Final- Integument Flashcards
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
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”)
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
Pustule
Palpable elevation filled with pus
Cause – leukocyte infiltrate
Pathological process: Inflammation and Repair
I.e. Pimples
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
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
Plaque- solid but with a flat top
Nodule
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
Scale
• Accumulation of loose keratinized cells
- dandruf
Causes:
– Disorders of keratinization
– Chronicdermatitis
Pathological Process: Inflammation/Repair or Disorders of Growth
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
Lichenification
• Thickening and hardening of the skin
- becomes hyperpigmented
Causes:
– Chronic irritation/inflammation
Pathological Process: Inflammation and Repair
What lesion terms can we use here?
- ulcers
- erthyema (skin term ONLY)
- paules
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
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
Flock of 300 merino ewes& lambs in the shade cuddling after a period of a lot of rainfall.
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
Pathogenesis of Photosensitization
Uv light absorbed by photodynamic chemicals(shouldn’t be there) in skin causes free radical damage causes e_pidermal necrosis of lightly pigmented or sparsely haired skin_
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)
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
Liver from a sheep with photosensitization due to red lantana toxicosis
REMEMBER- THE LIVER CAN BE NORMAL
Liver from a sheep with photosensitization due to Tribulus toxicosis
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
Most Degeneration&Necrosis skin cases have these features…
pink storm= necrosis
Skin healing by primary and seconary intention
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
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
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.
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
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).
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
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
Is Degeneration&necrosis the primary pathological process in our unknown case?
Erythema Multiforme & Toxic Epidermal Necrolysi
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
Gross Features of Dermatitis
Early
Gross Features of Dermatitis
– Edema
– Erythema
– +/‐ pustules, crust, vesicles
Later
– Scaling
– Ulceration
– Alopecia
– Lichenification
– Pigmentary change
– Fibrosis/scarring
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
Pyoderma
• “pus in the skin” – usually bacterial infection involved
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
Dog with superficial spreading pyoderma, a superficial pyoderma with bacterial folliculitis
Dog with chin acne, a deep pyoderma with bacterial furunculosis
hair explodes and bacteria then forms chin acne
Bacterial infection of skin
Portals for:
Pores (follicular openings)
Hematogenous spread- less common
Direct entry through damaged skin
Predisposing factors for bacterial infection of the skin
Allergy
Disorders of keratinization (seborrhea)
Immunodeficiency
Anatomic predisposition
Why are bacterial infections extremely common in dogs?
- Thin stratum corneum,
- lack of lipid seal of hair follicles,
- high skin pH
Skin infections often involve
Often involve Staphylococcus spp.
Exception: opportunistic gram negatives, and cases of dermatophilosis
Produce exfoliative toxins that cause intraepidermal splitting
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
Puppy with pustular dermatitis “impetigo”
Intertrigo
• Skin fold pyoderma
Intertrigo
• Pathogenesis: closely apposed skin surfaces → frictional trauma → moisture → opportunistic bacterial infections
You need histo to confirm dx
Intertrigo
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!
crusts and papules
Papule or if it gets bigger nodule
Pyotraumatic Dermatitis (“Hot Spots”)
Pyotraumatic Dermatitis (“Hot Spots”)
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
Greasy Pig Disease (Exudative Epidermitis)
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”
Dermatophilosis
Also called ‘lumpy wool’ in sheep
Dermatophilius
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
Canine superficial spreading pyoderma
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.
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
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!
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?
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!
Acantholytic keratinocytes
consistent with Pemphigus foliaceous
MDx: Eosinophilic pustular dermatitis with intralesional acatholytic keratinocytes
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
Piglets at a zoo display have come down with skin lesions…
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
Thickening of the epidermis(2-3x normal)
Histopathology report:
Mdx: Proliferative dermatitis with “ballooning degeneration” & intracytoplasmic inclusion bodies
Comment: Consistent with swine-pox infection
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
Lamb with contagious exanthema, early papular to vesicular phase
pox virus
Lambs with contagious exanthema, late crusty phase
Seeing lameness, anorexia, ptyalism in some backyard livestock…
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!
What else causes cutaneous vesicles?
Herpesviruses can cause cutaneous vesicles!
herpes virus in cows
4 year old mixed breed with multiple skin lesions…
Papules, plaques, and nodules in multiple foci. What is the most likely pathological process?
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
Histopathology report
Multifocal granulomatous dermatitis
No infectious agents or foreign material seen with special stain
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
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
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?
Actinomycete Mycetomas
- 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)
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
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
What is this and species it is common in?
Mycobacterial Dermatitis Canine Leproid Granuloma
BOXER!
Puppy Strangles
“Lick Granuloma” Acral lick dermatitis
year old mixed breed itching constantly, especially in the middle of the night, and driving everyone crazy…
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
Histo report:
Eosinophilic dermatitis with epidermal hyperplasia; no cause evident. Consistent with ALLERGIC SKIN DISEASE. Must distinguish clinically.
Atropy in a dog: MDx: chronic dermatitis
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
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
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)
Dog with flea bite hypersensitivity;
Remember: pyotraumatic dermatitis (secondary self‐trauma associated pyoderma) very common with this condition.
“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.
“Eosinophilic granuloma complex” in Cats
“Eosinophilic granuloma complex” in Cats
“Eosinophilic granuloma complex” in Cats
Degenerate collagen fibers within an eosinophilic granuloma
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.
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
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.
Pigmentary incontinence
MDx: Multifocal cutaneous ecchymotic hemorrhages
Cause = Primary hemostasis defect (Vasculitis vs thrombocytopenia)
hemorrage WILL NOT BLANCH OUT
Pig with “diamond skin disease”. MDx: Cutaneous infarcts
Cause: E. rhusiopathiae bacteremia, associated thrombosis & vasculitis.
MDx: Multifocal cutaneous infarcts.
Disease: Diamond skin disease
Cause: Erysipelothrix rhusiopathiae
DDx: Salmonellosis (+ African swine fever, hog cholera viruses)
Sharp demarkcation on the ears
MDx: Vasculitis and thrombosis (with cutaneous hemorrhage and necrosis)
see a lot of hemmorrage
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.
pig with “diamond skin disease”.
MDx: Cutaneous ecchymotic hemorrhages
Cause: E. rhusiopathiae bacteremia and associated vasculitis.
Purpura hemorrhagica
Horses with purpura hemorrhagica. Ecchymotic hemorrhages (above) and subcutaneous edema (below).
Fig. 20-30 Auricular infarction, frostbite, goat. Note that the distal (upper) half of the ear has dry gangrene from frost-bite.
12yo TB gelding with acute onset of ‘welts’. These are transicent.
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. T_hese 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
Wheal = Elevated, irregular-shaped area of cutaneous edema; solid, transient (arrows)
MDx
MDx: multifocal cutaneous edema and congestion
My dog “Jessie” with hives in St Kitts (in the middle of the night) due to suspected centipede bite reaction
My dog “Jessie” with hives in St Kitts (in the middle of the night) due to suspected centipede bite reaction
what’s the MDx?
MDx: Generalized subcutaneous edema.
Calf with hypotrichosis (“Singy calf”) Due to in utero BVD infection
born without hair
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.
Epitheliogenesis Imperfecta
fatal due to 2ndary infections
skin has not developed
Ichthyosis
calf
extra thick stratum corneum
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.
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.
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
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
Primary Idiopathic Seborrhea
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.
Normal wombat (above)
Wombat with sarcotic mange (below)
MDx: chronic dermatitis
MDx: chronic dermatitis
Sarcoptes mites burrowed beneath the stratum corneum, and associated hyperkeratosis.
Callus
Raised, irregular patch of thickened skin developing from chronic friction, usually over pressure points
Histo: epidermal hyperplasia
May develop secondary pyoderma
Follicular cyst
Nodular sebaceous hyperplasia
Collagenous hamartoma
skin tags
8 yo MN lab “Harley”…
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?
Pathologist report:
MDx: Grade II soft tissue sarcoma
Comment: excision does not appear complete
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.
Equine Sarcoid
Squamous cell carcinoma
Bilateral squamous cell carcinoma in ear tips of sheep, site of chronic fly strike (R);
Eyelid squamous cell carcinoma in a cow due to UV exposure.
Sebaceous adenoma
Lipoma
Mast Cell Tumor
Histiocytoma
junctional change in melanomas
melanoma
Hemangioma
Hemangiosarcoma.
Epitheliotropic
CD3 (T-cell) immunohistochemistry
Non-epitheliotropic
Melanin Synthesis
tyrosainse requires copper
Dog with Cushing’s disease (hyperadrenocorticism). MDx:cutaneoushyperpigmentation
Dog with chronic flea allergy dermatitis.
MDx: Chronic dermatitis and cutaneous hyperpigmentation.
Regional——> dermatitis
MDx: Leukoderma.
Dog with discoid lupus (below).
MDx: Focal leukoderma/leukotrichia
Horse acquired hypomelanosis (depigmentation) due to freeze branding
Cow with acquired hypomelanosis (depigmentation) due to copper deficiency
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
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
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
MDx?
Excessive mucin deposition (mucinosis) in the shar pei.
MDx: cutaneous micinosis or cutaneous mucin
