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393 Cards in this Set
- Front
- Back
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Equine Pruritic Dermatitis |
-Most common reason for equine dermatologic exam |
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Ectoparasites on horses
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-Mites
-Lice -Fleas -Ticks |
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Mites on horses
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-Chorioptes (most common)
-Psoroptes -Sarcoptes -Demodex -Dermanyssus gallinae -Trombicula -Tyroglyphus |
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Lice on horses
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-Haematopinus asini (sucking louse)
-Damalinia equi (biting louse) -Most commonly appear in winter, unsanitary conditions, or in immunosuppressed horses |
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Chorioptic mange
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-Chorioptes equi
-Pruritic -Contagious to other horses -Most commonly occurs in winter months -Common in draft horses with feathered fetlocks -Affects Pasterns, abdomens, axillae, groin |
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Clinical signs of Chorioptic mange
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-Alopecia, scales, crusts
-Exudative, proliferative dermatitis with secondary infections -Stamping, rubbing, biting at affected areas -Crusts and scales within feathers of draft horses |
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Chorioptic Mange Diagnosis and treatment
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-History and clinical signs
-Superficial skin scrapings (multiple) -Clip affected areas and remove scales -Antiparasitics may be helpful --permethrin, fipronil spray, lime sulfur spray, ivermectin -Treat all animals in contact, may have asymptomatic carriers -Clean environment and dispose of bedding etc. --do not put animal back into infested environment |
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Pediculosis clinical signs
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-Lice
-Host-specific -varies animal to animal -Erythema, excoriations, focal alopecia -Anemia, especially in foals -Haematopinus asini is in mane, tail, limbs/fetlocks, or inner thighs -Damalinia equi affects head, neck, dorsum, dorsolateral trunk of animal |
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Diagnosis of Pediculosis and treatment
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-Clinical exam, may find eggs
-Microscopic exam to find eggs or adults -Treat in-contact animals, blankets, tack, etc. -Often have multiple horses affected, need to treat everyone -Antiparasitics --lime sulfur, permethrin, fipronil spray, systemic ivermectin (more effective for sucking lice) |
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Dermatophilosis in horses
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-Bacterial cause of pruritus
-Dermatophilus congolensis -Common bacterial cause of skin disease -Actinomycete gram+ bacteria -Looks like railroad tracks on cytology, chains of paired cocci -“Paintbrush” appearance of hairs, held together by crusts -Contagious! Need to properly dispose of crusts --chronically infected animals can act as carriers -Pathogenesis is not completely understood -Infective zoospores |
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Dermatophilosis predisposing factors
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-Presence of bacteria or carrier animal
-Humidity and moisture, fall and winter -Cutaneous trauma (insect bites) |
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Dermatophilosis Clinical presentations
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1. Rain rot/Rain scald: on dorsal trunk
2. Greasy heel/mud fever, pastern dermatitis: pasterns --hind more common than front 3. Focal lesions: face or perineum |
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Dermatophilosis Diagnosis
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-Cytology of minced crust
-Look for groups or branching chains, may see bacterial organisms -“Railroad tracks” -Bacterial culture: takes a long time to grow organism |
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Dermatophilosis Treatment
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-Depends on how severely the horse is affected |
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Staphylococcal Folliculitis
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-“Summer rash” “saddle sores” “summer eczema”
-Most common in summer months -Usually in sites where there is sweating or moisture trapping, sites where tack sits --breaks in skin barrier allow infection -Clinical presentation is variable --papules, scaling, crusting, alopecia -Diagnose via skin cytology, bacterial culture, biopsy |
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Staphylococcus follucilitis in horses common isolates
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-S. pseudointermedius
--not as common as it is in dogs --Isolated in skin and soft tissue infections -S. aureus -S. hyicus -S. delphini -S. xylosus and S. sciuri: non-pathologic, present on normal skin |
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Methicillin Resistant Staph Aureus in Horses
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-Normal horses may be colonized
--nasal passages are primary site of colonization --0-10.9% of horses are affected -Skin, joint, surgical infections -Genotype “USA 500” is most common in horses -Zoonotic infections! --veterinarians are at higher risk of MRSA |
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Treatment of Staphylococcal Folliculitis
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-Good hand hygiene |
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Dermatophytosis in Horses
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-Transmitted by affected animals or infected fomites (tack, brushes)
-Contaminated environment -Young or sick animals -T. equinum is most common --M. equinum, M. gypseum, T. mentagrophytes, T. verrucosum can also cause infections |
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Clinical signs of Dermatophytosis in Horses
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-Papules, wheals
-Alopecia, focal or multifocal -Crusting, scaling -Short, broken hairs -Pruritus is variable |
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Dermatophytosis in horses Diagnosis
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-History
-Clinical signs -Trichogram -Culture (and culture all in contact horses) --Add niacin for T. equinum for culture -Skin biopsy |
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Treatment for Dermatophytosis in horses
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-Many spontaneously recover in 2-3 months |
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Insect Hypersensitivty in horses
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-Most common cause of equine Pruritus
-Type I hypersensitivity: immune mediated, IgE mediated -Type IV hypersensitivity: delayed hypersensitivity -Seasonal disease, spring and summer more common -Recurrent -Familial predisposition -Inhalation and percutaneous absorption of allergens |
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Culicoides
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-Most common cause of insect hypersensitivity in horses |
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Insects causing hypersensitivity in horses
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-Culicoides (most common)
-Tabanus (horse fly) -Stomoxys (stable fly) -Stimulium (black fly) --associated with viral induced aural plaques -Haematobia (horn fly) -Chrysops (Deer fly) -Wasps, mosquitos |
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Clinical signs of Insect hypersensitivity
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-Primary lesions: papules and/or wheals (urticarial)
-most often secondary lesions are seen, animal is not seen until it gets bad --Alopecia, crusts, excoriations, hyperpigmentation, lichenification -Irritability, restlessness, weight loss -Secondary bacterial infections |
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Insect Hypersensitivity Diagnosis
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-History
-Clinical signs -Response to insect control -Intradermal allergy test and serology |
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Treatment of Insect Hypersensitivity
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-Avoidance:
--antiparasitics, fly control in feed or as topical repellent --permethrin products -Move animals away from standing water -Stable horses from dusk to dawn, keep horses in during culicoides feeding time -Fine mesh screens -Fans, keep flies off -Cover horses with fly sheets -Antihistamines (hydroxyzine, cetirizine) -Tapered dose of steroids (Prednisolone, dexamethasone) -Essential fatty acids -Hyposensitization, allergen-specific immunotherapy |
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Atopy in Horses
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-Type I hypersensitivity
--IgE and IgG mediated -Familial disposition, quarter horses, thoroughbreds, arabs, morgans -Age of onset 5-6.5 years -Initially recurrent seasonal signs, may progress to non-seasonal -Allergens -Forage mites -Molds -Pollens (trees, grasses, weeds) -Dust mites -Epithelials |
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Clinical signs of Atopy in Horses
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-Pruritus
-Secondary lesions --alopecia, excoriation, lichenification, hyperpigmentation -Urticaria (usually chronic) -Chronic bronchitis -head shaking -Tail rubbing |
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DDx for Atopy in horses
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-Ectoparasites
-Ear disease -Guttural pouch disease -Mycosis -Malassezia dermatitis -Vaginitis -Endoaprasites (pinworms) -Insect dermatitis |
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Diagnosis of Atopy in Horses
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-Diagnosis of exclusion
-Intradermal Allergy test on side of the neck --Can have irritant reactions in normal horses --Need experience to perform and interpret the test -Test for type I (immediate) hypersensitivity reactions AND Late-phase immediate hypersensitivity reactions (4-24 hours) -Blood allergy test (serology) --not as reliable in the horse as it is in small animals --Tissue bound IgE does not correlate with circulating levels --False positives |
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Treatment for Atopy in horses
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-Avoid or reduce allergen exposure, hard to do! |
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Food allergy dermatitis in Horses
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-Uncommon in horses
-Causes: cereals, hay, preservatives -Diagnose based on history and seasonality -Clinical signs: Urticaria, pruritus especially on tail/tailhead, GI sign -hard to do food trials in horses, but can do with food exclusion trial |
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Immune-mediated Causes of Urticaria in horses
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-Very common in horses
-Immune mediated -Food -Environmental allergens -Drugs: sulfa drugs, penicillins, phenylbutazone, insect control, topicals, dewormers -infections: strangles, encephalomyelitis -Systemic diseases -Insect bites, insect hypersensitivity (common) |
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Non-immune mediated causes of Urticaria in horses
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-Stimulate mast-cell degranulation without allergen specific IgE production
-Genetic factors -Physical factors --dermatographism (pressure induced hives) --cold temperatures -Physiological factors --exercise, stress-induced -Idiopathic is common |
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Clinical signs of urticaria in Horses
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-Can be focal or multifocal
-Variable in size -papular, giant, hyrate, exudative -Always look for pitting edema! --differentiates from erythema multiforme, no pitting edema with EM -Rapid in onset, come on quickly -Should fade in 48 hours, do not persist for long periods of time -Angioedema -Pruritus is variable |
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Diagnosis of Urticaria
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-History
--look for changes in environment or exposure to possible allergens -Clinical signs -Cold, pit on pressure (pitting edema) -Rule out physical factors -Skin biopsy if they are persistent -Intrademral allergy testing -RULE OUT ERYTHEMA MULTIFORME -Rule out physical factors |
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Treatment for Urticaria
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-1st episode: steroids
-Recurrent cases: identify predisposing factors -Immunotherapy if there is underlying atopy -Persistent form: steroids (prednisolone) --antihistamines |
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Pastern Dermatitis
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-“Grease heel” or “Scratches”
-One of the most common dermatologic diseases seen in horses -Diagnostic and therapeutic challenge -Descriptive term for a variety of diseases --predisposing, primary, and perpetuating factors --NOT a stand-alone diagnosis |
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Predisposing factors for Pastern dermatitis
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-Genetic
--non-pigmented skin --excessive hair --keratinization defect -Conformation -Environmental factors --moisture, stable/pasture hygiene -Iatrgoenic factors: --topical medication --tact -Neoplasia: sarcoids, squamous cell carncinoma |
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Primary factors for pastern Dermatitis
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-Physical or chemical irritants
--blistering agents, creosote, chemically treated bedding causing contact dermatitis -Immunologic --contact allergy --photosensitization --vasculitis --pemphigus -Primary infections: --dermatophytosis --spirochetosis -parasites: --Chorioptes --Pelodera --strongyloides --Habronemiasis |
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Perpetuating factors causing pastern dermatitis
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-bacterial infections (staph, Dermatophilus)
-Chronic changes -Proliferative tissue formation --trauma, insect, granulation tissue, fibrosis -Treat underlying cause!!! |
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Photosensitization and pastern dermatitis
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-UV light (UVA) activated photodynamic agents within the skin
-Non-pigmented skin is most commonly affected, lack of melanin protective effect --Face and limbs -Production of free radicals --circulate through vessels, cause local tissue injury --erythema, pruritus, edema, fissure formation |
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Types of Photosensitization and pastern dermatitis
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1. Primary photosensitization
2. Hepatogenous photosensitization 3. Sensitization due to abnormal pigment synthesis (porphyria) 4. Contact sensitization: most common with exposure to clover pastures --photoactivated alkaloids |
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Primary photosensitization in horses
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-Ingestion of plants containing photo-activated alkaloids
-St. John’s wort -Buckwheat -Perennial ryegrass -Medications/chemicals --potentiated sulfonamides, tetracycline |
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Hepatogenous Photosensitization
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-Accumulation of chlorophyll metabolite, photodynamic metabolite
--Phylloerythrin -Primary liver disease (liver failure, neoplasia, abscess) -Ingestion of plants containing pyrrolizidine alkaloids --alsike clover, fireweed, ragwort, kale |
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Pastern Leukocytoclastic Vasculitis
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-Photo-activated/aggravated vasculitis
-Leukocytes have broken apart -Exudative dermatitis and crusting, limited to the distal extremities and pastern -Non-pigmented skin is more susceptible --can target pigmented skin as well -Type III hypersensitivity reaction, immune complex deposition |
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Diagnosis of Photosensitization in horses
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-History
-Change pastures for more than 2 weeks --ingesting new agent that could contribute to photosensitization -Clinical signs -Biochemistry profile, systemic health -Skin biopsy |
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Treatment for Photosensitization in horses
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-Prevent exposure to sunlight
--stable horse, wrap horse -Avoid exposure to photodynamic agents -Antibiotics -Pentoxifylline for vasculitis --softens RBC membranes, makes them more deformable --lets RBCs into ischemic areas -Steroids, higher doses for Pastern leukocytoclastic vasculitis |
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Sarcoidosis
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-Rare, severe, multisystemic granulomatous disease
-Pathogenesis may be due to response to self-antigen --mostly unknown pathogenesis -No infectious agent identified -Lesions can develop on face, legs, trunk, progress to generalized form |
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Systemic signs of Sarcoidosis
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-Fever
-Weight loss -Anorexia -Exercise intolerance -Scaling and crusting form, with or without alopecia (most common) -Nodule form (rare) |
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Internal organ involvement of sarcoidosis
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-Granulomas in lungs (most common)
-Lymph nodes -GI tract -Liver -Kidneys -May contribute to clinical signs |
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Diagnosis and treatment of Sarcoidosis
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-Histopathological diagnosis
-Mild form may spontaneously resolve --may wax and wane -Come cases respond to immunosuppressive corticosteroids or systemic antibiotics -Prognosis decreases with severe systemic involvement --overall prognosis is poor |
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Pemphigus Foliaceus in horses
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-Most common autoimmune disease in the horse
-Autoantibodies target desmosomal agents -Occurs in adults over 5 or foals under 1 --bimodal presentation -Appaloosa, thoroughbreds, and quarterhorses are predisposed |
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Clinical signs of Pemphigus Foliaceus in horses
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-Intact pustules (rare)
-Crusting (more common) -Alopecia -Lesions can be diffuse or localized --coronary band is common site -Systemic clinical signs: depression, weight loss, anorexia -ventral pitting edema is common |
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Pemphigus foliaceus in Horses Diagnosis and treatment
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-Diagnose via cytology, definitive diagnosis via histopathology
--look for acantholytic keratinocytes -Need to rule out dermatophytosis before treatment --fungal culture -Response to therapy varies based on age of onset -Young horses: may spontaneously resolve -Older horses: may need immunosuppressive corticosteroids, pentoxifylline --May need to be treated for life --worry about laminitis! Pentoxifylline may increase blood flow and avoid laminitis |
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Non-pruritic Alopecia in horses
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-Alopecia areata
-Mane and tail dysplasia -Anagen/telogen defluxion -Follicular dysplasia -Injection reaction -Selenium toxicosis |
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Alopecia Ateata in horses
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-Immune-mediated disease
--CD4 and CD8 T-lymphocytes and auto-antibodies against hair follicle -Breed predisposition in Appaloosa and quarterhorses -Lesions are a non-progressive alopecia, skin looks smooth -NOT pruritic -Face, mane, tail, trunk -Can wax and wane -Diagnose via histopathology --hard to catch disease in active phase --bulb of hair follicle is infiltrated by lymphocytes, “swarm of bees” |
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Nodular Diseases in horses
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-Eosinophilic granuloma
-Dermoid Cysts -Unilateral popular dermatosis -Axillary nodular necrosis -Amyloidosis -Sterile nodular panniculitis/steatitis |
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Eosinophilic Granulomas in Horses
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-Most common non-neoplastic nodular skin disease in horses |
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Diagnosis of Eosinophilic Granuloma
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-Fine needle aspirate |
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Metabolic diseases affecting the skin
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-Superficial necrolytic dermatitis
-Zinc responsive dermatosis -Vitamin A responsive dermatosis |
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Superficial Necrolytic Dermatitis
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-AKA Metabolic epidermal necrosis, necrolytic migratory erythema
-Caused by hepatocutaneous syndrome or glaucoma syndrome (rare) -Can affect any dogs -Skin lesions due to underlying metabolic disease -Profoundly low circulating amino acids -Low serum albumin -Increased liver enzymes, increased blood glucose are possible -Abdominal ultrasound of liver will look “swiss cheese” or “honeycomb” --liver looks mottled -Diagnose via biopsy of paw pad |
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Zinc responsive Dermatosis
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-Nordic dogs/arctic dogs
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Vitamin A dermatitis
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-Cocker spaniels
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Cat Paraneoplastic syndrome
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-2 options
--due to thymoma --due to carcinoma in pancreas, biliary tract (pancreatic paraneoplastic alopecia) |
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Dog Paraneoplastic Syndrome
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-Not that many well-defined skin conditions
-Paraneoplastic pemphigus -Erythema multiforme -Nodular dermatofibrosis of german shepherd dogs |
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Superficial necrolytic Dermatitis Presentation
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-Present for lameness! And not feeling well
-Hyperkeratosis along margins of paw pads -Will see erosions, ulcerations -NOT allergic skin disease, this is on the paw pads -Localized |
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DDx for lesions on paw pads
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-Pemphigus foliaceus (vulgaris is mucus membranes)
-Cutaneous T-cell lymphoma -Caustic contact dermatitis -Adverse drug reaction, erythema multiforme -Superficial necrolytic dermatitis |
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Causes of Superficial necrolytic Dermatitis
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1. Hepatic metabolic dysfunction, hepatocutaneous syndrome
-low circulating amino acids -Common 2. Glucagonoma -rare -Differentiate based on skin biopsy, biopsy is usually diagnostic |
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Pathogenesis of Superficial necrolytic dermatitis
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-Underlying hepatocutaneous syndrome or glucagonoma results in increased catabolism of amino acids
--decreased amino acids in circulation -Results in nutritional deprivation of skin, leads to altered cornification and necrosis -Failure to form a normal stratum corneum, response is parakeratosis --nucleated keratin, abnormal cornificaion |
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Superficial necrolytic Dermatitis Skin lesions
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-Footpads are always affected
--hyperkeratosis with erosions/ulcers --crusting with surrounding alopecia, usually on footpad margins -Mucocutaneous junctions --lips, eyes, nail folds, anus, scrotum -Secondary bacteria, malassezia, candida |
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Hepatocutaneous Syndrome
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-Dogs, 10 years or older
-Small breed dogs are over-represented -Lameness, lethargy, anorexia, weight loss -PU/PD may be present -History of anti-convulsant therapy may be present -Rarely seen in cats, clinical presentation in cats is not consistent |
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Features of Hepatocutaneous Syndrome
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-Increased liver enzymes, increased bile acids
-Decreased albumin -Hyperglycemia, may see diabetes mellitus -Skin biopsy shows red-white-blue, parakeratosis --necrosis in spinous layer -Hepatic ultrasound shows “swiss cheese pattern” -Specific vacuolar hepatopathy on liver biopsy |
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Glucagonoma Syndrome
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-Identical lesions to hepatocutaneous syndrome
-Extremely rare, only a few cases reported -heaptic ultrasound should be normal -Functional tumor of alpha islet cells --hyperglycemia, increased breakdown of glucose stores -Diagnose via exploratory laparotomy |
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Glucagon
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-Catabolic
-Maintains glucose levels during states of metabolic stress --liver gluconeogenesis --glycogenolysis, inhibits glycogen synthesis -Promotes amino acid catabolism -Glucagonoma results in protein deficiency results in impaired cornification |
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Prognosis of Superficial necrolytic Dermatitis
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-BAD
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Superficial necrolytic Dermatitis treatment
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-Treat secondary infections with topicals or soaks
-Nutritional therapy --increase dietary protein intake, give egg whites -Supplement with zinc and fatty acids -IV amino acid therapy |
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Zinc Responsive Deramtosis type I
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-Mild disease of arctic breeds
-Stress exacerbates lesions? -Usually affects young dogs -Genetic defect -Hyperkeratosis, crusts, and erythema -Usually periocular or perioral --can also affect pressure points, footpads, pinnae, nasal planum -Biopsy is diagnostic --do not scrub before biopsy -Hard to recognize, need to do dermatologic database -Easy to treat! |
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Zinc Responsive Dermatosis Treatment
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-Zinc supplementation
--Zinc methionine is usually most effective, dose on elemental zinc --zinc gluconate --zinc sulfate can be used, but might cause vomiting and diarrhea -Fatty acid supplementation may be helpful -Treat secondary skin infections -Minimize stress |
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Zinc-responsive dermatosis type II
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-Can occur in any breed
-“Generic dog food disease” -Large-breed dog on a crappy diet -High cereal diet results in poor zinc absorption due to high phytate --phytate binds to zinc -Excessive calcium supplementation prevents zinc absorption |
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Vitamin A responsive Dermatosis
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-Not a true deficiency
-Cocker spaniels, occasionally other breeds are affected -Adult-onset -Hyperkeratotic plaques on ventral and lateral chest and abdomen --can be very big -Greasy hair coat, ceruminous otitis, follicular plugging -Follicular casts -Treatment: give vitamin A! |
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Feline Paraneoplastic Syndrome
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-Paraneoplastic pancreatic alopecia
-Thymoma-associated dermatosis -May see interface dermatitis -Take chest X-ray, may see thymoma (mass in cranial mediastinum) --remove thymoma and condition improves, can be cured |
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Thymoma
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-Epithelial tumor that arises in thymus
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Thymoma associated dermatitis
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-Middle aged to older cats
-Erythema with marker hyperkeratosis --large sheets of scaling -Easily exfoliated hair -Skin lesions precede systemic signs -May or may not have respiratory signs, are usually subtle --cough, dyspnea, lethargy, weight loss -Skin biopsy shows interface dermatitis with keratinocyte apoptosis and hyperkeratosis --Biopsy is NOT diagnostic! Need to do chest X-ray -Treat by removing thymus --skin lesions regress if thymoma is excised |
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Pathogenesis of Thymoma associated dermatitis
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-Thymoma cells produce populations of auto-reactive CD4 T-cells
-CD4 T-cells attack keratinocytes |
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Thymoma associated dermatitis DDx
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-Erythema multiforme
-Sebaceous adenitis -Cutaneous lymphoma -Severe ringworm -Biopsy cannot distibguish erythema multiforme from thymoma associated dermatitis |
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Paraneoplastic Pancreatic Alopecia
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-Skin disorder that develops on conjunction with pancreatic exocrine carcinoma
-Causes animal to lose all hair on the ventrum -Old cats -Ventrally distributed symmetrical alopecia -Glistening sheen to the skin -Paw pads may be dry or scaly -Excessive grooming -Weight loss, lethargy, inappetence -Removal of tumor may cause clinical signs to decrease, but tumor may be metastatic at time of diagnosis -Unknown pathogenesis |
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Feline Pancreatic Paraneoplastic Alopecia DDx
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-Demodex gatoi
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Canine Paraneoplastic Syndromes
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-Paraneoplastic syndromes are rare in dogs
--paraneoplastic pemphigus --Erythema multiforme --Nodular dermatofibrosis and renal carcinomas -Chemotherapy-induced alopecia |
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Nodular Dermatofibrosis of the German Shepherd Dog |
-Multiple fibrous nodules in the dermis and subcutis |
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Scaling
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-“Dandruff”
-Need to find out if it is a primary scaling or secondary scaling -Primary: heritable problem in ability to form top layer of skin --uncommon --only diagnose if all other DDx have been ruled out --not many treatments! -Secondary scaling disorders: everything else (80%) --treat underlying cause |
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Cats with Severe scaling
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-Have some underlying condition
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Dog with Severe Scaling
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-Need to know signalment
--usually young, pure-breed dog -History is important, but take with a grain of salt -Lesion type and pattern can indicate the type of disease --subtle things change appearance -Can be localized or generalized |
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Crust vs. Scale
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-Crusts: cell debris, erosions
--pyoderma -Scales: dandruff --follicular casts |
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Follicular Cast
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-Primary lesion of sebaceous adenitis
-Hair shafts are annealed by keratin |
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Minimum Dermatologic database
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-Skin scrapings
-Impression smears --help differentiate scale vs. crust -Dermatophyte culture -Cytology of direct impression or tape impression -Trichogram -Skin biopsy if needed |
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Parasite causing generalized scaling
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-Cheylitiella
-Very superficial |
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Process of Cornification
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Modified form of programmed cell death
-Keratinocytes undergo dramatic change in shape, size, and function -Abnormalities in cornification lead to hyperkeratosis, clinical scaling, and decreased barrier function |
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Epidermal anatomy layers
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1. Corneal layer
2. Granular cell layer 3. Spinous layer 4. Basal cell layer |
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Cornification steps
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1. Lipid formation
2. Dissolution of nucleus and organelles 3. Aggregation of intermediate filaments 4. Formation of cornified envelope 5. Desquamation |
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Disorders of Cornification
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-Stratum corneum abnormalities: altered barrier function
--loss of integrity or elasticity --water loss --inflammation --pathogen entry |
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Secondary disorders causing scaling
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-Allergies
-Parasites -Metabolic -Endocrine -Infectious -Autoimmune |
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“Seborrhea”
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-“Excessive scaling”
-Often misused term -Primary and secondary seborrhea -Cannot use character of scale as sole basis of therapy --use history, PE, dermatology database to determine cause and make therapeutic choices |
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Clinical aspects of Seborrhea
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-Seborrhea sicca: dry scaling
--dull, dry coat with grey to white scale -Seborrhea Oleosa: greasy scaling --malodorous greasy coat --abundant keratosebaceous debris -Seborrheic dermatitis --scaling with skin infection |
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Causes of Generalized scaling
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-Flea infestation
-Demodicosis -Scabies -Dermatophytosis -Endoparasitism -Pyoderma -Malassezia |
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Diagnosis of generalized scaling
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-Flea comb
-Skin scrapings -Ivermectin trial -Wood’s lamp -Fecal -Check for pyoderma and malassezia -Skin biopsy! |
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Pruritic Scaling
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-Flea allergy
-Atopy -Food allergy, do dietary trial -Scabies, cheyletiella, do scraping, tape impression, response to treatment |
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Non-pruritic scaling
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-Hypothyroidism
-Hyperadrenocorticism (cushing’s) -Metabolic disease -Demodicosis -Sex hormone abnormality -Pemphigus foliaceus -Skin lymphosarcoma -Low humidity moisturizer |
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Primary cornification disorders
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-Primary idiopathic seborrhea
-Sebaceous adenitis -Vitamin A responsive dermatiosis -Zinc responsive dermatosis -Schnauzer comedo -Ichthyosis |
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Primary disorders of Cornification in Dogs
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-Primary idiopathic seborrhea
-Ichtyosis -Sebaceous adenitis -Schnauzed comedo syndrome -Nasodigital hyperkeratosis -Ear margin dermatosis -Vitamin A and Zinc responsive (metabolic) -Acne -Epidermal dysplasia syndrome |
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Breeds disposed to Canine Primary Idiopathic Seborrhea
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-Cocker spaniel
-English springer spaniel -Basset hounf -WHWT -Doberman -Lab -Irish setter -Chinese shar Pei -German Shepherd -Dachshund |
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Breeds predisposed to Feline Primary Idiopathic Seborrhea
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-Persian
-Himalayan |
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Breeds predisposed to Ichthyosis
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-Golden retriever
-Americal bulldog -Jack Russell terrier -Norfolk terrier -Rhodesian Ridgeback -WHWT -Yorkshire terrier |
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Ichthyosis
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-Inability to form normal stratum corneum
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Sebaceous Adenitis type I
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-Long-coated dogs, poodles
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Sebaceous Adenitis type II
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-Short-coated dogs, vizsla
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“Epidermal Dysplasia”
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-No longer considered cornification defect, actually a severe hypersensitivity reaction
-WHWT -Hypersensitivity to environmental allergens, food, malassezia |
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Primary Idiopathic Seborrhea in Dogs
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-Not a well-defined disorder
-Old terminology, most cases are classified into other disorders -Overlap with vitamin A responsive dermatosis |
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Goldern Retriever Ichthyosis
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-Mild form of ichthyosis
-Abnormality of lipid processing --genetic? Autosomal recessive? -Large white scales, dogs are “walking snow globes” -Diagnosed in puppies and adult dogs -Relatively common -Pigmentation ventrally, large white scales dorsally -Need to rule out sebaceous adentitis -Biopsy is diagnostic |
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Treatment for Golden Retriever Ichthyosis
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-Do not need to workup for allergic skin disease
-Oil baths with keratolytic rinses (topical therapy) |
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American Bulldog Ichthyosis
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-Keratin causes hair shafts to stand on end
-Can see in very young puppies -Ventrum has burnt orange appearance, looks like allergic skin disease -Associated with abnormal lipid? -May become pruritic due to development of Malassezia dermatitis -Follicular casts are common -More severe form of ichthyosis than golden retriever -Hyperkeratosis |
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Jack Russell Terrier Lamellar Ichthyosis
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-heritable disease
-Defective cornified envelope due to transglutaminase defect -Lots of scaling -Young dogs, puppies -Severe form of ichthyosis, “dinner plate” scales |
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Sebaceous Adenitis
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-Disease of standard poodles
-Immune mediated attack on sebaceous glands -has been diagnosed in 52 breeds, can happen in any dogs -lesions start on dorsal midline near face, extends back across dorsum -Scales are “silvery” -Owner complains of excessive dandruff, animal smells bad, mildly itchy -Not prednisone responsive |
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Sebaceous Adenitis DDx
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-Pyoderma
-Demodicosis -Dermatophytosis -Sebaceous adenitis -Pemphigus foliaceus -Idiopathic seborrhea |
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Diagnosis of Sebaceous Adenitis
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-Skin scrapings
-Impression smears -Dermatophyte culture/Wood’s lamp -Trichogram -Skin biopsy -CBC/Chem screen -Histopathology is Diagnostic |
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Sebaceous Adenitis Signalment
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-Young adult dogs
-Standard poodle -Vizsla -Dachshund -Akita, very greasy with marked pyoderma -Chow chow -Samoyed -Divided into type I and type II |
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Pathogenesis of Sebaceous Adenitis
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-Poodle: autosomal recessive
-4 theories --developmental and inherited defect --immune-mediated attach on sebaceous glands --keratinization defect with secondary sebaceous duct obstruction --abnormal lipid metabolism |
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Type I Sebaceous Adenitis
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-Long-coated breeds
-Sebaceous glands are rapidly destroyed -Partial alopecia with scaling that begins on dorsal midline, dorsal nasal planum, head, and neck --progresses caudally -Dull, brittle hair with tightly adherent silvery white scale -Follicular casts -Secondary pyoderma may develop |
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Type II Sebaceous Adenitis
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-Vizsla and other short-coated breeds
-Slow sebaceous gland destruction -Minimal progression of disease -Patchy areas of hair loss that looks like folliculitis -Lesions will begin on head and pinna, progress to truncal area -Typically has more granulomatous inflammation in sebaceous gland region |
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Treatment of Sebaceous Adenitis type I
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-Oil therapy
-Oral fatty acids -Keratinolytic shampoo -Moisturizers -Prednisone is NOT effective |
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Treatment of Sebaceous Adenitis Type II
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-Fatty acid supplementation
--omega-3, Omega-6 -Synthetic retinoids -Cyclosporine -Prednisone is NOT effective |
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Nasodigital Hyperkeratosis
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-Older dogs
-Increased horny tissue projecting from and adherent to footpad or nasal planum |
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Familial Footpad Hyperkeratosis
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-Rare, restricted to footpads
-“Elephant feet” due to production of keratin |
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Nasal parakeratosis of Labrador retrievers
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-Young dogs, less than 1 year
-Looks like discoid lupus -Tx: Vaseline -biopsy is diagnostic |
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Ear margin Seborrhea
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-Common in Dachshunds, can be seen in ohther breeds
-Scaling and follicular casts along ear margin |
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Schnauzer Comedo
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-Big blackheads on dorsal thorax
-Not common anymore |
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Canine Acne
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-Short-coated breeds
-Common in young adults -Chin and lips -Ingrown hairs -Probably not a true disorder or cornification -more likely due to traumatic insult that leads to folliculitis and furunculosis |
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Feline chin Acne
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-Disorder of follicular cornification |
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Feline Idiopathic Facial Dermatitis |
-Persian and Himalayan cats |
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Erosion
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-Disruption of the epidermis
-Pathologic process leading to a lesion -Any process causing loss of keratinocyte cohesion, adhesion to the basement membrane, apoptosis, or necrosis |
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Ulcer
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-Disruption of the epidermis and basement membrane, with exposure of the dermis
-Any physical, chemical, inflammatory, ischemic, or structural damage that leads to disruption of the dermal-epidermal junction, complete necrosis of the epidermis, or necrosis of the underlying dermis or subcutis |
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Self-tolerance
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-Mediated by B-cells and T-cells
-recognize “self” proteins as non-threatening -No reaction to selg |
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Loss of Self tolerance
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-Genetic predisposition
-Antigenic mimicry, self-protein and antigen are very similar -Traumatic alteration of immune privileged proteins -Hormonal influences -UV light exposure |
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Pemphigus Complex
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-Group of 4 autoimmune diseases of the skin
-Affect epidermis -Epidermis= brocks, mortar, and steel rods --keratinocytes=bricks --intracellular lipid= mortar --desmosomes= steel rod reinforcements |
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Desmosomes
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-Specialized intercellular junctions
-Provide adhesion between keratinocyrtes -Composed of 3 types of proteins --desmogleins, desmocollins, plakophilin -Anti-antibodies against adhesion molecules cause desmosomes to break apart --keratinocytes separate -Intrinsic factors: genetics -Extrinsic factors: drug reactions, infections, neoplasia |
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Pathophysiology of Pemphigus
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-Autoantibody is generated towards specific desmosomal adhesion molecules
--Dogs: DSC1 (p. foliaceus) DSG3 (p. vulgaris) -Binding of autoantibody to extracellular epitope on Dsg molecule sends intracellular signal for release of proteinases (plasminogen) -Structural integrity is disrupted, desmosomal function is weakened -Causes intercellular separation --acantholysis --keratinocytes separate from each other, forms clefts |
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Acantholytic cells
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-Orphaned keratinocytes
-Separated from other keratinocytes -Seen with pemphigus diseases |
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Pemphigus foliaceus and pemphigus erythematosus
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-Superficial disease
-Acantholysis and clefting occurs within granular cell layer -Limited to the skin -DSC-1 in dogs -DSG-1 in humans -Cleft fills with pus, form pustules -Intra-epidermal pustule, sub-corneal -Acantholytic cells in pustule |
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Pemphigus vulgaris and pemphigus vegetans
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-Acantholysis and clefting occurs just above the basal cell layer
-In skin and mucus membranes -Deep autoantibody target --DSG-3 -Basal cells remain attached to the basement membrane --forms “row of tombstones” histologically |
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History of Pemphigus diseases
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-Occur in wave-like fashion
-Often begin on face and progress caudally in a wave-like fashion -Acute flare-ups occur within hours or overnight -Intrinsic cyclicity bay be observed, especially in cats --can almost predict when animal will have a flare-up -Relationship to season and UV light exposure --sunny climate and high elevation |
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Clinical Presentation of Pemphigus
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-Lesions in sparsely haired areas
-Lesions can begin as pustules centered on erythematous macules -Pustules are very fragile, rupture and dessicate to form superficial crusts --hard to find intact pustules -Traumatic removal of crusts results in erosions --“Nikolsky sign” -Large diameter pustules -Suppurative crusts and depigmentation are hallmark -Painful erosions with removal -Facial involvement includes muzzle, pinnae, periocular skin --“pemphigus mask” -Localized pustules are possible, especially in groin and axillae --DDx: bacterial pyoderma, need to do pustule cytology to differentiate -Footpad lesions may be only clinical sign in some dogs -May rapidly progress to more generalized disease |
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Drug-induced Pemphigus foliaceus
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-Triggered by application of spot-on topical flea/tick products
-Promeris-duo, Certifect, and Vectra 3D -No known single active ingredient -Lesions may occur in localized drop pattern or may be generalized pattern -Immunosuppressive therapy may be required --may only be needed temporarily |
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Clinical Presentation of pemphigus in Cats
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-Facial, periocular, and pinnal lesions are common
-May also have footpad lesions -May be localized to nail beds or periocular skin -Can look like mosquito-bite allergy -Need to do cytology to definitively diagnose |
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Pemphigus DDx
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-Other pustular, scaling, and crusting diseases
-Varies according to species -infectious (bacterial, fungal) -Parasitic (demodicosis) -Zinc-responsive dermatosis (dogs only) -Mosquito bite hypersensitivity (cats) -Herpes facial dermatitis (cats) |
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Diagnosing Pemphigus Foliaceus
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-History and physical exam
-Direct impression smear of exudate --acantholytic cells with neutrophils and no bacteria -Dermatophytosis and severe pyoderma can also produce acantholytic cells -May be contamination by secondary bacterial overgrowth --presence of bacteria does NOT exclude diagnosis of Pemphigus -NEED BIOPSY CONFIRMATION FOR DIAGNOSIS! |
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Confirming a diagnosis of Pemphigus
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-Histopathology is the only reliable method for definitive diagnosis
-Site selection and technique are very important --lesions lave “lifespans,” old, dried crusts are least productive place -Best is pustules or moist crusted lesions -Sometimes old dry crusts contain acantholytic cells, even when there is no active epidermal clefting -Immunohistochemistry and immunoperoxidase tests are NOT useful for diagnosis of Pemphigus in animals --too unreliable |
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Pemphigus Erythematosus
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-Features of lupus erythematosus and pemphigus foliaceus
-Lesions across face in “butterfly” pattern -In dogs and cats, animal is rarely anti-nuclear antibody positive --lesions are usually limited to the face --histopathology has features of lupoid inflammation |
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Pemphigus Vulgaris
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-Separation occurs at apex of basal keratinocytes
-Lesion is a vesicle or bulla -Non-suppurative exudate -Clinically distinguishable from pemphigus foliaceus by bullae/ulcers vs. pustules/crusts -Acantholytic cells are stuck on basement membrane -May affect mucus membranes, especially oral cavity -MUCH less common than pemphigus foliaceus |
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History and clinical signs of Pemphigus vulgaris
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-Acute onset
-Oral ulcers may cause halitosis or ptyalism -Painful -Anorexia, pyrexia, depression -Vessicles or bullae rulture to form ulcers -Nails may slough off -Nikolsky sign, can peel skin off near lesion with gentle pressure -Usually have oral lesions -Footpads and face are common sites for lesions |
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DDx for Pemphigus vulgaris
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-Other bullous diseases
-Ulcerative drug reactions -Other causes of ulcerative stomatitis --uremia, viral diseases -Mosquito bite hypersensitivity (cats) -Herpes facial dermatitis (cats) |
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Diagnosis of P. vulgaris
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-Cytology: aspirate of vesicular fluid when available
--may have acantholytic cells -Histopathology: suprabasilar clefting --“row of tombstones” |
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Pemphigus vulgaris therapy
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-Often needs more aggressive immunosuppressive therapy than Pemphigus foliaceus
-Combination regimes are always recommended -Prognosis is usually guarded -Some cases can do well, despite bad reputation |
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Bullous Pemphigoid and Cicatrical pemphigoid
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-Autoimmune diseases that disrupt dermal-epidermal junction
-Autoimmunity against specific molecules within the hemidesmosomes -Hemidesmosomes are attacked by immune system -Structure that thethers epidermis to dermis is defective -Vesicles rupture to create ulcers -Looks identical to Epidermolysis Bullosa acquisita |
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Epidermolysis bullosa acquisita
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-Autoimmune disease that disrupts dermal-epidermal junction
-Acquired immune disease -Mostly affects great danes -Autoimmunity against type VII collagen (anchoring fibrils) -Deep lesions, rupture to create ulcers -Looks identical to Bullous pemphigoid |
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Canine Uveodermatologic Syndrome
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-VKH-like syndrome
-Autoimmunity to melanin and melanocytes of pigmented epithelium -Dogs develop inflammation of skin and uveal tract -Most common in arctic breeds/northern breeds --siberians, akitas, samoyeds -No age or sex predilections |
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Clinical features of Canine Uveodermatologic Syndrome (VKH)
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-Acute onset of uveitis
--Photophobia, squinting, corneal edema -Concurrent depigmentation of nose, eyelids, footpads, genital skin -Erosions and ulceration/crusting may develop -Detmatitis without uveitis is uncommon --Be sure to check eyes carefully! Look for uveitis and glaucoma --If there are no ocular lesions, consider discoid lupus |
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Diagnosis of Canine Uveodermatologic Syndrome (VKH)
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-History, breed, clinical signs
-Skin biopsy is needed to differentiate from lupus and pemphigoid diseases -Ocular pathology should how granulomatous panuveitis and retinitis --may see secondary glaucoma |
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Treatment of Canine Uveodermatologic Syndrome (VKH)
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-Eyes: refer to ophthalmologist!
--Cycloplegics and subconjunctival glucocorticoids -Skin: prednisone and azathioprine together in combination |
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Therapeutics for Autoimmune dermatoses
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-Glucocorticoids
--topical or systemic -Cytotoxic agents --azathioprine, chlorambucil, cyclophosphamide -Chrysotherapy: gold salts --oral, parenteral, not used very often too expensive -Non-cytotoxic immunosuppression: --Cyclosporine A --Mycophenolate mofetil --Leflunomide |
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Current therapy in Dog for Pemphigus and VKH
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-Immunoregulatory therapy!
--oral prednisone or methylprednisolone -Topical glucocorticoids for localized lesions -Adjunct immunosuppressive agents --azathioprine --chlorambucil --cyclosporin (not greatly effective in dogs) --Topical tacrolimus -Systemic antibiotics directed against staphylococci greatly improves survival |
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Current therapy in Cats for Pemphigus and VKH
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-Immunosuppressive doses of glucocorticoids alone are often sufficient
--methylprednisolone or triamcinolone -Cyclosporine may be effective for maintenance -Chlorambucil has been traditional drug of choice -Oral gold salts are rarely used, too expensive -Topical corticosteroids for localized lesions -Azathioprine is NOT used in cats! Causes liver issues |
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Lupoid Syndromes
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-Discoid lupus erythematosus
-Exfoliative cutaneous lupus erythematosus of the german short-haired pointer -Vesicular cutaneous lupus erythematosus of the rough collie and Shetland sheep dog -Symmetrical lupoid onychodystrophy |
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Discoid Lupus Erythgematosus
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-Unknown mechanism
--likely autoimmune -Skin-limited form of lupus in humans -No progression to Systemic lupus erythematous in dogs -ANA negative -Poor clinical and histologic homolog to human disease -Early signs of depigmentation of nasal planum and alae -Loss of cobblestone architecture and erosions/crusting on nose -Chronic signs include erosion and ulceration and crusting of nasal planum --may progress to haired skin of the muzzle and lips -May affect periocular skin, footpads, genital skin -Photo exacerbater, avoid UV exposure during peak daylight hours |
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Discoid Lupus Erythematosus in Cats
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-VERY rare! One case
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Discoid Lupus Erythematosus in Dogs DDx
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-Mucocutaneous pyoderma
--give antimicrobial therapy before biopsy! -Pemphigus -Mycosis fungoides (T-cell lymphoma) -Drug eruption -Uveodermatologic syndrome |
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Skin Biopsy for Discoid Lupus Erythematosis
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-Interface dermatitis with pigmentary incontinence
--derma;/epidermal junction is obscured -Apoptotic keratinocytes -Thickening and vacuolization of basement membrane |
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Treatment for Discoid Lupus Erythematosis
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-Tetracycline/Niacinamide
-Topical glucocorticoids -Sunscreens, spf 30 or higher -Topical tacrolimus -Antioxidants, vitamin E and omega-3 fatty acids -Avid systemic steroids if possible! Cause tissue atrophy |
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Exfoliative cutaneous Lupus Erythematosis of German Short-haired Pointers
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-ONLY occurs in german short-haired pointers
-Autosomal recessive? -Marked scaling beginning on head/pinnae --progresses caudally, may progress to heavy crusting or ulcerations -Severe phenotype, may behave like a patient with systemic lupus --anemia, thrombocytopenia, lymphadenopathy, pyrexia --severe non-localized pain with back arching and altered gait -Diagnose via signalment and skin biopsy --Skin biopsy is very specific --lymphocytic interface dermatitis, mural folliculitis, loss of sebaceous glands, individual keratinocyte apoptosis |
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Therapy for Exfoliative Cutaneous Lupus Erythematosis
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-Palliative therapy with anti-seborrheic shampoos
-Immunosuppressive therapy --glucocorticoids, cyclosporine A -Severe phenotype has poor prognosis, many are euthanized due to lack of response to treatment |
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Vesicular Cutaneous Lupus Erythematosus of the Rough Collie and Shetland Sheepdog
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-Exclusive to collies and Shelties
-Presents as polycyclic erythema, with vesicles and erosions of glaborous skin -Vesicles rupture easily -Diagnose via signalment and skin biopsy --lymphocyte rich interface dermatitis, intra-basilar vesiculation doe to cytolysis of keratinocytes |
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Pathophysiology of Vesicular Cutaneous Lupus
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-Photoexacerbated!
-UV exposure causes translocation of Ro and La antigens from nucleus of keratinocytes to cytoplasm and cell membrane -Antigens cause antibody-dependent cell-mediated cytotoxicity |
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Treatment for Vesicular Cutaneous Lupus
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-U.V. avoidance and sunscreens
-Localized/topical immunosuppression --tacrolimus or pimecrolimus --glucocorticoids -May need systemic immunosuppression in severe cases --oral steroids in combination with azathioprine or cyclosporine -Keep animal out of direct light! |
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Symmetrical Lupoid Onychodystrophy
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-Idiopathic disease
-Mostly seen in large-breed dogs -Results in sloughing of the claws, all toes and feet! -Histology of affected tissue has “lupoid” indlammatory pattern -NO evidence that it is an autoimmune disease! -Histological changes are thought to be caused by ischemia -Small minority of cases respond to hypoallergenic diets -Can remove nail if it is hanging off, but do not want to pull off too early |
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Perianal Furunculosis/Fistula
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-Incompletely known pathophysiology
-Affects German shepherds, almost exclusively -No furunculosis involved, really just a fistula -Causes severe inflammation with fistulous tracts peri-anally -Dyschezia, tenesmus, pain, large bowel diarrhea |
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Treatment of Perianal Fistulas
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-Used to be a surgical disease, now surgery is just for cases that do not respond to medical treatment
-Immunosuppressive therapy with cyclosporine is standard -Topical tacrolimus can be used for mild cases or chronic maintenance -Secondary infections are rare --no antibiotic therapy is usually needed --Metronidazole may improve associated colitis in some cases -Must rule out dietary hypersensitivity |
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Cutaneous Vasculitis
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-Disease process characterized by inflammation and necrosis of blood vessels
-can be skin-limited or in combination with systemic effects -Bleed into skin! -Severity of signs is based on which organ systems are affected most -Petechiae or ecchymoses on skin -Hemorrhagic papules, plaques, and urticaria that may ulcerate -Crateriform ulcers -Dependent edema -Panniculitis -Systemic signs: --arthropathy, gastroenteritis, hepatopathy, nephropathy are most common in dogs |
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Hypersensitivity Vasculitis
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-Antigen-antibody complex disease, type III hypersensitivity
-Can be due to drugs, vaccines, infectious agents, biting insects, dietary antigens -Neoplasia -50% of cases are idiopathic -Food allergy provoked, unless proven otherwise -Breed predilection for Jack Russell Terriers --affects pressure points --very resistant to therapy! |
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Diagnosis of Vasculitis
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-Good history is needed, rule out drug-induced and poly systemic disease
-Multi-system exam -Baseline CBC, serum chemistry, UA -Look for neoplasia if indicated, based on other clinical signs -SKIN BIOPSY! -Rule out infectious disease --rickettsiae in dogs --viral diseases in cats (FIV, FIP, FeLV) |
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Treatment of Vasculitis
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-Remove inciting cause when possible
-Stop all drugs or change drug classes if possible -Rule out adverse food reaction via diet trial -Glucocorticoids can be used short-term -Non-steroidal alternatives for the long-term --tetracycline/niacinamide --Sulfonamides (Sulfasalazine) --Pentoxifylline --Immunosuppressive therapy |
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Sulfasalazine
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-Most effective therapy for neutophilic vasculitis
-Bacteria in the colon break the azo-linkage --releases 5-amino-salicylic acid (anti-inflammatory in colon) and sulfapyridine (absorbed systemically) -Interferes with neutrophil cytotoxic systems -Can cause hepatotoxicity and keratoconjunctivitis sicca (KCS) |
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Anti-leukocyte properties of Doxycycline and Niacinamide
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-Tetracyclines: inhibit neutrophil chemotaxis, degranulation, and phagocytosis
--Inhibit lymphocyte transformation and proliferation -Niacinamide: stabilizes leukocytes from degranulation -Side effects: GI upset, hepatotoxicity with extended use |
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Vasculopathy
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-Diagnosis that is inferred when histologic evidence of vessel wall damage is not present, but tissue is ischemic
-Atrophy of the skin and hair follicles -“Ischemic dermatopathy” |
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Ischemic dermatopathies
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-Canine juvenile dermatomyositis
-Focal rabies vaccine associated vasculopathy -Rabies vaccine associated ischemic dermatopathy -Pinnal margin vasculopathy |
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Canine Juvenile Dermatomyositis
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-Hereditary inflammatory disease of collies, Shetland sheepdogs, and beaucerons
-Onset within 6-8 months of age -Progression is unpredictable, usually complete by 1 year of age -Periocular, muzzle, ear tip, tail tip, dorsum of toes may have skin lesions -Soft nails -Alopecia, erythema, scaling, mild crusting -Vesicles and ulceration in severe cases, vasculitis -Chronic cases show atrophy and scarring alopecia -Myositis: ranges from undetectable to severe --head, pelvic limbs, and megaesophagus |
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Diagnosis of Dermatomyositis
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-Signalment and clinical signs are suggestive
-Diagnose via skin biopsy, changes will be typical of vasculopathy -Muscle pathology will show necrosis or atrophy of muscle fibers on histopathology |
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Dermatomyositis DDx
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-Demodicosis
-Staph folliculitis -Dermatophytosis -Discoid lupus -Other autoimmune diseases |
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Dermatomyositis Treatment
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-Soft bedding, skin lesions are exacerbated by trauma
-Steroidal anti-inflammatory drugs for severe flares only --long-term use of steroids promotes additional atrophy -Vitamin E or Omega-3 fatty acids for very mild cases -Pentoxifylline for long-term management of more severe cases |
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Focal rabies vaccine associated vasculopathy
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-Flat, alopecic, hyperpigmented focal lesion
-Variable erythema and scales -Lesions appear 3-6 months after vaccination -Breed predilection for little, white, fluffy dogs --genetic predisposition? -May occur repeatedly if re-vaccinated |
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Diagnosis of Rabies Vaccine Reactions
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-Histology is typical of ischemic insult
-“Fading” hair follicles -Basal cell degeneration -Mononuclear cell infiltrate -Basophilic foreign material will sometimes be obvious --vaccine adjuvant |
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Rabies Vaccine associated ischemic dermatopathy
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-Wide-spread ischemic insult, beyond focal site of injection
--should still have vaccine site lesion, and should show up before other lesions -Skin becomes cyanotic and atrophic -Affects facial skin, tail tip, toes -Histology may be indistinguishable from other ischemic insults --dermatomyositis, focal RV-associated vasculopathy |
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Treatment for Rabins vaccine induced vasculopathies
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-Generalized lesions: Pentoxifylline and vitamin E |
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Pseudomonas Otitis Clinical findings
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-Opportunistic invader in chronic otitis
-Yellow/green purulent discharge -Moist and exudative consistenct -Malodorous, painful ulcers in the ear canal |
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Dermatologic exam for patient with Otitis
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-Look for concurrent dermatitis
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Otoscopic Exam
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-Evaluate the complete ear canal
-Evaluate integrity of the tympanic membrane -Look at amount and character of the exudate, look at debris/cerumen -Pull pinna away, up and out from body to straighten ear canal -Hand-held otoscope is usually most common --video otoscopy can be helpful, better optics and visualization --connected to a monitor --working channel for instruments |
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Ear Cytology
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-DO for EVERY case of Otitis!
-First diagnostic test on patient with otitis -Use cotton swabs, glass slides, heat source, stain, and microscope --can really be done anywhere -Sample junction between horizontal and vertical ear canal -Sample both ears, may have different cytologic findings -Look at sample under a microscope, start at low power |
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Ear Mite preparation
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-Direct microscopy, no stain or heat fixation
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Otitis Bacterial culture and sensitivity Indications
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-Not done in every otitis case
-Otitis externa with rods on cytology --pseudomonas is frequently drug-resistant -Chronic or recurrent otitis externa that does not respond to appropriate empirical therapy -Systemic therapy --otitis media, extensive ulceration, severe stenosis |
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Limitations of Bacterial Culture and Sensitivity for Otitis
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-Results are based on serum concentrations via systemic treatment
-Topical concentrations are much higher than serum levels -Not all topicals are available on culture and sensitivity profile |
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Ear Culture technique
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-Sample junction between horizontal and vertical ear canals
-Sample of middle ear cavity requires anesthesia -Sample both ears! Culture findings may be different |
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Myringotomy
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-Incision into the tympanic membrane
-Need animal to be under general anesthesia -Proper placement of incision is important --go in the right location! --Caudo-ventral portion of the tympanic membrane, Pars tensa --avoid stria mallearis, promontory, and blood vessels -Can be hard to place inicision in a very infected ear |
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Bullae Radiography
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-Good for cases where otitis media is suspected
-Less commonly performed by specialists, more common in general practice -Most helpful for looking at bony changes -May not be as helpful as CT |
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Management of Chronic Otitis externa
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-Resolve or minimize predisposing factors, if possible
-Reduce inflammation -Identify and resolve secondary infections -Look for underlying disease/primary disease |
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Otitis Externa Treatment
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-Topical treatment is most ideal, mainstay of treatment
-Make choice of treatment based on cytologic evaluation -Most commercially produced products contain combination of active ingredients --antibacterial --antifungal --anti-inflammatory -Systemic antibicrobials are not usually indicated --do not reach appropriate levels to be effective |
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Treatment of Cocci otitis externa
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-Usually staph bacteria
-Aminoglycosides -Polymixin B -Silver Sulfadiazine Fluoroquinolones |
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Aminoglycosides for otitis externa
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-First choice for cocci otitis externa
-Can be ototoxic, but rare -Neomycin 1st -Gentamicin 1st or 2nd -Amikacin 3rd, use for resistant staph based on culture and sensitivity |
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Polymixin B for Otitis externa
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-1st or 2nd for cocci otitis externa
-Surolan otic -Also contains miconazole and prednisolone acetate --anti-fungal and steroid --work synergistically to have antibacterial effect -Can be inactivated in pus --flush out purulent material before treatment |
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Silver sulfadiazine
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-2nd for cocci otitis externa
-Mild to moderate anti-yeast activity -Not present in form that is readily used in ears --1% cream -Some anti-fungal activity, particularly helpful for pseudomonas |
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Fluoroquinolones
|
-3rd treatment for cocci otitis externa
-Enrofloxacin, marbofloxacin, orbifloxacin -NOT 1st line! -Use based on culture and sensitivity |
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Treatment of Rod Otitis Externa
|
-Aminoglycosides
-Polymixin B -Silver sulfadiazine -Fluoroquinolones -Carboxypenicillins |
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Aminoglycosides for Rod Otitis externa
|
-Gentamicin 1st
--increasing resistance in gram- rods, especially pseudomonas -Amikacin 3rd -Tobramycin 3rd -Use 3rd therapies based on culture and sensitivity |
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Polymixin B for rod otitis externa
|
-1st or 2nd treatment for rods
-Includes pseudomonas |
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Silver Sulfadiazine for rod otitis externa
|
-1st or 2nd
-1% cream, concentrations as low as 0.1% can be effective against staph and pseudomonas -Safe to use with ruptured tympanic membranes |
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Fluoroquinolones for rod otitis externa
|
-2nd or 3rd for rods, more useful for rods than for cocci
-Use based on culture and sensitivity -Enrofloxacin, marbofloxacin, and orbifloxacin -Often used as systemic option |
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Carboxypenicillins for Rod Otitis externa
|
-3rd for rods
-Extended spectrum penicillins -Injectible product that can be made into an otic formulation -Mostly used for pseudomonas |
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Treatment options for Yeast otitis externa
|
-Antifungal
-Nystatin -Benzimidazoles, thiabendazole -Imidazoles --clotrimazole, miconazole, ketoconazole, posaconazole -Use with acificying cleaner |
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Treatment for Ear Mites
|
-Pyrethrin
-Rotenone -Thiabendazole -Ivermectin -Milbemycin -Selamectin -Imidacloprid/Moxidectin -Keep ears clean! -Always look for secondary infections with bacteria and yeast |
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Otitis Externa Treatment Strategy
|
-Category of disease is important for therapy
-Acute otitis externa 1st time infection: --topical treatment for 7-14 days with cleaning -base therapy on cytologic findings --yeast only: topical imidazole --cocci or cocci and rods: Neomycin or gentamicin --Rods only: gentamicin -Use high volume of therapy! Don’t be frugal! |
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Volume of therapy for Otitis
|
-do not be frugal!
-Dogs and cats have long ear canals -large breed animals should get 10-12 drops per application (1ml) MINIMUM -Small breed dogs 4-6 drops (0.5ml) MINIMUM |
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Treatment for Chronic Otitis Externa
|
-Weeks to months in duration
-Prior attempts may have been attempted -Require longer treatment duration, minimum of 4 weeks -Re-check every 2-4 weeks until resolved --cytology, otoscopy -Look for predisposing factors, primary factors, and perpetuating factors -Check status of the tympanic membrane -Rule out otitis media! -base therapy on history, otoscopy, cytology --cocci or cocci and rods: Gentamicin, Polymixin B, silver sulfadiazine --refractory rods: Amikacin, Tobramycin, Fluoroquinolones, Ticarcillin |
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Tris-EDTA
|
-Adjuvant topical therapy
-Tris: buffer, causes alkaline environment -EDTA: chelating agent, helps poke holes in cell membranes of gram- bacteria -Allows for better penetration of antibacterial therapy --enhances activity of aminoglycosides and fluoroquinolones -Give before giving topical treatment |
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Ear cleaning
|
-Essential component of treating ear disease
-Fill ear canal with a large volume -Clean 2-3x weekly at first, reduce to 1-2x per week -Depends on nature and severity of exudate or debris -Most are cleaning and drying agents and acidifying as well -Antiseptics also exist, are chlorhexidine based |
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Ear cleaning technique
|
1.fill up ear canal
2. Squish around 3. Dog shapes head 4. Clean out debris |
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Ceruminolytic cleansers
|
-Break up waxy debris
-Potentially ototoxic, not given to owners unless you are sure it all gets out of ear canal -Squalene is the only safe ceruminolytic for the middle ear |
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Anti-inflammatory drugs for Otitis externa
|
-Steroids
-Goal is to decrease inflammation, production of cerumen and ebum, epidermal and glandular hyperplasia, pruritus and pain -Will not remove irreversible changes like mineralization -Systemic absorption can occur even with topical use, be careful -Most topical corticosteroids are combined with antimicrobials in ear products |
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Treatmentof Otitis media
|
-Requires topical and systemic therapy
-Treat concurrent otitis externa -Systemic antibiotic choice is based on middle ear culture -Give 6-8 weeks minimum -Often need middle ear lavage -If neurologic signs are present, CT/MRI is strongly suggested -If there is no resolution with medical therapy, consider surgical intervention --Bulla osteotomy with or without TECA |
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Important points for successful management of otitis
|
-identify and manage predisposing factors |
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Ear Anatomy
|
-External ear:
--horizontal and vertical ear canals --Lined by skin -Middle ear: --Tympanic bullae --Lined by mucus membranes, respiratory membrane -Inner ear: Behind tympanic membrane --composed of hearing and balance structures, neurologic structures |
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Pinna
|
-Funnels sound vibrations towards the ear cannal
-Broad, leaf-shaped auricular cartilage -transmits sound down the ear canal to the tympanic membrane -Covered in normal skin |
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External ear canal
|
-Vertical ear canal: made of auricular cartilage
--continuous with the pinna -Horizontal ear canal: annular cartilage --separated from vertical canal by prominent cartilaginous ridge -Lined by skin -Conducts air vibrations to the tympanum -Contains hair follicles, sebaceous glands, and ceruminous glands |
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Cerumen
|
-Ear wax
-normally found in the ear canals of dogs -Secretions of sebaceous and ceruminous glands and sloughed epithelial cells -Traps debris, parasites, and microorganisms -Immune function -Protects tympanic membrane from desiccation -Increased production can be detrimental |
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Tympanic Membrane
|
-Tympanum: ear drum
--separates external ear canal from the middle ear -2 sections --pars flaccida, dorsal portion --pars tensa, ventral portion, looks like the drum --Stria mallearis, manubrium of the malleus, C-chaped, points towards the nose -Dog tympanic membrane may be oriented 45 degrees -Cat membrane is usually perpendicular |
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Middle Ear Cavity Anatomy
|
-Dorsal portion: acoustic ossicles and tympanic nerve
-Middle portion: adjacent to tympanic membrane --contains Promontory opposite mid-dorsal aspect of tympanic membrane -Ventral portion: “Bulla” --protected by bone --cat tympanic bulla is separated by bony septum -Auditory tube (Eustachian tube), opens into middle ear |
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Acoustic ossicles
|
-Malleus
-Incus -Stapes -Located in the dorsal portion of the middle ear cavity |
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Promontory
|
-IN Middle portion of the middle ear cavity
-Caudal end is the cochlear (round) window |
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Inner ear Structures
|
-Cochlea (hearing apparatus)
-Vestibule and semi-circular canals (balance apparatus) -Vestibulocochlear nerve (CN VIII) -Cochlear and vestibular functions can be damaged by ototoxic medications or internal ear infections |
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Otitis
|
-Inflammation of the ear
-pattern of cutaneous disease -Otitis externa: inflammation of the external ear canal -Otitis media: inflammation of the middle ear -Otitis interna: inflammation of the inner ear |
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Etiology of Ear Disease
|
-Often multifactorial
--Can be hard to identify all of the causes --necessary for management of otitis -Causes are divided into predisposing factors, primary factors, and perpetuating factors |
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Multifactorial Etiology of Ear Disease
|
1. Predisposing factors:
--conformation, excessive cerumen, excessive moisture, iatrogenic 2. Primary Factors: --parasites, hypersensitivity, foreign bodies, keratinization, autoimmune diseases, masses 3. Perpetuating Factors: --bacteria, yeast, inappropriate treatment, progressive pathologic changes, otitis media |
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Primary causes of Ear Disease
|
-Directly initiate inflammation
-Must be addressed for therapy to be successful -Ectoparasites -Hypersensitivity and allergic disorders -Obstruction: foreign bodies, tumors, polyps -Autoimmune disease -Keratinization disorders |
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Ectoparasites as cause of Primary ear disease
|
-Otodectes cynotis (ear mite)
-Most common cause of otitis externa in cats, 50% -5-10% of otitis in dogs -Not species specific -Demodex, otobius megnini, and chiggers are also possible |
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Allergic Skin disease and ear disease
|
-Most common underlying cause of otitis externa in dogs
-Atopic dermatitis, food allergy, or combination -May present with otitis as only clinical sign or in combination with other signs --pruritus and inflammation -Most commonly bilateral disease --may present as primary, one ear is more predisposed |
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Allergic/irritant contact dermatitis as cause of primary ear disease
|
-Suspect if the ear gets worse after treatment
-Can be due to any active topical ingredient or vehicle -Look at skin of concave pinna, may appear sunburnt or scaly -Neomycin, propylene glycol are common causes |
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Foreign Bodies as cause of Otitis
|
-Usually cause unilateral otitis
-Very painful, acute onset -Can become chronic if overlooked -Worry about tympanum perforation -Plant material, dirt, sand, dried medication, ceruminoliths, dead insects |
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Obstructive disease as primary cause of otitis
|
-Neoplasia
-Usually unilateral -Most commonly arise from ceruminous glands of external ear canal -Dogs: usually benign, ceruminous gland adenoma -Cats: 50% malignant, ceruminous gland adenocarcinoma -Allow accumulation of cerumen and debris, lead to secondary infections |
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Inflammatory/Nasopharyngeal polyps
|
-Usually unilateral
-Young adult cats -May have history of upper respiratory infection -Originate from middle ear or auditory tube, respiratory epithelium -Extend down into nasal cavity or up into ear canal -Perform oral exam! Often requires general anesthesia |
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Cornification disorders and Otitis
|
-Primary cause of otitis
-Hyperadrenocorticism -Hypothyroidism -Sebaceous adenitis -Primary or idiopathic seborrhea |
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Autoimmune or Immune mediated diseases causing Primary Otitis
|
-Lupoid diseases
-Pemphigus foliaceus -Vasculitis -Bullous diseases -Erythema multiforme -Juvenile Cellulitis |
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Otitis Predisposing Factors
|
-Increase risk of developing Otitis
-Alter microenvironment -Often do not cause clinical disease alone -Must be recognized and controlled for resolution of otitis -Anatomic and conformational factors -Excessive cerumen production -Excessive moisture -Treatment factors -Systemic Disease --immune suppression, debilitation, catabolic states |
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Anatomic/Conformational Predisposition to Otitis
|
-Pendulous Pinna (Basset hound)
-Stenotic ear canals (Shar Pei, Pug) -Natural ventilation and cleansing mechanisms are diminished -Hypertrichotic canals, increased hair in ear canal --poodles, Yorkshire terriers, Schnauzers |
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Excessive Cerumen Production and Otitis
|
-Predisposing factor for Otitis
-Increased ceruminous gland density --cocker and springer spaniels -Cerumen --nutrient rich medium for organisms --hydrophobic lipid material -Treatment includes ceruminolytic flushes |
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Excessive moisture and Otitis
|
-Humid environments
-Swimming, bathing -Overzealous cleaning -Sets up environment for microorganism development |
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Iatrogenic otitis
|
-Irritating cleanser
-Trauma from cotton-tipped applicators -Plucking of hairs |
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Immunosuppression and Otitis
|
-Predisposes animals to skin infections, therefore predisposes to otitis
-FeLV/FIV -Hypothyroidism -Hyperadrenocorticism |
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Otitis Perpetuating Factors
|
-Sustain inflammation, prevent resolution
-Responsible for the establishment of perpetuating factors -MAJOR reason for poor response to therapy -Progressive pathologic changes -Otitis media |
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Progressive Pathologic Changes and Otitis
|
-Glandular Hyperplasia
-Stenosis: harder to clean, harder to get treatment into ear canal -Fibrosis -Mineralization: irreversible change |
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Otitis Media
|
-Direct extension of infection through compromised tympanic membrane
-Extension of infection from nasopharynx via auditory tubes -Up to 89% of dogs with chronic otitis externa have concurrent otitis media -Can be a diagnostic challenge --Otoscopic examination, 70-80% of dogs have intact tympanic membranes --Radiographs or CT can be helpful, identify soft tissue in middle ear cavity |
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Indications for Total Ear Canal Ablation (TECA)
|
-Irreversible proliferative changes
-Severe mineralization, ossification -Bulla osteomyelitis with or without abscessation -Severe infections that do not respond to appropriate medical therapy -Severe discomfort -Neoplasia |
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Treatment errors as perpetuating factors of Otitis
|
-under-treatment:
--owner compliance --patient resistance -Over-treatment: --maceration of canal epithelium |
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Secondary infections of the Ear canal
|
-Opportunistic microorganisms
-Must be addressed for successful treatment -Identified with cytologic exam --#1 diagnostic test for a case of otitis -Bacteria and yeast |
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Microorganisms causing secondary otitis
|
-Cocci: staphylococcus, streptococcus, enterococcus
-Rods: Pseudomonas aeruginosa, E. coli, Proteus, Klebsiella, Corynebacterium -Yeasts: Malassezia pachydermatis, other Malassezia, Candida albicans |
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Clinical manifestations of Ear Disease
|
-Head shaking
-Ear scratching, ear rubbing -Exudate, odor -Discomfort -Excoriations, alopecia -Pyotraumatic dermatitis at base of the ear -Aural hematoma -Neurologic signs |
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Neurologic signs associated with Otitis
|
-Representative of Otitis media or Otitis interna
-Peripheral vestibular signs, head tilt towards affected side, nystagmus -Deafness -Facial nerve paralysis -Horner’s syndrome -Extension into CNS can lead to signs of brain stem dysfunction |
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Systemic approach to Otitis Externa
|
-What are the infections?
-Why are they there? -Signalment -Swimming -Systemic evidence of metabolic or endocrine disease -Pruritus or recurrent infections elsewhere on the body -Seasonality -Previous therapies -Response or bad reaction to therapy -COMPLETE physical exam is important! -Note color, odor, and consistency of aural exudates -Palpate ear canals and perform neurologic exam -Oral examination! |
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Otodectes Otitis Clinical Findings
|
-Black color |
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Malassezia Otitis Clinical Findings |
-Brown to black color |
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Hair Cycle
|
-Anagen (growth)
-Catagen (regression) -Telogen (resting) -Exogen (shedding -Hair growth is influenced by: --body region and genetics --photoperiod and ambient temperature --Hormonal changes |
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Important aspects of Hair Cycle
|
-Small animal hairs are in teolgen most of the time
-Old English sheepdogs, poodles, schnauzer have hairs that stay in anagen for longer --continuously growing hair -Anything that changes hair cycle will induce hypotrichosis or alopecia -Biopsy and histopathology is the best way to evaluate the hair cycle --trichogram may be helpful |
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Etiologic categories of Alopecia
|
-Congenital: not common
-Acquired: most common -inflammatory is most common, due to pruritus or self-trauma or infection and folliculitis -Non-inflammatory has many causes --not due to inflammation or pruritus --Endocrine --Follicular dysplasia --Immune-mediated --Sebaceous adenitis --Misc. |
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Trichogram
|
-Can differentiate anagen and telogen hairs by the bulb
--anagen has rounded club at root --telogen has rough end -May not be able to identify catagen hairs |
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Alopecia work-up
|
-Signalment
-History -Physical Exam -Dermatological examination -Diagnostic tests |
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Signalment for Alopecia patients
|
-Breed:
--sebaceous adenitis: Standard poodle, Akita, Vizsla --Pattern baldness: Dachcshund -Age: --Young: demodicosis, dermatophytosis, congenital hypotrichosis --Young-middle: allergic dermatitis, follicular dysplasia --middle-old: endocrine, neoplasia -Sex: intact male dogs and testicular neoplasia -Coat color: color dilution alopecia or black hair follicular dysplasia |
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History for an Alopecia patient
|
-Onset
-Duration -Persistence -Severity -Concurrent changes -Distribition -Most important question: IS THIS ANIMAL ITCHY --if so, did pruritus precede or follow hair loss --If animal is itchy, diagnose for pruritus and consider DDx for self-induced alopecia --Consider DDx for folliculitis |
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DDx for Folliculitis
|
-Demodex
-Dermatophytosis -Staphylococcal infection |
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Bald Cats
|
-Cats can be secretive groomers
-Good at licking all of their hair off -Create well-demarcated areas of alopecia -Look at trichogram! Broken distal ends of hairs indicates self-trauma |
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Generalizations about Alopecia
|
-Focal or multi-focal alopecia is associated with inflammatory and infectious disease
-generalized or bilaterally symmetrical alopecia is typically associated with non-inflammatory disease -Initial work-up of an alopecic patient should include diagnostic tests for common inflammatory causes --deep skin scrapings --cytologies --Trichograms --Dermatophyte culture |
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Patchy/Multifocal Alopecia
|
-Rule out causes of folliculitis before doing more advanced diagnostics
-Cytology, trichograms, skin scrapings, wood’s lamp exam, fungal culture |
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Diffuse/regional Alopecia
|
-Rule out causes of folliculitis (skin scrapings, cytology, trichogram, Wood’s lamp exam, fungal culture)
-Consider non-inflammatory alopecia causes --Endocrinopathies --Cyclic flank alopecia --Pattern baldness --Color dilution alopecia --Black hair follicular dysplasia --Alopecia X --Anagen/Telogen effluvium |
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Diffuse or bilaterally symmetric non-inflammatory alopecia DDx
|
-Endocrine or systemic disease
-Cushing’s disease -Hyperthyroid, hypothyroid -Biopsy after endocrine testing is non-conclusive |
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Endocrine Alopecia
|
-Usually bilaterally symmetrical
-Usually associated with hyperadrenocorticism or hypothyroidism -Can also have sex hormone associated alopecias --hyperestrogenism, secondary to testicular neoplasia or exogenous exposure -Skin histopathology is rarely diagnostic for hypothyroidism or cushing’s -False positive and negative results can occur with endocrine testing --interpret with clinical signs |
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Alopecia due to Hyperadrenocorticism (Cushing’s) vs. Hypothyroidism
|
-Age:
--Cushing’s: older, 10+ --Hypothyroid: middle age, 7 years -Breed: --Cushing’s: small sized dog, less than 20kg --Hypothyroidism: large size |
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Hyperadrenocorticism (Cushing’s) and Alopecia
|
-Thin skin
-Poor wound healing -Easy bruised -Comedones, milia -Calcinosis cutis -PU/PD/PP -Excessive panting -Lethargy -Muscle wasting -Pot belly -Neurologic signs |
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|
Hypothyroidism and Alopecia
|
-Lichenification
-Recurrent pyoderma -Loss of guard hairs, “puppy coat” -Wear area hypotrichosis --tail, bridge of the nose, head, lateral extremities -Myxedema, “tragic face” -Weight gain -Lethargy -Sex cycle abnormalities -Heat-seeking -Corneal lipidosis -Bradycardia |
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CBC/Chem to diagnose Cushing’s hyperadrenocorticism
|
-Stress leukogram
-Thrombocytosis -Increased ALP -Bacteriuria -Increased glucose -Increased cholesterol |
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|
Hypothyroidism CBC/Chem
|
-Mild anemia
-Hypercholesterolemia -Low T4 |
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|
Cyclic Flank Alopecia
|
-Idiopathic
-localized follicular dysplasia -Cyclic or recurrent --may be seasonal --season and photoperiod may be triggering factors -Bulldogs, boxers, Airedales, schnauzers -Lateral thorax and flank alopecia -Alopecia and marked hyperpigmentation -No detectible underlying disease -Resolves on own, then recurs yearly or at random -Diagnose via breed and clinical signs --rule out DDx: endocrine alopecia -Definitive diagnose via histopathology -Cosmetic disease! |
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Cyclic flank alopecia treatment
|
-Cosmetic disease, has no significant impact on health
-Do not harm! Do not give something that will damage the animal -Try melatonin supplementation -Can just ignore |
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|
Pattern baldness in dogs
|
-Dachshunds, boston terriers, Chihuahuas, greyhounds
-Progressive, non-inflammatory alopecia -Usually occurs at specific sites --pinnae --pre and post auricular --ventrum --caudal thighs -Cosmetic issue |
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Pattern Baldness Diagnosis
|
-Breed and clinical presentation are usually sufficient
-Histopathology can confirm -See miniaturized hair follicles -Cosmetic issue! |
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|
Color related alopecia
|
-Color dilution alopecia: blue or fawn colored dogs
-Black hair follicular dysplasia: dogs with dark hair -Congenital, age of onset is variable -Error in melanosome handling --abnormal storage or transfer of melanin --Hairs have clumped melanin and will break or fracture in clumped areas |
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Diagnosis of Color related alopecia
|
-Compatible lesions, breed, and trichogram
-Definitive diagnosis: histopathology -Color dilution and black hair follicular dysplasia have same histology, need do differentiate clinically |
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Treatment for Color related alopecia
|
-None
-Avoid harsh bathing/grooming -Treat secondary bacterial folliculitis |
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Alopecia X
|
-Growth hormone responsive alopecia
-Castration responsive alopecia -Adult-onset growth hormone deficiency -Pesudo cushing’s -Congenital adrenal hyperplasia-like syndrome -Black skin disease -Coat funk -Hair cycle arrest --failure of anagen initiation |
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|
Alopecia X recognition
|
-Failure of anagen initiation
-Plush coated breeds --Pomeranian --Chow, miniature poodle, Keeshond, Samoyed, malamute -3-6 years old -Dogs look like they have endocrine alopecia -Happy, healthy dogs -Alopecia with or without hyperpigmentation -Neck, caudal thighs, central and lateral trunk |
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Alopecia X Diagnosis
|
-Hematology and biochemical profile are within normal limits
-Regular adrenal and hormonal testing is normal -Histopath can be helpful, but is not definitive --indicates endocrine-like alopecia |
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|
Alopecia X Therapy
|
-Neutering
-Melatonin -Lysodren -Trilosane -No treatment, “sweater therapy” |
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|
Alopecia X Client education
|
-Essential!
-Expensive endocrine testing is unnecessary -Use of possible lethal drugs needs to be weighed against benefits -Generally only a cosmetic concern, dog is otherwise healthy |
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|
Anagen and Telogen Effluvium
|
-Disruption of anagen
--chemotherapy, infectious agents --Hair loss occurs after days -Synchronized telogen --stress, illness, pregnancy, lactation, chemotherapy --hair loss in 1-3 months -Usually due to drug or underlying disease |
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|
Summary of Alopecia
|
-Most is inflammatory |
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|
Flea Biology
|
-Life cycle takes 3-8 weeks, can be up to 6 months
-Adults are permanent ectoparasites, spend entire life on the host -Eggs are laid within 1-3 days of taking a blood meal -1 female flea can lay 40-50 eggs per day for 100 days -2 larval stages, then form pupae -Pupae are encased and difficult to kill -No stage survives prolonged freezing --need more than 10 days below freezing -Urban wildlife and feral cats continue lifecycle |
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|
Flea Larvae vs. Pupae
|
-Larvae are easy to kill
-Pupae are not easy to kill, encased in a shell and isolated --resistant to heat and desiccation |
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|
Flea bite myth
|
-“one flea bite is enough to cause clinical signs in a hypersensitive patient”
-Fleas feed within seconds to minutes, most within 5 minutes -Want to prevent repeated feeding |
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|
Flea resistance myth
|
-“Product is not working because fleas are resistant”
-Resistance is possible to develop -Really more resistance vs. tolerance -Ned to consider re-emergence of adult fleas due to environmental infestation -Poor application is a possibility -Poor understanding of the flea life cycle |
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|
Flea Tolerance
|
-Inherent difference in flea populations susceptibility to a specific product
|
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|
Flea adulticides
|
-Pyrethroids
-Fipronil -Imidacloprid -Metaflumizone -Dinotefuran -Indoxacarb -Nitenpyram -Spinosad -Spinoteram -Afoxolaner -Fluralaner |
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|
Juvenile flea control agents
|
-Insect development inhibitors: Lufenuron
-Insect growth regulators: --Pyriproxyfen --S-methoprene |
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|
Lufenuron
|
-Juvenile flea control agent
-Insect development inhibitor -Chitin synthesis inhibitor -Low mammalian toxicity, mammals do not have chitin -No adulticide activity, not appropriate for use as a sole flea control option --unless there is a low burden area |
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|
Insect Growth Regulators
|
-Juvenile hormone analogs, prevent flea eggs from hatching and prevent larvae from pupating
-No adulticide activity -Pyriproxyfen -S-methoprene |
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|
Rapid Flea Knock-down products
|
-Nitenpyram: starts killing in 30 min, full kill in 3-4 hours
--paralyzes flea mouthparts --“Capstar” -Spinosad: starts killing within 30 minutes, full kill in 4 hours --“comfortis” and “trifexis” -Imidacloprid: stops feeding in 3-5 minutes, full efficacy in 6-12 hours --“Advantage” -Afoxolaner: starts killing in 2 hours, full kill in 6 hours --“Nexgard” -Fluralaner: starts killing within 2 hours, full kill in 12 hours --“Bravecto” |
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|
Heartworm Prevention and Flea Control
|
-Selamectin: otodectes, Sarcoptes, and roundworms/hookworms
--Better efficacy and speed of kill in cats --“Revolution” -Imidacloprid/Moxidectin: Otodectes, sarcoptes scabiei, roundworms, hookworms, whipworms --“Advantage Multi” -Milbemycin oxime/Spinosad: roundworms/hookworms/whipworms --“Trifexis” (dogs only) |
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|
Flea control with Tick preventative
|
-Fipronil
-Imidacloprid/Dinotefuran/Indoxacarb/Permethrin (not in cats!) -Imidacloprid/Flumethrin -Fipronil/Cyphenothrin -Fipronil/S-methoprene/Amitraz -Afoxolaner -Fluralaner |
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|
Permethrin in cats
|
-TOXIC! Do not use in cats!
|
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|
Flea control for frequent bathing/swimming animals
|
-Nitenpyram, every 24-48 hours
-Monthly spinosad -Monthly afoxolaner -Fluralaner every 3 months -Fipronil: concentrates in sebaceous glands, is redistributed over the skin surface |
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|
Goals of Flea control
|
-Prevent flea life cycle establishment in home or yard
-Monthly adulticide with or without juvenile control agent is usually sufficient -Therapy depends on geography, local flea burden, swimming/bathing, number of animals, client preference |
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|
Flea Allergy Dermatitis Goals of Flea Control
|
-Prevent prolonged exposure to flea saliva
-Prevent flea infestations and egg laying -Integrated flea control: --On-animal adulticides --Insect growth regulators and development inhibitors --Quick-kill adulticides -Want to rapidly kill adult fleas before they can lay eggs or bite -Provide residual activity -Prevent egg laying -Prevent insecticide resistance by using multiple methods |
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Successful management for Flea Allergy Dermatitis flea control
|
-Treat all pets in-contact with each other
-Keep cats indoors -Environmental treatment for fleas --powders, foggers, sprays --vacuuming --professional exterminator -Avoid contact with wildlife or feral cats |
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|
Considerations for managing Flea Allergy Dermatitis
|
-Presence of an environmental infestation
-Single or multiple pets -Concurrent allergic dermatoses --food allergy -Degree of exposure -Environment -Frequency of swimming or bathing -Owner compliance |
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|
Techniques for managing Flea Allergy Dermatitis flea control
|
-Increased frequency of topicals, every 1-2 weeks
-Alternating topical treatments every 1-2 weeks -Monthly spinosad -Nitenpyram with topical -Monthly afoxolaner -Seresto collar with monthly selamectin |
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Tick control
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-Ticks are harder to kill
-Not a permanent ectoparasite, spend part of life off of host -Resistant to many insecticides, need to use specific products -Insect growth regulators are not helpful -No agent provides 100% control -Owner surveillance is essential, physical removal may be necessary -Need to address owner’s expectations |
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Rhipicephalus sanguineus
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-Brown Dog Tick
-Dog is host for all developmental life stages -Local/environmental control and on-dog control may be effective -Professional extermination is often required if there is an infestation |
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Tick Control for Dogs
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-Permethrin (Advantix, Vectra 3D)
-Deltamethrin (Scalibor collar) -Flumethrin (Seresto collar) -Amitraz (Certifect, Preventic collar) -Fipronil (Frontline) -Afoxolaner (Nexgard) -Fluralaner (Bravecto) |
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Tick Control for Cats
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-Fipronil (frontline)
-Flumethrin (Seresto collar) |
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Techniques for Tick Control
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-Use two agents at the same time
-increased frequency of application -Increase product weight rage -Lots of combinations are safe and effective |
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Pruritic Mites
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-Sarcoptes scabiei, Notoedres cati
-Otodectes cyanotis -Cheyletiella -Demodex gatoi |
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Non-pruritic mites
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-DEmodex
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Elimination of surface mites
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-Selamectin (revolution)
--approved for dogs and cats --Applied topically, absorbed systemically --Also covers for heartworm -Imidacloprid and Moxidectin (Advantage multi) -Address all surface mites except demodex gatoi -Ivermectin 1% --lower than typical dose for demodex --highly effective and inexpensive --need to use with caution in sensitive breeds and cats -Fipronil Spray --very sage, very useful for Chiroptes --can be expensive for large animals --toxic to rabbits -Lime sulfur dip: --effective, inexpensive, safe for young animals --antipruritic |
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Treating Pruritic surface mites
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-Identify and treat secondary infections!
-Short tapering course of anti-inflammatory corticosteroids -Pruritus may intensify as mites die -Avoid corticosteroids in follicular demodicosis |
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Demodex Gatoi
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-Lives in stratum corneum, not in hair follicle
-Pruritic, itchy! -Can be hard to find -hard to kill -Only proven treatment is lime sulfur dip 2% --weekly for 6-8 weeks |
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Lice control
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-Lice are uncommon in small animals |
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Antimicrobial Therapy of the Skin: Approach
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-What are the infections
-Why are the infections there |
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Indications for Topical therapy of Pyoderma
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-Removal of bacteria and debris from skin surface
--crusts --decrease bacterial load on the skin -Can be used as sole treatment in localized, mild, antimicrobial resistant infections -Used to be though of as an adjunct treatment, now is seen as primary treatment -Helps with preventing recurrent infections |
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Types of topical therapy for pyoderma
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-Shampoos are most common
--detergent is antimicrobial --helps dispersion -Lotions, creams, ointments, sprays, and dips can also be useful (or necessary) --harder to get full coverage with dogs |
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Benzoyl Peroxide Shampoo
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-Potent antibacterial
-Helpful in cases where there is folliculitis AND demodex -Flushes plugged hair follicles -Comedolytic -De-greasing effect, but can also have drying effect -2-5% in veterinary formulations --higher percentage can be irritating on animal skin -Keratolytic, breaks up keratinocytes -Available in shampoos, gels, pads, wipes -May bleach fabrics and hair |
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Ethyl Latate
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-Etiderm
-Benzoyl peroxide alternative -Antimicrobial -More gentle antimicrobial, hydrolyzed at the skin surface into ethanol and lactic acid --lowers pH on skin, makes less favorable for bacteria -Mild follicular flushing and comedolytic agent, mildly degreasing |
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Chlorhexidine Shampoo
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Potent antibacterial
-Mild anti-fungal -2-4% formulations --4% or higher is better for fungal infections -Less irritating or drying than benzoyl peroxide when used frequently -Persists when used regularly, can give long-lasting anti-bacterial activity |
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Chlorhexidine formulations
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-Comes in almost any form you can think of
-Potent antimicrobial! -Effective against resistant staph species -Can be mixed with anti-fungals to increase potency |
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Topical Therapy for Focal Pyoderma
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-Mupirocin ointment
-Has novel mechanism of action -Good efficacy against gram+ bacteria -Good penetration, can be used with deep infections -Limited to treating focal areas of infection |
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Iodine as treatment for skin infections
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-Broad-spectrum activity against bacteria and fungi
-Mostly used on horses -Has drying and staining effects -Highly irritating and drying, can stain -Not used on small animals very often |
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Sodium Hypochlorite
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-Bleach!
-Broad-spectrum antimicrobial activity -Dilute bleach bath, 0.5-1 cup of 6% bleach per bathtub of water (40 gallons) -Decreases S. aureus colonization -“Non-bleaching” veterinary products |
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Nisin
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-Antimicrobial protein
-Produced by Lactococcus lactis -Used in the foot industry and in cattle teat wipes -Effective in small trial for surface and superficial pyoderma -Also help prevent recurrent infections |
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Silver Sulfadiazine
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-Broad-spectrum antimicrobial
-Effective against pseudomonas and staph -Mild anti-fungal activity, used to treat fungal keratitis in horses -Available as 1% cream -Can be combined with Baytril, enrofloxacin -Promotes re-epithelialization and is soothing --used to treat burns |
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Challenges to using Systemic Antibiotics
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-Stratum corneum barrier function may prevent penetration of topical ointments
--diffusion DOWN -Basement membrane slows diffusion of systemic antibiotics to avascular deep epidermis --diffusion UP -Often need to treat longer for skin infections because area is not well-vascularized |
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Ideal Antibiotic
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-Effective:
--narrow spectrum, covers staphylococci for the most part --Cheap, easy to administer --bactericidal -Safe for extended use --limited potential for side effects --low incidence of induced resistance with repeated use |
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Duration of Dosing Antimicrobials
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-Dermatological dosing typically requires extended duration
-Superficial pyoderma: --3 weeks minimum, 1 week past clinical resolution -Deep pyoderma: --6 weeks minimum, 2 weeks past clinical resolution |
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Frequency of dosing antimicrobials
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-Frequency is drug-dependent
-Time dependent: beta-lactams, bacteriostatic drugs --maintain plasma concentration aboce MIC for entire inter-dose interval --BID to TID dosing -Concentration dependent: fluoroquinolones --greatly exceed MIC once during dosing interval --once daily dosing |
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Staphylococcal resistance
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-Methicillin resistance (oxacillin)
--mecA gene carried on staphylococcal chromosome cassette mec --encodes for altered penicillin binding protein (BPB2a) --if BPB2a is produced, no beta-lactam antibiotics will be effective -Resitance to all beta-lactam derivatives --penicillin, potentiated penicillins, cephalosporins, carbapenems -Prevalence of methicillin resistance is increasing in clinical isolates --S. aureus, S. pseudintermedius, S. schleiferi -Resistant staph infections also have additional genes that convey resistance to other antibiotics -Antibiotic changes should be based on culture and susceptibility |
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Antimicrobials with PBP2a resistance
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-Penicillin
-Potentiated penicillns -Cephalosporins -Carbapenems |
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Antibiotics that are poor choices for pyoderma treatment
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-Natural penicillins, potentiated penicillins
--penicillin, amoxicillin, ampicillin --majority of S. pseudointermedius resistant beta lactamases --use with beta-lactamase inhibitor -Tetracyclines --significant presence of tetracycline resistance genes in staph --doxycycline and minocycline may be used, based on culture and sensitivity |
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First tier antibiotics for pyoderma
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-Use with First occurrence pyoderma
-Good for Some recurrent infections based on culture and sensitivity -Clindamycin, lincomycin, erythromycin -Potentiated sulfonamides -beta-lactams -First generation cephalosporins Clavamox |
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Clindamycin
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-First tier antibiotic
-Good for first occurrence pyoderma -Narrow spectrum, bacteriostatic -Well tolerated, has good tissue penetration -May be used every 24 hours for superficial pyoderma -Inducible resistance gene, can cause treatment failure |
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Potentiated Sulfonamides
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-Trimethroprim sulfa
-Ormetoprim-ssulfadimethoxine -Adverse effects are a concern, especially with long-term use -Some adverse effects are idiosyncratic -KCS is most common side effect -Hypothyroidism is predictable side effect -Sterile polyarthropathy, blood dyscrasias, cutaneous drug eruptions or erythema multiforme can also occur -Dobermans are predisposed |
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Beta-lactams as 1st tier drugs for pyoderma
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-Cephalosporins
-Amoxicillin with clavulanate acid -Has concerns about selecting for colonization by methicillin resistant strains --Animal will probably develop recurrent infections |
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First generation cephalosporins
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-Cephalexin, cefadroxil
-Resistant to beta-lactamases -Bactericidal |
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Clavamox
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-Clavulanate, beta-lactamase inhibitor included
-Expensive for larger dogs |
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Second tier antibiotics for pyoderma
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-3rd generation cephalosporins
-Chosen in limited cases, have some benefit over -Cefpodoxine -Cefovecin |
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Cefpodoxine
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-once a day formulation, increased convenience
-also has increased gram- spectrum |
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Cefovecin
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-Repositol formulation, given every 14 days
-Long half-life, 5-6 days --very tight protein binding -Very convenient for fractious cats -Expensive! Especially for large breed dogs -Cannot be stopped if there are side effects -Prolonged exposure of GI flora to antibiotic --increased gram- exposure |
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Third tier antibiotics for pyoderma
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-Chosen based on culture and sensitivity
-ONLY chosen when other drugs are ineffective and culture indicates susceptibility -Have adverse effects, public health concerns, or are expensive or expensive to monitor -Fluroquinolones -Chloramphenicol -Rifampin -Aminoglycosides |
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Fluoroquinolones
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-3rd tier antibiotic
-Enrofloxacin, marbofloxacin, pradofloxacin, orbifoxacin -Broad spectrum antibiotic -Well-tolerated, has good penetration -bactericidal -Expensive! -Some resistance exists |
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Ciprofloxacin
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-Inexpensive, generic formulation
-Be careful for use in dogs! --not all dogs absorb tablets well -may see poor bioavailability |
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Chloramphenicol
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-3rd tier antibiotic
-Use only based on culture -Methicillin resistant staph are often susceptible -Bacteriostatic, needs to be given 3x daily -Adverse effects are rare but exist --idiosyncratic pancytopenia in humans (fatal), causes dose-dependent bone marrow suppression --vomiting, weight loss, inappetence -Inhibition of P450 microenzymes in cats |
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Rifampin
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-3rd tier antibiotics
-Rarely resistant to staphylococci, but can arise rapidly -Adverse effects are a concern --idiosyncratic hepatotoxicity, can be fatal --GI upset, hemolytic anemia, thrombocytopenia -Causes orange discoloration of body tissues -Potent inducer of P450 enzymes |
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Aminoglycosides
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-3rd tier antibiotics
-Amikacin -Methicillin resistant staph are usually susceptible -Parenteral only -Adverse effects are a concern --nephrotoxicity, ototoxicity --causes proximal tubular necrosis -Expensive, needs expensive monitoring --monitor via urinalysis |
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Topical Antifungals
|
-Treatment of uncomplicated or localized Malassezia dermatitis
-“Spot” therapy for focal dermatophytosis in dogs ONLY --Cats need systemic and topical treatment -Can be used as adjunctive therapy to systemic therapy of generalized Malassezia dermatitis and dermatophytosis |
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Topical treatment for dermatophytosis
|
-Lime sulfur dips
-Excellent activity against dermatophytes -Reduces environmental contamination via shedding of infected hairs into environment -Also kills spores -Cheap, safe, anti-pruritic -Stinky, dries skin, stains/tarnishes, irritating to mucus membranes -Caustic if undiluted! Need to dilute according to label! |
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Treatment for Malassezia pachydermatitis
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-Systemic and topical therapy
-Miconazole, chlorhexadine shampoo |
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Miconazole
|
-cream, lotion, spray, shampoos, conditioners, otic products
-Can be in combination with chlorhexidine |
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Antifungal Azoles
|
-Ketoconazole
-Clotrimazole (older azole, may see more resistance) -Posaconazole --new generation azole, used in Posatex otic formulation |
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Terbinafine
|
-Allylamine antifungal
-Squalene epoxidase inhibitor -Cream, solution, spray, and gel (Lamisil) -Treats focal dermatophytosis in dogs -Localized Malassezia dermatitis treatment |
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Systemic Antifungals
|
-Imidazoles:
--ketoconazole --Miconazole --Clotrimazole --Thiabendazole --Enilconazole -Triazoles: --Itraconazole (oral, IV, ophthalmic) --Fluconazole (oral, IV) --Posaconazole (oral, otic) --Voriconazole (oral, IV) |
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Azole mechanism of action
|
-Inhibits lanosterol 14-alpha demethylase
-Inhibits key fungal enzyme that converts lanosterol to ergosterol -Ergosterol is required for fungal cell membrane integrity -Decreased ergosterol results in osmotic disruption of the cell, fungistatic effects -CYP450 toxicity -Inhibition is possibly embryotoxic |
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Lanosterol in Humans
|
-Converted into cortisol, cholesterol, and some sex hormones
-Inhibition results in reduced hormone levels -May interfere with liver metabolic pathways -Inhibition is Possibly embryotoxic |
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Ketoconazole
|
-“Nizoral”
-First commonly used azole antifungal -Rough on cats -Most commonly used for Malassezia dermatitis --not often used for dermatophytosis -Is becoming superseded by newer drugs -Absorption needs acidic environment, give with food --Avoid concurrent use of antacids and H2 blockers -Highly protein bound, poor penetration of CSF -Delivered to epidermis via secretion in sebum -Extensively metabolized by the liver --strongly inhibits CYP3A4, causes hepatotoxicity --results in drug interactions |
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Ketoconazole and Cyclosporine
|
-Ketoconazole inhibits cyclosporine drug metabolism
-Give together, can give less cyclosporine |
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Adverse effects of Ketoconazole
|
-Nausea, vomiting
-Liver toxicity is uncommon but possible --monitor liver enzymes with long-term daily use -Be aware of drug interactions --CYP450 inhibition -Suppression of cortisol and sex hormones when given in high doses --was an old treatment for cushing’s disease, suppresses cortisol production |
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Itraconazole
|
-Most commonly used azole antifungal for dermatophytosis in cats
-Expensive -Often is compounded, but when compounded has poor bioavailability --Stick with brand-name! Sporanox -VERY expensive -Give liquids on an empty stomach, give capsules on a full stomach -Mostly used for dermatophytosis and Malassezia dermatitis -Also effective against deep cutaneous and systemic fungal infections |
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Itraconazole mechanism of action
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-Lipophilic
-Absorption is increased in acidic environment -Avoid concurrent use of antacids and H2 blockers, give with fatty meal -Solubilized by cyclodextrins in oral solution --special helper molecules -Give liquids on an empty stomach, give capsules on a full stomach -Highly keratinophilic, delivered to epidermis via secretion in sebum --Remains in skin 204 weeks after stopping -Pulse dosing is possible for superficial fungal infections like dermatophytosis -Highly protein bound, may have poor penetration of CSF |
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Itraconazole Adverse effects
|
-Nausea and vomiting are rare
-Extensively metabolized by the liver --liver toxicity is uncommon --monitor liver enzymes with long-term use or if clinical signs indicate monitoring -May have dose-related drug-induced cutaneous vasculitis --only reported in dogs, not cats -Negligble effect on P450 enzymes of mammals |
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Fluconazole
|
-“Diflucan”
-Used more commonly since is available as generic -Water soluble -Not protein bound, not lipophilic -Readily absorbed -Excreted in kidneys in active form --concentrated in urine -Good penetration of CNS and aqueous humor -Very low affinity for mammalian P450 enzymes -Excellent safety profile -Higher MIC for dermatophytes and Malassezia compared to other azoles, but is still often clinically effective --sometimes see failure -Not sure if pulse dosing is an effective option |
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Fluconazole adverse effects
|
-Nausea and vomiting are very rare in dogs and cats
-Excreted largely unchanged by kidneys --need to adjust dose with renal insufficiency |
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Terbinafine
|
-“Lamasil” |
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Terbinafine Adverse effects
|
-Nausea, vomiting |
