Conditions leading to photosensitization

Photosensitization depends on the absorption of ultraviolet light within a specific range of wavelengths (280-790 nm) and the presence of a photodynamic agent in the skin.  Photodynamic agents form unstable high energy molecules when exposed to ultraviolet light.  When the photodynamic agents return to the ground state, the energy released causes the molecule to fluoresce.  The released energy damages epidermal cell membranes and forms free radicals that can initiate a chain reaction of membrane damage.

Photosensitization is most prominent on areas of the body where protection from sunlight is least effective.

·        Dorsal and lateral areas of the body

·        Thin or non-pigmented skin (e.g., the sclera, escutcheon, udder and teats, muzzle). 

·        Photosensitization is most likely to occur in sunny climates and during the spring and summer when sunlight is more intense or of longer duration each day.

Clinical effects of photosensitization

ü      Early signs are erythema and edema.

ü      Pruritus, photophobia, and hyperesthesia follow.

ü      Serious signs that occur later in the course of the disease include exudation, ulceration, exfoliation of damaged epidermis develops and possibly blindness.

ü      In sheep, severe edema of the ears and face develops, resulting in a condition known as "big head". 

ü      Moderate to serious signs often are accompanied by reduced feed intake and cessation of nursing and breeding.

Types of photosensitization

Primary photosensitization occurs when a photodynamic agent is directly ingested, absorbed through the skin, or injected, or when a chemical is biotransformed to a photodynarnic metabolite

·        The major effects of primary photosensitizers occur in the skin; other organs are usually spared.

·        Prompt removal of the photosensitizer and supportive treatment often results in recovery with few sequelae.

Secondary (hepatogenous) photosensitization occurs as a result of compromised liver function, which reduces the excretion of plant pigment metabolites from the body.  Several toxic plants are known to cause hepatogenous photosensitizers.

·        Normally, chlorophyll is metabolized to phylloerythrin by intestinal and colonic bacteria.  Phylloerythrin reabsorbed from the gut is conjugated by the liver and excreted in the bile.

·        Failure of the liver to conjugate or excrete phylloerythrin allows it to accumulate in the dermal vasculare where it is activated to a photodynamic state by UV light.

·        Liver damage and involvement of other organ systems may accompany the expected skin-related signs and lesions of photosensitization.

Agents Associated with Photosensitization

            Primary Photosensitization

            Secondary Photosensitization