Combating Facial Eczema In Dairy Herds

Facial Eczema (FE) is a disease which can have a significant impact on dairy cattle production and health. It appears in Gippsland in summer and early autumn and though not always easy to manage, there are useful strategies to help reduce the risk of cows ingesting large numbers of spores and in minimizing the effects of the disease if an outbreak occurs.

FE is a hepatogenous photosensitisation disease caused by mycotoxins sporidesmin, contained in spores produced by fungus which grows in the dead and dying litter of pastures. When ingested by ruminants it causes liver damage often resulting in severe dermatitis of light-skinned areas such as the face and udder. The photosensitivity presents as severe ‘sunburn’ to areas of non pigmented skin causing, redness, swelling and eventually a peeling of the skin.

The disease in Gippsland is usually seen during or after periods of warm, humid weather which favours fungal growth. It can occur in cattle of all ages but is particularly common in lactating dairy cows and young growing stock. FE quite commonly occurs on irrigated pasture in late summer or early autumn as a result of the growth of fungus, Pithomyces chartarum. Pithomyces chartarum lives in dead or dying vegetative matter in the bottom of pasture and in ideal conditions of warm, wet, humid weather, can grow quite rapidly producing spores which contain the toxin sporidesmin. Ingestion of this sporidesmin results in quite severe liver damage, which in turn sees an inability for the liver to process phylloerthrin and a photosensitive reaction to occur effecting the non pigmented areas of skin on the animal including the udder. Once the reaction is seen it is often too late and much of the damage has been done with many of the spores being ingested 10-20 days prior. Not all animals with liver damage show the photosensitive effects but some research suggests that for every animal that does, another 10 may have quite severe damage to its liver.

The disease is mainly associated with perennial ryegrass because of its ability to produce dead litter. The greatest concentration of spores, and hence the most toxic part of the pasture, tends to be at the base of the sward. Liver biopsies to determine amount of sporidesmin may be the only real way to determine a facial eczema event or a photosensitive reaction of another source. Mycotoxins from moulds found in silage and other feedstuffs can also have an effect on the liver presenting as a photosensitive reaction. Photosensitivity from grazing crops is not always as well defined and may be due to other bacterial or fungal toxins or if the crop is introduced too quickly into the diet. Using a toxin binder may help reduce the impact of these other micotoxins on the liver during FE.

Control & Prevention
FE can be a very unpredictable disease and hard to manage. There are a number of strategies available for control and prevention of FE including: a) Avoid the toxin; b) suppress the toxin; c) protect the animal with zinc if toxin is ingested; and d) breed for FE tolerance. Here are some tips which may assist.

It is important to note that the spores are produced into the lower section of the plant and require consecutive days of high minimum temperatures and humid conditions. Preventing over grazing at these times as best as possible can help limit exposure. By identifying pasture which may be toxic, you can adopt grazing strategies for reducing the likelihood of FE including selecting paddocks known to have lower spore counts, providing alternative feeds such as silage, hay and grain rations during danger periods and minimizing the build up of dead or dying litter (no topping of pasture). Toxicity of pastures can be reduced or minimized by spraying them with commercial fungicides. Be sure to check indication for use and applicable withholding. We also recommend commercial testing to monitor pasture spore count.

One of the most effective preventative measure to liver damage from FE is through Zinc inclusion in feed. Using a higher dose rate of Zinc Oxide in feed is very effective in the prevention of liver damage. Zinc Oxide must be fed prior to spore exposure and should be limited to no more than 100 consecutive days of feeding, as the dose levels required to be effective are very close to those toxic to the animal. Provided that correct procedures are followed and animals receive around 20mg elemental Zinc/kg liveweight/day, the risk of toxicity is minimal. However, administering Zinc acts as a preventative and not a cure. Cows that do show signs of FE including a rapid decline in milk production, shade seeking, presenting redness and irritation of the non pigmented sections of skin especially the udder, although too late to prevent these effects, must be looked after to limit further stress. These animals should be kept where there is adequate provision of shade and fed feedstuffs with low levels of chlorophyll such as hay. Application of appropriate ointments to affected areas can also assist.

Speak to our nutrition and sales representatives about your options. We also recommend that you seek additional advice from your veterinarian. Dairy Australia may also assist with further material on the disease - dairyaustralia.com.au