Feed rations should be evaluated to determine if they are providing adequate levels of selenium and vitamin E. If dietary levels of selenium are inadequate, lambs can be given an injection of selenium and vitamin E shortly at birth. Dietary supplementation of selenium is usually preferred to selenium injections.

White muscle disease in sheep and goats 

tiff lamb disease – nutritional muscular dystrophy

What is it?
White muscle disease (WMD) is a degenerative muscle disease found in all large animals. It is caused by a deficiency of selenium and/or vitamin E. Generally, it is not known which. Selenium (Se) deficiency is associated with selenium deficient soils and the inadequate uptake of selenium by forages grown on these soils. Certain areas of the U.S., including the Northeast, are considered low in selenium levels. Selenium deficiency occurs when the soil contains less than 0.5 mg Se/kg of soil and locally harvested feeds contain less than 0.1 mg Se/kg of feed.

Vitamin E deficiency is independent of soil type and more closely reflects forage quality. Grazing animals usually consume adequate amounts of vitamin E. This is because fresh legumes and pasture are good sources of vitamin E, whereas silage, oil seeds, root crops, cereal grains, and dry hays tend to be poor sources of vitamin E. Prolonged storage of feedstuffs results in a degradation of Vitamin E activity, as much as 50% per month.

In addition to WMD, selenium and vitamin E deficiencies can produce symptoms of ill thrift and reproductive losses: lower conception rates, fetal reabsorption, dystocia, retained placenta, reduced milk production, and reduced semen quality. They can cause poor rate of growth or ill thrift in young lambs throughout the growing period. Sheep consuming selenium-deficient diets produce low wool yields and have increased incidence of periodontal disease. Selenium and vitamin E also play key roles in the animal’s normal immune response.

Symptoms
All breeds of sheep and goats are suceptible to WMD, and the condition may develop under extensive or intensive management systems. WMD is most commonly found in newborns or fast growing animals. Kids are believed to be more susceptible than lambs, possibly because they have a higher requirement for selenium. The disease can affect both the skeletal and cardiac muscles.

When the skeletal muscles are affected, symptoms vary from mild stiffness to obvious pain upon walking, to an inability to stand. Lambs/kids may tremble in pain when held in a standing position. A stiff gait and hunched appearance are common. Affected lambs/kids may remain bright and have normal appetites, but eventually they become too weak to nurse. When the problem occurs in newborns, they are born weak and unable to rise. Sudden exercise may trigger the condition in older lambs and kids.

When the disease affects the heart, the animal shows signs similar to pneumonia, including difficult breathing, a frothy nasal discharge (may be blood stained), and fever. The heart and respiratory rates are elevated and often irregular. Skeletal and cardiac muscle disease may occur concurrently.

Selenium deficiency can be confirmed by measuring selenium levels in whole blood or tissues. A diseased animal will have less than 0.04 ppm of selenium in its blood. Breeding ewes require more selenium, and their blood levels should be over 0.5 ppm. At necropsy, the muscles of affected animals appear paler than normal and may show distinct longitudinal striations or a pronounced chalky appearance due to abnormal calcium deposition.

Treatment
Treating the heart form of WMD is usually ineffective and those that survive often do not thrive because of the residual cardiac damage. The muscle form of the disease can be successfuly treated with supplemental selenium and/or vitamin E. Producers need to follow label directions carefully when using selenium for treatment. The concentrations of selenium (per ml) vary greatly with each product, and excessive or repeated injections can result in selenium toxicity and possibly death.

The commercially available selenium/vitamin E product(s) commonly used in the U.S. do not contain therapeutic levels of vitamin E. Additional vitamin E may need to be provided through an injection of vitamin E alone or through oral vitamin E products. Affected animals usually respond favorably to a single treatment of vitamin E and/or selenium in 24 hours, though recovery may not be complete, depending upon the severity of the condition. Animals which do not respond to treatment may be treated a second time. Treatment should not exceed two doses.

Prevention
Deficiencies occur when animals are fed poor-quality hay or straw or lack access to pasture. High concentrations of other minerals (e.g. calcium, sulfur, copper) and feed contaminants (e.g. nitrate, unsaturated fats, sulfates) may decrease absorption of selenium in the small intenstine. Diets high in polyunsaturated fatty acids or deficient in Vitamin C and/or beta-carotene increase vitamin E requirements, whereas adequate dietary selenium is almost completely protective against vitamin E deficiency.

WMD can be prevented by supplementing the diet of susceptible animals with selenium and vitamin E. Since it occurs mostly in lambs and kids whose mothers were fed a selenium-deficient diet, supplementation of pregnant animals helps reduce disease in newborns. This is because selenium is transferred from dam to fetus across the placenta and also is present in the colostrum. While not much Vitamin E is transmitted across the placenta, colostral levels of Vitamin E increase with ewe/doe supplementation.

While pasture, hay, grain, and other supplements can be analyzed to determine the amount of selenium to be added to supplemental feeds, it is important to note that selenium supplementation is controlled by law. For sheep, selenium can be supplemented in a complete ration at a level up to 0.3 ppm, in a feed supplement so that the intake of selenium does not exceed 0.7 mg per head per day, and in salt/mineral mixes at 90 ppm as long as total daily consumption does not exceed 0.7 mg/head/day. Selenium supplementation of feed has not been approved specifically for goats.

Injectable selenium compounds are available to prevent WMD in at risk-animals; however, injections are a poor alternative compared to routinely providing adequate selenium and vitamin E in the diet. Ideally, the total diet for sheep and/or goats should contain 0.10 to 0.30 ppm of selenium.

The exposed vagina of affected ewes should be washed with soapy disinfectant solution and forced back into the ewe. A bearing retainer or “spoon” can be inserted and secured in the ewe to prevent further prolapsing. In a ewe that has lambed, sutures are used to secure the prolapse. Affected ewes and their offspring should probably not be kept in the flock for breeding animals due to the possibly hereditary nature of the problem.

The uterus should be cleaned with a warm, soapy, disinfectant solution prior to replacement and should be replaced before the tissues become dry or chilled. Pouring water into the uterus will help to ensure that the tips of the horns are unfolded. Affected ewes should be given antibiotics and oxytocin. Unlike ewes that prolapse their vaginas, it is okay to keep a ewe that has prolapsed her uterus.

The most common cause of urinary calculi is feeding rations with high phosphorus levels. Grain products tend to be very high in phosphorus relative to calcium, whereas forages, especially legumes, have a much more desirable ratio. The ratio of calcium to phosphorus in the ration should be at least 2:1. Providing the proper balance of minerals in the ration is preferred to offering minerals free choice, since there is no guarantee animals will consume adequate amounts of free choice mineral.

The addition of ammonium chloride to the ration will aid in preventing urinary calculi. It is also important that animals have an ample supply of clean, potable water. The addition of salt to the ration will increase water intake and decrease stone formation.

Urinary calculi in sheep and goats

a.k.a. Urolithiasis – Water Belly – Calculosis

What is It?
Urinary calculi or “water belly” is a common metabolic disease of male sheep and goats. The disease occurs when calculi (stones), usually comprised of phosphate salts, lodge in the urinary tract and prevent urination. Normally, phosphorus is recycled through saliva and excreted via feces in ruminants. High grain, low roughage diets decrease the formation of saliva and therefore increase the amount of phosphorus excreted in the urine.

The primary cause of urinary calculi is feeding concentrate diets which are excessive in phosphorus and magnesium and/or have an imbalance of calcium and phosphorus. Lack of water and water sources that are high in minerals are also contributing factors.

Who’s at Risk?
While urinary calculi can occur in intact males, wethers are at greatest risk because castration of young males removes the hormonal influence (testosterone) necessary for the penis and urethra to reach full size.

Lambs castrated within the first month of life are most vulnerable. For this reason, some veterinarians advocate delaying castration until after puberty. If castration is performed after puberty, it should be done under anesthesia by a veterinarian.

It is generally recommended that lambs and kids be castrated between 1 and 7 days of age, especially if rubber bands are used. The better recommendation might be for producers to carefully consider whether it is necessary or desirable to castrate ram lambs and buck kids. Intact males grow faster and produce leaner carcasses, and there is no difference between the meat from a young intact male and a castrated lamb or kid.

In females, calculi are formed, but excreted due to anatomic differences in the male and female urinary tract.

What are the Symptoms?
Clinical signs vary. They usually start with restlessness and anxiety. Affected animals may experience abdominal pain, urine dribbling, distention and rupture of the urethra. They will usually experience a loss of appetite. They may have a humped-up appearance and edema under their belly. They may kick at their belly and strain to urinate. Dribbled urine may be bloody.

As pain and discomfort increases, affected animals will isolate themselves. In goats, there may be increased vocalization and tail twitching. If left untreated, affected animals will die when the bladder bursts and urine fills the peritoneal cavity and is absorbed into the bloodstream. Sometimes, it may be necessary to humanely destroy an affected animal to avoid further suffering.

How to You Treat It?
Treatment of urinary calculi depends upon the location of the obstruction and could be as simple as snipping off the urethral process to allow calculi at the end of the penis to dislodge. Tranquilizers and antispasmodics may help to naturally dislodge some calculi. In more advanced cases, surgical intervention may be necessary to save valuable animals or pets. Veterinary advice should be sought in this case.

How Do You Prevent It?

Like most disease conditions, it is better to prevent urinary calculi than to treat it. It can be prevented by feeding rations which contain a calcium-to-phosphorus ratio of at least 2:1. The ratio of Ca:P should never be allowed to go below 1:1. High calcium diets are effective at reducing the absorption of phosphorus from the GI tract.

Neither magnesium or phosphorus should be added to concentrate diets. Diets should also contain adequate amounts of vitamin A. Supplements should not be haphazardly added to otherwise balanced rations. Horse feed should not be fed to small ruminants because horse diets are not balanced for ruminants and can lead to stone formation

Extra calcium is well tolerated by sheep, so where rations are unbalanced, they can be counterbalanced by adding ground limestone (not dicalcium phosphate!). Legume hays (alfalfa, clover, lespedeza, etc.) are good sources of calcium. In addition, roughage will increase salivation and rumination which will increase the amount of phosphate excreted in the urine.

Cereal grains (corn, barley, etc.), on the other hand, have an abnormally low calcium-to-phosphorus ratio: 1:4 to 1:6. Therefore, rations containing cereal grains need to be balanced with other feeds or mineral sources to form a complete ration that has the proper ratio of calcium and phosphorus.

When formulating your own feed rations, you need to include minerals in the ration or a source of calcium (such as legume hay).  Free choice minerals may not be adequate to prevent urinary calculi in male goats and sheep, since you do not know if they are consuming sufficient quantities of the mineral. Minerals should be force-fed. When feeding textured feeds or mixed rations (e.g. whole grain + pellets), you need to make sure the animals are not picking at certain feed ingredients. This can also lead to an imbalance of Ca and P being consumed.

Adequate water intake is also necessary to prevent urinary calculi. Inadequate water intake causes the urine to be more concentrated, which makes the formation of stones more likely. Water should be proper temperature and clean. Force feeding salt (up to 4% of the ration) will help to increase water intake. However, salt should not be added to the water source, since lambs and kids will find it unpalatable and drink less water.

The use of ammonium chloride at a level of 0.5 percent of the total diet will help to acidify the urine and prevent the formation of calculi. Most commercial lamb and meat goat diets contain ammonium chloride, as well as the proper ratio of Ca:P.

The cause of the condition appears to be genetic alteration due to selection for extreme length and height in show sheep. The disease is found predominantly in black-faced lambs: 75% Suffolk and 25% Hampshire. In order to have this disease, lambs must inherit a recessive gene from each parent. Several labs offer genetic testing for spider lamb disease.

While the occurrence of scrapie in the U.S. sheep flock is low, it is a disease of regulatory concern. This is because scrapie is a member of a family of diseases called “transmissible spongiform encephalopathies (TGE’s), which also includes chronic wasting disease (in mule deer and elk), mad cow disease (bovine spongiform encephalopathy) and classic and new variant Creutzfeldt-Jacob’s Disease (in humans).

Producers of breeding stock are encouraged to enrolled in the voluntary scrapie flock certification program, which after five years of scrapie-free monitoring, enables a flock to be certified “scrapie-free.” Furthermore, while scrapie is not a genetic disease, a sheep’s genetic make-up influences its susceptibility to scrapie if exposed to the infective agent. Therefore, sheep can be tested for scrapie resistance.
Scrapie is an always-fatal disease affecting the central nervous system (CNS) of sheep and goats. It is a member of a family of diseases called Transmissible Spongiform Encephalopathies (TSE’s).

Other TSE’s include bovine spongiform encephalopathy (BSE), better known as “mad cow” disease; chronic wasting disease (CWD) in deer and elk; transmissible spongiform encephalopathy in mink; feline spongiform encephalopathy in cats; and in humans: Kuru, Gerstmann-Straussler-Scheinker syndrome, fatal familial insomnia, and both classical (CJD) and new variant Creutzfeldt-Jakob disease (nvCJD).

TSE’s cause sponge-like spaces in the brain of the affected animal. They affect the brain’s ability to control body functions and eventually cause death.

During the “mad cow” scare in Great Britain, scrapie was theoretically linked to “mad cow” disease which was linked to new variant CJD. It was proposed that cattle contracted BSE when they consumed meat and bone meal derived from scrapie-infected sheep carcasses and that humans developed nvCJD when they ingested BSE-infected beef.

The link between scrapie and mad cow disease has long since been discounted by scientists, as BSE is believed to be a new disease. The link between BSE and nvCJD has never been proven, despite its widespread acceptance as “fact.” Alternative theories have never received the same consideration as the infected feed theory.

While scrapie has been recognized as a disease for more than 250 years in Europe and the United Kingdom and has been in the United States since 1947, there is still much we do not know about it and how it is transmitted. Research continues to increase our understanding of what causes scrapie, how scrapie is transmitted, how it can be detected in the live and asymptomatic animal, and how genetics affects an animal’s susceptibility (and resistance) to the disease.

Cause(s)

The exact cause of scrapie and other TSE’s remains known. The causative agent has not been completely characterized. The popular theory is that the infective agent is a prion, an abnormally-shaped protein. Other theories maintain it is a virus with unusual characteristics or a virino ( a sub-viral particle).

The infective agent — whatever it is — is resistant to heat and other sterilization processes. It does not evoke an immune or inflammatory reaction in the host animal. It has a long incubation period. Infected sheep and goats usually do not show symptoms until 2 to 5 years after infection.

Symptoms can mimic other diseases, including ovine progressive pneumonia (OPP), pregnancy toxemia, listeriosis, rabies, toxins, and external parasites. Scrapie was so-named because affected sheep often scrape themselves against objects.

Transmission

Scrapie is thought to be spread most commonly from dam to offspring via infected placenta and placental fluids. Genetically-susceptible ewes and lambs in the same lambing environment are considered at-risk for developing the disease. While rams and bucks can get scrapie, they are not believed to be involved in the transmission of the disease. Semen is not known to transmit infectivity.

Other oral routes of transmission are possible. It was recently learned that infective scrapie prions can be transmitted to lambs through the milk. Soil may also serve as a reservoir for the disease. In Iceland, scrapie has re-occurred on farms that were depopulated and disinfected, as long as 16 years after the last sheep left the farm.

Feed is not considered to be a significant factor in the transmission of scrapie. Scrapie is not known to pose a human health risk.

Environmental factors

Organic farmer and scientist Mark Purdey (now deceased) hypothesized that BSE (and other TSE’s) is the result of environmental pollutants and chemical imbalances. The prion protein needs copper to keep its structure. If copper is not available, the prion protein can take up manganese and unfold, causing disease.

In scrapie-infected areas of Iceland, researchers determined bioavailable manganese to be very high, whereas soluble and free copper were very low. In other studies, sheep infected with scrapie have been shown to have higher manganese levels in their blood before clinical symptoms developed, leading scientists to theorize that manganese levels could serve as a diagnostic marker for prion diseases.

Genetically-resistant sheep show similar high levels of manganese when challenged with the disease, suggesting that changes in blood manganese are a result of scrapie challenge and not a consequence of scrapie pathology. Purdey postulated that high levels of manganese and low levels of copper favor the occurrence of natural scrapie.

Genetic testing

Scrapie is not a genetic disease; but a sheep’s genotype (DNA) affects whether it will develop the disease if it is exposed to the infective agent. A simple blood or tissue test, done at any age, can be used to determine a sheep’s resistance or susceptibility to scrapie. It is important to note that genetically-susceptible sheep are not carriers for the disease. Nor will they develop the disease if they are not exposed to the infective agent.

Sheep have one pair of genes that affect scrapie resistance and susceptibility, called PRNP. A lamb receives one copy of the gene from each of its parents. All genes are made up of codons. Four codons are known to affect scrapie resistance and susceptibility. As there are different strains of scrapie, codon 171 is the major one that determines scrapie resistance and susceptibility in the United States.

Sheep that are RR at codon 171 are very resistant to scrapie. Sheep that are QQ are the most susceptible to scrapie and almost all known cases of scrapie have been QQ sheep. Sheep that are QR are usually resistant to scrapie. Some states have programs to help producers get their rams tested for scrapie resistance/susceptibility. RR rams (or ewes) will not produce any offspring that are susceptible to scrapie.

So far, there doesn’t appear to be any negative correlation between scrapie resistance/susceptibility and any important production traits. Resistant genotypes have not been identified in goats yet.

Live animal testing

For many years, the only way to detect scrapie was to perform a necropsy and examine the brain tissue of the dead animal. It wasn’t until 1998 that a pre-clinical test for live animals was developed. The third eyelid test extracts lymph tissue from the third eyelid. Prions collect in the lymphoid tissue in the sheep’s third eyelid.

In early 2008, rectal biopsies were approved as another live animal test for scrapie. As compared to the third eyelid test, rectal biopsies are easier to perform, have less complications, and are just as accurate.

Also in 2008, a company in Europe announced the detection of exogenous prions in the blood plasma of asymptomatic scrapie-infected sheep. Amorfix Life Science, Ltd. is currently in discussions with potential partners to get regulatory approval and commercialize the test. A simple blood test to detect scrapie would aid greatly in the worldwide eradication of scrapie.

Slaughter surveillance

The incidence of scrapie in the United States is considered low. Slaughter surveillance studies conducted from February 2001 to March 2002 revealed a scrapie incidence of only 2/10 of one percent in the U.S. sheep population (1 in 500 sheep). States east of the Mississippi River have a higher incidence of scrapie (0.52 percent) than other regions in the U.S. While scrapie can affect any breed of sheep or goat, it is most commonly diagnosed in black-faced sheep and their crosses.

Though goats are just as susceptible to scrapie as sheep, only 21 goats have ever been diagnosed with scrapie in the U.S. Surveillance of scrapie incidence in goats is currently underway. None of the first 685 goats in the surveillance study (from Texas) have tested positive for scrapie. However, in December 2007, a 3-year old Nubian goat from a farm in Michigan tested positive for scrapie. Four additional goats were diagnosed with scrapie. It is not known how the original goat contracted the disease. Sheep had previously been kept on a farm where the goat was kept, but the goat did not have any direct contact with sheep. Goat-to-goat transmission most likely occurred.

Atypical scrapie

Last year, the first case of Nor98 atypical scrapie was diagnosed in a sheep in the United States. Four additional cases have followed. Nor98 is so-named because it was first discovered in 1998 in Norway. It has been diagnosed in sheep and goats in numerous countries in Europe, though fewer than 300 cases have been reported worldwide.

Nor98 differs from classical scrapie. It occurs mostly in sheep that are over 5 years of age. Twenty-five percent of the cases occur in sheep that are over 10 years of age. Nor98 seldom occurs in more than one sheep in a flock, unless it is a very large flock.

It is not known if and how Nor 98 is transmitted. It may occur sporadically. Horizontal transmission has not been ruled out. Nor98 can affect sheep that are genetically resistant to classical scrapie. The distribution of prions in sheep affected with Nor98 is different from classical scrapie. The current live animal tests do not detect Nor98.

Nor98 complicates scrapie eradication efforts. The World Organization for Animal Health has not yet decided how Nor98 will affect international trade.

Ryegrass staggers has not been recorded in goats. Affected animals have a stiff gait or are unable to walk. They may injure or kill themselves in transit. The toxins can induce high body temperatures thus animals will try to cool themselves. Younger animals tend to be worst affected. The symptoms of ryegrass staggers usually develop 7-14 days after livestock stock start grazing the toxic parts of the plant. Prolonged exposure to toxic pasture can lead to permanent neurological damage.