Flashcards in Skin Pathology 3 Deck (33):
A non-specific cutaneous inflammatory reaction, with concomitant changes in the epidermis AND dermis.
Can be caused by a variety of agents.
Changes are not always visible.
KERATINOCYTES release PRIMARY CYTOKINES (including interleukins, TNFa etc.)
These activate DENDRITIC CELLS, MAST CELLS, Th2 CELLS, EOSINOPHILS, DERMAL FIBROBLASTS, which go on to produce further chemokines and "further reinforce proinflammatory circuits through their massive release of potent cytokines and chemokines".
Downstream activation cascades are stimulated.
An 'inflammatory soup' is produced.
CARDINAL SIGNS OF INFLAMMATION
LOSS OF FUNCTION
NORMAL VS INFLAMED CAPILLARY
Normal- Central axial flow of cells (RBCs, WBCs), zone of plasma around edge. Tight junctions between endothelial cells.
Inflamed- CONGESTION/STASIS, LOSS OF AXIAL FLOW, MARGINATION, PAVEMENTING and EMIGRATION of POLYMORPHONUCLEAR LEUKOCYTES.
If inflammation is severe, RBCs can leak through gaps that form between endothelial cells.
Vasodilation leads to hyperaemia (increased blood flow).
Increased permeability leads to inflammatory oedema
Cell emigration of neutrophils, macrophages (scarce in urticaria).
DERMATITIS- ACUTE MACROSCOPIC LESIONS
Acute dermatitis not often seen in veterinary medicine- most clinical cases have chronic skin disease, and most lesions have been self-traumatised.
DERMATITIS- ACUTE MICROSCOPIC LESIONS
SUPERFICIAL DERMAL OEDEMA
PERIVASCULAR INFLAMMATORY CELLS
Not all changes will be present in every case.
DERMATITIS- CHRONIC MACROSCOPIC LESIONS
Chronic cases are most common. Most lesions have been traumatised.
DERMATITIS- CHRONIC MICROSCOPIC LESIONS
MILD-MODERATE DERMAL OEDEMA
PERIVASCULAR INFLAMMATORY CELLS.
Character of cell infiltrate varies with time- in chronic cases, neutrophils and plasma cells can be seen in follicles.
Widened, fluid filled spaces between keratinocytes in the epidermis.
Intracellular space increases due to oedema.
Mechanism uncertain- increased hyaluron and altered E-cadherin adhesion suggested.
Fluid comes from the dermis, but the change is not explained by hydrostatic pressure alone (little/no spongiosis is seen in urticaria- hives)
SUPERFICIAL DERMAL OEDEMA
Minimal erpidermal change.
Some spongiosis and sparse cellular infiltrate seen.
eg. Reaction to folliculitis in adjacent field.
Results in SCARRING.
Scar tissue is aligned parallel to skin surface.
Hyperplasia, compact hyperkeratosis, hypergranulosis can be seen.
Moderate cell infiltrate.
An example of physicochemical trauma
eg. Reaction to Tradescantia (spiderworts- certain species).
This is via DIRECT ACTION of the plant chemical.
NOT an allergic reaction- most contacts will be affected.
IRRITANT CONTACT DERMATITIS vs. ALLERGIC CONTACT DERMATITIS
Irritant Contact Dermatitis (ICD) can become Allergic Contact Dermatitis (ACD).
If the animal has been exposed before, a much lower second exposure to the irritant can illicit and allergic response.
INNATE immunity must be activated- irritant contacts skin, which stimulates irritation/inflammation -> leukocyte recruitment, dendritic cell activation.
Activated dendritic cells take up cutaneous haptens (small molecules that can only elicit an allergic response when bound to a larger carrier), then migrate to the draining lymph nodes.
Here, specific T cells are activated and leave the lymph nodes for the circulation.
EFFECTOR T CELLS- CD8+
REGULATORY T CELLS- CD4+
Subsequent contact with the same hapten:
Hapten penetration induces cutaneous irritation, which permits recruitment of EFFECTOR T cells (CD8+).
Effector T cells are activated by presentation of haptenated peptides by MHC I, II on the surface of skin cells.
Can be an aid to diagnosis. Consider lesions:
PERIVASCULAR, VESICULAR AND PUSTULAR, INTERFACE, VASCULAR, FOLLICULAR, NODULAR AND DIFFUSE, FIBROSING, PANNICULITIS, ATROPHIC (non-inflammatory dermatosis)
Perivascular reaction is common. In the abscence of other changes, it provides little clue as to definitive diagnosis.
It just tells us that there IS inflammation.
Subtypes are based on changes in the epidermis and what any cellular infiltrate is based on:
EPIDERMIS- Spongiotic or hyperplastic
CELL INFILTRATE- Neutrophilic, eosinophilic, mononuclear.
May be superficial, deep, or both.
Perivascular dermatitis eg. canine atopic dermatitis. Histologically we can see superficial perivascular dermatitis with epidermal hyperplasia and dermal oedema.
VESICULAR AND PUSTULAR
Vesicles arise by- SPONGIOSIS, ACANTHOLYSIS, HYDROPIC DEGENERATION.
They may evolve in to vesicopustules.
PUSTULES contain INFLAMMATORY CELLS- NEUTROPHILS, EOSINOPHILS.
Pustules may be sterile or indicative of inflammation
lesions are transient and become scale/crust eg. collarettes.
Vesiculopustular dermatitis eg. orthopoxvirus infection- bovine teats become ulcerated and crusted. Histologically, intra-epidermal vesiculation can be seen due to severe ballooning degeneration.
Common reaction pattern, usually indicative of infection (bacterial, parasitic, fungal etc.)
FOLLICULITIS- Inflammation of follicle, wall remains intact.
FURUNCULOSIS- Rupture of follicle wall releases follicle contents.
eg. 'short haired breed folliculitis'. Bacterial, dog.
NODULAR TO DIFFUSE
Characterised by CELL TYPE- granulomatous/pyogranulomatous, eosinophilic, lymphoplasmacytic, neutrophilic (uncommon).
Granulomatous/pyogranulomatous nodular dermatitis is a common reaction pattern.
In many sterile cases, the cause is idiopathic and thus difficult to determine. Such cases are difficult to treat.
eg. Feline Eosinophilic Granuloma complex- nodular to diffuse dermatitis with oedema and numerous eosinophils. Sterile lesions around the mouth/lips (oral mucosa), inguinal region. Characterised by eosinophilic infiltrate. Lesions can extend deeply.
CAUSES OF INFLAMMATORY SKIN DISEASE
-PHYSICOCHEMICAL TRAUMA- mechanical, thermal, electrical, radiation (UV light), chemical irritants, caustics.
-INFECTIONS- bacterial, fungal, viral, parasitic.
-IMMUNE MEDIATED REACTIONS- allergic dermatitis.
ACTINIC (SOLAR) DERMATITIS
Caused by exposure to UV(B) radiation- physicochemical trauma; has a direct phototoxic effect on cells.
-> photodermatitis (sunburn), inflammation, increased apoptosis, reactive hyperplasia, progressive dysplasia leading to neoplasia.
Structural damage to DNA occurs.
If this is passed on to daughter cells, there will be progressive dysplasia -> neoplasia.
Apoptosed keratinocytes- 'SUNBURN CELLS.'
eg. Squamous cell carcinoma on the nasal planum of the dog. Similar lesions can be seen on the ears of cats.
Lesions are locally aggressive, but metastasis is uncommon.
Indirect process, where photodynamic agents in the skin are activated by light.
They then release damaging compounds or react with oxygen to form free radicals:
-Free radicals + singlet oxygen
-Release of inflammatory mediators.
-> erythema, oedema, exudation/crusting and necrosis of sparsely haired, unpigmented skin.
Has been applied to tumour therapy- tumour is injected with photosensitising agent, light is applied, leading to tumour necrosis.
These are activated by light, leading to photosensitisation.
-HYPERCIN- primary photosensitisation- ingested preformed eg. St John's Wort.
-PHYLLOERYTHRIN eg. ragwort. Secondary photosensitisation- animals with liver damage cannot excrete these chlorophyll breakdown products via the liver like normal, so they build up in the skin and cause photosensitisation.
-PORPHYRINS- products of aberrant pigment synthesis. Cause CONGENITAL photosensitisation eg. congenital porphyria in cattle.
PHOTOSENSITISATION IN CATTLE
Unpigmented skin is cold, dry and parchment like, and will eventually slough.
Also seen in sheep- can cause massive oedema- 'big head'.
A cause of skin disease; bacteria can infect skin (superficial infection) secondary to physical trauma.
-SKIN FOLD DERMATITIS aka INTERTRIGO- frictional damage and maceration of skin in moist environment can lead to secondary bacterial infection- pus etc.
-ACUTE MOIST DERMATITIS aka PYOTRAUMATIC DERMATITIS- self trauma (scratching, excoriation), associated with flea bite hypersensitivity and sometimes seen with other pruritic disorders.
Trauma is often localised before secondary bacterial infection.
eg. Hotspots- repeated scratching leads to ulceration and necrosis of skin surface, inflammation, then bacterial colonisation of skin surface (visible histologically).
BACTERIAL SKIN DISEASE
Normal skin of healthy individuals is highly resistant to bacterial invasion, as normal resistant microflora inhibit colonisation by other bacteria.
Bacterial adherence is a KEY factor in pathogenesis.
Adherent bacteria are lost through normal continuous desquamation.
ANY CHANGE TO THE CUTANEOUS MICROENVIRONMENT CAN PREDISPOSE TO THE OVERGROWTH OF RESIDENT OR TRANSIENT BACTERIA
SUPERFICIAL BACTERIAL INFECTIONS (SUPERFICIAL PYODERMA)
-Pyoderma- a skin disease characterised by purulence.
-DERMATOPHILOSIS (Streptothricosis)- Dermatophilus congolensis.
-IMPETIGO (Superficial pustular dermatitis)- Coagulase-positive staphylococci.
-EXUDATIVE EPIDERMITIS (Greasy pig disease)- Staph hyicus.
-OVINE FLEECE ROT (exudative dermatitis)- P. aeruginosa.
aka. Rain rash, lumpy wool (sheep).
-Prevalent in subtropical/tropical climates.
-Substantial economic loss- hide damage, loss of condition, meat and milk.
-Mortality 10%- due to debility, loss of condition
-Predisposing factors are NECESSARY for infection- prolonged wetting, mechanical damage (in particular body areas), tick infestation, hyphae penetrate living epidermis- keratolytic enzymes then act.
Caused by Dermatophilus congolensis- Gram positive, pleomorphic filamentous bacteria.
Coccoid zoospores survive in dried exudates- can aid transmission.
Attracted by skin CO2.
Healthy carriers can act as a source of infection.
Commonest skin disease of crocodiles in Australia!
'Puppy pyoderma'- seen particularly in young animals.
Bacterial infection of the skin characterised by superficial interfollicular pustules.
Pustules become intercorneal as keratinocytes mature.
Very common in dogs, almost always secondary to an underlying problem/disease/predisposing factor.
-Caused primarily by S. pseudintermedius infection.
-Occasional isolates of other Staphylococci are seen eg. S. aureus.
-Host factors are important regarding susceptibility- thin/compact stratum corneum, limited lipid layer, relatively high pH.
-PREDISPOSING FACTORS- altered skin microenvironment, self trauma
-UNDERLYING SKIN DISORDERS- atopic dermatitis
-SYSTEMIC DISEASE- endocrine disturbance.
Bacterial infection can cause folliculitis/furunculosis- superficial or deep.
Involves skin down to level of the intact hair follicles.
Extends to tissues deeper than hair follicle, may involve hypodermis.
Can be caused by follicle rupture and extension of lesion to deeper structures- furunculosis.
eg. Canine acne- multiple nodules of deep pyoderma.
TRICHOGRANULOMA may be seen- pyogranulomatous inflammation around hair fragments in the deep dermis.
DEEP BACTERIAL INFECTIONS
-Staphylococcal folliculitis/furunculosis- dogs, horses, goats, sheep.
-Subcutaneous abscesses- cats (P. multocida), horses/sheep (C. pseudotuberculosis), cattle/sheep/pigs (A. pyogenes).
-Cellulitis- deep spreading infection along fascial planes. Dogs- staphylococcal, streptococcal (necrotising fasciitis).