Selenium Toxicity in Farm Animals
Treatment and Prevention

(Irish Veterinary Journal 1990, 43, 151-153)

PAM Rogers(1), SP Arora(1), GA Fleming(1), RAP Crinion(1), & JG McLaughlin(1)

(1) Grange Research Centre, Teagasc, Dunsany, Co. Meath

(2) National Dairy Institute, Himachal Pradesh Krishi Vishna Vidyayiya, Palpamur 176062 (HP), India

(3) Johnstown Castle Research Centre, Teagasc, Wexford, Co Wexford

(4) (Deceased) Veterinary Faculty, University College Dublin, Ballsbridge, Dublin 4

(5) Veterinary Research Laboratory, Abbotstown, Dublin 15

Abstract
Selenium (Se) toxicity in livestock occurs sporadically in counties Dublin, Limerick, Meath and Tipperary. Se-toxic soils occur also in counties Carlow, Kerry and Kilkenny. Most affected farms are also high in Mo.

Soil and herbage levels of Se exceed 9 mg/kg and 6 mg/kg DM respectively in 50% of toxic fields and exceed 5 mg/kg and 3 mg/kg DM respectively in 90% of toxic fields.

Clinical signs of Se toxicity are discussed. High oral doses of mineral sulphates antagonise Se. They were used successfully to treat clinical cases in India. Irish colleagues may wish to try this method in early clinical cases. Methods of prevention of Se toxicity are discussed.

While Se toxicity is uncommon, Se deficiency is very common. It can arise in stock within 1 km of toxic farms. For safety, mineral supplements high in Se should not be given to livestock within 5 miles of known toxic farms unless blood samples from the stock are found to be low in Se.

Introduction
Selenium (Se) toxicity in domestic animals can be acute or chronic. Acute toxicity, with high mortality in sheep, has been described following incorrect use of sodium selenite injections (Kyle and Allen 1990), or of anthelmintic drenches containing Se compounds.

Toxicity due to high Se levels in soil and herbage is usually chronic but can be acute. It has been confirmed in cattle and horses (and to a lesser extent in sheep) in a few locations in the Republic of Ireland. Horses are more susceptible than cattle. Toxicity occurs in buffaloes and cattle in India and in domesticated and wild animals (including fowl) in Australia, China, Eastern Europe, Israel, Mexico, North and South America.

The purpose of this article is to alert Irish colleagues to a possible method of treating chronic clinical Se toxicity. The method has been successful in India (Arora 1985). To our knowledge, it has not been attempted in Ireland. Methods of prevention are outlined also.

Background data on Se toxicity
In contrast to Se-deficiency, which is widespread in cattle and sheep in most counties of Ireland, Se-toxicity is rare, probably affecting not more than 50 farms in the State.

The origin of Se in Irish soils may be traced to leaching of Se compounds from Se-rich parent materials and their subsequent deposition in low-lying areas, such as old glacial lake beds or river flood plains. The most important Se-bearing rocks are the black shales of the Namurian (mid-Carb-onaceous) Period. These occur mainly in Co. Meath and north Co. Dublin but also in Counties Limerick and Tipperary. Although high-Se, high-Mo soils from Namurian black shale occur in Co. Clare (from Newmarket to Lisdoonvarna), we are unaware of Se toxicity in stock in Clare. Other sources of Se are the Calp limestones. These are earthy limestones which occur in mid to north Leinster. They are often interbedded with Namurian black shale.

The areas where the highest levels of Se are to be found are low-lying peaty swamps of high pH. Se-rich rocks are also molybdenum (Mo)-rich but the resulting molybdeniferous soils are far more widely dispersed than seleniferous soils in Ireland. The neutral to alkaline milieu favours the formation of the Se6+ or selenate form of Se. This form is very readily assimilated by plants. Fuller discussion on Se in Irish soils may be found in Walsh et al (1951), Fleming & Walsh (1957), Fleming (1962) and Atkinson (1967).

Animals on Se-toxic farms may develop signs of toxicity within 21-90 days of being confined to these fields (Twomey et al 1977; Crinion & O'Connor 1978; Crinion 1980). Animals which are left for only a short time on the affected fields seldom develop toxic signs. Nearby fields, typically more elevated than the toxic fields, are often safe and usually have much lower to safe levels of Se.

Soil Se levels in Se-toxic Irish fields (Fleming and Parle 1990), average 21 mg/kg (range 3.2-132.0 mg/kg, with occasional values above this; 50% of values exceed 9 mg/kg and 90% exceed 5 mg/kg).

Se in herbage and cereal grain is associated with the protein fractions. It substitutes for sulphur (S) in S-containing amino-acids, such as cysteine and methionine. Se in Se-methionine is thought to be more bio-available than equal amounts from e.g. sodium selenite. Herbage Se levels in Se-toxic Irish pastures average 18 mg/kg (range 1.6-140 mg/kg DM, with a few values above this; 50% of values exceed 6 mg/kg DM and 90% exceed 3 mg/kg DM).

In India, Se poisoning in cattle may arise within 10-42 days of feeding rice straw, lucerne or berseem with Se levels 0.50-6.7 mg/kg DM and the problem soils have Se levels of 1.0-10.5 mg/kg (Arora 1975, 1985). Thus, the toxic levels of Se in feed and soil in India are lower than the usual toxic levels in Ireland. International standards for Se requirement in cattle are usually given as 0.10-0.18 mg/kg DM but the Se requirement of cattle in the Irish Republic is considerably higher (0.24-0.48 mg/kg DM). A higher Se requirement (and, possibly, higher tolerance) may explain the higher Se levels needed to produce toxicity in Irish cattle, as compared with Indian cattle.

Within affected Irish farms, high soil Se levels are confined to specific fields, often just one field or part of a field, usually the most low-lying part where fog and mist linger in winter. In large farms, as in some parts of Co. Meath, the Se-toxic areas, or "hot-spots" may occupy only a small fraction of the total farm area and may arise as sporadic localised pockets through the farm. Occasionally, Se-deficient fields occur less than half a mile from a Se-toxic field.

If allowed to range freely, stock tend to avoid the Se-toxic areas. (This may be due to the unpalatable nature of Se-toxic herbage). Therefore, there is less danger to stock on large than on small farms, in which Se-toxic areas may form a considerable part of the farm area, as in the case of west Limerick. If stock are confined to toxic areas, they have little option but to eat high-Se herbage. Se volatilizes as dimethyl mono selenide (H3C-Se-CH3) or dimethyl diselenide (H3C-Se-Se-CH3) from high-Se soils and is excreted in the breath of cattle eating high-Se forage.

Apart from possible toxicity from incorrect use of high-Se supplements or environmental pollution by Se compounds, high Se intake in grazing animals can arise in two main ways: (a) by ingesting herbage or other plants high in Se and (b) by soil ingestion.
a. On good pasture, herbage DM intake by healthy cows may exceed 3% of liveweight, i.e. >16.5 kg/day for cows of 550 kg liveweight. Herbage with 3 or 6 mg Se/kg DM would supply >49.5 or >99.0 mg Se/cow/day respectively.
b. In periods of drought, or on heavily stocked pasture in late autumn or winter, soil ingestion by cattle can reach 15% of total DM intake, i.e. cows could ingest up to 2.5 kg soil/day. Soil with 5 or 9 mg Se /kg would supply 12.5 or 22.5 mg Se/cow/day respectively (in addition to Se in the ingested herbage).

Location of Se-toxic soils in Ireland
The location of Se-toxic soils is sporadic. Most are in Counties Carlow, Dublin, Kerry, Kilkenny, Limerick, Meath and Tipperary. Most affected farms are also high in Mo. Mo-induced copper deficiency is common in cattle on these farms. Small areas extend eastward from south Co. Limerick, through Clonmel (south Co. Tipperary) to Piltown (Co. Kilkenny). These are related to sporadic pockets of Namurian shale deposits, which influence soils in the immediate vicinity. However, the high-Se soils near Piltown are not molybdeniferous. This is the only instance of a seleniferous but not molybdeniferous soil known to date in Ireland.

Co. Carlow: near Castletown.
Co. Dublin: Pockets of high-Se, high-Mo soils from Namurian black shale occur near Garristown.
Co. Kerry: near Ardfert.
Co. Kilkenny: near Piltown.
Co. Limerick: The area between Foynes and Ardagh contains high-Se, high-Mo soils from the Clare shales.
Co. Meath: Many fields in the flood plain of the Skane river are Se-toxic. Stock in the Dunsany-Warrenstown area have shown sporadic signs of Se-toxicity for decades and similar signs were noted in stock in the area more than 100 years ago (Fream 1890). Mo-induced copper deficiency is common in the area also. Other Se-toxic areas occur in localised fields south of the Boyne and Blackwater rivers near Athboy, Navan, Slane, Drogheda, Dunshaughlin, Grange and Trim.
Co. Tipperary: near Boulick, Clonmel, Clogheen, Rathronan.

There may be a few other locations, as yet unknown.

Clinical signs of Se toxicity
In Ireland, the main signs are lameness; horizontal grooves or cracks in the hooves; occasional sloughing of hooves; reluctance to move and long periods of recumbency; severe illthrift or loss of body condition, especially if lameness is severe; hair loss, especially from the tail and parts that rub against external surfaces. Other occasional signs include constipation, abortion, infertility. In severe cases, animals may die of subacute poisoning.

In India gangrene of distal extremities (below the tarsus or carpus, tips of ears, muzzle, tip of tail or tongue) occurs occasionally. Such skin lesions are rare in Ireland but decubital ulcers can arise in animals recumbent for long periods.

In Ireland, the disease is sporadic, arising in some years and not in others. It occurs frequently in the autumn. Once the clinical disease has occurred on a farm, it is likely to re-occur in following years. New outbreaks are recorded each year on farms where the condition has not been observed previously. Some of these are explainable, for instance following land-spreading of high-Se drainage spoil. Other cases have no obvious explanation.

When the disease occurs, many animals may be affected. In Ireland, the course of the disease is usually chronic, developing over a period of 3 weeks to 3 months on the problem fields. Although silage or hay from the problem fields can contain high Se levels, the clinical problem seldom arises for the first time on winter feed and dilution of forage from toxic fields can lower the Se level and lower the risk of poisoning. Hay is not as toxic as fresh grass of the same Se content.

Treatment of Se toxicity
Se toxicity in buffaloes was treated successfully in India by Arora (1985), using a daily oral dose consisting of a mixture of sulphates. Sulphur (S) and Se are Group VI elements, closely related crystallographically and geo-chemically. Thus, S antagonises Se in soil and in the body. The mixture contained:

Ingredient (sulphate salt) in dose     

Magnesium sulphate
Ferrous sulphate
Copper sulphate
Zinc sulphate
Cobalt sulphate

Total

(kg)

1.000
0.166
0.024
0.075
0.015

1.280

Daily dose to adult cattle (g)

23.44
3.89
0.56
1.76
0.35

30.00

The dose was given daily until recovery was noted (21-50 days). If recovery was incomplete at 50 days, treatment was discontinued. Of 517 buffaloes treated, 430 (83%) were cured in 21-50 days. Recovery time and clinical outcome were related to the severity of signs and lesions at the time of treatment. Cattle which had lost hooves did not recover fully. They did not regrow new hooves and they remained lame. As gangrene of the extremities often occurs in Indian outbreaks, it is unclear if secondary disorders (ergotism, salmonellosis etc) complicate the condition there.

If they are removed from Se-toxic fields as soon as lameness is seen, many Irish cattle recover spontaneously (without shedding the hooves) within 60 days (J.G. McL, unpublished). Also, the Se levels in feed and soil in Indian outbreaks are often lower than in Irish outbreaks. Therefore, we are not sure that the syndromes and aetiology are identical in the two countries nor are we sure that Arora's sulphate cocktail can reduce recovery time under Irish conditions. However, we suggest that the method might be tried in affected or at-risk Irish cattle, should cases arise in future. As Se toxicity is usually accompanied by Mo-induced Cu deficiency in Ireland, we suggest that the copper sulphate part of the mixture might be increased to 0.064 kg and the magnesium sulphate be decreased to 0.960 kg. Thus, the 30 g dose would provide 1.5 g copper sulphate/head/day. To reduce the labour of dosing individual stock, the daily dose (say 30 g) could be fed in a 300 g of palatable carrier (6% molasses, 94% rolled barley). Alternatively, trough water could be medicated (using medication dispensers, as for control of hypomagnesaemia) with 30 g/head/day. As Cu sulphate may precipitate in trough water, the farmer should agitate the water in the trough a few times daily.

The dose for young stock and horses can be taken pro rata by body weight with cattle. If sheep are to be treated, it would be safer to exclude copper sulphate from the mixture. The dose for adult sheep can be taken as 10% of the adult bovine dose, i.e. 3 g/sheep/day. (If Cu deficiency is known to exist in the flock, administration of copper oxide boluses would be safer than oral copper sulphate).

Prevention of Se toxicity

1. Intensive sampling of herbage for Se analysis can be used to identify the most dangerous parts of the farm. If these are very localised, as is often the case, consideration should be given to fencing them off and excluding them permanently from use for grazing/cutting.
2. Graze the less dangerous fields. Where possible, the more dangerous seleniferous fields should be used for purposes other than grazing, i.e. for conservation for hay or silage. Silage or hay made from the toxic fields should be diluted with material from safer areas.
3. Application of sulphur-containing materials e.g. sulphate of ammonia or gypsum, can reduce the levels of Se in herbage. In a cutting trial in Co. Meath, heavy applications of gypsum (12 tonnes/ac) reduced herbage Se from 18 to 2 mg/kg DM. Sulphate of ammonia (1 tonne/ac) reduced herbage Se from 10 to 1.4 mg/kg DM. Sulphate of ammonia probably acts in three ways: dilution effect from increased grass growth; SO42-/SeO42- antagonism and NH4+/SeO42- antagonism.
4. In the absence of herbage Se reduction by S fertilisation, if stock must graze known Se-toxic fields, they should not be allowed to graze the toxic area for more than 2 weeks in any 6 week period.
5. At the first sign of clinical toxicity on known problem farms, all stock should be removed from the problem fields. The oral sulphate dose can be tried for 21-50 days, or until clinical signs disappear.
6. Should signs of toxicity arise on winter-feed, additional safe feed should be used to dilute the toxic feed and the oral sulphate-dosing regime can be tried.
7. Se should be removed from all mineral supplements of concentrate rations used on Se-toxic farms.
8. In Counties Carlow, Limerick and Meath, Se-deficient areas were identified within short distances of Se-toxic or Se-subtoxic areas. However, for safety, herds within 5 miles of known Se-toxic farms should not get high levels of Se in mineral supplements or concentrate rations unless clinical signs and blood (or herbage) tests confirm Se deficiency in those herds.
9. Land-spreading of drainage spoil should be avoided if there is any suspicion that the spoil may contain high Se levels.
10.  Horses are more susceptible than cattle. If other measures can not be used, cattle should be grazed in preference to horses in potentially toxic areas.

References

• Arora SP, Parvinder K, Khirwar SS, Chopra RC & Ludri RS (1975) Se levels in fodders and its relationship with Degnala Disease. Indian J. Dairy Sci., 28, 249-253.
• Arora SP (1985) Livestock problems related to geochemistry in India including selenium toxicity and goitre. Proc. 1st International Symposium on Geochemistry and Health (London). pp 164-180.
• Atkinson WJ (1967) Regional geochemical studies in Co. Limerick, Ireland with particular reference to selenium and molybdenum. Ph.D. Thesis, Royal School of Mines, Imperial College, London.
• Crinion RAP & O'Connor JP (1978) Selenium intoxication in horses. Irish Vet. J., 32, 81-86.
• Crinion RAP (1980) Distribution of selenium intoxication in Co. Meath: A retrospective study. Irish Vet. J., 33, 123-127.
• Fleming GA & Walsh T (1957) Selenium occurrence in certain Irish soils and its toxic effects on animals. Proc. of the Royal Irish Acad., 58B, 151-166.
• Fleming GA (1962) Selenium in Irish soils and plants. Soil Sci., 94, 28-35.
  
• Fleming GA & Parle PJ (1990) Unpublished observations on soil and herbage selenium levels on selenium-toxic farms.
  
• Fream W (1890) The herbage of pastures. J. Roy. Agr. Soc. of England 1, Sect. 3, 384.
  
• Kyle R & Allen WM (1990) Accidental selenium poisoning of a flock of sheep. Vet. Rec., 126, 601.
  
• Twomey T, Crinion RAP & Glazier DB (1977) Selenium toxicity in cattle in Co. Meath. Irish Vet. J., 31, 41-46.
  
• Walsh T, Fleming GA, O'Connor R & Sweeney A (1951) Selenium toxicity associated with an Irish Soil Series. Nature, Lond., 168, 881.
  

Phil Rogers MRCVS, Lucan, Dublin, Ireland​
THE NYCAVMA IS HONORED TO HOST & MANAGE THE PHIL ROGERS ARCHIVE