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primarily a condition of sheep, cattle and horses but other species may also be susceptible.  

primarily a condition of sheep, cattle and horses but other species may also be susceptible.  

The condition can be divided into two categories, primary and secondary photosensitisation. Primary photosensitisation occurs due to the ingestion of lush green plants containing photodynamic agents. Secondary (hepatogenous) photosensitisation is the most commmon type of photosensitivity seen in animals and occurs as a result of liver or bile duct damage. The photosensitising agent, phylloerythrin (a breakdown product of chlorophyll) accumulates in the blood, body tissues and skin due to insufficient conjugation and excretion by the liver. This accumulation in the skin leads to absorption and release of UV light, leading to a phototoxic reaction.

The condition can be divided into two categories; primary and secondary. Primary photosensitisation occurs due to the ingestion of lush green plants containing photodynamic agents. Secondary (hepatogenous) photosensitisation is the most commmon type of photosensitivity seen in animals and occurs as a result of liver or bile duct damage, often due to ingestion of hepatotoxic plants such as Ragwort. Due to insufficient hepatic conjugation and excretion, the photosensitising agent phylloerythrin (a breakdown product of chlorophyll) accumulates in the blood, body tissues and skin. This accumulation in the skin leads to absorption and release of UV light, resulting in a phototoxic reaction.

==Clinical signs==

==Clinical signs==

The history and clinical signs of affected animals are important in order to differentiate whether the condition is primary or secondary.  In the case of primary photosensitisation there is often a history of exposure to plants containing photodynamic agents such as St. John's Wort or clover. Alternatively, there may be a history of administration of drugs such as phenothiazines, sulphonamides or tetracyclines. Signs of liver disease are usually absent.

The history and clinical signs of affected animals are important in order to differentiate whether the condition is primary or secondary.  In the case of primary photosensitisation there is often a history of exposure to plants containing photodynamic agents such as St. John's Wort or clover. Alternatively, there may be a history of administration of drugs such as phenothiazines, sulphonamides or tetracyclines. Signs of liver disease are usually absent.

In contrast, in animals affected by secondary photosensitisation the classic skin lesions are accompanied by the signs of liver disease listed above. Serum biochemistry often reveals increased liver enzymes (ALP, GGT, SDH and ALT) but bilirubin and bile acid concentrations are usually normal. Ultrasonography may be useful in evaluating the hepatic structure and identifying pathological changes indicative of secondary disase. Definitive diagnosis may be obtained by liver biopsy.

In animals affected by secondary photosensitisation the classic skin lesions of the condition are often generalised rather than localised, and are accompanied by the signs of liver disease listed above. Serum biochemistry often reveals increased liver enzymes (ALP, GGT, SDH and ALT) but bilirubin and bile acid concentrations are usually normal. Ultrasonography may be useful in evaluating the hepatic structure and identifying pathological changes indicative of secondary disase. Definitive diagnosis may be obtained by liver biopsy.

==Treatment==

==Treatment==

Affected animals should be removed from pasture suspected to contain the photodynamic agent. Any drugs given at the time of the condition developing should be stopped. Affected animals should only be allowed access to grazing at night. Anti-inflammatory drugs such as flunixin meglumine and topical steroid creams may be useful to decrease the severity of cutaneous lesions in the acute stage of the disease.

Affected animals should be removed from pasture suspected to contain the photodynamic agent. Any drugs given at the time of the condition developing should be stopped. Affected animals should only be allowed access to grazing at night. Anti-inflammatory drugs such as flunixin meglumine and topical steroid creams may be useful to decrease the severity of cutaneous lesions in the acute stage of the disease.

If the animal is affected by secondary photosensitisation, a low-protein, high-energy diet rich in branched-chain amino acids such as beet pulp is recommended. Intravenous fluid therapy with 5% dextrose may be necessary in hypoglycaemic patients with signs of hepatic encephalopathy.

If the animal is affected by secondary photosensitisation supportive treatment should be provided. A low-protein, high-energy diet rich in branched-chain amino acids such as beet pulp is recommended. Intravenous fluid therapy with 5% dextrose may be necessary in hypoglycaemic patients with signs of hepatic encephalopathy. Severely affected animals with liver failure carry a grave prognosis and are not usually treatable.

Secondary bacterial infections of cutaneous lesions are common and should be treated with antimicrobials and correct wound management. Lesions generally heal well, and surgical debridement is reserved for only the most severly necrotic lesions.

Secondary bacterial infections of cutaneous lesions are common and should be treated with antimicrobials and correct wound management. Lesions generally heal well, and surgical debridement is reserved for only the most severly necrotic lesions.