Acne is a disease of young dogs of short-coated breeds. Dobermans, bulldogs,
Great Danes, boxers, German shorthaired pointers and
rottweilers appear to be over-represented.
This disease is a localized folliculitis, which is an inflammation of the hair follicle, and furunculosis or rupture of the hair follicle restricted to the chin and lips. Comedones are the first lesions noted on the chin. They result from follicular dilation and plugging with excessive keratin formation. Erythema and
alopecia may be present in more advanced cases.
Papules, pustules, firm nodules and fistulous tracts may develop as a consequence of a bacterial infection such as folliculitis and furunculosis. Lesions ulcerate and discharge a purulent exudate. Swelling of the chin is variable but it could be severe in some animals.
Regional lymphadenopathy may be prominent and pain and itchiness may be intense in animals with a secondary skin infection. Cysts may develop in chronic cases.
Clinical Presentation Onset of the disease occurs between 5 and 12 months of age. Acne in dogs tends to improve with age. Occasionally, it may persist in adulthood.
Erythema (redness), crusted papules and furuncles develop on the chin and lips. Hair follicles appear to be plugged (comedones or black head) with keratin.
With secondary infection, draining tracts may develop and exudate may be present.
In chronic cases secondary depigmentation may develop.
Differential diagnoses for this presentation include juvenile onset demodicosis with a secondary bacterial infection, dermatophytosis, contact dermatitis, and early stages of mild juvenile sterile granulomatous dermatitis and lymphadenitis (puppy strangles).
In contrast with juvenile cellulitis, dogs with acne do not have lymphadenopathy, and lesions are not present on the pinnae. In addition, dogs with acne are not systemically ill.
Causes
Onset of the disease occurs between 5 and 12 months of age. Acne in dogs tends to improve with age. Occasionally, it may persist in adulthood. The exact pathogenesis (development of disease) is unknown, but several theories have been formulated, such as the following:
Hormones. Hormones, more specifically androgens (male sex hormones), have been hypothesized to play a role. However, this disease does not seem to have a sex predilection and both females and neutered males may be affected. In addition, hormones would not explain why only short-coated breeds tend to develop acne.
Genetics. Genetics have also hypothesized to play a role to explain why some breeds are at increased risk.
Trauma. It may lead to hair follicle disruption and release of free keratin in the dermis. Keratin, in turn, could trigger an inflammatory response (foreign body response), and the bacteria present in the hair follicle would cause a deep bacterial infection (furunculosis).
Bacteria. The role of bacteria appears to be secondary, because at the onset of the disease the lesions are sterile, and antibiotic therapy does not significantly improve the clinical signs.
Keratinization. Canine acne does not appear to be a disease of keratinization. Excessive sebum production and sebum breakdown to free fatty acids was hypothesized to induce inflammation and comedo formation. However, in one study, where the lipids obtained form the skin of healthy controls and dogs with acne were evaluated, it was found that the lipids obtained from the acne lesions, such as free sterols, fatty acids, and ceramides, are characteristic epidermal lipids and that sebaceous gland contribution is minimal.
