INTRODUCTION

1. General functions of the skin: barrier and protector, sensory organ, temperature regulation, immunosurveillance, vitamin production, electrolyte regulation, hair

2. Stages of hair growth: anagen (growth phase), telogen (rest phase) and catagen (stage in between). The normal hair coat consists of primary hairs (coarse guard hairs) and secondary hairs (fine hairs). Secondary hairs are more numerous than primary hairs

3. During illness most of the hairs are in the telogen phase. Sick animals are observed to have a poor hair coat because the anagen phase is shortened and most hairs are in telogen, which are lost more easily. Severe illness may result in “telogen defluxion” a condition whereby many hairs synchronously enter telogen and are shed together.

4. The root of hairs plucked in anagen show a large expanded square root and have a root sheath, whereas hairs plucked in telogen show a tapered root and have no root sheath. In patients with alopecia hairs can be plucked and evaluated to determine what stage they are in.

5. The epidermis produces the protein keratin, which acts as a major barrier between the animal and the environment. There is a normal population of resident microflora on the skin that helps to prevent colonization by pathogenic organisms.

6. The dermis allows for the diffusion of nutrients and electrolytes to the upper avascular epidermal layer and acts to maintain and repair the skin. The subcutis is the deepest and thickest layer of the skin. It contains fat and connective tissue and serves primarily as protection, insulation and as an energy reserve.

7. The three types of glandular structures found in the skin include the sebaceous glands, apocrine sweat glands, and eccrine sweat glands. The sebaceous glands produce an oily secretion (sebum), which spreads over the stratum corneum. The eccrine glands are located in the footpads and likely play a role in thermoregulation and heat dissipation.

8. When taking a history on a dermatologic patient signalment, history of the skin lesion and presence of any other underlying disease should be noted. The dermatologic exam should include the animal being evaluated from a distance then up close and personal. The hair and skin should be evaluated and the skin lesions should be evaluated if they are primary or secondary.

Telogen

Anagen

9. Primary skin lesions develop as a direct reflection of underlying disease and may suggest a specific dermatosis. Secondary skin lesions evolve from a primary lesion or result from artifacts induced by the patient or the client (licking, scratching, medications etc).

10.

A. Primary lesions

1.  Macule: a flat circumscribed spot up to 1 cm in diameter characterized by a change in color.

2.  Patch: a macule >1 cm in size.

3.  Purpura: a type of macule caused by bleeding into the skin.

4.  Papule: a small, solid elevation of the skin up to 1 cm in diameter. Many are pink or red in color.

5.  Plaque: a larger flat-topped elevation formed by the coalition of papules.

6.  Nodule: a small circumscribed solid elevation > 1 cm in diameter that usually extends into the dermis or subcutis.

7.  Tumor: neoplastic enlargement.

8.  Cyst: an epithelial-lined cavity containing fluid or solid material.

9.  Pustule: a small, circumscribed elevation of the epidermis filled with pus.

10.  Abscess: a demarcated fluctuant lesion resulting from the dermal or subcutaneous accumulation of pus.

11.  Wheal: a sharply circumscribed raised lesion consisting of edema that tends to resolve quickly.

12.  Vesicle: a sharply circumscribed elevation of the epidermis filled with clear fluid.

13.  Bulla: a vesicle > 1 cm in diameter.

B. Secondary lesions

1.  Scale: an accumulation of loose fragments of the horny layer of the skin.

2.  Epidermal collarette: a type of scale arranged in a circular rim of loose keratin flakes - represents the remnants of a vesicle, bullae, or pustule.

3.  Crust: occurs when dried exudate, serum, pus, blood, etc. adheres to the surface of the skin and hairs.

4.  Scar: an area of fibrous tissue that has replaced damaged dermis or subcutis.

5.  Excoriation: abrasion of the skin - usually superficial and traumatic in origin.

6.  Erosion: a shallow ulcer that does not penetrate the dermis.

7.  Ulcer: a break in the epidermis with exposure of the underlying dermis.

8.  Lichenification: a thickening and hardening of the skin frequently resulting from chronic friction. Note exaggerated skin markings.

9.  Hyperpigmentation: increased melanin in epidermis and sometimes dermis. Often occurs with chronic inflammation, post-trauma or in association with endocrine disorders.

10.  Comedo: a dilated hair follicle filled with cornified cells and sebaceous debris.

11. Fissure: linear cleavage (cracks) in the epidermis or dermis caused by disease or injury.

EAR

1. Outer ear: vertical and horizontal ear canals, sebaceous and modified apocrine glands. Middle ear: tympanic membrane, tympanic cavity, tympanic bulla, auditory ossicles, and auditory tube. Inner ear: cochlea, vestibule, semicircular canals. The facial nerve along with branches of the sympathetic and parasympathetic nerves course near the middle ear.

2. Otitis media often results from spread of infection across a ruptured tympanum, which often is common in dogs with longstanding otitis externa.

3. Otitis externa is usually multifactorial in nature. Cats often suffer otitis externa due to Otodectes cyanotic and dogs often due to underlying atopy, food allergy and keratinization disorders. In the case of dogs anatomical, environmental, secondary microorganism proliferation and changes associated with chronic otitis are often present and confound treatment.

Otitis externa: multifactorial disease

Predisposing factors Primary causes Perpetuating factors

Conformation of ear Parasites: Otodectes, mange, ticks

Bacteria: (Staph interm, Pseud

Excessive moisture Microorganisms: dermatophytes

Proteus, E. coli, Klebsiella)

Excessive hair Allergies: atopy, food allergy, contact

Yeast: (Malassezia

Treatment: irritating topicals, etc.

Idiopathic seborrhea, hypothyroidism

pachydermatis, Candida alb.)

Obstruction: tumors, polyps

Foreign bodies: foxtails, hair, debris

Ear pathology (hyperplasia

Systemic disease: debilitation, etc.

Glandular hyperplasia keratinization, edema, fibrosis)

  Autoimmune diseases, other

Otitis media

4. Clinical signs of the patient with otitis externa include head shaking, aural pruritis, otic discharge and malodor, wheras otitis media head tilt, facial nerve paralysis, horners syndrome and deficient tear production may also be noted. Otitis interna often shows signs of peripheral vestibular disease due to damage of the vestibulocochlear nerve.

5. The appearance of otic discharge can provide clues as to the possible underlying etiology for example “coffee grounds” tend to be ear mites, moist brown exudates indicates staph or year, a prurulent cream-yellow colored exudates is often gram negative bacteria and oily yellow-tan discharge is ceruminous otitis which is from glandular disorders or hypersensitivities. Examination of the inflamed ear is often uncomfortable and painful for the patient so adequate sedation or general anesthesia can be used. The good ear should be examined first which will increase the chances of getting a good look and will minimize risk of spreading infectious agents from the bad ear to the good ear.

6. Culture and sensitivity is indicated in cases of chronic otitis externa/media to guide systemic antibiotic therapy. Bulla radiographs are indicated in cases of chronic otitis externa or suspected otitis media/interna.

7. It is very important to do a thorough physical exam and look for evidence of underlying disease or generalized dermatopathy because if the patient is suffering from an underlying cause of otitis externa, treatment will likely only temporarily ameliorate clinical signs. Hypersensitivity disorders, Keratinization defects and endocrinopathies often predispose to recurrent otitis.

8. Treatment of otitis includes cleaning the ear, removing excess hair, application of ceruminolytics, drying the ear canal, applying drying agents and topical glucocorticoids. Topical glucocorticoids decrease inflammation, pain, swelling, pruritis, exudation and proliferative changes.

9. Topical antibacterial agents and antiseptics can be used to treat otitis externa due to a bacterial cause. Oral antibiotics are indicated for severe otitis externa or otitis media/interna due to bacterial causes. The appropriate antibiotic should be selected based on culture/sensitivity results.

10. The most common cause of yeast infection in the ear is due to Malassezia pachydermatis. Antifungal agents and antiseptics are often used to treat yeast infections in the ear.

11. Otodectes cyanotic is the cause of about 50% of cases of otitis externa in the cat and 10% of cases in the dog. The mites induce a hypersensitivity reaction by injecting mite antigen while they feed on lymph and epidermal debris. As few as 2-3 mites can cause severe clinical signs. This mite is highly contagious so all in contact animals should be treated. Since mites can migrate elsewhere the ears and

entire haircoat should be treated. Systemic ivermectin is an alternative therapy but since it is not approved for this use it not the first line treatment. Owners must be educated as to the chronic nature of this disease since may animals with otitis externa require continued ear care at home due to a persistence of predisposing factors.

12. Surgical treatment is indicated in more chronic or severe cases of otitis. The total ear canal ablation with bulla osteotomy is most likely to be effective however this procedure typically results in hearing loss

FUNGAL SKIN DISEASES

1. Dermatophytes are fungi that invade and grow in dead keratinized tissue and dermatophytosis is an infection of the keratinize tissues, nail, hair and stratum corneum by dermatophytes. The most common cause of fungal skin disease in the dog and cat is dermatophytosis.

2. Microsporum canis is the most common cause of dermaphytosis in the dog and cat. M. canis is usually acquired by exposure to an infected cat although environmental contamination or fomites can also be responsible.

3. Exposure does not necessarily result in infection. Mechanical disruption of the stratum corneum aids in establishing an infection. Fungi prologerate and produce keratinases, which digests dead keratinized tissue and allows for hair penetration. The growing hair provides nutrition to the fungus, which is necessary for fungal growth. Turnover of the epidermis, shedding of infected telogen hairs and strengthening of the immune response results in elimination of infection in most healthy animals.

4. Many cats are inapparent carriers with minimal lesions of broken hairs and patchy alopecia. The classic “ringworm” lesions are focal circular to patchy areas of alopecia with minimal scaling and inflammation. These lesions tend to predominate on the head and forelimbs and pruritis is usually mild. Most infections are follicular and can closely resemble bacterial folliculitis. In dogs folliculitis or furunculosis may be noted.

5. The zoonotic potential of dermatophytosis is high with about 50% of exposed humans developing skin lesions. Dermatophytosis is diagnosed via woods light, microscopic exam or fungal culture. About 50% of M canis strains fluoresce under woods light. Positive fluorescence of hairs usually indicates M canis but a culture is needed to confirm. Negative fluorescence does not rule out disease since 50% of M canis doesn’t fluoresce. Hairs are evaluated for infection and hyphae or grape like clusters may be noted. However, as with wood’s light, negative finding does not rule out disease. Dermatophyte test media will inhibit bacterial growth but allow for fungal growth. A sample is added to the medium and checked daily for color change (may take 2-3 weeks to see growth).

6. The technique of choice for diagnosis of dermatophyte infection is via DTM plating. Dermatophytes use the protein first in the media, which turns the plate red. Most non-pathogenic fungi use CHO first, which will not cause a color change in the media. The plates must be checked daily for 2-3 weeks to notice the color change.

7. Treatment goals for M canis include promoting the host’s immune response, hastening resolution of infection and minimizing environmental contamination. Due to risk of contagion, re infection and zoonosis most people agree all cases of confirmed dermatophytosis should be treated.

8. In general “spot therapy” is not recommended because infective spores can be found as far as 6cm away from clinical lesions or in other normal appearing areas. General topical therapy is recommended for all cases of confirmed dermatophytosis and certainly in all cases with multifocal or generalized lesions. The entire haircoat including whiskers should be clipped since hair can serve as a major source of reinfection. Chlorhexidine shampoo is recommended for those with secondary pyoderma prior to dips. Lime Sulfur dip is the most effective dip available for management of feline dermatophytosis. All in contact animals must be treated as well as the environment to insure therapeutic success.

9. Systemic therapy is indicated in infected catteries or in dogs and cats that do not respond to topical therapy within 2-4 weeks. Systemic therapy shortens duration and severity of clinical disease. Topical therapy decreases environmental contamination and minimizes reinfection. Griseofulvin is the systemic drug of choice. If griseofulvin treatment fails itraconazole and ketoconazole should be used.

10. There is an M canis vaccine but there are no published scientific studies to document efficacy, and it does not have FDA approval. Environmental control is crucial to prevention of reinfection and absolutely necessary in the elimination of infection from a cattery. Mechanical clean up involves removal of hairs from the environment, fomite disposal or treatment of fomites. The best solution for treatment of walls, floors and counters is a 1:10 dilution of household bleach.

11. M pachydermatis is often associated with underlying disease that increases skin moisture or cerumen production. This often results in otitis externa and generalized seborrheic dermatitis. M. pachydermatis is usually diagnosed via cytology from a skin scrapings. Excessive numbers of budding “peanut shaped” yeast may be noted.

12. The SQ mycoses are fungal infections that have invaded viable tissues of the skin. They are typically acquired by traumatic inoculation of saprophytic organisms into the skin. Many of the SQ mycosis result in localized nodular lesions that exhibit variable swelling, ulceration and drainage. These lesions can resemble a

granuloma, foreign body reaction, the common abscess or focal neoplasm. Cytology, culture and biopsy are used to diagnose SQ mycosis. Biopsy is usually required for definitive diagnosis. Treatment is variable depending the specific fungal pathogen, but often it entails complete surgical excision or systemic anti-fungal therapy.

13. The clinical signs for sporotrichosis include firm, raised nodules that often ulcerate. The cutaneous lymphatic form also has lymphadopathy, ulceration and draining. Exudates containing infectious organisms are transferable to people without skin penetration.

14. A systemic mycosis is a fungal infection of the internal organs that may disseminate secondarily to the skin. These fungal diseases are not contagious. Infection typically occurs via inhalation since the causative fungi exist as saprophytes. The dermatological manifestations of systemic mycoses include papules, plaques, ulcers and nodule formation. Diagnosis is usually made by demonstration of the organism on aspiration or biopsy of the affected organ. The most common systemic mycoses associated with dermatologic signs are Cryptococcus neoformans, and Blastomyces dermatitidis.

BACTERIAL SKIN DISEASES

1. Resident microflora is a commensal population that plays an important role in inhibiting colonization by pathogenic organisms. Pathogenic microflora are the bacteria on the skin that will cause clinical signs in the host. Folliculitis is infection confined to the hair follicle, whereas furunculosis is rupture of the follicle and spread to the dermis.

2. The most common bacterial pathogen in canine and feline pyoderma is Staph intermedius. A primary pyoderma is a skin infection that occurs in otherwise healthy skin with no apparent cause. Most pyodermas are secondary in nature. They are skin infections that have an underlying cause, occurs in diseases skin and is often less responsive to therapy. Underlying diseases include allergies, mites, dermatophytosis, seborrhea, endocrinopathies and diseased skin.

3. Surface pyoderma is bacterial colonization or overgrowth that is present on the skin surface but the skin is not infected. Superficial pyoderma is an infection of the skin that involves the epidermis and/or intact hair follicles. Deep pyodermas are skin infections that are deeper and often serious, extending further down into the hair follicle, dermis or subcutis. History and physical exam is crucial in determining if the skin infection is primary or secondary and gathering clues as to possible causes. Basic tests used in the evaluation of all patients with pyoderma include dermatologic exam, a skin scrapping to look for mites, DTM culture to look for dermatophytosis, and cytology. Tests that can be pursued in deep, non-responsive or recurrent pyodermas are skin biopsies, skin culture and sensitivity.

Contributory hypersensitivities, underlying metabolic disease and underlying endocrine or immunologic disease should also be investigated.

4. Treatment of skin infections should begin with addressing any underlying causes. Antibacterial shampoos will help to remove tissue debris and to aid in eliminating bacteria in the more superficial layers of the skin. Soaks and hydrotherapy may be helpful in the initial management of deep pyoderma to remove crusts and decrease surface bacteria. Topical antibiotics may be helpful if applied to focal lesions, however oral antibiotics are necessary to reach effective antibiotic levels in the skin in most pyodermas since the stratum corneum is a major barrier to effective topical penetration.

5. A patient with intertrigo (skin fold pyoderma) has skin lesions on the body where there are excessive skin folds and are characterized by local erythemia, oozing, erosion and odiferous discharge. Treatment involves reducing obesity, antibacterial shampoos and surgical excision of excessive skin folds. Hot spots are painful, red moist and exudative lesions with a yellowish center that can progress to a more severe infected form. Treatment involves eliminating the trigger, clipping the hair, cleaning with an antibacterial shampoo, applying a drying agent and providing a short course of oral anti-inflammatory glucocorticoids.

6. Impetigo (puppy pyoderma) is a mild superficial pustular rash and crusts in inguinal and axillary region of young puppies. This disease is usually self-limiting, but topical antibacterial shampoos often help. Superficial folliculitis is the most common form of canine pyoderma. The classic primary lesion is a tiny intact papule or pustule with a hair emanating from the center. It may also present as papules, pustules, crusts, epidermal collarettes and hyperpigmented or erythematous macules. When treating these patients the underlying cause should be addressed. Topical antibacterial shampoo therapy and oral antibiotics should also be instituted. Glucocorticoids are contraindicated in this disease. Juvenile cellulitis (puppy strangles) is an acute swelling of the face and submandibular lymph nodes followed by papules, pustules, oozing serum or pus and crust formation. Treatment involves immunosuppressive doses of glucocorticoids, antibiotics (if there is a secondary infection) and topical drying agents.

7. Deep pyodermas are often serious, extending further down into the hair follicle, dermis or subcutis. It may be associated with systemic signs of illness, however it is less common than superficial pyodermas and rare in cats. Deep pyodermas do not occur spontaneously, they are usually a continuation of superficial pyoderma associated with underlying disease. Characteristic lesions may include red/purple nodules, hemorrhagic bullae, ulcerative lesions and draining purulent fistulous tracts. Treatment involves identifying and treating underlying disease which adding whirlpool soaks with antiseptic agents, antibacterial shampoos, appropriate antibiotic therapy for a minimum of 8-10 weeks, and surgical excision where indicated.

Pyotraumatic folliculitis: infected hot spot; lesions resemble hot spots only they are more erythematous and plaque like and have surrounding papules and pustulesCallus pyoderma: occurs when calluses become secondarily infectedNasal folliculitis: painful localized deep infections of the nose found most often in GSD and other doliocephalic breedsAcne: Interdigital pyoderma: painful, red, swollen feet w nodules and exudative draining fistulas. Variable pruritis, lameness and lymphadenopathyGeneralized deep pyoderma: folliculitis, nodules, crusts and open deep purulent fistulas with ulceration. Distributed over trunk, abdomen and pressure pointsAnaerobic Cellulitis: often initiated by trauma, FBs etc; CS: fever, crepitus; Tx: surgical debridement, lavage, AB’s

8. Abscesses are characterized by single to multiple cutaneous nodules, which may ulcerate to form fistulous tracts with purulent exudates. If the patient is not responding to symptomatic treatment for presumptive abscess, then such lesions should be biopsied, cultured and special stains applied to look for causative etiology. In many cases complete surgical excision of affected lesion is necessary to affect a cure. In other cases, specific detailed antimicrobial protocols are indicated. Cat bite abscesses occur when the skin seals over a puncture site rapidly and the abscess develops within 2-4 days. The likely causative organisms are anaerobes from the oral microflora. Treatment involves surgical debridement, antiseptic lavage and appropriate antibiotics.

9. Sterile granulomas are lesions characterized by firm, painless cutaneous nodules, plaques or papules that may become secondarily infected. They are diagnosed by biopsy and negative bacterial cultures. Treatment includes surgical excision of solitary lesions or immunosuppressive doses of glucocorticoids if there are multiple lesions.Panniculitis are solitary lesions that ulcerate to drain an oily, yellowish brown to bloody discharge. Definitive diagnosis requires biopsy. As with sterile granulomas surgical excision is the treatment for solitary lesions and immunosuppressive disease of glucocorticoids for animals with multiple nodules.

PARASITIC SKIN DISEASES I

1. The clinical signs for hookworm dermatitis include skin lesions on parts of the body in contact with the ground, including pruritis and papules. The disease is contracted by percutaneous entry. Treat all in contact dogs with anthelmintics and remove feces from the environment. Symptomatic treatment for secondary bacterial infection should also be instituted. This disease is of zoonotic concern therefore all puppies and kittens should be given prophylactic anthelmintic therapy at 2-3 weeks.

2. Otobius megini is the only soft tick that is of concern in the small animal patient. The larva and nymphs feed on the lymph in the ear canal and tend to cause acute

otitis externa. This disease is diagnosed by identifying the parasites in the ear canal. The otitis externa should be treated symptomatically and typically tick infestation treatment should also be pursued.

3. Two common pathogenic hard ticks are Rhipicephalus sanguineus and Dermacentor variabilis. Rhipicephalus can transmit babesiosis, anaplasmosis, E. canis, F tularensis and tick paralysis, whereas Dermacentor can transmit RMSF, St louis encephalitis, tularemia, anaplasmosis and tick paralysis.

4. If the number of ticks is relatively few they should be removed manually. After removal the animal should be treated with appropriated topical insecticides including Frontline (fipronil), amitraz collars, and various insecticide dips and sprays. The premises should also be treated with organophosphate insecticides.

5. The entire life cycle of sarcoptes is completed on the host. The adult burrows in the horny layer of the epidermis and lays its eggs there. The eggs hatch into larva and burrow into the surface where both larvae and nymphs feed. The larva mold to nymphs and then to adults within the tunnels. Mites prefer the hairless regions on the body and these areas are typically affected first (elbows, ears, ventrum etc). The hallmark feature of sarcoptes is intense pruritis. Scabies incognito is a form, which occurs in the meticulously groomed dogs with minimal skin lesions but severe pruritis. Sarcoptes is diagnosed by skin scrapings and response to therapy. Mites are difficult to find on numerous skin scrapings therefore choose an area that is not excoriated and make multiple skin scrapings, ear margins, elbows and hocks are good sites. The finding of one mite or mite pellet is diagnostic of scabies. Sarcoptes can only be excluded in a patient that fails to respond to treatment.

6. Sarcoptes can be treated using dip solutions or systemic anti-miticide treatment. Prior to dipping the whole body should be clipped with animals that have a dense or long haircoat. Bathe with antibacterial/antiseborrheic shampoo prior to dipping to remove crusts and allow for adequate skin contact with dip. Dips should be applied to every inch of skin to be effective.

7. Effective dip solutions include lime sulfur dips, or amitraz (mitaban) dips. Lime sulfur dips are non-toxic but have an unpleasant odor and will stain light colored coats. Amitraz dips are not licensed for use against sarcoptes and cannot be used in dogs less than 4 months of age. Organophosphate dips can also be used but tend to be less effective. Ivermectin is not approved for use against sarcoptes but is shown to be very effective. Ivermectin can not be used in collies or related breeds or in patients less than 4 months old. Animals must be heartworm negative to avoid anaphylactic complications. Interceptor (milbemycin) may be as effective as ivermectin but is not licensed for use in sarcoptes infections. Currently the number one treatment of choice is Revolution (salemectin). Revolution is the only drug licensed against sarcoptes infestation.

8. Glucocorticoids may be used in the initial management of sarcoptes to alleviate severe pruritis. Antibiotics can also be used if indicated for secondary pyoderma. Sarcoptes is highly contagious so all other in contact dogs as well as premises should be treated regardless if they show clinical signs.

9. Feline scabies is caused by Notoedres cati. Clinical signs include intense pruruitis and scrusty papules with alopecia. Skin scrapings readily identify mites unlike sarcoptes which tends to yield few if any mites.

10. Treatment of notoedres includes either dip therapy or systemic ivermectin. Amitraz (mitaban) dips and systemic ivermectin are not approved for use in the cat. As with sarcoptes this disease is highly contagious so all other cats in the household as well as the premises should be treated.

PARASITIC SKIN DISEASES II

1. Demodicosis is not a contagious disease. All dogs typically have a small number of these mites on their skin. D. canis lives within the hair follicle and associated glands.

2. Many dogs with chronic generalized demodicosis have depressed T cell function, however current data suggests that immunosuppression is mite-induced and proportional to the number of mites present. There may be a hereditary predisposition in certain breeds of dog, therefore dogs with generalized demodicosis should not be bred. Glucocorticoids are contraindicated in demodex infestations because it is induced in dogs in association with immunodeficient states, including high dose glucocorticoid therapy.

3. There are three types of demodicosis based on distribution of skin lesions, localized, generalized and pododemodicosis. Localized demodicosis is characterized by 1-5 focal lesions noted most often on the face and forelegs. The localized form usually occurs in the young animal (3-6 months old). About 10% of cases progress to the generalized form of the disease. Generalized demodicosis is characterized by greater than 5 lesions or involvement of an entire body region. Most cases of generalized demodicosis starts during puppyhood. Generalized adult onset demodex is uncommon and occurs in dogs who first experience generalized demodicosis at 4 years or older. This forms is very serious as it usually signals the presence of underlying internal disease, immunosuppression or neoplasia. Pododemodicosis is demodicosis of the feet, it can occur alone or may result from the generalized form of demodex which can also involves the feet.

4. The classic signs of demodex infections include variable degrees of folliculityis, furunculosis, erythema, crusting, hyperpigmentation and alopecia. In more severe cases deep folliculitis, furunculosis and marked peripheral lymphadenopathy with secondary pyoderma may be noted.

5. Skin scrapings allows for a definitive diagnosis. The occasional mite in a skin scrapping is normal. Animals with demodicosis will have either increased numbers of mites or increased immature forms.

6. Animals with true adult onset generalized demodicosis should be screened for the presence of underlying disease. Initially a CBC, serum biochemistry profile, UA, fecal and heartworm test should be performed. Further testing may be indicated to rule out concurrent allergies, hypothyroidism and hyperadrenocorticism.

7. Localized demodicosis can be treated with benign neglect, since most cases will spontaneously resolve within 6-8 weeks. These patients should be monitored via serial skin scrapings. Therapy for generalized demodicosis can be pursued if the lesions are seen to progress.

8. Prior to treatment, patients with demodicosis should be prepared by addressing any underlying factors which contribute to poor health and treating secondary pyoderma. The entire haircoat should be clipped and they should be bathed thoroughly with an antibacterial/anti-seborrheic shampoo and allowed to thoroughly dry. The only licensed product for this disease is amitraz (mitaban) dips. Owners of puppies that have demodex should be warned that about 10% of cases will relapse and told not to breed recovered dogs.

9. In patients that fail amitraz therapy there are several extralabel drugs that may be used including amitraz at higher doses, milbemycin (interceptor) and ivermectin.

10. Patients with generalized demodicosis should be monitored every 2-4 weeks with repeat skin scrapings, while therapy is continued at least 30-90 days past the first negative skin scrapping. Patients cannot be considered cured of demodex until 12 months after treatment has stopped. The animals should be monitored monthly to bimonthly for evidence of relapse.

11. Feline demodicosis is a rare disease in cats caused by D.cati and another unnamed demodex mite species. Predilection sites include the face, eye and ears.

12. Clinical signs of demodex include variable scaling, erythema, alopecia, hyperpigmentation and pruritis with the localized form. The generalized for shows signs of predominant folliculitis, secondary pyoderma and peripheral lymphadenopathy. Mites of either species are readily found on skin scrapings. Lime sulfur dips and systemic ivermectin are usually effective for eliminating demodex infections in the cat.

13. Cheytiella is called the walking dandruff mite because it causes scaling and flaking of the skin and as it moves so does the dandruff causing the appearance of walking dandruff. Transmission occurs via direct contact and these mites are highly contagious. Clinical signs include dry scaling with minimal pruritis, however as the disease progresses scaling becomes more severe and hair loss,

pruritis and military dermatitis (cat) may develop. In most dogs visual inspection will readily give a diagnosis, but in 15% of infected dogs and 58% of infected cats treatment must be used to rule out the mite. Most topical parasiticides including lime-sulfur dip along with systemic ivermectin will be effective. Humans can get a transient pruritis associated with cheytiella.

14. Chiggers tend to cause disease in the summer or fall when animals are outdoors with larvae. The chigger bite usually causes severe irritation and pruritis with secondary papules, crusts and scaling.

PARASITIC SKIN DISEASES- INSECTS

1. Ctenocephalides felis is the most common flea found on both the dog and the cat. The adult flea lays its eggs on the host. These eggs fall off into the environment and hatch into larva. The larva feed on fecal casts then undergo molts to enter the pupal phase. The larva pupates and the adult emerges.

2. The flea is a permanent and obligate parasite of dogs and cats. Flea-free animals do not pick up fleas by contact with infested animals-they pick up fleas by contact with an infested environment.

3. The major clinical effects of flea infestation includes flea allergic dermatitis, anemia, tapeworm infestation. FAD occurs when animals that have a hypersensitivity to flea saliva get bitten. FAD is the most common hypersensitivity disorder in dogs and cats. The clinical signs of FAD in the dog include pruritic papules, crusts, erythema, and diffuse alopecia typically on the dorsum, tail, perineum etc. Secondary manifestations include pyoderma, hot spots, seborrhea, hyperpigmentation and lichenification. The cat typically shows signs of military dermatitis, which involves crusted papules, scales, alopecia and pruritis with a haircoat that often feels “bumpy” on exam.

4. Anemia due to flea infestation occurs typically in very young animals.

5. Fleas serve as an intermediate host for Dipylidium canunum. Animals become infected when they ingest an infected flea. The clinical signs associated with tapeworms include anal pruritis and scooting.

6. A diagnosis of FAD is made on history and by noting fleas, flea dirt, and the distribution of skin lesions on exam. The absence of fleas on exam does not rule out FAD, intradermal skin testing may be required for a diagnosis (injecting flea antigen intradermally).

7. Adequate control of fleas necessitates aggressive and continuous treatment of the indoor and outdoor environment, all in contact animals and the patient. Treatment of the environment involves using an insect growth regulator to render eggs and larvae in the environment nonviable, control of pet access to flea breeding sites,

mechanically cleaning all areas flea eggs, larvae and pupae collect and application of residual pesticides. Perform premise treatment every month until good flea control is achieved, then every 3-4 months thereafter. Borate treatment of carpet and Biopesticide Interrupt may help to eliminate flea infestation. A professional exterminator may be the most cost efficient means of eliminating fleas from the environment.

8. Topical formulations of powders, sprays and shampoos made of pyrethrins, carbamates or organophosphates are the old method of flea control. The are effective against only the adult flea, which includes about 5% of the total flea population.

9. Lufeneron (Program): insect development inhibitor, inhibits chitin synthesis which prevents flea eggs from hatching and larvae from maturing. No effect on adult fleas.Fipronil (Frontline): adulticide for fleas and ticks, collects in sebaceous secretions of hair follicle for continueal re-application. Inhibits GABA, mode of action is highly specific to invertebrates. Has no effect on flea eggs or larvae. Imidacloprid (Advantage): adulticide, binds to insect’s nicotinic receptor sites and disrupts nerve transmission causing death. Kills on contact. Has no effect on flea eggs or larvae.Selamectin (Revolution): adulticide and prevents eggs from hatching. Produce neuromuscular paralysis of target organisms by increasing chloride permeability

10. The most important part of therapy against FAD is flea control. Medical relief of pruritis (prednisolone, antihistamines and omega 3 fatty acids), and flea hyposensitization can also be used to treat for FAD. Flea hyposensitization involves intradermal injections of flea salivary extracts given once weekly for up to 9-12 months. The efficacy of flea hyposensitization is unproven and debated.

11. Anoplura and mallophaga are the two types of lice that can affect the small animal patient. Anoplurans can cause anemia whereas Mallophagans tend to cause irritation and pruritis but might also draw blood. Lice produce few direct lesions but secondary excoriations, scaling and crusting may occur. Lice infestation is diagnosed usually on physical exam by seeing fleas or the acetate tape test to immobilize lice. It is treated by shampooing and treating all in contact animals (repeat in 2-3 weeks), along with cleaning and disinfecting bedding and fomites. Ivermectin is also shown to be effective, but this is an off-label use.

12. Fly dermatitis is pruritis caused by the attack of Stable flies and black flies. Most animals also develop a pruritic papule at the site of a bite from mosquitoes.

13. Myiasis is usually a disease of neglect, where the adult fly lays eggs in wounds or in urine and feces soaked coats of debilitated animals. Fly larva are highly destructive and tunnel extensively under the skin and in the subcutis. Myiasis is treated by clipping the haircoat and providing daily wound care. The larva must

be removed manually and the diseased tissue should be debrided. Apply topical antibiotics and pyrethrin sprays. Keep all affected patients indoors away from flies.

ALLERGIC SKIN DISORDERS

1. The clinical signs of urticaria, which are discrete wheals with variable pruritis, and angioedema, which is a deeper and more severe vascular response with localized to generalized edematous tissue swelling are usually due to a type 1 hypersensitivity reaction. Treatment involves prednisolone and epinephrine (prednisolone is the initial treatment of choice).

2. Contact hypersensitivity is a type 4 hypersensitivity reaction, which occurs in response to contact with topical medications, plants, plastic food dishes etc. Treatment is aimed at the avoidance of the causative allergen. Symptomatic therapy with anti-inflammatory agents may also be necessary.

3. Atopy accounts in about 10% of the canine population and is the second most common hypersensitivity disorder after FAD. Atopy is a heritable disorder in dogs, however a hereditary disposition has not been documented in cats, although there are case reports of a genetic component. Atopy is caused by a Type 1 hypersensitivity reaction to environmental allergens. Genetically predisposed dogs percutaneously absorb or inhale various allergens, which incite allergen specific IgE production. IgE binds to mast cells, which causes mast cell degranulation. This results in the release of inflammatory mediators that cause pruritis, inflammation and characteristic cutaneous signs.

4. Commonly implicated allergens include house dust, house dust mites, molds, human dander, feathers, kapok, weeds, pollens, grasses and trees. Most animals are sensitive to multiple allergens.

5. Pruritis is the hallmark sign associated with atopy. Manifestations of pruritis in the atopic dog may include face rubbing along the floor, feet licking, salivary staining, chewing and armpit scratching. Clinical signs in the dog associated with atopy include pururitis without skin lesions or with mild erythema. Other skin lesions occur secondary to pruritis and self-trauma. Otitis externa and conjunctivitis occurs in about 50% of atopic animals and may be the only manifestation of atopy. Some atopic cats exhibit self-induced alopecia without skin lesions. Skin lesions in atopic cats include eosinophilic granuloma complex and military dermatitis.

6. A diagnosis of atopy involves evaluating history and signalment, ruling out other likely causes of pruritis and intradermal skin testing. FAD and sarcoptes are the main two types of pruritic dermatoses that need to be ruled out. Any other pruritic disease should be ruled out first because of the specialty and expense of doing intradermal skin testing.

7. The test of choice to establish a definitive diagnosis is intradermal skin testing. This test is best performed by a boarded dermatologist because of the experience needed for allergen selection, administration and interpretation of the test.

8. Approximately 50 allergens are usually tested when doing intradermal skin testing. The allergens are injected intradermally with a small gauge needle. A positive test is when there is a wheal with a diameter equal to or larger than half way between the control and the histamine. False positive reactions may occur due to irritant test allergens, poor technique and irritable skin. False negative reactions may occur due to failure to use appropriate challenge allergens or prior drug therapy (glucocorticoids, antihistamines, fatty acids).

9. Serological assays can also be done to detect levels of allergen specific IgE in the serum. This test cannot be used alone to diagnose atopy. Negative results likely rule out atopy, however positive results should be confirmed by intradermal skin testing.

10. Hypersensitivity threshold is when concurrent pruritic diseases are treated to lower the patients “pruritic threshold.” The concept of avoidance rests on the principle that if the allergen can be identified and avoided, this is the best treatment. Topical therapy for the atopic patient involves anti-prurutic shampoos and rinses and other topical antipruritic agents.

11. Medical therapy for the atopic patient includes glucocrticoids, anti-histamines and omega 3 fatty acids. Antihistamines work to prevent binding of histamine to the effector cells, however they are only effective if given prophylactically. The most common side effect of antihistamines is sedation. Omega 3 fatty acids are used to decrease production of inflammatory mediators. They are effective alone for control of pruritis in only about 15% of atopic dogs, but they can allow for a decrease in glucocorticoids or anti-histamine dose. Systemic glucocorticoids can be used to decrease inflammation but they should not be used long term. Anti-inflammatory doses of glucocorticoids in the dog are 0.5-1.5 mg/kg/day and 1-3 mg/kg/day for the cat.

12. Hyposensitization is recommended for the year-around atopic patient or for the patient that has an unsatisfactory response to medical therapy. Allergens are administered SQ in gradually increasing concentration over a 4-6 week period of time. This treatment is aimed at desensitizing the patient to the offending allergens. 50-80% of atopic dogs and cats can benefit from hyposensitization.

13. The typical inciting food allergen is usually a protein. Food allergies often develop to those foods most commonly fed. Oral tolerance breaks down by injured mucosa allowing penetration of antigens across the GI mucosa. A defect in local (GALT) immunity results in immunoglobulin synthesis and sensitization of peripheral lymphocytes. The Type 1 hypersensitivity reactions are mediated by

IgE induced degranulation of mast cells. The two most common food allergens in the dog and cat are beef and dairy. Patients with dermatologic manifestations often have a single food allergy.

14. Pruritis is the hallmark complaint with food allergies. The skin lesions can mimic any pruritic dermatosis, papules, pustules, crusts, plaques, wheals, erythema, excoriation and pigmentary changes may be noted. Secondary pyoderma, seborrhea, malassezia dermatitis and pyotraumatic dermatitis are common. Just like in the dog, the hallmark complain in the cat is pruritis. Skin lesions in the cat most often involve the head, face, pinna and neck. Self induced alopecia with or without skin lesions such as military dermatitis and eosinophilic granuloma may be seen. As food allergy can mimic any other pruritic dermatosis, it is prudent to rule out more common disorders. Neither serological assay nor intradermal skin testing is very helpful in the diagnosis of food allergies.

15. The method of choice for diagnosing food allergy is the dietary elimination trial.

16. The dietary elimination trial should be fed for 10-13 weeks. A highly digestible single protein source the patient has never been exposed to before and a simple easily digestible carbohydrate source is utilized. Cats should be kept indoors during the dietary trial so that they don’t consume possible allergens.

17. The hallmark sign of a positive response to the diet is a decrease in pruritis. The concept of a rotation diet with sacrificial protein source is that if an elimination diet is fed during a period of mucosal compromise the patient may develop a food hypersensitivity to that novel protein. Therefore the first protein source is considered sacrificial as it is fed when the bowel is inflamed and the patient may develop hypersensitivity.

18. The protein hydrolysate diet is based on the principle that the more complete the pre-digestion of a protein source, the less allergenic it is. In this diet the proteins are hydrolyzed to less than 10,000 daltons to escape detection by the immune system. It provides an alternative option to dietary elimination trial for diagnosis and treatment of food allergy. The most common ingredient in the protein hydrolysate diet is hydrolyzed chicken therefore it is not important to determine a novel protein source, any hydrolyzed protein should be non immunogenic. Hill’s hydrolysate diet is z/d.

19. The key component to the dietary elimination trial is to feed the elimination diet and nothing else for 10-13 weeks. A decrease in pruritis is a positive response to the elimination diet. Food allergy pruritis is often non responsive to most medical therapies. Omega 3 fatty acids may be helpful to reduce production of inflammatory mediators.

20. The feline eosinophilic granuloma complex is a cutaneous reaction pattern often associated with hypersensitivities. The feline indolent ulcer, eosinophilic

granuloma and eosinophilic plaque are the three disorders that occur under this title. Treatment involves addressing the underlying hypersensitivities and systemic glucocorticoids. Some refractory lesions may respond to antibiotics.

21. The clinical signs associated with canine eosinophilic granuloma are lingual masses or ulcerated palatine plaques. The classic signalment is a young male Siberian husky. These lesions often respond to glucocorticoid therapy.

IMMUNE MEDIATED DISORDERS

1. All of the immune mediated dermatoses are characterized by an inappropriate immune response. They are separated into two forms- primary and secondary. Primary or autoimmune is when the immune response is directed against normal body tissues. Secondary or immune mediated is when the inciting antigen is foreign, but the subsequent immunologic reaction destroys the host tissue. Immune mediated skin diseases are uncommon. They account for about 1.3% of dermatoses seen.

2. Skin biopsy and demonstration of characteristic dermatopathologic changes are necessary to establish a definitive diagnosis. Samples are best evaluated by a boarded dermatologist or by a veterinary pathologist with interest in dermatopathology. In order to obtain the best samples possible gently clip and minimally prep the area to be biopsied. Infiltrate SQ the area with 2% lidocaine. Using very gentle technique harvest multiple samples. Try to biopsy the newly formed lesions and avoid the secondarily infected lesions. Obtain these samples prior to placing the patient on steroids or other immunosuppressive drug therapy. Immunopathology (ie direct immunifluorescence) is not routinely performed. The basis for this study is that biopsy samples are evaluated for autoantibody within the skin. There is a high incidence of false positives as many other inflammatory dermatoses also yield positive results.

3. The key to treating these immune mediated skin dermatoses is the use of immunosuppressive agents. Systemic glucocorticoids are typically the initial drug of choice in the management of many immune mediated dermatoses. Immunosuppressive doses of glucocorticoids are usually required to induce remission of disease (Dog: 2-6 mg/kg/day; Cat 4-8 mg/kg/day). Once the patient has attained clinical remission, glucocorticoid therapy is slowly tapered. Some patients can be gradually weaned off steroids, however many patients need continued therapy to maintain clinical remission. Glucocorticoids alone are ineffective in some patients, whereas in other patients the undesirable side effects of glucocorticoids preclude its use. Azathioprine (Imuran) is often used in conjunction with glucocorticoids. It is typically the second additional agent of choice in the dog for treatment of immune mediated dermatoses. Chlorambucil is often used as the second agent of choice in cats for the management of immune mediated dermatoses. Chrysotherapy (gold salts) acts, by an unknown mechanism, to modulate both inflammatory and immune responses. Tetracycline

plus niacinamide has both anti-inflammatory and immunomodulatory properties, which makes it helpful in canine discoid lupus and pemphigus erythematosis. Vitamin E has anti-inflammatory and anti-oxidant properties, which may also be helpful in treating canine discoid lupus and pemphigus erythematosis. Photoprotection including applying sunscreen may help prevent secondary photodermatitis. Topical steroids may be beneficial in the treatment of focal inflammatory lesions.

4. Pemphigus is caused by the production of an autoantibdy to the normal components of the skin. The initiating trigger is unknown in most cases but genetic predisposition, chronic skin disease, drug provocation, UV light exposure, emotional upset or viral infection may play a role in some cases. The primary skin lesions are fragile and transient and consist of intraepidermal vesicles and bullae (p.vulgaris) and pustules (all other forms). The secondary lesions consist of erosions/ulcerations bordered by epidermal collarettes, crusting and alopecia. Variable pain, pruritis, lymphadenopathy and secondary pyoderma may be present. Some cases show nasal depigmentation and photodermatitis. The most severely afflicted animals may exhibit systemic signs such as fever, depression, and anorexia.

Pemphigus foliaceous is the most common immune mediated dermatosis in dogs and cats and the most common form of pemphigus. Characteristic findings include a predominantly pustular crusting dermatosis on the face and ears with uncommon mucocutaneous and oral lesions. Later lesions involve the feet and groin and can become generalized.

Pemphigus erythematosus shows similar clinical signs to P. foliaceous, however it seems to be a more benign form. Collies and German Shepherds are thought to be predisposed.

Pemphigus vulgaris is characterized by lesions that affect the oral cavity, mucocutaneous junctions and skin. This form is a severe, erosive to ulcerative dermatopathy often associated with systemic signs.

In the more severely afflicted patients, leukocytosis, anemia, hypoalbuminemia and hyperglobulinemia may be noted on lab work. Acantholytic keratinocytes are keratinocytes that are disrupted from their intracellular connections between the epidermis. The definitive diagnosis is made using histopathologic findings.

Pemphigus vulgaris and the severe forms of pemphigus foliaceous may be fatal without treatment. Treatment usually requires immunosuppressive drug therapy, however glucocorticoids alone are effective in only about 50% of cases. P. erythematous, P. vegetans and mild forms of P. foliaceous can often be managed with sun avoidance and topical steroids.

5. Bullous pemphigoid is a very rare autoimmune vesicobullous ulcerative disease. It is characterized by autoantibody production against an antigen at the basement membrane zone of skin and mucosa. Primary lesions invlude vesicles and bullae whereas the secondary lesions are similar to P. vulgaris. This disease tends to be

severe and associated with systemic signs. Immunosuppressive drug therapy should be used to treat Bullous pemphigoid and sun exposure should be avoided.

6. SLE is an uncommon multisystemic autoimmune disorder of dogs and cats. The etiology is multifactorial including genetic predilection, immunologic disorder, drugs, viral infection and hormonal or UV light modulation. Autoantibody production occurs against a variety of tissues. The tissue damage is mediated by a type 3 hypersensitivity reaction. The current hypothesis on the development of cutaneous lesions states that in genetically predisposed individuals, UV light may induce expression of sequestered antigens or keratinocytes. The injured keratinocytes then start an inflammatory response. Collies, Shetland sheepdogs and German shepherds are predisposed. Polyarthritis, proteinuria, anemia and fever are some of the more common systemic manifestations of SLE. SLE does occur in the cat but it is fairly rare. No single lab test is diagnostic for SLE. Screening bloodwork will show variable anemia, thrombocytopenia, hyperglobulinemia and proteinuria. The ANA titer will be positive in 90% of cases of SLE but many other diseases may also cause a positive titer. Treatment involves immunosuppressive drug therapy.

7. Discoid lupus erythematosus is an autoimmune dermatitis, which is thought to be a benign variant of SLE. It is the second most common immune-mediated dermatosis of the dog, but is rare in the cat. Photosensitivity may play a role in the pathogenesis since sun exposure aggravates the disease in 50% of cases. DLE is a relatively benign cutaneous disease with no systemic involvement. There is an increased incidence in the female with the collie, german shepherd, Shetland sheepdog and Siberian husky being predisposed. Skin lesions mostly occur on the face and less often the distal limbs and genitalia. The early signs often consist of nasal depigmentation, erythema and scaling, whereas later signs progress to erosions/ulcerations, secondary pyoderma, scarring and leukoderma. Nasodigital hyperkeratosis and punctuate oral ulcers are occasionally noted. Affected animals should avoid sunlight and have sunscreens applied. Topical glucocorticoids can be used for their anti-inflammatory effects, but immunosuppressive agents may be indicated for more severe cases.

8. Cutaneous drug reactions, erythemia mutiforme, toxic epidermal necrolysis and vasculitis can all be caused by exposure to a drug. These reaction can be mediated by type 1, 2, 3 or 4 hypersensitivity reactions. Drug reactions can occur with any drug but the sulfonamides, penicillins, cephalexin and levamisole are more commonly implicated.

9. Drug eruptions can occur within days or years of drug administration, can mimic an dermatosis and may be associated with oral, cutaneous or mucocutaneous lesions. Erythema multiforme occur acutely and are characterized by symmetrical erythematous macules or papules that spread peripherally and clear centrally.

There are two forms of erythema multiforme, E. minor and E. major. Toxic epidermal necrolysis is characterized by vesicles and bullae with secondary epidermal collarettes, ulceration and necrosis. Systemic signs of illness are often present. TEN is considered by some to be a continuation of or closely related to EM major. Vasculitis is uncommon in the dog and rare in the cat. The skin lesions are usually distributed along the vascular pathways and are characterized by palpable purpura, hemorrhagic bullae, necrosis and ulceration. Systemic signs of illness may also be present. Most cases of drug reactions and EM are mild in nature and will undergo spontaneous resolution within several weeks of removing the inciting trigger so an effort should be made to try to identify and eliminate the primary cause. Immunosuppressive doses of glucocorticoids may be helpful in cases of severe drug reactions and vasculitis, but not all cases will be responsive to glucocorticoid therapy. Supportive therapy may be needed for signs of systemic illness. The prognosis for EM major and TEN is guarded to poor because its similar to that of a patient with a massive second degree burn. The mortality is also higher where a causative trigger cannot be identified and eliminated.

10. Cold agglutinin disease is idiopathic but it is characterized by RBC auto-antibodies that bind at lower temperatures to cause hemagglutination. The cutaneous lesions result from vascular stasis and obstruction. Lesions are often precipitated by exposure to cold, which is why they usually occur on the distal extremities. The lesions are characterized by localized erythema, purpura, ulcers and necrosis.

11. VKH (Vogt-Koyanagi-Harada Syndrome) is an idiopathic disease that is thought to have an autoimmune etiology. The Akita, Samoyed and Siberian husky seen to be predisposed. This disease is characterized by depigmentation of the nose, lips, eyelids, footpads and anus and sometimes secondary photodermatitis. Granulomatous uveitis often occurs acutely and may be associated with blindness.

12. The clinical signs associated with feline plasma cell pododermatitis include multiple non-painful swellings on the footpads, which can become ulcerated and infected.

KERATINIZATION DEFECTS AND HEREDITARY DERMATOSES

1. Seborrhea is a keratinization defect that can be separated into primary or secondary groups by etiology. Primary seborrhea is an inherited disorder, most common in Cocker spaniels, springer spaniels, West highland white terriers and basset hounds. Secondary seborrhea is caused by any disease that alters normal epidermal growth or turnover. There are three distinct clinical forms of seborrhea, seborrhea sicca (dry form), seborrhea oleosa (oily form), and seborrhea dermatitis (inflammatory form).

2. Animals with primary seborrhea may have a dull coat, dry flaky skin, greasy malodorous skin, follicular casts and crusty pruritic patches. Ceruminous hyperplastic otitis externa, and digital hyperkeratosis may also be seen. Secondary seborrhea usually has signs of flakiness, greasiness, seborrheic dermatitis, ceruminous otitis externa or some combination. Seborrhea is diagnosed on physical exam.

3. Primary seborrhea is clinically indistinguishable from secondary seborrhea, in order to diagnose primary seborrhea all of the causes of secondary seborrhea must first be ruled out. In all cases the preliminary evaluation should include skin scrapings, cytology and DTM culture. As appropriate skin biopsy and evaluation of underlying allergies, systemic disease and endocrinopathies should be pursued. On skin biopsy marked keratinization defects should be noted in both forms of seborrhea. Primary seborrhea is a controllable but not a curable disease, however secondary seborrhea is a curable disease if the underlying cause is identified and resolved. The dry forms of seborrhea are easier to manage and should be treated with a topical shampoo that moisturizes the skin. For mildly flaky skin use a moisturizing hypoallergenic shampoo, but for more severe flaking sulfur and salicylic acid products or mild tar products may need to be used. The greasy forms of seborrhea are harder to manage. For the mild to moderate cases use a sulfur and salicylic acid or mild tar product, whereas for more severe cases use stronger tar products, selenium sulfides or benzoyl peroxides. These products can cause dry seborrhea if overused.

4. If topical therapy is ineffective or not possible there are several systemic therapies that can be tried. Retinoic acid, omega 3 fatty acids and glucocorticoids may be tried.

5. The most common type of seborrhea in the cat is secondary seborrhea sicca. It is diagnosed the same as in the dog. Treatment involves addressing the underlying cause, grooming and using a topical anti-seborrheic shampoo therapy. Do not use tar, selenium, phenol or quaternary ammonium compounds in cats due to their toxic effects.

6. The clinical signs of vitamin A responsive dermatosis is severe seborrhea and frequently concurrent otitis externa. It is characterized by hyperkeratotic plaques, dull haircoat, follicular plugging and rancid skin odor. This disease is found most often in cocker spaniels. Affected animals respond to oral Vitamin A, improvement should be noted within 3 weeks.

7. Nasodigital hyperkeratosis is a marked hyperkeratosis and epidermal hyperplasia of the nose and digits. It may occur due to hereditary keratinization defect in association with an underlying disease or it can be idiopathic.

8. Canine tail gland hyperplasia is when the oval tail gland area becomes swollen, alopecic, greasy, scaly, and hyperpigmented. In cats a local greasy accumulation with matted hairs, crusts, hyperpigmentation, alopecia and rarely infection may be noted. In dogs treatment involves castration (to decrease testosterone), local cleaning and rarely surgical management. Castration does not help in cats since this form is not testosterone driven. Local shampoo therapy and encouraging self-grooming is often enough to treat this disease.

9. Feline acne shows comedones as its initial signs. Papules, pustules, bacterial folliculitis and furunculosis may follow. Benign neglect may be enough for asymptomatic cases, whereas topical therapy should work for mild cases. The refractory cases may benefit from fatty acid supplements or oral isotretinoin.

10. Epidermal dysplasia of West highland white terriers is an uncommon condition in which affected dogs have epidermal dysplasia and an inflammatory dermatitis associated with Malassezia overgrowth. The lesions initially occur on the feet, legs and ventrum but later become generalized. Skin lesions are characterized by a greasy odiferous coat, then erythema, hyperpigmentation, lichenification and pruritis. Most cases are euthanized due to poor response to therapy.

11. Schnauzer comedo syndrome is a hereditary developemental dysplasia of hair follicles. The main lesion is multiple comedones that occur primarily on the back. Mild cases are typically managed with topical therapy with anti-seborrheic agents.

12. fMISCELLANEOUS DERMATOSES