Canine and Feline Demodicosis
World Small Animal Veterinary Association World Congress Proceedings, 2010
Didier-Noël Carlotti, Dr vét, DECVD
Eysines, Bordeaux, France, EU

Read the French translation: Démodécie du Chien et du Chat


Demodex spp. are host specific mites that are normal inhabitants of the hair follicles in most species of domestic animals and man. Demodectic mites are indeed part of the normal fauna of canine and feline skin, where they are present in small numbers in many healthy individuals. Recently, superficial short-tailed Demodex have been recognized in dogs and cats.

Demodex canis

Canine demodicosis or demodectic mange is a non-contagious skin disease usually seen in young dogs where the population of the follicular mite Demodex canis is present in much larger than normal numbers. Localized and generalized demodicosis are very different diseases. Demodex canis (Leydig, 1859) is a small (200-300 µ) elongated cylindrical mite with 4 pairs of short legs and a tapering abdomen. Transmission is made by direct contact from the bitch to the nursing puppies during the first 2 or 3 days after birth. The life cycle occurs completely on the host: fusiform egg 6 legged larvae 8 legged protonymph adult. In the normal puppy, a low multiplication of the mite will not generate lesions, whereas a moderate multiplication will lead to localized demodicosis with a spontaneous healing. In severe clinical demodectic mite infestations, a cutaneous environment exists that is somehow ecologically favourable for intense colonization with mites. It is likely that generalized demodicosis is an immunological disease. The following hypothesis is realistic: "Generalized demodicosis of the young dog is the consequence of a specific and hereditary T-lymphocyte deficiency (suppressor T-cells?), allowing the multiplication of Demodex canis (a normal host of canine skin), inducing the production of a humoral factor (parasitic antigen-antibody complex) which is the cause of a secondary generalized T-lymphocytes immunosuppression". This cell-mediated immunodeficiency leads to severe deep pyoderma (cellulitis).

There is no sex predilection. Demodicosis is usually a disease of young dogs (less than 2 years of age): < 12 months of age for localized demodicosis, and usually < 18 months for generalized demodicosis. Adult-onset demodicosis may appear in the older dog. Demodicosis is reported to be more common in purebred dogs, e.g., in Dobermans, Great Danes, Chihuahuas, Old English Sheepdogs and Shar-Peis. There are several forms of localized demodicosis. In the nummular form, one or more areas of well circumscribed alopecia with erythema and scaling (arbitrarily up to five) are commonly found in several sites: face (periorbital, commissures of the mouth), forelimbs, rarely trunk, abdomen and hind legs. This form is usually non-pruritic. There is no lymphadenopathy. 90% of the cases undergo spontaneous remission within a few weeks to a few months (puberty?). The diffuse form is more extensive and characterized by erythema, hyperpigmentation, comedones and seborrhoea. It is sometimes pruritic. It can lead to the generalized form but may regress spontaneously. Pododemodicosis is a form of pododermatitis, sometimes exclusive, with erythema, oozing and at the end cellulitis, leading to pain and lameness. In otodemodicosis there is an erythemato-ceruminous otitis externa, sometimes exclusive, with moderate pruritus. In generalized demodicosis the lesions become generalized with commonly secondary furunculosis/cellulitis. There are erythema, oedema, seborrhoea (scaling and crusting), necrosis (cellulitis), oozing, bloody suppuration along with pain, lymphadenopathy (regional or generalized) and depression. The prognosis is guarded without appropriate treatment (spontaneous death or euthanasia).

Diagnosis is based on history (young dog, lack of pruritus, non contagious disease, and familial disease), clinical signs (lesions and topography), skin-scrapings with mineral oil or lactophenol, squeezing the skin prior to scraping (trichograms and surface biopsies are less sensitive). Cutaneous histopathology shows mites inside hair follicles, with follicular interface dermatitis, furunculosis and cellulitis.

Localized nummular demodicosis requires no treatment but a thorough and regular follow-up is necessary to identify cases in which lesions will extend and generalize. Treatment is necessary in localized diffuse and generalized demodicosis, as well as in pododemodicosis and otodemodicosis. Antidemodectic properties have been attributed to numerous topical agents. Ch. LEBLOIS wrote in 1926: "Tous les topiques vantés ont ceci de remarquable, de donner des résultats étonnants entre les mains de leur auteur et d'échouer lamentablement entre les mains des autres." Scott listed in 1979 reports on the efficacy of 74 substances... that were all active in localized demodicosis, which heals spontaneously! Therapy, when indicated, includes indispensable preparatory measures. Clipping is often necessary. Cleaning of lesions must be done, antiseborrheic and antibacterial shampoos being appropriate. Benzoyl peroxide shampoos have a follicular flushing effect and are consequently beneficial. Amitraz used topically in frictions (with a sponge) at 0.025% to 0.05% is active on Demodex canis. Percentages of cure vary from 50 to 86%. Unfortunately relapses are relatively common. The use of a spot-on containing amitraz, applied every 2 to 4 weeks (20 mg kg-1) has lead to a clinical improvement and a decrease of parasite counts. The current treatment of choice of canine generalized demodicosis is based on the administration of systemic antidemodectic agents belonging to the macrocyclic lactones group. Ivermectin is an avermectin with a gamma-aminobutyric acid (GABA) agonist activity. A daily oral administration (0.3 to 0.6 mg kg-1) is very effective, even in amitraz failures. The injectable form of the drug is administered orally or the equine paste is given via the same route. This treatment is contra-indicated in Collies, Shetland sheepdogs, Old English sheepdogs, Australian sheepdogs, Swiss white shepherds and their crossbreds. This is due to a homozygote mutation, common in these breeds, of the MDR 1 gene (multidrug resistance 1) which allows the penetration of the drug through the blood-brain barrier. A genetic DNA test is now available (heterozygotes are not at risk). Doramectin, injected subcutaneously or given orally at the dose of 0.6 mg kg-1 once a week, was effective in two limited studies. Interceptor® is a mixture of milbemycin A3 oxime and milbemycin A4 oxime, in a 20:80 ratio, with potent anthelmintic and negligible antibiotic activity. The anthelmintic activity is believed to result from disruption of invertebrate gamma amino butyric acid (GABA) neurotransmission. The toxicity of Interceptor® in mammals is low including in Collies. Several studies have shown that dogs affected with generalized demodicosis can respond to daily doses of 0.5 to 1 mg kg-1 (and even up to 3.1 mg kg-1 SID). The rate of clinical and parasitological cure varies from 60 to 96% in a few months (up to about 1 year), the highest rate being obtained with high doses (> 1 mg kg-1 SID). Moxidectin is also effective when given daily by mouth. The injectable solution for ruminants (1%) is used per oral route at the dose is 0.2 to 0.4 mg kg-1 per day and give good results with up to 96% of cure in 2 to 6 months, with parasitological negativation in 2 to 7 months. A 2.5% spot-on recently launched on the market (Advocate®) has given a relatively better success in dogs with less severe disease than in dogs with more severe disease when applied every 2 weeks. Weekly application of the product is probably more effective than biweekly or monthly application. Pododemodicosis and otodemodicosis can be treated with systemic macrocyclic lactones, or amitraz locally. No study has demonstrated the value of "immunomodulators" in the treatment of generalized demodicosis. Antidemodectic treatment is continued until negative skin scrapings (and/or cerumen examination) are obtained in several areas (always the same in each dog), at least twice one month apart. The author controls the cured patients 3 and 12 months after discontinuation of therapy. In pyodemodicosis, the pyoderma must be treated urgently and vigorously with systemic antibiotics, after bacteriological culture and sensitivity testing (particularly if cytological examination has shown rods). Multi-resistant staphylococci and gram-negative bacteria (particularly Pseudomonas spp.) are often cultured. Antibiotic therapy is usually given on a long term basis, in association with an appropriate topical treatment, notably benzoyl peroxide shampoos. Glucocorticoids are absolutely contra-indicated, even topically. In the absence of realistic data on the transmission of juvenile demodicosis, particularly the generalized form, neutering of animals with localized or generalized demodicosis (even if it has been cured) is recommended. The same applies to animals having cases of demodicosis in their descendants.

Demodex injai

A new canine mite was called D. injai in 2003. The adult mite is very long (350 to 400 µm) due to a particularly long opisthosoma. A few reports were published or presented in meetings. History and clinical examination reveal a greasy keratoseborrhoeic disorder mainly on the dorso-lumbar area, in young adults (older than 2 years and a half years) of terrier breeds and more rarely others. Alopecia and pruritus are variable. Secondary bacterial folliculitis and Malassezia dermatitis may be seen. The diagnosis of this newly recognized disease is based on the history, clinical signs and the demonstration of the mite. Mites can be found in multiple deep skin scrapings. Therapy is the same as for demodicosis caused by D. canis.

Demodex cati

This mite was discovered in 1859 by Leydig who named it Demodex folliculorum var cati. It was renamed Demodex cati by Hirst in 1919. It is similar to D. canis (about 200 µm in length). Localized lesions are alopecic, with erythema, comedones, scaling and/or seborrhoea, follicular papules and/or pustules, erosions/ulcers, crusts and are located on the head (particularly eyelids), ear pinnae and neck. Generalized lesions have the same appearance with a common involvement of the trunk and limbs. Lichenification and hyperpigmentation can be seen. Pruritus is variable, usually absent or mild. Rarely, secondary bacterial cellulitis can occur. Otodemodicosis due to D. cati is commonly associated with the skin disease but it can also occur by itself. Diagnosis of feline demodicosis due to D. cati is based on the history, clinical signs and demonstration of the mite by microscopic examination of skin scrapings, trichograms and cerumen. Mites can be readily found in lesions of multiple squamous cell carcinoma in situ. Localized demodicosis due to D. cati is self-limited and can heal spontaneously. However therapy can be envisaged as for the generalized form. Feline otodemodicosis can be treated with amitraz in mineral oil (1:9, 1 ml amitraz 5% in 9 ml mineral oil) but Demodex mites can persist in spite of treatment. Two (2)% lime sulfur dips weekly, amitraz rinses at 0.0125-0.025% weekly and doramectin at 600 µg kg-1 weekly subcutaneously are effective. Milbemycin oxime or moxidectin orally seem to be effective. Secondary pyoderma should be treated appropriately.

Demodex gatoi

Demodex gatoi was discovered in cats in 1981 and was named in 1999. It is a short mite, living in the stratum corneum (not the hair follicles) and morphologically similar to Demodex criceti, the Demodex found in the Syrian hamster (Mesocricetus auratus). History and clinical examination reveal a pruritic skin disease in usually young short-haired cats, with alopecia (broken hair), erythema, scaling, excoriations and crusting, particularly on the head, neck and elbows and/or flanks, ventrum and rear legs. Hyperpigmentation can occur and the disease may be symmetrical. Also history may be suggestive because of the existence of the disease in a particular area (e.g., southern United States such as Texas) and/or contagiousness. The disease can occur in several cats at the same time, including asymptomatic carriers on which the mite is present in high numbers. In contrast, in pruritic cats the mite can be difficult to find even with many skin scrapings, which render the diagnosis difficult. This is based on history, physical examination and identification of the mite. Treatment is based mainly on topical lime sulfur in the USA, but topical amitraz (0.0125 to 0.025%) or systemic ivermectin are also used. These could be used in Europe, and perhaps milbemycin oxime and moxidectin as well.

Other "New" Demodex Mites

In the cat, an unusual species of Demodex mite was found along hair shafts from clumps of easily epilated hairs and was longer (and wider) than D. gatoi but shorter than D. cati. Biopsies were taken from 7 cats and showed no mites, but only signs of a hypersensitivity reaction. Weekly lime sulfur rinses plus daily oral ivermectin (300 µg kg-1) were successful.

In the dog, a short-bodied Demodex mite has been found in a few cases. It may be living exclusively in the stratum corneum, as Demodex gatoi. It has been found in fact in 4 countries over 3 continents and could be a mutant of D. canis or a new species. Anecdotally, it has been called Demodex cornei (K. Mason). It seems that the mite is present only in cases of simultaneous infestation with Demodex canis.


References are available upon request.

Speaker Information
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Didier-Noël Carlotti, Dr vét, DECVD
Eysines, Bordeaux, France

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