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Spotlight on: Photosensitisation in livestock

What is Photosensitisation?

Photosensitisation arises when sensitive skin becomes highly susceptible to UV light. All livestock species, breeds and classes can be affected by photosensitisation, although it is most evident in livestock with unpigmented (white/pink) skin, recently shorn sheep and young lambs.

Areas exposed to sunlight and lacking protective hair, pigmentation or wool cover are most vulnerable.





There are 2 types of photosensitisation:

1. Primary Photosensitisation

Primary Photosensitisation results from animals grazing plants containing light sensitive (photosensitising) compounds. Following their ingestion, these compounds accumulate in the blood vessels at the surface of the skin. Sun exposure activates these compounds into toxins causing local tissue death and swelling. This results in intense irritation and serious skin damage. This form of photosensitisation usually occurs with ingestion of lush, rapid growing plants that are the dominant species in a pasture. Clinical signs are usually noted 3-5 days after access to the toxic plants. This type of photosensitisation is often associated with livestock grazing:

i) St John’s wort (Hypericum perforatum)

St John’s wort is easily identified by its characteristic yellow flowers, each with 5 petals. Though animals will only graze it if other feed is scarce, St John’s wort competes with useful plants in pastures and can expand in size rapidly. St John’s wort contains the photosensitising toxin hypericin, and is most potent in Spring once in full flower with stems exceeding a height of 5-10cm. Seeds of St John’s Wort are prolific in the environment and spread by water, wind, livestock or feral animals. The roots can also grow fragments, resulting in spread during crop cultivation unless roots are brought to the surface.






ii) Buckwheat (Polygonum fagopyrum)

Recognisable by its petite white flowers, the leaves of the Buckwheat plant are thought to contain the most potent levels of photosensitising compounds.






iii) Perennial ryegrass (Lolium perenne)





2. Secondary (hepatogenous) photosensitisation

Secondary photosensitisation occurs as a secondary result following liver damage, which can occur following the consumption of toxic plants. When chlorophyll (the green pigment in plants) is broken down in the liver, the compound phylloerythrin is produced. This product is normally excreted in the bile produced by the liver. When the liver is damaged or the biliary system gets blocked, phylloerythrin cannot be excreted and accumulates in the bloodstream. Once it reaches levels in the skin that make it sensitive to light it results in subsequent photosensitisation.

Secondary photosensitisation can be associated with grazing of:

i) Hairy Panic (Panicum effusum)

Characterised by the ‘hairy’ appearance of leaves, leaf sheaths and nodes. Hairy Panic is a short-lived perennial grass standing up to 0.5m high. It is highly drought tolerant and in abundance in native pastures, woodlands and undisturbed areas such as roadsides. If eaten in large quantities it can cause photosensitisation.











ii) Caltrop (Tribulus terrestris)

iii) Sweet grass (Panicum laevifolium)

iv) Heliotrope (Heliotropium europeaum)

v) Lantana (Lantana camara)

vi) Patterson’s curse (Echium plantagineum)

Clinical Signs

Only the areas of skin exposed to sunlight will be affected. In sheep, the face, ears and muzzle are worse affected. Although any recently shorn areas and lambs (who have thinner skin) are also susceptible. Cattle may display signs on the udder, vulva and in any white areas of skin.

The extent of damage depends on the amount and type of plant ingested, stage of plant growth and degree of sun exposure. Clinical signs of primary photosensitisation appear within 3-5 days of plant ingestion. In comparison, signs of secondary photosensitisation may not occur until weeks after exposure to toxic plants.

Classic signs include:

  • Reddened, crusty, weeping skin
  • Severe swelling of the ears, eyelids, lips and nose. This swelling may result in distinctive ear drooping, swelling below the jaw, difficulty eating (if lips are swollen) and breathing (if the nostrils are swollen shut)
  • Shade-seeking behaviour
  • Restlessness, irritation, rubbing and shaking of the head and ears
  • Resentment to feeding of lambs and calves
  • Watery/weeping eyes with increased squinting, some animals may appear blind if they are not able to close their eyes due to damage of the eyelids
  • In severe cases the skin may slough and scab
  • Some animals may die due to extensive tissue damage and shock
  • Neurological signs may include unsteady gait, weakness in the hind limbs, depression or in some cases excitement
  • Jaundice (yellow appearance of gums, skin and whites of eyes) may be evident in secondary photosensitisation



A diagnosis of photosensitisation is based on clinical signs, a history of toxic plant exposure and characteristic lesions on unpigmented skin. Shade-seeking or agitated behaviour strengthens this association. If an animal is suffering from suspected liver damage, blood tests for liver function or post-mortem examination can confirm the diagnosis. The disease must be distinguished from other causes of dermatitis, rain scald or bighead in rams. 

Treatment & Prevention

The prognosis for secondary photosensitisation or severe clinical signs is poor, although mild episodes of primary photosensitisation can recover in a few days. Treatment primarily focuses on palliative measures. Affected livestock should be immediately removed from toxin exposure and housed in full shade, preferably in dark sheds. Secondary bacterial skin infections should be bathed and treated to prevent fly strike contamination. Most skin lesions will heal well with basic nursing care. Cereal hay or lower quality pasture hay should be provided to minimise consumption of chlorophyll. Veterinary advice must be sought for severe cases, as euthanasia must be considered for livestock with extensive tissue damage.

Prevention of photosensitisation centres on the removal of toxic plant species from grazing pastures. Ensuring root fragments are destroyed during crop cultivation will minimise the growth of toxic plants to potent levels. Regular pasture examination will minimise the growth of dangerous species, and supplementary feeding in instances of low ground cover will reduce the likelihood of preferential grazing.

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