Was she out grazing that fall rye?
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.
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.
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.
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.
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.
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.
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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See Also
