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Poisoning
Sweet Clover Poisoning
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  • Introduction to Poisoning
  • Metabolism of Poisons
  • Factors Affecting the Activity of Poisons
  • Diagnosis of Poisoning
  • General Treatment of Poisoning
  • Algal Poisoning
  • Arsenic Poisoning
  • Bracken Fern Poisoning
  • Cantharidin Poisoning (Blister Beetle Poisoning)
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  • Ethylene Glycol (Antifreeze) Poisoning
  • Fluoride Poisoning
  • Food Hazards
  • Fungal Poisoning
  • Gossypol Poisoning
  • Halogenated Aromatic Poisoning (PCB and Others)
  • Herbicide Poisoning
  • Household Hazards
  • Insecticide Poisoning
  • Lead Poisoning
  • Mercury Poisoning
  • Metaldehyde Poisoning
  • Nitrate and Nitrite Poisoning
  • Nonprotein Nitrogen Poisoning (Ammonia Poisoning)
  • Pentachlorophenol Poisoning (Penta Poisoning)
  • Petroleum Product Poisoning
  • Plants Poisonous to Animals
  • Poisoning from Human Over-the-Counter Drugs
  • Poisonings from Human Prescription Drugs
  • Poisonings from Illicit and Abused Drugs
  • Pyrrolizidine Alkaloidosis (Senecio Poisoning, Ragwort Poisoning)
  • Quercus Poisoning (Oak Bud Poisoning, Acorn Poisoning)
  • Rodenticide Poisoning
  • Ryegrass Poisoning
  • Salt Poisoning
  • Selenium Poisoning
  • Snakebite
  • Sorghum Poisoning (Sudan Grass Poisoning)
  • Spider Bites
  • Strychnine Poisoning
  • Sweet Clover Poisoning
  • Toad Poisoning
  • Zinc Poisoning
 
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Sweet Clover Poisoning

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Sweet clover poisoning is seen when animals eat spoiled sweet clover hay or silage. Any method of hay storage that allows sweet clover to mold increases the chance of a toxin forming in the hay. Weathered, large round bales, particularly the outer portions, usually contain the highest levels of toxin. When toxic hay or silage is eaten, blood clotting may be delayed and spontaneous bleeding may result (see Blood Disorders of Dogs: Blood Clotting Disorders). Instances of poisoning have involved mainly cattle and some horses.

Signs are caused by faulty clotting of blood and loss of blood from ruptured blood vessels. The amount of time between eating toxic sweet clover and appearance of signs varies greatly. If the sweet clover has a low level of toxin, animals may eat it for months before disease appears.

The first signs may be stiffness and lameness, caused by bleeding into the muscles and joints. The animal may bleed from the nose or into the gastrointestinal tract. Death from massive bleeding after injury, surgery, or giving birth can occur suddenly without other signs.

Diagnosis is based on a history of eating sweet clover hay or silage over relatively long periods, signs, and a prolonged blood clotting time. Sweet clover poisoning is usually a problem in all animals in a herd. It is unlikely if bleeding or slow blood clotting are seen in a single animal from a group.

Blood transfusions are usually needed and can be repeated if necessary. Severely affected animals are also treated with vitamin K1, which reverses the effects of the toxin. Several hours are needed for significant improvement, and more than 24 hours is needed for clotting to return to normal.

The only certain method of prevention is to avoid feeding sweet clover hay or silage. However, variations of sweet clover, low in the toxin and safe to feed (for example, Polara), have been developed.

A simple management technique is to alternate feeding (every 7 to 10 days) sweet clover hay suspected of containing the toxin with other roughage such as alfalfa or a grass-legume hay mixture. Pregnant animals should not receive sweet clover hay for at least 2 to 3 weeks, and preferably 4 weeks, before giving birth. Similarly, animals should not receive sweet clover hay for 3 to 4 weeks before castration or other surgery.

Last full review/revision July 2011 by Barry R. Blakley, DVM, PhD; Cheryl L. Waldner, DVM, PhD; Rob Bildfell, DVM, MSc, DACVP; William D. Black, MSc, DVM, PhD; Herman J. Boermans, DVM, MSc, PhD; Cecil F. Brownie, DVM, PhD, DABVT, DABT, DABFE, DABFM, FACFEI; Raymond Cahill-Morasco, MS, DVM; Keith A. Clark, DVM, PhD; Gregory F. Grauer, DVM, MS, DACVIM; Sharon M. Gwaltney-Brant, DVM, PhD, DABVT, DABT; Larry G. Hansen, PhD; Safdar A. Khan, DVM, MS, PhD, DABVT; Garrick C. M. Latch, MASc, PhD; Gavin L. Meerdink, DVM, DABVT; Lisa A. Murphy, VMD; Frederick W. Oehme, DVM, PhD; Gary D. Osweiler, DVM, MS, PhD, DABVT; Mary M. Schell, DVM; David G. Schmitz, DVM, MS, DACVIM; Norman R. Schneider, DVM, MSc, DABVT

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