SA Med Exam 2

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vfritsch
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197039
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SA Med Exam 2
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2013-02-09 14:19:05
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  1. What is the mechanism of pemphigus foliaceus?
    Antibodies targeted against desmocollin-1 or desmoglein-1 in the desmosomes
  2. What type of hypersensitivity is pemphigus foliaceus?
    type 2
  3. What are the CS of PF?
    • crusts and pustules of nasal planum, eyes, feet (including claws) and pinna
    • pruritus, febrile, depressed
    • can also be generalized
  4. In which animals is generalized PF common?
    retrievers, chows, cats
  5. How is PF dx, and what are the results?
    • histopathology - don't clean the site!
    • see acantholytic cells, subcorneal pustules with neutrophils
    • CBC shows neutrophilia
  6. How is drug-related pemphigus treated?
    remove drug, may need immunosuppressive therapy
  7. Wat is drug-related pemphigus caused by?
    TMS, abx, griseofulvin
  8. In which breeds is exfoliative cutaneous lupus erythematosus found?
    GSP
  9. In which breeds is vesicular cutaneous lupus erythematosus found?
    collies, shelties
  10. Which types of lupus erythematosus can be found in all dog breeds?
    systemic and discoid
  11. What is the pathophysiology of discoid lupus erythematosus?
    Ag-Ab complexes form at the BMZ
  12. What type of hypersensitivity is DLE?
    type 3
  13. What are the CS of DLE?
    • Depigmentation and alopecia around the eyes, nasal planum, muzzle and pinna
    • Can be very crusty, or loss of "cobblestone" appearance on nose
  14. In which dogs is DLE more likely?
    • dolicocephalic or mesaticephalic, but not brachycephalic
    • e.g. Siberian Husky, Sheltie, Collie, GSD
  15. How is DLE dx?
    histopathology
  16. What age dogs are most commonly affected by DLE and PF?
    2-6 years old
  17. If the CS look like DLE or PF, but it's a dog 8+ years old, what should be on your diff dx?
    cutaneous lymphoma, hepato-cutaneous syndrome
  18. What is seen on histopathology of DLE?
    • "interface dermatitis"
    • thickening of BM because of Ag:Ab complexes
    • pigmentary incontinence
    • hydropic degeneration (vacuolated areas)
  19. What is an important medical management tool for DLE and PF?
    reduce exposure to sunlight!
  20. What is the tx for PF in dogs?
    • Pred (2x allergy dose) then taper
    • azathioprine for a month, then taper (steroid sparing drug)
    • Abx at same time medium acting steroids are started
    • Gold (esp if endogenous steroids)
  21. What are the AE of azathioprine?
    bone marrow suppression (esp in cats!)
  22. What is the tx for PF in cats?
    • Pred
    • Dex
    • Triamcinolone
    • Chlorambucil (because can't give azathioprine)
    • Cyclosporine
    • Gold (esp if endogenous steroids)
  23. What is the tx for DLE?
    • niacinamide + tetracycline for 1-2 months
    • tacrolimus ointment
    • topical bethamethasone
    • topical sunscreen
  24. What are the AE of tetracyclines + niacinamide?
    vomiting (rare)
  25. What is tacrolimus ointment?
    expensive ointment that works like cyclosporine but has better skin absorption
  26. What is the most common flea?
    Ctenocephalides felis felis
  27. What is the average life span of a flea?
    • 21 days
    • Can be 12-190 days
  28. What are ideal environment conditions for fleas?
    75F and 78% relative humidity 
  29. How quickly are flea eggs laid on the host?
    24-36 hours after the first blood meal
  30. When do flea eggs hatch?
    1-10 days
  31. How many flea eggs can be laid by a flea in a month?
    >1,000
  32. What are the characteristics of flea larvae?
    • 3 stages total, last 5-11 days each
    • feed off flea poop
    • negatively phototaxic and positively geotaxic
    • highly susceptible to heat dryness
  33. What are the characteristics of flea pupae?
    • cocoon stage
    • most resistant to dessication / elimination
    • sticky, so get covered in dust and camouflage
    • adults emerge in response to heat, CO2, vibrations, physical pressure
  34. What are adult fleas attracted to?
    body heat, CO2, vibrations, light, air, host movement
  35. When do adult fleas feed and mate?
    • Feed every 3 minutes
    • Mate 8-24hours after emergence
    • Lay eggs 24-36 hours after feeding
  36. Where can adult fleas be found?
    Permanent ectoparasite
  37. What is FAD?
    hypersensitivity (type 1 and 4) to flea saliva
  38. What are the CS of FAD?
    pruritus on caudal half of body
  39. What makes flea saliva pruritic?
    • Histamine-like compounds
    • Proteolytic, cytolytic and anti-coagulant enzymes
    • Complete protein antigens
  40. What makes a FAD have a greater or lesser immunological response?
    • genetic predisposition
    • duration of exposure
    • degree of exposure
  41. What are the immunological responses to flea saliva?
    • type 1 hypersensitivity (immediate, IgE mediated)
    • type 4 hypersensitivity (delayed, T cell mediated)
    • cutaneous basophil hypersensitivity
  42. Which animals are predisposed to FAD?
    animals with AD
  43. How is FAD dx?
    • hx (are they giving flea meds, does the animal go in the water a lot, recent boarding)
    • finding flea dirt (= flea poop, stains red on paper)
    • PE (pruritus and alopecia caudal to "belt")
  44. How is feline FAD slightly different?
    • can have neck and face alopecia
    • can see miliary dermatitis and eosinophilic skin disease
  45. What dx can be used for FAD, and what results would you expect?
    • CBC (regenerative anemia, eosinophilia)
    • biopsy (r/o other diseases)
  46. What are the three objectives when managing FAD?
    • eradicate fleas in the environment
    • symptomatically tx the patient
    • prevent further infestations (must tx all animals!)
  47. What are the symptomatic txts for FAD?
    • tx secondary infx (malassezia and superficial pyodermA)
    • corticosteroids (short course)
  48. What are the characteristics of the ideal flea control?
    • quick kill (reduces allergic rxn)
    • acts against >1 life stage, but esp gets adults
    • non-irritating, non-toxic
    • residual effects
  49. What are some disadvantages of topical flea control?
    • re apply every 2-4 weeks
    • come off with bathing / swimming
    • malodorous
  50. What are the advantages to oral flea control?
    • doesn't get washed off
    • quicker speed of kill
  51. What are the disadvantages of flea control?
    • expensive
    • give once monthly
    • +/- flavored
  52. What do adulticides do?
    kill adult fleas
  53. What do IGRs do?
    kill non-adult flea life stages
  54. What are the two type of IGRs?
    • Juvenile Hormone Analogues (JHAs)
    • Insect Development Inhibitors (IDIs)
  55. What do Juvenile Hormone Analogues (JHAs) do?
    synthetic hormones that cause incomplete larval molts, disrupt embryogenesis
  56. What are some examples of Juvenile Hormone Analogues (JHAs)?
    • pyriproxyfen (Vectro3D, AdvantixII)
    • S-methoprene (Frontline+)
  57. What do Insect Development Inhibitors (IDIs) do?
    malformation of chitin cuticle, incomplete larval ecdysis (flea can't emerge, or dies soon after emerging)
  58. What are some examples of Insect Development Inhibitors (IDIs)?
    Lufenuron (Program, Sentinel)
  59. What is imidacloprid effective against?
    flea adulticide + larvicide
  60. How does imidacloprid work?
    • inhibits post-synaptic nicotinic receptors
    • distribution via translocation
  61. How does fipronil work?
    disrupts chloride channels in CNS -> neurotoxicity
  62. What is fipronil effective against?
    • adult fleas and ticks
    • can't use on rabbits!
  63. How does selamectin work?
    increase Cl- permeability in Glu-gated neuronal Cl- channels -> paralysis
  64. What is selamectin effective against?
    • fleas - adults, larvae and eggs
    • HWP
  65. What are the advantages of pyrethrins and pyrethroids?
    Repellant, fast kill
  66. What are the disadvantages of pyrethrins and pyrethroids?
    • variable efficacy and duration
    • *toxic to cats*
    • breaks down in uv light
  67. How does dinotefuran work?
    neonicotinoid adulticide
  68. What is dinotefuran effective against?
    adult fleas, ticks, mosquitos
  69. How does spinetoram work?
    activates nicotinic AchR
  70. How does nitenpyram work?
    neonicotinoid
  71. What is nitenpyram effective against?
    adult fleas
  72. What are the advantages of nitenpyram?
    • most effective flea adulticide
    • *very safe*
    • gold standard txt for FAD
    • starts killing in 30 minutes
  73. What are the disadvantages of nitenpyram?
    only 24 hour effect
  74. What are the advantages of spinosad?
    100% effect in 4 hours
  75. What is the mechanism of action of spinosad?
    neonicotinoid
  76. What are the disadvantages of spinosad?
    • apply once monthly
    • give with a full meal
    • AE: vomiting
    • *do not give with ivermectin!*
  77. What are some botanical flea control products?
    • rotenone (rare)
    • -inhibits oxidative phosphorylation
    • d-limonene
    • -inhibits peripheral sensory n.
    • pyrethrins / pyrethroids
    • -inhibits Na channels
    • carbamates
    • -inhibits cholinesterase (reversible)
    • organophosphates
    • -inhibits cholinesterase (irreversible)
  78. What are the common etiologies for feline eosinophilic granuloma complex and miliary dermatitis?
    • infection, infestation, allergy
    • -also consider heavily perfumed litter boxes, and the role genetics
  79. What are the three forms of feline eosinophilic granuloma complex?
    • eosinophilic granuloma
    • lip ulcer (aka rodent, eosinophilic)
    • eosinophilic plaque
  80. What are the CS of eosinophilic granulomas?
    • see on caudal thighs, oral cavity
    • +/- peripheral lymphadenopathy
  81. How are eosinophilic granulomas dx, and what results do you expect?
    • CBC: eosinophlia
    • histopathology: eosinophilic-derived granulomas that coat collagen fiber (*not collagen degeneration*)
  82. What are the CS of mosquito bite granulomas?
    crusts, vesicles, ulcers and swelling on the nasal planum, pinna and footpads
  83. What are the histopathology results of mosquito bite granulomas?
    eosinophils + eosinophilic-coated collagen
  84. What is the txt for mosquito bite granulomas?
    • corticosteroids
    • keep the cat indoors
  85. How can you dx a lip ulcer?
    • PE: ulcerative dermatitis on upper lip
    • blood and tissue eosinophilia (but will be neutrophils if biopsy early)
    • +/- peripheral lymphadenopathy
  86. What are the differential dx of a lip ulcer?
    • SCC
    • herpes virus dermatitis
    • rare: staph, dermatophytes, deep fungal infx
  87. What are the CS of an eosinophilic plaque?
    • VERY puruitic
    • see on abdomen and medial thighs
    • +/- peripheral lymphadenopathy
  88. How can you dx eosinophilic plaques, and what results would you expect?
    • impression smear: eos
    • histopathology: eos in epidermal vacuoles
  89. What hypersensitivities can cause eosinophilic granuloma complexes?
    fleas, food, AD, contact (perfumed litter box)
  90. What is the txt for eosinophilic granuloma complex?
    • tx underlying hypersensitivity
    • methylprednisolone q2wks x 3 txts
    • cyclosporine (better for eos plaque and granuloma)
    • ~EFAs (better for granulomas)
    • clavamox (better for plaque, maybe for ulcer)
  91. What are the AE of cyclosporine?
    • V
    • lethargy
    • secondary infx / pyoderma
    • papillomas
    • hypertrichosis
    • gingival enlargement
  92. What are the CS of miliary dermatitis?
    encrusted papules reaction pattern
  93. What can cause miliary dermatitis?
    • fleas - most common
    • Cheyletiella
    • lice
    • food allergy
    • AD
    • dermatophytes
    • pyoderma
  94. How do you tx miliary dermatitis?
    • tx underlying cause
    • anti-inflammatory oral corticosteroids if idiopathic
  95. What are the three most common allergies, in order?
    FAD > AD > food allergy
  96. What is AD?
    • genetically predisposed inflammatory and pruritic skin disease with characteristic clinical features
    • IgE abs to environmental allergens
  97. What are allergens?
    Ag that favors development of hypersensitivity
  98. What are some common allergens?
    • house dust mites - most common
    • pollens
    • molds
    • storage mites
    • epithelial cells
  99. What is the pathophysiology of AD?
    • defective epidermal barrier function -> exposure and absorption of allergens + water loss
    • usually due to abnormal lamellar bodies
  100. What provides normal cutaneous barrier function?
    • epidermal lipids (esp in stratum corneum)
    • ceramides
    • cholesterol
    • fatty acids
    • sphingosine
  101. How does allergen sensitization happen?
    • defective cutaneous barrier
    • -> naive Langerhans cell (LC) processing of allergen
    • -> LC migrates to LN
    • -> naive T helper cell (Th0) presentation ->
    • activate Th2 cell
    • -> production of cytokines IL4, IL13
    • -> cytokines stimulate B cell production of AS IgE
    • -> AS IgE + Th2 cells migrate to dermis
    • -> cycle of itch and inflammation
    • -> ->
    • re-exposure of allergen
    • -> LC bound to AS IgE bind allergen and migrate to dermis
    • -> present allergen to TH2
    • -> cytokines like IL31 released
    • -> activate sensory neurons
    • -> pruritus
  102. Why does AD get worse with further exposure of Ag?
    • pruritus and inflammation
    • -> stratum corneum thickening
    • -> worsened barrier function
    • -> increased allergen penetration
  103. What breeds are commonly affected with AD?
    Goldens, labs, WH fox terrier, dalmation, westie, small terriers, weimaraner, irish setter, shar peis, spaniels
  104. When does onset of AD usually happen?
    • 1.5-3 years old
    • can be 6mo-6yrs
  105. What is the speed of onset of AD?
    insidious and gradual
  106. What is the seasonality of AD?
    will often start at a certain season, then progress to being year round
  107. What are the site predilections for AD?
    face, paws, distal extremities, ears, ventrum and especially caudal carpi
  108. What are the CS of AD in dogs?
    self trauma -> excoriation, erythema, alopecia, lichenification, hyperpigmentation, secondary infx at site predilections
  109. What are the two most common pathogens causing secondary infx?
    • Staph pseudintermedius
    • Malassezia pachydermatis
  110. How is AD tx in dogs?
    • systemic: corticosteroids (pred, temaril-P), EFAs, cyclosporine
    • topical: corticosteroids (triamcinolone spray), EFA shampoo and spray, oatmeal, tacrolimus
    • tx secondary infx
  111. How does secondary infx with Staph pseudintermedius and Malassezia make AD worse?
    • They have greater affinity for keratinocytes of atopic dogs
    • -> hypersensitivity to secondary pathogen
    • -> increased pruritus
    • -> CS e.g. collarettes, papules, pustules
  112. What are the CS of a secondary Malssezia infx?
    • waxy brown exudate on proximal claws
    • interdigital erythema
  113. What is the dx criteria for AD?
    • must have 5 or more:
    • -age of onset <3 years
    • -mostly indoor dog
    • -front feet affected
    • -inner pinna affected (not margins)
    • -dorso lumbar region unaffected (FAD)
    • -chronic or recurrent Malassezia infx
    • -responds to corticosteroid therapy
    • -pruritus before skin lesions at onset
  114. How accurate is the dx criteria for AD?
    • 85% sensitivity
    • 79% specificity
  115. What are the CS of AD in cats?
    • face, neck and head pruritus
    • miliary dermatitis
    • -eosinophilic granuloma complex
    • -over grooming alopecia
  116. How is AD dx?
    • signalment
    • eliminate food allergy, FAD
    • allergy testing (ELISA or intradermal)
  117. What are the advantages of intradermal testing for AD?
    • considered gold standard
    • can customize allergens
  118. What are the disadvantages of intradermal testing for AD?
    • must have corresponding CS to be meaningful
    • many false + and -
    • can't be on anti-histamines or steroids
    • chronic skin changes interfere
    • need sedation or GA -> day hospitalization
    • subjective results (and no standard)
    • need experience
  119. What are the most common allergens?
    house dust mites, house dust, grasses
  120. How does an ELISA for allergy testing work?
    measurement of serum AS IgE with standardized results
  121. What are the advantages of ELISA for AD testing?
    • results are standardized
    • no sedation, GA or hospitalization
    • can run if there are chronic skin changes
    • results less affected by anti-histamines and steroids
  122. What are the disadvantages of ELISA for AD testing?
    • the Ags aren't as pure
    • can't customize Ags
    • more false + (maybe)
  123. How does ASIT work?
    • hyposensitization to specific allergens
    • takes 4-6mo of weekly shots for improvement in 70% of cases
  124. What is the ASIT mechanism of action?
    • Th2 -> Th1 cytokine profile switch
    • IgE -> IgG switch
    • Induce T cell tolerance by generation of allergen specific Treg cells -> decreased Th1 & Th2 cytokine response to allergen
    • decrease APCs, T & B cells & effector cells
  125. What are the effects of corticosteroids in AD tx?
    • decreased production of pro-inflammatory cytokines
    • decreased T cell activation
    • decreased eosinophilic function
    • decreased mast cell degranulation
    • decreased APCs in skin
    • decreased vascular permeability (-> decreased effector cells)
    • decreased LT and PgI (-> decreased arachidonic acid cascade)
  126. How is AD tx in cats?
    • systemic: corticosteroids (pred, triamcinolone), EFAs, cyclosporine
    • topical: corticosteroids (triamcinolone spray), EFA shampoo and spray, oatmeal, tacrolimus
    • tx secondary infx
  127. What is the safe annual dose of glucocorticoids in dogs?
    15 x lbs = mg pred / year
  128. What kind of long term monitoring do you need to do for glucocorticoid therapy?
    urine culture
  129. What drug can spare atopica (cyclosporine) in AD therapy?
    ketoconazole, reduces dose by 50%
  130. How does cyclosporine work?
    • calcineuron inhibitor blocks IL2
    • decrease T cell activation
    • decrease cytokines
    • decrease function of effector cells
  131. How do anti-histamines work?
    • blocks histamine receptors on blood vessels
    • prevents erythema, vasodilation and swelling due to histamine
  132. How effective are anti-histamines, and why?
    • not very effective
    • other inflammatory mediators besides histamine
  133. How do EFAs work?
    • improve barrier function
    • reduces trans-epidermal water loss
    • omega 3s compete with arachidonic acid, which reduces breakdown to pro-inflammatory mediators
  134. How does Sogeval DuoxoCalm spray work?
    • phytosphingosine (improves barrier function)
    • and
    • hinokitiol (plant metal chelator = anti-infective)
  135. What is the common hx of CAFR?
    • same diet last 2+ years
    • acute onset
    • not seasonal
    • +/- response to glucocorticoids
  136. What is the common signalment of CAFR?
    • young or old (middle aged tends to be AD)
    • Goldens, terriers, GSD
  137. What are the CS of CAFR in dogs?
    • generalized pruritus
    • pododermatitis
    • bilateral otitis externa (>80% at presentation)
    • -only CS in 20% cases
    • scaling
    • papules
    • erythema
  138. What are the CS of CAFR in cats?
    • pruritus and alopecia of neck and face
    • papules
    • miliary dermatitis
    • eosinophilic granuloma complex
  139. Are there extracutaneous CS of CAFR?
    • maybe, maybe not
    • V, increased pooping
  140. How do you dx CAFR?
    • elimination diet trial 8-12 weeks
    • rechallenge with old food
    • should see CS return within 2 weeks
  141. What are common canine food allergens?
    beef, dairy, chicken, lamb, corn, soy
  142. What are common feline allergens?
    fish, dairy, beef, lamb
  143. Where does contact dermatitis occur?
    • poorly haired regions
    • interdigital, axilla, inguinal, muzzle, pinnae, perineal
  144. What are the two types of contact dermatitis, and which is more common?
    allergic and irritant (more common)
  145. What is the difference between allergic and irritant contact dermatitis?
    • allergic requires sensitization
    • irritant dermatitis happens on first exposure to allergen
  146. What is the relationship between FAD, AD and CAFR?
    • 5-25% of dogs have AD and CAFR
    • 10-50% of dogs have FAD and AD
    • AD predisposes dogs to have FAD
  147. What is the most common agents causing canine pyoderma?
    • Staph pseudintermedius - most common
    • Staph schleiferi
    • Staph aureus
    • Proteus
    • Pseudomonas
    • E. coli
  148. Why do animals develop pyoderma?
    • less efficient stratum corneum allows bacterial invasion
    • lack of ostial plug in entrance of hair follicle
  149. In which animals is Staph schleiferi seen?
    more in cats, less in dogs
  150. In which animals is Staph aureus seen?
    humans and horses, not dogs
  151. Where is Staph pseudintermedius most often found?
    nares and perianal
  152. What are predisposing factors for canine pyoderma?
    • pruritus
    • inflammation
    • disorders of cornification
    • diseases of the hair follicle
    • endocrinopathy
    • poor grooming
    • immunological defects
  153. What are the types of surface pyoderma?
    • acute moist dermatitis aka hotspot aka pyotraumatic deramtitis
    • intertrigo (skin fold pyoderma)
    • muco-cutaneous pyoderma
  154. What are the types of superficial pyoderma?
    • impetigo
    • superficial folliculitis
    • superficial spreading pyoderma
  155. What are the types of deep pyoderma?
    • deep folliculitis
    • deep furunculitis
    • cellulitis
    • deep pyoderma aka muzzle folliculitis aka canine acne
  156. What is the treatment for acute moist deramtitis?
    clip, no need for abx initially
  157. Why is intertrigo common?
    • effect of temperature, pH, frictional microtrauma
    • obesity can create skin folds
  158. What is an impetigo?
    • a non-follicular subcorneal pustule
    • often seen in less haired areas
    • seen in puppies
  159. What is superficial folliculitis?
    follicular pustule
  160. How can you tell a pyoderma is deep?
    hemorrhagic crusts
  161. What is the initial treatment for cellulitis?
    • Look for underlying cause
    • Systemic abx
    • Abx shampoo
  162. When would you be sure to use bacteriocidal systemic antibiotics?
    • deep infx
    • immunodeficiency
  163. What are the common results for culture and sensitivity of pyoderma?
    • Resistance to penicillin, ampicillin, amoxicillin, sulfonamides
    • -staphs have a beta lactamase enzyme
    • More resistant bacteria in deep pyodermas
  164. What is the most common risk factor for development of MRS?
    prior administration of abx
  165. What are the first line abx for pyoderma?
    • cephalosporins
    • lincomycin
    • amoxicillin / clavulanate
  166. What are the second line abx for pyoderma?
    • fluoroquinolones
    • -marbofloxacin
    • -enrofloxacin
    • -ciprofloxacin
  167. What is the abx regime for pyoderma?
    • use abx for 4 weeks
    • monitor lesions and pruritus
  168. When must you culture be performed on a pyoderma?
    • lesions are not improving
    • abx in last 6-12mo
  169. What abx should be used against MRS?
    • TMs maybe
    • doxycycline
    • chloramphenicol
    • amikacin
  170. What are the AE of chloramphenicol?
    aplastic anemia when taken by humans
  171. What are the AE of amikacin?
    renal monitoring
  172. What are some good agents for antibacterial shampoo for pyoderma, and what are the directions for use?
    • chlorhexidine - best choice
    • benzoyl peroxide
    • BP and sulfur
    • ethyl lactate
    • triclosan
    • Give 2x a week with 10-15 min contact time
  173. What are the characteristics of Malassezia furfur?
    lipid dependent, humans only
  174. What are the characteristics of Malassezia pachyderamtis?
    • lipophilic (not lipid dependent) non-mycelial yeast
    • found on animals
    • reproduces by unipolar budding
    • peanut shaped
  175. Where can Malassezia be found on a dog as a commensal?
    • skin
    • ear canal
    • anal sacs
    • vagina
    • rectum
  176. How do you know if the cytology has a significant amount of Malassezia or you're seeing commensal organisms?
    • 5+ Malassezia whole slide for skin cytology is significant
    • Slightly more expected for ear cytology
  177. How is Malassezia a facultative pathogen?
    • underlying host disease -> microclimate and defense changes
    • barrier disruption (e.g. moisture accumulation)
    • excess sebum or cerumen production
    • defect in innate immunity (e.g. antimicrobial peptides, CMI, IgA)
    • enzymes (lipases, proteases, zymosan)
    • hypersensitivity?
  178. What is the pathogenesis of Malassezia opportunistic infx?
    • IgE (type 1) Malassezia hypersenstitivity
    • type 1 and 4 seborrheic dermatitis
  179. What conditions can predispose a dog to Malassezia infx?
    • AD
    • cornification disorders
    • chronic inflammation
    • previous abx or steroids
    • breed predilection
  180. Which canine breeds are predisposed to Malassezia infx?
    • Westie, Basset, Springer, GSD
    • -Basset normally has intense colonization with no lesions unless becomes immunosuppressed
  181. Which feline breeds are predisposed to Malassezia infx?
    Devon Rex, Sphinx
  182. What are some underlying immunosuppressive causes of feline malassezia?
    • paraneoplastic skin disease (paraneoplastic alopecia, feline thymoma-associated)
    • erythema multiforme
    • FeLV
    • FIV
    • DM
    • Neoplasia
  183. What does primary canine malassezia infx look like?
    generalized inflammatory skin disease, rapid onset, odor, pruritus, rapid response, no recurrence (rare)
  184. What does secondary canine malassezia infx look like?
    associated with chronic, inflammatory skin disease, odor, pruritus
  185. What does a malassezia skin lesion look like?
    sharply demarcated margins
  186. Where do you see malassezia infx?
    • Ventral neck
    • Ventral abdomen, axilla
    • Face, ears (pinna)
    • Feet, forelegs
    • Any skin folds
    • Claw beds
  187. How do you dx malasezzia infx?
    • culture
    • biopsy
    • cytology
  188. What is the therapy for malassezia infx?
    • tx the underlying disease
    • systemic antifungals (ketoconazole, fluconazole, itraconazole, terbinafine)
    • topicals (twice weekly shampoo or wipes with miconazole, ketoconazole, >2.5% chlorhexidine, 2.5% acetic acid, 2% boric acid)
  189. When would you use extended antifungals?
    uncontrolled recurrent malassezia infx
  190. What is the extended regimen for treating recurrent malassezia infx with systemic antifungals?
    azole given on three consecutive days, try to reduce to twice weekly
  191. Is canine demodex contagious?
    only from dam -> puppies
  192. Where does canine demodex live?
    hair follicles
  193. What are the common canine demodex species, and what are the characteristics?
    • Demodex canis: most common
    • D. injai: large bodied, in hair follicle and sebaceous glands
    • D. cornei: Short-bodied stratum corneum, a sub-species of D. canis
  194. How can you define demodicosis as localized vs. generalized?
    • localized: <5 regions on body affected, or a paw affected
    • generalized: 5 or more regions affected
  195. How can you define demodecosis as juvenile vs adult onset?
    • juvenile: <2 years old, average <1 year old
    • adult: >2 years old, but average is >7 years old
  196. What is the txt for juvenile onset localized demodicosis?
    • self limiting
    • can add on mupirocin to avoid secondary infx
  197. What is the pathophysiology of juvenile onset generalized demodicosis?
    • Defective immune response: demodex specific
    • T cell dysfunction: maybe
    • Hereditary: predisposed
    • Sex hormones: females in estrus or pregnancy
  198. What is the txt for juvenile onset generalized demodicosis?
    • spay if intact
    • ivermectin PO (in ice cream)
    • milbemycin
    • moxidectin
    • amitraz dip after clipping hair coat and bathing in antibacterial shampoo
    • tx secondary pyoderma (cephalosporins, lincomycin, fluoroquinolones, clindamycin)*
    • must monitor with deep skin scrapings once monthly*
    • *must tx until 1mo after 2 negative skin scrapings done 1 mo apart*
  199. How do you dx demodicosis?
    • deep skin scraping
    • hair pluck
    • cytology of pustules (might see mites)
    • biopsy (chronically inflammed and thickened lesions)
    • minimum database for underlying diseases
  200. What can predispose dogs to adult onset generalized demodicosis?
    • immunosuppressive corticosteroids
    • hypothyroidism (beware sick euthyroid)
    • hyperadrenocorticism
    • Leishmania
    • neoplasia
    • idiopathic (25%)
  201. What is the txt for adult onset demodicosis (either localized or generalized)?
    • spay if intact
    • ivermectin PO (in ice cream)
    • milbemycin
    • moxidectin
    • amitraz dip after clipping hair coat and bathing in antibacterial shampoo
    • tx secondary pyoderma (cephalosporins, lincomycin, fluoroquinolones, clindamycin)
    • *must monitor with deep skin scrapings once monthly*
    • *must tx until 1mo after 2 negative skin scrapings done 1 mo apart*
  202. What are the AE of ivermectin?
    lethargy, anorexia, mydriasis, edematous wheals
  203. What drugs should not be given at the same time as ivermectin for demodicosis txt?
    ketoconazole
  204. Which canine breeds are predisposed to abcb1-1Δ defect?
    Collie, Shetland Sheepdog, Old English Sheepdog, English Shepherd, Australian Shepherd, McNab, Longhaired Whippet, Silken Windhound
  205. What are the AE of milbemycin?
    Stupor, ataxia, trembling, transient vomiting (rare)
  206. What drugs must be avoided if an animal on avermectin develops neurological signs?
    • diazepam
    • barbituates
  207. What is the txt for severe pododermatitis from demodicosis?
    • 1ml of 12.5% amitraz concentrate in 30 ml mineral oil q24hrs
    • -must have owners wear gloves
  208. What are the AE of amitraz?
    lethargy, hypoglycemia, hyperglycemia, V
  209. How can amitraz AE be reversed?
    give yohimbine or atipamazole
  210. What is the tx for demodicosis that persists >6mo?
    Need lifelong miticidal txt, but try to drop dose over time
  211. What are the common feline demodex species, and where are they found?
    • Demodex cati (hair follicles)
    • Demodex gatoi (stratum corneum)
  212. What conditions commonly underly feline generalized demodicosis?
    • DM
    • FeLV
    • FIV
    • hyperadrenocorticism
  213. What are the CS of feline demodicosis?
    • alopecia
    • otitis externa
  214. Is feline demodex contagious?
    D. gatoi is contagious
  215. How is demodicosis dx in felines?
    • D. cati - deep skin scraping
    • D. gatoi - superficial skin scraping (esp of other cats in household)
  216. How is feline demodicosis tx?
    • moxidectin applied weekly
    • lime sulfur if D. gatoi
    • amitraz
    • milbemycin
  217. What are the characteristics of canine scabies?
    • highly contagious
    • *intensely pruritic*
  218. What causes canine scabies?
    Sarcoptes scabiei canis
  219. What is the pathogenesis of canine scabies infestation?
    • Direct transmission from infected animals (mites are obligate parasites, so fomite transmission is less likely)
    • Female burrows and lays eggs
    • Complex hypersensitivity rxn
  220. Is canine scabies zoonotic?
    • Yes, but humans are a dead-end host
    • Can have continuing signs of pruritus if constantly re-infested by dog with scabies
  221. How is canine scabies tx?
    • *Must tx every animal (including humans) in the contact*
    • selamectin (adulticide, requires 2 txt/month for 2 months)
    • ivermectin (same as selamectin)
    • 2% lime sulfur (2x / week for a month)
    • milbemycin oxime
    • topical moxidectin
  222. What animals are most likely to get canine scabies?
    young (exposed to more infested environments like shelters, breeders, pet stores)
  223. What are the CS of canine scabies?
    • *intense pruritus*
    • dramatic erythematous maculopapular eruption (red rash) with crusts and alopecia on the ventrum, around the pinna and lateral elbows
  224. How is canine scabies dx?
    • Hx: contagion, pruritus and zoonosis
    • Skin scraping (50% sensitive)
    • Response to txt
  225. What causes feline scabies?
    Notoedres cati
  226. What are the characteristics of feline scabies?
    • highly contagious
    • *intensely pruritic*
  227. What is the pathogenesis of feline scabies infestation?
    • direct transmission from infested cat (obligate parasite)
    • Female burrows, lays eggs
    • Complex hypersensitivity rxn
  228. Is feline scabies zoonotic?
    Rarely, and humans are a dead end host
  229. What are the CS of feline scabies?
    crusting, scaling, lichenification, erythema, alopecia, excoriation on the head and pinna, maybe see on the feet too
  230. How is feline scabies dx?
    • Hx: pruritus, contagion, zoonosis
    • PE
    • skin scraping (>50% sensitivity)
    • Response to txt
  231. How is feline scabies tx?
    • selamectin
    • ivermectin
    • 2% lime sulfur
    • amitraz
    • milbemycin oxime
    • *treat all animals (including humans) in contact
  232. What are the characteristics of Cheyletiella dermatitis?
    • Contagious
    • Variably pruritic
  233. Where is Cheyletiella dermatitis seen?
    • Areas with poor flea control (prevented by Frontline and Advantage multi)
    • On rabbits
  234. What is the pathogenesis of Cheyletiella dermatitis?
    • Directed transmission from infested animals (obligate parasite)
    • Stay on epidermal surface (no burrowing)
    • Hypersensitivity rxn
  235. Is Cheyletiella zoonotic?
    Likely under-dx
  236. What are the CS of Cheyletiella dermatitis?
    • Scaling and crusting
    • Variable pruritus
    • See on the dorsum, but varies with species
    • -dog have dorsal scale
    • -cats have miliary dermatitis
    • -rabbits have crusts on head, neck and ears plus scale on the dorsum
  237. How is Cheyletiella dx?
    • Hx: contagion, pruritus, zoonosis
    • PE
    • skin scraping
  238. How is Cheyletiella dermatitis tx?
    • selamectin
    • ivermectin
    • 2% lime sulfur
    • amitraz
    • milbemycin oxime
    • *must tx all in contact animals (including humans)*
    • Wash and dry the bedding (heat kills them)
  239. What species of lice can infest dogs?
    • Linognathus setosus (Anoplura sucking louse)
    • Trichodectes canis (Mallophaga biting louse)
  240. Where is lice infestation seen?
    • Areas of poor flea control
    • Flea adulticides = lice adulticides
  241. What species of lice can infest cats?
    Felicola subrostratuas (Mallophagia biting louse)
  242. What is the tx for lice infestation?
    • selamectin
    • *must tx all animals in the house of the same species (lice are very species specific)
  243. What is the definition of keratinization?
    Genetic program of keratinocytes in the basal cell layer to mature, die, & produce the stratum corneum
  244. What is the definition of cornification?
    Keratinization + formation of lipid interstitium holding the dead keratinocytes together
  245. What is the definition of scale?
    excess stratum corneum
  246. What is the definition of a crust?
    scale + blood, pus, microbes, cells
  247. How is the stratum corneum described?
    corneocytes plus filaggrin, ceramides, other lipids
  248. How is the stratum granulosum described?
    Production of keratohyaline granules (keratin, pro-filaggrin) and lamellar granules (ceramindes, other lipids)
  249. How is the stratum spinosum described?
    keratinocytes begin to ‘flatten’; cytoplasmic attachments via desmosomes
  250. How is the stratum basale described?
    Keratinocytes undergo mitosis several times before becoming nonmitotic and progressing ‘upwards’
  251. What are the primary keratinization / cornification disorders?
    • genetic (aka breed-related aka idiopathic)
    • congenital
    • nutritional
  252. What are the secondary keratinization / cornification disorders?
    Parasitic, endocrine, infectious, neoplastic...
  253. Are primary or secondary keratinization / cornification disorders more common?
    Secondary
  254. What is the current term for sebhorrhea?
    primary keratinization / cornification defect (PKD)
  255. What breeds are predisposed to PKD?
    cocker spaniel, irish setter
  256. What are the CS of PKD?
    • scale and crust on pinna and trunk
    • ceruminous otitis externa
    • rancid odor
    • variable pruritus
    • secondary bacterial or yeast infx
  257. How is PKD tx?
    • Shampoos with sulfur or salicylic acid
    • treat the secondary infx
    • retinoids, VitA
    • maybe corticosteroids, cyclosporine
  258. What is canine ichthyosis?
    Rare, congenital, hereditary group of diseases that causes excessive scaling
  259. What breeds get canine ichthyosis?
    Breeds: Norfolk terriers (autosomal recessive disorder of keratin 10), Golden Retrievers, Cavalier King Charles spaniels, American Bulldogs
  260. How is canine ichthyosis dx?
    skin biopsy
  261. How is canine ichthyosis tx?
    Can't, so neuter to prevent
  262. What breeds get idiopathic regional cornification defects?
    • Kerry blue terriers and Dogue de Bordeaux: excessive foot pad fronding
    • Spaniels and brachycephalics: nasal planum
    • Labs: parakeratosis of nasal planum
  263. What breeds get sebaceous adenitis?
    Vizla, Akita, Standard Poodle, Lhasa Apso
  264. What is sebaceous adenitis?
    idiopathic granulomatous destruction of sebaceous glands
  265. What are the CS of sebaceous adenitis?
    • scaling and alopecia
    • secondary infx
  266. How is sebaceous adenitis dx?
    • signalment: predisposed breeds
    • CS: alopecia and scale
    • skin scraping: follicular casting
    • skin biopsy: shows absence of hair follicles - need good pathologist
  267. How is sebaceous adenitis tx?
    • VitA - expect improvement in 6weeks
    • *will need to monitor tear production with STT*
    • cyclosporine can help
  268. What is Zn responsive dermatitis?
    • syndrome I: Huskies and white GSDs get crusting and scaling of muco-cutaneous junctions, elbows and footpads
    • syndrome II: any breed fed excessive Ca or plant protein. See crusting plaques, fissured foot pads, fever and malaise
  269. What is the pathophysiology of Zn responsive dermatitis?
    • syndrome I: defect in  Zn absorption
    • syndrome II: excessive Ca or plant protein in diet
  270. How is Zn responsive dermatitis dx?
    • Hx: breed predisposition
    • histo: follicular and epidermal parakeratotic hyperkeratosis
  271. How is Zn responsive dermatitis tx?
    • syndrome I: elemental Zn and OVH
    • syndrome II: balance diet, can add Zn supplementation to get faster resolution
  272. What is an acral lick dermatitis?
    • Thickened, slightly depressed hyperpigmented erythematous, alopecic lesion
    • Left front leg
    • Large breeds predisposed
    • Young - middle aged dogs
  273. What causes acral lick dermatitis?
    • behavior
    • deep pyoderma
    • allergy (AD)
    • Rare: neoplasia, orthopedic devices, osteomyelitis, other infections
  274. What CS do you NOT expect with acral lick dermatitis?
    lameness
  275. How is acral lick dermatitis dx?
    • Hx
    • CS
    • rads
    • biopsy
    • culture (both deep and superficial)
  276. How is acral lick dermatitis tx?
    • Antibiotics
    • Psychoactive medications (Amitryptiline, Clomipramine)
    • Narcotic antagonists (Naltrexone, Hydroxycodone)
    • Fluocinolone acetonide in DMSO base (SynoticTM)
    • Flunixin meglumine (BanamineTM)
    • Capsaicin cream
    • Heet ® - OTC, contains capsaicin
  277. What is a common secondary pathogen from grass awns?
    Actinomyces
  278. When are grass awn FB more likely to be seen?
    summer and fall
  279. How are foxtails tx?
    • Remove if possible
    • Abx (empircial or C&S)
  280. What are the types and causes of ischemic dermatosis?
    • Dermatomyositis
    • Ischemic dermatitis due to vaccines or other medications
    • Idiopathic ischemic dermatoses
  281. What are the characteristics of dermatomyositis?
    • Unknown etiology
    • Collies, shelties = autosomal dominant transmission
    • Early onset, < 6 months
  282. What are the CS of dermatomyositis?
    • Alopecia, depigmentation, erythema, scarring
    • Myositis (if present) affects muscles of mastication and limb girdles
    • Severe cases = megaesophagus
  283. What is a strong CS that points you toward dermatomyositis / ischemic dermatosis?
    Inner pinna affected but no otitis externa
  284. How is dermatomyositis / ischemic dermatosis dx?
    • Hx: breed
    • Skin histopathology: ischemic dermatosis
    • Muscle histopathology: myositis
  285. How is dermatomyositis / ischemic dermatosis tx?
    • Pentoxifylline (methylxanthine family)
    • Tacrolimus
    • Cyclosporine
  286. What are the AE effects of pentoxifylline (methylxanthine family)?
    Vomiting, hyperexcitability
  287. What causes ischemic dermatosis?
    • Drug
    • Idiopathic
    • Rabies vaccine frequently implicated or suspected
    • -vx rxns may occur 6 months later
  288. What are the characteristics of juvenile cellulitis aka (sterile) juvenile pyoderma aka puppy strangles?
    • Idiopathic
    • Dogs < 3 months old (rarely, adults)
    • Breed: any, but commonly retrievers, dachshunds, and Brittany spaniels
  289. What are the CS of juvenile cellulitis?
    • Suggestive of infection, but NO organism identified (sterile pyogranuloma)
    • Mandibular lymphadenopathy (may fistulate)
    • Edema, pustules, papules, or crusts around the eyes, mouth, muzzle, ears
    • Lethargy, fever and anorexia
    • Sterile arthritis
  290. How is juvenile cellulitis tx?
    • Pred (because it's sterile) + abx (cephalosporin, but it's not infectious...more CYA)
    • Dogs feel and look better within 24 hours of txt
  291. How is juvenile cellulitis dx?
    Clinical sx, aspirates if needed
  292. What is the px for juvenile cellulitis?
    • Approximately 10% of dogs will relapse after the month of treatment is stopped
    • Older dogs may require longer Rx, sometimes with other drugs (azathioprine)
    • Cyclosporine has been used in a few dogs with good success ($$$)
  293. What is the definition of otitis externa?
    • Inflammation of the external ear canal epithelium
    • + / - pinnal dermatitis
  294. What are the characteristics of the external ear canal?
    • Vertical and horizontal canals
    • Modified squamous epithelium
    • Numerous large sebaceous & ceruminous glands
    • Hair follicles
  295. What is the tympanic membrane, and why is it important?
    • White, oval shaped membrane that relays vibrations to ossicles
    • Has two parts: pars flacida (dorsal, vascular) and pars densa (ventral)
    • Divides external ear from the middle ear
    • TM rupture -> otitis media
  296. What are the most common age and etiology of otitis externa in dogs and cats?
    • Dogs: 5–8 years of age from allergic dermatitis
    • Cats: 1–2 years of age from ear mites
  297. What are some predisposing factors of otitis externa?
    • Alter microenvironment of the ear canal
    • Breed ear conformation
    • High humidity in ear canal
    • Obstructive ear disease
    • Treatment errors
  298. What aspects of breed conformation can predispose to otitis externa?
    • Pendulous pinnae
    • Hairs within ear canal (hirsutism)
    • Narrow canal conformation
    • Increased # of apocrine glands
  299. What can cause increased humidity in the ear canal?
    • Poor anatomical ventilation
    • Frequent swimming / bathing
    • Obstruction of ear canal (tumors or polyps, inflammation -> epithelial swelling)
  300. What therapies should you not do to tx otitis externa?
    • Mechanical trauma (plucking hair, use Q-tips that push debris towards TMb)
    • Irritant topical products
    • Improper antibiotic usage
  301. What are some primary causes of otitis externa?
    • Allergy (AD, CAFR)
    • Contact allergy
    • Parasites
    • Foreign bodies
    • PKD
    • Neoplasia
    • Immune–mediated diseases
  302. What otic rx commonly causes a contact reaction?
    neomycin
  303. What parasites can cause otitis externa?
    • Otodectes cynotis (50% in cats, 10% in dogs)
    • Demodex canis
    • Otobius megnini
  304. What neoplasia can cause otitis externa?
    • Ceruminous gland ademomas
    • Adenocarcinomas
    • SCC
  305. What immune-mediated diseases can cause otitis externa?
    • PF
    • Systemic lupus erythematosis
    • Erythema multiforme
    • Ischemic dermatopathy
    • Juvenile cellulitis
  306. What factors can perpetuate otitis externa?
    • Bacterial organisms
    • Fungal organisms
    • Otitis media
    • Chronic pathologic change (irreversible)
  307. What are the common bacterial pathogens in otitis externa?
    • Staph pseudintermedius
    • Strep sp.
    • Pseudomonas sp.
    • Proteus sp.
    • *Often have resistance*
  308. What are the common fungal pathogens in otitis externa?
    • Malassezia (but also normal ear flora)
    • Candida sp. (rare)
    • Aspergillus (rare)
    • Dermatophytes & systemic fungal mycoses (cause pinnal dermatitis, not directly otitis externa)
  309. When should you suspect otitis media?
    With otitis externa EVEN if TMb intact
  310. How is otitis media tx?
    • Systemic abx
    • +/- surgery (bulla osteotomy)
  311. How can otitis media be dx?
    • CS
    • Imaging (CT)
  312. What are the clinical sequela to otitis externa?
    • Epithelial hyperplasia & glandular hyperplasia
    • Calcification of auditory canal
    • Fibrosis of dermis & subcutis
  313. How is otitis externa dx?
    • Hx + PE
    • Otoscopic examination
    • Cytology
    • Culture & sensitivity
    • Imaging studies
    • Myringotomy (incise TMb)
    • Biopsy
  314. When is it more necessary to perform culture & sensitivity in ear disease?
    • otitis media
    • cytology with lots of rods
    • poorly responsive cases
  315. What are the tx principles for otitis externa?
    • Make a specific diagnosis & identify all factors involved
    • Use ear cleaner prior to treating with appropriate topical +/- systemic therapies
    • Instruct owners how to clean ears & apply medications
    • Re-evaluate frequently
  316. What are the characteristics of ear cleaners for otitis externa?
    • Modified cleaning / drying solutions : antimicrobial properties & mild ceruminolytic agents
    • Examples: Epi-Otic® , Oti-clens®, Chlorhexi Derm®, Malacetic Otic® Douxo micellar solution®
    • Potent ceruminolytic agents so always flush with saline after use
  317. What do the common combination otitis externa preparations have?
    • topical antibiotic, glucocorticoid & an anti-fungal
    • E.g. Tresaderm®, Otomax®
  318. When are glucocorticoids used for otitis externa txt?
    • Antipruritic + anti-inflammatory
    • Decrease sebaceous & apocrine gland secretion
    • Often in combination products
    • Used as sole topical agent in allergic or ceruminous otitis
  319. What are the systemic therapies for otitis externa?
    • Antibiotics: cases of otitis media or severe inflammation
    • Glucocorticoids: short course to diminish inflammation
    • Anti-fungals: refractory otitis externa or otitis media due to yeast

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