Canine demodicosis: Serious disease requires aggressive therapy
The immune system plays a role in the development of juvenile- and adult-onset demodicosis.
Generalized adult-onset demodicosis, which clinically can appear as squamous or pustular, has been produced using immunosuppressives in adult dogs in which genetic factors are unlikely. A natural decline in non-specific immunity in older dogs can incite the emergence of demodex.
Reports of underlying internal medicine disease, such as Cushing's disease (naturally occurring or iatrogenic), hypothyroidism or neoplasia, can also incite demodicosis. Other studies suggest that development of demodicosis secondary to a concurrent disease is rare. Despite these conflicting reports, studies show that there may be a link between steroid use and emergence of adult-onset demodicosis.
However, cellular immunity appears compromised with affected patients having depressed in vitro lymphocyte blastogenesis; lymphopenia and hypocellularity of T-cell areas of the lymph nodes and spleen; and a lower percentage of IL-2 receptors and IL-2 production when compared with control dogs (TH1 cells synthesize IL-2, gamma interferon, and lymphotoxin, and use IL-2 as an autocrine growth factor and drive the immune response toward cell-mediated pathways).
To summarize, generalized juvenile-onset demodicosis is hereditary (probably autosomal recessive) with certain breeds at risk (Collie, Doberman Pinscher, Boxer, Staffordshire Terrier, Scottish Terrier, West Highland White Terrier, English Bulldog, Shar pei and Great Dane), resulting in a specific T-cell defect whereby the mites multiply to large numbers. A secondary bacterial pyoderma develops, which induces formation of a humoral substance causing generalized T-cell suppression. The suppression leads to further increase in the number of mites.
Localized demodicosis is usually limited to the face and occasionally extremities of immature dogs and involves five or less areas. The clinical signs include focal areas of alopecia and erythema on the face, head or legs. The patient should be checked for intestinal parasites, be fed a good-quality diet, and not be administered glucocorticoids. The diagnosis is made by skin scrapings or trichograms, and observing the Demodex canis mite in oil under low-power. Treatment includes benign neglect (90 percent will resolve without therapy) or benzoyl peroxide gel. Goodwinol is a known irritant and can make the patient appear worse. There is some controversy about whether to use topical amitraz on these dogs because some are concerned the localized lesions will become generalized. It is best to treat locally and recheck the patient to closely observe for development of additional areas. Avoid steroid use either systemically or topically.
Along with Demodex canis, two other species of canine demodex mites have been reported — one with a blunted terminal end and the other, an unnamed long-bodied mite. Demodicosis may be more common in the Southeast and Southwest, possibly due to the increased temperature and humidity. The four stages include egg, larvae, nymph and adult. Clinical signs include scaling, comedones and papules, or with the pustular form, crusting and a deep folliculitis/furunculosis. Lymphadenopathy may be present as well as a deep bacterial pyoderma. Otitis externa may be the only presenting sign or a pododermatitis that is often accompanied by pain, swelling and furunculosis. Often a yeast nail-bed infection is diagnosed, but the primary pododermatitis caused by demodex is missed. A cure for juvenile-onset demodicosis is usually more likely than with adult-onset.