Management of Demodicosis
World Small Animal Veterinary Association World Congress Proceedings, 2014
Ralf S. Mueller, DACVD, FACVSc, DECVD
Center for Clinical Veterinary Medicine, Ludwig Maximilian University, Munich, Germany

Demodex mites are transmitted from the dam to the pups in early life and in some dogs excessive proliferation of these mites leads to clinical disease. Predisposing factors for such proliferation includes genetic makeup, stress, endoparasites, malnutrition and debilitation in young dogs and underlying neoplastic or hormonal diseases in adult dogs. Such predisposing factors should be recognized and addressed as far as possible to optimize treatment efficacy. Almost all publications evaluating treatment of generalized demodicosis are in the form of case reports or case series, but overall results achieved with the various drugs are very similar.

Localized Demodicosis

This is a mild disease that usually heals spontaneously in 6 to 8 weeks but may wax and wane in a localized area for months. Anecdotally, there is no difference between treated and untreated cases. If a therapeutic intervention is desired, benzoyl peroxide gel can be gently massaged into the alopecic area once daily or antimicrobial shampoo used weekly. I do not treat the localized form at all with ectoparasiticides.

Generalized Demodicosis

Although the prognosis of demodicosis has improved dramatically over the last decades, successful treatment may still be a challenge in some cases. About 90% of patients can be cured, but it may take up to 12 months of treatment. However, the average time to clinical and microscopical remission in reported studies is approximately 2–4 months. The most common problem in the treatment is premature cessation of therapy.

In intact females, ovariohysterectomy is strongly recommended, because the dog may deteriorate or the disease may recur. In dogs older than 1 to 2 years of age or dogs with adult-onset generalized demodicosis, systemic disorders can be the cause of demodicosis and the reason for an unfavorable treatment response. Some dogs may recover without miticidal therapy if the underlying disease is treated successfully.

Dogs with generalised demodicosis need to be reevaluated typically every 2 to 4 weeks, and skin scrapings need to be obtained to monitor success of therapy. To determine the efficacy of treatment, the skin scrapings should always be done at the same sites. If there is no clinical improvement or if skin scrapings show the same high number of mites or especially immature stages such as nymphs, larvae or eggs, change of treatment should be considered.

Secondary pyoderma is almost always present in dogs with generalized demodicosis. The most common bacterial isolate is Staphylococcus pseudintermedius. Treatment with oral antibiotics in addition to topical antibacterial shampoos and oral ivermectin did not decrease the time to negative cytology and first negative skin scraping in a recent randomized study. The most common gram-negative bacteria found in canine demodicosis are Pseudomonas aeruginosa or Proteus mirabilis. If rods predominate or a dog was pretreated with antibiotics, and systemic antibiotics are considered, bacterial culture and sensitivity is recommended. Commonly used miticidal therapies include amitraz and macrocyclic lactones such as ivermectin, moxidectin and milbemycin oxime.


Amitraz is widely used for the treatment of generalized demodicosis. Dogs with medium-length or long coats should be clipped to allow the solution to contact the skin and penetrate the hair follicle better. All crusts should be removed. Before using amitraz, the entire dog is washed with a medicated shampoo designed to kill bacteria and remove scales. Amitraz is then applied by wetting and sponging. The solution must be applied to the entire body. Adverse effects such as respiratory problems have been observed in humans, so the washing procedure should be performed outside or in a well-ventilated area, and protective gloves should be worn.

The recommended treatment protocol in the USA is 0.025% amitraz used every 2 weeks. Higher concentrations and/or frequencies seem to be associated with a higher success rate. Daily therapy with 0.125% amitraz on alternating halves of the body was reported to be efficacious for dogs with generalized demodicosis resistant to conventional therapy. Amitraz at 1.25% weekly was used successfully to treat generalized demodicosis in eight dogs that had failed to respond to amitraz at lower concentrations. These dogs were premedicated with atipamezole at 0.1 mg/kg intramuscularly once and yohimbine 0.1 mg/kg once daily orally for a further 3 days in an attempt to counteract the α2-adrenergic activity of amitraz which results in bradycardia, a decrease in rectal temperature and hyperglycemia.

Adult-onset demodicosis may respond less favourably to therapy. Adverse effects with amitraz therapy were depression, sleepiness, ataxia, polyphagia/polydipsia and vomiting and diarrhoea. With 1.25% amitraz, generalized erythema, scaling and an unpleasant odour were noted.

Avermectins (e.g., ivermectin, doramectin) and milbemycins (milbemycin oxime and moxidectin) are antiparasitic agents produced by the fermentation of various actinomycetes. They bind selectively to glutamate-gated chloride channels resulting in increased cell permeability for chloride ions and cause neuromuscular blocking resulting in paralysis and death of the parasite. They also interact with gamma-aminobutyric acid (GABA) sites. Mammalian safety is due to mammals not having glutamate-gated chloride channels in the peripheral nervous system. In mammals, GABA is a central nervous system neurotransmitter, and these drugs do not cross the blood-brain barrier.


Milbemycin is used for monthly heartworm and intestinal parasite prevention in dogs at 0.5 mg/ kg. Dogs with generalized demodicosis were treated with dosages varying from 0.5 to 3.8 mg/kg given daily. The mean duration to achieve negative skin scrapings was 8–26 weeks; mean treatment duration was 12–30 weeks. Clinical cure rates varied from 15% to 92%, depending on the dosage used and the age at onset of disease. Several studies have shown a better success rate with higher doses. Dogs with adult-onset disease respond more poorly to treatment than dogs with juvenile-onset disease. There are some rare adverse effects, including stupor, ataxia and trembling in two dogs at 3.8 mg/kg/day, transient vomiting and lethargy.


Ivermectin is not licensed for treating demodicosis in any country, to the author's knowledge. It was first reported as a treatment of generalized demodicosis almost 20 years ago. The dose usually varies from 0.3 to 0.6 mg/kg/day. The mean duration time with daily therapy to achieve negative skin scrapings was 6.5 to 28 weeks, the mean treatment duration 10–33 weeks. The rate of clinical cure varied from 83% to 100% in the individual studies.

Side effects of ivermectin include lethargy, oedematous wheals, ataxia and mydriasis. These developed as late as 10 weeks into treatment. Collies are particularly sensitive. One report recommended to gradually increase the dose of ivermectin administered from 0.05 mg/kg to 0.1, 0.2 and 0.3 mg/kg during the first days of treatment to identify sensitive animals. Because of the relative long half-life of ivermectin, serum concentrations of ivermectin administered daily continue to increase for weeks before reaching equilibrium at much higher levels than with weekly therapy. Thus, chronic toxicity due to cumulative therapy may develop with prolonged daily ivermectin treatment.

Today, some veterinary laboratories offer a gene test to recognise dogs with a defect of the MDR-1 gene encoding for the multidrug-resistance transport protein P-glycoprotein. This gene was reported to be associated with ivermectin toxicity in the Collie. The MDR-1 defect is autosomal recessive. However, in a recent study, 26 of 27 non-Collie dogs with chronic ivermectin toxicity had a normal MDR-1 gene!


Combining the studies, 52 dogs with generalized demodicosis, 41 with juvenile-onset, and 11 with adult-onset demodicosis were treated with oral moxidectin in a dose of 0.2 to 0.4 mg/kg/day. Thirty-one (76%) of the dogs with juvenile-onset demodicosis were in remission after 8–14 weeks, seven were lost to followup. Of the 11 dogs with adult-onset demodicosis, nine were in remission after 8–16 weeks. All dogs were cured, but details on long-term followup were unavailable. Transient side effects included lethargy, anorexia, ataxia, vomiting and stupor. More studies with longer follow-up periods are needed to identify potential benefits and disadvantages of this drug. Moxidectin as part of a spot-on approved for the treatment of many endo- and ectoparasites, including demodicosis, has become recently available in many countries. Weekly application of the spot-on has a clearly better success rate than monthly application, and dogs with severe demodicosis seem to respond less favourably than dogs with mild disease.


Doramectin is also a macrocyclic lactone. In one study, 23 dogs were injected weekly with 0.6 mg/kg subcutaneously for 5–23 weeks. Ten of the dogs were cured, seven relapsed after 1–24 months (two of which responded to repeat doramectin treatment), and six were lost to followup. In another study, doramectin was given weekly or twice weekly orally at the same dose with good success. More studies are needed to evaluate the efficacy and optimal dosing of doramectin for the treatment of canine demodicosis.

A number of other drugs were evaluated as treatment for canine demodicosis, but at this point in time insufficient evidence for the treatment of canine generalised demodicosis is available for amitraz collars, closantel, deltamethrin, doramectin, herbal and homeopathic preparations, muramyl dipeptide, Phoxime, vitamin E and fair evidence against the use of pour-on ivermectin, levamisole, lufenuron, oral selamectin and ronnel.


1.  Bissonnette S, Paradis M, Daneau I, Silversides DW. The ABCB1-1Delta mutation is not responsible for subchronic neurotoxicity seen in dogs of non-collie breeds following macrocyclic lactone treatment for generalized demodicosis. Vet Dermatol. 2009;20:60–66.

2.  Mueller RS, Bensignor E, Ferrer L, Holm BR, Lemarie S, Paradis M, Shipstone MA. Treatment of demodicosis in dogs: 2011 clinical practice guidelines. Vet Dermatol. 2012;23:86–96 (available as free download under


Speaker Information
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Ralf S. Mueller, DACVD, FACVSc, DECVD
Center for Clinical Veterinary Medicine
Ludwig Maximilian University
Munich, Germany

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