By Ralph Chain
I’ve had some pretty interesting experiences in my acquaintance with Jake Graham. At one time we use to feed sheep. Jake ran a feed grinder for George Kech. He would grind hay for our sheep operation.
Sue, Jake’s wife, had inherited a large ranch east of Bouse Junction, Okla., when her father died. They wanted to stock this ranch with cattle. Jake came to grind feed and told of hearing about this really good herd of Angus cows for sale in the sand hills of Nebraska. Jake and Sue were wanting to look at the cows and probably try to buy them to stock their ranch. They needed a partner because there were more cows than they needed. Jake wanted to know if we would be interested in buying these cows with them, so Jake and I drove up to O’Neill, Neb., and looked at the cows.
They belonged to Alfred Drayton. He was building this herd up for a long time. They showed these calves in Chicago at the International Livestock Show and did well. The calves off of this group of cattle were sold to Eli Peterson and Bob Letkey in Truman, Minn. The Peterson’s bought the calves from the Drayton’s for several years.
When Alfred Drayton decided to sell out the herd, a fellow by the name of Dale Hewitt, a cattle dealer who was sending the Drayton calves to the Peterson’s and Bob Letkey in Minnesota, contacted Jake and I.
He wanted to know if we would be interested in selling the calves off of this group of cows to the Peterson’s in Minnesota when the calves got ready to wean in the fall. We said we might be interested. He said that they also might be interested in our other calves.
We bought this group of cattle and sent them to Oklahoma and split them up. There were about 300 commercial Angus cows and about 50 or 60 registered cows. We bought everything that he had — yearling heifers, bred heifers, his registered herd — we bought the entire group. We split the commercial cows up, and kept the registered cows together as a partnership and ran them on land south of Fairview that Jake’s mother owned.
The Peterson’s wanted to come and look at our calf crop, so Lee and his dad and Bob Letkey, flew to Oklahoma. We picked them up and showed them around, and they bought the calves, plus other calves.
We became well-acquainted with the Peterson’s and the Letkey’s and dealt with them for several years. They bought our calves every fall, and we shipped them to Minnesota. They visited us, and we visited them. It was a real good relationship between us and the Peterson’s.
A fellow by the name of Frank Bringham had a flying service and sprayed weeds and brush for us.
He said, “If you ever want to go anywhere just call us, we’ve got a Cessna 172, and would be happy to fly you.” He said, “You’ve done so much business with us, it won’t cost you anything.”
It was late summer, and my dad was still alive. We decided to go to see the Peterson’s in Minnesota and look at the cattle and see if they were interested in buying our calf crop again that fall, and, also, go on in to Canada and go fishing.
I told my dad about our plans and told him we might do this. I told him that Frank Bringham would fly us for nothing. That made it all the more interesting to him, because he was going to get a free trip out of the deal. We decided to get Frank to fly us to Canada and fish for three or four days. I made the arrangements and called Frank and told him what we wanted and asked him if he would be interested. He said he would be happy to go.
On a Sunday night he called and said he couldn’t go. He was the chairman for the hospital board at Geary, and they planned a meeting so he couldn’t fly us, but said his son, Davey, could fly us if that was all right. I knew that Davey had been flying one of the spray planes and I figured he was a guy about 24 or 25 years old. I said, “That’s fine as far as I’m concerned, he’s a good pilot.” Frank asked me how big we all were. I told him we were all pretty good size. He thought his 172 plane might not be big enough so he was going to borrow an airplane from his mechanic who lived in Elk City. It was a Beech Bonaza, which was bigger and flew faster. He said we could take that plane instead of his smaller one. So we made the arrangements, Davey was going to meet us at the Fairview Airport Monday morning. We gathered up our suitcases and fishing tackle. My dad, mom, Darla, and I had all went to the Fairview airport. Jake and Sue were there. The wives were going to see us off on our trip.
We were supposed to meet the pilot of the plane about 8 a.m. We went to the airport and waited and waited and waited. He was about 45 minutes to one hour late. When the plane finally came in and landed, it looked like a fairly decent airplane. We were standing on the runway with our suitcases and fishing tackle ready to leave.
The plane taxied up to us, the door opened, and the pilot got out. The pilot was a kid, about 15 or 16 year old, we were dumbfounded. My dad began to swallow and began to have mixed emotions.
We didn’t know what to say. We didn’t want to tell him that we were afraid to go with him. So, we walked around the airplane and kind of discussed things to his back. We discussed whether we ought to go with this kid or not.
I know he wasn’t over 16 years old, but he had flown spray planes because he had sprayed for us. When he was spraying, I didn’t know how old he was, but I just figured he was 25 or 26 years old. Here he was, this 16 year old kid, and we debated.
My dad walked up to this kid and asked, “Are you sure you can fly this airplane?” And this kid said, “Well, yeah I think I can fly it.” That didn’t help matters any. He didn’t act like he was really sure whether he could fly it or not.
My dad asked. “Have you flown this before?” This kid said, “Well, no not really, this morning was the first time I had flown it.” We didn’t know what to do. We decided maybe the Lord would be with us, and we would go. So, we put all of our stuff in the plane and took off.
Read the March issue to learn more!
Barry Whitworth, DVM
Area Food/Animal Quality and
Health Specialist for Eastern Oklahoma
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.
Dropping Like Flies-Prussic Acid in Cattle
As the year progresses many producers look to move cattle to alternative pasture. Unfortunately, certain weather conditions, including drought or freezing, can set up some plants in the sorghum family, including Johnson grass, to become toxic. Even after limited grazing, deaths may be seen due to the ingestion of prussic acid, also known as hydrocyanic acid or cyanide. A classic call to the veterinarian is, “My cattle are dropping like flies.”
Prussic acid toxin is created when the harmless hydrocyanic glycosides in plants are stressed and breakdown. Once the hydrocyanic glycosides in the plants are damaged through actions like cattle chewing or a swather and crimper, they quickly convert to prussic acid. Following ingestion, the prussic acid is released in the rumen and rapidly absorbed into the blood stream.
Once in the circulatory system, the toxin prevents cells from taking up oxygen. The blood therefore becomes saturated with oxygen leading to blood that appears bright cherry red. The clinical signs most often seen include excitement, muscle tremors, increased respiration rate, excess salivation, staggering, convulsions, and collapse. Asphyxiation at the cellular level is the cause of death due to deprivation of oxygen.
When producers encounter animals displaying clinical signs of prussic acid toxicity, they should immediately remove all the animals that appear normal to a new pasture and contact their veterinarian. The veterinarian will treat the sick animals with two drugs (sodium nitrite and sodium thiosulfate) that can reverse the toxicity. Treatment must be initiated quickly but can prove difficult due to the rapid progression of the toxin.
The drugs used to treat prussic acid toxicity can be difficult to obtain. It is advisable to contact your veterinarian before grazing potential toxic plants to make sure that your veterinarian will have availability to respond and the necessary drugs on hand to treat the cattle if a problem arises.
Read more in the August 2022 issue of Oklahoma Farm & Ranch.
A question sometimes asked by backyard poultry enthusiasts is “Can turkeys and chickens be raised in the same area?” A simple answer is that many backyard poultry producers do; however, many poultry experts would caution poultry producers about comingling these two species. The reason for this is a small protozoan parasite called Histomonas meleagridis.
H. meleagridis is a flagellated ameboid protozoan. The survival of this protozoan is dependent on Heterakis gallinarum, commonly referred to as the cecal worm of poultry. The cecal worms eat the protozoans. Once inside the cecal worm, the female cecal worm incorporates the protozoan in her eggs. The contaminated cecal worm eggs are shed in the bird’s droppings. At this time, H. meleagridis can be transmitted to domestic birds by ingestion of the contaminated cecal worm eggs or intermediated host (earthworms) that has ingested the contaminated eggs. Also, the protozoan can be transmitted directly from one bird to another bird. Unless protected in the cecal worm eggs or earthworms, H. meleagridis only survives a short period of time in the environment.
Several different species of birds (turkeys, chickens, ducks, geese, game birds, zoo birds) have been infected with H. meleagridis. Turkeys are considered the most susceptible with high morbidity and mortality rates. Young turkeys seem more susceptible than older turkeys. Blackhead can be rapid with birds appearing healthy in the morning and sick and/or dead by the afternoon. This makes control difficult. Chickens are easily infected but unlike turkeys, they have a milder form of the disease. Although not as deadly as in turkeys, production losses can be substantial with chickens. The difference between the severity of disease between turkeys and chickens may be explained by the turkey’s poor immune response compared to chickens. Lastly, some studies indicate that the development of disease is dependent on the presence of bacteria (Clostridium perfringens, Escherichia coli) or other microorganisms such as coccidia (Eimeria tenella).
Once a bird is infected with H. meleagridis, the protozoan penetrates the intestinal cecal wall of the bird. They will multiply and enter the bloodstream. Eventually, the protozoans infect the liver. The protozoans can be found in other tissues as well. Clinical signs will develop in one to two weeks.
Infected turkeys will display clinical signs such as yellow stained feces, anorexia, drooping wings, drowsiness, and problems walking. Eventually, turkeys will become emaciated. Studies have found sickness rates greater than 80% and death rates up to 100% in turkeys. As mentioned earlier, chickens tend to have milder forms of the disease; however, mortality rates around 30% have occurred.
Diagnosis of blackhead disease should be based on laboratory testing; however, poultry producers can make a presumptive diagnosis based on clinical signs, morbidity/mortality rates, and viewing the internal tissues. The primary internal lesions seen are in the ceca and liver. The cecal lesions are thick cecal walls with a cheesy like core and inflamed surfaces with an occasional ulcerated area. The liver will have circular dead depressed areas surrounded by red raised areas (bulls-eye-like lesions).
All previous approved drugs used to treat/prevent/control blackhead disease have been banned by the United States Food and Drug Administration. Several different prevention and control practices have been suggested with few being thoroughly researched. One key is to start with healthy chicks and turkey poults. Studies have shown that beginning with high quality young reduces issues with blackhead disease. Some recommended practices by poultry experts are confirming the diagnosis of blackhead disease, maintain a proper environmental (wet moist conditions favor the development of the protozoan), control coccidiosis, control internal parasites (cecal worm) through deworming, do not comingle chickens and turkeys, and follow biosecurity protocols. Development of resistant genetic lines of birds has the potential to reduce the incidence of the disease. Several different natural treatments/preventions (essential oils, oregano, garlic, rosemary, etc.) have shown promise in laboratory conditions, but have not been researched in the field situations.
Fortunately, blackhead disease has not been found to be a major cause of death in backyard poultry operations; however, backyard poultry enthusiast should be careful when commingling turkeys and chickens. If a producer would like more information about blackhead disease, they should contact their local veterinarian and/or their local Oklahoma State University Cooperative County Extension Agriculture Educator.
Cadmus, K. J., Mete, A., Harris, M., Anderson, D., Davison, S., Sato, Y., Helm, J., Boger, L., Odani, J., Ficken, M. D., & Pabilonia, K. L. (2019). Causes of mortality in backyard poultry in eight states in the United States. Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc, 31(3), 318–326.
Clark, S., & Kimminau, E. (2017). Critical Review: Future Control of Blackhead Disease (Histomoniasis) in Poultry. Avian diseases, 61(3), 281–288.
Swayne, D.E. and Halvorson, D.A. 2003 Influenza. In Y. M. Saif (ed.). Diseases of Poultry, 11th ed. Iowa State Press: Ames, Iowa, 135-160.
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