Skin Disorders

Urticaria (Hives or nettle rash)

• Definition

It is nodular skin disease, type 1 hypersensetivity

reaction characterized by multiple edematous
dermal swelling that appear and disappear
suddenly.
• Etiology
• Exogenous hives: as insect bites, stings, topical
applications, drugs and vaccines
• Endogenous hives by inhalation as pollens, mold
spores and fungi, or ingestion of certain antigenic
substance.
• Dermatographism: occur in purebred horses
in which rubbing produce urticaria-like lesion.
 Clinical Signs
• Lesions appear within few minutes to hours after
exposure to the allergin
• Lesion may be localized or generalized
• No age, sex, breed predilections
• Lesions may be at any part of the body but
particularly in eyelid, legs, flank and back
• Purities varied
• Lesion are elevated flat-topped 1-20 cm in diameter,
pit under pressure cool to touch.
 Diagnosis

• Although it is usually recognized, the

identification of cause may be difficult
• Cause of acute urticaria (less than 6 week
duration) is more likely to be identified than
chronic urticaria (more than 6 week duration)
• History of diet, management and recent drug
administration should be checked
• Interdermal skin allergic test may be applied
 Treatment

• Elimination of primary cause if possible

• Often spontaneous recovery occur
• Parentral administration of glucocorticoid is
useful especially in acute uritcaria
• Chronic urticaria: Hydroxyzine may be used
 Photodermatitis
• Cutaneous exposure to sun light resulting in dermatitis
of varying severity.
• 2.1.1. Photo toxicity (sunburns)
• - It is a photochemical reaction involving the dermis
and epidermis
• -Produced by direct exposure to sunlight (powerful
UV rays)
• - Causing erythema, inflammation and tissue damage
• - The severity of the changes depends on: Time of
exposure, degree of exposure, skin area involved
 2.1.2. Photo sensitization

• Severe cutaneous reaction following the

penetration of UV rays into unprotected
dermis and epidermis, which contain photo-
reactive molecules, derived from either
circulation or topical application.
 Classification and Etiology

• Primary photo sensitization

• Secondary (hepatogenous) photo sensitization

• Photo- contact reaction

• Photo-allergic reaction.
• Primary photosensitization
• Photosensitizing agent being deposited
unchanged in the skin after injection or
ingestion as:
• Some posture plants containing photo-
dynamic agents as:Fogopyrin in buck wheat,
Furocumarin in wild carrot , Hypercin in St.
John's weed, Some drugs can cause
photosensitization as :phenothiazine,
tetracycline and sulphonamides.
• Secondary (hepatogenous photosensitization

• It is resulting from liver dysfunction/damage or

biliary stasis allowing certain compound (photo-
dynamic agents) which usually eliminated from the
body via bile or break down in liver to accumulate
and deposit in the skin

• The most important compound is "Phylloerythrin"

which produced by breakdown of chlorophyll by
bacterial action in bowel.
• Phylloerythrin circulate in body and deposit in
the skin, when exposed to UV rays, photo-
dynamic molecules become sensitizing and
unstable, emission of light energy leading to
phototoxic reaction.
• Photo- contact reaction
• It is resulting when photo-dynamic agent come
in direct contact and absorbed by the skin,
when exposed to UV rays leading to
phototoxic reaction.
• Some posture plants containing essential oils
(as some types of clover) may be incriminated
• Contact with certain coal tar products such as
acridine or creosote.
• Photo- allergic reaction
• It is very rare and not yet confirmed in horses, it is
of unknown pathogenesis.
• Other Classification:
• Type 1 (primary photosensitization)
• Type 2 (abnormal pigment metabolism): occur in
cattle and cat, congenital or acquired defect in
enzyme involved in heme synthesis (erythropiotic
prophoria).
• Type 3 (secondary or hepatogenous
photosensitization).
• Type 4 photosensetization: of unknown pathogenity
 Clinical signs:

• Cutaneous changes can occur in non-

pigmented and pigmented skin
• Skin inflammation and edema
• Skin splitting and exudation
• In severe cases: skin necrosis and sloughing
• Animal scratch and rub the lightly pigmented
area especially eyelid, muzzle and ear
• Animal became photophobic and discomfort
• Animal may be icteric
 Diagnosis

• Depends mainly on history and clinical signs

• Period from exposure to onset of clinical signs
can vary from several hours up to 10 days.
• Increase the activity of SDH, ALP and direct
Bilirubin.
• Some evidence of liver dysfunction as
anorexia, depression, malaise and jaundice
• Increase phylloerythrin levels
 Treatment

• Animal should be shaded immediately

• Parental administration of corticosteroids may
be helpful in early stages
• Antibiotic for the skin lesion with appropriate
dressing of the lesion
• Prognosis
• Secondary is usually of poor prognosis
• Primary is usually of favorable prognosis and
skin lesions are healed remarkably well even
in area of extensive skin necrosis.