About Facial Eczema
Facial eczema (FE) is a type of sunburn (sometimes called photosensitisation) affecting exposed areas of pale skin of cattle. It is caused by a poisonous substance called "sporidesmin" that causes liver damage. Sporidesmin is produced on pasture plants, including rye grass, by a fungus called Pithomyces chartartum. This fungus is widely distributed and occurs naturally within dead plant material at the base of standing pasture. The fungus producing sporidesmin is normally not visible to the naked
eye. It multiplies by producing millions of spores which are coated with the
toxin sporidesmin.
FE has been recorded in sheep and cattle on mainland south eastern Australia. These cases appear to be rare, sporadic and vary between years. Although no cases of FE have been reported in Tasmanian sheep, the Department has identified a number of suspect cases in Tasmanian dairy herds. The disease is seasonally common in New Zealand.
Signs of disease
The disease may be seen in stock between several days and several weeks following pick-up of sporidesmin from the pasture. The toxin is absorbed from the intestine and reaches the liver, where it causes severe damage to bile ducts and liver cells. All the outward signs of FE result from the liver damage caused by sporidesmin.
The signs of FE range from mild photosensitisation (sunburn) to severe jaundice and death, depending on the amount of sporidesmin consumed. Sunburn is the most consistent sign, and usually affects the exposed areas of the skin of the face, ears, teats, and vulva, and areas of skin lacking dark pigmentation, ie. areas covered by white hair. The skin over these areas becomes reddened, and then goes crusty and dark. It eventually peels off leaving large raw areas, which are susceptible to infections. The sunburn is often accompanied by watery swelling of the underlying tissues. Jaundice (yellowing of mucous membranes) is often seen at this stage.
Affected animals lose weight rapidly. Most animals recover from the acute phase, but tend to be unthrifty, often taking many months to regain condition. Some never recover, and either die or are culled. In dairy cattle, the udder and teats are often severely affected, and milk production drops sharply. Loss of weight and general illness are often severe, and death, although uncommon, can occur sometimes months after the initial liver damage occurs.
Occurrence
Outbreaks of FE typically occur when weather conditions suitable for
rapid fungus growth and spore production are combined with abundant dead,
recently killed plant material, which favours fungal growth. The fungus
requires warm, humid weather and light rain (or irrigation) for growth. This is
most likely to be a problem in autumn when the summer has been hot and dry, the
pasture well eaten back, and rains fall when the ground is still warm. In such
conditions both pasture and grass grow rapidly.
The fungus will grow on most pasture plants, but it grows best on perennial
ryegrass. It grows in the dead pasture litter at the base of the plants. When
the fungus reaches toxic levels, animals grazing short pasture at high stocking
rates are at greatest risk. Freshly produced
spores are the most toxic; if fungal growth stops after a change in the
weather, the residual spores on the pasture lose their toxicity within one or
two weeks.
Prevention and control
It is important to. Although the basis of
prevention of FE is stock management, one of the difficulties in preventing FE
is predicting the occurrence of the disease. During high risk periods or during
an outbreak, the following actions may help to minimise the intake of toxic
pasture:
Shift stock to the longest pasture possible, and try to avoid very
close grazing.
Avoid paddocks cut for hay or late-topped. These are likely to be
more toxic because of greater quantities of pasture litter. If topping
must be carried out, ensure topped material is removed.
In general, paddocks sheltered by windbreaks or hills are more
dangerous and should be avoided.
It is believed that warmer northern slopes may carry higher spore
numbers and should be avoided in favour of cooler southern slopes during
outbreaks.
Feed hay or other supplements to preserve ground feed and minimise
close grazing of pasture. Don't push stock to eat into the base of the
sward where spore concentration is highest.
Summer-growing crops are generally safer than pastures, and stock
should be given as much access to these as possible where they are
available.
On irrigated farms, if pasture is short and grazing pressure is
heavy, farm irrigation may be valuable if used immediately.
Alternate grazing between native and improved pastures if feasible.
Fungicides have been used in New Zealand where FE
commonly occurs, but probably cannot be justified economically in Australia.
High doses of zinc can be used to reduce liver damage and production losses,
however this must be administered at the time of, or before, animals ingest
sporidesmin. Daily drenching, in-feed and drinking water have been used to
administer zinc. Slow-release intra-rumen zinc boluses are also used overseas,
but are currently not available in Australia. There are potential side effects
with prolonged zinc dosing and these should be discussed with your
veterinarian.
Monitoring of pastures by undertaking spore counts is used in some countries to
provide an early warning system.
Treatment
If FE is suspected, a veterinary practitioner should be called promptly. Although there is no primary treatment for FE, a veterinarian will be able to provide supportive treatments, such as antibiotics to control secondary infections and provide advice on longer term care of affected stock.
Importantly, affected animals should be sheltered from direct sunlight if possible. In dairy herds, affected cows should be dried off and shifted to low-risk pasture to ensure recovery and satisfactory future production.
Further information
For further information on this condition, contact your veterinary practitioner or NRE Tas at: