Photosensitisation in ruminants
Photosensitisation occurs in ruminants when a compound that reacts to light accumulates in the skin. These ‘photodynamic’ agents are altered by the action of UV light into highly unstable molecules which damage the skin. These compounds accumulate throughout the skin, however, sparsely haired and/or unpigmented skin are more likely to be affected because they are exposed to more UV light.
Acute cases of photosensitisation present with reddening and thickening of the skin; in some situations there can be irritation, pain or itchiness. Lesions will usually progress into oozing and ulcerative wounds, before affected skin is sloughed. Acute lesions can result in bacterial infections or fly strike, whilst chronic lesions can result in skin cancer. Wounds can take several months to heal, depending on the thickness of skin that has been lost.
There are two main types of photosensitisation: primary or secondary. Primary photosensitisation occurs when a ‘photodynamic’ agent is ingested, injected or absorbed through the skin. These compounds are circulated around the body via the bloodstream and accumulate in the skin, inducing photosensitisation when the animal is exposed to UV light. A large variety of plants are known or suspected to cause primary photosensitisation. Some plants include: St John’s Wort, buckwheat and some species of ryegrass, clover and lucerne. Several chemicals that are commonly used to treat animals can also result in the development of photosensitisation, such as tetracyclines and some sulphonamide antibiotics.
Secondary photosensitisation only occurs through the action of one ‘photodynamic’ agent: phytoporphoryn. Micro-organisms in the rumen convert chlorophyll, ingested in plants, into phytoporphoryn. Normally, this compound is metabolised by the liver and harmlessly excreted in the bile. However, any condition that damages the liver or impairs bile excretion can culminate in the collection of phytoporphoryn in the skin and consequently results in photosensitisation. Plants that produce toxins which affect the liver include Paterson’s curse, fireweed, and Lantana.
Liver abscesses, liver fluke, Leptospira infections in calves and neoplasia can also be associated with secondary photosensitisation. Due to the nature of this disease, other clinical signs often accompany photosensitisation as a result of the liver damage. Such signs include: weight loss, decreased milk production and jaundice.
Diagnosis of photosensitisation is simple, due to the characteristic nature and distribution of lesions. It is important to identify the underlying cause of any photosensitisation problem. Clinical pathology is often required to determine between the two types of photosensitisation. Liver enzymes and liver biopsy samples may be required to assess liver function. Prognosis for animals with primary photosensitisation is generally good. Whilst, the prognosis for those with secondary photosensitisation depends on the extent of liver damage; severely affected animals may die or are likely to suffer from reduced production for the rest of their lives.
Management and Prevention
There is no cure or antidote that alleviates the effects of photosensitisation; therapy involves identifying and removing the source of the photodynamic agent, or in the case of secondary photosensitisation, the toxin that is damaging the liver. Affected animals should be kept away from direct sunlight, in barns, and allowed to graze at night. NSAIDs (non-steroidal anti-inflammatory drugs) and antihistamines can be used to decrease pain and inflammation, whilst antibiotics are indicated if bacterial infections occur. Sun blocking ointments can be applied to affected areas, such as the teats, to minimise further damage.
Categories: Production Animals
Posted on 27th January 2021, last updated 22nd November 2021