Mouldy sweet clover poisoning in cattle is caused by the ingestion of sweet clover hay or ensilage containing dicoumarol. Poisoning is characterized by extensive hemorrhages into tissues throughout the body and severe blood loss after injury, surgery or parturition.
Coumarol, a normal constituent of many sweet clover cultivars, is converted to dicoumarol through the action of moulds common in sweet clover. Not all sweet clover contains dicoumarol and the degree of spoilage does not reflect the degree of toxicity in feed. Varieties of sweet clover differ in the content of coumarol they contain and their potential toxicity. The only way to know for sure what risks exist is to have feed tested.
Wet-hay seasons increase the incidence of spoilage, which is often accentuated by storage conditions. The presence of dicoumarol in feed does not diminish with time. The shortage of feed during drought means bales get pulled from older stacks and used for feed. Managing the risk of toxicity means managing sweet clover-based feed appropriately.
All ages of cattle are susceptible. Yearlings and calves are more susceptible than mature cows. Sweet clover poisoning is insidious, often becoming a herd problem that may involve 25 to 30 per cent of animals consuming affected feed. Clinical signs might appear spontaneously, but uncontrollable and life-threatening bleeding often follows procedures like dehorning and castration. Cows on feed containing dicoumarol during calving season are particularly at risk. New calves may succumb to hemorrhage during the first few days of life without the cows showing clinical signs. Animals already prone to bleeding often show severe bruising and fatal bleeding during transport. In cattle already suffering prolonged bleeding times, parasites can initiate serious hemorrhagic episodes.
During the process of spoiling, coumarin in sweet clover is converted to toxic dicoumarol, a potent vitamin K antagonist and anticoagulant. The weathered, outer portions of large round bales usually contain the highest concentration of dicoumarol. Dicoumarol alters proenzymes required for synthesis of vitamin K-dependent coagulation factors like prothrombin, and factors VII, IX and X, constituents necessary in the biological cascade of clotting. Dicoumarol concentrations of 20 to 30 mg/kg of hay ingested throughout several weeks are required to cause poisoning. The toxic agent crosses the placenta in pregnant animals, affecting the newborn. All species of animals studied are susceptible, but instances of poisoning are most common in cattle and, to a limited extent, sheep, pigs, and horses.
Clinical Findings and Lesions
Cattle develop bleeding problems as early as two weeks and as late as three to four months on feed containing mouldy sweet clover. Pockets of spoilage in bale stacks or silage pits influence the amount of dicoumarol consumed by animals.
Hemorrhage causes clinical signs. Preliminary symptoms often include stiffness, lameness, dullness, and swellings beneath the skin (hematomas or blood clots) primarily over the hips, brisket, and neck. Mucous membranes are often pale — indicating anemia. Because hemorrhage decreases the quantity of red blood cells available to transport oxygen, respiratory distress is not uncommon. Feces, urine, and milk frequently contain blood and blood often oozes from the nostrils. Parturition is often accompanied by extensive hemorrhage. Dicoumarol crosses the placenta causing hemorrhage in the fetus leading to fetal reabsorption and stillbirths. Newborn calves often become weak during the first few days of life due to internal bleeding. Calves can die suddenly without displaying noticeable signs.
The first indication of dicoumarol poisoning may be the sudden death of one or more animals. Animals showing clinical signs display stiffness and lameness due to bleeding into muscles and joints. Death caused by massive hemorrhage after injury, surgery, or parturition is a definite warning sign. Neonatal deaths rarely occur without noticeable signs in mother cows.
Sweet clover poisoning is easily diagnosed on post mortem examination by identifying signs compatible with widespread hemorrhage and prolonged clotting times. Producers need to be working with a veterinary practitioner at the first suggestion of dicoumarol poisoning. Disasters can be prevented through early treatment and prompt changes in herd and feed management.
Treatment and prevention
Immediate removal from the affected feed is the first step in minimizing losses. New cases may appear for up to six days because of the persistent effect of ingested dicoumarol. The journey from this point onward needs to be discussed and co-ordinated with a veterinarian.
Intravenous administration of whole blood (10 ml/kg b.w.), though not always practical, is a consideration in the case of individual animals. Parenteral administration of natural vitamin K1 (expensive) is one option, the other being the use of synthetic vitamin K3, available as both injectable and premix.
Longer-term options include:
- Use of sweet clover cultivars of sweet clover low in coumarin.
- Mouldy portions of hay and silage can be discarded; however, the absence of visible spoilage is insufficient evidence of safety.
- Feed should be submitted for analysis of dicoumarol content. Animal health professionals can provide guidance on sampling and testing.
- Alternating sweet clover hay suspected of containing dicoumarol with other roughage such as alfalfa or grass-legume hay mixtures can be used to avoid severe poisoning. A seven- to ten-day period on sweet clover hay, followed by an equal time on alternative hay mixtures, will prevent poisoning in most situations even though bleeding times remain prolonged. Animals in higher risk categories (surgical candidates, pending parturition) should not receive sweet clover hay or silage for a minimum of three weeks (preferably four weeks), before surgery or parturition.
- Stack or bale sweet clover only when it is well cured and dry.