Aetiology, Impacts and Identification of Mites

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Ectoparasitic infections: aetiology, impacts and identification of mites

Author : Filippo De Bellis

Categories : Vets

Date : July 5, 2010

FILIPPO DE BELLIS gets under the skin of how infections involving mites of the Cheyletiella, Sarcoptes, Demodex and Otodectes species affect popular pets

CHEYLETIELLOSIS is an uncommon and usually mild dermatitis caused by an infestation of Cheyletiella species mites.

Cheyletiella species are common non-burrowing mites on dogs and rabbits, but are uncommon in cats. They are commonly zoonotic. Cheyletiella yagsuri is the species most frequently isolated from dogs, with C blakei and C parasitivorax isolated from cats and rabbits respectively; however, they are not believed to be host specific1. The entire life cycle lasts for five weeks and is completed on one host, going through the typical stages of egg, larva, nymph and adult.

Lesions include scaling (Figure 1), crusting, erythema and alopecia on dorsal areas, particularly on the shoulder blades. Dogs may develop pyotraumatic dermatitis – young animals are particularly susceptible. Although any breed may be affected, in the author’s experience canine infestations appear to be more prevalent in cocker spaniels and cavalier King Charles spaniels. The level of pruritus is variable, and may increase with the number of parasites.

Cats may develop miliary dermatitis, and differential diagnoses vary according to the predominant clinical signs. When pruritus is present, sarcoptic acariasis, flea allergy dermatitis, notoedric acariasis and allergic skin diseases should be considered. With absent or little pruritus or poor coat quality due to poor nutrition, systemic disease (cats) or cornification disorders (dogs) should be

1 / 7 considered. Diagnosis is confirmed by finding the mites (Figure 2) and/or eggs (Figure 3) in skin scrapes or acetate tape preparations. These parasites, although normally present in large numbers, can occasionally be difficult to detect and, therefore, therapeutic trials with acaricides may be needed.

In rabbits, gently vacuuming the animal with a pipette attached to a suction unit or a small commercial vacuum can be helpful – using a filter paper to trap the debris, which can be examined on light microscopy2.

In the UK, no licensed veterinary products are specifically indicated for treating Cheyletiella infestations. However, a variety of antiparasitic treatment protocols have been successfully used for ectoparasitic mite infestations in small animal veterinary practice. In the literature, efficacy using fipronil3,4 and selamectin5,6 is evident. Alternative treatment includes weekly lime sulphur dips, or weekly bathing with one per cent selenium sulphide shampoo over three consecutive weeks7.

Larvae, nymphs and adult males are not resistant and die after two days in the environment, but adult females can survive for at least 10 days off the host1. Eggs shed into the environment may be important re-infestation sources. Environmental treatment with an insecticidal product may be helpful to reduce the contamination.

All species can be transmitted to humans, but it is unusual to report lesions – which normally consist of papules and erythema, often accompanied by pruritus, vesiculobullous eruptions or excoriated erosions – in body areas that have been in close contact with the infested pet, such as the forearms, chest and abdomen8.

Canine sarcoptic acariosis

Canine sarcoptic acariasis is a non-seasonal, highly pruritic and contagious canine skin disease caused by infestation with the burrowing mite Sarcoptes scabiei var canis. The mite is transferable by direct contact, or indirectly to other species, including foxes, cats and humans1. The entire life cycle lasts for three weeks and is completed on one host; it goes through the typical stages of egg, larva, nymph and adult. Age, sex or breed predilections have not been reported.

Clinical signs consist of erythematous maculopapular eruptions with crusting and alopecia. Extensive alopecia, lichenification and hyperpigmentation may be seen in chronic cases9. The distribution of the lesions usually shows a typical pattern, with involvement of the ventral abdomen, chest, legs and especially the margins of the pinnae (Figure 4) and the elbows (Figure 5)9. Extreme pruritus due to a hypersensitivity reaction10 is a common feature, with selftrauma and, in long-term cases, demeanour changes1.

Differential diagnoses include pruritic skin diseases, such as flea-allergy dermatitis or other ectoparasitic diseases (cheyletiellosis and otodectic dermatitis), atopic dermatitis, food hypersensitivity and contact dermatitis. The sudden onset and distribution of the lesions may aid

2 / 7 differentiation.

Although nonspecific, a positive pinnal-pedal scratch reflex may be helpful11. Definitive diagnosis is based on demonstrating the presence of the mites (Figure 6) and/or their eggs by skin scrapings or faecal flotation of ingested mites and eggs. However, as these mites can be difficult to show, trial therapy is very important in suspect cases. Alternatively, serological enzymelinked immunosorbent assay (ELISA) is a useful diagnostic aid12.

Canine scabies treatments include topical (amitraz, lyme sulphur dip and fipronil spray) and systemic therapy (moxidectin and selamectin)7.

Selamectin and moxidectin are licensed to be used twice at four-week intervals; published studies show these two molecules allow elimination of the mites after two applications 28 to 30 days apart13,14. According to Scott et al1, Sarcoptes mites can live in the environment for up to 21 days, and environmental treatment has been recommended as part of an overall management plan to prevent possible re-infestations7.

Canine and feline demodicosis

Canine demodicosis is a common parasitic disease of dogs characterised by the presence of larger- than-normal numbers of Demodex canis, which is part of the normal fauna of canine skin1.

Two other mites with different morphologic features have been recognised in some dogs with generalised demodicosis: Demodex injay (long-bodied)15 and Demodex cornei (shortbodied)16. D canis is a cigar-shaped mite with short legs (Figure 7). Although a considerable number of studies -23, the precise pathogenesis is still unclear. The entire life cycle is completed on the dog’s skin, and it goes through the typical stages of egg, larva, nymph and 17 adulthave 1been. conducted

Several breeds are predisposed to juvenile onset of generalised demodicosis1. Although the Staffordshire bull terrier is not reported to be at risk1, it is the author’s clinical impression that this breed is commonly affected in the UK. Two forms are recognised: a localised form, most common in young dogs; and a generalised form, occurring in either young (less than one year of age) or adult animals. It requires a cutaneous environment ecologically and immunologically favourable for colonisation by demodectic mites24.

Clinical signs of generalised demodicosis initially consist of multifocal, erythematous and partially alopecic crusted maculae with a tendency to coalescence (Figure 8). Follicular papules, comedones and follicular plugs are common, and hyperpigmentation and lichenification occur with chronicity (Figure 9). Secondary bacterial infections are extremely common – severe pedal lesions (Figure 10) are often seen. Pruritus, pain and lymphadenopathy are frequent features.

3 / 7 Differential diagnoses of canine demodicosis include deep folliculitis and furunculosis due to other causes, dermatophytosis and, in exfoliative forms, primary keratinisation disorders.

Pruritic forms are often misdiagnosed as allergic skin diseases, but the nature of the lesions, along with the absence of responses to anti-inflammatory therapy, may aid differentiation. Definitive diagnosis is based on demonstrating the presence of the mites and/or their eggs by skin scrapings or hair plucks1.

Generalised canine demodicosis treatment includes amitraz rinses and amitraz or moxidectin spot- on. Until recently, amitraz rinses were the only licensed product for treating canine demodicosis in the UK and, according to Mueller25, good evidence supports recommending it for weekly to fortnightly rinses at 0.025 to 0.05 per cent. It is commonly accepted that therapy should be continued until two negative skin scrapings have been obtained1, each two to four weeks apart.

Moxidectin is available as a spot-on preparation licensed for treating D canis infestations, and the manufacturer recommends a monthly treatment, repeated two to four times.

A multicentre study26 evaluated the success rate of this spoton method for treating canine demodicosis. The moxidectin spot-on had a better success rate in dogs with less severe disease, but the spot-on did not receive the success rate reported in the literature for other therapies. In this study, the spot-on was applied every two weeks.

A spot-on product containing amitraz plus metaflumizone is licensed for treating canine demodicosis, but little clinical data is currently available.

Feline demodicosis is rare. It is caused by D cati (follicular mite), D gatoi (a short-bodied, nonfollicular species that inhabits the stratum corneum) and a third, unnamed species. Alopecia, scaling and crusting are commonly seen. The pathogenesis, transmission and immunology of demodicosis caused by D cati resemble those of canine demodicosis27. It has been reported in association with diabetes mellitus, feline immunodeficiency virus infections, feline leukaemia virus infections, hyperadrenocorticism, squamous cell carcinoma in situ and toxoplasmosis. Infestation caused by D gatoi is contagious, transmissible and normally pruritic. It has been reported in association with adverse food reactions, diabetes mellitus and actinic dermatitis25.

In cats, no licensed products are available for treating this condition, but some good evidence recommends weekly two per cent lime sulphur dips25.

Canine and feline otoacariosis

Canine and feline otoacariosis is a common disease characterised by otitis externa associated with Otodectes cynotis infestation.

4 / 7 O cynotis belongs to the Psoroptidae family, and is an obligate parasite that mainly inhabits the vertical and horizontal ear canal of dogs and cats. It is commonly considered to be an infestation of young animals, and it causes both mechanical and chemical irritation; additionally, hypersensitivity reactions have been reported in cats28.

The entire life cycle takes place in the ear canal, lasts for three weeks and is completed on one host. The life cycle goes through the typical stages of egg, larva, nymph and adult.

Otodectes mites can survive on the coat for some time, and infest other parts of the body. The mites can survive in the environment for up to 12 days29. The mites in the ear canal feed on epithelial debris and tissue fluids from the superficial epidermis. This results in irritation and the canal filling up with cerumen, debris and blood, producing the classic “coffee-ground” discharge. Definitive diagnosis is based on demonstrating the mites in samples taken from the external ear canal (Figure 11).

Treatment options f o r otoacariasis include topical and systemic products. In the UK, an aural preparation containing thiabendazole is licensed to be used twice daily for seven days. Topical products require pre-treatment with a ceruminolytic to remove exudates. Systemic products have a longer residual action, and are easy to apply. Based on the results of field studies, moxidectin and selamectin spoton are licensed for otoacariasis treatment in dogs and cats30,31. A single dose should be administered, although a re-examination is warranted 30 days afterwards, as some animals may need a second application. In-contact animals and the environment should be concurrently treated.

References

1. Scott D W, Miller W H and Griffin C E (2001). Parasitic skin diseases. In (eds), Small Animal Dermatology (6th edn), W B Saunders, Philadelphia: 423-516. 2. Laber-Laird K, Swindle M M and Flecknell P (1996). Rabbits, Handbook of Rodent and Rabbit Medicine, Pergamon Veterinary Handbook Series (2nd edn), Pergamon: 202-203. 3. Scarampella F, Pollmeier M, Visser M, Boeckh A and Jeannin P (2005). Efficacy of fipronil in the treatment of feline cheyletiellosis, Vet Parasitol 129: 333-339. 4. Chadwick A J (1997). Use of a 0.25 per cent fipronil pump spray formulation to treat canine cheyletiellosis, J Small Anim Pract 38: 261-262. 5. Chailleaux N and Paradis M (2002). Efficacy of selamectin in the treatment of naturally acquired cheyletiellosis in cats, Can Vet J 43: 767-770. 6. Mueller R S and Bettanay S V (2002). Efficacy of selamectin in the treatment of canine cheyletiellosis, Vet Rec 151: 773. 7. Curtis C F (2004). Current trends in the treatment of Sarcoptes, Cheyletiella and Otodectes mite infestations in dogs and cats, Vet Dermatol 15: 108-114. 8. Wagner R and Stallmeister N (2000). Cheyletiella dermatitis in humans, dogs and cats, British Journal of Dermatology 143(5): 1,110-1,112.

5 / 7 9. Lee Gross T, Irkhe P J, Walder J and Affolter V K (2005). Perivascular diseases of the dermis, Skin Diseases of the Dog and Cat: Clinical and Histopathological Diagnosis(2nd edn), Blackwell Science, Oxford: 200-237. 10. Bornestein S and Zacrisson G (1993). Humoral antibody response to experimental Sarcoptes scabiei var vulpes infection in the dog, Vet Dermatol 4: 107-110. 11. Mueller R S, Bettanay S V and Shipstone M (2001). Value of the pinnal-pedal scratch reflex in the diagnosis of the canine scabies, Vet Rec 148: 621-623. 12. Lower K S, Medleau L M, Hnilnica K and Bigler B (2001). Evaluation of an enzymelinked immunosorbent assay (ELISA) for the serological diagnosis of sarcoptic mange in dogs, Vet Dermatol 12: 315-320. 13. Six R H, Clemence R G, Thomas C A, Behan M G B, Benchaoui H A, Clements P J M, Rowan T G and Jernigan A D (2000). Efficacy and safety of selamectin against Sarcoptes scabiei and Otodectes cynotis on dogs and cats presented as veterinary patients, Vet Parasitol 91: 291-309. 14. Krieger K, Heine J, Dumont P and Helmann K (2005). Efficacy and safety of imidacloprid 10 per cent plus moxidectin 2.5 per cent spot on in the treatment of sarcoptic mange and otoacariosis in dogs: result of a European field study, Parasitol Res 97 (1): S81-88. 15. Desch C E and Hillier A (2003). Demodex injai: a new species of hair follicle mite (Acari: Demodecidae) from the domestic dog (Canidae, J Med Entomol 40(2): 146-149. 16. Chestney C J (1999). Short form of Demodex species mite in the dog: occurrence and measurements, J Small Anim Pract 40(2): 58-61. 17. Scott D W, Farrow B R H and Schultz R D (1974). Studies on the therapeutic and immunologic aspects of generalized demodectic mange in the dog, Journal of the American Animal Hospital Association 10: 233-244. 18. Scott D W, Farrow B R H and Baker E B (1976). Further studies on the therapeutic and immunologic aspects of generalized demodectic mange in the dog, Journal of the American Animal Hospital Association 12: 203-213. 19. Barta O, Waltman C, Oyekan P, Mcgrath R K and Hribernic T N (1983). Lymphocytes transformation suppression caused by pyoderma – failure to demonstrate it in uncomplicated demodectic mange, Comparative Immunology, Microbiology and Infectious Disease 6: 9-18. 20. Barriga O O, Al Khalidi N W, Martin S and Wyman M (1992). Evidence of immonosuppression by Demodex canis, Veterinary Immunology and Immunopathology 32: 37-46. 21 Caswell J L, Yager J A, Parker W M and Moore P F (1997). A prospective study of the immunophenotype and temporal changes in the histologic lesions on canine demodicosis, Vet Pathol 34: 279-287. 22. Lemarie S L and Horohov D W (1996). Evaluation of interleukintwo production and interleukin-two receptor expression in dogs with generalized demodicosis, Vet Dermatol 7: 213-219. 23. Linder K E, Kunkle G A, Parker W M and Yager J A (2000). Application of the skin

6 / 7 xenograft-mouse model in veterinary dermatology research: modelling canine demodicosis. In Thoday K L, Foil C S and Bond R (eds), Advances in Veterinary Dermatology, Iowa State University Press: 76-84. 24. Lee Gross T, Irkhe P J, Walder J and Affolter V K (2005). Pustular and nodular diseases with adnexal destruction, Skin Diseases of the Dog and Cat: Clinical and Histopathological Diagnosis (2nd edn) Blackwell Science, Oxford: 420-459. 25. Mueller R S (2004). Treatment protocol for demodicosis: an evidence-based review, Vet Dermatol 15: 75-89. 26. Mueller R S, Meyer D, Bensignor E and Sauter-Louis C (2009).Treatment of canine generalized demodicosis with a “spot-on” formulation containing 10 per cent moxidectin and 2.5 per cent imidacloprid (Advocate, Bayer Healthcare), Vet Dermatol 20(5-6): 441-446. 27. Lee Gross T, Irkhe P J, Walder J and Affolter V K (2005): Diseases of the dermis, Skin Diseases of the Dog and Cat: Clinical and Histopathological Diagnosis (2nd edn), Blackwell Science, Oxford: 200-237. 28. Powell M B, Weisbroth S H, Roth L and Wilhelmsen C (1980). Reaginic hypersensitivity in Otodectes cynotis infestation of cats and mode of mite feeding, Am J Vet Res 41(6): 877-882. 29. Otranto D, Milillo P, Mesto P, De Caprariis D, Perrucci S and Capelli G (2004). Otodectes cynotis (Acari: Psoroptidae): examination of survival off the host under natural and laboratory conditions, Exp Appl Acarol 32(3): 171-179. 30. Krieger K, Heine J, Dumont P and Hellmann K (2005). Efficacy and safety of imidacloprid 10 per cent plus moxidectin 2.5 per cent spot-on in the treatment of sarcoptic mange and otoacariosis in dogs: results af a European field study, Parasitol Res 97(Suppl one): S81-88. 31. Blot C, Kodjo A, Reynaud M C and Bourdoiseau G (2003). Efficacy of selamectin administered topically in the treatment of feline otoacariosis, Vet Parasitol 112(3): 241-247.

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