Photosensitivity in Cattle

Photosensitivity in Cattle

This condition is primarily caused by compounds in the blood that react with sunlight, causing damage to the skin. There are 4 categories of photosensitisation (PS), however most clinical cases are seen to be caused by the same category (Type III).

PS occurs when skin (especially areas exposed to light and lacking significant protective hair, wool, or pigmentation) becomes more susceptible to UV light because of the presence of photodynamic agents (chemicals which increase susceptibility to UV light). PS differs from sunburn and photodermatitis because both of these diseases occur without the presence of a photodynamic agent.

In PS, unstable, high-energy molecules are formed when photons (in UV light) react with a photodynamic agent (present in the body usually as a result of ingestion). These high-energy molecules initiate reactions with substrate molecules of the skin, causing the release of free radicals (very reactive and highly charged particles). These free radicals in turn increase the permeability of outer cell and lysosomal membranes. The damage caused to the outer cell membranes releases lytic (breaking down) enzymes into the cell. This can lead to skin ulceration, necrosis and oedema. The time interval between exposure to the agent and the onset of clinical signs depends on the type and dose of the agent as well as the exposure to sunlight.

PS is classified typically according to the source of the photodynamic agent. These categories are:

1.       Type I : Primary Photosensitisation

2.       Type II : Aberrant Endogenous Pigment Synthesis Photosensitisation

3.       Type III : Hepatogenous (secondary) Photosensitisation

4.       Type IV : Idiopathic Photosensitisation

In general, the photodynamic agents are derived from plant material. The most affected species are cattle, sheep, goats and horses.

General Overview

Photosensitivity is caused by compounds in the blood react to sunlight. Liver function is the key.

Anything affecting the liver’s ability to metabolise or excrete harmful compounds predisposes an animal to photosensitivity. If the liver is not functioning, toxic compounds build up in the blood. When toxins reach the skin and react with sunlight, they cause photosensitisation.

The source of these compounds can be primary, through the animal’s diet or an inherited defect in the animal’s metabolism of its red blood cells; or secondary, due to liver damage from facial eczema, leptospirosis or anything that interferes with normal metabolism.
The main signs of photosensitivity include:

·         Twitching, flicking of ears and tail

·         Irritability, stomping and kicking at self

·         Swelling around the eyes, ears, udder and feet

·         Hair loss, reddening, thickening and peeling of affected skin

In order to diagnose the disease the clinical signs must be observed and if necessary, liver function can be assessed using a blood sample.

Type I: Primary Photosensitisation…

This occurs when the photodynamic agent is ingested, injected or absorbed through the skin. The agent enters the systemic circulation (bloodstream) in its native form, where it results in skin cell membrane damage after the animal is exposed to UV.

Examples of these agents include hypericin (from St. John’s Wort) and fagopyrin (from buckwheat). Coal tar derivatives such as polycyclic aromatic hydrocarbons, tetracyclines and some sulfonamides have been reported to also be agents. However, most of the time the agent is ingested and derived from plants.

Some phenothiazine anthelmintics have been implicated in causing some cases.

Type 2: Aberrant Pigment Metabolism

Type II PS is known to occur in cattle and cats. In this syndrome, the PS chemical agents are endogenous pigments (pigments produced in the body, from genes that hold their coding) that arise from inherited or acquired defective functions of enzymes involved in haem synthesis.

In other words, the substances in the blood that cause this type of PS to occur, are a result of faulty/mutated gene sequences which produce enzymes with incorrect functions, which usually help with producing haem substances (involved in blood), but instead will produce these harmful photodynamic agents.

Bovine congenital erythropoietic porphyria and bovine erythropoietic protoporphyria are the most common diseases seen in this category of PS.

Type 3: Secondary (Hepatogenous) Photosensitization

This PS is by far the most common.

The photosensitizing agent, phylloerythrin/PE (a porphyrin/chemical with a particularly circular structure) accumulates in the plasma because of impaired hepatobiliary excretion (hepato- meaning liver and biliary- referring to bile production and excretion).

PE is derived from the breakdown of chlorophyll by microorganisms in the GI tract. PE, but not chlorophyll, is normally absorbed into the circulation and is effectively excreted by the liver in the bile fluid. The lack of ability to complete this excretion of PE due to liver dysfunction of bile duct lesions increases the amount of PE in the general circulation. Thus, when it reaches the skin absorbs UV and starts the phototoxic reaction.

PE has been noted as the causal agent of PS in the following conditions: common bile duct occlusion; facial eczema; lupinosis; congenital PS and plant poisoning.

Type 4: Unknown

This is when neither the photodynamic agent nor cause can be identified.

Clinical Signs & Lesions

Dermatological signs associated with photosensitivity are similar regardless of cause.

Affected 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.

Severe phylloerythrinemia and bright sunlight can induce typical skin lesions, even in black coated animals. 

Erythema (raw, inflamed skin) develops rapidly and is soon followed by oedema (fluid). If exposure to light stops at this point, the lesions will soon resolve. If exposure is prolonged, lesions may progress to include vesicle and bulla formation, serum formation, serum exudation, ulceration, scab formation, and skin necrosis. The final stage involves the skin sloughing. In cattle and deer, exposure of the tongue when licking may result in glossitis, characterised by ulceration and deep necrosis.

Treatment

Animals affected with the Hepatogenous PS have poor prognosis; however, the prognosis for animals with Primary PS is generally good.

Treatment involves mostly palliative measures. While PS continues, animals should be shaded fully, or preferably housed and allowed to graze only during darkness. The severe stress of PS 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 preventions.

Primarily supportive therapy is usually the most achievable and necessary therapy.

Topical treatments with zinc oxide-based sunblock and necessary fly control should be used in both early and chronic cases.  Depending on the cause, antibiotics for secondary skin infection and/or prevention of hepatitis may be useful. Early use of anti-inflammatory drugs can reduce severity and improve welfare of the animal.

Prevention

Preventing PS depends on the cause. Facial eczema, spring eczema and certain plant ingestion are the 3 most common causes.

Facial Eczema causes PS and/or death due to liver injury. Humid conditions trigger growth and formation of fungal spores on pastures. These produce the toxin, sporidesmin, which when ingested, causes liver damage (especially to the bile system) and impairs the excretion of phylloerythrin.

At high-risk spore times it is important to make sure that cattle do not graze right down to the base level as this is where the spores are – to prevent this, rotation times can be increased. Spraying pastures with fungicide and using zinc salts in water troughs or zinc oxide for oral drenching can help give resistance against the toxin.

The cause of spring eczema is uncertain.

Maintaining vigilance on pastures to ensure the incidence of plants that may cause PS is relatively low can also help to reduce the number of cases seen.