Barry Whitworth, DVM
Senior Extension Specialist Department of Animal & Food Science Ferguson College of Agriculture

Scrapie is a chronic, progressive disease of the central nervous system that affects sheep and goats. Scrapie is the oldest of the group of neurodegenerative diseases known as transmissible spongiform encephalopathies (TSE). Some of the other TSE are Bovine Spongiform Encephalopathy known as mad cow disease, Chronic Wasting Disease which is found in deer, and Creutzfeldt Jacob Disease which is found in humans. TSE are protein-misfolding diseases that lead to brain damage and are always fatal.

The cause of Scrapie is not completely understood, but evidence indicates that an infectious protein referred to as a prion is responsible for the disease. These infectious prions cause damage to the normal prion proteins found in the brain. The mis-folding of the proteins lead to brain damage and the presentation of clinical signs of the disease. Prions are very resistant to destruction, so once in the environment, they are difficult to remove.

Scrapie is believed to primarily be transmitted by the oral route. Typically, lambs and kids might ingest the prion when they come in contact with the infectious agent through placentas and birthing fluids from infected ewes and does. Older animals may be exposed to the prions this way as well. Colostrum and milk are also sources of prions. Other secretions such as urine, feces, saliva, and nasal secretions may contain infectious prions as well. Once ingested, the prions cross into the lymphoid system. The prions will incubate for a long time usually two to five years before entering the nervous system.

Genetics plays a part in Scrapie infections. Certain breeds are more susceptible to the disease due to genetic composition. Genetic testing is available for producers to help them select breeding stock with resistant genes.

Clinical signs most commonly associated with Scrapie are intense pruritis, ataxia, and wasting. Early in the disease, small ruminant producers may notice slight changes in behavior with sheep and goats infected with Scrapie. Initially, animals may have a staring or fixed gaze, may not respond to herding, and may be aggressive towards objects. As the disease progresses, other clinical signs noticed are progressive weight loss with normal appetite, incoordination, head tremors, and intense pruritis. In the terminal stages, sheep are recumbent and may have blindness, seizures, and an inability to swallow. Once initial clinical signs are notice, death usually occurs in one to six months.

The gold standard for postmortem (dead animals) diagnosing of Scrapie is the use of immunohistochemistry test on brain tissues as well as microscopic examination of brain tissue for characteristic TGE lesions. Live animal diagnosis is possible by testing lymphoid tissues from the third eyelid and rectal mucosa scrapings.

There is no treatment available for Scrapie, so prevention is key to controlling the disease. Following biosecurity protocols is a good starting point for preventing Scrapie. Part of the biosecurity plan is to maintain a closed flock and only buy replacement animals from certified Scrapie free flocks. Producers should limit visitors’ contact with their animals. Sanitation is important in lambing and kidding areas. Manure and bedding contaminated with birthing fluids and placentas should be disposed of properly. Genetically resistant animals should be used for breeding to produce genetically resistant offspring.

It should be noted that there is a novel or atypical form of Scrapie. This disease may also be referred to as Nor98 variant. This atypical version of Scrapie was initially found in Norway. It has been diagnosed in the United States as well. The disease is usually only found in a single old animal in the flock or herd. The brain lesions in atypical Scrapie are different from classical Scrapie. Currently, experts believe that natural transmission of atypical Scrapie is not likely.

The United States Department of Agriculture (USDA) has been battling Scrapie for decades. According to recent information from the USDA, the United States (US) is close to accomplishing eradication of the disease. In order for the United States to achieve Scrapie free status, no sheep or goats can test positive for classical scrapie for seven years and a certain level of testing needs to be done each year that represents the sheep and goat populations within the country. Small ruminant producers can assist the USDA eradication efforts by contacting the USDA when they have an adult sheep or goat exhibiting clinical signs of Scrapie or an adult animal dies or is euthanized. Producers should contact the Oklahoma State Veterinarian, Dr. Rod Hall at 405-522-6141 or the USDA Veterinary Services at 405-254-1797. This will aid the USDA in reaching sampling testing goals. There is no charge for the collection or testing of the samples for scrapie. 

Scrapie is a disease that needs to be eliminated from the US. Once eliminated, the US will have additional export markets for sheep and goat products. Oklahoma State University Cooperative Extension Service has an informative fact sheet on Scrapie. Please visit the Local County Extension Office and asked for fact sheet VTMD-9135 or producers may view the fact sheet online at  https://extension.okstate.edu/fact-sheets/scrapie.html. Also, the USDA National Scrapie Eradication Program website has valuable information as well at https://www.aphis.usda.gov/aphis/ourfocus/animalhealth/animal-disease-information/sheep-and-goat-health/national-scrapie-eradication-program. 

References Cassmann, E. D., & Greenlee, J. J. (2020). Pathogenesis, detection, and control of scrapie in sheep. American journal of veterinary research, 81(7), 600–614. https://doi.org/10.2460/ajvr.81.7.600

Barry Whitworth, DVM

Area Food/Animal Quality and Health

Specialist for Eastern Oklahoma

With the prolonged drought, most pastures in Oklahoma are in poor condition. With the lack of available forage, animals may go in search of alternative foods. If oak trees are in the pastures, acorns may be a favorite meal for some livestock this fall. This may result in oak poisoning.

Oak (Quercus species) leaves, twigs, buds, and acorns may be toxic to some animals when consumed. Obviously, acorns can be a problem in the fall and green acorns can be more toxic than mature acorns. When acorns form only a small portion of the diet, there are usually no signs of problems. However, consumption of large quantities may result in toxicity. Tannins in the acorns cause the toxicity. The most common tissue damaged by the tannins are the digestive tract and kidneys. Cattle and sheep appear to be more susceptible to toxicity than goats. Other animals such as horses, rabbits, and chickens have succumbed to the toxicity of oak poisoning as well. Interestingly, some individual animals are more tolerable of the toxins and show no ill effects when consuming acorns.

Clinical signs of oak toxicity usually appear a few days after consumption of acorns. Initially, the animals are weak, listless, emaciated, and anorexic. This is followed by ventral edema (swelling of lower parts of the body such as legs, chest, ventral abdomen), urinating large amounts of urine, abdominal pain, and constipation. The animal may pass hard mucus covered fecal material which may change to black tarry or bloody feces as the disease progresses. If the animal is not treated, kidney failure is likely.

A tentative diagnosis of acorn poisoning may be based on clinical signs and access to acorns. Blood tests that indicate kidney disease is another clue to the condition. A necroscopy with examination of tissues for characteristic lesions of the disease is the standard to confirm a diagnosis of oak toxicity.

Treatment of oak toxicity starts with removing the animals from the area where the acorns are located. Those animals displaying signs of the disease should be given fluids to correct dehydration and electrolyte imbalances. Mineral oil and/or activated charcoal may be given to reduce toxin absorption. If animals survive the initial toxicity, they may recover, but it may take several weeks for kidney function to return to normal.

As always, prevention is better than treatment. Producers should be very careful allowing livestock to graze in areas where acorns are present. Livestock should be fed plenty of hay and feed this fall to avoid over consumption of acorns. For those producers who cannot avoid grazing areas with large numbers of oak trees, feeding a grain mixture with 10% to 20% of calcium hydroxide has been successful in preventing problems with acorn poisoning.

Two thousand twenty-two has not been the best year for livestock producers. The drought has produced poor pasture conditions as well as very little hay. On top of those problems, feed costs continue to increase. The last problem a producer needs is a large number of sick cows. For those that graze an area with a large number of oak trees, prevention may be worth the cost this year. At the very least keep a close watch of your animals this fall. Producers wanting more information about oak toxicity, should consult with their local veterinarian or visit with their Oklahoma State University Cooperative Extension County Agriculture Educator.

Barry Whitworth, DVM | Area Food/Animal Quality and Health Specialist for Eastern Oklahoma 

*Article originally printed in the October 2022 issue of Oklahoma Farm & Ranch.

Since most of Oklahoma experienced drought conditions and with fall fast approaching, producers with fescue pastures should closely observe their livestock for any signs of fescue toxicity. According to Mike Trammel, Pottawatomie County Ag Educator and Muti-County Agronomist, fescue toxins (ergot alkaloids) tend to increase in Kentucky-31 tall fescue pastures in the fall. Some reports indicate more problems with fescue toxins following a summer drought and limited fall rains. All of this may put Oklahoma cattle at a greater risk of fescue toxicity.

One issue that cattle experience with fescue toxins is fescue foot. Fescue foot is thought to be caused by ergot alkaloids such as ergovaline. These alkaloids are produced by endophyte fungus (Epichloë coenophiala) which is in tall fescue. Ergovaline has been proven to be a vasoconstrictor which might be responsible for fescue foot and heat intolerance also known as summer slump in cattle. Other issues that may be seen with the ergot fescue toxins are reduced milk production and reproductive issues.

Clinical signs of fescue foot appear within a few days of cattle being turned on to tall fescue pastures or it may take weeks if toxins in the pasture are low. Producers will initially observe cattle with arched back, rough hair coats, and sore feet. These symptoms are more noticeable early in the morning and with cold weather. This is followed by reddening and swelling in the area between the dewclaws and hooves. The lameness usually becomes more severe with time. If no action is taken, gangrene will result in loss of tissues distal to the coronary band and declaws. If the weather remains mild, other signs such as increase respiration rate, increase heart rate, and higher body temperature are more common.

Other causes of lameness in cattle must be differentiated from fescue foot. One simple method that will help differentiate fescue foot from footrot is to check the temperature of the foot. If the foot is cold, this is an indication that the problem is more likely fescue foot.

Since there is not a specific treatment for fescue foot, the condition must be managed. Cattle need to be observed daily for any signs of lameness or stiffness during the first few weeks on fescue pastures. This should be done early in the morning before cattle walk off the stiffness. Producers should pay close attention during cold weather, especially when rain, snow, or ice are present. Any animal showing clinical signs of fescue foot should be removed from the pasture and placed in a clean environment. The animal should be fed a ration with no fescue toxins.  

The best but most costly solution to reduce fescue toxicity is to renovate old pastures with new endophyte friendly varieties. If this option is not possible, producers might try interseeding fescue pastures with clovers or other grasses. This should dilute fescue toxins. Nitrogen fertilization may increase ergot alkaloids, so producers should avoid fertilizing fescue pastures with high amounts of nitrogen. Researchers have demonstrated that feeding a supplement while grazing fescue pastures reduces clinical symptoms. Some studies indicate a difference in susceptibility to fescue toxicity in some cattle. Selecting cattle based on genetic tolerance of fescue toxins is an option. (For more information go to www.agbotanica.com/t-snip.aspx)

With large areas in Oklahoma covered with Kentucky-31 fescue pastures, fescue foot as well as other fescue toxicities are not going away any time soon. Livestock producers will need to watch their livestock closely for any signs of fescue toxicity and manage their pastures to keep toxins as low as possible. If producers would like more information on fescue foot, they should consult their veterinarian and/or visit their local Oklahoma State University Cooperative County Extension Agriculture Educator.