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Flashcards in Final- Integument Deck (201):
1

Vesicle/Bulla

• Palpable elevation filled with clear fluid( fragile and they don't stick around for long)

Degeneration and Necrosis or Inflammation and Repair

NAME DEPENDS ON SIZE:

– Vesicle < 1cm

– Bulla > 1cm

 Causes:
– Auto‐immune dermatoses

– Viral infections
– Chemical irritants

– Burns

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What can lead to the formation of  vesicle/bulba?

-Intercellular edema ( histologically called “spongiosis”)- inflammatory process

-Intracellular edema (“hydropic degeneration”- loose osmotic balance)

-Disruption of intercellular junctions (“acantholysis”)

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How vesicles form

Fig. 17‐17 Schematic diagram of the sites of vesicle formation in the skin. A, In a subcorneal vesicle, the stratum corneum forms the roof of the vesicle (as in impetigo or pemphigus foliaceous). B, In a suprabasal vesicle, a portion of the epidermis (stratum spinosum) forms the roof (as in pemphigus vulgaris). C, In a subepidermal vesicle, the entire epidermis separates from the dermis and forms the roof (as in bullous pemphigoid).

 

Need to know-- you can get a lot of information by knowning where the vesicle is forming- SAMPLE IT

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Pustule

Palpable elevation filled with pus

Cause – leukocyte infiltrate

Pathological process: Inflammation and Repair

I.e. Pimples

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Crust

 can be when a pustule ruptures

• Dried exudate, serum, blood, and scale that is adhered to the skin surface

Causes:
– Severe disorders of keratinization

– Severe pustular dermatitis( when pustules burst)

– Secondary to ulcers

Pathological Processes: Degeneration/Necrosis, Inflammation/Repair, or Disorder of Growth

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Papules

• Palpable, solid (no fluid), elevated mass < 1cm diameter

i.e. mosquito bite

 Causes:
– Infiltrate of inflammatory cells

– Infiltrate of neoplastic cells

– Epidermal hyperplasia
– Deposit of mineral

Termed Based on Size:

Nodules = >1cm diameter and deeper- usually thinking about tumors

Plaques = coalesced papules- has a flat surface

Pathological Process: Inflammation/Repair, Disorder of Growth, Deposits and Pigmentations

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Plaque- solid but with a flat top

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Nodule

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Ulcers

• Loss of epidermis with exposure of dermis- VERY NON-SPECIFIC

Cause: 2ndaryto...

– Epidermal necrosis

– Inflammation

– Infarction(cut off of blood supply)
– Neoplasia

Pathological processes: degeneration/necrosis, inflammation/repair, cirulatory disorders, or disorder of growth

Erosion--- no dermis exposed

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Scale

• Accumulation of loose keratinized cells

- dandruf

Causes:
– Disorders of keratinization

– Chronicdermatitis

Pathological Process: Inflammation/Repair or Disorders of Growth

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Epidermal collarette

a circular rim of scale that occurs secondary to rupture of a vesicle, pustule, or papule

 

FORM OF SCALE- vesicle, papule or pustule has ruptured

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Lichenification

• Thickening and hardening of the skin

- becomes hyperpigmented

Causes:
– Chronic irritation/inflammation

 

Pathological Process: Inflammation and Repair

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What lesion terms can we use here?

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-ulcers

-erthyema (skin term ONLY)

-paules

 

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When collecting a skin biopsy...

• DO
– Biopsy early, before treatment
– Be gentle
– Collect multiple samples, range of changes – Include crusts

• DO NOT
– Surgically prep the site
– Grasp with forceps
– Biopsy the center of a lesion

– Hold out on history/DDx

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Pathological Processes of degeneration and necrosis

 

Can be difficult to grossly tell from other groups

- Degenerative/Necrotic lesions tend to ulcerate, but other pathological processes lead to ulceration too

- Degenerative/Necrotic lesions become inflammation&repair over time – normal response to injury, and secondary infections common

- Primary circulatory disorders often lead to degeneration/necrosis

THINCK BURNS

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Flock of 300 merino ewes& lambs in the shade cuddling after a period of a lot of rainfall.

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The skin lesions indicate something is injuring the epidermis because there are crusts and ulcers

The pathological process is likely epidermal degeneration&necrosis or inflammatory (infectious)

Differential Diagnoses

• Photosensitization

• Dermatophilus

• Viral infections – bluetongue, pox (orf), vesicular disease (FMD, VS

What can we do to determine the cause?

BIOPOSY,  serum chem(NSF), bluetongue (negative), virus isolation(negative), plant id- st. john's wort, histopath results- epidermal necrosis and ulceration(unknown etiology) comment- bacterial dermatitis which appears secondary



 

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Pathogenesis of Photosensitization

Uv light absorbed by photodynamic chemicals(shouldn't be there) in skin causes free radical damage causes epidermal necrosis of lightly pigmented or sparsely haired skin

 

 

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2 Types of Primary photosensitization

Primary photosensitization

 

Type I (Exogenous)
– Plants containing photosensitive chemicals

– St Johns Wort, lucerne, perennialryegrass

-TMS, quinolones, griseofulvin

Type II (Intrinsic)

– Porphyria

– Inherited deficiency of proporphyrinogen III cosynthetase leads to defect in heme synthesis leads to  buildup of porphyrins(PINK TEETH)

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Secondary Photosenitization

Pathogenesis of Photosensitization

Light activates agents leads to free radical damage  leads to epidermal necrosis of lightly pigmented or sparsely haired skin

Secondary (Type III, hepatogenous photosensitization)

– Poor hepatic clearance of phylloerythrin (product of rumenal chlorophyll transformation).

– Toxins causing biliary obstruction: nothing in these plants- phylloerythrin just can not clear the liver
• Lantadenes – Red Lantana
• Steroidal saponins – Tribulus, Pancium

• Sporodesmin (Facial Eczema) ‐ Lolium perenne + Pithomyces chartarum--->sporodesmin toxicosis

• Other hepatotoxins: Pyrrolizidine alkaloids, aflatoxin, phomopsin

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Liver from a sheep with photosensitization due to red lantana toxicosis

 

REMEMBER- THE LIVER CAN BE NORMAL

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Liver from a sheep with photosensitization due to Tribulus toxicosis

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A couple learning points

• Important to use clinical clues to come up with differentials for likely pathological processes of skin pathology

• Not always going to get definitive answers from your tests, including histology (gasp!)

• How did we rule out type III photosensitization in this case?

We found the plant and we did a serum chemistry(if it was type III, then hyperbillirubia should show up)

• How do we know this simply wasn’t just too much sun exposure (i.e. not photosensitization)? History is different; photosensitization happens a lot faster

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 Most Degeneration&Necrosis skin cases have these features...

pink storm= necrosis

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Skin healing by primary and seconary intention

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 Acute Solar injury

• Acute UV light exposure leads to “sunburn”

–  erythema leads to blistering/vesicles leads to sloughing of necrotic skin

–  potentially due to uv‐mediated endothelial damage and cytokine production

 

MDx: chronic locally extensive ulcers

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Chronic Solar Injury

• Chronic (years of) UV light exposure leads to “solar/actinic keratosis”

– Chronic injury leads to epidermal hyperplasia and dermal fibrosis and elastosis

– Increased risk for neoplasia due to direct DNA injury and subsequent mutations- SQUAMOUS CELL CARCINOMA

MDX: epidermal hyperplasia, dermal fibrosis and elastosis

increased risk for neoplasia due to direct DNA injury and subsequent mutations

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dermal fibrosis and comedones

The epidermis is thickened by acanthosis, and three comedones (follicular distention and hyperkeratosis) are present. If comedones rupture, a large amount of endogenous foreign material (stratum corneum, hair shafts, and sebum) is released into the dermis, causing a foreign‐body inflammatory response. Bacteria are also released and cause a secondary bacterial infection.

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Thermal burns

• Caused by exposure to excessive heat – hot liquids, flames, friction, electricity, heating pads, blow dryers, drying cages, and lightning

1st degree
– epidermis

–  Reddened/darkened necrotic epidermis

–  Complete healing

2nd degree
– epidermis and dermis

–  Vesicle formation

–  Some adnexa are preserved allowing epidermal

3rd degree

– full thickness epidermis and dermis +/‐ subcutis

– Sloughing of necrotic tissue, followed by granulation tissue

– Scar; life threatening (fluid/protein loss and portal for sepsis)

Examples:

1st degree burn from my savvy cooking skills- Mdx: focal acute epidermal degeneration and necrosiss

regeneration with some scarring

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Thermal burn, full thickness (third‐degree) skin, dog. A, There is necrosis of the epidermis (arrow), follicular epithelium, and dermis. Because of increased capillary permeability, fluid has accumulated between the dermis and epidermis, forming vesicles (V). H&E stain. B, The dry necrotic skin is the site of the burn (arrow).

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Chemical burns

• Caused by body or wound secretions, application of drugs, exposure to acids, alkalies, soaps, detergents, or irritant plants

Most cases mild (“irritant”)

Exposure via direct application

– Must penetrate hair and protective epidermal layers

– Adsorptive medium may facilitate

• Main issue differentiating vs contact hypersensitivity dermatitis

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Erythema Multiforme & Toxic Epidermal Necrolysis

THIS TYPE IS HISTOLOGICALLY AND GROSSLY DISTINCT!

• Pathogenesis thought to involve type IV hypersensitivity towards antigens on the surface of keratinocytes inducing apoptosis

– induced via antigenic mimicry from drug administration, underlying infection, neoplasia, dyes/preservatives in pet foods?

–  Histologically distinct

–  Widespread coalescing erythematous macules(spots that are not elevated or depressed, but they are a different color) that leads to vesicles and ulcers

EM
– Milder

macules leads to vesicles and ulcers

– Single cell apoptosis +/‐ lymphocyte satellitosis

TEN
– More severe

– Sheets of apoptotic/necrotic cells resembling a burn

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Is Degeneration&necrosis the primary pathological process in our unknown case?

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Erythema Multiforme & Toxic Epidermal Necrolysi

 

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Ways to tell the difference between Inflammation & Repair

Tips for differentiating

- Look for ‘cardinal signs of inflammation’ – erythema, edema, exudate, heat, pain; + itching!

- If there are pustules/crust, there is an inflammatory component to the lesion

-  Depigmentation – immune mediated inflammatory lesions

-  If inflammatory infiltrate is severe enough, will see papules, plaques, nodules, but disorders of growth (neoplasia) can also result in these changes

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Gross Features of Dermatitis

Early

Gross Features of Dermatitis

–  Edema

–  Erythema

–  +/‐ pustules, crust, vesicles

 Later

–  Scaling

–  Ulceration

–  Alopecia

–  Lichenification

–  Pigmentary change

–  Fibrosis/scarring

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Inflammation & Repair

Inflammation and Repair- DERMATITIS

– Suppurative/Pustular/Exudative/Neutrophilic – bacterial, auto‐immunity

– Proliferative – viral

– Vesicular – viral, auto‐immunity

– Granulomatous – ‘higher’ bacteria, mycobacteria, fungal, foreign substance

–  Eosinophilic – allergy, parasitic

–  Interface – auto‐immunity- HISTOLOGICAL DX

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Pyoderma

• “pus in the skin” – usually bacterial infection involved

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Superficial vs deep pyoderma

• Superficial – epidermis and hair follicles

– Examples

• Canine superficial spreading pyoderma / Bacterial folliculitis

• Impetigo (superficial pustular dermatitis)

 

Greasy pig disease

Dermatophilosis

• Deep – deep dermis

– Examples

• Bacterial furunculosis • Abscesses

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Dog with superficial spreading pyoderma, a superficial pyoderma with bacterial folliculitis

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Dog with chin acne, a deep pyoderma with bacterial furunculosis

 

hair explodes and bacteria then forms chin acne

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Bacterial infection of skin

Portals for:

Pores (follicular openings)

Hematogenous spread- less common

Direct entry through damaged skin

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Predisposing factors for bacterial infection of the skin

Allergy

Disorders of keratinization (seborrhea)

Immunodeficiency

Anatomic predisposition

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 Why are bacterial infections extremely common in dogs?

-Thin stratum corneum,

-lack of lipid seal of hair follicles,

-high skin pH

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Skin infections often involve

Often involve Staphylococcus spp.

Exception: opportunistic gram negatives, and cases of dermatophilosis

Produce exfoliative toxins that cause intraepidermal splitting

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Impetigo

(Superficial pustular dermatitis)- bacteria colonize WHEREVER in the epidermis

 

• Nonfollicular pustules which develop into crusts

• Prepubescent puppies – healthy otherwise

• Adults – look for underlying disease

 

can be from poor over all condition

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Puppy with pustular dermatitis “impetigo”

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Intertrigo

• Skin fold pyoderma

Intertrigo

• Pathogenesis: closely apposed skin surfaces → frictional trauma → moisture → opportunistic bacterial infections

 

You need histo to confirm dx

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Intertrigo

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Pyotraumatic Dermatitis

Pyotraumatic Dermatitis (“Hot Spots”)

• Very common in dogs

Pathogenesis

Self trauma ---->bacterial infection

Gross: moist, alopecic, slightly raised, red well‐ circumscribed lesions -----> ulceration/crusting

• Underlying pruritis – especially flea allergy dermatitis!

Usually Staph!

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crusts and papules

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Papule or if it gets bigger nodule

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Pyotraumatic Dermatitis (“Hot Spots”)

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Pyotraumatic Dermatitis (“Hot Spots”)

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Greasy Pig Disease (Exudative Epidermitis)

Fatal in neonatal pigs

Caused by Staphylococcus hyicus

Gross: erythema-->pustules--->crusts

• Predisposing factors – other skin lesions, poor nutrition/husbandry, lacerations

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Greasy Pig Disease (Exudative Epidermitis)

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Dermatophilosis

• Caused by Dermatophilus congolensis(Train tracks!) – gram positive filamentous bacteria which subdivide longitudinally and transversely

• Lesions on back or distal extremities

• Stimulate neutrophilic exocytosis: pustules-->exudate-->matting of hair/wool ---> alopecia

 Predisposing factors:

Wet weather in humid climates (“rain rot”) – prolonged wetting of skin/hair/wool allows penetration of epidermis by “zoospores”

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Dermatophilosis

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Also called ‘lumpy wool’ in sheep

Dermatophilius

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Canine superficial spreading pyoderma

Usually secondary condition

Bacterial infection of superficial follicles and adjacent skin- Follicultis- when we have inflammation of the hair follicle before the hair follicle ruptures

furunculosis- when the hair follicle ruptures

Gross: scaling, erythematous macules (often circular-->ring shaped), papules, pustules, crusts, epidermal collarettes, alopecia

DDx:
– Dermatophytosis (‘ring worm’)

– Demodicosis

 

 Diagnostics:
– Cytology of pustule/crust

-------------neutrophils with cocci

– Woods lamp

–  Fungal culture

–  Skin scraping

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Canine superficial spreading pyoderma

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Fig. 17‐27 Folliculitis and furunculosis, skin, haired, dog.
A, The wall of the follicle has become disrupted, resulting in the release of follicular contents (a hair shaft, stratum corneum of the follicle, and exudate) into the dermis. The follicular lumen also contains numerous coccoid bacteria (arrow). The hair shaft has variably sized and shaped melanin pigment granules, indicating that this dog also has coat color dilution. H&E stain.

B, A circular area of erythema, scaling, and crusting is caused by follicular inflammation and rupture (furunculosis). The inflammation in the perifollicular dermis has extended into the surrounding dermis and formed a draining sinus to the epidermal surface. The exudate on the surface has dried to form a crust.

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Demodicosis

Two Conditions Grossly Indistinguishable from Canine Superficial Spreading Pyoderma

(because they also have folliculitis; erythematous macules--->alopecia and scaling)

Demodicosis

Cause: Demodex spp. mite

Lesion vary by host/mite species

–  Distribution on body

–  Neutrophilic to granulomatous

(exudative vs nodular grossly)

• In dogs

– Localized form

– face, forelegs

– Generalized form

– Adult‐onset demodicosis is often associated with systemic disease such as neoplasia, endocrinopathy, or immunosuppressive therapy

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Dermatophytosis

Two Conditions Grossly Indistinguishable from Canine Superficial Spreading Pyoderma

(because they also have folliculitis; erythematous macules--> alopecia and scaling) Dermatophytosis

• Cause: Epidermophyton, Microsporum, and Trichophyton spp. (keratinophilic fungi)

Contagious(only one that is) – acquired by contact with scales shed from infected animals

• Colonize keratin, do not need to invade tissue to cause disease

• Self‐limiting in healthy animals, can become chronic/generalized in immunocompromised animals

 Predisposing factors:
– Youngorimmunosuppressed

– Hot/humid environments

 

Cattle have a different lesion!

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5 yo FS dog has acutely developed some nasty skin lesions...

How do we describe these changes?
What can we do to determine the pathological process and cause?

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There is a leukocyte infiltrate of the epidermis...

The pathological process is likely inflammatory

Differential Diagnoses??

What can we do to determine the cause?

Skin scraping:

• No mites or fungus seen

Wood’s lamp:

• No fluorescence

Fungal culture:

no growth

Cytology of a pustule:

• Eosinophils

• Some bacteria, but not within cytoplasm of leukocytes, and not many neutrophils- NOT A LOT OF BACTERIA THOUGH!

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Acantholytic keratinocytes

consistent with Pemphigus foliaceous

 

MDx: Eosinophilic pustular dermatitis with intralesional acatholytic keratinocytes

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Pemphigus foliaceous

• “Pemphigus” – group of auto‐immune diseases involving type II hypersensitivity against cell adhesion proteins (desmosomes)

• PF is the most common and milder form of pemphigus (reported in horses, dogs, cats and goats) – others are rare but covered in text

• Often involves face, ears, footpads, clawbeds

• Vesicles, pustules, crusts, ulcers

Can be spontaneous, drug‐induced, or associated with allergic skin disease

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Piglets at a zoo display have come down with skin lesions...

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Something is being added to the epidermis...

The pathological process is likely a disturbance of growth or inflammatory- MDx: papular dermatisis

Proliferative- Viral etiology

Differential Diagnoses??

What can we do to determine the cause?

Skin scraping:

• No mites or fungus seen

Cytology (aspirate a papule):

• A few lymphocytes, some keratin

• Staph. sp

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Thickening of the epidermis(2-3x normal)

Histopathology report:
Mdx: Proliferative dermatitis with “ballooning degeneration” & intracytoplasmic inclusion bodies
Comment: Consistent with swine-pox infection

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Pox Viruses

• Sequence of lesions: macule → papule → vesicle → umbilicated pustule → crust → scar

• Poxviruses have a gene whose product is similar to epidermal growth factor → epidermal hyperplasia

• Many cutaneous lesions only, some systemic and fatal

• Some are foreign animal diseases

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Lamb with contagious exanthema, early papular to vesicular phase

pox virus

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Lambs with contagious exanthema, late crusty phase

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Seeing lameness, anorexia, ptyalism in some backyard livestock...

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Something is injuring keratinocytes...

The pathological process is likely degeneration&necrosis or inflammatory

Differential Diagnoses??

• Early herpesvirus

• Early poxvirus

Viruses!!

• Vesicular diseases – FMD, VSV, SVD, VES

What is the next best step in our diagnostic process??

This was VSV.

• The only sure way to distinguish these diseases is by laboratory testing

• Producers and private practitioners, are the first line of defense against these economically devastating diseases.

• WHENEVER YOU SEE ULCERS – LOOK FOR VESICLES!

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What else causes cutaneous vesicles?

Herpesviruses can cause cutaneous vesicles!

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herpes virus in cows

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4 year old mixed breed with multiple skin lesions...

 

Papules, plaques, and nodules in multiple foci. What is the most likely pathological process?

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Something is being added to the epidermis...

The pathological process is likely a disturbance of growth or inflammatory

Differential Diagnoses??

What can we do to determine the cause?

Skin scraping:

• No mites or fungus seen – how helpful is this with nodular disease? NOT VERY HELPFUL!

Cytology (aspirate a papule):

• Macrophages; inflammatory, cause not apparent

• Staph. sp

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Histopathology report

Multifocal granulomatous dermatitis

 

 No infectious agents or foreign material seen with special stain

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Examples of Granulomatous Dermatitis w/o Agents (“sterile”)

Pathogenesis is not understood- treat with immunosupressives

• Juvenile sterile granulomatous dermatitis and lymphadenitis

• Sterile pyogranuloma syndrome (idiopathic sterile granuloma and pyogranuloma)

Canine reactive histiocytosis

Canine Langerhans’ cell histiocytosis

Feline dendritic cell histiocytosis

Idiopathic sterile nodular panniculitis

Xanthoma (xanthogranuloma)

• Equine generalized granulomatous disease (see the section on Vetch Toxicosis and Vetch‐Like Diseases)

• Feline nutritional pansteatitis (see the section on Vitamin E Deficiency

Don't need to memorize all of these! Just know that we don't quite know why this happens

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Idiopathic Sterile Granuloma and Pyogranuloma Syndrome

• Rare

• Esp. dogs

Pathogenesis

• Pathogenesis – cause unknown

– Caused by fastidious unrecognized organisms?

– Abnormal immune response to unidentified microbial antigen?

– Variant of histiocytic neoplasia?

• Diagnosis of exclusion

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Fungal dermatitis

• Uncommon

Fungal dermatitis

• Pythium, Lagenidium spp.

“Swamp Cancer” ‐ clinically resembles neoplasia...invasive lesions, involvement of regional lymph nodes

• Dx with Culture + PCR – why?

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Actinomycete Mycetomas

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• Bacteria introduced by traumatic injury

• Nocardia and Actinomyces sp.

• Can form large clumps (grossly evident as ‘sulfur granules’)

• Gross ‐ Nodules, ulceration, draining sinuses, involvement of underlying bone(Actinomyces bovis- lumpy jaw)

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Mycobacterial Dermatitis

Feline

Mycobacterial Dermatitis Feline leprosy

• Cause ‐ Mycobacterium lepraemurium, obligate intracellular organism (potentially other strains)

• Cats in cold, wet areas

• Transmission unknown – biting insects?

• FIV/debilitation may be predisposing factors

• Numbers of mycobacteria in lesions can be low – might not see on histo

• DOES NOT GROW IN CULTURE – Must use PCR

– Can not get sensitivity results

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Mycobacterial Dermatitis

Opportunistic mycobacteriosis

Mycobacterial Dermatitis Opportunistic mycobacteriosis

• Cause – “atypical mycobacteria”, facultative saprophytes (inhabitants of soil, water, and decomposing vegetation)

– Rapid‐growing (more common) – M. fortuitum, M. smegmatis, M. chelonae, M. abscessus, M. thermoresistible

Dermatology for Animals

– Slow‐growing – M. avium‐intracellulare complex, M. kansasii, M. ulcerans

• Infection tends to occur via wound contamination or traumatic implantation

Usually localized, but can disseminate

Can do culture and sensitivity

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Mycobacterial Dermatitis

Canine Leproid Granuloma

• Cause – saprophytic mycobacteria

• Transmission – fly bites?

• Nodules involving dorsal pinna, less commonly other distal extremities- EARS IN DOGS

Short coated breeds, esp Boxer

Self‐limiting in immunocompetent dogs but may last months

• Difficult to culture, may need PCR; but usually can find organisms with histo

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What is this and species it is common in?

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Mycobacterial Dermatitis Canine Leproid Granuloma

 

BOXER!

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Puppy Strangles

Puppy Strangles

(Juvenile sterile granulomatous dermatitis)

Day 1 – pustules, enlarged LN

• Pups<4mosold

• One or more in litter

Pathogenesis unknown

• Gross – pustules, nodules, swelling of face, ears, mucocutaneous junctions

• Histo – (pyo)granulomatous dermatitis and panniculitis +/‐ lymphadenitis

• Fever, joint pain

 

STARTS WITH PUSTULES ON THE FACE!

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Puppy Strangles

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“Lick Granuloma”

“Lick Granuloma” Acral lick dermatitis

Common in dogs

Cause – persistent

licking/chewing

• Underlying factors – boredom? Sensory polyneuropathy?

• Gross – extremities; circumscribed, hairless, and ulcerated

• Histo

Not really a granuloma!

– Epidermal hyperplasia, granulation tissue, fibrosis

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“Lick Granuloma” Acral lick dermatitis

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year old mixed breed itching constantly, especially in the middle of the night, and driving everyone crazy...

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eryethema on the ventrum and inter-digitally

The pathological process is likely

inflammatory BECAUSE IT'S ITCHY!

Skin scraping:

• No mites or fungus seen

Bacterial Culture:

• Staph. sp

Fungal culture:

• negative

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Histo report:

Eosinophilic dermatitis with epidermal hyperplasia; no cause evident. Consistent with ALLERGIC SKIN DISEASE. Must distinguish clinically.

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Atropy in a dog: MDx: chronic dermatitis

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Web Fig. 17‐2 Atopic dermatitis, skin, dog.
A, This Golden retriever has erythema, alopecia, and erosions in the skin around the eye and muzzle. The lesions are caused by self‐trauma from rubbing and scratching as a result of pruritus.

 

DX WITH INTRADERMAL SKIN DISEASE

TYPE I HYPERSENSITIVITY TO ENVIRONMENTAL ALLERGENS

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Contact Dermatitis

• Pathogenesis: Type IV hypersensitivity reaction; exposure via direct contact

– Plastics in food bowls
– Dyes in carpets
– Plant residues in bedding

• Low molecular weight haptens present in chemicals require binding to cell‐associated proteins prior to being recognized by CD8+ (cytotoxic) T lymphocytes

• Distribution ‐ depends on site of contact, often in poorly haired areas

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Insect Bite Hypersensitivity

• Pathogenesis: Type I and/or IV hypersensitivity reaction

• Examples
– Culicoides saliva ‐ horses

–  Flea saliva ‐ dogs and cats

–  Mosquito saliva ‐ cats

• Distribution: depends on areas favored by insect, but can become generalized

–  Culicoides – tail base, withers, head

–  Fleas – tail base (dog), neck (cats)

–  Mosquito – nose and face

• Gross: often includes papules

• Histo: may have eosinophilic pustules, folliculitis, or granulomas

IN the picture:Horse with culicoides hypersensitivity (above); Cat with mosquito bite hypersensitivity (below)

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Dog with flea bite hypersensitivity;
Remember: pyotraumatic dermatitis (secondary self‐trauma associated pyoderma) very common with this condition.

 

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“Miliary dermatitis” in Cats- Clinical Term not patholgical term

Not a disease, a pattern of lesions.

Small crusty erythematous papules.

Commonly seen in cats with allergic skin disease.

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“Eosinophilic granuloma complex” in Cats

ALSO not a disease, a pattern of lesions.

Indolent ulcer – ulcers on upper lips.

Eosinophilic plaque – discrete red to ulcerated plaques on abdomen or medial thighs.

Eosinophilic granuloma – nodules (may be ulcerated) on thighs, face or mouth.

Commonly seen in cats with allergic skin disease.

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“Eosinophilic granuloma complex” in Cats

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“Eosinophilic granuloma complex” in Cats

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“Eosinophilic granuloma complex” in Cats

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Eosinophilic Granuloma

• Grossly similar to non‐eosinophilic granulomas

• Often see collagenolysis – due to proteolytic enzymes of eosinophil granules?

• Causes:
– Parasite reaction

–  Insect bite hypersenstivity

–  Foreign body reaction

–  Underlying mast cell neoplasia

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Degenerate collagen fibers within an eosinophilic granuloma

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Case of cutaneous habronemiasis (“Summer sores”):
Cutaneous eosinophilic granulomas caused by larval migration of Habronema or Draschia sp. deposited into a wound by house or stable flies

Fig. 17‐59 Cutaneous habronemiasis, Habronema sp., skin, horse. A, Face. Multiple coalescing nodular granulomatous and ulcerated areas are present on the skin of the medial canthus, skin immediately ventral to the eye, and the skin of the lateral surface of the face. Lesions of cutaneous habronemiasis develop in areas of the skin that are traumatized (often the legs) or in soft moist skin (around the genitalia or eyes). In this case, moisture from ocular secretion (tears) may have predisposed to bites of house or stable flies, with subsequent emergence and migration of Habronema sp. larvae into the dermis. B, Note sections of larvae within necrotic debris bordered by macrophages and mixed inflammation including eosinophils. H&E stain.

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Discoid Lupus Erythematosis

• 2nd most common autoimmune skin disease

• Induction/exacerbation by UV light

• Dorsal nose and nasal planum >>> pinnae, lips, periocular region >>> oral mucosa

• Gross: depigmentation, erythema, scaling, erosion, ulceration, and crusting

Dermatology for Animals

• Histo: interface dermatitis

• DDx: Uveodermatologic syndrome – auto‐ immune disease against dermal and uveal melanocytes; esp arctic breeds

 

Uveodermatological Syndrome in an Akita

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Mononuclear leukocytes infiltrate at the epidermal junction and obscure the basal lamina

Basal keratinocyte apoptosis

 

There are several other immune-mediated dermatoses with similar interface dermatitis.

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Pigmentary incontinence

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Tips for differentiating Circulatory Disorders

-  Discrete reddened areas (hemorrhage)!

-  Lesions follow a linear pattern

-  Lesions are in geometrical shapes (indicating mapping to a vascular

supply)

-  Vascular lesions which result in ischemia ----->see gross features of

degeneration/necrosis

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What are the 4 main mechanisms of subcutaneous edema?

  1. increased vascular permeability
  2. decreased oconotic pressure(loss of protein)
  3. increased hydrostatic pressure(hypertension or chronic congestion)
  4. lymphatic obstruction

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MDx: Multifocal cutaneous ecchymotic hemorrhages

Cause = Primary hemostasis defect (Vasculitis vs thrombocytopenia)

 

hemorrage WILL NOT BLANCH OUT

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Infarcts

No blood supply to the area- this is how you get the pigmentation

Gross:

–  Sharply demarcated geometrical shaped dark red to blue area

–  As time goes by becomes firm, dry, sunken, darkened (features of necrosis begin to predominate over hemorrhage)

Causes:

–  Vasculitis

Gram negative septicemias

- Erysipelothrix rhusiopathiae, Salmonella, Pasteurella, E. coli

E. coli shiga toxin 2e (damages endothelium) “Edema Disease”

Spider/snake bite

hypersensitivity

Drug reaction

Secondary to ulceration

–  Frost bite- distial extremidities

–  Toxins causing extreme vasoconstriction (ergot)

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Pig with “diamond skin disease”. MDx: Cutaneous infarcts
Cause: E. rhusiopathiae bacteremia, associated thrombosis & vasculitis.

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MDx: Multifocal cutaneous infarcts.

Disease: Diamond skin disease

Cause: Erysipelothrix rhusiopathiae

DDx: Salmonellosis (+ African swine fever, hog cholera viruses)

 

Sharp demarkcation on the ears

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MDx: Vasculitis and thrombosis (with cutaneous hemorrhage and necrosis)

 

see a lot of hemmorrage

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Erysipelothrix rhusiopathiae infection, skin, haired, pig.
B, The epidermis and dermis are necrotic from infarction. The only normal dermis and epidermis are at the extreme left. H&E stain.

 

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pig with “diamond skin disease”.
MDx: Cutaneous ecchymotic hemorrhages
Cause: E. rhusiopathiae bacteremia and associated vasculitis.

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Purpura hemorrhagica

Pathogenesis: Type III hypersensitivity immune-mediated vasculitis

Cause: Streptococcus equi infection (rarely with other infections or vaccinations)

Gross: Red or purple macules or patches (hemorrhage or infarct) in the skin or mucous membranes

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Purpura hemorrhagica

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Horses with purpura hemorrhagica. Ecchymotic hemorrhages (above) and subcutaneous edema (below).

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Frost bite

Cause: exposure to cold temperature

Pathogenesis:

–  Formation of ice crystals which physically disrupt cells

–  Vasoconstriction and endothelial damage---> reduced blood flow---> thrombosis --->infarction

Lesions in cold exposed extremities

Fig. 20-30 Auricular infarction, frostbite, goat. Note that the distal (upper) half of the ear has dry gangrene from frost-bite.

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Fig. 20-30 Auricular infarction, frostbite, goat. Note that the distal (upper) half of the ear has dry gangrene from frost-bite.

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12yo TB gelding with acute onset of ‘welts’. These are transicent.

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Something is being added to the dermis...

The pathological process is a

vascular disorder

What can we do to determine the cause?

These are called WHEALS. These are trascient. These are from a vascular disorder from edema. These are a Hyper I and III hypersentivity. These are itchy.

Wheal = Elevated, irregular-shaped area of cutaneous edema; solid, transient

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Wheal = Elevated, irregular-shaped area of cutaneous edema; solid, transient (arrows)

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Urticaria (“Hives”)

Dogs, horses

Localized areas of edema

– Urticaria – superficial dermis

– Angioedema – dermis + subcutis- when head is swelling

Pathogenesis: Type I and III hypersensitivity; mast cell degranulation  focal edema, congestion, pruritis

Triggers – foods, drugs, antisera, insect stings

Histo – subtle (don’t waste your time!)

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MDx

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MDx: multifocal cutaneous edema and congestion

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My dog “Jessie” with hives in St Kitts (in the middle of the night) due to suspected centipede bite reaction

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My dog “Jessie” with hives in St Kitts (in the middle of the night) due to suspected centipede bite reaction

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Allergic Skin Disease

Food Allergy

Contact Hypersensitivity

Insect Bite Hypersensitivity

• Distribution of lesions vary

• Gross

– Lesions due to self‐inflicted trauma: erythema, alopecia, excoriation

– Lesions due to secondary pyoderma: papules, pustules, crusts

– Lesions due to chronicity: lichenification, hyperpigmentation, scaling

 

Dog with atopy.

• Histo
– Lymphocytic and eosinophilic dermatitis

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Atopy

• Affects 10‐15% of dogs

 

• Pathogenesis: Type I hypersensitivity to environmental allergens (“inhalant allergy”)

Diagnose with intradermal skin testing

Distribution ‐ ventrum, face, distal

extremities

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129

what's the MDx?

 

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MDx: Generalized subcutaneous edema.

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Causes of developmental anomalies

Things that injure cells at a critical stage of development. The defect depends on tissue tropism and timing.

Genetic defect – inherited mutation, spontaneous somatic mutation

In utero infection – BVD, bluetongue, border disease, akabane, panleukopenia, classical swine fever

In utero exposure to teratogens – toxic plants, griseofulvin in cats

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Hypotrichosis

Less than the normal amount of hair

Hereditary most common

More susceptible to environmental extremes and infections

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Calf with hypotrichosis (“Singy calf”) Due to in utero BVD infection

 

born without hair

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Collagen Dysplasia (Cutaneous Asthenia, Dermatosparaxis, Ehlers-Danlos)

Fig. 17-36 Collagen dysplasia, skin, dog.
A, The skin is hyperextensible. In this dog, the skin can be stretched more than the skin of a normal dog.
B, The collagen bundles are irregular in size and shape and are arranged haphazardly. The abnormally formed collagen is responsible for the hyperextensibility of the skin, which predisposes to tearing with normal handling and activity. H&E stain.
C, Deeper level of the sample shown in B. Collagen bundles are stained blue. The variation in diameter and shape of the collagen bundles and their haphazard arrangement is accentuated with this stain. Masson's trichrome stain.

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Epitheliogenesis Imperfecta

 

fatal due to 2ndary infections

 

skin has not developed

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Ichthyosis

calf

extra thick stratum corneum

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Disorders with Alopecia

Endocrine disorders

–  Hypothyroidism

–  Hyperadrenocorticism

–  Hyperestrogenism (sertoli cell tumor)

–  Alopecia X

Hair cycle abnormalities

–  Postclipping alopecia

–  Telogen effluvium

–  Antimitotic drugs - chemotherapeutics, immunosuppressants

 

Excessive grooming – feline psychogenic alopecia

Self-trauma (pruritis- most common) – ectoparasites, dermatitis of any cause, but particularly allergic skin disease

Autoimmune - alopecia areata (antibodies made against hair follicle)- only one that is HISTOLOGICALLY DISTINCT

General poor nutrition - hairs are produced weak

Hyperkeratosis - interferes with the hair follicle decreasing hair production

Cicatricial alopecia (scar)

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Fig. 17-65 Truncal alopecia, hyperadrenocorticism, skin, dog. A, Note the alopecia, distended abdomen, and thin skin in which blood vessels are faintly visible (arrow). The distended abdomen and visibility of blood vessels are a result of protein catabolism and loss of muscle and dermal collagen, respectively. The distended abdomen and thin skin with greater visibility of blood vessels in conjunction with symmetric alopecia suggest that a catabolic endocrine disease, such as hyperadrenocorticism, is likely. B, Atrophy of dermal collagen fibers is so severe that the collagen has almost disappeared, leaving the adnexa and arrector pili muscles readily visible. Hair follicles are in the telogen (resting) stage of the hair cycle. H&E stain.

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Fig. 17-67 Symmetric alopecia and hyperpigmentation, hyperestrogenism (iatrogenic from diethylstilbestrol therapy), skin, dog.
A, Note the symmetric alopecia and hyperpigmentation over the caudal dorsal trunk and caudolateral hind legs. In male dogs, the symmetric alopecia in conjunction with enlargement of nipples, pendulous prepuce, and attraction of other male dogs suggest the possibility of hyperestrogenism.

B, Note epidermal orthokeratotic hyperkeratosis (arrowhead), follicles dilated with keratin (F), and small atrophic follicles (arrows) in the telogen (resting) stage of the hair cycle. H&E stain.

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Epidermal Hyperplasia

Acanthosis – increased thickness of stratums basale and spinosum

------ very active areas which is why they thickenss

Hyperkeratosis – increased thickness of stratum corneum

–  Parakeratotic - nuclei retained

–  Orthokeratotic - anuclear

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Hyperkeratosis

Gross – scaling “seborrhea”

Primary (Idiopathic seborrhea) - especially Cockers, Springers, Westies

Secondary

–  Endocrine imbalances – hyperadrenocorticism, hypothyroidism, hyperestrogenism

–  Chronic dermatitis – especially allergy and ectoparasitism

–  Zinc responsive

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Primary Idiopathic Seborrhea

Inherited disorder of keratinization or cornification

Pathogenesis: thought to involve hyperproliferation of the epidermis, hair

follicle infundibulum, and sebaceous glands

Clinical presentations:

–  Dry form (seborrhea sicca) → dry skin and white-to-gray scales that exfoliate

–  Greasy form (seborrhea oleosa) →excessive brown to yellow lipids

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Primary Idiopathic Seborrhea

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Zinc responsive dermatosis

• Types

–  Arctic breeds – inherited defect in zinc absorption

–  Rapidly growing large-breed dogs fed low zinc diet

• Gross: scaling around mouth, chin, eyes, pressure points, pawpads

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Fig. 17-70 Zinc-responsive dermatosis, skin, dog.
A, Siberian husky. Periocular skin is thickened, alopecic, pigmented, and covered by tightly adherent scale. In Siberian huskies and Alaskan malamutes in particular, scaling and crusting develop in the skin around the mouth, chin, eyes, external ears, pressure points, and pawpads.
B, Note the papillary epidermal hyperplasia (H) with marked parakeratosis (P). The parakeratotic hyperkeratosis and acanthosis form the thickened adherent scale. Although epidermal hyperplasia and parakeratosis are features of zinc-responsive dermatosis, they also occur in other conditions (such as superficial necrolytic dermatitis, chronic surface trauma, and nasal parakeratosis). Therefore breed, lesion distribution, and other features in the clinical history or clinical chemistry analysis are important in differential diagnosis. H&E stain.

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Sarcoptic Mange

Caused by Sarcoptes scabiei

Highly contagious and zoonotic

Pathogenesis: burrow into stratum corneum ---->intense pruritis through hypersensitivity mechanism---->self trauma, chronic irritation---->hyperkeratosis, lichenification, alopecia

Characteristic of a chronic dermatitis that ends in hyperkeratosis

VERY ITCHY

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Normal wombat (above)

Wombat with sarcotic mange (below)

 

MDx: chronic dermatitis

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MDx: chronic dermatitis

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Sarcoptes mites burrowed beneath the stratum corneum, and associated hyperkeratosis.

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Callus

Raised, irregular patch of thickened skin developing from chronic friction, usually over pressure points

Histo: epidermal hyperplasia

May develop secondary pyoderma

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Are many skin tumors neoplasms?

Many skin tumors are not true neoplasms...

They are other benign disorders of growth such as:

–  Nodular hyperplasia

–  Hamartoma–redundant disorganized tissue normally present at the site

–  Cysts

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Follicular cyst

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Nodular sebaceous hyperplasia

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Collagenous hamartoma

skin tags

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8 yo MN lab “Harley”...

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How do we describe these changes?
What can we do to determine the pathological process and cause?

Something is being added to the epidermis... papules

The pathological process is likely a disorder of growth or inflammatory

Differential Diagnoses??

What can we do to determine the cause?

Cytology:

• Low numbers of spindle cells, some mixed leukocytes.

– Probably not a round cell tumor or carcinoma.

What next?

Excisional vs incisional biopsy?

How big of margins?

Histopathology or not?

Surgical margin assessment?

want 1 fasical plane under the tumor and about 1 cm for margins

Culture?

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Pathologist report:
MDx: Grade II soft tissue sarcoma
Comment: excision does not appear complete

 

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Cutaneous Soft Tissue Sarcomas (spindle cell tumors)

Very common in dogs

Types-- cells that have several different possible origins that can not be distinguished pathologically

–  Fibrosarcoma

–  Nerve sheath tumor

–  Malignant fibrous histiocytoma

–  Liposarcoma

–  Myxosarcoma

Have overlapping histological features and similar prognosis -->treat the same

Prognosis predicted by grade and margins

Locally invasive, slow to metastasize

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Papillomas

Caused by papilloma virus

Pathogenesis: viral genes inactivate host tumor-suppressor proteins

Benign, spontaneously regress

Gross: horny cauliflower-like masses

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Fig. 17-45 Cutaneous papillomas, skin.
C, The papillary projections (arrows), often called fronds, are composed of hyperkeratotic epidermis covering a collagenous core. H&E stain.

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Equine Sarcoid

Very common in young adult horses

Thought to be caused by bovine papilloma virus

Frequently involve sites of previous wounds

Invasive, high rate of recurrence, but do not metastasize

Gross: variable range from nodular to plaque-like to wart-like

Histo: composed of both epithelial and dermal components – need a biopsy that is not ulcerated to diagnose!

 

Remember that it looks like proud flesh, so you have to do a biospy to tell the difference.

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Equine Sarcoid

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Squamous cell carcinoma

Pathogenesis: solar radiation, chronic injury commonly involved

Gross:

– Verrucous and ulcerated

– Poorly pigmented,sparsely haired, sun-exposed areas

Histo: keratinizing squamous cells gone wild

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Squamous cell carcinoma

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Bilateral squamous cell carcinoma in ear tips of sheep, site of chronic fly strike (R);

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Eyelid squamous cell carcinoma in a cow due to UV exposure.

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Sebaceous adenoma

• Benign growth of dogs

• Gross:

– White-yellow , greasy, cauliflower- like

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Sebaceous adenoma

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Lipoma

• Benign growth of dogs >>> cats

• Gross:

– Looks and feels like fat,only forming a nodule

• Histo:
– Looks like normal fat

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Lipoma

169

Mast Cell Tumor

Dog - behavior varies with grade but all considered potentially malignant

Cats, horses - benign---- NO GRADING SYSTEM DEVELOPED!

• Gross:

– Can look like anything
– Often resembles inflammation

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Mast Cell Tumor

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Histiocytoma

Dogs, mostly young, but any age

Head, ears, neck, distal forelegs

Gross: dome-shaped

Cyto: round cells

Langerhans’ cell origin (epidermal dendritic antigen-presenting cell)

Benign, often spontaneously regress

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Histiocytoma

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Melanoma

Dog, horse, angora goat

Gross: usually dark brown

Histo: characteristic “junctional change” (in nonulcerated biopsies!)

Location, size, mitotic index, and cell morphology may help predict behavior

– Canine:

oral, mucocutaneous, subungual,- often malignant

haired skin often benign

– Gray horses
• usually progressive and multicentric

WANT EPIDERMIS IN THE BX

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Hemangioma / Hemangiosarcoma

Pathogenesis: solar radiation

Hemorrages everywhere

Young adult dogs

• Hemangiosarcoma

–  Not as malignant as visceral counterparts

–  Primary to skin or metastatic from visceral tumor

–  Metastatic potential may vary with depth of tissue invasion

 

these bleed a lot

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junctional change in melanomas

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melanoma

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Hemangioma / Hemangiosarcoma

Pathogenesis: solar radiation

Young adult dogs

• Hemangiosarcoma

–  Not as malignant as visceral counterparts

–  Primary to skin or metastatic from visceral tumor

–  Metastatic potential may vary with depth of tissue invasion

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Hemangioma

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Hemangiosarcoma.

180

Cutaneous Lymphoma

Many species, esp. dogs

Poor prognosis

• Epitheliotropic – T-cells

• Nonepitheliotropic

– T or B cells

 

BAD PROGNOSIS

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Epitheliotropic

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CD3 (T-cell) immunohistochemistry

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Non-epitheliotropic

184

185

Deposits & Pigmentations Tips for differentiating

Tips for differentiating

- Look for color change

-  Melanin – darker color (added), lighter color (lost)

-  Calcium – chalky white, gritty to hard texture

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Melanin

The pigment which imparts skin color

Factors that influence production:

– Hormones
– Genes
– Age
– Inflammation

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Melanin Synthesis

tyrosainse requires copper

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Hyperpigmentation (Hypermelanosis)

• Usually increase in amount of melanin rather than number of melanocytes

• Generalized

–  Endocrine dermatosis (Cushing’s, Hypothyroidism, Hyperestrogenism)

–  Acanthosis nigricans– genetically determined disease of young dachshunds

• Localized

–  Chronic inflammation or physical irritation (rubbing/friction)

–  Congenital (freckles)

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Dog with Cushing’s disease (hyperadrenocorticism). MDx:cutaneoushyperpigmentation

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Dog with chronic flea allergy dermatitis.

MDx: Chronic dermatitis and cutaneous hyperpigmentation.

 

Regional------> dermatitis

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Hypopigmentation

(Hypomelanosis)

 

• Causes

Numbers can decrease or amount of melanin can decrease

Congenital

–  Inherited lack of melanocytes – various conditions of horses, dogs, cats; associated with deafness

 Piebaldism – foci of lack of melanocytes

–  Albinism – melanocytes are present but defect to synthesize melanin (usually tyrosinase gene); color dilution is a mild form

Acquired

–  Copper deficiency

–  Destruction of melanocytes or melanin-containing keratinocytes (“pigmentary incontinence”) – scars,

autoimmune dermatoses, vitiligo

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MDx: Leukoderma.

Dog with discoid lupus (below).

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MDx: Focal leukoderma/leukotrichia

Horse acquired hypomelanosis (depigmentation) due to freeze branding

Cow with acquired hypomelanosis (depigmentation) due to copper deficiency

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vitiligo

Horses with vitiligo, an idiopathic acquired melanocytopenic hypomelanosis (depigmentation).

Gradually expanding pale macules,

often symmetrical.

Genetic inheritance.

Pathogenesis of melanocyte death? not understood but genetic predisposition

Micheal Jackson

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Calcification

The most common forms observed in the skin are both classified as dystrophic calcification, but pathogenesis not understood for both!

Calcinosis cutis

–  Associated with hyperadrenocorticism(Cushing's Disease)

–  Erythematous to white gritty plaques and nodules

Calcinosis circumscripta

–  Young, rapidly-growing, large-breed

dogs

–  Single hard subcutaneous nodule, usually over pressure points or at previous site of trauma/injection

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Fig. 17-66 Calcinosis cutis, hyperadrenocorticism( CUSHING"S DISEASE- PATHONUERMOTIC LESIONS) skin, dog.
A, Dorsal neck. The skin is partially alopecic, ulcerated, and crusted. It is also palpably thickened. B, Subcutis. Mineral deposits are visible as white nodular foci..

 

chalky foci in the skin

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Dog with calcinosis circumscripta. Mild granulomatous inflammation surrounds deposits of calcium within the dermal and subcutaneous connective tissue.

young, large bred dogs often over pressure points

MDx: Cutaneous calcification

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Mucinosis

• Mucin is normally in the dermis (protein bound to hyaluronic acid)

• Gross:
– Thickened/puffy gelatinous skin

–  If severe can exude viscous fluid when pricked with needle

–  Prone to injury

Seen with:

–  Inherited mucinosis in the Chinese Shar-Pei

–  Myxedema with hypothyroidism

 

When you squeeze out fluid, it's still a nodule(opposite of a papule)

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MDx?

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Excessive mucin deposition (mucinosis) in the shar pei.

 

MDx: cutaneous micinosis or cutaneous mucin

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201

Looking at the organism in a crust in ___ will be benefical

DERMATOPHILIUS