Demodex cati

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Demodex cati Hirst, 1919

(Figures 5-22 and 5-24)

ETYMOLOGY:Demos = tallow and dex = woodworm; along with cati for the feline host.

SYNONYMS:Demodexfolliculorum var. cati Megnin, 1877.

HISTORY: In 1859, Leydig stated that the cat was host to a species of Demodex. In 1877, Megnin described the species in the cat as Demodexfolliculorum var. cati and gave the description: “This is a dimimuitive of the caninus variety having exactly its features with all dimensions reduced by one fourth.” Hirst (1919) elevated the mite to specific status and presented a brief description of the species. In 1979, Desch and Nutting redescribed Demodexcati Hirst, 1919 and provided illustrations of all life cycle stages.

GEOGRAPHICAL DISTRIBUTION: Cases of feline demodicosis due to Demodexcati have been described from North America, Europe, Australia, New Caledonia, Africa, and India (Beugnet & Chardonnet, 1993; Chesney, 1989; Yathiraj et al., 1994). Foley (1995) describes feline demodicosis as “the least commonly diagnosed disease associated with mites in cats.”

LOCATION IN HOST: The mites live within the hair follicles of the the cat (Fig. 5-22). The hair follicles that are most often infested include those of the eyelids, face, chin, or neck.

IDENTIFICATION: The mites are cigar shaped with very short legs (Desch & Nutting, 1979) (Fig. 5-23). The adult mites and nymphs possess eight very short legs, while the larval stage and protonymph possess six legs. The adult male mite is 182 μm long and 20 μm wide. The adult female is 220 μm long and about 30 μm wide. The eggs are 70.5 μm long and about 21 μm wide. In both the male and female, the opisthosoma makes up two-thirds of the total body length [the body is composed of the opisthoma (tail), the podosoma (body with legs), and the gnathosoma (anterior end with jaws)]. The opther species of Demodex that occurs in the cat has a much shorter opisthosoma relative to the total body length.

LIFE CYCLE: Although all life-cycle stages were described by Desch and Nutting (1979), there has been no specific work on the life cycle of Demodexcati. It is assumed that it is similar to that of Demodexbrevis of humans. Basically, eggs are laid within the epidermal cavity, and the eggs hatch to produce a six-legged larval stage. The larva then develops to a six-legged protonymph, and finally to an eight-legged nymph. The adults also have eight legs, and it appears that the female is diploid and the male is haploid.

PATHOGENESIS AND CLINICAL SIGNS: Two forms of feline demodicosis, localized and generalized, are recognized (Foley, 1995). The localized form typically is associated with lesions that appear as acne or as erythematous patches of alopecia on the eyelids, face, chin, or neck (Fig. 5-24). The generalized form of the disease is considered by Foley (1995) to be represented by cats that have more than five lesion sites or more than one affected body region. Chesney (1989) reviewed 35 published cases of demodicosis in cats. There was no apparent predisposition of disease to develop in young animals, cases were reported in cats between 1 to 18 years of age. There seemed to be no correlation with breed or sex, although it is possible that demodicosis may be slightly more common in Siamese and Burmese cats. Unlike dogs, pyoderma is rare in generalized feline demodicosis.

It is believed that generalized demodicosis is more apt to appear in cats with underlying immunologic disorders or as sequelae to other infections (Chalmers et al., 1989). Systemic illnesses associated with generalized demodicosis include diabetes mellitus, Cushing’s disease, feline leukemia virus infection, systemic lupus erythematosus, feline immunodeficiency virus infection, and toxoplasmosis (Guaguère, 1993).

TREATMENT: Treatment of feline demodicosis is usually successful (Foley, 1991). Treatments include 2.5% lime-sulfur dips, carbaryl shampoos, and malathion dips. Half-strength amitraz dips (0.0125%) have been found effective againsty feline demodicosis (Cowan and Campbell, 1988). Foley (1995) finds that localized infestation with Demodexcati responds well to parenteral ivermectin (300 ug ivermectin/kg body weight) and 2.5% lime-sulfur immersion in the same protocol. In addition, he has treated with topical follicular flushing with 5% benzoyl peroxide gel which he believes hastens resolution of the infestation. Foley (1995) believes generalized Demodex cati infestations have a more guarded prognosis if the cat is immunocompromized or has underlying severe disease. Therapy for the generalized form includes patenteral ivermectin again at 300 ug ivermectin per kg body weight. It has also been shown that extralabel amitraz immersion can be used in cats at half strength (0.0125%) at weekly intervals to minimize the toxic side effects of sedation, salivatrion, hyperglycemia, and insulin resistance. The side effects of amitraz preclude its use in diabetic cats or in cats owned by diabetic clients without appropriate gloves and barriers being used during dipping (Foley, 1995). In one case of generalized demodicosis, ivermectin seemed to reduce mite numbers, but fresh lesions continued to appear in spite of ivermectin treatment (Yathiraj et al., 1994). In this case, treatment with 0.0125% amitraz baths (3 treatments, at weekly intervals) caused the lesions to regress and the resolution of lesions by 50 days after the beginning of weekly amitraz therapy.

EPIZOOTIOLOGY: Very little is known about the epizootiology of feline demodicosis. It is suspected that the mite is highly host specific and that most cats obtain their infections while nursing as kittens. However, none of these questions have been carefully analyzed experimentally.

HAZARDS TO OTHER ANIMALS: The mite is believed to be highly host specific and to be restricted to the domestic cat. Demodicosis in snow leopards, Pantherauncia, has recently been described as a new species, Demodexuncii, which is said to closely resemble Demodexcati (Desch, 1993).

HAZARDS TO HUMANS: It is not believed that Demodexcati is transmissible to humans.

CONTROL AND PREVENTION: It is believed that many cats are infested with these mites at birth and that transmission between cats is unlikely.

REFERENCES:

Beugnet F, Chardonnet L. 1993. Otite demodecique chex un chat. Rev d’Elev Med Vet Nouvelle Caledonie. 17:5-7.

Chalmers S, Schick RO, Jeffers J. 1989. Demodicosis in two cats seropositive for feline immunodeficiency virus. JAVMA 194:256-257.

Chesney CJ. 1989. Demodicosis in the cat. J Small Anim Pract 30:689-695.

Cowan LA, Campbell K. 1988. Generalized demodicosis in a cat responsive to amitraz. JAVMA 192:1442-1444.

Desch CE. 1993. A new species of hair follicle mite (Acari: Demodecidae) from the snow leopard, Patherauncia (Schreber, 1775) (Felidae). Int J Acarol 19:63-67.

Desch C, Nutting WB. 1979. Demodexcati Hirst 1919: a redescription. Cornell Vet 69:280-285.

Foley RH. 1991. Parasite mites of dogs and cats. Comp Cont Ed Pract Vet 13:783-800.

Foley RH. 1995. Feline Demodicosis. Comp Cont Ed Pract Vet 17:481-487.

Guaguère E. 1993. Démodécie féline: étude réetrospective de 9 cas. Prot Med Chir Anim Comp 28:31-36.

Hirst S. 1919. Studies on Acari. I. The genus Demodex, Owen. Brit Mus (Nat Hist) 53 pp.

Leydig F. 1859. Ueber Haarsakmilben und Krätzmilben. Arch Natur Berlin 1:338-354.

Megnin P. 1877. Memoire sur le Demodexfolliculorum Owen. J Anat Physil 13:97-122.

Yathiraj S, Thimmappa Rai M, Madhava Rao P. 1994. Treatment of generalised demodicosis in a cat - a case report. Ind Vet J 71:393-395.

Figure 5-22. Demodexcati. Section through a hair follicle containing numerous sections through mites.

Figure 5-23. Demodex. Note the elogate body and very short legs.

Figure 5-24. Feline demodicosis. Cat with demodicosis (Image provided by Dr. Robert Foley).

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