redazione@vetpedia.it +39-0372-40-35-36/37/47

Canine demodicosis

Details
Category: Schede
Hits: 10
  • Disciplina: Dermatologia
  • Specie: Cane

Canine demodicosis, also known as demodectic mange, is a very common dermatological disease in dogs. It is a non-contagious parasitosis caused by mites of the genus Demodex. Three species of mites have been recognized in the dog: Demodex canis, responsible for almost all cases of demodectic mange, Demodex cornei and Demodex injai, although some researchers believe that these are three variants of the same species.

 

MORPHOLOGY AND BIOLOGICAL CYCLE OF THE  PARASITE

Demodex canisis a mite about 150-250 µm long with an elongated body and a short, square rostrum. The four pairs of limbs are atrophied, ending with small claws and grouped at the anterior extremity of the body (podosoma), while the distal part (opisthosoma) forms two-thirds of the body of the parasite (Fig. 1).

Demodex canis  is a species-specific, follicular mite, which lives as a commensal in the hair follicles and sebaceous glands of dogs. Its life cycle is passed entirely on the host (permanent parasitism): the females lays eggs (with the characteristic shape of a lemon or pistachio) within the hair follicle from which the hexapod larvae originate before transforming into octopod nymphs and then into adult mites (Fig. 2). The cycle is completed in 18-24 days and the mite cannot survive away from its host. The disease is not contagious and the mites are transferred by direct contact from the mother to her puppies exclusively in the very first few days of life.

Demodex corneilives in the stratum corneum of the epidermis (from which it derives its name) and the posterior part of its abdomen (opisthosoma) is shorter than that of Demodex canis (Fig. 3). Demodex injai, in contrast, has a much longer opisthosoma and lives in hair follicles and, in particular, in sebaceous glands (Fig. 4).

 

PATHOGENESIS

Canine demodicosis can be divided into forms with a juvenile onset or adult onset. Juvenile-onset demodicosis is much more frequent and is observed in young dogs up to the age of 2 years. Adult-onset demodicosis is less common and is seen in adult or elderly dogs with systemic infestations (for example, leishmaniasis), hormonal disorders (for example, hypercortisolism), or neoplasms (for example, lymphoma) or in animals receiving immunosuppressive treatment (for example, corticosteroids); however, it is not always possible to identify an underlying cause in elderly dogs with demodicosis.

The clinical classification of canine demodicosis divides this disease into a localised form and a generalised form. At present localised demodicosis is defined as the clinical condition in which there are no more than five lesions and these involve less than 10% of the total skin area; generalised demodicosis is the term used for demodicosis that involves more than 10% of the total skin surface (with more than five areas involved) or affects whole body districts such as the face or feet (pododemodicosis). This clinical distinction is of considerable importance because the juvenile-onset, localised form is considered self-limiting and tends to regress spontaneously in 90% of dogs within 6 months, while the generalised form does not regress and must, therefore, be treated pharmacologically.

The immunopathogenic mechanism responsible for the development of the infestation has not yet been clarified. It is probable that in young animals there is a genetically determined defect in immunity that enables multiplication of the mites, which can be favoured by the concomitant occurrence of transient stressful events (endo-ectoparasitosis, estrus, etc.). In contrast, it is thought that in adult animals there is an acquired defect of the immune system secondary to the presence of immunosuppressant diseases (spontaneous or iatrogenic hypercortisolism, leishmaniasis, neoplasms etc.) or treatment with corticosteroids or cytotoxic drugs.

Since some pedigrees and breeds (West Highland White Terrier, Scottish Terrier, Shih Tzu, Bulldog, Shar Pei, Pug, Bobtail) are predisposed to the development of generalised demodicosis it has been hypothesised that a genetic factor could be responsible for a mite-specific defect in immunity such that an efficient cell-mediated immune response is not raised against the mites. On the basis of this consideration, in 1981 the American Academy of Veterinary Dermatology (AAVD) released a directive recommending sterilisation of all dogs with generalised demodicosis in order to reduce the incidence of the disease.

 

CLINICAL SIGNS

Canine demodicosis is one of the skin diseases with the greatest variety of clinical presentations which can differ considerably also in relation to the breed and type of coat of the affected animals.

The clinical signs consist of focal and multifocal alopecia, localised predominantly to the head, muzzle (perilabial and peri-ocular areas) and limbs (Figs. 5 and 6). Confluence of areas of multifocal alopecia can lead to widespread alopecia (Fig. 7). The lesions may or may not be accompanied by erythema which, in some subjects with non-pigmented skin, is so extensive as to justify the name “red mange” which was widely used in the past to describe the disease (Fig. 8). There may be disorders of cornification, such as comedones, or less frequently, keratinised hair sheaths or diffuse desquamation (Figs. 9 and 10).

Some subjects develop a characteristic cutaneous hyperpigmentation that gives the skin a slate-grey colour (Fig. 11). Intrafollicular multiplication of the mites is often the cause of a bacterial folliculitis that is initially manifested by the formation of papules, pustules and epidermal collarettes (pyodemodicosis) (Fig. 12). Following the rupture of the hair shaft, a deep pyogranulomatous form of pyodermatitis develops which is characterized clinically by papulo-nodular lesions, haemorrhagic pustules, fistulae and bloody crusts (Figs. 13 and 14).

Pododemodicosisexclusively affects the interdigital spaces and dorsal and ventral surfaces of the paws and can cause severe lameness as a result of the intense pain (Fig. 15); the Shih Tzu and West Highland White Terrier breeds are particularly predisposed to this form of demodicosis (Fig. 16).

On rare occasions the external auditory system can be involved (otodemodicosis). Pruritus is generally mild, but can be intense in pyodemodicosis. In the severe forms of generalised  demodicosis complicated by deep pyodermitis, systemic clinical signs such as fever, loss of appetite and dejection are possible.

The rare infestations by Demodex injai are reported to occur with a higher frequency in Terriers: the lesions are predominantly localised along the dorsal line of the trunk and are characterized by desquamative dermatitis with a greasy skin (Fig. 17). The lesions observed in these animals are usually mild and circumscribed, unless they are complicated by pyodermatitis; furthermore, the number of mites demonstrable in deep skin scrapes is usually small. The presence of mites on skin biopsies from healthy subjects raises some doubts about the pathogenic role of these mites in the course of infestations. The role of Demodex cornei is particularly controversial and indeed this species is almost always reported in association with Demodex canis. In cases in which D. cornei is found, there is always a desquamative dermatitis to explain the extrafollicular localisation of the mite (Fig. 18).

 

DIAGNOSIS

The diagnosis of demodicosis is made from observing the adult parasite, instars or eggs under a microscope. The technique of choice for finding Demodex spp. is deep skin scraping (Fig. 19). Another diagnostic method that can be used is microscopic examination of the skin, which is the technique exploited in particular for sampling sensitive regions such as the peri-ocular area and feet (Fig. 20). This method is less sensitive than deep skin scraping and so a negative result does not exclude demodicosis; for this reason microscopic examination of the fur is not a suitable technique for monitoring therapy.

In some cases cytological examination of the contents of a pustule can lead to the diagnosis of demodicosis by showing directly the unstained bodies of the Demodex spp. (Fig. 21). During severe infestations by Demodex canis and in cases caused by Demodex cornei the parasites can also be seen by microscopic examination of material collected on a piece of transparent adhesive tape (Fig. 22). Rarely, the diagnosis may require histopathological examination of a skin biopsy (Fig. 23).

 

DIFFERENTIAL DIAGNOSIS

  • Pyodermatitis
  • Ringworm
  • Pemphigus foliaceus
  • Sebaceous adenitis
  • Leishmaniasis
  • Endocrine disorders
  • Epitheliotropic lymphoma

 

TREATMENT

Localised demodicosis resolves spontaneously in almost all cases, so no acaricide treatment is necessary; indeed, in some cases, acaricide therapy could mask the evolution from a localised to generalised form. The recommended treatment for animals with localised demodicosis is exclusively control of bacterial infections through the use of topical antibiotics (for example, fusidic acid, chlorhexidine, benzoyl peroxide).

In contrast, generalised demodicosis requires specific acaricide treatment which can be administered topically or systemically. The drugs currently registered in Italy for the treatment of canine demodicosis include amitraz, milbemycin oxime and moxidectin, available in association with imidacloprid.

Amitraz was the first compound registered for the treatment of canine demodicosis and has been the treatment of choice for more than 20 years. This drug is administered topically by sponging and is registered for application at a concentration of 0.025%. Over the years amitraz has been used at different dilutions and frequencies of administration in various studies. The final dilution ranges from 0.025% to 0.125%, depending on the country of use and the authors, with a frequency of administration from once a day to once a fortnight. 

The dose of milbemycin oxime is 0.5-2.2 mg/kg/die per os.

The recent registration of moxidectin, available in association with imidacloprid for the treatment of canine demodicosis requires further investigation although recent studies seem to indicate that it has moderate efficacy as a spot-on formulation administered at a higher frequency and at a higher dose than indicated by the manufacturer (weekly rather than monthly).

There are numerous other protocols describing the use of compounds not registered for the treatment of canine demodicosis such as injectable ivermectin 1% (0.4-0.6 mg/kg/die per os). It should be remembered that ivermectin has been associated with severe neurotoxic adverse reactions, often fatal and not only in Collies but also in a growing number of other breeds. Indeed, various authors suggest typing the abcb1 gene (also known as mdr1), since homozygous mutations of this gene are responsible for sensitivity to ivermectin.

Other compounds that have been used off-label with success are doramectin (subcutaneous injections of 0.6 mg/kg/die) and injectable moxidectin (0.4 mg/kg/die per os).

Independently of the type of acaricide used, the treatment must be continued until two deep skin scrapes, carried out 1 month apart,  are negative (absence of live or dead mites, no eggs or instars). Although not based on scientific evidence, it is considered that the infection has been resolved if no recurrences occur in the 12 months following treatment interruption.

An equally important aspect of the management of demodicosis is to control the various factors that can, directly or indirectly, influence the course of the disease; for example, it is of the utmost importance to eliminate associated bacterial infections by using topical and/or systemic antibiotics. It is also essential to identify and treat any underlying diseases in cases of adult-onset demodicosis.  

 

Suggested readings

  1. Albanese F, Leone F. Demodicosi canina. In Manuale pratico di parassitologia cutanea del cane e del gatto. Ed. Pfizer 2007; 24-31
  2. Albanese F, Ferrara L. Utilizzo di un prodotto spot-on a base di moxidectina 2,5% - imidacloprid 10% per il trattamento della demodicosi generalizzata: studio aperto non controllato su 17 cani. Veterinaria 2011; 25(3): 17-22
  3. Barta O et al. Lymphocyte transformation suppression caused by pyoderma--failure to demonstrate it in uncomplicated demodectic mange.  Comp Immunol Microbiol Infect Dis, 1983; 6(1):9-18
  4. Bensignor E, Guaguère E, Prelaud P. Demodicosis due to Demodex injai in dogs: eight cases. Vet Dermatol 2006; 17(5):356-7
  5. Carlotti DN. Demodex injai, Demodex cati and Demodex gatoi (and others…): diagnosis and treatment. In Proceedings 21st  Annual Congress of the ESVD-ECVD, Lisbon 2006; 194-8
  6. Caswell JL et al. A prospective study of the immunophenotype and temporal changes in the histologic lesions of canine demodicosis. Vet Pathol 1997; 34(4):279-87
  7. Chen C.  A Short-tailed Demodectic Mite and  Demodex canis infestation in Chihuahua dog.  Vet Dermatol 1995; 6(4):227-9
  8. Chesney CJ. Short form of Demodex species mite in the dog: occurrence and measurements. J Small Animal Pract 1999; 40(2):58-61
  9. Curtis CF. Diagnostic techniques and sample collection. Clin Tech Small Anim Pract 2001; 16(4): 199-206
  10. Day MJ. An immunohistochemical study of the lesions of demodicosis in the dog.  J Comp Pathol 1997; 116(2):203-16
  11. DeBoer DJ. Treatment for demodicosis: old and new. In Proceedings ESVD Workshop on Dermatology Therapy 2008; 38-41
  12. Desch CE, Hillier A.Demodex injai: a new species of hair follicle mite (Acari: Demodecidae) from the domestic dog (Canidae). J Med Entomol 2003; 40(2):146-9
  13. Dimri U et al. Changes in oxidative stress indices, zinc and copper concentrations in blood in canine demodicosis. Vet Parasitol 2008; 154(1-2):98-102
  14. Fondati A et al. Prevalence of Demodex canis-positive healthy dogs at trichoscopic examination. Vet Dermatol 2010; 21(2):146-51
  15. Genchi M, Traldi G, Genchi C. Demodex canis. In Manuale di Parassitologia Veterinaria. Casa Editrice Ambrosiana, Milano 2010; 130-1
  16. Ghubash R. Parasitic miticidal therapy. Clin Tech Small Anim Pract 2006; 21(3): 135-44
  17. Greeve JH, Gaafar SM. Natural Transmission of Demodex canis in Dogs. J Am Vet Med Assoc 1966; 148(9):  1043-5
  18. Gross TL, Ihrke PJ, Walder EJ, Affolter V. Canine demodicosis. In: Skin Disease of the Dog and Cat. Clinical and Histopathologic Diagnosis. 2nd edn. Oxford, UK: Blackwell Publishing, 2005: 442-7
  19. Hillier A, Desch CE.Large-bodied Demodex mite infestation in 4 dogs. J Am Vet Med Assoc 2002; 220(5):623-7
  20. HirshDC et al.Suppression of in vitro lymphocyte transformation by serum from dogs with generalized demodicosis. Am J Vet Res 1975; 36(11):1591-5
  21. Holm BR. Efficacy of milbemycin oxime in the treatment of canine generalized demodicosis: a retrospective study of 99 dogs (1995-2000). Vet Dermatol 2003; 14(4):189-95
  22. Hugnet C, Bruchon-Hugnet C, Royer H, Bourdoiseau G. Efficacy of 1.25% amitraz solution in the treatment of generalized demodicosis (eight cases) and sarcoptic mange (five cases) in dogs. Vet Dermatol 2001; 12(2):89-92
  23. It V Barrientos L et al. Association of canine juvenile generalized demodicosis with the dog leukocyte antigen system. Tissue Antigens 2010; 76(1):67-70
  24. Lemarie SL, Horohov DW. Evaluation of interleukin-2 production and interleukin-2 receptor expression in dogs with generalized demodicosis. Vet Derm 1996; 7(4):213-19
  25. Linek M. Folliculitis with intraluminal organism. In Mecklenburg L, Linek M, Tobin DJ. Hair Loss Disorders in Domestic Animals. ed. Wiley-Blackwell 2009; 193-214
  26. Littlewood JD. Management of demodicosis. In Proceedings 22nd Annual Congress of the ESVD-ECVD, Mainz 2007; 147-49
  27. Mueller RS et al. Treatment of canine generalized demodicosis with a 'spot-on' formulation containing 10% moxidectin and 2.5% imidacloprid (Advocate, Bayer Healthcare). Vet Dermatol 2009; 20(5-6):441-6
  28. Mueller RS. Treatment protocols for demodicosis: an evidence-based review. Vet Derm 2004; 15(2):75-89.
  29. Murayama N, Shibata K, Nagata M. Efficacy of weekly oral doramectin in canine demodicosis. Vet Rec 2010; 167(2):63-4
  30. Noli C, Toma S. Demodicosi canina. In Dermatologia del cane e del gatto seconda ed. Poletto editore 2011; 275-83
  31. Ordeix L et al. Demodex iniaj infestation and dorsal greasy skin and hair in eight wierehaired fox terrier dogs. Vet Dermatol 2009; 20(4):267-72
  32. Page SW. Antiparasitic drugs. In Maddison JE, Page SW, Churh DB. Small Animal Clinical Pharmacology. second edition, Saunders Elsevier 2008; 198-260
  33. Paradis M. Macrocyclic lactones in canine and feline dermatology: 25 years later.In Proceeding 6th World Congress of Veterinary Dermatology, Hong Kong, 2008; 170-8
  34. Paterson TE et al. Treatment of canine-generalized demodicosis: a blind, randomized clinical trial comparing the efficacy of Advocate(Bayer Animal Health) with ivermectin. Vet Dermatol 2009; 20(5-6):447-55
  35. Saridomichelakis M et al. Adult-onset demodicosis in two dogs due to Demodex canis and a short-tailed demodectic mite. J Small Anim Pract. 1999; 40(11): 529-32
  36. SaridomichelakisMN et al.Relative sensitivity of hair pluckings and exudate microscopy for the diagnosis of canine demodicosis. Vet Dermatol 2007; 18(2):138-41
  37. Schnabl B et al. Oral selamectin in the treatment of canine generalised demodicosis. Vet Rec 2010; 166(23):710-4
  38. Scott DW, Miller WH, Griffin CE. Canine demodicosis. In Scott DW, Miller WH, Griffin CE: Muller and Kirk’s Small Animal Dermatology, 6th ed. WB Saunders Company, Philadelphia 2001; 457-74
  39. Tamura Y et al. Scanning electron microscopy description of a new species of Demodex canis spp. Vet Dermatol 2001; 12(5):275-8
  40. TaylorMA, Coop RL, Wall RL. Demodex canis. In Parassitologia e Malattie Parassitarie degli Animali. EMSI, Roma 2010; 450-2
  41. Wall R, Shearer D. Demodicidae. In Veterinary Ectoparasites: biology, pathology & control. Second edition, Blackwell Science, Oxford 2001; 44-5
  42. Wall R. Designation of new’s mite species. Vet Rec 2005; 157:600
  43. Wilkie BN, Markham RJ, Hazlett C. Deficient cutaneous response to PHA-P in healthy puppies from a kennel with a high prevalence of demodicosis. Can J Comp Med 1979; 43(4):415-9