Farm & Ranch
Histomoniasis (Blackhead)
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.
References
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.
Farm & Ranch
External Parasites in Backyard Poultry
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 entomology, 53(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 entomology, 109(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.
Farm & Ranch
Scrapie
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
Farm & Ranch
Acorn Toxicity
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.
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