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107 Cards in this Set
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How might you differentiate b'twn spontaneous & self induced alopecia? ****
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spontaneous
-well demarcated -usually less inflammation -hair epilates easily -intact hair tips self-induced -not well-demarcated -usually more inflammation -hair does NOT epilate easily -broken hair tips: can feel |
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What are the phases of the hair follicle cycle?
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early anagen --> late anagen --> catagen --> telogen --> early anagen
-anagen: growing phase -telogen: resting phase -in most dogs, most hairs are in telogen -in dogs like poodles, most hairs are usually in anagen |
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What is the diagnostic approach to spontaneous localized alopecia? ****
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skin scrape
trichogram +/- fungal culture (if appropriate) skin bx |
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What are some disorders of follicular cycling that produced generalized alopecia?
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endocrine diseases w/ follicular arrest: Cushing's, hypothyroidism, hyperestrogenism
genetic diseases w/ follicular arrest: alopecia X, recurrent flank alopecia, color dilution alopecia, black hair follicular dysplasia diseases of cycling synchronization: telogen effluvium, anagen defluxion |
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Cushing's in dogs
a. pathogenesis of alopecia b. common skin lesions |
a. glucocorticoid excess (endogenous or exogenous) --> anagen phase terminated --> hair follicles stop cycling & undergo atrophy --> spontaneous expulsion of hair shafts --> alopecia
b. bilaterally symmetric truncal alopecia, skin atrophy (steroids interfere w/ collagen production in dermis), comedones (dilated follicles: contents not expelled --> comedones), calcinosis cutis (hydroxyapatite deposition; pathognomonic), variable scaling -predisposes to demodicosis d/t chronic immunosuppression |
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hypothyroidism
a. pathogenesis of alopecia b. common skin lesions |
a. ↓ availability of thyroid hormones --> hair follicle cycling slows down --> predominance of telogen phase (w/o atrophy: no shedding) --> slow hair growth --> friction alopecia (hair fails to regrow)
b. seen in 60-80% of affected dogs -spontaneous alopecia (25-55%), scaling +/- greasy coat (10-40%), hyperpigmentation (20%), myxedema (very rare: accumulation of mucin in skin) -predisposes to bacterial skin infections: if hair fails to regrow following tx of infection, think of hypothyroidism |
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hyperestrogenism
a. common causes b. clinical signs c. common skin lesions |
a. intact females: estrogen producing cystic or neoplastic ovaries
-intact males: estrogen producing testicular neoplasms (ex. Sertoli cell tumor) -exogenous estrogen administration b. feminization: very sensitive/specific sign for this condition -females: enlarged vulva, gynecomastia -males: pendulous prepuce, gynecomastia - myelosuppression c. +/- alopecia, seborrhea, hyperpigmentation of caudomedial thighs, abdomen, flank, & neck |
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color dilution alopecia ****
a. pathogenesis b. breeds affected c. common skin lesions d. tx |
a. dilute coat color phenotype related to disturbances of transport of melanosomes from melanocytes to hair bulb keratinocytes
-dilute phenotype assoc. w/ focal to diffuse hair loss d/t to insufficient production of hair b. individuals w/ dilute coat color (most common: Dobermans, yorkies, dachshunds) c. varies w/ breed: focal to generalized alopecia at areas of dilute coat color, variable scaling, variable predisposition to bacterial skin infections (esp. Dobermans) d. objective: induce hair cycling non-specifically -drug of choice: melatonin (doesn’t always work) |
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alopecia X
a. pathogenesis b. breeds affected c. common skin lesions d. tx |
a. genetic defect of hair cycling: no re-entry into anagen (stuck in telogen)
b. Nordic breeds w/ plush coat (ex. Pomeranians, Keeshonds, Samoyeds, Chows, etc.) -these breeds have hair that normally doesn’t cycle often c. spontaneous bilaterally symmetric alopecia affecting caudomedial thighs, abdomen, flanks, neck, ears (starts on neck, ventrum) -friction alopecia: hair doesn’t grown back d. objective: induce hair cycling non-specifically drug options -melatonin: cheap, no side effects, works in most dogs -other: sex hormones, inflammation, low dose mitotane, trilostane |
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recurrent flank alopecia ****
a. pathogenesis b. breeds affects c. common skin lesions d. tx |
a. photoperiod dependent localized telogen arrest (waxes & wanes)
b. boxers, bulldogs, Airedales, etc. c. patchy alopecia & hyperpigmentation affecting flank, rump d. objective: induce hair cycling non-specifically -drug of choice: melatonin or no tx |
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What is the pathogenesis of black hair follicular dysplasia?
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white hair normal, alopecia in black hair: melanocytes cannot distribute melanosomes to keratinocytes
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What is the pathogenesis of telogen effluvium?
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significant systemic insult (ex. high fever, pregnancy, severe illness, sx) --> synchronization of all follicles in telogen --> dramatic shedding of hairs during next anagen (1-3 mo. after initial insult) --> alopecia
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What is the pathogenesis of anagen defluxion?
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significant systemic insult (ex. chemo) --> abrupt disruption of normal follicular activity (hair follicles damaged in early anagen) --> alopecia develops during same anagen (w/in 1-3 d. of insult)
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What are some disorders of follicular growth +/- cycling that produce generalized alopecia?
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congenital/hereditary alopecias:
hairless breeds (ex. Chinese crested, Mexican hairless): follicular ectodermal dysplasias X-linked anhydrotic ectodermal dysplasia: very uncommon -follicular + apocrine + dental ectodermal dysplasia (ED1) |
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How is canine demodicosis diagnosed?
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deep skin scrape: almost 100% sensitivity
trichogram: start here b/c least traumatic, but low sensitivity, esp. w/ local dz if infected, collect pus & look for organisms on unstained slide (new method) skin bx sample from center of alopecic patches |
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What are some etiologies of post-folliculitis alopecia in dogs & cats?
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dogs
-#1: bacterial folliculitis (~80%) -#2: demodectic folliculitis (~19%) -#3: dermatophytic folliculitis (~1%) cats -#1: dermatophytic folliculitis -#2, 3: bacterial, demodectic folliculitis (very rare) immunological folliculitis (alopecia areata): rare to extremely rare rhabditic folliculitis (Pelodera): rare to extremely rare |
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What are common skin lesions seen w/ bacterial folliculitis?
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may present as alopecia, pustules, pruritis
alopecia more common in short coated breeds & is usually located on thorax & abdomen (macules, papules, pustules) |
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juvenile onset canine demodicosis ****
a. pathogenesis b. common skin lesions c. px |
a. genetic predisposition
b. focal areas of alopecia in 3-6 mo dogs lesions common on face, feet c. most recover w/o tx, ~10% become generalized |
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adult onset demodicosis ****
a. pathogenesis b. common skin lesions |
a. d/t underlying immune suppression: steroid administration, Cushing’s, hypothyroidism, chemotherapy
-cannot determine underlying cause in 20-30% of cases b. usually present w/ alopecia +/- 2º pyoderma -severe cases: furuncles (boils), draining tracts, lymphadenopathy, hyperthermia, anorexia |
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What are some clinical features & distributions of canine demodicosis? ****
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-not usually pruritic unless accompanied by 2º bacterial infection
-dog w/ grayish pigmented skin w/ comedones: usually demodicosis -deep pyoderma: think demodicosis localized: 90% juvenile onset, 10% adult onset generalized: 10% juvenile onset, 90% adult onset pododemodicosis: > 90% adult onset (hardest to tx: guarded px) |
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What is the tx for canine demodicosis? ****
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investigate & tx underlying conditions
tx 2º bacterial infections -swelling or draining tracts = infection initiate parasitcidal therapy -amitraz dip q 1-2 wks -milbemycin or ivermectin SID: if amitraz not effective *seem more effective than amitraz, but expensive conduct monthly evaluations continue tx until at least 2 consecutive negative scrapes/plucks may take 3-6 mo. for clinical resolution + additional 3 mo. for negative scrapes |
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What is the pathogenesis of dermatophytosis?
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infection of hair shaft +/- stratum corneum w/ keratinophilic fungi (require keratin to survive)
infestation --> hair shaft invasion --> dermatophytic folliculitis --> spontaneous alopecia |
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What are the etiologic agents of dermatophytosis? ****
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Microsporum canis
-90-95% of cases in dogs, 100% of cases in cats -reservoir: cat (may carry as inapparent infection) Microsporum gypseum -reservoir: dirt (may see in dogs that root in dirt) Trichophyton metagrophytes -reservoir: small rodents |
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What are the clinical signs of dermatophytosis?
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variable pruritis
if you see focal alopecia & inflammation in a cat (esp. long haired): think dermatophytosis 1st -spontaneous remission occurs in most cats, except long haired cats |
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How is dermatophytosis diagnosed? ****
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Wood’s lamp exam: most strains of M. canis fluoresce a green apple color
trichogram: microscopic exam of plucked hair shafts may reveal fungal spores & hyphae *Wood’s lamp + trichogram: pluck fluorescing hairs to confirm dx fungal culture: pluck fluorescing hairs, brush w/ toothbrush, pluck hairs from edge of a lesion skin bx sample from edge of lesions |
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tx for dermatophytosis
a. animal b. environment |
a. topical therapy: miconazole (shampoos, lotions, creams, sprays: safe & well tolerated), ketoconazole, enilconazole (excellent for dogs, toxicity reported in cats), chlorhexidine?, terbinafine
-systemic therapy: griseofulvin (teratogenic, idiosyncratic BM suppression) , ketoconazole, itraconazole ($$), terbinafine, lufenuron? b. very contagious d/t spores -remove fomites -chlorine bleach disinfection: 1:10 dilution -enilconazole |
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canine alopecia areata
a. pathogenesis b. common skin lesions c. px |
a. lymphocytic destruction of hair bulb
b. usually bilaterally symmetrical facial alopecia c. many cases spontaneously regress |
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What are some disorders of follicular ischemia that produce local or multi-focal alopecia?
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rabies vaccine rxns
canine juvenile dermatomyositis |
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rabies vaccine rxns
a. pathogenesis b. common skin lesions c. breeds affected |
a. at site of injection: Ag induced lymphocytic arteritis --> ischemia --> follicular involution
b. focal alopecia, thickening in center of lesion (2-3 mo. after vaccination) -rarely, may be generalized: common sites are ear tips, tail tip c. usually small dogs |
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canine juvenile dermatomyositis
a. affected breeds b. common skin lesions c. tx |
a. young collies, shelties
b. transient vesicles followed by ulceration & scarring alopecia (bilaterally symmetric), hypopigmentation -affected areas: bridge of nose, peri-ocular skin, anterior forelimbs, ear & tail tips -myositis can occur concurrently c. pentoxyfylline OR topical tacrolimus ointment BID for 3 mo. (topical immunosuppressant: very good results) |
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What is the diagnostic approach to superficial pustules? ****
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-aspiration cytology of intact pustule
-tx for bacterial skin dz -if cytology does not support superficial pyoderma or animal fails to respond to ABs *bacterial culture of pustule contents *fungal culture of hair & scales *skin bx of intact pustule |
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What is the mechanism of pustule formation?
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pustule: elevated, circumscribed lesion full of granulocytes
infectious agents (~95%) OR Ab binding to auto-Ags --> granulocyte chemotaxis |
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What are causes of superficial pustular dermatoses in dogs & cats? ****
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dogs
-bacterial folliculitis & impetigo: ~90% -pemphigus foliaceus (PF): ~8% -pustular dermatophytosis: ~2% cats -pustules are uncommon in cats: likely PF -PF > bacterial folliculitis & impetigo very uncommon (immunologic): subcorneal pustular dermatosis, eosinophilic pustular folliculitis |
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What are the 2 main forms of superficial pyoderma & what is the difference b'twn them?
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bacterial folliculitis
-infection confined to hair follicle --> small, scattered lesions -don’t R/O if you don’t see pustules: commonly see many lesion types (macules, crusts, papules) bacterial impetigo -infection in b’twn hair follicles --> large round pustules that tend to spread & may become confluent -crusts & epidermal collarettes: may be d/t exfoliative toxins from Staph intermedius |
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What is the pathogenesis of superficial pyoderma?
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-superficial pyoderma implies that infection has not extended beyond level of follicular isthmus (where sebaceous gland enters hair follicle)
-majority of cases caused by Staph intermedius -any condition that disruputs normal cutaneous barrier function or compromises immune system may predispose to development of pyoderma |
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What are some causes of recurrent episodes of superficial pyoderma?
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glucocorticoid administration
endocrine dz: Cushing’s, hypothyroidism allergic dz: atopic dermatitis, flea allergy, food rxn parasitic dz: most ectoparasites |
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How is superficial pyoderma diagnosed? ****
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-cytology: aspiration, smear, swab (collect pus from intact pustule)
-cytology: numerous degenerate neutrophils w/ intracellular cocci -bacterial C/S -response to ABs: may do for a single isolated episode -skin bx: if all else fails |
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How is superficial pyoderma treated? ****
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topical antimicrobial agents
-shampoos: 1-2x / wk (if generalized) *chlorhexidine, benzoyl peroxide, ethyl lactate, triclosan -ointments, gels, creams: SID-BID *mupirocin, erythromycin, clindamycin oral ABs -SID to BID for 3-6 weeks & at least 1 wk. beyond resolution of clinical signs -1st round: TMS, Clavamox, Cephalexin *cheapest, best chance to work, fewest side effects -2nd round: Clindamycin -3rd round: enrofloxacin, marbofloxacin *indications: unusually severe non-Staph (ex. Pseudomonas) pyoderma OR proven resistance to other ABs -Staph NOT susceptible to Amoxicillin d/t β-lactamase production: NEVER use for skin infections in dogs! if recurrent (w/in a few wks, NOT months later): ID & correct any underlying dz |
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How is recurrent idiopathic pyoderma treated?
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prophylactic use of antibacterial shampoos
bacterial vaccines -staphage lysate: Staph aureus extract -immunoregulin: Propionibacterium acnes extract intermittent (“pulse”) AB therapy -DON’T use chronic low dose ABs --> bacterial resistance |
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pustular dermatophytosis
a. etiologic agent b. clinical signs c. dx d. tx |
a. Trichophyton spp.
b. uncommon: may see in hunting terriers usually presents as small pustules on face c. hard to dx: easily confused w/ PF -submit scales & hair from affected area for fungal culture d. same as regular dermatophytosis |
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pemphigus foliaceus ****
a. predisposed breeds b. pathogenesis c. suspected triggers |
a. Chows, Akitas
b. auto Abs against keratinocyte proteins --> cell-cell separation in superficial epidermis (acantholysis) massive neutrophil immigration --> pustule formation c. sun exposure (#1), possibly some drug rxns |
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pemphigus foliaceus ****
a. clinical forms b. common skin lesions |
a. classical form
generalized form pedal form: foot pad crusting & pustules is fairly unique to PF (rarely, dog may have only foot pad lesions) feline PF: crusts, papules inside ear pinna: almost pathognomonic b. progress from erythematous macules & papules to large irregular & coalescing pustules (bilaterally symmetric), scales, erosions, & crusts -face, feet &/or abdomen -severity often waxes & wanes |
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What is the tx for pemphigus foliaceus?
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oral glucocorticoid monotherapy: start here, try for minimum of 4-6 wks
-start w/ very high doses for just a few days, then ↓ dose sharply -drug options: pred, methyprednisolone, triamcinolone, dexamethasone oral combination immunosuppression: used if steroids alone don’t help -glucocorticoid + azathioprine OR chlorambucil OR cyclophosphamide -tx until remission, then slowly withdraw drugs (stop steroids 1st) -~20% of dogs can come off all drugs w/o relapse -monitor liver values q 1-2 wks if on azathioprine: causes hepatitis in 60% of dogs UPenn study: 60% of dogs using standard tx regimen died during study -adverse effects d/t very high dose steroids for long periods & hepatic effects of azathioprine |
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How is pemphigus foliaceus diagnosed? ****
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cytology: aspiration, smear, swab
-cytology: neutrophils w/ acantholytic keratinocytes -neutrophils are non-degenerate, no bacteria -lots of free floating keratinocytes (acanthocytes): can also see w/ impetigo, dermatophytosis skin bx of intact pustule for histopath: often diagnostic +/- lack of response to AB therapy +/- bacterial C/S +/- immunologic tests: available at NCSU only -skin fixed auto Abs -serum auto Abs against keratinocytes |
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What is the most common autoimmune skin dz in dogs & cats?
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pemphigus foliaceus
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What is the diagnostic approach to erosions & ulcers? ****
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cytology
skin bx -elliptical excision encompassing center, edge, & periphery of lesion -deep punch bx of center of ulcer if deep vasculitis suspected -may also bx erythematous areas (early lesions) |
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What is the difference b'twn an ulcer & an erosion? ****
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both are non-specific lesions
erosion: interruption of epidermis only (does NOT bleed) ulcer: loss of epidermis & disruption of basement membrane (bleeds easily) |
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What are some mechanisms of erosion formation? ****
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secondary to pruritis & self trauma (#1): pyotraumatic dermatitis (hot spots)
secondary to mechanical trauma: intertrigo (skin fold pyoderma) secondary to superficial pustules: bacterial impetigo, PF secondary to superficial epidermal edema: necrolytic migratory erythemai secondary to epidermal necrosis: erythema multiforme complex |
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What are some predisposing factors for pyotraumatic dermatitis (hot spots)? ****
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allergic skin dz (FAD most common), otitis externa, ectoparasites
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What are some breed predilections, predisposing factors for intertrigo (fold pyoderma)? ****
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common in breeds w/ generalized or focal abundance of skin: Shar Pei, Basset, Bulldog, etc.
focal problems can be found in lip folds of Spaniels or “screw tail” of some brachycephalic breeds obesity predisposes 2 skin surfaces being rubbed together --> accumulation of moisture, bacteria, yeast |
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What is the treatment for surface pyodermas (hot spots, skin fold pyoderma)?
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clip & cleanse
topical therapy: should suffice -chlorhexidine solutions: Malaseb is a good choice (chlorhexidine + miconazole) -AB gels oral AB therapy?: only if lack of response to topicals, or deeper infection present (suggested my presence of edema, draining tracts) glucocorticoid therapy?: not usually needed -can use topical &/or systemic steroids for 5-14 d. depending on severity of lesion tx underlying dz/defect |
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necrolytic migratory erythema
a. etiology b. pathogenesis c. skin lesions d. tx |
a. chronic fibrosing hepatitis: 80%
-skin lesions occur late in course of dz phenobarb/primidone hepatopathy: 10% glucagonoma: < 10% mycotoxic hepatopathy: 1 case reported b. metabolic cause(s): deficiency of AAs?, FAs?, zinc? c. mucocutaneous scaling, crusting, erosions, ulcerations genitals usually involved most erosions occur in friction areas ~80% of dogs have characteristic footpad lesions: crusting lesions become infected w/ variety of agents d. AA, FA, zinc supplementation: remission of skin lesions for 1-6 mo. if d/t glucagonoma: sx --> quick remission of skin lesions |
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erythema multiforme complex
a. 3 syndromes b. pathogenesis c. distribution of lesions |
a. erythema multiforme major/minor: post-infectious?, rarely caused by drug administration
Stevens-Johnson syndrome: drug administration toxic epidermal necrolysis: drug administration (most severe, least common) b. lymphocytes kill keratinocytes --> dead layer sloughs off c. lesions on face, oral cavity, ears, abdomen |
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What are some mechanisms of ulcer formation? ****
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secondary to pruritis & self trauma: common
secondary to chemical or thermal injury secondary to deep epidermal vesicles: pemphigus vulgaris, vesicular cutaneous lupus, SLE secondary to dermo-epidermal separation: bullous pemphigoid, mucus membrane pemphigoid secondary to ischemia: vasculitis & thrombosis, neoplastic or severe inflammatory dermal nodules |
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What skin lesions may be assoc. w/ systemic lupus erythematosus?
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usually d/t vasculitis: erosion, ulcerations, depigmentation, panniculitis, scaling, hyperkeratosis
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vasculitis ****
a. etiology b. possible clinical signs c. organization of cutaneous vasculature |
a. post-infectious: Ehrlichia, Rickettsia, Bartonella, etc.
post-drug administration systemic lupus erythematosus b. classic lesion of vasculitis is a circular punched out defect representing segment of skin suppled by affected vessel (deep vessel arteritis) if superficial vessels (venules) affected or inflammatory process is slowly progressive, ulceration does not occur & these diseases can present as focal alopecia or ecchymoses lesions often on extremities (paws, tail, ear tips, nose) & may be accompanied by pain & edema when lesion has healed, scarring is common & focal alopecia or losses of pigment are permanent c. capillaries: just below epidermis superficial plexus deep plexus: if obstructed --> ulcers |
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What are the general principles of therapy for scaling disorders?
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ID & tx underlying disorders
ID & tx 2º infections use topical antiseborrheic shampoos |
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What is the difference b'twn crusts & scales? ****
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crusts: “scabs”; corneocytes + fibrin + blood cells, external covers of underlying erosions or ulcers
scales: “flakes”; excess amts. of stratum corneum that does not exfoliate in a normal fashion -no underlying defect of epidermis -nonspecific lesion: ~90% of all skin dz may have scaling |
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What are some dermatoses w/ primary scaling? ****
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primary seborrhea of cocker spaniels
ichthyosis |
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What are some dermatoses w/ secondary scaling? **
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infectious (bacterial, fungal), parasitic, immunological, metabolic, neoplastic
sebaceous adenitis zinc responsive dermatoses exfoliative pyoderma Malasezzia dermatitis Demodex injai |
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primary seborrhea of cockers
a. pathogenesis b. common skin lesions |
a. normal dog: takes 21 d. for basal epidermal cell to be desquamated as a corneocyte
affected cocker: takes 7 d. -more basal keratinocytes dividing more often than normal dogs --> excessive epidermal turnover -↑ basal cell division pushes up keratinocytes --> abnormal cornfication & desquamation -excess cell division also occurs in earl canal epithelium & basal cells of sebaceous glands b. excessive scaling & follicular casts (squames around hair shafts), 1st seen around nipples & on back usually excessive scaling & greasiness on ventral neck, b’twn digits, in skin fold areas scales are adherent otitis externa common more sebum --> more contamination by yeast, bacteria |
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What is the pathogenesis of ichthyosis?
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very rare genetic disorders of epidermal differentiation/ cornification/desquamation
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dermatoses w/ 1º scaling: genetic disorders of cornification (primary seborrhea of cockers, ichthyosis)
a. dx b. tx |
a. signalment, hx, clinical signs
-R/O dermatoses w/ 2º scaling -skin bx b. shampoos: sulfur + salicylic acid, sulfur + salicylic acid + tar, sulfur + benzoyl peroxide -facilitates shedding of scales systemic therapy -vitamin A PO SID-BID *helps in regulation of epidermal differentiation -ABs/antifungals to tx 2º infections |
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sebaceous adenitis
a. predisposed breeds b. pathogenesis c. common skin lesions |
a. standard poodle, akita, samoyed
b. inflammation of sebaceous glands --> destruction of glands lack of sebum --> epidermal scaling & abnormal lubrication of hair follicle openings --> excessive corneocyte accumulation in hair follicle openings c. lesions occur on dorsum & move from cranial to caudal, then ventrally lots of follicular casts: adherent scaling at base of hair shaft -stratum corneum requires sebum to separate from hair shaft loss of undercoat, diffuse alopecia, matted fur 2º bacterial/yeast infections common |
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sebaceous adenitits
a. histopath findings b. tx |
a. bx normal skin slightly beyond scaly edge
early: inflammation of sebaceous glands late: absence of sebaceous glands b. shampoos: sulfur + salicylic acid, sulfur + salicylic acid + tar, sulfur + benzoyl peroxide cyclosporine SID: tx of choice -commonly use ketoconazole to ↓ cyclosporine dose -only 1 study done: very good results, dogs produce new sebaceous glands ABs/antifungals to tx 2º infections vitamin A/ retinoids: somewhat helpful, but no longer recommended d/t success of cyclosporine |
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zinc responsive dermatoses
a. 2 syndromes b. pathogenesis c. common skin lesions d. histopath findings |
a. syndrome I: Nordic breeds (mostly Huskies, Malamutes)
syndrome II: young dogs (often d/t poor diet) b. genetic defect in Zn absorption dietary interference: minerals, phytates (vegetal products) unknown cause(s) c. bilaterally symmetrical adherent scales: pressure points, mucocutaneous junctions footpad scaling & hyperkeratosis (ddx: necrolytic migratory erythema, pemphigus foliaceus) d. marked parakeratosis: early poorly differentiated stratum corneum that’s not going to shed |
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exfoliative pyoderma
a. etiologic agent b. common skin lesions c. tx |
a. exfoliating toxin producing Staph
b. expanding epidermal collarettes +/- pustules, papules c. very responsive to ABs |
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Malassezia dermatitis ****
a. most common organism b. predisposed breed c. pathogenesis |
a. Malasezzia pachydermatis
-normal skin flora: inhabits oral cavity, lip commisures, external ear canals, interdigital webs, perineum, anal sacs b. basset hound c. any cause of skin inflammation --> abnormal cornification, ↓ epidermal defense system, excessive sebum secretion --> overgrowth of commensal yeast +/- bacteria |
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Malassezia dermatitis ****
a. common skin lesions b. dx c. tx |
a. erythema, scaling, greasiness, esp. in fold areas
b. cytology: swab, smears, imprints, surface scrapes, tape strips -don’t rely on # of organisms to make dx dx based on clinical signs & ID of yeast --> tx --> no more yeast on cytology, resolution of signs c. topical therapy -degreasing shampoos -miconazole-chlorhexidine (Malaseb) shampoo, wipes, spray -miconazole shampoos, sprays, lotions -chlorhexidine shampoos, solutions systemic therapy -ketoconazole SID-BID for 2-4 wks -itraconazole |
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Demodex injai
a. predisposed breeds b. common skin lesions c. dx, tx |
a. terriers
b. dorsal scaling & greasiness -no alopecia: doesn’t live in hair follicle c. same as for D. canis (but 2x as long) |
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3 ddx for foot pad hyperkeratosis
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pemphigus foliaceous
necrolytic migratory erythema zinc responsive dermatosis |
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What is the diagnostic approach to canine pruritis? ****
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R/O parasitic dz
-skin scrapes: scabies, other ectoparasites -response to acaricidal tx: scabies, other ectoparasites -response to flea control: fleas, other parasites -fecal float: endoparasites, ectoparasites R/O infectious dz -cytology: bacterial pyoderma, Malassezia -response to ABs: bacterial pyoderma -response to antifungal agents: Malassezia R/O allergic dz -elimination dietary trial: adverse food rxn -refer to dermatologist if clinical signs compatible w/ atopic dermatitis & owner willing to consider immunotherapy -if seasonal: consider seasonal medical therapy OR refer |
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How can you determine if a dog is pruritic or not?
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presence of 2º lesions: d/t self trauma
-excoriations: self induced erosions or ulcers -self induced alopecia -lichenification, hyperpigmentation: if chronic presence of broken hair tips on trichograms presence of hair embedded b’twn teeth presence of hair in feces: esp. in cats |
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What are the 3 main causes of canine pruritis? ***
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parasitic dermatoses
infectious dermatoses: bacterial pyoderma, Malasezzia dermatitis allergic dermatoses |
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scabies ****
a. etiologic agent b. transmission c. skin lesions |
a. Sarcoptes scabiei
b. highly contagious b’twn affected dogs: healthy cats generally not affected zoonotic superficial burrowing skin mite c. erythematous macules, patches, & crusted papules that are very pruritic commonly found on face, ear margins, ventral aspect of body & lateral limbs |
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scabies ****
a. dx b. tx |
a. skin scrapes: superficial, extensive & numerous
-look for crusted papules -not very sensitive method fecal float?: ingestion of mites (serological test): very sensitive, but no longer available in US response to acaricidal therapy: if suspicion for dz is high & skin scrapes negative b. topical acaricides -selamectin spot on (Revolution): total of 3 doses 2 wks apart (tx of choice: cheap, safe, good efficacy) -organophosphate dips: q 1 wk x 4 -lime sulfur dips: q 1 wk x 4 -amitraz dips: q 1 wk x 4 systemic acaricides -ivermectin SQ, PO q 1 wk x 4 -milbemycin PO q 1 wk x 4 or EOD for 15-21 d. pruritis will ↑ when tx starts: OK to give steroids for 1st week or so of tx |
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cheyletiellosis
a. derm lesions b. dx |
a. pruritis, scaling on dorsolumbar area (trunk)
b. demonstration of parasites &/or response to parasiticidal tx (ex. fipronil) |
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trombiculidiasis
a. derm lesions b. dx |
a. folds (b'twn digits, behind ears), poorly haired areas
b. demonstration of parasites &/or response to parasiticdal tx (ex. fipronil) |
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What derm lesions are assoc. w/ Malasezzia dermatitis?
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erythmatous patches & seborrhea affecting primarily face, ears, intertriginous areas (ventral neck, axillae, groin, interdigital area)
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flea allergy dermatitis ****
a. derm lesions b. dx c. tx |
a. papules, pruritis, 2º lesions on dorsolumbar area, hind legs, & abdomen
b. demonstration of fleas or flea dirt intradermal injection of flea extracts allergen specific IgE serology response to flea control c. short term oral glucocorticoid therapy -allergic rxn lasts for several days flea control: adulticides + growth regulators BEST -animals: spray or spot on formulations -environment: sprays -to ↓ flea resistance, change products frequently |
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What is the definition of atopic dermatitis? How does it differ from "atopic like dermatitis"? ****
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atopic dermatitis: genetically predisposed inflammatory & pruritic allergic skin dz w/ characteristic clinical features assoc. w/ IgE Abs against environmental allergens
atopic like dermatitis: inflammatory & pruritic skin dz w/ clinical features identical to those seen in canine atopic dermatitis in which an IgE response to environmental or other allergens cannot be documented |
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atopic dermatitis ****
a. usual age of onset b. primary skin lesions c. secondary skin lesions d. distribution of skin lesions |
a. 6 mo-3 yrs
b. acute: erythematous macules & patches, “micro” papules seen in poorly haired ventral areas (abdomen, concave pinnae), & friction zones (axillae, groin, flexural aspect of legs) 1º lesions often masked by 2º lesions b. excoriations, lichenification, hyperpigmentation, self induced alopecia -allergic rhinitis, allergic conjunctivitis, otic inflammation may be present d. around eyes, muzzle, inside ear, b’twn toes, ventral neck, groin, axilla, abdomen, inside legs, spares back -friction & flexion probably important in formation of lesions |
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atopic dermatitis
a. possible flare factors b. dx |
a. mites, pollens, molds, foods, fleas, bacteria, yeast, contact?, other?
-conditions that trigger relapse of dz or worsening of signs -AD often complicated by Malassezia &.or Staph infection: patients may produce IgE against yeast or bacteria b. suggestive hx compatible signalment characteristic clinical signs R/O resembling pruritic diseases perform intradermal testing/serology +/- diet trial to differentiate AD from ALD -other indications: for allergen avoidance measures, for immunotherapy allergen selection -these tests are NOT diagnostic tests for AD: often (+) in normal dogs |
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What is the tx for atopic dermatitis? ****
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1º goal: ID & eliminate all flare factors (allergens, bacteria, yeast)
-includes excellent flea control, elimination diet, allergen avoidance, frequent bathing, antimicrobial therapy PRN 2º goal: ↓ clinical signs w/ drugs -top 3: oral steroids, oral cyclosporine, topical tacrolimus -other: topical steroids, oral FAs, oral antihistamines, immunotherapy 3º goal: prevent relapses w/ immunotherapy +/- allergen avoidance immunotherapy: administration of gradually increasing quantities of an allergen extract to an allergic subject to ameliorate symptoms assoc. w/ subsequent exposure to causative allergen immunotherapy indicated for use in patients (~10% of dogs w/ AD): -w/ demonstrable & clinically relevant allergic specific IgE Abs -in which allergen contact is unavoidable -w/ clinical signs that respond poorly to antiprurtic drugs, or in which cost or side effects of therapy are unacceptable -whose owners are ready to afford the time, expense & technical aspects of this regimen |
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cutaneous adverse food rxn ****
a. classification b. dx |
a. food intolerance: non-immunologic
food allergies: immunologic -GI -pruritis -otitis -atopic dermatitis -urticaria b. elimination diets -ingredients not fed before -homemade or commercial available -novel ingredients > hydrolysates -trial should last at least 4-10 wks |
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What are some less common allergic dermatoses?
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insect bite allergies
drug allergies |
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What is the diagnostic approach to nodules & draining tracts? ****
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cytology
-nodules: FNA -draining tracts: swabs, smears histopath: if cytology not helpful cultures for infectious organisms: swabs, skin bx -only do after cytology, bx: need an idea of what to culture for |
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What is a:
a. nodule b. draining tract |
a. circumscribed elevation of skin > 1 cm in diameter
b. MF areas of punctate draining ulcerations overlying nodules |
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How are nodules formed?
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cells: inflammatory, neoplastic (90%)
foreign material: exogenous, endogenous |
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What is the algorithm of ddx for nodules & draining tracts? ****
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neoplastic
inflammatory -non-infectious -infection: bacterial, fungal |
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What are some infectious causes of nodules & draining tracts?
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bacterial furunculosis (deep pyoderma)
acne (skin furunculosis) German Shepherd pyoderma? acral lick furunculosis Mycobacterial infection Pythiosis |
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bacterial furunculosis (deep pyoderma)
a. most common organism involved b. derm signs c. other possibles signs d. possible assoc. condition |
a. Staph intermedius
b. may be localized or generalized: lesions (nodules, draining tracts) often b’twn digits, around pressure points c. fever, anorexia, pain, local lymphadenopathy d. demodicosis |
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acral lick furunculosis
a. pathogenesis b. tx |
a. chewing/licking of anterior carpus --> epidermal hyperplasia --> bacterial folliculitis & furunculosis --> more chewing/licking (vicious cycle)
b. systemic ABs for 6 wks or longer (up to 2-3 mo) |
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acne
a. pathogenesis b. tx |
a. large sebaceous glands on chin: hair follicles into which they open become plugged w/ sebaceous & cornified cells --> comedones
occ. bacterial or yeast folliculitis & furunculosis develops --> localized areas of draining tracts (acne) b. topical ABs |
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What is the tx for bacterial furunculosis?
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topical therapy: for localized dz (ex. chin acne)
-antibacterial shampoos? -ointments, gels, creams: focal lesions systemic therapy: needed for most cases -same ABs as for superficial pyoderma: 6 wks (3 wks beyond remission) -bacterial C/S if recurrent R/O demodicosis |
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What are some sterile nodular diseases?
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FB granulomas
calcinoses sterile panniculitis juvenile cellulitis sterile (pyo)granulomas/ histiocytoses eosinophilic granulomas cutaneous neoplasia |
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sterile panniculitis
a. what is it b. causes c. derm signs d. tx |
a. inflammation of hypodermis (cutaneous fat)
b. trauma, infection (ex. Mycobacterium, Pythium), pancreatic (pancreatitis, pancreatic neoplasia), idiopathic c. : firm to fluctuant nodules that rapidly evolve into tracts draining a lipid rich material (opaque, oily), may be painful d. idiopathic: often use broad spectrum ABs before putting on steroids -immunosuppressive doses of corticosteroids may be beneficial |
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juvenile cellulitis
a. derm lesions b. tx |
a. large coalescing pustules & suppurative lymphadenitis develop rapidly on anterior aspect of body; usually marked swelling of face, fever
b. pred (14-21 d.) |
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What are some common cutaneous neoplasms?
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sebaceous adenoma
MCT SCC cutaneous LSA |
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What is:
a. otitis externa? b. otitis media? |
a. acute or chronic inflammation of external ear canal( a problem, NOT a dx; ≠ infection)
b. inflammation of middle ear canal |
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What are some predisposing factors for otitis externa?
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ear canal conformation: stenotic canal, pendulous pinna, hair in ear canal
excessive moisture in ear canal: frequent swimming or bathing high relative environmental humidiity tx effects: hair plucking, grooming powders, overuse of cleaning agents systemic dz: immune suppression, viral, endocrine |
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What are some primary factors that directly cause otitis externa?
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parasites: Otodectes (ear mites), Otobius (spinous ear tick), Demodex
hypersensitivities: AD, adverse food rxn, contact hypersensitivity to ear meds keratinization disorders: primary seborrhea of cockers, hypothyroidism foreign bodies: plant awns, hair, impacted wax, tumors, polyps autoimmune dz (usually pinnal involvement more common) |
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What are clinical ear signs assoc. w/ atopic dermatitis or adverse food rxn?
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erythema of pinna & vertical ear canal, ceruminous otitis, usually assoc. w/ pruritis in other regions of body
2º bacterial &/or yeast infections common |
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What are some perpetuating factors for development of otitis externa?
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maintain & exacerbate inflammatory process; often main reasons for tx failure
bacteria yeast progressive pathologic changes: epidermal hyperkeratosis & hyperplasia, dermal edema & fibrosis, ceruminal gland hyperplasia, stenosis of canal lumen, skin folding, fibrosis, calcificaiton otitis media |
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What are the most common bacterial agents assoc. w/ otitis externa?
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Staph intermedius: 30-50%
Pseudomonas aeruginosa (worst: painful, pus, erosion, malodorous): 5-35% Proteus mirabilis: 4-21% Streptococcus: 4-9% other: Klebsiella, E. coli, Corynebacterium |
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How is otitis externa diagnosed?
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hx
clinical signs PE, incl. otoscopic exam cytology +/- otic cytology (rarely done), CT |
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What are indications for CT in patients w/ otitis externa?
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refractory or recurrent OE, when OM &/or mineralization of external ear canal is suspected, when sx is contemplated
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