Canine demodicosis is a common skin disease resulting from a proliferation of Demodex spp. mites within hair follicles or, depending on the species of mite involved, in the stratum corneum. The disease usually presents as focal or multifocal patches of alopecia, with or without secondary pyoderma. This case report describes a case of demodicosis in an adult West Highland terrier that had a long history of glucocorticoid-responsive pruritus and concurrent respiratory disease.
The disease is most commonly seen in puppies and young dogs, with no history suggestive of systemic involvement. In around 50% of adult-onset cases there is some underlying immunosuppressive disorder and the history may reflect this. There may be a history of long-standing pruritic skin disease that has been reasonably well controlled by the use of glucocorticoids, but therapy has recently been ineffective and the skin lesions have become more severe. Demodicosis is not zoonotic and only very rarely contagious.
Demodicosis usually presents as focal or multifocal patches of alopecia with variable crusting, scaling and pruritus. Canine localized demodicosis (CLD) is usually defined as involving up to five individual patches of alopecia, while generalized disease (CGD) involves six or more patches, an entire body region, or presents as pododemodicosis. Squamous demodicosis is characterized by patches of alopecia, scaling, erythema, folliculitis and comedone formation. Pustular demodicosis is diagnosed when secondary bacterial infection is present, and is characterized by lesions of deep pyoderma and cellulitis. Most cases of CLD are squamous, whereas CGD may initially present as squamous, but frequently progresses to the pustular form of the disease. Exten-sive pustular demodicosis is a severe, potentially life-threatening systemic disease. Secondary infection with Staphylococcus intermedius is common and more rarely Pseudomonas aeruginosa or Proteus mirabilis may be involved. Peripheral lymphadenopathy is usually present in pustular demodicosis.
There was a long history of glucocorticoid-responsive pruritus that was very suggestive of a hypersensitivity disorder. The recent exacerbation of skin disease associated with multifocal alopecia, crusting and scaling was consistent with the development of an additional disease such as pyoderma or demodicosis. Additionally, there were signs of systemic disease, probably related to hypercortisolaemia and also respiratory involvement.
The diagnosis of demodicosis is generally made on the microscopic demonstration of mites or eggs. Skin scrapes are the most sensitive method of finding mites, although they may also be found on examination of exudate or on trichography (see Chapter 2). Skin scrapes and cytology should always be the first diagnostic tests performed where there is evidence of alopecia, crusting and scaling.
Further investigation of the respiratory disease was indicated because not only was the disease affecting the patient’s quality of life, but also because any treatment required to control the respiratory symptoms could have a bearing on the management of the demodicosis. The dog was thus referred to a cardiologist.
Adult-onset demodicosis is usually associated with underlying immunosuppression and, in this case, the long-term use of glucocorticoids to control pruritus was very likely to be the cause. Additionally, the chronic respiratory disease and secondary pyoderma would have lead to further immunosuppression. The long-term pruritus was suggestive of a hypersensitivity disorder. There was evidence of cardiac enlargement and a heart murmur but no clinical signs suggestive of congestive cardiac failure. The provisional diagnosis for the thoracic disease was pulmonary interstitial fibrosis.