pathology of the integumentary systempeople.upei.ca/hanna/skin3/skinl3-webf17.pdf · pathology of...

Pathology of the Integumentary System

Lecture 3 Congenital / Environmental / Infectious

(Web review)

Paul Hanna Fall 2017

CONGENITAL AND HEREDITARY SKIN DISEASE

Congenital Hypotrichosis

• all domestic species

• absence of hair follicles &/or abnormal follicular development

Cattle: • hereditary vs acquired (BVD, iodine, pituitary hypoplasia, teratogens)

• r/o telogen or anagen defluxion

Dogs and Cats: • several hereditary forms

Congenital Hypotrichosis

Congenital hypotrichosis in an Ayrshire calf

(note: thin hair coat due to failure of normal

development of many hair follicles)

Anagen or Telogen Defluxion (Effluvium)

eg anagen defluxion following severe neonatal diarrhea / sepsis

[For information only] Hereditary collagen dysplasia

Ichthyiosis

Hereditary collagen dysplasia

(note: distensible skin which tears easily)

Calf with ichthyosis - a congenital keratinization disorder

[For information only] Epidermolysis Bullosa

Various forms of epidermolysis

bullosa are recognized in humans

and domestic animals that are

associated with inherited defects

of adhesion molecules in the

hemidesosomes / basement

membrane.


Epidermolysis bullosa is

described in Belgian foals.

In the first few days of life

see skin / oral ulceration

and also separation /

sloughing of the hooves.


Extensive subepidermal clefting causing vesicle / bulla

formation in the skin

Note, extensive subepidermal clefting / separation also

occurs in oral cavity & esophagus

Canine Recurrent Flank Alopecia

aka = Seasonal (cyclic) flank alopecia

Also:

Color dilution alopecia

Black hair follicular dysplasia

Other follicular dysplasias

[For information only] Pattern alopecia (Pattern baldness)

Idiopathic bald thigh syndrome,

a form of pattern baldness seen in greyhounds

ENVIRONMENTAL INDUCED SKIN DISEASE

I. ACTINIC (SUN) INJURY

II. CHEMICAL INJURY

III. PHYSICAL INJURY

ACTINIC (SUN) INJURY

Epidemiology

• amount of light reaching skin:

Environmental Factors (atmosphere / latitude / altitude / shelter)

Host Factors (quantity of hair / pigmentation / stratum corneum / genetics)

Path of sunlight through atmosphere.

In general the farther you are from the equator

the farther the suns radiant energy has to travel

through the atmosphere with greater amount of

filtering / absorption of the radiation.

Etiopathogenesis

• visible light vs UV-A vs UV-B vs UV-C

• UV-B free radicals damages nucleic acids, proteins & lipids cell death

www.skin-science.com


Note, arrows indicate apoptotic

keratinocytes (“sunburn cells”) due to

UV-B radiation. These can be induced

within 30 minutes of sun exposure.

Sunburn

• due to: direct endothelial damage

damage to keratinocytes with release of inflammatory mediators

Solar dermatitis

• chronically see thickened inflamed skin +/- dysplasia / neoplasia


Sunburn on

udder of a goat

Fig 14-5 (Hnilica – Sm An

Derm) Feline Solar

Dermatosis. Alopecia,

erythema, erosions, and

crusting on the ear pinna.

As the disease progresses,

papules will develop, with

erosion and ulceration that

suggest progression to

squamous cell carcinoma.

• Mutagenesis:

pyrimidine dimer formation; esp in mutation “hot spots” on P53 gene

impaired P53 protein function no delayed replication & no apoptosis if not repaired

also promoter preferential replacement of damaged cells with mutated P53 cells



UV induced dimer results in permanent mutation

Sci Am, 1996

Pyrimidine dimer

formation

Sci Am, 1996


Pyrimidine dimers are efficiently corrected by Nucleotide Excision Repair

(NER) mechanisms. Even if it was 99.99% effective, the more exposure to

sunlight, the more pyrimidine dimers are formed which will increase the

risk of a dimer remaining unrepaired and going on to form a somatic

mutation. Also certain individuals can have defects in their NER repair

mechanism which would greatly increase the risk of mutations (eg

xeroderma pigmentosa).

Nucleotide Excision Repair (NER)

ADDITIONAL

SUNBURNS


UV light can not only cause somatic mutations of the cells (left image), it can also act as a cancer promoter, ie sunburns

injures/kills keratinocytes which results in hyperplasia. Hyperplasia is fertile ground for replicating / amplifying / inducing

additional mutations → neoplastic transformation.

Sci Am, 1996

UV light as a cancer promoter


Photosensitization after treatment with a phenothiazine anthelmintic

Many plants contain chemicals which are

photoreactive, eg St John’s wort (above)

Photosensitization

• photodynamic substances in skin are activated by UV-A or visible light

Type I exogenous origin of photodynamic agents

Type II aberrant heme pigment synthesis

Type III (hepatogenous type) failure to remove phylloerythrin

Type IV idiopathic

Photosensitization

Photosensitization associated with liver disease; note

only poorly haired &/or white haired areas affected

Photosensitization in cattle; note only white areas affected. There

is enough pigment in the colored hair to absorb / block the light and

prevent activating the photodynamic agents.

CHEMICAL INJURY

Local application

• agent must penetrate hair & stratum corneum; enhanced by moisture &/or damage

Systemic absorption

• ingestion of toxins with systemic effects on the skin and usually other organs

1. Primary Contact Irritant Dermatitis

• skin contact by substances expected to cause irritation:

caustic chemicals (eg acids, alkalis)

concentrated drugs (eg insecticides)

soaps / detergents

body excretions (eg anal sac, urine)

CHEMICAL INJURY

Contact irritant dermatitis (eg concentrated lye solution) Contact irritant dermatitis (eg concentrated pour-on insecticide)

2. Gangrenous Ergotism and Fescue Toxicosis

3. Many Others: thallium, selenium, mercury, arsenic, etc

CHEMICAL INJURY

gangrenous necrosis of distal limbs due to

severe peripheral vasoconstriction with ergotism

Acral Lick Dermatitis

• esp large active breeds, esp < 5 yrs

• psychogenic boredom &/or anxiety

PHYSICAL INJURY

Acral lick dermatitis, note focal area of

alopecia, erythema, erosion / ulceration

PHYSICAL INJURY

Abrasion / Laceration / Ulceration / Foreign Bodies

Radiation

Extremes in Temperature

Callus / Hygroma

Feline Psycogenic Dermatitis

Burn victim – note epidermal

necrosis / ulcers, crusts

INFECTIOUS SKIN DISEASE

VIRAL SKIN DISEASES

BACTERIAL SKIN DISEASES

MYCOTIC SKIN DISEASES

PARASITIC SKIN DISEASES

PROTOZOAL SKIN DISEASES

VIRAL SKIN DISEASES

Contagious Pustular Dermatitis (= contagious ecthyma = "Orf“)

• common / worldwide parapoxvirus infection of sheep & goats.

• typical pox phases (vesicles / pustules / crusts), but more hyperplastic

Fig. 17-31 (Zachary) Schematic diagram of the development of a poxvirus lesion over time.

Local Infection

• intact skin resistant to local infecting viruses (eg papillomaviruses, parapoxviruses)

• requires abrasion or arthropod bite

Contagious Pustular Dermatitis

• lesions on lips; ± eyelids, feet, oral cavity; rarely GI tract / viscera

Contagious Pustular Dermatitis

Note, ballooning degeneration and

intracytoplasmic inclusion bodies.

Contagious pustular dermatitis is a relatively common

zoonosis in individuals handling sheep & goats

Systemic Viral Infection

• epitheliotropic

• other, eg 2o to pruritus

• pantropic

Canine distemper – “hard pad”

Scrapie Vesicular exanthema

Diagnosis

• history & clinical signs / lesions

• skin biopsy

• serology

• virus isolation or identification

VIRAL SKIN DISEASES

Raccoon – scale / crust on

distal limbs due to canine

distemper virus infection

CANINE

Papilloma virus

Canine distemper virus

CATTLE

Bovine mammillitis virus

Pseudocowpox

Papilloma virus

SWINE

Swinepox

HORSES

Papilloma virus

VIRAL SKIN DISEASES

Swinepox

BACTERIAL SKIN DISEASES (PYODERMAS)

healthy skin is resistant to bacterial infection due to:

lack of moisture

stratum corneum forms physical barrier + continuous desquamation

antibacterial effects of sebum / sweat and the normal microflora

• result depends on agent pathogenicity / host defence mechanisms

factors assisting bacterial colonization / proliferation:

moisture and dirt

altered cornification

physical damage

PRIMARY SECONDARY

SKIN Otherwise healthy Not healthy

BACTERIA One species > 1 species

PATTERN Characteristic Not characteristic

ANTIBIOTICS Successful Not successful

• pyodermas are common in dogs


SUPERFICIAL DEEP

INVOLVE epidermis dermis / subcutis

REPAIR no scarring scarring

DURATION short chronic

LYMPH NODE no yes

SYSTEMIC no +/-

GROSS pustules, crusts pustule, nodule, abscess, sinus

HISTOLOGY pustular &/or perivascular dermatitis

with neutrophils

folliculitis / furunculosis

&/or nodular to diffuse

dermatitis / panniculitis,

suppurative to granulomatous,

± bacterial agent


Diagnosis

history & lesions

culture

skin biopsy


Fig 3-14 (Hnilica – Sm An Derm) Superficial

Pyoderma. Erythematous dermatitis with

epidermal collarettes formation is apparent.

CANINE

Pyotraumatic dermatitis ("hot spots” or “acute moist dermatitis”)

• intense pruritus➞ self-trauma ➞ secondary bacterial infection.

focal alopecia, excoriation (erosion / ulceration), exudation

CANINE

Impetigo

• primary superficial pustular dermatitis, esp dogs (“puppy pyoderma”)

• predisposed by moist / dirty environments, abrasions, parasitism, poor nutrition

Note, pustules and epidermal collarettes

CANINE Skin fold pyoderma

FELINE

Subcutaneous Abscesses

Note, bite wounds overlying area of inflammation (panniculitis / cellulitis and abscessation), which is not

obvious on external visual examination, ie often need to dissect to find the underlying inflammation.

RUMINANTS

Papillomatous Digital Dermatitis (“hairy heel warts”)

Initially an erosive / ulcerative plaque-like lesion, which is intensely painful and progresses

to a proliferative / papillomatous (with long, thin papillae), less painful lesion

Papillomatous Digital Dermatitis

See epidermal hyperplasia & prominent papillae extending

from the surface. Basophilic material at base of papillae is

composed of myriads of bacteria (H&E stain).

Note, see myriads of spirochete bacteria along the

epidermal surface with silver staining.

Papillomatous Digital Dermatitis

Transmission electron micrograph showing numerous spirochetes in an advanced

stage of a typical digital dermatitis lesion. Int J Syst Bacteriol. 1997 Jan;47(1):175-81]

RUMINANTS

Dermatophilosis (D. congolensis)

• a superficial exudative dermatitis, seen most commonly in hot, humid areas.

Characteristic branching

filaments of D. congolensis.

Filaments undergo

longitudinal & transverse

septation to form parallel

rows of coccoid bodies

which will mature into

zoospores.

PORCINE

Exudative Epidermitis (Greasy Pig Disease)

• acute, rapidly spreading, often fatal exudative pyoderma of suckling to weaner pigs.

• infection with Staphylococcus hyicus, which have exfoliative exotoxins.

Note: cell crusts composed of

degenerate inflammatory cells

admixed with keratin, bacteria

In the common acute form see

greasy brown-black exudate /

crust which typically starts on

face &/or limbs and quickly

spread to the entire body.

PORCINE

Septicemia

Salmonella

"Diamond Skin Disease"

“Diamond Skin Disease” in pig with Swine Erysipelas

Note rhomboid / ‘diamond shaped’ erythematous

plaques typical of infection with Erysipelothrix rhusiopathiae.

Salmonellosis - or other endotoxemias; note venous

infarction of extremities due to endotoxin induced venous

thrombosis.

Diagnosis

history & lesions

fungal id / culture

skin biopsy

Cutaneous Mycoses

Subcutaneous Mycoses

Systemic Mycoses

Dermatophytosis (Ringworm)

Malasseziasis

Candidiasis

Cutaneous Mycoses of Wildlife

MYCOTIC SKIN DISEASES


• common / worldwide distribution; mainly Microsporum & Trichophyton

• young / immunocompromised

• predisposing factors: overcrowding, high humidity, poor sanitation / nutrition

• contagious direct or fomites

• dermatophytes attack keratinized layers inflammation due to proteases

Cutaneous Mycoses


• circular patches of scaling / alopecia to papules / pustules / furunculosis / crusting

Canine pinna, note focal alopecia,

erythema and scaling Bovine head, note mulifocal alopecia with scaling / crusting


note multiple, often coalescing, areas of alopecia with scale & crust


Arthrospores surrounding and hyphae within hair shaft.

Ringworm is the most commonly reported zoonosis in people

working with cattle. Although less common in small animals, one

study indicated ~50% of people exposed to either symptomatically

or asymptomatically infected cats develop lesions.

Malasseziasis (Malassezia pachydermatis)

• yeast that are part of the normal microflora proliferate & cause dermatitis

secondary to underlying skin disease (eg allergies, seborrhea)

Malasseziasis in a couple of Westies (above) and same dogs following treatment (right). Vet Dermatol. 2001 Oct;12(5):285-90.

Malasseziasis

Fig. 17-54B (Zachary) Stratum corneum contains numerous Malassezia pachydermatis yeast (arrows), which are bilobed (“peanut”-shaped). The

dermis is mildly edematous—note the mild separation of the collagen bundles by nonstaining to lightly amphophilic extracellular fluid. Gomori's

methenamine silver stain–H&E counter stain. [note: cytologic methods are much more sensitive than histology in detecting yeast]

austriantribune.com

wikimedia.org

http://www.nwhc.usgs.gov

news.berkeley.edu

Chytridiomycosis of frogs and salamanders

White-nose syndrome of bats Snake fungal disease

Cutaneous Mycoses of Wildlife

• traumatic implantation of a wide variety of saprophytic fungi

primarily by inhalation; esp Blastomycosis & Cryptococcosis

host usually has compromised resistance to infection

Subcutaneous Mycoses

Systemic Mycoses

Papular / nodular dermatitis, due to Blastomycosis

note: crusted papules / nodules on nostril and lip.

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