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Farm & Ranch

The Barn

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By Ralph Chain

In 1935 and 1936, when we used to work a lot of mules, my granddad and dad decided to build some mule barns. So, in 1935, we built the first barn where my dad lived and in 1936 we built a barn where my granddad lived. All the work on these barns was done by hand, back before we had cement mixers and the conveniences of life. The work was done by hoe or shovel.

Our neighbors, Sale and Dwight Bennett, and their dad, Claude, helped build the barns. The old man who laid the tile on the barn was Bill Hopper. He was an old bachelor and where he came from or where he went I do not know. But he stayed with my mother and father all during this time while building the west barn. It probably took two or three months to build a barn. He was particular about what he ate. My mother always had to cook for him, and she was glad to see him leave. He also laid the tile for my granddad’s barn. My grandmother cooked for him while he was building that barn.

We used the barn for mules until the late 1940s or early 1950s, when tractors took the place of our mules. I remember my dad trading a team of mules for a D John Deere tractor, which had steel wheel lugs on the back wheel, and you cranked it by hand. I think John Deere built these tractors and called them Argentine, because they were built for sale in Argentina.

When the mules left we converted the west barn. We took out the oat bins and mule stalls and moved our cattle working equipment inside the barn. Each barn had a long oat bin that ran the length of the barn. We filled these bins by scoop shovel with oats that were fed to our work mules.

We converted the east barn the same way but instead of moving our cattle working equipment I converted it to a sheep barn. We used to feed a lot of sheep, and we put the sheep feeders in the barn. Then we quit feeding sheep and the barn was converted into calving pens for our two-year-old heifers.

One day Newley, my grandson, approached me. He and Mandy Hill were getting married and he wanted to have the wedding in our converted school house. I asked him, “Why don’t you have your wedding in the barn?” He nearly fainted when I mentioned the barn. But I told him we would clean the barn up if he wanted to have the wedding there.

He needed to talk to Mandy’s mother, Glenda Hill, and see what she thought about it. She came and looked the barn over and said it if was cleaned up it would be all right. One of the biggest jobs was cleaning the hay out of the hay loft. Some of it had been there ever since the barn had been built. The only way to get it out was using pitchforks through a little door in the north part of the barn. It took three guys several months to get all the hay out of the loft.

It was amazing what they found in the hay. They found collars, harnesses and all kinds of mule and horse equipment. One of the main things they found was whiskey bottles, which had been hidden by some of the hands. They had hid them there because we didn’t believe in drinking.

Then the work started downstairs removing all the calving pens, and we poured a new cement floor. We got a steam cleaner and cleaned the walls, which helped a lot, and repaired some of the windows. On May 16, 1997, the wedding took place, and the reception was held in the hay loft. It went off great.

The barn has been used for all sorts of things from family reunions, hunting business, and special events for handicapped children. We have had people come from New York, California and even the Vice-President of Ecuador.

There is something always going on in the barn. The main event now is the Red Angus Sale that we have had for the past seven or eight years. There will be from 150 to 200 people in and out of the barn during the sale. Both barns are as good as they’ve ever been after 80 years. I don’t know of any other barns anywhere that are still standing after the horsepower went away and people starting using tractors. I can see no reason that the barns shouldn’t last another 80 years. Of course, a tornado or fire could destroy them in a matter of seconds.

Time changes things.

This article originally appeared in the September 2016 issue of Oklahoma Farm & Ranch. 

Farm & Ranch

Fescue Foot

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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.  

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Farm & Ranch

External Parasites in Backyard Poultry

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By Barry Whitworth, DVM, MPH | Senior Extension Specialist Department of Animal & Food Sciences | Ferguson College of Agriculture | Oklahoma State University

According to the 11th edition of Poultry Diseases, external parasites of poultry are arthropods that live on or in the skin and feathers. Essentially, parasites are freeloaders that live at the expense of the host. Backyard birds are infested with a variety of pests. Ticks, fleas, mites, and lice are some of the most common external parasites found in chickens, turkeys, and ducks. Several of these parasites are bloodsuckers. If not controlled, they can cause weight loss, decreased egg production, unthriftiness, and death in severe cases.

According to a study conducted by Dr. Amy Murillo and associates in California, the most common external parasites in backyard flocks were lice, fleas, and mites. Lice were the most frequently observed parasites, with the chicken body louse (Menacanthus stramineus) found on half of the premises inspected. The fluff louse (Goniocotes gallinae) was found in 35% of operations. The wing louse (Lipeurus caponis) and sticktight flea (Echidnophaga gallinacea) were present in 20% of flocks. Northern fowl mites (Ornithonyssus sylviarum), which are the most common mites found in commercial poultry operations, were detected in only 15% of flocks. However, the survey was conducted in the summer, which may have influenced the low number of northern fowl mites, since they are most active in the winter.

Birds infested with external parasites often become agitated due to skin irritation. They will spend more time preening and scratching. Their feathers may become damaged, and they may appear unhealthy. Birds showing these signs should be examined.

When examining birds for external parasites, producers should focus on the breast, back, head, vent region, and wings. Lice may be found on different parts of the body. They are yellowish in color and lie flat against the skin. Their eggs are typically found attached to the shafts of feathers. The vent area is the primary location to check for mite infestations and may appear “dirty.” Sticktight fleas are usually found embedded in the comb.

Birds should be monitored regularly. When producers are unable to examine all birds, they should focus on the young, the old, and any bird that appears unhealthy. The coop should also be inspected. Producers should examine the bedding, walls, and roosts, with close attention given to crevices and cracks where pests may hide.

Before parasite control can begin, the parasite must be correctly identified. Producers can use books or other publications for this purpose, or they may consult a veterinarian. Contacting the local Oklahoma State University Extension office is also a useful option. An agricultural extension educator may be able to identify the pest or submit samples to the Plant Disease and Insect Diagnostic Laboratory at Oklahoma State University for identification.

Prevention and control of external parasites require an integrated approach. The first line of defense is a strong biosecurity program to prevent parasites from entering the operation. Sanitation is also critical, keeping the coop and surrounding area clean helps prevent infestations.

Maintaining healthy birds is essential in preventing parasite infestations. Producers should focus on proper nutrition and disease prevention as they are key factors in maintaining a healthy flock. A strong immune system can help birds better withstand some external parasites.

Selecting the proper pesticide and using it correctly is essential. Many pests described in this article can be controlled with appropriate pesticides; however, their eggs are not killed, which requires repeated applications to target newly hatched larvae. Producers should read and follow pesticide label directions.

Alternative methods for external parasite control are also available such as providing diatomaceous earth mixed with sand for dust bathing or using sulfur bags to control mites and lice. For more information on these methods, see references below.

Finally, early identification and treatment greatly increase the chances of successful control. If infestations are allowed to become established, control becomes much more difficult.

For more information on external parasites in backyard poultry, producers may visit https://www.veterinaryentomology.org/ or contact their local veterinarian or Oklahoma State University County Agriculture Extension Educator.

References

Arends, J., J. (2003). External parasites and poultry pests. Diseases of Poultry. 11th Edition.

Murillo, A. C., & Mullens, B. A. (2016). Diversity and Prevalence of Ectoparasites on Backyard Chicken Flocks in California. Journal of medical entomology53(3), 707–71.

Murillo, A. C., & Mullens, B. A. (2016). Timing Diatomaceous Earth-Filled Dustbox Use for Management of Northern Fowl Mites (Acari: Macronyssidae) in Cage-Free Poultry Systems. Journal of economic entomology109(6), 2572–2579.

Murrillo, A.C., Mullens, B.A. (2016). Sulfur Dust Bag: A Novel Technique for Ectoparasite Control in Poultry Systems: Journal of Economic Entomology, 109(5), 2016, 2229-2233.

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Farm & Ranch

Scrapie

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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 research81(7), 600–614. https://doi.org/10.2460/ajvr.81.7.600

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