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.  

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

A ranch in Australia experienced an abnormally high number of stillbirths and weak born calves in 2004-2005. An investigation revealed that the usual infectious causes were not the problem. After additional testing, veterinarians diagnosed low levels of vitamin A as the cause.

According to Dr. Greg Hanzlicek, with the Kansas State Veterinary Diagnostic Laboratory (KSVDL), Kansas had an unusually high number of stillbirth cases and weak born calves in the spring of 2019. After many laboratory tests, it was concluded that the problem stimmed from a lack of energy, protein, Vitamin A, or combinations of all of these.

Both of the above examples demonstrate the importance of vitamin A in reproductive efficiency. Research has shown that low vitamin A levels during pregnancy are associated with abortions, stillbirths, and weak born calves. In addition to playing an important role in reproductive efficiency, vitamin A is essential for vision, bone growth, and maintaining epithelial tissue such as skin and hooves.

Animals obtain vitamin A from consuming green forage and/or the addition of vitamin A supplements to the diet. Lush green pastures contain high amounts of vitamin A. As plants mature and during times of drought, the amount of vitamin A decreases. The ranch in Australia experienced below average rainfall in the previous two years prior to the calving season. During the calving season, rainfall was below average with very dry conditions and little green forage was available.

In general, animals obtain adequate amounts of vitamin A by grazing green forage. Animals grazing green pastures will build a healthy store of vitamin A in the liver. When vitamin A is in short supply, the stores in the liver prevent deficiencies. According to Dr. Lalman, Extension Beef Cattle Specialist Oklahoma State University, the stores should last 2 to 4 months during times of deficiency. During times when green forage is not available, vitamin A supplements need to be added to the diet to prevent deficiencies.

When vitamin A levels are deficient, night blindness is one of the earliest clinical signs. Other eye issues include clouding of the cornea, ocular discharges, and possible ulcerations. Skin issues found when levels of vitamin A are deficient include a dry rough coat, scales on the skin, and dry cracked hooves. Other neurological signs include incoordination or gait problems. Seizures may occur due to the increase cerebrospinal fluid pressure. Birth defects have also been attributed to low vitamin A levels.

Animals displaying vitamin A deficiency should be treated immediately with vitamin A injections. If treated early, response is usually rapid and complete. However, delaying treatment may result in irreversible damage. Even with treatment, cattle with vision impairment due to vitamin A deficiency may not regain their sight.

Preventing Vitamin A deficiency depends on producers being attentive to the environmental conditions that favor low vitamin A levels in forage. During these times, producers need to supplement the diet with vitamin A. Producers need to be aware that Vitamin A supplements degrade rapidly, so vitamin A supplements should not be stored for long periods of time. In addition to vitamin A supplementation, research indicates that diets low in protein result in poor absorption of vitamin A. It is important that producers ensure that the rations have sufficient protein levels. Lastly, since colostrum contains high levels of vitamin A, producers need to ensure that newborns obtain adequate amounts of colostrum at birth.

Similar to the Australian example, most of Oklahoma had below average rainfall for the year of 2022. This resulted in pasture quality decreasing earlier than normal. Due to this year’s lack of green forage, liver stores of vitamin A may be inadequate for the animal’s needs. Producers need to ensure that the diets of their cattle have adequate amounts of vitamin A, energy, and protein. For more information about Vitamin A, producers should contact their veterinarian and/or visit with their Oklahoma State University County Ag Educator.

References

Hanzlicek, G. (2019, May). Difficult Calving Season Findings:2019. Diagnostic Insights. www.ksudl.org/resources/news/diagnostic_insights/may2019/difficult-calving-season2019.html.

Hill, B., Holroyd, R., & Sullivan, M. (2009). Clinical and pathological findings associated with congenital hypovitaminosis A in extensively grazed beef cattle. Australian Veterinary Journal, 87(3), 94–98.

Parker, E. M., Gardiner, C. P., Kessell, A. E., & Parker, A. J. (2017). Hypovitaminosis A in extensively grazed beef cattle. Australian veterinary journal, 95(3), 80–84.