Photosensitization is an increased susceptibility of skin to damage caused by ultraviolet light. Agents that cause the hypersensitivity include a variety of plant compounds, aberrant pigments, and compounds that accumulate after aberrant hepatic metabolism. Affected animals are photophobic and develop skin bullae, ulcers, and necrosis. Diagnosis is based on signalment and clinical signs, along with measurement of porphyrins in blood, urine, and feces. Treatment is primarily supportive and palliative care.
Photosensitization occurs when skin (especially areas exposed to light and lacking significant protective hair, wool, or pigmentation) becomes more susceptible to ultraviolet light because of the presence of photodynamic agents. Photosensitization differs from sunburn and photodermatitis, because both of these conditions result in pathologic skin changes without the presence of a photodynamic agent.
In photosensitization, unstable, high-energy molecules are formed when photons react with a photodynamic agent. These high-energy molecules initiate reactions with substrate molecules of the skin, causing the release of free radicals that in turn result in increased permeability of outer cell and lysosomal membranes. Damage to outer cell membranes allows for leakage of cellular potassium and cytoplasmic extrusion. Lysosomal membrane damage releases lytic enzymes into the cell. This can lead to skin ulceration, necrosis, and edema. The time interval between exposure to the photodynamic agent and the onset of clinical signs depends on the type of agent, its dose, and the exposure to sunlight.
Photosensitization is typically classified according to the source of the photodynamic agent. These categories include primary (type I) photosensitivity, aberrant endogenous pigment synthesis (type II) photosensitivity, and hepatogenous (secondary, type III) photosensitivity. A fourth category termed idiopathic (type IV) photosensitivity has been described.
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 animals are plant-derived. Photosensitization occurs worldwide and can affect any species but is most commonly seen in cattle, sheep, goats, and horses.
Primary Photosensitization in Animals
Primary photosensitization occurs when the photodynamic agent is either ingested, injected, or absorbed through the skin. The agent enters the systemic circulation in its native form, where it results in skin cell membrane damage after the animal is exposed to ultraviolet light. Examples of primary photosensitizing agents include 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 photosensitizing agents. Many other plants have been suspected, but the toxins responsible have not been identified (eg, Cynodon dactylon [Bermudagrass]).
Additionally, coal tar derivatives such as polycyclic aromatic hydrocarbons, tetracyclines, and some sulfonamides have been reported to cause primary photosensitization. Phenothiazine anthelmintics have been reported to cause primary photosensitivity in cattle, sheep, goats, and swine.
Aberrant Pigment Metabolism in Animals
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 ( see Congenital Erythropoietic Porphyria Congenital Erythropoietic Porphyria ) and bovine erythropoietic protoporphyria ( see Cutaneous Manifestations of Multisystemic and Metabolic Defects in Animals Cutaneous Manifestations of Multisystemic and Metabolic Defects in Animals ) are the most commonly reported diseases in this category.
Secondary (Hepatogenous) Photosensitization in Animals
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 plasma because of 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 in Animals Facial eczema, also known as sporidesmin toxicosis and pithomycotoxicosis, is a disorder of grazing livestock caused by the fungus Pithomyces chartarum growing on dead plant material... read more ; lupinosis Mycotoxic Lupinosis in Animals Lupinosis is a liver disease or hepatotoxicosis caused by ingestion of lupine plants infected with Diaporthe toxica (previously identified as Phomopsis leptostromiformis). Lupinosis... read more ; congenital photosensitivity Congenital Photosensitization in Sheep Southdown and Corriedale sheep may inherit a hepatobiliary incompetence that results in photosensitization. In mutant Southdown sheep, the inherited defect involves hepatic uptake of unconjugated... read more of Southdown and Corriedale 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 alkaloids Pyrrolizidine Alkaloidosis (eg, Senecio spp, Cynoglossum spp, Heliotropium spp, Echium spp)
cyanobacteria (Microcystis spp, Oscillatoria spp)
Nolina spp (bunch grass)
Agave lechuguilla (lechuguilla)
Tetradymia spp (horse brush or rabbit brush)
Trifolium pratense and T hybridum (red and alsike clover)
Phylloerythrin is likely the phototoxic agent in many of these poisonings.
Type IV Photosensitivity in Animals
Photosensitivity in which the pathogenesis is unknown or the photodynamic agent is not identified is classified as type IV. One such example involved a case of primary photosensitivity in cattle presumed to be caused by Thlaspi arvense (field pennycress), even though field pennycress has not been reported to cause photosensitization. Outbreaks of photosensitization have been reported in cattle exposed to water-damaged alfalfa hay, moldy straw, and foxtail-orchardgrass hay. These cases were suspected to be hepatogenous in origin. Ranunculus bulbosus (buttercup) has also been presumed to be a cause of hepatogenous photosensitization. Other plants associated with photosensitization include winter wheat (cattle), Medicago spp (alfalfa), Brassica spp (mustards), and Kochia scoparia (fireweed). Many of these plants are believed to be type I photosensitizers. Forages such as oats, wheat, and red clover have been suspected in cases of photosensitization and may be associated with specific environmental conditions such as heavy rainfall.
Clinical Findings and Lesions of Photosensitivity in Animals
Dermatologic signs associated with photosensitivity are similar regardless of the cause. Photosensitive animals are photophobic immediately when exposed to sunlight and appear agitated and uncomfortable. They may scratch or rub lightly pigmented, exposed areas of skin (eg, ears, eyelids, muzzle).
Lesions initially appear in white-haired, nonpigmented, or hairless areas such as the nose and udder. However, 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, lesions may progress to include vesicle and bulla formation, serum exudation, ulceration, scab formation, and skin necrosis.
The final stage involves skin sloughing. In cattle, and especially in deer, exposure of the tongue while licking may result in glossitis, characterized by ulceration and deep necrosis. Irrespective of coat color, cattle may develop epiphora, corneal edema, and blindness.
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 Congenital Erythropoietic Porphyria Congenital erythropoietic porphyria (CEP) is a rare, hereditary disease of cattle, pigs, cats, and people that results from a significant yet variable decrease in uroporphyrinogen III synthase... read more , discoloration of dentin, bone (and other tissues), and urine often accompanies the skin lesions. Photodermatitis is the sole manifestation seen in bovine erythropoietic protoporphyria.
Diagnosis of Photosensitivity in Animals
Based on signalment and clinical signs, confirmed by measuring porphyrin in blood, urine, and feces
Diagnosis of photosensitization is based on clinical signs, evidence or history of exposure to photosensitizing agents or hepatotoxins, and characteristic lesions. Photophobia in combination with erythema and edema of hairless, nonpigmented areas of skin is strongly suggestive of the disease. The period from exposure to photodynamic or hepatotoxic agents to the onset of clinical signs can vary from several hours up to 10 days. Clinical signs; increased serum biochemical measurements, including sorbitol dehydrogenase, gamma glutamyltransferase, alkaline phosphatase, and direct bilirubin; and gross or histologic signs of liver disease help support a diagnosis of hepatogenous photosensitization. A presumptive diagnosis of porphyria is based on signalment (sex, breed, age) combined with clinical signs, and a definitive diagnosis can be made by measuring porphyrin levels in blood, feces, and urine.
Treatment of Photosensitivity in Animals
Palliative and supportive care
The prognosis for animals with hepatogenous photosensitization and porphyria is poor; however, the prognosis for animals with primary photosensitization is generally good. 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.
Photosensitization is caused by production or ingestion of photodynamic agents, which lead to increased susceptibility to skin damage following exposure to sunlight.
Secondary (type III) photosensitization caused by abnormal hepatic metabolism of phylloerythrin is the most common type seen in livestock.
For More Information
Also see pet health content regarding photosensitization in dogs Photosensitization in Dogs Photosensitization is a clinical condition in which skin is oversensitive to sunlight; this condition is not sunburn. Certain molecules present in the skin are energized by light. When the molecules... read more and photosensitization in cats Photosensitization in Cats Photosensitization is a condition in which skin is overly sensitive to sunlight; it is not the same as sunburn. Certain molecules present in the skin are energized by light. When the molecules... read more .
Photosensitization is a serious skin condition in horses and cattle caused by a hazardous combination of certain plants and ultraviolet (UV) light. Certain plants contain photodynamic agents, which then cause a reaction in the animal's body that leads to ultra-sensitive skin.Which pigment is responsible for Photosensitization? ›
The photosensitizing agent, phylloerythrin (a porphyrin), accumulates in plasma because of impaired hepatobiliary excretion. Phylloerythrin is derived from the breakdown of chlorophyll by microorganisms present in the GI tract.What causes the liver dysfunction that results in photosensitization? ›
It occurs following liver damage from consuming plant toxins. In all cases the photosensitising compound is phylloerythrin, produced in the breakdown of chlorophyll in the gastrointestinal tract. Normally, phylloerythrin is absorbed into the blood, then removed by the liver and excreted in the bile.How do you treat photosensitivity in horses legs? ›
Typically, treatment for photosensitivity starts by taking the horse off all pasture that may contain alsike clover or other phototoxic plants and keeping him indoors, shielded from the sun, until his skin heals.What is Photosensitization explain with example? ›
photosensitization, the process of initiating a reaction through the use of a substance capable of absorbing light and transferring the energy to the desired reactants.What is for examples of Photosensitization? ›
The type of photosensitivity produced due to direct ingestion of photodynamic substances or metabolically activated agents is called primary photosensitization For example, plants belonging to species such as Hypericum (Fig. 15.14), Fagopyrum (Fig. 15.15), and Parthenium produce primary type of photosensitivity.What is the most common type of photosensitization? ›
Secondary (Hepatogenous) Photosensitization in Animals. Secondary or type III photosensitization is by far the most frequent type of photosensitivity observed in livestock.What are the two types of photosensitizing reactions? ›
Photosensitized reactions involving oxygen are framed as either as type I or type II. Type I and II photosensitized oxidation reactions require oxygen as a reagent. The type I and II photosensitized mechanisms apply to photoreactions including initial electron or hydrogen atom abstraction as an oxidizing step.What is the importance of photosensitized reaction? ›
In this sense, PAS is an excellent tool for studying the photophysical properties of the drugs and their interaction with biological molecules. The photophysical properties of the photosensitizers are usually monitored to determine the efficiency of the treatments.What organ is damaged with secondary photosensitization? ›
Photosensitisation is inflammation of the skin, and occasionally the conjunctiva and cornea of the eye. Primary photosensitisation can arise as a result of eating a range of plants that contain photosensitising substances. Secondary photosensitisation occurs as a result of liver damage.
Photosensitization is a condition caused by the accumulation of a photodynamic agent in the skin that sensitizes it to ultraviolet radiation (Fowler 1993). Exposure of nonpigmented skin to UV radiation (e.g., the sun) results in dermatonecrosis.
(Examples by Generic Name)
- Coal Tar and Derivatives.
- Contraceptives, Oral and Estrogens.
- Non-Steroidal Anti-Inflammatory Drugs.
To treat chemical photosensitivity reactions, corticosteroids are applied to the skin and the substance that is causing the reaction is avoided. Solar urticaria can be difficult to treat, but doctors may try histamine (H1) blockers (antihistamines), corticosteroids applied to the skin, or sunscreens.How can skin photosensitivity be reduced? ›
Sun protection basics
Wear a broad-brimmed hat and sun-protective clothing. Use a broad-spectrum sunscreen with an SPF of at least 30 on all exposed skin. Don't forget the backs of your hands and reapply sunscreen every two hours. Find sunscreen products with our Seal of Recommendation.
- Gradually increase light exposure. ...
- Get rid of fluorescent light bulbs, and be wary of LEDs too. ...
- Fully open your window blinds (or close them altogether) ...
- Double check your medications. ...
- Wear sunglasses with polarization when outside.
A condition in which the skin becomes very sensitive to sunlight or other forms of ultraviolet light and may burn easily. Photosensitivity usually causes a rash or sunburn, especially on areas of the skin that are exposed to ultraviolet light. The affected areas may be painful and may itch, blister, or peel.Which of the following characteristics is correct for good photosensitizer? ›
The ideal photosensitizer would be a chemically pure drug with specific uptake by the target tissue, minimal dark toxicity (i.e., activated only upon irradiation), high photoactivity (high quantum yield of ROS), rapid clearance to avoid phototoxic side effects, and strong absorption at relatively long wavelengths (∼630 ...Which of the following is used as a photosensitizer *? ›
Anthraquinones (AQs, Figure 12) have been used as dyes, antibiotics, solar energy-storing materials and photosensitizers. Some of these compounds have a high yield of triplet states upon excitation by light, and form reactive oxygen species (ROS), including singlet oxygen.What are the different types of photosensitivity? ›
Photosensitive conditions are classified into five categories, which include primary or autoimmune photodermatosis, exogenous or drug/chemical-induced photodermatosis, photo-exacerbated or photo-aggravated dermatoses, metabolic photodermatosis, and genetic photodermatosis.What type of reaction is photosensitivity? ›
Photosensitivity, sometimes referred to as a sun allergy, is an immune system reaction that is triggered by sunlight. Sunlight can trigger immune system reactions. People develop itchy eruptions or areas of redness and inflammation on patches of sun-exposed skin. The diagnosis is usually based on a doctor's evaluation.
When a drug induces photosensitivity, exogenous molecules in the skin absorb normally harmless doses of visible and UV light, leading to an acute inflammatory response. In phototoxic reactions, the damage to tissues is direct; in photoallergic reactions, it is immunologically mediated.What is the difference between phototoxicity and photosensitivity? ›
|Onset after exposure||Minutes to hours||24-48 hours|
|Dose of agent needed for reaction||Large||Small|
A catalyst does not change in itself or being consumed in the overall chemical reaction. This definition includes photosensitization, a process by which a photochemical alteration occurs in one molecular entity as a result of initial absorption of radiation by another molecular entity called the photosensitized.What is an example of a photochemical reaction? ›
What is a photochemical reaction example? Photosynthesis: plants convert carbon dioxide and water into glucose and oxygen using solar energy. Human vitamin D production by sunlight exposure. Bioluminescence: for example, Luciferase an enzyme in the abdomen catalyses a light-producing reaction in fireflies.What are photosensitizers explain photosensitized reaction *? ›
Photosensitization is a reaction to light that is mediated by a light-absorbing molecule, which is not the ultimate target. Photosensitization can involve reactions within living cells or tissues, or they can occur in pure chemical systems. In photobiology, we are concerned with the reactions in living systems.What is photosensitized oxidation? ›
Photosensitized oxidations are involved in a multitude of phenomena triggered by the excitation of photosensitizer molecules by light, yielding excited states and other reactive species that ultimately elicit oxidative reactions.What are the laws of photochemistry? ›
The law may be stated as: “When light falls on any substance, only a fraction of it is absorbed whereas the rest is either reflected or transmitted. It is only the absorbed light which is effective in bringing about a chemical reaction.”What disease increases photosensitivity? ›
Chronic Actinic Dermatitis
Chronic actinic dermatitis (CAD) is a photosensitivity disorder in which outbreaks of eczematous rashes develop most often on exposed skin. Patients suffering from the disorder often suffer form papules, or inflamed bumps, and plaques, which are scaly, raised patches of skin.
Photosensitivity is an extreme sensitivity to ultraviolet (UV) rays from the sun and other light sources. Most people are at risk of developing sunburn during long exposure to sunlight. Exposure to UV rays can also lead to skin damage and skin cancer.Which of the following drugs may cause photosensitivity? ›
- Alpha-hydroxy acids in cosmetics.
- Antibiotics (ciprofloxacin, doxycycline, levofloxacin, ofloxacin, tetracycline, trimethoprim)
- Antifungals (flucytosine, griseofulvin, voricanozole)
- Antihistamines (cetirizine, diphenhydramine, loratadine, promethazine, cyproheptadine)
“Photosensitivity generally presents as a rash,” she says. “It may look like a sunburn or eczema. Blistering may be present, and affected areas may be hot or painful.”What causes photosensitivity in cattle? ›
Photosensitivity reactions in cattle occur when light reactive plant components (called phototoxins) enter the skin and are exposed to ultraviolet light. The phototoxin reacts to UV in light coloured or thin-skinned or hairless areas such as around the eyes, nose or teats.How do you protect photosensitive drugs? ›
Protect from light. Store the vial in the original carton to protect from light. Keep ampules in package until time of use. Drug can be stored in a syringe for up to 8 hours prior to administration but must be protected from direct sunlight.What antibiotic class causes photosensitivity? ›
Although sulfonamide antibiotics are safe in terms of photosensitivity, sulfur-containing diuretics and diabetic drugs are the common culprits. Sulfamethoxazole, a component of the commonly used antibiotic cotrimoxazole, has been implicated as a cause of phototoxicity, as well as dapsone.What vitamins help with photosensitivity? ›
Vitamin B6 has been used to successfully reduce reactions to sunlight. Cases have been reported of people with photosensitivity who responded to vitamin B6 supplementation. Amounts of vitamin B6 used to successfully reduce reactions to sunlight have varied considerably.What deficiency causes sun sensitivity? ›
If you do not get enough of some nutrients, your skin can become sensitive to sunlight. Pellagra, for example, is caused by a niacin deficiency and leads to photosensitivity. Other nutrients, particularly antioxidants and flavonoids, may help protect skin against sun damage in healthy people.Can vitamin D help with photosensitivity? ›
Vitamin D deficiency is more common in people with photosensitivity due to their efforts to avoid sun exposure. Oral vitamin D supplementation (2000 or 5000 IU per day) is inexpensive and should be prescribed for these patients.How can photosensitivity be improved? ›
Staying out of sunlight and keeping the lights dimmed inside can help make photophobia less uncomfortable. Keeping your eyes closed or covering them with dark, tinted glasses can also provide relief.How do you prevent Photodermatitis? ›
- Limit sun exposure, especially intense midday sun.
- Use PABA-free sunscreens that protect against UVA and have a sun protection factor (SPF) of 30 to 50.
- Cover up with a long sleeved shirt, long pants, and a wide brimmed hat.
- Beware of using any product that causes sun sensitivity.
If you're naturally sensitive to light, avoid bright sunlight and other harsh lighting sources. Wear wide-brimmed hats and sunglasses with ultraviolet (UV) protection when outdoors in daylight. Also, consider wearing eyeglasses with photochromic lenses.
In general, riboflavin deficiency causes aversion to light (photophobia), inflammation of the mouth, face, and tongue (glossitis), excessive oiliness of face and scalp (seborrhea), and angular stomatitis (fissures and inflammation of the lower lip).Can photosensitivity reversed? ›
Adverse photosensitivity responses to drugs occur predominantly as a phototoxic reaction which is more immediate than photoallergy, and can be reversed by withdrawal or substitution of the drug.What is photosensitivity in biology? ›
Photosensitivity is an abnormal cutaneous reaction to solar ultraviolet radiation. This reaction may clinically manifest as greater propensity toward sunburn or development of a rash upon exposure to solar radiation.What is Photosensitisation in cattle? ›
Photosensitisation occurs when the skin becomes extremely sensitive to sunlight, leading to what is effectively very severe sunburn, even in cloudy conditions. It is very painful, and affected animals may be dull and depressed, or show signs of pain and irritation in the affected areas.What can trigger photosensitivity? ›
Examples of Triggers
Intense strobe lights like visual fire alarms. Natural light, such as sunlight, especially when shimmering off water, flickering through trees or through the slats of Venetian blinds. Certain visual patterns, especially stripes of contrasting colors.
Photosensitivity, sometimes referred to as a sun allergy, is an immune system reaction that is triggered by sunlight. Sunlight can trigger immune system reactions. People develop itchy eruptions or areas of redness and inflammation on patches of sun-exposed skin. The diagnosis is usually based on a doctor's evaluation.What are the five drugs that are attributed to photosensitivity? ›
- Coal Tar and Derivatives.
- Contraceptives, Oral and Estrogens.
- Non-Steroidal Anti-Inflammatory Drugs.
Secondary (Hepatogenous) Photosensitization in Animals. Secondary or type III photosensitization is by far the most frequent type of photosensitivity observed in livestock.Which areas of the body will be affected by photosensitisation in cattle? ›
Affected cattle may show skin damage along the back and on the sides of the udder, depending on where non-pigmented skin is located. Clinical signs are usually adequate for diagnosis but must be differentiated from sunburn.What causes photosynthesis in cattle? ›
Direct photosensitisation occurs when the chemical comes from a defect in the animals metabolism of its red blood cells, or, more commonly, from plants such as St. John's wort. Secondary photosensitisation occurs in animals with liver damage.
Because light sensitivity can be difficult to diagnose, there are two new diagnostic tools that have been introduced: the ocular photosensitivity analyzer (OPA) and the visual light sensitivity questionnaire-8 (VLSQ-8). The OPA is an automated instrument that determines your light sensitivity threshold.Does photosensitivity affect eyes? ›
But photosensitivity doesn't just affect skin. Your eyes can also become sun sensitive from using certain medications. This light sensitivity can cause inflammation, squinting, burning, excessive eye watering and can make going outside — even for a few moments or while it's overcast — difficult and painful.