Demodex spp. mites are part of the normal skin fauna of healthy mammals.
Demodicosis results from the excessive proliferation of Demodex spp. mites in the skin and is commonly encountered in dogs. Differing clinical presentations are recognized and new presentations of canine demodicosis have been described.
Canine Demodex Mite Species
Three species of Demodex mites are recognized in dogs.
The female is approximately 300 µm in length and the male 250 µm. Mites are acquired from nursing bitches in the first few days of life. The entire lifecycle of the mite is spent on the host. Demodex canis is present on all dogs, albeit in very small numbers. In histopathological sections, D. canis may be found in hair follicles, sebaceous glands and ducts.
Short-Tailed Mite (Unofficial Name D. cornei)
A short-tailed species inhabits pits in the stratum corneum. It is invariably found in association with D. canis.1 Phylogenetic studies suggest that this is a morphologic variant of D. canis.
A longer mite (350–400 microns) is recognised. On histopathological sections, this mite has been found in hair follicles and sebaceous glands.
Pathogenesis of Demodicosis
It is thought the main mechanism for control of mite proliferation is a host immune response associated with recognition of mite chitin by toll-like receptor 2 on keratinocytes. The resulting immune response is poorly understood but is likely to involve both cellular and humoral mechanisms.2 Dogs susceptible to demodicosis are thought to have an inherited, Demodex-specific immunodeficiency, although the primary defect is unknown. Once disease is advanced, a state of T-cell exhaustion develops that is reversible following treatment.2
Underlying immunosuppressive disease or drug therapy plays a role in some adult onset cases. Hyperadrenocorticism, hypothyroidism, glucocorticoid administration and cancer chemotherapy have all been implicated, although a possible underlying cause is only identified in 50% of cases.3
Typically, demodicosis results in severe inflammation characterised by interface mural folliculitis, perifolliculitis, folliculitis, furunculosis and nodular dermatitis.
Disease Associated with D. canis
Various terms have been used to describe disease caused by D. canis.
Squamous demodicosis is characterised by folliculitis with patches of alopecia, scaling, erythema, follicular casts and comedone formation.
Pustular demodicosis occurs with secondary bacterial infection and is characterised by deep pyoderma and cellulitis. Peripheral lymphadenopathy is usually present. Extensive disease may be life threatening.
Localised disease has recently been defined as involving no more than four individual patches up to 2.5 cm diameter.4 Most cases are squamous.
Generalised disease involves five or more patches, an entire body region, or presents as pododemodicosis. May initially be squamous but frequently progresses to pustular disease.
Juvenile onset starts between 3 and 18 months of age. Many cases spontaneously resolve.
Adult onset demodicosis is defined as disease appearing at four years or older. There are many predisposed breeds.5 Adult onset cases should be evaluated for underlying disease.
Nodular disease is seen most commonly in short coated breeds (Shar pei and boxer).
Demodicosis is a rare cause of otitis externa.
Disease Associated with D. injai
A dermatosis characterised by intense dorsal pruritus along with variable greasiness, hypotrichosis, erythema, scaling, crusting and papule formation has been reported in terrier breeds (Border, Fox and West Highland) in association with D. injai infestation.6 Sebaceous hyperplasia was a common finding.
Additionally, a syndrome of intense facial pruritus in the Shih Tzu and Scottish Terrier has been reported.7
Multiple deep skin scrapings are the diagnostic test of choice. Trichograms are useful in areas that are difficult to scrape but deep skin scrapings should be taken to rule out demodicosis if trichograms are negative. Finding one mite should raise the index of suspicion for demodicosis. Histopathological examination may be required to confirm the diagnosis in the nodular form of D. canis, in pododemodicosis and in thick-skinned breeds such as the Shar Pei.
Ninety percent of juvenile onset localised demodicosis cases will resolve spontaneously. However, treatment should be started if additional lesions develop.
Treatment of Canine Generalized Demodicosis4
Some CGD cases may undergo spontaneous remission, but treatment is generally recommended. Owners should be made aware of the time, commitment and expense involved. The general health status of cases of generalized demodicosis should be evaluated. Wherever possible, immunosuppressive therapies should be withdrawn.
Reports and clinical experience suggest that treatments effective against D. canis are effective for D. injai.
Clinical resolution precedes parasitological cure and treatment should continue until two negative sets of scrapings at a month interval.
In some cases it can be difficult to achieve negative skin scrapes despite clinical improvement. More aggressive therapy may result in a parasitological cure but long-term maintenance therapy may be required to maintain clinical improvement.
Antimicrobial therapy was considered mandatory in pustular disease but may have less effect on the outcome than previously thought.1 If required, systemic drug selection should be based on the results of cytology and perhaps culture and sensitivity testing.
Affected animals should not be bred.
Amitraz is effective for treatment of canine demodicosis used at 0.025%–0.05% applied every 7–14 days depending on local licensing regulations.
The 5% w/v liquid is diluted in water prior to use and sponged onto the entire integument. Clipping long-haired dogs aids contact and penetration. Avoid wetting between treatments.
Adverse effects including bradycardia, hypotension, ataxia, sedation and hyperglycaemia may be reversed by atipamezole (50 µg/kg i/m). Generalized erythema, pruritus and urticaria can occur following initial treatment which is related to the presence of large numbers of dead mites. This effect diminishes with subsequent treatments. Guidelines for safe use and disposal should be observed.
Avermectins and milbemycins are active against a wide range of nematodes and arthropods. They induce a tonic paralysis of the musculature of susceptible organisms via potentiation and/or direct activation of glutamate gated chloride channels, found only in invertebrates. They also stimulate release and enhance binding of γ-amino butyric acid (GABA). In mammals, GABA receptors are found only in the CNS and macrocyclic lactones do not readily cross the blood brain barrier due to the action of p-glycoprotein transmembrane pumps in CNS endothelial cells. However, around 50% of collies and related breeds are homozygous for a mutation in the ABCB1-D1 gene that encodes for p-glycoprotein, rendering them highly susceptible to macrocyclic lactone neurotoxicity. Testing for the ABCB1-D1 mutation is possible but it appears that other mechanisms of toxicity also exist.4
Ivermectin is effective for CGD at a dosage of 0.3–0.6 mg/kg per os q24h. The injectable form is used and may be added to food. This should not be administered to susceptible breeds and is an unlicensed product in many countries including the UK. Toxicity is mainly seen in collies but can occur in other breeds. Signs include anorexia, ataxia, blindness, tremors, seizures, coma and ultimately death. There is no specific antidote apart from withdrawal of treatment and supportive care. To minimise the risk, an initial dosage of 0.03–0.06 mg/kg is gradually increased to the full therapeutic dosage over the first week to 10 days.
Milbemycin oxime is effective for CGD given orally at a dosage of 1–2 mg/kg/day and is licensed in some European countries. Fewer adverse effects are seen compared to ivermectin. Dogs homozygous for the ABCB1-D1 mutation developed ataxia with milbemycin oxime at a dose of approximately 1.5 mg⁄kg/day, but tolerated the drug at 0.6 mg⁄kg⁄day.
Moxidectin, a milbemycin, is available in a spot on formulation combined with imidacloprid licensed for the treatment of canine demodicosis. Clinical experience has shown that this only effective when administered weekly in mild disease.4 The injectable formulation is effective in the treatment of CGD at a dosage of 0.2–0.5 mg/kg/day with similar success and adverse effects to ivermectin. No firm conclusions can be drawn as to the safety of moxidectin in ivermectin-sensitive breeds.
1. Kuznetsova E, Bettenay S, Nikolaeva L, Majzoub M, Mueller R. Influence of systemic antibiotics on the treatment of dogs with generalized demodicosis. Vet Parasitol. 2012;188(1–2):148–155. Epub 2012 May 12.
2. Ferrer L, Ravera I, Silbermayr K. Immunology and pathogenesis of canine demodicosis. Vet Dermatol. 2014;25(5):427–e65. Epub 2014 June 10.
3. Duclos DD, Jeffers JG, Shanley KJ. Prognosis for treatment of adult-onset demodicosis in dogs: 34 cases (1979–1990). J Am Vet Med Assoc. 1994;204(4):616–619. Epub 1994 Feb 15.
4. Mueller RS, Bensignor E, Ferrer L, et al. Treatment of demodicosis in dogs: 2011 clinical practice guidelines. Vet Dermatol. 2012;23(2):86–96, e20–21. Epub 2012 Feb 15.
5. Lemarie SL, Hosgood G, Foil CS. A retrospective study of juvenile- and adult-onset generalized demodicosis in dogs (1986–1991). Vet Dermatol. 1996;7(1):3–10.
6. Ordeix L, Bardagi M, Scarampella F, Ferrer L, Fondati A. Demodex injai infestation and dorsal greasy skin and hair in eight wirehaired fox terrier dogs. Vet Dermatol. 2009;20(4):267–272.
7. Forsythe PJ, Auxilia ST, Jackson HA, eds. Intense facial pruritus associated with Demodex injai infestation: a report of 10 cases. In: Proceedings from the 24th North American Veterinary Dermatology Forum; 2009; Savannah, GA.