Ann Rashmir-Raven, Rebecca S. McConnico
Photosensitization
Photosensitization is an uncommon cause of dermatitis but a potentially serious problem in horses. The spectrum of disease associated with photosensitization ranges from being a simple nuisance associated with pasture plant contact to a life-threatening crisis of hepatogenous origin. Clinical signs typically begin a few hours after exposure to intense sunlight and include erythema, edema, exudation, scab formation, and skin necrosis. Photosensitization occurs when skin is sensitized by a photodynamic agent and then is exposed to ultraviolet (UV) light. Photosensitization differs from sunburn or photodermatitis, both of which develop independently of a photodynamic agent. Veterinarians’ ability to recognize and treat photosensitization in the early stages will provide their equine patients optimal comfort in all cases and enhanced survival in cases of hepatogenous origin.
Photodynamic Agents
Photodynamic agents responsible for photosensitization can be either phototoxic or photoallergic in nature. Phototoxic agents are capable of inducing a photosensitivity reaction in almost all animals under suitable conditions. Photoallergic agents require the animal to first be sensitized to the compound. Both phototoxic and photoallergic compounds are able to reach the skin through the bloodstream or by direct contact, with the most common route being through the systemic circulation. The chemical configuration of a photodynamic agent enables it to absorb specific wavelengths of UV or visible light. Many of these agents absorb spectrums of light that exceed the UV-B range. In these cases, exposure to actinic radiation that would normally be incidental severely damages the horse’s skin. The photodynamic agent becomes activated when it is exposed to photons. The high-energy molecules that are produced can react with the biologic substrate or with molecular oxygen. This reaction results in production of reactive oxygen intermediates such as superoxide anion, singlet oxygen, and hydroxyl radical. The release of these reactive molecules leads to damage of certain macromolecules, including nucleic acids, proteins, and lipoproteins. The nucleus, cell membrane, and organelles, especially lysosomes and mitochondria, are the major targets of phototoxic reactions. Superficial blood vessels and the epidermis are primarily affected.
Four types of photosensitization are recognized in animals, including primary photosensitivity (also known as type 1 photosensitivity), hepatogenous photosensitivity (also known as type 2 photosensitivity), photosensitivity secondary to aberrant pigment synthesis (porphyria), and photosensitivity of uncertain etiology.
Primary Photosensitization
Primary photosensitization results when the photodynamic agent is ingested and absorbed directly from the digestive tract, reaching the skin through the circulation. These agents are chiefly encountered through plants, in particular St. John’s wort (Hypericum perforatum), buckwheat (Fagopyrum spp), spring parsley (Cymopterus watsoni), and Ammi spp. Although it is a rare occurrence, the classic example of this is seen in horses that graze in pastures containing St. John’s wort, which contains a red fluorescent pigment, hypericin, in its leaves. The hypericin acts as a photodynamic agent. St. John’s wort is an invasive noxious weed that is common to the United States, South America, Europe, New Zealand, and Australia. Hypericin is contained in the plant’s leaves in areas that appear as small clear dots and is present during all stages of the plant’s growth. St. John’s wort has orange-yellow flowers with five petals; the petals occasionally have black dots along the edges. Horses only consume significant amounts of this weed when the plant is prolific or has young tender shoots, when feed is scarce, or when the plant is dried and mixed with hay. Therefore photosensitization caused by St. John’s wort may also occur during winter. Clinical signs appear within 21 days from the onset of ingestion. Horses that ingest substantial quantities develop signs in as little as 2 days.
Primary photosensitization from other plants such as buckwheat (fagopyrum toxicosis), which has several toxins similar to hypericin in St. John’s wort, is uncommon in horses. Similarly, photosensitization caused by spring parsley, Bishop’s weed, and Dutchman’s breeches (furocoumarin toxicosis) is more common in sheep, cattle, and pasture-raised swine.
Cases of contact photosensitization most commonly have been reported in horses that graze in pastures that contain various legumes, most commonly clovers. It is unclear why the occasional pasture accumulates a photodynamic agent. Because some clovers can cause hepatic photosensitization, it is imperative that horses with signs of photosensitization be evaluated for liver disease.
In addition to photosensitization from plants, an uncommon side effect of many drugs and chemicals is primary photosensitization through a variety of mechanisms (Table 128-1). In the author’s experience, certain fly sprays, antimicrobial soaps, and tetracycline antimicrobials are the most commonly encountered substances in equine practice. In addition to photosensitization from the substances previously mentioned, ingestion of gluten from a dairy concentrate formulation has been linked to primary photosensitivity in the horse.
TABLE 128-1
Causes of Primary Photosensitization
| Substance | Photodynamic Agent |
| Hypericum perforatum (St. John’s wort, goat weed, Klamath weed), H pseudomaculatum (large St. John’s wort), H punctatum (spotted St. John’s wort) | Hypericin (ingested) |
| Fagopyrum esculentum, F sagittatum, F tatoricum (buckwheat) | Fagopyrin, photofagopyrin, pseudohypericin (ingested) |
| Cymopterus watsonii (spring parsley) | Furocoumarins |
| Ammi majus (Bishop’s weed) | Furocoumarins |
| Thamnosma texana (Dutchman’s breeches) | Furocoumarins (ingested) |
| Lolium perenne (perennial rye grass) | Perloline (ingested) |
| Froelichia humboldtiana | Naphthodianthrone derivative |
| Medicago denticulate (burr trefoil) | Aphids |
| Trifolium hybridum (alsike clover), T pretense | Ingested, and possibly contact with unknown photo and hepatotoxin |
| Medicago spp (alfalfa) | Unidentified |
| Sphenociadium capitellatum (whiteheads, ranger’s buttons) | Ingested—unidentified agent |
| Heracleum mantegazzlanum (giant hogweed) | Furanocoumarin (contact) |
| Cooperia pedunculata (rain lily) | Unidentified agent |
| Avena sativa (oats) | Unidentified agent |
| Brassica napus (rape) | Unidentified agent |
| Brassica rapa (mustard) | Unidentified agent |
| Vicia spp (vetches) | Unidentified agent |
| Mycotoxins | |
| Fungi on celery and parsnips | Phytoalexins (xanthotoxin, tripsoralen) |
| Drugs and Chemicals | |
| Phenothiazine | Phenothiazine sulfoxide |
| Thiazides | Unidentified agent |
| Retinoids, therapeutic photoagents | Tazarotene (surface application) |
| Promazines | Unidentified agent |
| Acriflavines | Unidentified agent |
| Rose bengal | Unidentified agent |
| Methylene blue | Unidentified agent |
| Sulfonamides | Unidentified agent |
| Tetracyclines | Unidentified agent |
| Chlorpromazine | Unidentified agent |
| Quinidine | Unidentified agent |
| Coal tar derivatives | Unidentified agent |
| Furosemide | Unidentified agent |
| Some antimicrobial soaps | Unidentified agent |
| Endogenous Metabolites | |
| Porphyrins | Genetic abnormality (porphyrin) |
| Phylloerythrin | Hepatic failure (ingested) |
| Bilirubin | Liver, blood disorders (endogenous) |
Adapted from Scott DW, Miller WH, eds. Equine Dermatology. 2nd ed. Maryland Heights, MO: Elsevier Saunders, 2011.
Treatment for primary photosensitization includes removal of the sensitizing agent and restricting the horse to stall confinement or to a stall with nighttime pasture access until the photosensitivity resolves. Alternatively, the use of fly sheets, masks, and boots to minimize UV light exposure may be sufficient in mild cases. Application of 30- to 55-SPF sunscreens may also be useful. The occasional horse may benefit from systemic glucocorticoids or nonsteroidal antiinflammatory agents; topical application of corticosteroids, pramoxine, or other soothing agents; and prevention and control of myiasis. Severely affected horses may need systemic antimicrobials for secondary bacterial infections and, rarely, debridement of affected areas.
Secondary or Hepatogenous Photosensitization
Hepatogenous photosensitivity is the most common type of photosensitization affecting horses and occurs secondary to hepatic injury. Hepatic injury results in increased phylloerythrin concentrations in the skin. Phylloerythrin is a degradation product of chlorophyll that is formed in the intestinal tract by enteric microorganisms and transported to the liver through the portal circulation. Phylloerythrin is subsequently absorbed by hepatocytes and excreted into the bile. When liver function has been compromised, the liver’s capacity to excrete phylloerythrin is similarly compromised, and phylloerythrin accumulates. Because phylloerythrin is a photodynamic agent, high levels in the skin render the animal photosensitive. Clinical signs generally develop when serum phylloerythrin concentrations are greater than 8.0 µg/dL. Hepatogenous photosensitization may occur from any disease process that results in severe liver damage and cholestasis, such as cholelithiasis, bacterial cholangitis, and parasite migration. However, hepatogenous photosensitization is most commonly caused by ingestion of toxic plants and mycotoxins (Table 128-2). The area in which the horse lives and the source of the hay that the horse consumes may provide clues to which toxin is responsible. For example, pyrrolizidine alkaloid toxicosis from ingestion of Senecio and Amsinckia spp is more prevalent in hay grown in the western United States, whereas alsike clover toxicosis is more common in hay from the Northeast. Horses will not usually eat hepatotoxic plants in a typical grazing situation if plenty of appropriate grasses and legumes are available.
TABLE 128-2
Causes of Hepatogenous Photosensitization
| Diseases | |
| Substance | Hepatotoxin |
| Plants | |
| Senecio jacobaea (tansy ragwort), S riddellii (Riddell’s groundsel), S douglasii (woolly groundsel), S vulgaris (common groundsel) | Pyrrolizidine alkaloids (retrorsine) |
| Amsinckia spp (tarweed, fiddleneck) | Pyrrolizidine alkaloids |
| Crotalaria spp (rattleweed) | Pyrrolizidine alkaloids |
| Echium plantagineum (Salvation Jane, Patterson curse) | Pyrrolizidine alkaloids |
| Heliotropicum europeaum (common heliotrope) | Pyrrolizidine alkaloids (lasiocarpine, heliotrine) |
| Cynoglossum officinale (hound tongue) | Pyrrolizidine alkaloids |
| Kochia scoparia (fireweed, burning bush) | Unidentified agent |
| Myoporum laetum (ngaio tree) | Ngaione |
| Lantana camara (lantana) | Lantadenes |
| Tribulus terrestris (goathead, puncture vine) | Unidentified agent |
| Nolina texana (bunchgrass, sacahuiste) | Unidentified agent |
| Narthecium ossifragum (bog asphodel) | Unidentified agent |
| Tetradymia canescens (horsebrush, rabbitbrush), T glabrata (spineless horsebrush, coal-oil brush) | Unidentified agent |
| Trifolium hybridum (alsike clover) | Unidentified agent |
| Medicago spp (Bermuda grass) | Unidentified agent |
| Holocalyx glaziovii (Alecrim) | Unidentified agent |
| Lippia spp (whitebrush) | Unidentified agent |
| Panicum antidotale (blue panicum), P coloratum (klein grass), P dichotomiflorum (smooth witchgrass), P maximum (guinea grass), P miliaceam (millet), P virgathum (switch grass) | Saponins (diosgenin, tamagenin, epismilagenin) |
| Agave lecheguilla (lecheguilla) | Saponins |
| Brachiaria brizantha (Australia grass), B decumbens (signalgrass), B humidicola, Brassica rapa (cabbage, kale) | Saponins |
| Mycotoxins | |
| Microcystis spp (blue-green algae in water) | Cyclic peptide |
| Phomopsis leptostromiformis (on lupins) | Phomopsins |
| Pithomyces chartarum (facial eczema, perennial ryegrass staggers, sporodesmin) | Unidentified agent |
| Lupinus spp (lupinosis, lupine) | Unidentified agent |
| Medicago sativa (moldy alfalfa) | Unidentified agent |
| Fusarium spp (moldy corn) | T-2 toxins |
| Aspergillus spp | Aflatoxin |
| Toxins and Chemicals | |
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