Parasitic Skin Disorders

CHAPTER | 5 Parasitic Skin Disorders

Ixodid Ticks (hard ticks)

Features

Ixodid ticks include the genera Rhipicephalus (i.e., brown dog tick), Dermacentor (i.e., American dog tick, Rocky Mountain wood tick, Pacific or West Coast tick), Ixodes (i.e., shoulder tick of North America, deer tick, British dog tick [Europe]), Amblyomma (i.e., black-legged tick, Lone Star tick), and Haemophysalis (i.e., yellow dog tick [Africa and Asia]). Ixodid ticks are more commonly found on dogs than on cats.

Symptoms of tick infestation include none (asymptomatic), inflamed nodule at the site of tick attachment, signs of tick-borne disease (e.g., ehrlichiosis, Rocky Mountain spotted fever, Lyme disease), and tick paralysis. Ticks are most commonly found on the ears or interdigitally, but they can be anywhere on the body.

Diagnosis

1 Direct visualization of ticks on the body.

Treatment and Prognosis

1 If infestation is mild, ticks should be carefully removed manually with forceps or fine-tipped tweezers. The tick should not be twisted or its mouth parts allowed to remain in the skin. Do not burn, puncture, squeeze, or crush the tick’s body to kill it because its fluids may be infectious.

2 For severe infestations, topical insecticide labeled for use against ticks should be applied. Amitraz-containing collars, fipronil, and permethrins (dogs) seem to be most effective. New generation veterinary insecticides seem to provide variable efficacy against ticks with a wide range of safety.

3 Concurrent tick-borne disease, if present, should be treated. Products that repel or kill ticks rapidly enough to reduce the transmission of Rickettsia diseases are preferred.

4 Periodically, the premises should be treated with appropriately labeled insecticides (in homes and kennels infested with Rhipicephalus sanguineus [brown dog tick]).

5 Spraying grassed and shrubbed areas every spring and midsummer with appropriately labeled pesticides may be helpful in controlling ticks.

6 The prognosis is good. Infected animals are sources of tick transmission to other animals and to humans.

FIGURE 5-1 Ixodid Ticks.

Multiple ticks attached to the inner ear pinnae.

(Courtesy D. Angarano.)

FIGURE 5-2 Ixodid Ticks.

This erythematous lesion developed at the site of tick attachment.

(Courtesy D. Gram.)

Spinous Ear Tick (Otobius megnini)

Features

Otobius megnini is a soft (argasid) tick primarily found in arid areas of North and South America, India, and southern Africa. Adult ticks are not parasitic, but larvae and nymphs infest external ear canals of animals. These ticks are uncommon in dogs and rare in cats.

The presence of O. megnini may be seen as acute onset of otitis externa with severe inflammation and waxy exudate, vigorous head shaking, and ear scratching.

Top Differentials

Differentials include other causes of otitis externa.

Diagnosis

1 Otoscopy: visualization of larval, nymph, and immature adult spinous ear ticks.

Canine Localized Demodicosis

Features

Skin lesions occur when there is a localized overpopulation of Demodex canis, a normal commensal inhabitant of canine skin. Demodectic overgrowth is often associated with a predisposing factor such as endoparasitism, poor nutrition, immunosuppressive drug therapy, or transient stress (e.g., estrus, pregnancy, surgery, boarding). Canine localized demodicosis is common in dogs, with highest incidence reported in puppies 3 to 6 months old.

Canine localized demodicosis may appear as one to five patchy areas of alopecia with variable erythema, hyperpigmentation, and scaling localized to one region of the body. Lesions are most common on the face, but they can be anywhere on the body. Lesions are not usually pruritic unless they are secondarily infected.

Top Differentials

Differentials include superficial pyoderma, dermatophytosis, and other causes of alopecia.

Diagnosis

1 Microscopy (deep skin scrapes): many Demodex sp. adults, nymphs, larvae, or ova.

2 Dermatohistopathology: intrafollicular demodectic mites with varying degrees of perifolliculitis, folliculitis, or furunculosis.

Treatment and Prognosis

1 Any predisposing factors and secondary pyoderma should be identified and treated.

2 Any secondary pyoderma should be treated with appropriate long-term (minimum 3–4 weeks) systemic antibiotics that are continued at least 1 week beyond clinical resolution of the pyoderma.

3 Most patients’ conditions will be resolved with infection control and topical shampoo therapy using a 1% to 3% benzoyl peroxide shampoo every 3 to 7 days. Topical creams and ointments do not demonstrate any additional benefit when compared with shampoo therapy alone.

4 Miticidal treatment may not be necessary because many cases resolve spontaneously.

5 If the localized lesion persists, the patient should be neutered and given miticidal treatment. Effective miticidal therapies include the following:

Ivermectin 0.2–0.6 mg/kg PO every 24 hours is often effective. Initially, ivermectin 0.1 mg/kg PO is administered on day 1, then 0.2 mg/kg PO is administered on day 2, with oral daily increments of 0.1 mg/kg until 0.2–0.6 mg/kg/day is being administered, assuming that no signs of toxicity develop. The cure rate for 0.4 mg/kg/day ivermectin is 85% to 90%.

Milbemycin oxime, 0.5–2 mg/kg PO every 24 hours. The cure rate is 85% to 90%.

Doramectin 0.2–0.6 mg/kg SC once weekly. The cure rate is approximately 85%.

For dogs weighing less than 20 kg, the use of 9% amitraz collars may be effective. In small dogs, use of 9% amitraz collars alone may be as effective as ivermectin (0.6 mg/kg/day PO).

Topical application of Promeris (topical metaflumizone and amitraz solution) every 2 weeks has demonstrated good efficacy.

Topical moxidectin has demonstrated variable efficacy when applied every 2 to 4 weeks.

6 Historical (traditional miticidal) treatment includes the following:

Total body hair coat clip if dog is medium- to long-haired.

Weekly bath with 2.5% to 3% benzoyl peroxide shampoo, followed by a total body application of 0.03% to 0.05% amitraz solution. The cure rate ranges from 50% to 86%.

For demodectic pododermatitis, in addition to weekly amitraz dips, foot soaks in 0.125% amitraz solution should be performed every 1 to 3 days.

7 The prognosis is good. Most cases resolve within 4 to 8 weeks, but a few may progress to generalized demodicosis. Systemic therapy or total body dips should not be used in intact animals, as this may mask the development of generalized demodicosis, which is thought to be an inherited disease. D. canis is not considered contagious to other dogs (except for newborn puppies), to cats, or to humans.

Author’s Note

Although localized demodicosis is not believed to be genetically predisposed, breeding of infected dogs should be discouraged.

Dogs with localized demodicosis may be more likely to develop adult-onset demodicosis if exposed to steroids later in life.

FIGURE 5-3 Canine Localized Demodicosis.

Multiple alopecic papular lesions on the face of an adult Shetland Sheep dog.

(Courtesy D. Angarano.)

FIGURE 5-4 Canine Localized Demodicosis.

Focal area of alopecia and hyperpigmentation typical of folliculitis.

FIGURE 5-5 Canine Localized Demodicosis.

Numerous comedones on the abdomen of a dog with hyperadrenocorticism. Comedones are often caused by demodicosis or Cushing’s disease.

FIGURE 5-6 Canine Localized Demodicosis.

Microscopic image of Demodex mites, as seen with a 10× objective.

FIGURE 5-7 Canine Localized Demodicosis.

This circular area of alopecia with central hair regrowth typical of folliculitis is often misdiagnosed as dermatophytosis.

FIGURE 5-8 Canine Localized Demodicosis.

Focal area of papular dermatitis caused by Demodex.

FIGURE 5-9 Canine Localized Demodicosis.

Focal area of alopecia on the muzzle of a young dog.

(Courtesy D. Angarano.)

FIGURE 5-10 Canine Localized Demodicosis.

Papular dermatitis with hyperpigmentation typical of demodicosis.

Canine Generalized Demodicosis

Features

Canine generalized demodicosis may appear as a generalized skin disease that may have genetic tendencies and can be caused by three different species of demodectic mites: D. canis, D. injai, and an unnamed short-bodied Demodex mite. D. canis, a normal resident of the canine pilosebaceous unit (hair follicle, sebaceous duct, and sebaceous gland), is primarily transmitted from mother to neonate during the first 2 to 3 days of nursing, but adult-to-adult transmission may rarely occur. D. injai, a recently described, large, long-bodied Demodex mite, is also found in the pilosebaceous unit, but its mode of transmission is unknown. Mode of transmission is also unknown for the short-bodied unnamed Demodex mite, which, unlike the other two species, lives in the stratum corneum. Depending on the dog’s age at onset, generalized demodicosis is classified as juvenile-onset or adult-onset. Both forms are common in dogs. Juvenile-onset generalized demodicosis may be caused by D. canis and the short-bodied unnamed Demodex mite. It occurs in young dogs, usually between 3 and 18 months of age, with highest incidence in medium-sized and large purebred dogs. Adult-onset generalized demodicosis can be caused by all three mite species and occurs in dogs older than 18 months of age, with highest incidence in middle-aged to older dogs that are immunocompromised because of an underlying condition such as endogenous or iatrogenic hyperadrenocorticism, hypothyroidism, immunosuppressive drug therapy, diabetes mellitus, or neoplasia. To date, only adult-onset disease has been reported with D. injai, with highest incidence noted in terriers.

Clinical signs of infestation with D. canis or the unnamed Demodex mite are variable. Generalized demodicosis is defined as five or more focal lesions, or two or more body regions affected. Usually, patchy, regional, multifocal, or diffuse alopecia is observed with variable erythema, silvery grayish scaling, papules, or pruritus. Affected skin may become lichenified, hyperpigmented, pustular, eroded, crusted, or ulcerated from secondary superficial or deep pyoderma. Lesions can be anywhere on the body, including the feet. Pododemodicosis is characterized by any combination of interdigital pruritus, pain, erythema, alopecia, hyperpigmentation, lichenification, scaling, swelling, crusts, pustules, bullae, and draining tracts. Peripheral lymphadenomegaly is common. Systemic signs (e.g., fever, depression, anorexia) may be seen if secondary bacterial sepsis develops.

D. injai infestations are typically characterized by focal areas of greasy seborrhea (seborrhea oleosa), especially over the dorsum of the trunk. Other skin lesions may include alopecia, erythema, hyperpigmentation, and comedones. Small breeds and terriers seem predisposed to D. injai infection.

Top Differentials

Differentials include pyoderma (superficial or deep), dermatophytosis, hypersensitivity (flea bite, food, atopy), and autoimmune skin disorders.

Diagnosis

1 Microscopy (deep skin scrapes): many demodectic adults, nymphs, larvae, and ova are typically found with D. canis and the short-bodied, unnamed demodectic mite, although D. canis may be difficult to find in fibrotic lesions and in feet. With D. injai, mites may be low in number and difficult to find, requiring skin biopsies.

2 Dermatohistopathology: minimal to mild suppurative perivascular dermatitis with mites in stratum corneum, or intrafollicular demodectic mites with varying degrees of perifolliculitis, folliculitis, or furunculosis.

Treatment and Prognosis

1 If adult-onset, any underlying conditions should be identified and corrected. All steroid-containing therapies should be discontinued, as steroid administration is the most common cause of adult-onset demodicosis.

2 Intact dogs, especially females, should be neutered. Estrus or pregnancy may trigger relapse.

3 Any secondary pyoderma should be treated with appropriate long-term (minimum 3–4 weeks) systemic antibiotics that are continued at least 1 week beyond clinical resolution of the pyoderma.

4 Topical shampoo therapy using a 1% to 3% benzoyl peroxide shampoo every 3 to 7 days will help speed resolution and will enhance miticidal treatments.

5 Effective miticidal therapies include the following:

Ivermectin 0.2–0.6 mg/kg PO every 24 hours is often effective against generalized demodicosis. Initially, ivermectin 0.1 mg/kg PO is administered on day 1, then 0.2 mg/kg PO is administered on day 2, with oral daily increments of 0.1 mg/kg until 0.2–0.6 mg/kg/day is being administered, assuming that no signs of toxicity develop. The cure rate for 0.4 mg/kg/day ivermectin is 85% to 90%.

Milbemycin oxime, 0.5–2 mg/kg PO every 24 hours. The cure rate is 85% to 90%.

Doramectin 0.2–0.6 mg/kg SC once weekly. The cure rate is approximately 85%.

For dogs ≤20 kg, the use of 9% amitraz collars may be effective. In small dogs, use of 9% amitraz collars alone may be as effective as ivermectin (0.6 mg/kg/day PO).

Topical application of Promeris (topical metaflumizone and amitraz solution) every 2 weeks has demonstrated good efficacy.

Topical moxidectin has demonstrated variable efficacy when applied every 2 to 4 weeks.

6 Historical (traditional miticidal) treatment includes the following:

Total body hair coat clip if dog is medium- to long-haired.

Weekly bath with 2.5% to 3% benzoyl peroxide shampoo, followed by a total body application of 0.03% to 0.05% amitraz solution. The cure rate ranges from 50% to 86%.

For demodectic pododermatitis, in addition to weekly amitraz dips, foot soaks in 0.125% amitraz solution should be performed every 1 to 3 days.

7 Regardless of the miticidal treatment chosen, therapy is administered over the long term (weeks to months). Treatments should be continued for at least 1 month beyond the time when the first follow-up skin scrapings become negative for mites (total of two negative skin scrapings).

8 The prognosis is good to fair. Relapses may occur, requiring periodic or lifelong treatment in some dogs. The use of glucocorticosteroids in any dog that has been diagnosed with demodicosis should be avoided. Because of its hereditary predisposition, neither female nor male dogs with juvenile-onset generalized demodicosis should be bred. D. canis is not considered contagious to cats or to humans. It is transmitted from bitch to newborn puppies during the first 2 to 3 days of nursing, and possibly between adult dogs that are close cohabitants. The mode of transmission for D injai and the unnamed short-bodied Demodex mite is unknown.

Author’s Note

Steroids are the most common cause of adult-onset demodicosis.

Products containing amitraz tend to be the most toxic usually because of the product vehicle.

Aggressive treatment should be tried for up to 6 months before giving up.

One of the most common causes of treatment failure is that the patient will look greatly improved before negative skin scrapes are achieved. Many owners therefore will discontinue treatment prematurely, resulting in relapse.

The average time to achieve clinical improvement is 4 to 6 weeks; the first negative skin scrape usually occurs around 6 to 8 weeks; most patients need approximately 3 months of treatment to resolve the infection based on two negative skin scrapes at least 3 weeks apart.

FIGURE 5-11 Canine Generalized Demodicosis.

Generalized alopecia and papules with crusts and scales on the head and neck of a juvenile dog.

FIGURE 5-12 Canine Generalized Demodicosis.

Multifocal alopecia over the head, trunk, and extremities of an adult dog with generalized demodicosis.

FIGURE 5-13 Canine Generalized Demodicosis.

Close-up of the dog in Figure 5-12. Multifocal areas of alopecia with mild hyperpigmentation are apparent.

FIGURE 5-14 Canine Generalized Demodicosis.

Diffuse alopecic, erythematous, crusting, papular lesions affecting the entire head and neck.

FIGURE 5-15 Canine Generalized Demodicosis.

Alopecic, erythematous, papular dermatitis on the axilla and ventral trunk of an adult dog with iatrogenic hyperadrenocorticism.

FIGURE 5-16 Canine Generalized Demodicosis.

Multiple patches of comedones on the abdomen of a dog.

FIGURE 5-17 Close-up of the dog in Figure 5-11. Multiple pustules on the ventral abdomen can be seen.

FIGURE 5-18 Canine Generalized Demodicosis.

Alopecia, crusting, and papular lesions typically of folliculitis and furunculosis caused by Demodex.

FIGURE 5-19 Canine Generalized Demodicosis.

Numerous comedones, papules, and pustules on the abdomen of a dog. Note the similarity to superficial pyoderma.

FIGURE 5-20 Canine Generalized Demodicosis.

Matting of the hair associated with an underlying crusting papular dermatitis.

FIGURE 5-21 Canine Generalized Demodicosis.

Severe alopecia, erythema, and hyperpigmentation with a papular rash on the feet of an adult dog with iatrogenic hyperadrenocorticism.

FIGURE 5-22 Canine Generalized Demodicosis.

Alopecia and papular dermatitis with a large erosive lesion.

FIGURE 5-23 Canine Generalized Demodicosis.

Alopecia, erythema, and crusting ulcerative lesions are typical of furunculosis caused by demodicosis.

FIGURE 5-24 Canine Generalized Demodicosis.

Alopecia and hyperpigmentation affecting the swollen nail beds (paronychia) of a dog with Demodex.

FIGURE 5-25 Canine Generalized Demodicosis.

Microscopic image of Demodex mites, as seen with a 10× objective.

FIGURE 5-26 Canine Generalized Demodicosis.

Microscopic image of Demodex mites, as seen with a 10× objective.

FIGURE 5-27 Canine Generalized Demodicosis.

Diffuse papular dermatitis with hyperpigmentation on the abdomen of an adult Cocker spaniel.

FIGURE 5-28 Canine Generalized Demodicosis.

Focal area of alopecia and papular dermatitis on the dorsum of an adult dog with Demodex injai. Note the location and severe seborrhea oleosa that are characteristic of this species.

FIGURE 5-29 Canine Generalized Demodicosis.

Same dog as in Figure 5-28. Clumping of the hair is caused by excessive sebaceous secretions.

FIGURE 5-30 Canine Generalized Demodicosis.

Microscopic image of Demodex injai, as seen with a 10× objective. The mite is larger than Demodex canis.

Feline Demodicosis

Features

Feline demodicosis is a skin disease that can be caused by two different species of demodectic mites—D. cati and D. gatoi, a short-bodied Demodex mite whose normal habitat is unknown. Skin disease may be localized or generalized. D. gatoi is contagious and usually causes pruritic skin disease. D. cati infections are often associated with an underlying immunosuppressive or metabolic disease such as feline immunodeficiency virus (FIV), feline leukemia virus (FeLV), toxoplasmosis, systemic lupus erythematosus, neoplasia, or diabetes mellitus. Localized or generalized demodicosis caused by D. cati infection is rare in cats. D. gatoi infections are emerging as a cause of pruritic skin disease in cats in the United States, especially in the southern United States.

Localized disease is characterized by a variably pruritic ceruminous otitis externa or by focal patchy alopecia and erythema that may be scaly or crusty. Localized skin lesions are most common around the eyes, on the head, or on the neck. Generalized disease is characterized by variably pruritic (none to extreme), multifocal, patchy, regional, or symmetrical alopecia, with or without erythema, scaling, crusts, macules, and hyperpigmentation. Lesions usually involve the head, neck, limbs, flanks, or ventrum. Ceruminous otitis externa and secondary pyoderma may be present.

Top Differentials

Differentials include dermatophytosis, other ectoparasites (Cheyletiella, Notoedres, ear mites), hypersensitivity (flea bite, food, atopy), psychogenic alopecia, and other causes of otitis externa.

Treatment and Prognosis

1 Any predisposing factors should be identified and corrected.

2 D. gatoi may be difficult to find on microscopy but respond well to lime sulfur dips.

2% to 4% lime sulfur dips applied q 3–7 days for 4 to 8 weeks. Clinical improvement is often observed within 3 to 4 weeks, but therapy should be continued for a total of 6 to 8 weeks to resolve the infection.

All cats in close contact must be treated to prevent reinfection.

Tags: Small Animal Dermatology A Color Atlas and Therapeutic Guide

Sep 10, 2016 | Posted by admin in SMALL ANIMAL | Comments Off

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