Pithomycotoxicosis(facial eczema) of ruminants must hold centre stage in any consideration of pasture based mycotoxicoses. In New Zealand it is by far the most important mycotoxicosis and ranks as one of the most destructive diseases of sheep. Its occurrence is seasonal, with most cases occurring during the autumn. Severe outbreaks of the disease, such as that of 1981, occur about every 6 7 years. The 1981 outbreak was estimated to cost about NZ$58m or about 0.25% of GDP (1981 values). The 1999 outbreak affected 60% of NZ dairy herds and cost the dairy industry over $40m. The disease occurs typically in warm temperate climates. In New Zealand the disease occurs in the lowland warm areas of the North Island but occasionally extends south to the northern areas of the South Island. The disease also occurs in some coastal areas of SE and SW Australia and in southern areas of South Africa. There have been reports of what may be facial eczema from USA, Uruguay, Brazil, Columbia and most recently from France and the United Kingdom.
During the severe NZ outbreak of 1981 surveys showed that 69% of sheep and beef cattle farms had outbreaks of facial eczema. On these farms, clinical cases of facial eczema occurred on average in 3.3% of adult sheep, 3.4% of lambs and 0.2% of beef cattle. Facial eczema also occurs in deer and camelids, the latter are particularly susceptible.
The disease is a hepatogenous photosensitization caused by the hepatotoxin sporidesmin which is produced by the saprophytic fungus Pithomyces (Leptosphaerulina) chartarum. Under the warm moist conditions of autumn, Pithomyces chartarum proliferates on pasture litter producing the toxin sporidesmin. At sporulation the sporidesmin is translocated into the spore and it is consumed by ruminants especially under close grazing conditions.
P.chartarum is a cosmopolitan saprophyte. It lacks special nutrient requirements and appears to grow on a wide range of substrates. It has large characteristic spores (photo), a feature invaluable in the recognition of "hot" pastures. The spores are produced most freely between 20° and 24°C, especially when night minimum temperatures exceed 14°C and the humidity is close to 100%. As P.chartarum sporulates it produces sporidesmin; the amount of sporidesmin being produced is directly proportional to spore numbers. Sporulation appears to be enhanced by ultraviolet light and with most New Zealand strains this sporulation correlates well with sporidesmin production. However many South African and North American strains, although they spore freely don't seem to produce sporidesmin.
In the field, increases in spore numbers commonly occur after a fall of at least 4mm of rain followed by high grass minimum temperatures. A significant grass minimum of 12°C is often quoted but higher minimums eg. 16° to 18°C for two or more nights are more commonly associated with significant rises in spore numbers. Under such conditions rapid and significant rises in spore numbers can occur within 48 hours. It is generally recognised that several such climatic periods, by enabling several generations of spores to occur, are required before major "hot" periods arise.
These "hot" or "danger" periods are recognised by pasture spore counting, a technique which appears to work in NZ where most field isolates are sporidesmin producers. Although toxin estimates are technically feasible, a simple field test of toxin concentrations has yet to be produced. In the meantime the spore counting technique, possible because of the readily identifiable spore, is used to identify toxic pastures.
Spore counts of 100,000 or more per gram of grass are often considered to be dangerous. However it is not possible to be absolute about the "danger" level. Stocking rate, the closeness of grazing, the type of stock, the age of the spores, the length of time spent grazing the pasture and previous exposure to toxic spores are all important considerations. Breeds of ruminants, species of sheep and individual sheep vary in their resistance or susceptibility to sporidesmin. Of the sheep breeds, the Merino is the most resistant. The individual variation in resistance is inherited and this is now being exploited commercially.
a. The disulphide bridge of the mycotoxin is reduced by GSH (glutathione).
b. The product formed is unstable in the presence of oxygen and autooxidises back to the parent compound but in the process produces a superoxide radical.
c. Zinc treatment stabilises the molecule by binding at the –SH site and forming a stable mercaptide thus preventing auto-oxidation.
The sporidesmin is rapidly absorbed from the upper gut, and is concentrated in the liver and hepatic bile. Here the molecule undergoes a glutathione linked, copper catalyzed cycle of oxidation and reduction to produce the toxic free radical superoxide, and other free radicals (see figure). This superoxide radical production causes necrosis of the ductular epithelium in the early stages, later the ducts become occluded by fibrous tissue, causing obstruction of the bilary system. The resulting liver injury, particularly of the biliary system, blocks the excretion of phylloerythin, the breakdown product of chlorophyll.
Endogenous porphyrins, e.g. haemoglobin and myoglobin, accumulate giving the clinical condition of jaundice. The concentration of the major liver enzyme, gamma glutamyltransferase (GGT) is used in the diagnosis of the disease and in the selection of F.E. resistant animals.
see photosensitisation diseases, photos
see photosensitisation diseases
Clinical signs, history and pasture spore counts. Measurement of liver enzymes (GGT) can help confirmthe diagnosis.
Other causes of photosensitivity.
Affected animals should be kept in a dark shed and allowed to graze at night. For further information refer to the treatment of photosensitivity.
Breeds of ruminants, species of sheep and individual sheep vary in their resistance or susceptibility to sporidesmin. Of the sheep breeds, the Merino is the most resistant. The individual variation in resistance is inherited and this is now being exploited commercially.A knowledge of weather conditions favouring Pithomyces chartarum growth together with a knowledge of habitats known to produce high spore counts (eg. north facing slopes, ridges, near hedges) can help to identify "hot" locations and periods. Spore counting on a regional basis can identify danger periods accurately and when conducted by farmers even on a paddock to paddock basis, may help them to identify local "hot spots". Such knowledge, together with a knowledge of the grazing and management conditions leading to more spore consumption, can be used effectively to prevent the disease.
Spraying Pastures with Benzimidazole Fungicidesto Prevent Fungal Growth
On some high risk farms especially where valuable stock are grazed, the toxicity of pasture can be reduced or minimised by spraying pastures with benzimidazole fungicides.
The fungicides commonly used include benomyl (150g active ingredient/ha) and thiophanate methyl and thiabendazole (both 140 g/ha). It is usual to spray sufficient pasture to last livestock for 7 days. Sprayed pastures can remain safe for 6 weeks. Respraying must be carried out if more than 25mm of rain in a 24h period occurs within 3 days of spraying.
Fungicides may make "hot" pastures safe but stock should not graze within 5 days of spraying. Spore counting should be carried out to check the safety of pastures. Other methods of control can be combined with this method.
Administration of zinc salts at the time ruminants are exposed to pasture with high spore counts will reduce the amount of liver injury and hence the number of animals affected by facial eczema. The dose rates of zinc required to prevent facial eczema are high (20 to 30 times the daily zinc intake necessary to meet normal nutritional needs). Zinc does not prevent facial eczema if given after the Pithomyces spore or sporidesmin challenge, nor does it appear to have a therapeutic effect when given orally to animals with the photodermatitis of facial eczema. The protective effect increases with increasing dose rates of zinc but at a diminishing rate. The daily dose rate of zinc determined to give the best protective effect without zinc toxicity or residue problems is 25 mg Zn/kg/d. See notes on zinc dosing under zinc toxicity.
Zinc sulphatein drinking water
Despite initial reservations, this method has been shown to be particularly effective in preventing facial eczema in dairy cattle. The method does not work effectively for sheep.
Drenching with a zinc oxide slurry
This method has given effective control of facial eczema in sheep and more so in dairy cattle where frequent drenching is possible. The problem with sheep has been that while weekly dosing of zinc oxide has given effective control of facial eczema, it is not popular because of the impracticability of mustering and handling sheep at such intervals. Increasing the interval between doses to 2 weeks has given inconsistent results and at dose rates beyond this hypocalcaemia is a risk and in conditions of stress, salmonellosis may occur. The slurry is made by mixing zinc oxide and water to such a consistency that it will pass through a drenching gun but not such that it will settle out too quickly. Settling out and flowability problems have been improved by adding seaweed fertiliser to the mixture.
Some farmers have circumvented the problem of frequent mustering and drenching of sheep by adding zinc oxide to a feed to which the sheep have become accustomed. The zinc oxide powder or slurry is poured or shaken onto such feeds as chopped maize or hay which is then fed out in the paddock. Some animals may not get enough and some too much but the safety margin for zinc oxide should be sufficient to prevent a problem, certainly the risk of not protecting against facial eczema may be worse.
Pasture spraying with zinc oxide
This method has been used effectively for dairy cows. It has potential for sheep but when there is a lack of feed for sheep, most of the sprayed material is lost between the pasture plants. For dairy cows the system requires that the animals to be protected are concentrated for 24 hours on a small area previously sprayed with zinc oxide. The appropriate zinc oxide spraying rate depends on the efficiency of pasture utilisation. The harder the grazing pressure the higher the proportion of applied ZnO that is actually ingested by the animals. Disadvantages with this system lie in the increased risk of disease because of the higher stocking rates and the need to estimate the pasture utilisation to ensure correct zinc oxide spraying.
Zinc bullets
Intraruminal zinc capsules provide a sustained release of zinc for the prevention of facial eczema. The capsules are available for use in sheep and cattle. The serum zinc levels afford protection for 4 to 6 weeks depending on the species. The product needs to be administered correctly to avoid injury. The use in underweight animals or too frequent administration may cause zinc toxicity.
A practical long term solution to the facial eczema problem in sheep would be to breed animals with greater resistance to the disease. For years it has been plain to both researchers and farmers alike that individual sheep in any one affected flock may differ in their susceptibility to the disease. Ruakura workers have shown that there is an inherited resistance to the disease and that this may be exploited through selective breeding to create relatively resistant flocks. The heritability for susceptibility to facial eczema in sheep has been calculated to be 0.42, certainly high compared to other heritable traits for which selective breeding is undertaken.
In 1982 two flocks, a control and a selected flock were established to measure the rate of genetic progress obtained when rams were selected using a performance test developed by Ruakura staff. Rams are challenged with small doses of sporidesmin and subsequent liver injury is measured by examining serum Gamma glutamyl transferase (GGT) activities. Resistant rams show no elevation of serum GGT. An analysis of the flock data using modern population genetic techniques showed that after 5 years of selective breeding there were 15% more resistant animals in the selected flock than in the control flock. Such findings encouraged the development of a commercial FE resistant ram breeding scheme.
The following is a brief summary of how a performance testing programme to select facial eczema resistant ram lambs is conducted.
Rams are selected as potential flock sires, on the basis of the sheep plan post weaning selection test. It is important that such animals be kept grazing on entirely safe pastures until test challenged. The animals are then dosed with a commercially prepared extracted sporidesmin preparation (Stock Safeti Ltd, now MAFTech). Blood samples from each ram under test are collected before testing commences and at weekly intervals until the test is concluded. The first samples after challenge are taken at 10 14 days.
Blood GGT is then determined to identify which rams have liver damage. Those rams which have elevated GGT are withdrawn from the trial and given a score. Rams are ranked, within scores, on GGT levels. The first and highest rises in plasma GGT indicate sensitivity to sporidesmin, while rams with the last and lowest rises in GGT are selected as the more resistant animals. The test is continued until the desired number of animals to be culled has been identified by their elevated GGT levels.
The welfare aspects of this technique need to be carefully watched and rams which are under test must be provided with adequate shade, water and good feed.
Having assisted in the initial establishment of a commercially based FE resistant sheep breeding scheme (Stock Safeti), MAFTech have purchased this business and are operating the now improved scheme under the MAFTech RAMGUARD banner. This business is operating from Ruakura Agricultural Centre and utilises MAFTech consultants and private veterinarians for the field aspects of the operation.Briggs, L.R. Towers, N.R. and Molan, P.C. (1993). Sporidesmin and ELISA technology. N Z vet J. 41:220.
Munday, R. Thompson, A.M. Fowler, E.A. Wesselink, C. Smith, B.L. Towers, N.R. O’Donnell, K. McDonald, R.M. Stirnemann, M. and Ford, A.J. (1997). A Zinc containing intraruminal device for facial eczema control in lambs. N Z vet J. 45:93 99.
Scheie, E, Ryste, E.V. and Flåøyen, A. (2003). Measurement of phylloerythrin (phytoporphyrin) in plasma or serum and skin from sheep photosensitised after ingestion of Narthecium ossifragum. NZ vet. J. 51:99-103.
Scheie, E, Smith, B.L, Cox, N. and Flåøyen, A. (2003). Spectrofluorometric analysis of phylloerythrin (phytoporphyrin) in plasma and tissues from sheep suffering from facial eczema. NZ vet. J. 51:104-110.
Scotland, T. and Davidson, P. (1999). Suspected facial eczema in ostriches. Vetscript XII 11. 4.
Smith, B.L. and Embling, P.P. (1991). Facial eczema in goats: The toxicity of sporidesmin in goats and its pathology. NZ vet. J. 39:18-22.
Smith, B.L. (1987). Mycotoxicoses of cattle and horses in Australia and New Zealand. Proceedings No.103 Veterinary Toxicology. The Post-Graduate Committee in Veterinary Science, University of Sydney, Australia. 270-276.
Smith, B.L. (1987). Mycotoxicoses in sheep: Proceedings No.103 Veterinary Toxicology. The Post-Graduate Committee in Veterinary Science, University of Sydney, Australia. 279-286.
Stafford, K.J, West, D.M, Alley, M.R. and Waghorn, G.G. (1995). Suspected photosensitisation in lambs grazing birdsfoot trefoil (Lotus corniculatus). NZ vet. J. 43:114-117.
Surveillance (1974) 1(4): 4 Cattle syndromes of chronic eczema hepatic encephalopathy
Surveillance (1974) 1(4): 4 Cattle syndromes of chronic eczema urinary incontinence.
Surveillance (1975) 2(3): 4 Spore counts
Surveillance (1975) 2(3): 8 Chronic sporidesmin toxicity in cattle
Surveillance (1975) 2(5): 10 Chronic sporidesmin toxicity in cattle
Surveillance (1976) 3(5): 11 Diagnosis of chronic facial eczema in cattle
Surveillance (1977) 4(1): 13 A facial eczema hoax
Surveillance (1978) 5(3): 10 Facial eczema in Northland
Surveillance (1978) 5(4): 11 Cattle foetal facial eczema
Surveillance (1979) 6(2): 4 Surveillance at meat works (1974 1979)
Surveillance (1979) 6(3): 3 Gaining information on facial eczema
Surveillance (1979) 6(4): 10 Genetic resistance in sheep possible
Surveillance (1980) 7(2): 9 Surveillance at meat works (1975 1980)
Surveillance (1981) 8(1): 6 Facial eczema in weaner stags
Surveillance (1981) 8(2): 12 Facial eczema in association with redwater
Surveillance (1981) 8(3): 3 Deer incidence of facial eczema increases
Surveillance (1982) 9(1): 2 Facial eczema publicity fails to move farmers
Surveillance (1982) 9(3): 13 Effect of sub clinical facial eczema on periparturient performance of cattle
Surveillance (1982) 9(3): 14 Monitoring spore counts on limed and unlimed pasture
Surveillance (1982) 9(3): 22 F.E. in cattle and sheep in the South Island
Surveillance (1983) 10(1): 3 Prevention only way to combat F.E.
Surveillance (1989) 16(3):23 Facial eczema in cattle on the West Coast
Surveillance (1991) 18(2):14 Prevention and costs of facial eczema on dairy farms
Surveillance (1994) 21(2): 4 Facial eczema in Mid Canterbury
Surveillance (1994) 21(3):30 Facial eczema in cattle
Surveillance (1995) 22(2): 4 Facial eczema in cattle
Surveillance (1999) 26(2):15 Facial eczema of deer
Surveillance (1999) 26(3):16 Facial eczema in Otago sheep and cattle
Surveillance (1999) 26(3):18 Facial eczema in cattle
Surveillance (2003) 30(3):31 Facial eczema in camelids
Surveillance (2005) 32(3):14 Sporidesmin toxicity in alpaca