezia.

Parasitic Blepharitis

Parasitic blepharitis most commonly is caused by infestation with Demodex mites. Demodex canis is the most commonly identified Demodex mite in dogs, but there also is a long-bodied mite, Demodex injai, and short-bodied mite, Demodex cornei. The most common form of demodicosis is localized disease, which is seen most frequently in animals younger than 10 months of age. Clinically dogs have focal areas of alopecia, erythema, and scaling, often involving the face and feet. Generalized demodicosis covers larger areas of the body and is more common in certain breeds such as the Staffordshire terrier, Chinese shar-pei, English bulldog, Boston terrier, boxer, and pug. Clinically there can be marked areas of alopecia and erythema. Complete alopecia of the eyelids and periocular regions develops in some dogs. A cause for generalized demodicosis in adult dogs, such as immunosuppression resulting from underlying disease or a history of long-term corticosteroid use, is found in about 50% of cases. Concurrent bacterial folliculitis or deep pyoderma almost always is present in generalized demodicosis and should be treated appropriately. Feline generalized demodicosis due to Demodex cati also often is associated with underlying systemic disease. Demodex gatoi is a short-bodied mite that lives in the stratum corneum and can be a cause of contagious pruritus in cats.

Diagnosis of demodicosis is based on identification of the mite on deep skin scrapings or hair pluckings. Multiple life stages and eggs also may be identified. For localized demodicosis no treatment is needed; it should resolve spontaneously as the dog matures. Dogs with generalized disease should be spayed because the disease may be exacerbated by estrus, and predisposition to disease likely is a heritable trait.

Generalized demodicosis can be treated with total body dips with amitraz, which is the only licensed therapy for canine demodicosis. Off-label systemic therapy with ivermectin (0.4 to 0.6 mg/kg daily), milbemycin (1 to 2 mg/kg daily), or moxidectin (0.4 mg/kg) can be effective for generalized demodicosis (see Chapter 99 for details regarding dosing frequency). The clinician must ensure that the patient is negative for heartworm microfilaria before treatment. Ivermectin or moxidectin should never be used in breeds known or suspected to be sensitive to this drug. Dogs can be tested for carriage of the ABCB1-1 mutation (previously called the multidrug resistance gene [MDR1]) that conveys sensitivity to ivermectin toxicity. Regardless of which treatment is used, therapy should be continued for 1 month past the second consecutive monthly skin scraping in which mites are not detected.

Feline Herpetic Ulcerative Dermatitis

Feline herpesvirus 1 (FHV-1) is a common pathogen of domestic cats worldwide that is associated with acute and chronic rhinitis, numerous ocular diseases, stomatitis, and ulcerative facial and nasal dermatitis. Cats with herpetic dermatitis develop ulcerative skin lesions most commonly on the dorsal muzzle and nasal planum, but lesions can involve the medial canthus and periocular regions. Pruritus is variable. Cats may not have any other concurrent signs of FHV-1 infection.

Diagnosis is based on compatible histopathologic findings on skin biopsy specimens from representative lesions. The presence of intranuclear viral inclusions in cells obtained from the face of a cat with marked ulcerative dermatitis is diagnostic. Eosinophilic inflammation also may be evident in affected tissues. If viral inclusions are not found, polymerase chain reaction (PCR) assay for FHV-1 or immunohistochemical testing for the virus can be performed on formalin-fixed tissue samples taken from skin biopsy specimens. In one study a negative PCR result had a 100% negative predictive value.

Treatments for herpetic ulcerative dermatitis can include subcutaneous interferon-α at 1 million U/m² or systemic antiviral drugs such as famciclovir. Secondary bacterial dermatitis may develop; thus appropriate systemic antibiotics may be warranted initially.

Atopic Dermatitis

Atopic dermatitis is a pruritic, inflammatory, allergic skin disease that occurs in genetically predisposed animals (see Chapter 90). The prevalence of canine atopic dermatitis has been estimated to be up to 10%. Breeds predisposed to atopic dermatitis tend to vary geographically. In general, boxers, retriever breeds, and terrier breeds are overrepresented among dogs affected with this disease. Most dogs show clinical signs of atopic dermatitis between 1 and 3 years of age, and initially the clinical signs often are seasonal. The most common clinical manifestation is pruritus, particularly involving the face and including the ears, feet, axillae, and ventrum. Dogs self-traumatize pruritic areas, which results in alopecia, erythema, and excoriations. Lichenification and hyperpigmentation can develop in chronic lesions.

Atopic dermatitis is diagnosed on the basis of appropriate signalment, history, and clinical findings and the exclusion of all other causes of pruritic skin disease. Treatment is aimed at decreasing the individual dog’s pruritic threshold. This often involves the elimination of any secondary bacterial and Malassezia infections; identification of any other concurrent allergic skin diseases; and judicious and prudent use of antihistamines, corticosteroids (topical and systemic), allergen-specific immunotherapy, and cyclosporine in various combinations (see Chapters 91 and 92).

Cutaneous Adverse Food Reaction (Food Allergy)

A cutaneous adverse food reaction (food allergy) is presumed to be a hypersensitivity reaction to ingested allergens. Food allergy occurs in both dogs and cats, and clinically affected animals demonstrate nonseasonal pruritus that results in lesions caused by self-trauma including erosions, ulcerations, excoriations with varying degrees of alopecia, lichenification, and hyperpigmentation or erythema. The face, ears, extremities (feet), and ventrum are affected most commonly. Otitis externa also is a common feature of canine food allergy.

Food allergy is diagnosed based on a compatible history and clinical signs as well as confirmation of improvement with consumption of a strict elimination diet containing a novel protein and relapse on challenge provocation with the original diet (see Chapter 96).