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Photosensitization: Introduction |  |
| Photosensitization is a clinical condition in which skin (areas exposed to light and lacking significant protective hair, wool, or pigmentation) is hyperreactive to sunlight due to the presence of photodynamic agents. Molecules of photosensitizing agents present in the skin are energized by light. When the molecules return to the less energized state, the released energy is transferred to receptor molecules that quickly initiate chemical reactions in various skin components. Tissue
injury is thought to result from the production of reactive oxygen intermediates or from alterations in cell membrane permeability. Photosensitization can be difficult to differentiate clinically from actual sunburn. |
| Photosensitization is often classified according to the source of the photodynamic pigment. These categories are primary or type I photosensitivity, aberrant endogenous pigment synthesis or type II photosensitivity, and type III or secondary (hepatogenous) photosensitivity. Sometimes a fourth category has been identified, labeled idiopathic type IV photosensitivity. (See also
congenital erythropoietic porphyria,
Congenital Erythropoietic Porphyria: Introduction, and protoporphyria,
Cutaneous Manifestations of Multisystemic and Metabolic Defects.) |
| A wide range of chemicals, including some that are fungal and bacterial in origin, may act as photosensitizing agents. However, most compounds that are important causes of photosensitivity in veterinary medicine are plant-derived. Photosensitization occurs worldwide and can affect any species, but is probably most commonly seen in cattle, sheep, goats, and horses.
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Primary Photosensitization: |
| Primary photosensitization occurs when the photodynamic agent is absorbed either through the skin or from the GI tract unchanged, reaching the skin in its native form. Examples of primary photosensitizers are hypericin (from
Hypericum
perforatum
[St. John’s wort]) and fagopyrin (from
Fagopyrum
esculentum
[buckwheat]). Plants in the families Umbelliferae and Rutaceae contain photoactive furocoumarins (psoralens), which cause photosensitization in livestock and poultry.
Ammi
majus
(bishop’s weed) and
Cymopterus
watsonii
(spring parsley) have produced photosensitization in cattle and sheep, respectively. Ingestion of
A
majus
and
A
visnaga
seeds has produced severe photosensitization in poultry. Species of
Trifolium
,
Medicago
(clovers and alfalfa),
Erodium
,
Polygonum
, and
Brassica
have been incriminated as primary photosensitizers. Many other plants have been suspected, but the toxins responsible have not been identified (eg,
Cynodon
dactylon
[bermudagrass]). Additionally, some coal tar derivatives, phenothiazine, sulfonamides, and tetracyclines have induced primary photosensitivity. |
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Aberrant Pigment Metabolism: |
| Type II photosensitivity due to aberrant pigment metabolism is known to occur in both cattle and cats. In this syndrome, the photosensitizing porphyrin agents are endogenous pigments that arise from inherited or acquired defective functions of enzymes involved in heme synthesis. Bovine congenital erythropoietic porphyria (
Congenital Erythropoietic Porphyria: Introduction) and bovine erythropoietic protoporphyria are the most commonly reported diseases in this category. |
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Secondary (Hepatogenous) Photosensitization: |
| Secondary or type III photosensitization is by far the most frequent type of photosensitivity observed in livestock. The photosensitizing agent, phylloerythrin (a porphyrin), accumulates in the plasma due to impaired hepatobiliary excretion. Phylloerythrin is derived from the breakdown of chlorophyll by microorganisms present in the GI tract. Phylloerythrin, but not chlorophyll, is normally absorbed into the circulation and is
effectively excreted by the liver into the bile. Failure to excrete phylloerythrin due to hepatic dysfunction or bile duct lesions increases the amount in the circulation. Thus, when it reaches the skin, it can absorb and release light energy, initiating a phototoxic reaction. |
| Phylloerythrin has been incriminated as the phototoxic agent in the following conditions: common bile duct occlusion; facial eczema (
Facial Eczema); lupinosis (
Mycotoxic Lupinosis ); congenital photosensitivity of Southdown and Corriedale sheep (see
Congenital Photosensitization in Sheep); and poisoning by numerous plants including
Tribulis
terrestris
(puncture vine),
Lippia
rehmanni
,
Lantana
camara
, several
Panicum
spp
(kleingrass, broomcorn millet, witch grass),
Cynodon
dactylon
,
Myoporum
laetum
(ngaio), and
Narthecium
ossifragum
(bog asphodel). |
| Photosensitization also has been reported in animals that have liver damage associated with various poisonings: pyrrolizidine alkaloid (eg,
Senecio
spp
,
Cynoglossum
spp
,
Heliotropium
spp
,
Echium
spp
;
Pyrrolizidine Alkaloidosis: Introduction), cyanobacteria (
Microcystis
spp
,
Oscillatoria
spp
),
Nolina
spp
(bunch grass),
Agave
lechuguilla
(lechuguilla),
Holocalyx
glaziovii
,
Kochia
scoparia,
Tetradymia
spp
(horse brush or rabbit brush),
Brachiaria
brizantha,
Brassica
napus,
Trifolium
pratense
and
T
hybridum
(red and alsike clover),
Medicago
sativa,
Ranunculus
spp,
phosphorus, and carbon tetrachloride. Phylloerythrin is likely the phototoxic agent in many of these poisonings. |
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Type IV Photosensitivity: |
| Photosensitivity where the pathogenesis is unknown is classified as type IV. Examples include winter wheat (cattle),
Medicago
spp
(alfalfa),
Brassica
spp
(mustards), and
Kochia
scoparia
(fireweed). Many plants that fall in this category may perhaps be type I photosensitizers. |
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| Clinical Findings and Lesions: |
| The clinical signs associated with photosensitivity are similar regardless of the cause. Photosensitive animals are photophobic immediately when exposed to sunlight and squirm in apparent discomfort. They scratch or rub lightly pigmented, exposed areas of skin (eg, ears, eyelids, muzzle). Severe phylloerythrinemia and bright sunlight can induce typical skin lesions, even in black-coated animals. Erythema develops rapidly and is soon followed by edema. If exposure to light stops
at this stage, the lesions soon resolve. When exposure is prolonged, serum exudation, scab formation, and skin necrosis are marked. In cattle, and especially in deer, exposure of the tongue while licking may result in glossitis, characterized by ulceration and deep necrosis. |
| Depending on the initial cause of the accumulation of the photosensitizing agent, other clinical signs may be seen. For example, if the photosensitivity is hepatogenous, icterus may be present. In bovine congenital erythropoietic porphyria, discoloration of dentin, bone (and other tissues), and urine often accompanies the skin lesions. Photodermatitis is the sole manifestation observed in bovine erythropoietic protoporphyria. |
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| Diagnosis: |
| Clinical signs are easily recognized in cases of marked photosensitivity but are similar to the primary actinic effects of sunburn in early or mild cases. Reference to the specific diseases in which photosensitization is an objective sign may assist in diagnosis of the underlying disease. Evaluation of serum liver enzymes and liver biopsies may be necessary to confirm the presence of hepatic disease. Examination of blood, feces, and urine for porphyrins can also be performed. |
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| Treatment: |
| Treatment involves mostly palliative measures. While photosensitivity continues, animals should be shaded fully or, preferably, housed and allowed to graze only during darkness. The severe stress of photosensitization and extensive skin necrosis can be highly debilitating and increase mortality. Corticosteroids, given parenterally in the early stages, may be helpful. Secondary skin infections and suppurations should be treated with basic wound management techniques, and fly
strike prevented. The skin lesions heal remarkably well, even after extensive necrosis. |
| The prognosis and eventual productivity of an animal is related to the site and severity of the primary lesion and/or hepatic disease, and to the degree of resolution. |
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