Dermatology Exam I

Front 1

Approach to a Dermatology case

Back 1

-Full patient history
-Physical and dermatologic examination
-Diagnostic tests
--scrapings, cytology, etc.

Front 2

Patient History for a dermatology work-up

Back 2

-Essential part of approach to dermatologic disease
-Perhaps the most important aspect
-Use checklist or clinical record form
--can ask owner to fill out form in the waiting room

Front 3

Important questions in dermatology history

Back 3

-Signalment
--LOTS of breed-related dermatoses
-Concurrent systemic signs
--skin is a good marker for internal organ health
-Travel history
--out of state, international
-Other animals in the household, other animals with skin lesions
--remember to ask about human lesions
-Any environmental changes
-Duration of clinical signs
-Initial lesions and distribution
-Progression of lesions and location of lesions
-Pruritus presence (cause or effect, severity, distribution)
-Seasonality of lesions
-Medications and response
-Flea and heartworm preventatives used
-Complete diet history

Front 4

Presence of an Itch

Back 4

-Did it start before lesions? (allergy)
-Lesion started first (endocrineopathy and secondary infection)
-be able to chart the progression of an itch
-Identify severity of scale of 1-10
-Distribution can help with diagnosis

Front 5

Medications and dermatoses history

Back 5

-Important to know previous medications and current medications and response to medication
-Drug, dose, frequency, duration of administration, response, side effects
-Know side-effects of drugs

Front 6

Dermatologic Exam

Back 6

-Be systematic and complete
--do each exam the same way each time
-Examine entire skin surface, ears, claws, mucocutaneous junctions, oral cavity, paw pads
-Describe all lesions in the medical record
-Use specific dermatology vocabulary/terminology
-note configuration, color, distribution of lesions
-Primary vs. secondary
-Take photos!!!

Front 7

Primary Skin Lesions

Back 7

-Primary lesions are changes direct result of disease process
-Have not changed due to disease process, are direct result
-Macules/patches
-Papules/plaques
-Pustules
-Vesicles/Bulla
-Nodule
-Wheal

Front 8

Secondary Skin lesions

Back 8

-Arise from primary lesion that was once present
-can also arise from chronic irritation or inflammation (itch)
-Epidermal collarette
-Erosion/ulcer
-Lichenification
-Excoriations
-Hylerkeratosis
-Fissures

Front 9

Skin lesions that can be primary OR secondary

Back 9

-Alopecia
-Scale
-Crust
-Follicular cyst
-Comedone
-Pigmentary abnormalities

Front 10

Macule/Patch

Back 10

-Primary skin lesions
-Non-palpable, flat areas of pigmentation
--do not stick up from skin
-Macules are smaller, less than 1cm
-Macules coalesce to form patches
-Can be red or other colors, hyperpigmented or hypopigmented
-FLAT lesions

Front 11

Pustules

Back 11

-Primary skin lesions
-“pimple”
-Puss-filled, purulent exudate
-Yellow or green in color
-bacterial skin infections (staph)
-Can be large, associated with hair follicles or not
-Fragile and can rupture
--Rupture to form epidermal collarettes

Front 12

Epidermal Collarette

Back 12

-Secondary lesion
-Result of a ruptured pustule, “footprint” of a pustule
-Circular rim of scale or crust
-Commonly seen with pyoderma/staph infection of skin

Front 13

Vesicle

Back 13

-Primary skin lesion
-Elevations of epidermis filled with clear fluid
-“Blister”
-Very fragile, rupture easily
-Can be seen with viral infections or other irritations of the skin
-Often seen with blistering diseases
--Epidermolysis bullosa inquisita

Front 14

Ulcer

Back 14

-Secondary skin lesion
-Defects in epidermis, epidermis is completely lost down to the basement membrane
-can be a burst vesicle
-Hard to clinically differentiate from erosion (not full thickness)
--can tell the difference histopathologically
-Erosion and ulcers are both surface defects in the skin where outer surface of skin is lost
--usually called erosions/ulcers

Front 15

Nodule

Back 15

-Primary skin lesion
-Not fluid-filled, solid elevations of the sikin
-Usually associated with some sort of infiltrative cell
--lymphocytes, inflammatory cells, inflammatory associated with infectious disease

Front 16

Crust

Back 16

-Secondary skin lesion
-“Scab”
-Accumulations of dried exudate on the skin
-Surface material that is adhered to the surface of the skin

Front 17

Papule

Back 17

-Primary skin lesions
-Solid elevations of the skin, raised lesions
-Usually less than 1cm in diameter
-Often erythematous, seen with inflammation of the hair follicle
-Often precede pustules, which can then become crusts or epidermal collarettes
-Can be present with parasitic infestations

Front 18

Plaque

Back 18

-Primary skin lesion
-“Coalescing papules”
-Area of skin that is raised and flat-topped, plateau
-Usually more than 1cm in diameter
-Usually associated with some infiltrative disease of the skin
--Inflammatory, neoplastic, infectious disease infiltration
-Can erode or ulcerate to become a secondary skin lesion

Front 19

Wheal

Back 19

-Primary skin lesion
-“Hives”
-Caused by dermal edema
-Fade quickly, within 24-48 hours
-Can recur, but are usually short-lived

Front 20

Hyperkeratosis

Back 20

-Secondary skin lesion
-Histopathologic term that is used clinically
-Thickening of the outer layer of the skin (sratum corneum)
--Orthokeratotic hyperkeratosis
--parakeratotoci hyperkeratosis
-Stratum corneum becomes thicker and less pliable, can have secondary fissures form

Front 21

Fissure

Back 21

-Secondary skin lesion
-Liner cracks in the stratum corneum
-Occurs when skin is thickened or less pliable
--can be due to hyperkeratotis

Front 22

Hyperkeratotic fissured foot pads

Back 22

-Can occur due to hepatocutaneous syndrome

Front 23

Scale

Back 23

-Primary or secondary skin lesions
--usually secondary to disease or inflammation
-Exfoliated stratum corneum
-“Dandruff”
-Usually due to something in the skin causing increased turnover of stratum corneum

Front 24

Alopecia

Back 24

-Primary or secondary skin lesion
-Loss of hair
-Primary: loss of entire length of the hair, whole hair fell out
-Secondary: Most commonly secondary to itch
--pruritus, self-trauma
--hair is fractured, bulb is still present but tapered end is gone

Front 25

Excoriations

Back 25

-Secondary skin lesion
-“Scratches”
-Linear configurations of crusts/erosions/ulcers

Front 26

Follicular Casts

Back 26

-Primary or secondary skin lesions
-Can be secondary to diseases causing hair follicle inflammation, accumultation of material in hair follicles

Front 27

Sequelae of chronic pruritis

Back 27

-Secondary alopecia
-Secondary lichenification
-Secondary hyperpigmentation, increased melanin deposition in skin

Front 28

Lichenification

Back 28

-Secondary skin lesion
-Thickened skin, “elephant skin”
-Whole epidermis is thick and hyperplastic
-more “nooks and crannies” in skin than normal

Front 29

Hyperpigmentation

Back 29

-Secondary skin lesion
-Increased melanin in the skin, increased deposition
-Post-inflammatory change, due to inflammatory cells in skin

Front 30

Comedones

Back 30

-Can be primary of secondary skin lesions
-Primary: disorder of skin turnover
-Secondary: secondary to another disease that causes plugging of hair follicles
-“Blackheads”
-Plugged hair follicles

Front 31

Loss of Pigment

Back 31

-Primary or secondary skin lesion
-Decreased pigment deposition
-Loss of pigment in the hair: leucotrichia
-Loss of pigment in the skin: Leucoderma
-Secondary due to inflammation or infiltration of other cells

Front 32

Leucotrichia

Back 32

-Loss of pigment in the hair

Front 33

Leucoderma

Back 33

-Loss of pigment in the skin

Front 34

Progression of Skin lesions

Back 34

-Progress from primary skin disease to secondary skin disease
-Commonly folliculitis progression due to bacteria on skin
-Papule becomes a pustule, pustule ruptures and becomes a crust or epidermal collarette
-Crust can also become an epidermal collarette

Front 35

Diagnosing Dermatologic Disease

Back 35

-Very systematic approach to diagnosis
-Impression cytology is one of most common diagnostic tests
-Acetate tape impression
-Wood’s lamp exam
-Skin scrapings (deep and superficial)
-Trichogram
-Flea combing

Front 36

Impression Cytology

Back 36

-Very common dermatologic diagnostic test
-Ear cytology and skin cytology

Front 37

Advanced dermatologic tests

Back 37

-bacterial culture and sensitivity
-Fungal culture
-Skin biopsy
-Diascopy
-Allergy testing
--intradermal and serology

Front 38

Skin Cytology

Back 38

-What infections are present?
-Why are those infections present?
-Almost always indicated
-Helps look for inflammatory cells and organisms
-Can get clues about more rare diseases
-80% of allergic cases have secondary skin infections

Front 39

Techniques for Skin Cytology

Back 39

-Moist lesion: direct impression with slide onto skin
-Dry or greasy lesion or difficult location: clear acetate tape against skin
-Pustule: rupture pustule with 25 G needle, smear material onto slide

Front 40

Slide preparation

Back 40

-Usually air dry
-Can blow dry, but be careful that tape does not shrink
-Greasy sample needs to be heat fixed with flame
--Do not heat fix tape slides!
-Diff-quik stain, 20 seconds in each

Front 41

Microscopic evaluation of Slide preparations

Back 41

-Start at low magnification, 10x
-Inflammatory cells are usually heterogenous population
-Neoplastic cells are usually homogenous population
-Oil immersion lens to identify organisms 1000x
--bacteria: cocci, rods
--yeast: Malassezia spp.

Front 42

Extracellular vs. intracellular bacteria on slides

Back 42

-Can see bacteria within neutrophils
-Important to note
--rough scale of 0-4+, mild, moderate, marked, severe
-Note intracellular vs. extracellular

Front 43

Malassezia

Back 43

-yeast commonly seen on slide preparations
-Look like little footprints
-Easily seen on tape preparations

Front 44

Acantholytic keratinocytes

Back 44

-Large cells with central nucleus
-Much larger than neutrophils
-Common in pemphigus foliaceus
-Keratinocytes have “broken free” of desmosomes and cellular bridges
--“free floating” keratinocytes

Front 45

Superficial pyoderma vs. pemphigus foliaceous

Back 45

1. Superficial pyoderma:
-Extracellular and intracellular bacteria
-Degenerated neutrophils with nuclear streaming
-Rare acantholytic cells, if any
2. Pemphigus foliaceus
-Numerous acantholytic cells
-Background of intact neutrophils
-Occasional intracellular bacteria

Front 46

Skin Scrapings

Back 46

-Indicated for almost every derm patient
-Helpful for alopecia, comedones, folliculitis
-Needed to identify Demodex and sarcopiform mites (surface mites)
-Minimal equipment needed
-Deep skin scrapings and superficial skin scrapings

Front 47

Deep skin scrapings vs superficial skin scrapings

Back 47

-Deep skin scrapings: Used to find demodex mites
--D-Demodex-deep
-Superficial skin scrapings: used to fins sarcoptes, superficial dwelling mites
--S-Scabies-Superficial

Front 48

Superficial skin-dwelling mites

Back 48

-Need superficial skin scrapings!
-Knowing which mite is suspected and where it lives increases mite retrieval
-Sarcoptes scabiei var canis
-Notoedres cati
-Cheyletiella
-Demodex gatoi (surface-dwelling demodex mite)

Front 49

Superficial skin scraping technique

Back 49

-Broad, superficial strokes
-Not focused on getting bleeding
-Put surface material onto a slide with mineral oil and coverslip
-Observe with 10x objective and diffuse dim illumination

Front 50

Deep dwelling mites

Back 50

-Demodex canis
-Demodex cati
-Find with deep skin scrapings
-Need to get down into hair follicles where mites hang out
-Scrape to get capillary oozing, need to go deep into the dermis

Front 51

Deep Skin Scraping Technique

Back 51

-Pinch skin
-Dull blade, do not need a sharp blade
-Scrape until there is capillary bleeding
--lay skin flat to scrape
-Scrape 3-4 sites for representative sample
-Put scraped material on slide with mineral oil and coverslip
-Examine with 10x objective an diffuse dim illumination

Front 52

Diffuse dim illumination

Back 52

-Want contrast
-Mites are an un-stained sample, will vanish in bright illumination
-Lower condenser, dim illumination, and adjust iris aperture for maximum contrast

Front 53

Trichogram

Back 53

-Hair plucking
-Indicated for alopecia, pruritus (rule out self-induced hair loss), parasites, dermatophytosis, hair follicle diseases
-Pluck hairs from periphery of lesion and place in mineral oil on slide
--use forceps to pluck
-Evaluate hair bulb, hair shaft, and distal end of the hair

Front 54

Trichogram Assessment

Back 54

-Ends: will be ragged/fractured with self-trauma
-Bulb: round during anagen, spear-shaped with telogen
-Hair shaft:
--look for melanin clumping abnormalities
--fungal hyphae or surrounding dermatophyte spores, “fuzzy hair”
--lice, Cheyletiella

Front 55

Flea Combing

Back 55

-Comb any animal with hair loss and pruritus
-Place dark material on wet paper towel
--material turns red if flea dirt
-Place scape on slide with mineral oil to look for Cheyletiella

Front 56

Wood’s Lamp Examination

Back 56

-Quick screening test for dermatophytosis
-Blacklight
-Alopecia, suspect dermatophytosis
-Tryptophan metabolite produced by dermatophytes causes illumination
-Only effective for microsporum canis (50% of cases)
--makes hair shafts fluoresce
-Screening technique, need to follow up with diagnostic tests
-Fast, inexpensive, screening tool
-Have false positives with scales, crusts, and topical medication

Front 57

Fungal Culture

Back 57

-Indications: alopecia, folliculitis, any cat with skin disease
--always rule out dermatophytoses in cats
-Gold standard!
-Collect hair and scale from periphery of lesion
--can also collect a hair that fluoresces
-Sterile toothbrush technique: brush all over the pet and embed collected hair

Front 58

Dermatophyte Test medium

Back 58

-Contains a color indicator, phenol red
-Has agents to reduce contaminant over-growth
--cyclohexamide, gentamicin, chlortetracycline
-Proteins, carbohydrates for nutrients allow fungal growth
-Dermatophytes use protein first, turn medium red concurrent with growth
-Saprophytes (contaminants) use carbohydrates first, no color change, and consume protein later

Front 59

Dermatophyte identification

Back 59

-Sab-dex allows conidia development
-Incubate 3-4 weeks in dark, humid place at room temp
-Check daily for white, fluffy growth with simultaneous change in color
-Apply acetate tape to surface of colony
-Place 1-2 drops of lactophenol or new methylene blue on slide, apply tape over stain
-Examine at 40-100x
-Identify pathogen species
-Helps confirm dermatophytosis diagnosis
-Helps identify source of infection

Front 60

Indications for Bacterial culture and sensitivity on skin

Back 60

-Empiric treatment fails
-Recurrent or relapsing pyoderma
-Suspected uncommon bacterial infection
--actinomycetic, nocardial, mycobacterial infection
-Deep pyoderma

Front 61

Bacteria culture and sensitivity for superficial pyoderma

Back 61

-Pustule: lance with sterile needle and culture exudate
--ideal situation, has not been open to the world
-Crust: lift crust with sterile needle, culture underlying area
-Epidermal collarette: leading edge
-Only aerobic culture is needed for superficial pyoderma
--look for Staph

Front 62

Bacterial culture and sensitivity for deep infections

Back 62

-Ideal to culture sterile tissue biopsy
-Sterile aspiration of furuncle
-Lumps, bumps, draining tracts
--submit tissue for a bunch of different cultures
--aerobic, anaerobic, atypical mycobacterial and fungal cultures

Front 63

Biopsy and Histopathology of skin

Back 63

-Suspected neoplasia, auto-immune, or metabolic disease
-If patient has not responded to appropriate empiric treatment
-Biopsy to confirm diagnosis before starting treatment with immunosuppressants, expensive or extensive treatment, or hazardous treatments
-Helps prioritize differentials and form prognosis for patient
-Punch biopsy is most commonly used
-Excisional or incisional can also be used

Front 64

Goals of skin biopsy

Back 64

-Establish a definitive diagnosis and prioritize DDx
-Rule out other diseases
-Determine prognosis

Front 65

Biopsy punch sizes

Back 65

-Size matters!
-4.0mm (small), used for difficult sites
--nasal planum, footpads, periocular skin
-6.0mm is minimal acceptable size, most commonly used
--more tissue for examination, fewer artifacts, more likely to give diagnostic section

Front 66

Punch Biopsy technique

Back 66

-Before procedure stop steroids for at least 2 weeks
--can mask diagnosis
-Treat secondary infections before procedure
-Local anesthesia is most often used with minor physical restraint
-Sedation is needed in some cases
-General anesthesia may be needed for difficult sites
--nasal planum, footpads, periocular skin, pinnae, claws
-Take multiple representative samples of lesions
-Clip hair carefully, do not scrub or disturb scales, crusts, surface debris
-Mark site, lesions tend to vanish with lidocaine
-Rotate gently in 1 direction, avoid damage from shearing forces
-Apply gentle pressure until blade enters SQ tissue
-Grasp pedicle of underlying SQ fat, cut pedicle with iris scissors
-Remoce excess blood, fix in formalin

Front 67

Local anesthesia for punch biopsy

Back 67

-Lidocaine 2%
-Lidocaine and epinephrine can be used for hemostasis
-Sodium bicarbonate can be used to buffer lidocaine
-inject SQ with 25 G needle

Front 68

Diascopy

Back 68

-Assessment of red macules
--erythema or hemorrhage/bruising
-Press glass slide firmly onto skin
-Erythema: RBCs are in blood vessels
--should see blanching
-Hemorrhage: RBCs are not in blood vessels
--no blanching

Front 69

Pruritus as a clinical problem

Back 69

-Clinical problem, NOT a diagnosis
-Can be caused by many underlying disease processes

Front 70

Pruritus

Back 70

-Unpleasant sensation that provokes the desire to scratch
-Associated with inflammation, but NOT an “itis”

Front 71

Rules when investigating Pruritus

Back 71

1. Start with Minimum database
-Skin scrapings, skin cytology, trichograms, wood’s lamp exam in cats
-Do not make shotgun diagnoses
2. Treat what you can see (parasites and infections)
-need to clear in order to focus on the primary cause
3. Common diseases occur commonly, uncommon diseases occur uncommonly

Front 72

Type I Hypersensitivity

Back 72

-Immediate hypersensitivity
-Genetic predisposition in animal to produce IgE against nonsense antigens, things that should be ignored
--IgE is normally directed towards parasites
-IgE and IgGd binds to surfaces of mast cells and basophils, cross-linking of 2 IgE receptors by allergen signals mast cell degranulation
-Cross-linking causes release of inflammatory mediators into surrounding tissue
--histamine, inflammatory proteases
-Response is immediate, occurs within minutes and reduces within an hour after the allergen is gone
-Mast cells are in skin, respiratory tract, GI tract

Front 73

Examples of Type I hypersensitivities

Back 73

-Urticaria and angioedema
-Anaphylaxis
-Atopic diseases
-Some Flea bite allergy
-Some drug reactions (not common in animals)

Front 74

Late phase reactions

Back 74

-Occur 2-4 hours after immediate hypersensitivity reaction
-Persists for up to 24 hours
-Mast cells continue to release chemical mediators and eosinophil chemotactic factors
--infiltrate tissue and contribute to tissue injury by releasing inflammatory mediators
-Common in atopic diseases and flea bite allergy

Front 75

Type IV hypersensitivity

Back 75

-Delayed hypersensitivity
-Something that is too small to be antigenic attaches to carrier protein and goes into tissue
--together form complete antigen
-T-cells are sensitized, next exposure results in elicitation phase and T-cell response
-Contact allergy, some insect reactions, reactions to mycobacteria

Front 76

Cutaneous Basophil Hypersensitivity

Back 76

-Characterized by marked basophil infiltration of the skin
-occurs 12-24 hours after antigen exposure
-Lymphocyte mediated, has features of type I and type IV hypersensitivities
-Tick bite hypersensitivity, flea allergy dermatitis

Front 77

Neuroanatomy of Pruritus

Back 77

-Free nerve endings of non-myelinated C-fibers at dermal-epidermal junction
-Not specialized for “itch”
--same receptors that detect pain

Front 78

Neurophysiology of Pruritus

Back 78

-Chemical mediators
-Inflammatory cell-derived: histamines and vasoactive amines, cytokines released by T-cells, prostaglandins and leukotrienes released from inflammatory cells
-Neuroendocrine-derived substances
--substance P, VIP
--induced by psychosocial stressors

Front 79

Clinical signs of Pruritus

Back 79

-Scratching
-Biting
-Licking or chewing
-Rubbing (common in horses)
-Excessive grooming (cats)

Front 80

Patient history for Pruritus

Back 80

-Duration
-Distribution
-Progression
-Seasonality
-Intensity
-Contagion/zoonosis, is it affecting humans in the house?
-Age of onset
-Dietary history
-Drug or insecticide history
-Response to therapy
-Exposure to other animals

Front 81

DDx for Pruritus

Back 81

-Allergic diseases
-Parasitic infections
-Primary infections
-Secondary infections
-Drug reactions

Front 82

The Allergic Patient

Back 82

-Allergies make skin more susceptible to secondary infections
--Malassezia, bacterial pyoderma
-Secondary infections can elevate disease dramatically
-Environment can play a major role

Front 83

Flea Allergy Dermatitis

Back 83

-Was once the #1 allergic skin disease of both dogs and cats
--has reduced due to modern insecticides and rapid kill times
-Atopic individuals are at increased risk for flea allergy dermatitis
-Intermittent/massive exposure favors flea-allergy dermatitis
-Chronic low-grade infestation favors tolerance
-Seasonal allergy in some climates
-Non-seasonal in tropical areas or when fleas over-winter in a home

Front 84

Pathophysiology of Flea Allergy Dermatitis

Back 84

-Allergic reactions to flea salivary antigens
--antigens are deposited into wounded skin as flea feeds on animal
-Type I hypersensitivity
-Type IV hypersensitivity
-Late phase reaction, makes it hard to find the fleas
-Cutaneous basophil hypersensitivity

Front 85

Clinical picture of Flea Allergy Dermatitis in Dogs

Back 85

-Pretty consistent clinical picture
-No age, sex, or breed predilections
-Pruritus and popular rash over caudal 1/3 of the body, predominantly on dorsum
--lumbo-sacral area
-“Flea triangle:” rump/tailhead, caudal thighs, and groin
-Most clinical signs are self-induced or due to secondary infections
--excoriation, lichenification, folliculitis, alopecia, crusts, hyperpigmentation, fibro-pruritic nodules (scar tissue)

Front 86

Fibro-pruritic nodules

Back 86

-Scar tissue
-Pathognomonic for flea bite allergy

Front 87

Flea Bite allergy and concurrent disease

Back 87

-Presents as severe pruritus of the feet, face, or ears
-Look for concurrent hypersensitivities
-Finding flea dirt is no necessary for flea allergy dermatitis!

Front 88

Flea dirt and flea bite allergy

Back 88

-Allergic animal can respond to very few flea bites
-Usually successful in grooming the fleas away
-Do not need to see flea dirt to have allergy!
-Most flea preventatives do not kill fleas quickly enough to get them before they bite
--will still get flea bite allergy even with complete flea and tick preventative

Front 89

History and clinical signs for Flea bite allergy in Cats

Back 89

-No age, sex, or breed predilections
-Miliary dermatitis or symmetrical alopecia are most common
--Caudal 1/3 of the animal, dorsal neck
-Any of the feline eosinophilic reaction patterns are possible

Front 90

Diagnosis of Flea Allergy Dermatitis

Back 90

-History, physical exam, flea combing
-No fleas does NOT constitute a negative diagnosis!
-Intradermal allergy testing with commercial flea allergen
--causes immediate wheal and flare reaction within 20 minutes
--delayed or popular or military rash in 6-48 hours
-No specific histopathologic indications

Front 91

Treatment for Flea Allergy Dermatitis

Back 91

-Aggressive flea control! Zero tolerance
-Address environment and all pets in the household
-Hyposensitization/allergy immunotherapy does not work for fleas
-Purified flea salivary antigen may be useful for severe cases
--not available in USA
-Treat secondary infections
-Steroid therapy to break cycle of pathogenic itch is NOT a substitute for adequate flea control
-Knowledge of flea biology and hypersensitivity manifestation is imperative
-Integrated flea control program for household with allergic pet needs a vet!

Front 92

Atopic Diseases

Back 92

-Characterized by IgE response to “non-sense” antigens
-Atopic dermatitis is most common in dogs
-Allergic rhinitis/sunisitis/conjunctivitis
-Allergic bronchitis (more common in dogs)
-Some forms of asthma

Front 93

Atopic Dermatitis

Back 93

-Multifactorial pathophysiology
-Reduced stratum corneum barrier function
--Likely due to gene mutations that result in reduced or abnormal protein expression
-IgE mediated allergic cascade and release of mast cell/eosinophil products
-Cytokine release from activated t-cells
-Neuro-endocrine release of pruritogenic mediators

Front 94

Atopic Dermatitis “Cascade”

Back 94

1. Sensitization
2. IgE production and priming of mast cells
3. Re-exposure to allergen and elicitation

Front 95

Atopic Dermatitis Cascade: Sensitization

Back 95

-First step in cascade
-Basically a symptom-free stage
-Reduced stratum corneum barrier function due to genetic mediated mutation
--“leaky” stratum corneum
-Allergens penetrate epidermis, run into Langerhans cells
--allergens are “presented” on cell surface
-Langerhans cells travel to regional lymph nodes and present allergen to T-cells
-Results in T-helper cell sensitization, T-cells activate B-cells to produce IgE

Front 96

Atopic Dermatitis Cascade: IgE production and priming of mast cells

Back 96

-Allergen-specific T-helper cells recognize and activate B-cells
-T-helper and B-cells migrate to the dermis
-B-cells mature to plasma cells and produce IgE, secrete IgE into derms
-IgE sticks onto the surface of mast cells
-Mast cells “hang out” in the dermis near small venules

Front 97

Atopic Dermatitis Cascade: Re-exposure to allergen and elicitation

Back 97

-Mast cells near small venules in dermis wait for allergen to re-appear
-When allergen appears IgE is cross-linked, mast cell releases mediators
--cytokines, histamine
-Causes vascular and smooth muscle response for immediate reaction
-Causes inflammation as late phase reaction

Front 98

Mast-cell mediated effects

Back 98

-Vascular dilation and “leaky vessels”
-Results in edema, forms wheal
-Cytokines produced by T-lymphocytes

Front 99

Cytokines produced by T-lymphocytes

Back 99

-IL-4 (promotes class switch in B-cell from IgM to IgE production)
-IL-2
-IL-5: enhances eosinophil replication, differentiation, adhesion, degranulation, improves survival time of eosinophils
-IL-6
-IL-13
-IL-31: Induces neuronal itch stimulation, causes nerve endings to fire

Front 100

History and signalment for Atopic Dermatitis

Back 100

-Affects about 10% of canine population
-May breeds predisposed
--french bulldogs, labs, goldens
-Age of onset between 1-3 yeas (can be from 6 months to 7 years)
-Many cases will be seasonal initially
--depends on climate and season of birth
--non-seasonal causes can occur

Front 101

Clinical signs of Atopic Dermatitis

Back 101

-Primary lesion: Pruritus and erythema or edema
-Visible lesions are due to self-trauma and secondary infections
-Sebaceous gland hypertrophy and increased secretions
--leads to greasy coat, seborrhea oleosa
-Recurrent secondary infections are common, hallmark
-Immuno-deficiency that is specific to skin allows infections to occur
-Rhinitis/sinusitis, bronchitis, asthma are rare in dogs

Front 102

Distribution of lesions in Atopic Dermatitis

Back 102

-Affects areas where hair is sparse or skin stays moist
--favorable to allergen penetration
--axillae, perineum, groin, periocular, muzzle, external ear canals, conjunctiva, interdigital areas
-Extensor surfaces of the forelimbs
-Flexural surfaces of the hindlimbs

Front 103

Diagnosis of Atopic Dermatitis

Back 103

-Diagnosis of Exclusion
-Supported by history, signalment, and clinical signs
-Seasonal causes: rule out insect hypersensitivity
-Non-seasonal causes: rule out food allergy, scabies, other parasites
-Non-seasonal atopy often has seasonal exacerbation in intensity of signs
-Clear infections with antimicrobial therapy before using anti-pruritic medication

Front 104

Allergen Testing for atopic dermatitis

Back 104

-Not a yes/no test for determining of dog has atopic dermatitis
-Look for specific allergens
-Allows for avoidance or immunotherapy
-Strengthens the clinician’s faith in clinical diagnosis of atopic dermatitis
-Concurrent food allergy should be ruled out in non-seasonal cases
--allergen testing is not reliable for diagnosing food allergies

Front 105

Intradermal Allergen Testing

Back 105

-Uses air-borne allergens and indoor allergens and common insects
-“Gold standard” of allergen tests
-Administered under sedation for patient comfort ant reproducible results
-0.05-0.1cc of each allergen is injected intradermally
-Wheal and flare response is graded on a 0-4 scale and compared to saline and histamine controls
-Wheal reaction causing antigen can be put into a vaccine and injected into patient

Front 106

Serologic Allergen tests

Back 106

-ELISAs: measure serum concentration of allergen-specific IgE in circulation
-Do not need sedation, clipping, drug withdrawl
-Lots of false positives
--cross-reactivity with IgG and non-specific IgE binding
--can have high baseline total IgE levels due to exposure to parasites
-Can have false negatives during off-season
--serum IgE levels fall more quickly than mast-cell bound IgE in tissue

Front 107

ELISA Serologic allergen tests available

Back 107

-Monoclonal, polyclonal
-IgE receptor based platforms
-False positive reactions are common with polyclonal antibody assays

Front 108

Secondary infections associated with Atopic Dermatitis

Back 108

-Hallmark of atopic dermatitis state
-Staphylococcal pyoderma
-Malassezia yeast
-Bacterial and yeast otitis externa
-Immunodeficiency is limited to the skin
-No increased susceptibility to infection in other organ systems
--drugs used to keep animal confortable may predispose animal to secondary UTIs

Front 109

Hypersensitivity to Microbes

Back 109

-Malassezia pachydermatis
-Staphylococcus pseudointermedius
-Provoke hypersensitivity reactions that are IgE mediated, part of atopic phenotype
-Infection and organisms produce proteins that patient recognizes as allergenic
--compounds effect and importance of infection

Front 110

Feline Atopy

Back 110

-“Catopy”
-No breed or sex predilections
-Age of onset between 6 and 24 months
-less common than in humans and dogs
-Pathogenesis is similar to canine atopy
-25% of cats with have concurrent food allergy or flea-associated dermatitis

Front 111

Clinical Features of Feline Atopy

Back 111

-Pruritus!
--scratching, biting, excessive grooming
-Respiratory signs are more common than in dogs
--sneezing, asthma/bronchitis, rhinoconjunctivitis
-Distribution of lesions: mostly face and neck
--abdomen, groin, perineum, head/neck, pinnae, periocular, anterior and medial forelimbs, posterior and lateral hindlimbs, feet, otitis externa
-Feline reaction patterns: any can be provoked with hypersensitivity component

Front 112

Diagnosis of Feline Atopy

Back 112

-History and clinical signs
-Seasonal appearance
-Non-seasonal: food allergy, flea allergy, parasitism, dermatophytosis, psychogenic (rare!)
-Intradermal allergen testing is more difficult and interpretation is more difficult
--more reliable than a blood test?
-Serologic allergy testing is preferred by some dermatologists
-Unknown what role IgG sub-classes play in cats

Front 113

Food Sensitivities

Back 113

-Any adverse reaction to dietary ingredient
-Can be allergic or non-allergic
-Cutaneous, GI, respiratory, or neurologic signs (seizures, rare)
-“Adverse food reaction”

Front 114

Types of food intolerance

Back 114

-Pharmacological reactions: histamine and other vasoactive cpds
-Metabolic problems: individual deficiencies in digestive enzymes
-Toxic reactions: spoiled or contaminated foods
-Idiosyncratic reactions: response on 1st exposure that cannot be explained by allergy (no initial sensitization phase)

Front 115

Pathophysiology of food allergies

Back 115

-Not well-understood
-IgE is not often produced against the food that makes animal itchy
--not IgE mediated allergy most often
-Immature gut epithelium? Allows protein absorption of particles of larger molecular mass?
-Presentation of incompletely digested food antigens to GALT?

Front 116

Evidence that food allergies are type I hypersensitivity reactions

Back 116

-Commonly occurs with atopic dermatitis
--suggests common mechanism
-Some patients show immediate reactions to food challenges
-Some cases present with urticarial
-Experimental models in IgE hyper-secreting dogs mimic clinical cases
-May find allergen-specific IgE in feces of dogs with protein-losing enteropathy

Front 117

Immunologic reactions with Food Sensitivity

Back 117

-Type IV reactions (delayed)
--suggested by delayed reactions to food challenges
--may explain lack of circulating food-specific IgE and poor specificity of intradermal testing with food extracts
-Type III reactions:
--urticarial vasculitis and pinnal margin vasculopathy can be exacerbated by food

Front 118

Food allergy signalment

Back 118

-Dogs: 2 months to 13 years, mean 2-4 years
-Cats: 3 months to 11 years, mean 405 years
-No breed or sex predilection in dogs
-Siamese cats may be over-represented
-Think food allergy when patients are very young or over 7 years when non-seasonal pruritus begins

Front 119

History for Food Allergies

Back 119

-Non-seasonal pruritus, usually constant over a period of months
--can be complicated by concurrent atopy or flea bite allergy
-GI signs:
--vomiting, diarrhea, flatulence, loose stools
-Most dogs and cats have been eating offending diet for months or years before developing a sensitivity
-Epileptic seizures are rare
-Respiratory signs are common in humans, unknown in animals
-Oral allergy syndrome is hard to document in animals
-Response to steroids is highly variable, good response does not rule out food allergy
--atopy is usually very responsive to steroids, ectoparasitism is not responsive

Front 120

Clinical Signs of Food Allergy in Dogs

Back 120

-non-seasonal pruritus
-May be worse immediately after eating, but hard to pin-point
-Distribution: similar to atopy
--feet, face, groin, axillae, perineum
--recurrent otitis externa
-Secondary infections are common
--staph pyoderma
--malassezia pachydermatis
--Yeast and bacterial otitis

Front 121

Clinical signs of Food Allergy in Cats

Back 121

-Non-seasonal Pruritus
-Head and neck excoriations may be severe
-Miliary dermatitis
-Symmetrical alopecia
-Eosinophilic granuloma complex
-Recurrent otitis is uncommon
-Distributed along face and neck, feet, perineum, groin, etc.

Front 122

Diagnosis of Food Allergy in dogs and cats

Back 122

-Allergy testing is highly unreliable!
-DO NOT do skin or blood tests for food allergies
- histopathology of the skin and gut shows non-specific mononuclear and eosinophilic inflammation
-Diet elimination trial is gold standard for diagnosis
--requires provocative food item challenge whenever possible

Front 123

Dietary Elimination Trial Protocol

Back 123

-Minimum trial period of 8 weeks, 10-12 weeks is ideal for cats
-resolve secondary bacterial and yeast infections during first 4 weeks of trial
--may relapse with infection, need to treat
-Glucocorticoids may be required during first month to break inflammatory and itch cycle
-patient should maintain healthy skin for 2-4 weeks off medications with test diet to prove cause
-Wait until animal is at least 1 year old

Front 124

Provocative Food item Challenge

Back 124

-Re-exposure to offending diet after clearing with food trial
-Important if only partial improvement has been achieved
--addresses concurrent hypersensitivities
-Challenge with prior complete diet is quickest way to prove cause
-Individual food items can be addressed, starting with known ingredients from whole diet
--2-day washout period between items

Front 125

Proteins implicated in food sensitivity in Dogs

Back 125

-Beef
-Dairy products
-Wheat
-Corn, pork, rice, fish
-Chicken is very common

Front 126

Proteins implicated in food sensitivity in Cats

Back 126

-Beef, dairy products, fish
-Account for 90% of reactions
-Poultry may be most common

Front 127

Trial Diet Conundrum

Back 127

-Commercial vs. home-prepared diet
-not all animals can be cleared with commercial foods
--manufacturer added ingredients?
-Novel proteins for home cooking is tough
--rabbit, venison, duck, salmon, whitefish, Kangaroo
-May have cross-reactivity, most cross-reactivities in animals are unknown

Front 128

Hydrolyzed proteins and food trials

Back 128

-Common proteins hydrolyzed to peptides less than 10kD
--smaller than most food allergens
-Can fool immune system by giving chopped up proteins
-Widely effective products

Front 129

Home prepared diets

Back 129

-Make sure diet is balanced by a nutritionist if possible!

Front 130

Maintenance diets

Back 130

-can be any commercial or home-prepared diet that controls clinical signs
-Most of novel protein and hydrolyzed protein products can be used for long-term feeding
-Sensitization to new diet seems to be rare
--may occur more commonly in very young patients

Front 131

Atopy and food sensitivity

Back 131

-Occur together in many dogs and some cats with allergic dermatitis
-Indistinguishable in most cases
--similar distribution patterns
--result in secondary infections and otitis externa
--may result in urticarial (rare)

Front 132

Atopy vs. Food sensitivity

Back 132

-Seasonality? Probably atopy, not just food
-GI signs with food allergy, none with atopic dermatitis
-Young or old animals affected, most likely food allergy
-Food allergy can mimic flea-allergy dermatitis, atopy will not
-“ears and rears” is common in food allergy and less in atopic dermatitis

Front 133

Allergic Contact Dermatitis

Back 133

-Type IV hypersensitivity
-Caused by incomplete antigen binding to a tissue protein, becomes a complete antigen
-Heavy metals, plant resins, lipid-soluble chemicals
-Rare in dogs, animals do not react to poison ivy, poison oak, or sumac
-Can be confused with atopic dermatitis due to similar distribution patterns

Front 134

Diagnosing Allergic Contact Dermatitis

Back 134

-Patch testing kits are used in people, not useful in animals (do not stick)
-Diagnosis in dogs is based on response to therapy
-Tx: avoidance if possible
--pentoxifylline can be used
-DDx: irritant contact dermatitis

Front 135

Malassezia Dermatitis

Back 135

-Yeast dermatitis
-Second most common cause of cutaneous infections in allergic dogs
-Occurs secondary to endocrinopathies and hyperkeratotic disorders
-Growth is promoted by:
--disruption of stratum corneum barrier function
--increased moisture on skin surface
--increased lipid content of sebum emulsion due to lipophilic organism

Front 136

Primary allergic diseases associated with Malassezia dermatitis

Back 136

-Any allergic skin disease can lead to
Malassezia pachydermatitis overgrowth
-Usually occurs on inflamed skin
--distribution pattern is identical to the underlying disease
-Yeast overgrowth causes major increase in pruritus
-Endocrinopathies can lead to yeast over-growth
--hyperadrenocorticism (Cushing’s)
--hypothyroidism
-Parakeratotic diseases:
--hepatocutaneous syndrome
--zinc-responsive dermatosis
--generic dog food dermatosis

Front 137

Malassezia Hypersensitivity

Back 137

-Malassezia provokes type I hypersensitivity reactions in atopic dogs
-Yeast infections need to be eliminated with topical or systemic anti-fungal therapy

Front 138

Lesions associated with Malassezia dermatitis

Back 138

-Identical to underlying allergic disease
-Erythema is earliest lesion noted
-Inflammation within skin folds (Intertrigo)
-Pruritus may be severe, self trauma results in excoriations, alopecia, lichenification, hyperpigmentation
-Chronic inflammation may result in seborrhea
--inflamed skin can be dry and flaky or greasy
-Paronychia (inflammation of the claw fold) and interdigital pododermatitis

Front 139

Pruritic Parasites

Back 139

-Scabies: Sarcoptes scabiei, Notoedres cati
-Cheyletiella
-Otodectes cynotis
-Demodex gatoi
-Trombiculosis (chiggers)

Front 140

Scabies

Back 140

-Average 21 day life cycle from egg to adult
-Caused by separate species of mites for each animal
--can parasitize other mammals than the usual host species
-All sarcoptid mites burrow through stratum corneum
-Feed on skin and lay eggs in tunnels in the skin
-Zoonotic! Do not reproduce on other animals, but will crawl around and cause itching

Front 141

Canine Scabies clinical signs

Back 141

-Most pruritic parasitic disease
-Papular rash, erythema, and excoriations are initial lesions
-Classic pattern: elbows, ears, and hocks
-Entire ventrum becomes involved as parasites progress
-Pinna-pedal response

Front 142

Scabies “incognito”

Back 142

-Hypersensitivity response within a few minutes clears mites
-Animal is in state of balance with the mites
-Hypersensitivity to mite poop
-Pruritus with no papules
-No mites on scrapings
-Easily confused with allergic dermatoses, food allergy or non-seasonal atopic dermatitis
-Need to treat with avermectin

Front 143

Norwegian Scabies

Back 143

-Hyperkeratotic/crusted scabies
-TONS of crusts all over the animal
-Massive numbers of mites with no pruritus
-Associated with immunosuppression

Front 144

Diagnosis of Canine Scabies

Back 144

-Broad, superficial scrapings needed
--hard to find mites! 50% of classic cases may have no mites found
-Avoid chronic or lichenified and traumatized skin
-Look for mites, eggs, and fecal pellets
-Many scrapings are often needed to find a single mite
-Positive pinnal-pedal reflex is sensitive but not specific
-Histopathology is rarely helpful
-Therapeutic trials should be done if there is a high index of suspicion
-If human is also itchy, likely dog has scabies

Front 145

Feline Scabies

Back 145

-Notoedres cati
-“Feline head mange”
-Usually begins on pinnae and progresses to head and dorsal neck
-Adherent crusts with thick or wrinkled skin
-Cats can inoculate other areas of skin via grooming behavior
-Intense pruritus
-mites are usually very easy to find on skin scrapings, incognito cases are rare
-DDx: other parasites, allergies

Front 146

Otodectes cynotis

Back 146

-Ear mites
-Psoroptid mite of dogs and cats
-Lives on surface of the skin
-Prefers ear canals
-Feeds on epidermal debris and interstitial fluid
-Most common in puppies and kittens
-21 day lifecycle

Front 147

Clinical signs of ear mites

Back 147

-Dogs: otic pruritus with minimal discharge
--mites on rump/trunk
--can mimic flea-allergy dermatitis
-Kittens: ear canals filled with cerumen, blood, and mite exudate
--may or may not be pruritic
-Adult cats: initially clear the mite infection, then hypersensitivity response to mite products
--chronic otitis externa with no mites
--miliary dermatitis of the neck and trunk

Front 148

Diagnosis of ear mites

Back 148

-Ear exudate in mineral oil at 10x objective
-Scrapings of local lesions

Front 149

Demodex gatoi

Back 149

-Short, stumpy mite
-Part of normal microflora?
-Live in stratum corneum, NOT in hair follicles
-Primarily associated with pruritus
--can mimic ant pattern of feline allergic skin disease
--most common with immune suppression or chronic steroid treatment
-Highly contagious between cats
--check all feline housemates for asymptomatic carrier status
-Cats lick hair in a symmetrical pattern, may see miliary dermatitis

Front 150

Diagnosis of Demodex gatoi

Back 150

-Broad and superficial scrapings from large surface area, similar to scabies diagnosis
--concentrate scraping material
-Occult cases are very common in endemic regions
--texas, southeast US
-Need therapeutic trials to evaluate response to therapy
-Cases in PA are rare
-Always on DDx list

Front 151

Treatment for Demodex gatoi

Back 151

-Lyme sulfur dips, weekly for 6 weeks
-ONLY cure, safe and effective
-Cats hate it, it smells bad, owner’s hate it, but it is the only thing that works
-Oral ivermectin in cats cannot be used due to propylene glycol
-Amitraz dips are highly toxic to cats

Front 152

Cheyletiellosis

Back 152

-Each mammal has own species, but one can affect all
-Form pseudo-tunnels in epidermal surface debris on the skin
-Pierce epidermis to feed on interstitial fluid
-Eggs are cemented to hair shafts
--environmental contamination when animal sheds
-VERY contagious
-Zoonotic potential

Front 153

Clinical signs of Chyletiellosis

Back 153

-Pruritus is variable, some are highly pruritic and some are not
-“Walking dandruff”
-Mites are so big they can be seen with naked eye, can find with flea combing
--HUGE compared to scabies
-May cause miliary dermatitis in some cats
-All rabbits should be assumed to be infested until proven otherwise?

Front 154

Diagnosis of Cheyletiellosis

Back 154

-Skin scrapings
-Flea combing
-Acetate tape
-Examine scraping material in mineral oil with 10x objective
--Always use coverslip!
-May find mite eggs on fecal float

Front 155

Diagnosing Pruritus A

Back 155

-Screen for ectoparasites
--skin scrapings, acetate tape, combings, fecal float
-Screen for dermatophytes
--Wood’s lamp, trichogram
-Screen for microbial overgrowth
--skin surface cytology
-ID testing with flea allergen

Front 156

Pruritus Treatment plan A

Back 156

-Treat secondary infections, treat what you can see
-Treat ectoparasites found
-Make sure flea control is tight
-Therapeutic trials with non-steroidal anti-pruritic drugs
--antihistamines, fatty acids, vitamin E for mild cases

Front 157

Diagnosis of Pruritus plan B

Back 157

-Rule out occult ectoparasitism with therapeutic trials
-Dietary elimination trials
-Corticosteroids, cyclosporine, oclacitanib for symptomatic relief
-Aeroallergen screening to formulate allergen-specific immunotherapy, allergy vaccines

Front 158

Diagnosis of Pruritus plan C

Back 158

-Skin biopsy
-Rarely useful in identifying a specific cause
-Can be helpful to determine lesion is eosinophilic in cats
-Refer!

Front 159

Urticaria and angioedema

Back 159

-Inflammation in the skin causes blood vessels in the skin to become leaky
--tight junctions loosen due to vasoactive mediators from mast cells and basophils
-Plasma leaks into interstitium
-Common in humans and horses
-Uncommon in dogs
-Rare in cats

Front 160

Urticaria

Back 160

-“Wheal and flare”

Front 161

Hemorrhagic Urticaria

Back 161

-leakage of whole blood, not just plasma
-Leaks into interstitial tissue and causes sheal
-Most commonly due to vasculitis
-Diascopoy can be used to differentiate inflammation from hemorrhage
--inflammation blanches, hemorrhage is always red

Front 162

Etiology of urticaria

Back 162

-Anything that causes pruritus can cause urticaria
-Immunologic: atopic dermatitis, food allergy, drug reaction
-Non-immune mediated in horses

Front 163

Urticaria DDx

Back 163

-Anything that causes hair follicles to stand up on end
-Can look like welts
-Folliculitis in short-coated dogs and horses
-Vasculitis
-Mast cel tumors
-Erythema multiforme (horses)
--need biopsy to differentiate

Front 164

Angioedema

Back 164

-Diffuse regional swelling
-Mostly seen in dogs
-Rare in cats, usually a response to a biting insect or IV injection that went out of the vein

Front 165

Angioedema DDx

Back 165

-Allergic reaction
-Lymphatic disease
-Vascular disease
-Congestive heart failure

Front 166

Treatment for Urticaria/angioedema

Back 166

-Eliminate inciting cause
-Pre-treat with antihistamines
-Immunotherapy
-Life-threatening angioedema may need high-dose IV soluble glucocorticoids or epinephrine
--anaphylactic reaction

Front 167

Eosinophilic Dermatoses

Back 167

-Very common in cats and horses
-Skin lesions are dominated by eosinophilic infiltrates
-Uncommon or rare in dogs

Front 168

Eosinophil structure and function

Back 168

-Developed as a mechanism to attack and eliminate parasites
-“Bag of noxious chemicals”
-Cause “innocent bystander” damage of tissues
-Anti-parasitic immune response is Th2-mediated response
-Allergic disease is also initially Th2-mediated
-Th2-cells contain granules of cationic proteins, pro-inflammatory cytokines, and lipids

Front 169

Eosinophilic Reaction Patterns

Back 169

-Occur in the skin of cats and horses
-Response to same stimuli that produce pruritus
-Anything that causes pruritus can cause eosinophilic infiltration
-Pruritus is usually a concurrent finding, but not always
-All eosinophilic reaction patterns in the skin are clinical problems, not final diagnoses
--does not explain etiology

Front 170

Eosinophilic reaction patterns in feline skin

Back 170

-May DDx for each cause
-Feline symmetrical alopecia
-Miliary dermatitis
-Eosinophilic dermatitis complex
--indolent ulcer of the lip
--Eosinophilic plaque
--eosinophilic granuloma
-Mosquito bite hypersensitivity is an etiologic diagnosis with predictable clinical reaction pattern

Front 171

Self-induced symmetrical alopecia in cats DDx

Back 171

-Cats over-groom in classic response to pruritus, hair falls out in symmetrical pattern
-Psychogenic over-groomin
-Non-pruritic acquired alopecia is rare
-Paraneoplastic/metabolic syndromes
-Immune-mediated follicular diseases
-Congenital pattern alopecia

Front 172

Self-inflicted Feline Symmetrical Alopecia

Back 172

-Majority of cases!
-Cat will lick hair out in pattern that is typical of atopic dermatitis in dogs
--abdomen/groin
--lumbosacral region
--caudal/medial thighs
--flanks
--anterior forelimbs (more likely to be non-flea, cheylitiella, immune-mediated)

Front 173

Diagnostic Dilemma of self-inflicted feline symmetrical alopecia

Back 173

-Is the cat removing the hair?
--YES until proven otherwise!
--rarely proven otherwise
-Some cats are seclusionary groomers, owner may not realize that the hair is being groomed/removed
-Check ends of hair for breakage, will see broken/jagged ends
-Apply E-collar and re-check in a few weeks (should not be necessary, but is an option)

Front 174

Pruritus vs. psychosis

Back 174

-“Stress” causes cats to lick out hair
-Rare, better to consider other pruritic diseases
--allergy (atopy, food allergy, insect hypersensitivity)
--parasitic (Demodex gatoi, Scabies, Otodectes, Cheyletiella)
--infectious (staph, dermatophytic, yeast)
-If ALL pruritic causes can be excluded, think about psychosis

Front 175

Diagnosing a cat with symmetrical alopecia

Back 175

1. Rule out ectoparasites
--Cheyletiella and Demodex gatoi
2. Rule out surface infections from yeast and bacteria
3. Screen for dermatophytosis via wood’s lamp and trichogram
-fungal culture may be needed if index of suspicion is high
4. Better flea control measures =
5. Consider food allergy or atopic dermatitis

Front 176

Feline Miliary Dermatitis

Back 176

-Clinical presentation: small, crusted papules
--can sometimes feel bumpy crusts before you see them
-Down the line of the back is most common distribution
-Can have intense pruritus at the same time
-DDx: folliculitis and neoplasia

Front 177

Diagnosing Miliary Dermatitis or Small crusted papules

Back 177

1. Rule out follicular diseases via screening tests
--dermatophytosis, Demodex cati, bacterial folliculitis
2. Determine if miliary dermatitis should be working diagnosis from history and distribution pattern
3. Skin scrapings
4. If neoplasia is suspected, recommend biopsy

Front 178

Feline Eosinophilic Dermatitis Complex

Back 178

-Group of reaction patterns that are eosinophilic in earliest stages
--as lesion progresses, eosinophils are replaced with mast cells or other inflammatory cells
-Probably share common pathophysiology and causes
-Indolent ulcer
-Eosinophilic plaque
-Eosinophilic granuloma

Front 179

Indolent Ulcer

Back 179

-“non-healing” ulcer
-Ulcers of upper lip and oral commissure
-Do not go away on own
-Begin as erythema/swelling, usually progress rapidly to erosions and ulcers

Front 180

DDx for lip ulcers

Back 180

-Eosinophilic reaction
--any pruritic disease (allergic, ectoparasitic, dermatophytosis)
-Toxicity and physical tissue damage
-Neoplasia (SCC)

Front 181

Pathophysiology of Indolent ulcers

Back 181

-Tissue damage by inflammatory cell products? Flea antigen? Flea bite? Food allergen?
-Self-trauma of rough tongue during excessive grooming with secondary bacterial infection?
-Chronicity can lead to fibrosis
--looks like SCC
-Can be infected and form crusted or abscessed lesions

Front 182

Features of Indolent Ulcers

Back 182

-Peripheral eosinophilia is rare
-Dx confirmed by biopsy, if needed
--cellular infiltrate by time of biopsy will not be eosinophilic anymore
-Typically good response to glucocorticoids if acute or antibiotics if chronic

Front 183

Eosinophilic plaques

Back 183

-Flat, raised, circumscribed, erythemic lesions
-Often extremely pruritic
-Similar to canine hotspots
-On abdomen and inner thighs most commonly, but can occur anywhere
-Can be really thick and raised
--can aspirate, will find eosinophilic infiltrate

Front 184

DDx for eosinophilic plaques

Back 184

-Caused by infiltration of upper dermis with inflammatory or neoplastic cells
-Eosinophilic plaques
-Neoplastic plaques (lymphoma, mast cell tumors)
-Mixed inflammatory cell plaques
--trauma or non-healing wounds with secondary infections
--primary infections (dermatophytosis)

Front 185

Features of Eosinophilic Plaques

Back 185

-Secondary bacterial overgrowth on surface
-Peripheral eosinophilia is common
-T-cell lymphoma and infectious diseases that may cause plaque lesions should be considered

Front 186

Diagnosis of Eosinophilic plaques

Back 186

-Direct impression spear
-Fine needle aspirate
-Skin biopsy

Front 187

Eosinophilic granuloma

Back 187

-Nodular lesion, thick and infiltrates deeply
-Yellow to pink in color
-May occur anywhere
--oral cavity, head, abdomen, thighs, feet
-Often occur in linear pattern on caudal thighs and abdomen
--due to linear pattern of grooming
-May present as swollen chin or “fat lip”/”pouting cat”

Front 188

DDx for nodules

Back 188

-Nodules are caused by deep infiltration of the dermis/subcutis with inflammatory or neoplastic cells
-Eosinophilic granulomas
-Neoplastic granulomas (lymphoma, mast cell tumors, sarcoma, metastatic disease)
-Primary infections (bacterial, fungal, mycobacterial)
-Trauma, non-healing sounds with secondary infections
-Sterile or mixed inflammatory cell granulomas at vaccine injection site

Front 189

Features of Eosinophilic Granulomas

Back 189

-Pruritus is highly variable
-Peripheral eosinophilia is variable
-Diagnosis may be made via cytology if Fine-needle aspirate is possible
--can also biopsy
-All 3 different eosinophilic patterns can occur on one animal at the same time!

Front 190

Diagnosis for Feline Eosinophilic Dermatoses

Back 190

1. Identify the clinical problem
--presentation, rule-out non-eosinophilic tissue reactions, biopsy or fine needle aspirate confirmation
2. Search for underlying cause
--idiopathic: rare
--flea bite allergy is common and top differential
--extoparasites: Demodex gatoi, Otodectes cynotis, Notoedres cati, Cheyletiella
--atopic dermatitis or food allergy
3. Sometimes cannot make diagnosis based on owner resources

Front 191

Eosinophilic dermatosis Treatment

Back 191

-Symptomatic treatment
--usually successful if disease is short-term seasonal disease
-Treat secondary infections
-Treat underlying disease
-Make sure there is excellent anti-parasitic control

Front 192

Mosquito-bite hypersensitivity in cats

Back 192

-Mostly affects outdoor cats
-Lesions are in areas where mosquitos can feed on animal without hair getting in the way
--muzzle, nasal planum, ear tips, footpads, pre-auricular areas, peri-areolar skin
-Acute lesions: miliary dermatitis, erosions and ulcers, edema
-Chronic lesions: leukoderma (loss of pigment) and scarring alopecia

Front 193

Diagnosis of Mosquito Hypersensitivity

Back 193

-Minimum database
-Rule out parasites and dermatophytosis
-Scrapings, trichogram, wood’s lamp exam, fungal culture, skin surface cytology
-Intradermal testing with whole mosquito extracts
-Skin biopsy is key to rule out DDx

Front 194

DDx for Mosquito Hypersensitivity

Back 194

-Pemphigus foliaceus
-Demodicosis
-Dermatophytosis
-Neoplasia
-Herpes-virus associated facial dermatitis
-Allergic dermatitis with secondary infections

Front 195

Treatment for Mosquito bite hypersensitivity

Back 195

-Steroids to break inflammatory cycle
--oral steroids most common, can also use injectable steroids
-Restrict to indoors, especially during mosquito hours
-Repellents are bad news!
--0.1% permethrin, never more than 0.1%
-NO DEET products!

Front 196

Canine eosinophilic reaction patterns

Back 196

-Canine eosinophilic furunculosis of the face
-Canine eosinophilic dermatitis with edema
--Well’s like syndrome

Front 197

Canine Eosinophilic furunculosis of the face

Back 197

-Insect bite causes massive eosinophilic infiltration into hair follicles
-Furunculosis results from rupture of hair follicles
-Keratin from hair follicles are in surrounding dermis, results in massive inflammatory response
-Common in young, medium-large breed dolicocephalic dogs
-No sex predilection
-Acute lesions on dorsal muzzle or nasal planum
-Lesions progress rapidly from papules and edema to ulcerative or hemorrhagic lesions that may crust
-Often very painful
-No response to antibiotic therapy

Front 198

Causes of Furunculosis

Back 198

-Staph folliculitis
-Parasites
-Fungal infection, dermatophytosis
-Canine Eosinophilic furunculosis on the face

Front 199

DDx for Eosinophilic furunculosis

Back 199

-Pemphigus foliaceus
-Muzzle pyoderma
-Dermatophytosis
-Demodex
-Neoplasia

Front 200

Diagnosis of Eosinophilic furunculosis

Back 200

-Surface impression smear
-Fine needle aspirate (will see lots of eosinophils)
-Skin biopsy is usually unnecessary if know insect sting occurred
-VERY steroid responsive

Front 201

Canine Eosinophilic Dermatitis with Edema

Back 201

-Wells’ like syndrome
-Hypersensitivity response to insect or arachnoid allergens, drugs, dietary or air-borne allergens

Front 202

Canine Eosinophilic Dermatitis with Edema Clinical signs and History

Back 202

-Lesions occur acutely, often with known antigen exposure
--drugs, insect bites or stings
-Bloody diarrhea happens 1st
-Association with metronidazole?
-Edema can be severe
-Purple macules, wheals, plaques can be bizarre shapes
--need to rule out erythema multiforme
-May not blanche with diascopy due to intense erythema
--looks like hemorrhage
-Systemic signs: pyrexia, malaise, hypoproteinemia
-Reactive eosinophilic lymphadenopathy

Front 203

Canine Eosinophilic Dermatitis with Edema diagnosis

Back 203

-Skin biopsy is mandatory!
--other differentials are deadly (erythema multiforme and vasculitis)
-Will see marked edema, pan-dermal interstitial eosinophilic dermatitis
-Peripheral eosinophilia is not common

Front 204

Canine eosinophilic dermatitis with edema treatment

Back 204

-Rapid and good response to steroids at anti-inflamamtory doses
--some may need higher doses
-Anti-histamines alone are not effective
--combined with steroids may lower dose of steroids or decrease treatment time
-Recurrent or chronic cases are rare

Front 205

Approach to Management of atopic dermatitis

Back 205

-Treat secondary infections (pyoderma, yeasts)
-Control ectoparasites
-Eliminate or avoid primary airborne allergen or desensitize with allergy shots
--hard to completely avoid airborne antigens
-Management with anti-pruritic techniques for life

Front 206

Therapeutic modalitis for pruritus

Back 206

-Regular bathing or rinsing
--remove all allergens from skin surface
--improve stratum corneum barrier function
-Spot therapy with topical steroids or anesthetics
-Non-steroidal anti-pruritic drugs
-Steroidal anti-inflammatory drugs
-Non-steroidal immunomodulators
-Immunotherapy (allergy shots)

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Goals for Topical therapy for Pruritis

Back 207

-Restore stratum corneum barrier function
--decrease penetration of allergens
--hydrate skin, reduce trans-epidermal water loss
--“soak and smear”
--dry skin when over-hydrated or exudative
-Remove allergen
-Direct anti-pruritic medications

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Actions of anti-pruritic medications

Back 208

-Block or inactivate pruritic mediators
-Topical anesthesia
-Substitute another sensation for itch
--cooling
-Protect/restore stratum corneum barrier function

Front 209

Active ingredients for anti-pruritic agents

Back 209

-Drying agents
-Protectants
-Cooling agents
-Antihistamines
-Anesthetics
-Allergen denaturing agents
-Glucocorticoids
-Non-steroidal immunoregulators

Front 210

Drying agents

Back 210

-Antistringents
-Aluminum acetate and colloidal sulfur
-One of main points of dermatology!
--if it is wet, dry it. If it is dry, wet it.

Front 211

Protection/hydration of the epidermis

Back 211

-reduce trans-epidermal water loss by using a protectant to seal in body water
--oils
-Hygroscopic agents to take up and retain moisture
--glycerin, propylene glycol, polyethylene glycol, urea, lactic acid, colloidal oatmeal
--L-Rhamnose
-Correct SQ lipid content, correct lipid abnormality
--ceramides, sphingolipids

Front 212

Topical anesthetics

Back 212

-Lidocaine
-Pramoxine
-Provide a few hours of itch relief

Front 213

Allergen denaturing agents

Back 213

-Contains proteases that denature allergens on the skin surface
-Break down allergens before they are absorbed/recognized by T-cells
-Expensive!

Front 214

Glucocorticoid anti-itch creams

Back 214

-Hydrocortisone: mildly antipruritic
-Triamcinolone: moderate potency, greater potential for local skin atrophy
-Betamethasone: high potency
-Mometasone fuorate lotion: high potency, soft steroid
--not absorbed systemically
-Potency depends on vehicle
--ointments are more potent than creams, lotions, gels, spray/rinse

Front 215

Non-steroidal anti-pruritics

Back 215

-Systemic treatment
-Essential fatty acids (omega-3 fish oil)
-Antihistamines
-Vitamin E
-Leukotriene inhibitors
-Misoprostol

Front 216

Omega-3 Fatty Acids for pruritus

Back 216

-Fish oil
-Eicosapentanoic acid
-Docosa-hexaenoic acid
-Gamma-linolenic acid
-Administered orally
-Incorporated into cell membranes
-Compete for enzymes that metabolize arachadonic acid
--shift metabolic products of arachadonic acid from pro-inflammatory to anti-inflammatory prostaglandins and leukotrienes

Front 217

Omega-3 Dosing

Back 217

-Medium-sized capsules (280mg)
-1 capsule for every 10lbs body weight in small dogs
-1 capsule for every 15-20lbs body weight in larger dogs

Front 218

Antihistamines for pruritus

Back 218

-Work best for allergic respiratory disease or mild atopic dermatitis
-Work very well in respiratory tract, do not work so well on skin
-Synergistic with omega-3 fatty acids
-Best used in combination
-Incredibly safe and inexpensive in generic form
-Need to use caution in glaucoma patients due to anti-cholinergic effects
-1st generation anti-histamines work best because they also act as a sedative
--dog sleeps more, scratches less
-Non-sedative antihistamines do not work as well
-Certirizine and fexofenadine do work well, inhibit eosinophil migration

Front 219

Leukotriene inhibitors for pruritus

Back 219

-Useful with HUMAN allergic respiratory disease
-Not helpful in dogs at all, not worth the effort or the cost

Front 220

Misoprostol for pruritus

Back 220

-PGE-1 analog
-Positive effects with type-I hypersensitivity
-Significantly reduces pruritus and skin lesions in dogs
-Disadvantages: vomiting, diarrhea, expensive!

Front 221

Vitamin E for pruritus

Back 221

-Potent anti-oxidant
-Decreases prostaglandin production and decreases serum IgE levels in atopic people
-Very safe
-May be synergistic with antihistamines, omega-3 fatty acids, and steroids
-“vitamin,” not sure of the form or formula
--cannot guarantee product equivalency
-Get “Natural” vitamin E
--dogs do not absorb synthetic vitamin E

Front 222

Steroidal anti-inflammatory drugs for pruritus

Back 222

-Steroids modify transcription of various genes
-Act at every single step in the inflammatory cascade
-Decreases production of pro-inflammatory cytokines, enzymes, and eicosanoids
-Increased production of anti-inflammatory cytokines, enzymes, and eicosanoids
-Inhibit inflammatory cells and tissue adhesion molecules
-Topicals are safest
-Injectable steroids should be used with great caution! Monitor blood glucose homeostasis
-Oral dosing is preferred
--allows quick withdrawal, closely approximates endogenous rhythms, less effect on HPA axis

Front 223

Indications for oral steroids

Back 223

-Give in patient that is having an acute flare
-Maintenance therapy for seasonal atopic dermatitis with 4 month duration
-Adjunctive treatment of chronic/refractory atopy
-Try to use lowest possible dose and least frequency
-Can decrease dose and frequency by combining with antihistamines, omega-3, topical therapy, allergen immunotherapy

Front 224

Choosing an oral steroid

Back 224

1. Short-acting:
-Prednisone in dogs
-Prednisolone in cats
-Methylprednisolone in dogs and cats
2. Longer acting:
-Triamcinolone in dogs and cats
3. Longest acting:
-Dexamethasone in cats, use with caution in dogs

Front 225

Parenteral Steroids

Back 225

-Methylprenisolone acetate

Front 226

Methylprednisolone acetate

Back 226

-Parenteral steroid
-Do no use in dogs as injection, destroys HPA axis and induces addison’s disease
-Clinical effect is usually shorter in duration
-DO NOT USE IN DOGS
-Use with caution in cats
--check blood glucose before administration
--used for problematic eosinophilic granulomas and lip ulcers

Front 227

Triamcinolone acetonide

Back 227

-Shorter acting parenteral steroid
-Potent HPA axis suppression
-Good choice for intra-lesional treatment
--single eosinophilic granulomas
--stenotic ear canals

Front 228

Steroid side effects

Back 228

-Polydipsia
-Polyphagia
-Tachypnea
-Behavioral changes
-G.I. upset
-Dermal thinning
-Comedones
-Bruising
-Demodicosis
-Secondary infections
-Calcinosis cutis
-Delayed or poor wound healing

Front 229

Non-steroidal immunomodulation

Back 229

-Pentoxifylline
-Macrolide immunosuppressants
-Janise kinase inhibitor (JAK inhibitor)
-Allergen-specific immunotherapy

Front 230

Pentoxifylline

Back 230

-Methylxanthine derivative
-Many immunomodulatory effects
-Alters cytokine production and inflammatory cell migration/adhesion molecule function
-Useful for contact allergy
-Synergistic with other steroids for treatment of atopic dermatitis
--inhibits late-phase reaction
-Side effects: nausea/vomiting, anxiety, hyperactivity

Front 231

Macrolide Immunosuppressants

Back 231

-Suppress cytokine production and proliferation of activated T-lymphocytes
-Decreases mRNA transcription
-Down-regulates T-cell receptors
-Inhibits IL-2
-Inhibits T-helper cells and leads to indirect inhibition of B-cells
-Non-selective immunosuppressive effect
--secondary infections and tumor growth are concerns

Front 232

Atopica Side-effects

Back 232

-Nausea/vomiting is most common
--administer with anti-emetic
-Secondary infections
-Gingival hyperplasia
-Papillomatosis
-Diabetogenic
-hepatic and renal toxicity at high doses or if animal is already compromised
-Monitor blood levels if something seems amiss

Front 233

Cyclosporine and ketoconazole

Back 233

-Give in combination, reduces amount of cyclosporine needed
-Ketoconazole inhibits P450 enzymes that metabolize cyclosporine quickly
--increases blood levels of cyclosporine
-DO no give ketoconazole in cats! Get liver toxicity!

Front 234

Tacrolimus

Back 234

-Similar mechanism to Cyclosporine, inhibits gene transcription in T-cells
-Used topically for inflammatory dermatoses
-Use in dogs:
--discoid lupus erythematosus
--localized atopic dermatitis
--perianal fistulas

Front 235

Janus Kinase Inhibitor

Back 235

-Oclacitanib
-Inhibits JAK enzymes involved in production of pro-inflammatory cytokines
--IL-2, IL-4, IL-5, IL-6, IL-13, IL-31
-Very specific to pruritus, does not treat autoimmune diseases
-Works rapidly after a single does
-Does not interfere with allergy test results like steroids do
-Works great for some dogs, not as effective for other dogs

Front 236

Janus Kinase Inhibitor Side effects

Back 236

-Oclacitanib
-Really side effects are unknown, drug is too new
-Vomiting and diarrhea
-Not approved for use in dogs less than 12 months old due to risk of demodicosis
-May increase susceptibility to infection and demodicosis, may exacerbate neoplastic conditions
-Not for use in breeding dogs, pregnant or lactating females

Front 237

Allergen-specific Immunotherapy

Back 237

-Best for atopic dermatitis patients that cannot be managed with non-steroidal or non-immunosuppressive regimens
-Mechanism of action is not completely understood
--induces production of IgG blocking antibodies specific to allergens within vaccine
-Benefits 50-66% of dogs

Front 238

Allergen-specific Immunotherapy formulation

Back 238

-Need to limit number of allergens per vial to 12-15 extracts
-Subcutaneous immunotherapy = “allergy shots”
-Sub-lingual immunotherapy = “allergy drops”
-No standardized frequency of administration
-Works for a good portion of dogs and cats

Front 239

Clinical appearance of folliculitis and popular/pustular skin diseases

Back 239

-Papules
-Pustules
-Collarettes
-Crusts
-Alopecia
-Most common cause of popular/pustular skin lesions in dogs and cats is folliculitis
--inflammation of the hair follicle
-IN most cases, numerous lesion types are resent in the same case
-Most epidermis in dogs and cats is in the hair follicle

Front 240

Progression of Lesions in Folliculits

Back 240

-Papule to pustule
-Pustule ruptures to form collarette or crust
-IN most cases, numerous lesion types are resent in the same case
--progresses from one lesion type to the netxt

Front 241

Alopecia and Folliculitis

Back 241

-Alopecia may be most common clinical sign
-Often circular and patchy, hairs can be pulled out easily from edges
-Short-coated breeds will have “moth eaten” appearance to coat
--can be mistaken as hives early in disease process
--crusting associated with lesion is common
--hair can stand up on end

Front 242

Ring-like lesions in dogs

Back 242

-bacterial until proven otherwise!
-Usually epidermal collarettes, often due to bacterial infections
--rarely due to ringworm

Front 243

Folliculitis Big 3

Back 243

1. Bacterial
2. Demodicosis
3. Dermatophytosis (ringworm)

Front 244

Folliculitis Diagnosis

Back 244

-Impossible to differentiate between causes of folliculitis based on clinical presentation alone
-Need to do diagnostic tests!

Front 245

Diagnostic approach to Folliculitis

Back 245

-Full history and exam
-Skin cytology in all cases, rule out for bacterial pyoderma
-Deep skin scrapings in all cases, rule out demodex
-Trichogram
-Flea combing
-Fungal culture in all cats and some dogs
--ALL CATS
--young or old dogs, facial lesions, patients with immunosuppressive disease, yorkies
--cases that do not respond to appropriate treatment when skin scraping are negative

Front 246

Folliculitis in Cats

Back 246

-Most common cause is dermatophytosis (ringworm)
-Bacterial is second most common
-Demodex is third

Front 247

Folliculitis in Dogs

Back 247

-Bacterial folliculitis is most common
-Demodex is second
-Dermatophytosis/ringworm is third

Front 248

Bacterial Pyoderma Diagnosis

Back 248

-Need cytology to diagnose
--Will see cocci, either inside or outside of the cell
-Degenerative and intact neutrophils will be present
-Bacterial culture and sensitivity can be helpful
-Biopsy for histopathology

Front 249

Bacterial Pyoderma/folliculitis

Back 249

-Most commonly caused by staph pseudointermedius
-presence of pustules along with papules indicates bacterial infection
-Primary pyoderma is rare
-Secondary pyoderma is MUCH more common
--always secondary to some underlying cause
--allergic skin disease is most common
--parasites, endocrine are also possible

Front 250

Superficial Bacterial pyoderma treatment

Back 250

-minimum of 3 weeks of systemic antibiotics
-continue antibiotics 1 week past clinical resolution
-topical therapy
-Look for underlying cause

Front 251

Deep Bacterial pyoderma treatment

Back 251

-Minimum of 6 weeks of systemic antibiotics
-2 weeks past clinical resolution
-Topical therapy
-Look for underlying cause!

Front 252

Dermatophytosis

Back 252

-Ringworm
-Fungal infection of keratin
-Hair, superficial layers of skin, claws
-more common in cats than dogs
-Classified by preferred host and location
--anthropophilic: humans
--zoophilic: animals
--Geophilic: in soil
-ZOONOTIC!

Front 253

Microsporum Canis

Back 253

-Dermatophytosis
-Most common isolate of ringworm
-90% of cases in cats
-70% of cases in dogs
-Zoophilic, cats are normal host

Front 254

Microsporum gypseum

Back 254

-Dermatophytosis
-Geophilic species
-Causes 20% of ringworm cases in dogs
-Acquired by digging or rooting in contaminated soil
-Usually appears on face where dog has been digging

Front 255

Trichophyton mentagrophytes

Back 255

-Dermatophytosis
-Zoophilic, lives on small mammals
-10% of canine cases
-Most common species in cows and other large animals

Front 256

Dermatophytosis Transmission

Back 256

-Contact with infected or carrier animals, fomites, or soil
--fomites: blankets, brushes, clippers, cages
-Spores stay infective Even after hair is shed from host for up to 18 months
-7-14 day incubation period
-After contact with skin, spores germinate and hyphae invade superficial layers of the skin, nails, and hair follicles
-Arthrospores produced, grow down follicle of actively growing hairs
--weakens hair shafts and causes breakage
-Fungus invades adjacent follicles in anagen phase, produces circular spreading pattern

Front 257

Clinical presentation of Dermatophytosis

Back 257

-Classic circular lesion
-Circular ring of hair loss with erythema and crusting or scaling
-Looks a lot like a bacterial folliculitis lesion, need to do diagnostic testing to tell apart

Front 258

Dermatophytosis in Dogs

Back 258

-Localized lesions are more common
-Circular alopecia
-Kerion (Furunculosis)
-generalized form is less common, occurs in certain breeds or in immunosuppressed animals
--Yorkies, Jack Russel terriers

Front 259

Kerion

Back 259

-Form of localized dermatophytosis in dogs
-Nodular due to rupture of hair shafts
-Furunculosis

Front 260

Yorkies and Ringworm

Back 260

-Yorkies are like cats and dermatophytosis
-Get ringworm often
-generalized ringworm
-May have underlying immunosuppression in some cases

Front 261

Dermatophytosis in Cats

Back 261

-More common in cats than dogs
-Should be a DDx for any skin disease in cats
-Many different clinical appearances
-Alopecia, crusting, and scaling are most common
-Long-haired cat breeds are predisposed
-Very common in young cats
-May or may not be accompanied by pruritus

Front 262

Dermatophytosis Diagnosis

Back 262

-Screening tests:
--direct microscopy trichogram
--Wood’s lamp and green fluorescence
-Culture:
--identification of the fungus
--Culture is gold standard for diagnosis
-Skin biopsy

Front 263

Wood’s lamp diagnosis for Dermatophytosis

Back 263

-Examine hair coat in dark room with Wood’s lamp
-Tryptophan metabolite of dermatophyte fluoresces under UV light
-Wavelength is temperature dependent, need to let lamp heat up for 5-10 minutes
-Look for green fluorescence in hairs
-Pro: fast, inexpensive, screening test, can look at specific hairs
-Cons: less than 50% of Microsporum canis strains fluoresce, false positives can be seen with scales, crusts, topical medications
-DO A CULTURE!

Front 264

Fungal Culture

Back 264

-Gold standard for diagnosis of dermatophytosis
-Active lesions: use hemostats to collect hair and scale from periphery of lesion
--inoculate hair onto media or send hairs in sterile red top tube to lab
--Make sure you autoclave hemostats!
-If there are no active lesions or want to test asymptomatic carriers, use sterile toothbrush culture

Front 265

Dermatophyte Test media and Fungal Culture

Back 265

-Need to check culture EVERY DAY
-DTM (media) has proteins and carbohydrates
-Dermatophytes use protein first
--produce alkaline by-products, turn phenol red in media to red color
-Saprophytes use carbohydrates first
--no color change
--protein consumption comes later, 10-14 days before color change

Front 266

Problems with Fungal cultures

Back 266

-Need to check every day for growth
--labor intensive
--forgetting to check can result in contaminant overgrowth and false negatives or false positives
-Color change may only be useful for 10-14 days
-Needs to be identified! Color change is not a sufficient diagnosis
-Avoid small slant jars or small DTM discs, need enough media

Front 267

Microsporum canis identification

Back 267

-More than 6 cells in spore
-Thick cell wall

Front 268

Micosporum gypseum

Back 268

-Thinner cell wall
-Fewer than 6 cells within macrocandidya

Front 269

Dermatophytosis Treatment

Back 269

-Most healthy animals with dermatophytosis will self-cure
-Treatment is recommended in all cases due to contagious and zoonotic nature
-No matter what drug is used, therapy must be continued until at least 2 consecutive fungal negative cultures are obtained

Front 270

Dermatophytosis treatment in Dogs

Back 270

-Localized:
--topical therapy is often acceptable if only 1 lesion
--miconazole, clotrimazole, terbinafine
-Generalized, kerions, or numerous lesions:
--systemic treatment is needed
--fluconazole, ketoconazole, itraconazole
--terbinafine

Front 271

Dermatophytosis treatment in Cats

Back 271

-Systemic therapy is needed in all cases
-Itraconazole
-Fluconazole
-Terbinafine
-Topical therapy:
--lyme-sulfur dips, decrease environmental contamination

Front 272

End treatment of Dermatophytosis

Back 272

-When 2 negative fungal cultures in a row
-3 negative fungal cultures in chronic cases and multi-cat households
-If there are no lesions, use sterile toothbrush to brush cat coat

Front 273

Dermatophytosis Management

Back 273

-Keep infected animals in area of the house that can be safely and easily cleaned/disinfected
-Isolate other animals if possible
-Culture all animals in contact with infected animal
-Zoonotic risk! Up to 60% of humans in household will develop lesions

Front 274

Itraconazole

Back 274

-Most commonly used azole antifungal for dermatophytosis in cats
-Highly keratinophilic, sticks to keratin and has residual effect
-Pulse-dosing is reported to be effective
--alternate week dosing is effective
-DO NOT COMPOUND!
-Side effects: GI, liver toxicity is rare but reported, cutaneous vasculitis in dogs

Front 275

Fluconazole

Back 275

-Increased use for dermatophytosis since it has become generic and more available
-Water soluble, do not need to give with food
-Excreted via kidneys in active form
--drug is concentrated in urine
-Very very low affinity for mammalian P450 enzymes
--VERY safe for liver issues

Front 276

Terbinafine

Back 276

-Newest class of antifungals: Allylamines
-Generic and cheap
-Need a higher dose, low doses do not work
-Concentrated in the hair
--stays above MIC90 for 5 weeks after 14 days of oral treatment
--pulse dosing is probably an option because it concentrates so well in the hair
-Side effects:
--GI, increased liver enzymes (rare), facial pruritus or cutaneous drug eruption

Front 277

Ketoconazole

Back 277

-In-vitro activity against Microsporum canis but decreased compared to other azoles
-Cats get sick from ketoconazole
--liver toxicity, do not use in cats!
-Beware of drug interactions, suppresses drug metabolism via down-regulation of P450 microsomal enzymes

Front 278

Topical Antifungals

Back 278

-Adjunct to systemic treatment, hastens resolution and decreases environmental contamination
-Whole-body topical treatment is preferred
--can get even non-visible lesions
-Lime-sulfur dips or sprays are topical treatment of choice
-Enilconazole is not available in US

Front 279

Lime Sulfur Treatment of Dermatophytosis

Back 279

-Most effective topical antifungal treatment
-Typically used as a dip
-Applied once weekly
-Side effects:
--strong odor, stains surfaces and fabrics and jewelry
--Can irritate mucus membranes
-Making lime sulfur into a spray and spraying entire coat can improve compliance
--dilute 1:32 in spray bottle and spray down cat
--cats tolerate better than dipping

Front 280

Environmental Decontamination of Dermatophytosis

Back 280

-Can be difficult aspect of treatment due to resistant spores
-Infective spores are contained within hairs that have been shed
-Infective spores can remain viable in environment for up to 18 months
--most live 3-6 months or shorter if there is more humidity
-Big issue in multi-cat households, catteries, or shelters
-Hard clean is most important part of decontaminating the environment!
--mechanical removal of organic debris and hairs from the environment
--follow with washing surface with detergent
--Electrostatic cleaners are preferred over sweeping
--follow with disinfectant

Front 281

Disinfectant use for Environmental decondamination of Dermatophytosis

Back 281

-Disinfectant is used after hard clean (step 2)
-10 minutes contact time
-Bleach is “best” disinfectant for ringworm
--some surfaces are not able to be bleached
-Enilconazole is approved for use in poultry houses
-Accelerated hydrogen peroxide products
-Any over-the-counter product that has label claim against T. mentagrophytes can be used against ringworm

Front 282

Environmental Decontamination of Fomites with Dermatophytosis

Back 282

-Discard fomites that cannot be thoroughly treated
--cat towels, collars, clothes
-Dry cleaning is effective against killing spores
-Washing machine on longest cycle with highest water level, was clothes twice
--use bleach if possible
-Carpets are one of most difficult surfaces to disinfect
--vacuum frequently!
--steam cleaning does not kill all infective spores, good for mechanical removal
--carpet shampoo can work

Front 283

Dermatophytosis Summary

Back 283

-Microsporum canis is most common
-Systemic treatment is mandatory in cases of feline dermatophytosis
--itraconazole, fluconazole, terbinafine
-Treat until you have at least 2 consecutive negative fungal cultures
--3 in chronic cases or multi-cat households
-Topical therapy: lime-sulfur dip
-Environmental decontamination is key

Front 284

Canine Demodicosis

Back 284

-3 species
--demodex canis (most common)
--demodex injai (long bodied)
--demodex cornei (short bodied)

Front 285

Demodex canis classifications

Back 285

1. Juvenile onset:
-less than 10 months
-localized or generalized form
2. Adult onset:
-more than 4 years at onset

Front 286

Localized demodicosis

Back 286

-Young dogs, less than 6 months
-Fewer than 6 lesions, usually limited to the face
-Treatment is not usually needed, more than 90% will resolve on own in 4-8 weeks
-Therapy is not recommended, want to know which ones will become generalized
-Topical antimicrobials
-Evaluate for other stressors including internal parasites
-Re-check every 3-4 weeks with deep skin scrapings

Front 287

Generalized demodex

Back 287

-More than 4 lesions
-Numerous life stages on scrapings
-1 entire body region
-Lesions involving feet
-Spreading or persisting for more than 6 months
-ANY adult onset demodex is generalized

Front 288

Generalized Demodex Juvenile Onset

Back 288

-Pathogenesis is unclear, involves mite-specific immunodeficiency
-Immunodeficiency is shown to be heritable
--dog should not be used for breeding

Front 289

Generalized demodex Clinical Signs

Back 289

-Alopecia, scaling, papules, comedones
-Pruritus is usually minimal, but can increase with secondary infections
-Secondary infection is very very common, 95% of cases
--pustules, crusts
-Deep pyoderma occurs as hair follicles rupture
-Deep secondary infectious complications can cause death (very rare)

Front 290

Generalized Demodicosis Adult Onset

Back 290

-Secondary to immunosuppressive disease
--Hypothyroidism, Cushing’s, Diabetes mellitus, Neoplasia
--immunosuppressive therapy
-Need to look for underlying cause
--CBC, chem, urinalysis, thyroid panel
--radiographs to rule out neoplasia
-Can be a sign of early immunosuppression

Front 291

Diagnosis of Demodicosis

Back 291

-DEEP skin scraping is diagnostic test of choice, need to get capillary bleeding
-Trichograms can be helpful, useful in difficult places to scrape
--can be used as a screening tool
-Cytology and Biopsy can also be helpful

Front 292

Mite Counts

Back 292

-Useful in monitoring response to therapy
-Number of adults
-Number of eggs
-Number of larva
-Percentage dead vs alive
-Ghosts

Front 293

Biopsy for Demodex

Back 293

-Sometimes is needed to find eggs
-Effective in breeds with thickened skin or fibrotic skin
--Shar-peis, bulldogs, or dogs within chronic dermatitis

Front 294

Treatment of Generalized Canine Demodicosis

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1. Antibiotics: all cases have secondary pyoderma until proven otherwise
-minimum 4 weeks, 6 weeks if deep
--culture based if deep pyoderma
2. Topical therapy
--shampoo 2-3x per week with anti-microbial shampoos (chlorhex, benzoyl peroxide, ethyl lactate)
--Benzoyl peroxide flushes follicles
--Hydrotherapy is often used 1x per day to help exfoliate crusts, decrease inflammation, and decrease secondary infection
3. Miticidal therapy

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Amitraz for Demodex

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-Monoamine oxidase inhibitor, alpha-2 agonist
-only FDA approved drug for demodex in dogs
-has lots of side effects
--lethargy, sedation, bradycardia, polyuria, hypothermia, and hyperglycemia in dogs
--Headaches, lethargy, dizziness, asthma attacks in humans
-Toxicity is reversible with atipamezole and yohimbine

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Macrocytic Lactones as treatment for Demodex

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-Avermectins
--ivermectin
--doramectin
-Milbemycins
--milbemycin oxime
--Moxidectin

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Ivermectin for Demodex

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-Macrocytic lactone
-GABA agonist
-Treatment of choice for demodex in dogs
-Extra-label treatment, not approved
--use injectable product orally
-0.4-0.6mg/kg per day
-400-600 ug/kg per day
-Graduallt increase dose over 10-14 days until therapeutic dose is reached
-Greater than 90% cure rate, less than 5% recurrence rate if treated appropriately

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Dosing Regimen for Ivermectin

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-Days 0-2: 50ug/kg
-Days 3-5: 100ug/kg
-Days 6-8: 200ug/kg
-Days 9-11: 300ug/kg
-Day 12: 400ug/kg, maintenance dose
-Can increase up to 600ug/kg if not responding
-Need to re-check weight and adjust dosing!

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Treatment duration for Demodex

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-Repeat skin scrapings every 4 weeks during treatment
-Sample at least 4-6 sites affected, including face and paws
--Take samples from same areas
-Finding any mites is considered positive!
--alive, dead, part of a mite, immature stages, etc.
-Treat until at least 2 sets of consecutive negative scrapings are obtained a month apart
--3 in more chronic or severe cases

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End-point for Demodex treatment

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-2 consecutive negative scrapings 1 month apart
-3 consecutive negative scrapings is chronic or severe case

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Ivermectin Side Effects

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-Ataxia, tremors, GI, Lethargy, mydriasis, blindness
-Severe side effects: stupor, coma, seizures, death
-MDR1 gene mutation encodes faulty P-glycoprotein
--Ivermectin builds up in brain and results in neurotoxicity
-MDR1 mutation test is available
-Do not use ivermectin with comfortis!

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Treatment failure for Demodex

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-Treatment failure is due to premature end of treatment!
-Educate clients
-Discuss side effects and longevity of treatment
-Spay/neuter juvenile onset generalized cases

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Milbemycin and demodex

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-“safe” for ivermectin-sensitive breeds
-No longer available
-DO NOT used Sentinel as alternative! Lufenuron is not safe for daily use

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Advantage Multi and Demodex

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-Imidacloprid 10% and moxidectin 2.5%
-Fleas, heartworm, hookworm, whipworm, roundworm
-Good for mild cases of demodex
--Efficacy increases with rate of application

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Moxidectin for Demodex

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-Give orally at 400ug/kg
-Similar protocol as ivermectin administration

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Demodex injai

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-Long-bodied follicular demodex
-Lives in sebacious gland and hair follicle
-Dorsal greasy skin and coat in terriers
--wire haired fox terriers, westis, other terriers
-Often have concurrent skin disease

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Demodex corei

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-Short-bodied Demodex mite in dogs
-Inhabits stratum corneum, NOT hair follicle
-Seen on scrapings of dogs with high levels of Demodex canis mites
-Clinical presentation and treatment is same as Demodex canis

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Feline Demodicosis

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-Demodex gatoi: superficial and pruritic
-demodex cati

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Demodex gatoi

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-Short and stubby mite
-Inhabits stratum corneum, found on superficial skin scrapings
-Can be difficult to find, may find on fecal exam due to over-grooming
-Cat will be pruritic on head, neck, ventrum
--symmetrical alopecia is common presentation
-More common in southeast US and gulf coast
-Contagious! Treat all in contact with cats!
-Asymptomatic carriers exist
-Tx: lime-sulfur dip 1x per week for 6 weeks

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Demodex cati

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-uncommon
-Follicular, long-bodied mite
-Alopecia, crusting, ceruminous otitis
-Underlying immunosuppression
--corticosteroid administration, FeLV/FIV, diabetes, Neoplasia
-Tx: weekly lime-sulfur dips are most effective

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Pyoderma

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-“Pus in the skin”
-Any pyogenic inflammation within the skin
-Typically used for bacterial skin infection, even though anything can cause pus in the skin
-Most commonly Staphylococcus
-Primary pyoderma is rare, secondary pyoderma is the rule
--Almost always an underlying cause for pyoderma
-Allergic skin diseases are most common
--endocrinopathies, immune-suppression, and ectoparasites are also possible causes

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Recognizing Pyoderma

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-Very essential skill
-Dogs more common than horses more common than cats
-Pyoderma is unusual if it presents with unique clinical lesion or pattern of lesions, or is caused by unexpected species of bacteria
-Even typical cases of pyoderma can take many different forms
--very variable clinical presentation

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Staphylococcal infections

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-Staph bacteria are normal inhabitants of the skin and mucus membranes in mammals and birds
-Also the most common pathogen causing skin and soft tissue infections worldwide
-Superficial infections result from disruption of skin/mucus membrane barrier
-Deep infections result from rupture through hair follicle walls, penetrating wounds, or hematogenous spread
-Normal bacteria on skin, makes it hard to vaccinate against, hard to manipulate body’s immune response

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Coagulase positive Staph

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-Pathogenic staphylococci
-Considered to be “true” pathogens
-S. aureus: humans are primary reservoir
-S. pseudointermedius: dogs are primary reservoir
-S. schleideri coagulans: dogs
-S. intermedius: pigeons
-S. delphinii: sea mammals
-S. hyicus: pigs

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Coagulase negative Staph

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-Non-pathogenic resident or transient commensal bacteria
-S. schleiferi schleiferi IS pathogenic
--need to speciate coagulase negative staph

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“Pathogenic” for clinical purposes

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-Most coagulase negative staph lack significant virulence factors
-Coag- are commensals of skin and mucus membranes
-Referred as “contaminants” when isolated from culture sample
-Coag- commonly express multiple drug resistance
-Hard to know if a coag- bacteria on clinical sample is significant or not

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Coagulase negative bacteria isolated on clinical sample

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-Staph Schleiferi Should ALWAYS be considered to be pathogenic
-If culture was from a sterile site or intact primary lesion, bacteria is probably causing infection
--joint fluid, blood, CSF, closed body cavity, cystocentesis, pustule, bulla
-Interpret findings from contaminated sites with caution
--skin surface swab, wound, external ear canal

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Classification Scheme for Pyoderma

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-Surface: bacteria is on the surface of the skin
--intertrigo: skin fold pyoderma
--hot spots: acute, moist, pyotraumatic dermatitis
--otitis externa
-Superficial:
--follicular
--subcorneal/non-follicular
-Deep: infection is outside of hair follicle wall
--Furunculosis, abscess, cellulitis, panniculitis

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Surface Pyoderma

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-Bacterial colonization of the epidermal surface only
-No invasion into the stratum corneum
-3 types:
--acute moist pyotraumatic dermatitis
--skin fold pyoderma.intertrigo
--otitis externa
-Should be treatable with topical therapy alone!

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Acute moist pyotraumatic dermatitis

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-“Hot spots”
-Self-induced lesion from pruritic insult
--usually flea bites, typically occur over “flea zone”
-Alopecic, erythemic, thick, eroded, or ulcerated skin
-Matted hair
-Can progress to folliculitis if left untreated
-Treatment: clip and scrub
--use drying agents (Domboro solution), topical steroids, topical antibiotics for 5-7 days
--identify and eliminate primary cause (usually flea bite allergy)

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Treatment for Severe or Advanced hot spots

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-Depends on severity of pruritus
-Always do skin scraping!
-Systemic anti-inflammatory doses of corticosteroids
--“itch buster” of steroids
-Systemic antibiotics in cases that have progressed to pyotraumatic folliculitis
--Satellite papules/pustules are a clue
-best treatment for hot spots is topical

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Intertrigo

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-Skin fold pyoderma
-Occurs where skin contacts or rubs on skin
-Deep skin folds maintain moisture, leads to bacterial or yeast overgrowth
-Occurs in obese dogs or breeds with skin folds
-Treatment: topical cleansing and antiseptics
--Medicated wipes, baby wipes, shampoos, gels/creams
--Weight loss is occasionally corrective
--Surgical correction for facial folds

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Superficial Pyoderma

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-Impetigo and bacterial folliculitis
-Culture and susceptibility testing is standard, need to know what to treat
-Some strains are resistant to all oral drugs
--aggressive topical therapy may be the only option

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Impetigo

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-Pustular, non-follicular form of superficial pyoderma
-Not contagious in dogs
-Usually occurs in young dogs or puppies
-Large non-follicular pustules (non-haired skin) and crusting in inguinal/ventral abdominal area
-May be seen in older dogs with underlying immunosuppression
--iatrogenic or endocrine diseases

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Bacterial folliculitis

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-Staph infection is most common
-Papules or pustules centered on hair follicles
-Follicular plugging
-Alopecia
-Crusts and epidermal collarettes, causes hair to fall out
--bacterial infection induces inflammation, kicks hair out of the follicle
-Very variable clinical picture, varies according to coat type, acute vs. chronic disease, location on body that is affected
-Need to do a skin scrape and diagnostics to diagnose effectively

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Silky coated breeds and Folliculitis

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-Obvious papular/pustular lesions, crusts, or collarettes may not always be present
-hair does not come out as easily
-Some cases are very subtle
--vague thinning of the hair, in patches
--sometimes can see dilated and inflamed hair follicles
-Peristent infections can lead to significant inflammation, extensive alopecia, and chronic changes (lichenification)

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Heavy-coated dogs and Folliculitis

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-May not see obvious papular or pustular lesions, crusts, collarettes
-Thinning of the undercoat
--animal is not as “fluffy” as it was
-Shaving hair may be needed to see full extent of lesions

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Deep pyoderma

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-Mostly furunculosis, perforating folliculitis
--hair follicle ruptures, spews keratin out into dermis
--keratin is attached by inflammatory cells
--Free hairs in dermis act as foreign body
-Staph is most common inciting etiology
-May also have secondary invasion by gram- bacteria (Proteus, Pseudomonas, E. coli)

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Folliculitis and Furinculosis

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-Often occur together
-Can be localized or regional

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German Shepherd Staph Infection

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-Seem to develop strong staph infections
-Develop strong inflammatory responses to staph infections
-Usually due to flea bite allergy, underlying atopic dermatitis, or some other underlying disease

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Callus pyoderma

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-Develops when dogs lie on hard surfaces
-Some can become nasty, deep infections
--especially in dogs that do not deal with staph infections normally (atopic dogs)
-Usually have underlying allergic disease

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Muzzle folliculitis and furunculosis

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-“Chin acne”

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Pedal/interdigital folliculitis and furunculosis

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-Common presentation
-Mostly in short-coated breeds with allergic disease
-Results in pain and lameness
-Hemorrhagic bullae may develop and rupture
-Most have underlying allergic disease

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Nasal folliculitis and furunculosis

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-Top of the nose, nasal planum and haired skin behind nasal planum
-

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Acral Lick Dermatitis/granuloma

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-Single lesion
-Most commonly on top of the carpus
-Self-induced by dogs licking and chewing at one site
-Most dogs have underlying primary allergic disease, causes dog to chew at the forelimbs
-Occasionally seen on the hind limbs
-Deep, boggy furunculosis
-Requires very long-term antibiotic therapy
-Can be very frustating to owners, destructive, and cause a lot of scarring

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Staphylococcal blepharitis

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-Staph infection of the hair follicles around the eyes
-Can become very involved if left unaddressed
-Can affect the eyelids only, without pruritic disease

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Post-grooming Furunculosis

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-Dogs are often systemically ill, febrile, anorexic, painful
--VERY painful!
-History of recent grooming, can see lesions on dorsal mid-line
-Pseudomonas and Serratia are often cultured (water borne bacteria)
-Diagnose with biopsy and histopathology
-Treatment: supportive care with pain meds
--Antibiotics, preferably with culture and sensitivity
--often start treatment of fluoroquinolones without culture

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Superficial Spreading Pyoderma

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-Rough-coated dogs with rapidly, peripherally expanding alopecia and crusting, collarettes
-Intense erythema at periphery
-Intense inflammation on leading edge of lesions
-May hyperpigment in center of lesions
-Often highly pruritic
-Sometimes referred to as “staph hypersensitivity”
-Staph undermines stratum corneum, goes down into hair follicles
-With chronic infections, will have large areas of “burned” hair follicles

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Mucocutaneous pyoderma

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-Erosions, ulcerations, crusting, depigmentation of mucocutaneous junctions
-Occurs around lips, nasal planum, eyelids
-May or may not be secondary infection
-Common in German Shepherds but occurs in all breeds
-Discoid Lupus is main DDx

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DDx for Pyoderma

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-Malassezia dermatitis (intertrigo and hot spots)
-Demodicosis, dermatophytosis, sebaceous adenitis (folliculitis, papules, crusts)
-Pustular diseases, esp. pemphigus foliaceus (pustules)
-Deep infectious process, fungal and mycobacterial infections

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Diagnosis of Pyoderma

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-Often clinical judgement
-Confirm via cytology, always worth pursuing
-Rule out presence of acantholytic cells and pemphigus
-Sometimes bacteria is too deep to culture, lack of culture does not rule out pyoderma as diagnosis
--could be deep down in hair follicle

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Acantholysis

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-Process in which keratinocytes become separated from each other
-Dissolution of molecular glue holding keratinocytes together
-Large cells with central nucleus and stained cytoplasm
-May be formed by enzymatic activity from pyoderma and dermatophytosis
--causes disruption of adhesion molecules

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Multi-Drug Resistance and Pyoderma

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-Spectrum of antimicrobial susceptibility was stable for LOOOOONNNGGG time
-Now there is increased resistance
-Probably developed due to suppression of normal flora and growth of resistant strains

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Specific pet populations experiencing Multi-drug resistance

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1. populations with prior antimicrobial exposure
--suppression of normal flora that leads to super-infection by resistant strains
--Mutations induced by dosing error or poor use
2. Pets with staph aureus infections: cross-transmission from people

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Indications for bacteria culture and sensitivity

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-Superficial pyoderma that fails to respond to appropriate empirical oral antibiotic therapy
-History of repeated antibiotic therapy
-Pyoderma with gram- rods on cytology
-Deep draining tracts, deep pyoderma
-Nodular granulomatous lesions
-When uncommon bacterial species are suspected
--actinomycetes, mycobacteriae

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Bacterial culture and sensitivity sampling

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-Sample primary lesions
--papules, pustules, intact abscesses
--lance with sterile needle, swab purulent exudate
-Secondary lesions are less than ideal
--crust: lift crust with sterile needle or blade and swab underneath
--epidermal collarette: swab under leading edge
-Deep granulomatous lesions or pure folliculitis may need tissue biopsy