A FAMACHA training session will be held at the Great Lakes Fiber Show at
the Wayne County fairgrounds in Wooster, OH, on May 23. The schedule and
more information about the event can be found at
http://www.greatlakesfibershow.com/shows-sales.htm
For information about registering for the FAMACHA training contact Marlene & Carl Gruetter: 740-256-1866 or e-mail at trf@trfohio.com.

Green grass is beginning to peek through the brown plant residues on many Ohio pastures. If our weather pattern is typical this spring, we will soon be enjoying warmer, but wetter, weather. Although we will welcome the flush of new forage that this weather will bring, this is the major transmission season for one of the most common of sheep diseases: contagious footrot. Warm wet weather softens the hoof and soft tissues between the toes making the foot more susceptible to infection. It also favors the transmission of the causative bacteria, Dichelobacter nodosus (formerly Bacteroides nodsus), from the hooves of carrier sheep to the hooves of unaffected animals. For a review of the causes of virulent and benign footrot in sheep, as well as “scald,” the reader is referred to the August 2003 issue of the Sheep Team Newsletter at http://sheep.osu.edu or the appropriate section in the latest edition of the SID Sheep Production Handbook (available from ASI at: http://www.sheepusa.org/index.phtml?page=site/text&nav_id=42c985d7b36d445107825b11f21ff35b. )

When footrot appears in a flock, it often seems to go away, or become less severe, as the weather gets hotter and dryer in mid to late summer. Sometimes this appears to be a positive response to a treatment effort, and the shepherd thinks he/she has “cured” it. Unfortunately, eradication of footrot usually takes a planned and concerted effort in most flocks, and many shepherds find that what they thought had disappeared, reappears at this time of year when weather conditions increase the irritation to the foot and favor transmission of the bacteria. If your flock experienced a footrot problem last year, you might wish to begin considering how to deal with it again this year to limit the labor and production costs it often creates. Scientists usually advise that attempts at eradication of footrot during times of high probable transmission is unwise, but that attempts to control the disease should help limit the number of animals affected and the numbers of cases that progress to severe disease. There are two main methods for controlling footrot during the transmission period – vaccination and topical treatment with a footbath.

Footvax® is used for vaccination for D. nodosus in the US. This product contains ten strains of this organism in an oil-based carrier. When one of these strains is present in a flock, the vaccine may stimulate a strong immune response that provides protection from infection in many sheep and a significant reduction in severity of foot damage in many others. Unfortunately, some strains of this bacteria exist in the US that are not present in the vaccine, and the lack of complete cross-protection across strains often leads to disappointing results. There currently is no easy way to determine which strain is present in a flock, but if footrot has been a recurring problem, it may be worth using the vaccine to evaluate its potential usefulness. The vaccine requires a primary series of two injections at least six weeks, and not more than six months, apart. Booster vaccinations can be given at six-month intervals or annually just prior to an expected period of transmission. It is important to try to stimulate the highest immune response to precede, or coincide with, an expected period of transmission. Because the vaccine contains an oil base, users should carefully follow the label precautions and avoid accidental human injection.

Zinc sulfate in a 10% solution (8 pounds of zinc sulfate powder [hepta hydrate] in 10 gallons of water) is the most commonly recommended solution for use in footbaths. A small amount of powdered laundry detergent, about a half cup, is usually added to improve the penetration of hoof horn. Although formalin (formaldehyde) solutions have been recommended for footbaths in the past, they are very irritating if inhaled or splashed in the eyes, are quite irritating to the skin between the hooves, can cause the hoof to become hardened and difficult to trim, are less penetrating than zinc sulfate, and formalin is now classed as a probable human carcinogen. Research has shown that footbathing in a control effort helps primarily in the early stages of infection where it is limited to the skin between the toes and before serious damage to the horny tissue has begun. Therefore, if it is likely that the flock has footrot, footbathing should start early in the transmission period to limit the number and severity of new cases. Numerous recommendations for the length of time animals should spend in the footbath, from walk-through baths to one-hour soaks, can be found in the scientific literature. Although one-hour soaks can result in higher “cure” rates and longer protection against re-infection, they can be difficult to accomplish with large groups of sheep. Some researchers have gotten good results with 2-5 minute soaks, but these will probably need to be repeated weekly during seasons of high transmission. It is generally agreed that footbathing success is improved if the sheep have relatively clean feet when they enter the footbath and if they are placed on a clean dry surface for a couple of hours after bathing.

It is believed that the combination of vaccination and footbathing is more effective than either administered alone. Footbathing may be especially useful if vaccine use was delayed until the onset of the transmission season.

Contrary to popular belief, the bacteria that cause contagious footrot do not survive outside the sheep’s foot for more than seven days. This fact is critical to the success of eradication efforts (which are most successful during dry periods when transmission is unlikely). However, because neither vaccination or footbathing are likely to be 100% successful in the short term, and because many flocks will not have enough separate pastures to allow a contaminated paddock to rest seven days, spelling pastures during a transmission period is seldom possible or recommended. The goal of footrot control during a transmission period is the reduction of the number and severity of cases, not eradicating the disease.

Another common misconception is that foot trimming prevents footrot. Foot trimming does not prevent sheep from getting footrot. Foot trimming will improve the success of footbathing in sheep which have more advanced disease with hoof separation, or under-running, of the horny tissues of the sole and wall. Foot inspection and appropriate paring are critical to an eradication effort, but inspection and trimming of every animal’s feet may not be necessary for control efforts during seasonal periods when the risk of transmission is high. Excessive trimming can reduce the effectiveness of footbathing and can lead to permanent damage to the hoof. It is usually adequate to remove only the excessive horny tissue to expose pockets of infection to the footbathing solution.

Severe cases of footrot are costly and may create an animal welfare concern. A review of a flock’s past history and a little planning can reduce the impact of this disease and is particularly relevant as we approach warm wet weather this spring.

In the previous article we described the basic signs and causes of mastitis in ewes. Mastitis caused by bacteria can be acute or chronic. Acute mastitis often results in obvious signs in the ewe such as being off feed, feverish, and depressed along with changes in the milk. Chronic bacterial mastitis may not result in obvious signs or changes in the milk but may lead to loss of secretory tissue and scarring in the udder with reduced milk production. We also discussed the so-called “hard bag” syndrome caused by the virus that is considered the cause of ovine progressive pneumonia (OPP). In this syndrome, the ewe is often not visibly ill and the producer may not realize that she doesn’t have much milk until the lamb(s) is starving or grow(s) poorly. A common characteristic of flocks that are infected with the OPP virus is the presence of excessive numbers of orphan lambs.

It is not always easy to determine whether ewes that don’t seem to have enough milk have nutritional problems, chronic bacterial mastitis, OPP, or some other condition. Generally speaking, when several ewes in the flock that appear to be healthy, well fed, and in good body condition have firm or swollen udders and unthrifty lambs, mastitis should be suspected. Bacterial mastitis often affects only one half of the udder, although both halves can be affected. The milk may be off-colored and have flakes, but it may appear normal. The udder may or may not be swollen or hot.

If the OPP virus is the primary cause of a firm, swollen udder, both halves are usually affected. The udder is not hot to the touch, and it may not be really hard. Often it may actually appear normal, but there is very little milk in the udder. The ewe often has no signs of illness.

When more than the occasional ewe seems to be milking poorly, udder problems are suspected, or too many lambs are starving or unthrifty, it is time for some diagnostic work and help from your veterinarian. This situation is a flock problem, and examining several ewes is most helpful in determining what the problem might be. Laboratory culture of milk samples from typical ewes is useful in determining whether bacterial mastitis is present. Staphylococcus infections in sheep seem to be the most common bacterial cause of chronic mastitis and udder damage leading to reduced milk production.

Infections during the dry period can cause damage to the udder, and frequently the bacteria are gone by lambing. If typical bacteria are isolated from milk samples from several ewes, it may indicate that the primary problem is bacterial. Often these result from unsanitary environmental conditions where the ewes are housed or damage to teat ends from trauma or soremouth (orf) virus. Damage to the teat end makes it easier for bacteria to get into the udder to cause mastitis. Improving the sanitation in the ewes’ environment and careful management of their nutrition at weaning time can reduce this problem. Treatment of the udder at dry off with dairy cow mastitis preparations has been used on some farms. However, there are no FDA-approved products for sheep, and this practice can result in drug residues. It should only be done in consultation with a veterinarian. Lastly, it is questionable whether this practice can be economically justified as a routine practice.

While sampling the ewes for bacterial mastitis, it is usually a good idea to collect blood samples for testing for OPP virus infection. As this blood test detects antibodies to the virus in the blood, it can tell us whether the ewe is infected. Because infected ewes are infected for life, the presence of test-positive ewes indicates the virus is present in that ewe and on the farm. However, a positive blood test does not tell us that the firm udder we are seeing has been caused by the OPP virus. It only indicates the infection is present, but infected ewes in an infected flock often have no visible signs. If most ewes with hard udders are test-positive for the OPP virus and few of them have bacteria in the milk, it is very likely that OPP virus is the culprit. In many flocks, a close inspection of the flock will reveal other signs of the presence of OPP virus. These include thin ewes that tire easily and ewes with swollen, painful joints.

We have used another technique to help determine whether these udder problems are caused by the OPP virus. Your veterinarian can use a biopsy tool (we use the TruCut biopsy needle) to get a sample of udder tissue. This sample can be placed in formaldehyde and sent to a laboratory where it can be microscopically examined for changes that are characteristic of the OPP virus infection. The ewe’s teat should be thoroughly cleaned and disinfected, and the biopsy needle can be inserted through the teat canal and on into the udder tissue for taking the sample. A sample from a single ewe may not be diagnostic of the flock problem, but samples from several ewes will usually provide evidence for OPP infection as the cause of “hard bag” if the virus is present. Often a problem flock will have several cull ewes that have had these udder problems and which can be sampled.

It is possible to find both bacterial mastitis and OPP virus infections in the same flock; perhaps even in the same udder. However, if enough samples are taken it is usually possible to sort out the real troublemaker. In assisting several veterinarians working with flocks with hard udder problems, we have frequently observed the following when OPP virus is the main problem: high rates of test-positive ewes on random sampling – usually 60% of ewes or higher; microscopic changes in udder tissue that are compatible with OPP virus infection; and the presence of other signs of OPP virus infection such as some thin ewes and some cases of swollen, arthritic joints. Post mortem examination of some of these cull ewes may provide additional evidence for OPP virus infection.

Every year some flocks will have ewes that deliver a live healthy lamb(s) that subsequently 1) suffers starvation, 2) must be bottle raised, or 3) grows poorly. There are several possible causes for this observation. Poor mothering ability; poor nutrition of the ewe; and systemic diseases in the ewe, such as chronic bacterial pneumonia, are several of these. However, udder disease is also a common cause of unthrifty lambs.

Mastitis is the name given to inflammation of the secretory tissue of the udder. The most common cause of mastitis is a bacterial infection, and the vast majority of these infections enter the gland through the teat end. We usually classify bacterial mastitis as acute or chronic based on appearance of the signs, the duration of the infection and the severity of the disease. Acute mastitis is often easily recognized. Usually the udder, one or both halves, is swollen, warm to the touch, and painful. The milk may be off color with flakes or chunks in it. The ewe may also show signs that she doesn’t feel good. She may have a fever, be off feed, and be depressed. In some severe cases, the infection may progress to gangrene with loss of an udder section and sometimes death of the ewe.

Chronic mastitis often produces no obvious signs in the ewe. The milk may appear slightly abnormal or grossly abnormal to the eye. These infections may occur anytime but are common at the onset of lactation and near dry off. These chronic infections, especially those in the dry period, may produce enough inflammation and scarring to reduce milk production in subsequent lactations. In some cases, enough damage is produced that the udder produces little or no milk.

Treatment of ewes with acute mastitis is usually done with antibiotics, frequent milking, and oxytocin. If the ewe shows signs of depression, a veterinarian should be consulted. Chronic mastitis, by its very nature, often is not diagnosed until after damage has been done. Although treatment of the udder at dry off (weaning the lambs) has been advocated by some in the past, there is little information to suggest that routine treatment is economically justified. There are no products labeled for this use in sheep.

Another infection that may cause severely reduced milk production, as well as other signs, is ovine progressive pneumonia (OPP) virus infection. This is a relatively common infection in sheep. Data from the 2002 NAHMS study is not yet completely analyzed, but it is expected that it will show that >30% of US sheep flocks are infected. This virus is often considered the cause of the so-called “hard bag” syndrome.

The virus infects certain cell types of the body including some found in the udder. The body’s reaction to these infected cells results in gradual replacement of the secretory tissue with immune system cells that are trying to get rid of the virus. This usually takes place over several months and doesn’t result in obvious signs in the ewe. At lambing time, the producer often sees a symmetrically full udder and assumes that it contains a lot of milk. However, there may be very little milk actually produced, the milk that is present usually looks normal, and the ewe usually shows no sign of illness.

Although the virus that causes OPP affects other areas of the body such as the lungs, joints, and brain, it is frequently the occurrence of several ewes with the signs described above that signal the producer that something is wrong. Although a blood test is available that shows whether a ewe is infected with the OPP virus, a positive blood test really can’t tell you that the udder disease you are seeing is the result of OPP virus infection. Many animals that are infected have no obvious signs or detectable disease. At this point a thorough investigation is warranted. This usually involves a diagnostic effort involving your veterinarian and the veterinary diagnostic laboratory. The next article in this newsletter will discuss diagnosis of the causes of mastitis, including OPP.

This O.S.U. Extension Coordinated Program is an effort to provide outreach programs in several areas of sheep production. We invite sheep and goat producers from around Ohio to come to one or more of the educational sessions to learn more about different areas of sheep and goat production.

Programs Sponsored by: Ohio Sheep Improvement Association, Roger A. High, Executive Director, contact (614) 246-8299 or rhigh@ofbf.org or visit our website at www.ohiosheep.org for more information. Contact Extension Educators for possible meeting fees.

When, Where and What?

Wednesday, January 14, 2009 “Mt. Victory Program”
Location: Mt. Victory Plaza Inn, Mt. Victory, OH
Time: 6:00 p.m. – PAID RESERVATION IS REQUIRED FOR MEAL
7:00 p.m. – Program begins
Registration for meal: $15.00/person: Paid Registration due by: January 5, 2009
Speaker: Bob Hendershot, USDA/NCRS Grazing Specialist, “Pasture Management”
Contact: Wesley Haun, Logan County Extension Educator at (937) 599-4227

Tuesday, January 27, 2009 “Springfield Program”
Location: Clark County Extension Office, 4400 Gateway Blvd., Suite 104, Springfield, OH
Time: 7:00 p.m.
Speaker: David O’Diam, OSU Meat Lab Manager, “Lamb and Goat Carcass Evaluation”
Contact: Jonah Johnson, Clark County Extension Educator at (937) 328-4607 or
Tim Fine, Miami County Extension Program Assistant at (937) 440-3945

Monday, February 9, 2009 “Burton Program”
Location: Geauga County Extension Office – Patterson Center, 14269 Claridon-Troy Rd, Burton, OH
Time: 7:00 p.m.
Speaker: Roger A. High, OSU Sheep Extension Specialist, “The Management Continuum”
Contact: Les Ober, Geauga County Program Assistant, (440) 834-4656

February 25, 2009 “Bryan Program”
Location: Williams County Extension Office -
Time: 7:00 p.m.
Speaker: Dr. Bill Shulaw, OSU Preventive Veterinarian, Beef and Sheep, “Internal Parasite Management”
Contact: Flo Chirra, Williams County Extension Educator at (419) 636-5608

Wednesday, March 4, 2009 “Fostoria Program”
Location: Ag Credit Services Corporate Office, 610 West Lytle St., Fostoria, OH
Time: 7:00 p.m.
Speaker: Dr. Steve Loerch, OARDC Ruminant Nutritionist”, “Ruminant Nutritional Programs utilizing Dried Distiller’s Grain’s (DDG’s)”
Contact: Ed Lentz, Seneca County Extension Educator, (419) 447-9722 or Gary Wilson, Hancock County Extension Educator, (419) 422-3851

Monday, March 16, 2009 “Licking/Muskingum Program”
Location: Licking Valley High School, Haynesview Drive, Hanover, OH
Time: 7:00 p.m.
Speakers: Roger A. High, OSU Sheep Extension Specialist, “What Market are You Breeding For?”
Katherine Harrison, General Manager, Blystone Farms, “Marketing to the Ethnic Population”
Contact: Howard Siegrist, Licking County Extension Educator, (740) 349-6900 or
Mark Mechling, Muskingum County Extension Educator, (740) 454-0144

Thursday, March 19, 2009 “Barnsville Program”
Location: “New” Farm Bureau Building, 100 Colonel Dr., Barnsville, OH
Time: 7:00 p.m.
Speaker: Roger A. High, OSU Sheep Extension Specialist, “Sheep Nutrition”
Contact: Steve Schumacher, Belmont Co. Extension Educator, (740) 695-1455 or
Mark Landefeld, Monroe County Extension Educator, (740) 472-0810

Wednesday, March 25, 2009 “Lisbon Program”
Location: Crestview Local School, 44100 Crestview Rd. , Columbiana, OH
Time: 7:00 p.m.
Speaker: Roger A. High, OSU Sheep Extension Specialist, “Lamb and Goat Quality Assurance”
Contact: Julie Herron, Columbiana County Extension Educator, (330) 424-7291

UNKNOWN DATE AT THIS TIME! 2009 “Bryan Program”
Location: Unknown at time of release – More details later
Time: 7:00 p.m.
Speaker: Dr. Bill Shulaw, OSU Preventive Veterinarian, Beef and Sheep, “Internal Parasite Management”
Contact: Flo Chirra, Williams County Extension Educator at (419) 636-5608

We are setting these programs up as “district” programs to reach as many sheep and goat producers around the state of Ohio as possible. We encourage you to come and to get your sheep and goat production questions answered.

The starvation/hypothermia complex usually comes about when multiple contributing factors are present and not just the simple occurrence of cold weather. Some of these include failure of the ewe to care for the lamb, difficult birth resulting in a weak lamb, bacterial mastitis in the ewe, “hard bag” in the ewe caused by ovine progressive pneumonia virus, and several infectious causes of abortions which also may result in live, but weak, lambs. Most producers will be confronted with the occasional hypothermic lamb.

A comprehensive source of information about problems occurring around lambing time is the Sheep Production Handbook published by the American Sheep Industry Association. The following is from the current edition of the Handbook:

“Rectal temperature is the primary guide to identification and treatment of hypothermia in lambs. Mild to moderate hypothermia is characterized by a body temperature between 37° and 39°C (98° and 102°F); severe hypothermia occurs when the body temperature is below 37°C (<98°F). Hypothermia is caused by excessive body heat loss coupled with reduced heat production. Newborn lambs are unable to regulate their body temperature for the first 36 hours after birth so environment and management practices greatly affect how much body heat newborn lambs may lose. Energy from body fat, colostrum, and milk is required by lambs to generate heat. Starvation depletes stored energy sources quickly and precludes the intake of adequate amounts of high energy nutrients. Common, but not necessarily routine, findings on necropsy that suggest starvation include: the absence of milk in the stomach and intestine, a change in the color and consistency of fat around the kidneys from light tan and firm to purple and gelatinous, and a complete absence of fat in the abdomen.”

There are multiple approaches to treatment of lambs that are hypothermic. Again quoting from the Sheep Production Handbook :

“Hypothermic lambs do not get better without assistance. For treatment of hypothermia, the following steps are recommended:
1. Move ewe and lambs to shelter or, if the hypothermia is severe, remove lambs from the ewe.
2. PRIOR TO WARMING, lambs more than five hours old with severe hypothermia (< 37°C, 98°F) should be given an intraperitoneal injection of a warm 20 percent dextrose (glucose) solution at a dose of four to five milliliters per pound of body weight. The injection can be given by the following procedure: (1) hold the lamb by the back legs in a hanging position, (2) disinfect the injection site that is located one inch either side and one inch behind the navel, (3) slowly insert a 20-gauge, one inch sterile needle, with the syringe containing the dextrose attached, into the abdomen, and 4) direct the injection toward the rump.
3. Towel-dry wet lambs. Supplement with heat or warm in a warming box using dry heat, e.g., a hand-held hair dryer or heat lamp. Temperature in the box should not exceed 103°F. Avoid overheating lambs by affixing a thermometer to the inside of the box and checking the lambs and the box thermometer regularly, at least every 30 minutes. Lambs should be warmed to 99°F.
4. Tube feed colostrum at the rate of 20 to 25 milliliters per pound of body weight per feeding after the lamb has been warmed (30 milliliters is approximately equal to one fluid ounce). Lambs unable to nurse on their own should receive this amount of colostrum by stomach tube three to four times during the first day of life.
5. Return the lambs to the ewe when rectal temperature is normal (usually one to three hours), and they can stand and nurse on their own. If lambs are still weak after treatment, they should be fed regularly by stomach tube until they are strong enough to join their mother.
6. If only one of a set of twin lambs is involved, remove both lambs from the ewe while warming is taking place and return both lambs simultaneously. Observe lambs frequently to check for relapses.”

Your veterinarian should instruct you in the technique of intraperitoneal injection and can provide you with sterile glucose solution. If you find yourself unprepared, tube feeding the lamb a warm (1020 F.) corn syrup solution (like Karo®) may be helpful. Two ounces of a 50:50 mix of corn syrup and warm water through a stomach tube will provide both heat and readily available glucose to a cold lamb. This can be repeated hourly or so if the lamb appears to be responding.

Moderately hypothermic lambs may respond to warming them and tube feeding with milk or colostrum. If the ewe has no milk and you can’t get milk from another ewe, milk from your refrigerator that has been warmed to body temperature can be substituted safely.

Much has been written about colostrum and its importance to the health of newborn mammals. Again from Sheep Production Handbook:

“Many infectious diseases occurring in the first few days of life occur because the lamb did not get enough colostrum during the first 12 hours after birth. The newborn lamb, unlike the human baby, is born without protective proteins, called antibodies, in the blood. Antibodies are necessary to protect the lamb from bacteria and viruses that gain entrance into the body by various means. The first milk of the ewe, called colostrum, contains antibodies necessary for lamb survival. Colostrum antibodies against some diseases, such as the clostridial diseases, can be increased by vaccinating the ewe a month before lambing. The antibodies consumed by the lamb pass from the intestines into the blood stream. However, a gradual closure of the intestine to the passage of antibodies occurs and is completed by approximately 12 hours after birth. Therefore, it is extremely important for the lamb to get colostrum as soon after birth as possible. Colostrum also contains concentrated levels of energy, protein, vitamins, and other nutrients needed by the lamb. To ensure survival, the lamb should consume an amount of colostrum equal to five percent of its body weight. For example, a 10-pound (160 oz.) lamb should receive eight ounces of colostrum within the first few hours after birth, four ounces immediately, and an additional four ounces within the next 12 hours. It is easier, quicker, and more effective to use a stomach tube rather than a bottle to feed colostrum to a weak lamb.”

Although it is possible to use cow or goat colostrum as a substitute for ewe colostrum, shepherds should carefully weigh the risks of doing so. Colostrum from outside sources, including other sheep flocks, can bring unwanted disease causing bacteria and viruses to the farm. Some examples include Johne’s disease and salmonella, and very recent research has suggested that scrapie may be transmitted by milk or colostrum.1,2

The above quotations are from pages 423, 424, and 426 of the SID Sheep Production Handbook, 2002 Edition, volume 7, published by the American Sheep Industry Association, 9785 Maroon Circle, Suite 360, Centennial, CO 80112. Phone: (303) 771-3500. (Email: info@sheepusa.org)

1. Lacroux C et al. Prions in milk from ewes incubating natural scrapie. PLoS Pathog. 2008 Dec;4(12):e1000238. Epub 2008 Dec 12.

2. Konold T et al. Evidence of scrapie transmission via milk. BMC Vet Res. 2008 Apr 8;4:14.

There are many factors that affect lamb survival. Serious shepherds should consult the Sheep Production Handbook, produced by the American Sheep Industry Association (www.sheepusa.org), for a more complete discussion of the various conditions and infectious diseases which impact lamb survival. However, if a pregnancy is carried to term, most losses occur in the first 3-4 days of life, and if lambs survive the first 4 weeks, most usually make it to market. Most losses can be grouped in 3 general categories – starvation/hypothermia, pneumonia, and scours (diarrhea). To a large degree, these losses are related to management factors we control, and therefore, a proportion of this loss is preventable.

Most small ruminant species are very hardy and have adapted well to their environment and available nutritional support. If one examines which mammals are found in the harshest of the world’s environments, you will find that small ruminants predominate over bovines and other large mammals. If left to themselves, many small ruminant species will deliver their young in the spring, or early summer, when the weather turns milder and forages are most nutritious and abundant. In wild small ruminant species, selection pressure eliminates extremes in birth weights and favors mothers with optimal characteristics in ease of birth, mothering ability, balanced milk production, and ability to thrive with available nutritional resources.

One only has to look as far as the white-tailed deer in Ohio to see these pressures at work. Data collected by the Ohio Division of Wildlife from 1997-1999 (published in 2004) indicate that greater than 90% of mature does will give birth to an average of about 1.86 fawns in May and June. (Tonkovich et al, 2004) Somewhere between 6% and 10% of mature does will have three or more fawns. Between 30% and 60% of those female fawns (depending on the region of Ohio) will conceive in the following fall when their live weight is about 85 pounds. They will give birth to about 1.21 fawns when they are themselves only one year old. These recent figures are actually somewhat lower than previous research conducted in 1981-82 and may reflect declining habitat quality (read nutrition) in some parts of the state where deer numbers have increased substantially since the early 1980s. Each fall we harvest over 30% of these animals during the hunting seasons (over 230,000 in 2007/2008), and car accidents account for many more. (http://dispatch.com/live/content/local_news/stories/2008/02/07/2008-09_deer_regs.ART_ART_02-07-08_B1_GT99IS2.html?sid=101) Except for the agricultural crops they use, deer provide Ohioans with considerable red meat production with no help from us, largely as a result of our relatively fertile soils and favorable climate.

The starvation/hypothermia complex is the leading cause of death in the Great Lakes region. This is a largely a function of the time of year when lambs are born. However, vigorous lambs that receive adequate colostrum and milk (5-10% of body weight) in the first few hours after birth can withstand a significant amount of cold. Some literature from other parts of the world refers to this problem as SME – starvation, mismothering, and exposure. This terminology emphasizes the ewe’s contribution to the problem. Research, and practical experience, indicates that selection for ewes with sound udders, desirable teat placement, and strong mothering instincts can significantly reduce the impact of this problem. Likewise, large birth weights and dystocia, also conditions we can select against, contribute to less vigorous lambs that don’t find the ewe’s udder without assistance. Because lambs have small body weight in relation to their surface area, hypothermia will always be a potential cause of loss, even in lambs born in mild or warm weather. However, we can reduce its impact in our flocks by altering our selection and management practices.

Pneumonia is the second leading cause of death in young lambs. Death is most often caused by bacterial infections, usually Mannheimia (Pasteurella) hemolytica and Mycoplasma ovipneumoniae. These bacteria are common in sheep flocks, and the problem strains usually can be found in the nasal passages and tonsils of adult, and often healthy appearing, ewes. Transmission to the lamb is usually by aerosolized droplets, containing the bacteria, originating from carrier ewes. This transmission is favored by inadequate exchange of air and moisture as is often seen in our barns. Poor ventilation, combined with a significant proportion of the ewe flock with chronic infection of the respiratory tract, generally results in pneumonia being a significant cause of mortality in young lambs. The same situation occurs in cattle and some other species. Producers should consider culling ewes with a chronic cough.

Increasing the rate of air exchange will, of course, tend to make the barn colder in winter and could increase the risk of hypothermia in lambs. However, starvation/hypothermia problems can be minimized with appropriate selection and management. Pneumonia not only causes significant mortality in young lambs, but also leads to chronic infections in older lambs and ewes. Pneumonia is a leading cause of death and reduced performance in feedlot age lambs. Many infections in these lambs are already established in the respiratory passages, long before lambs reach the feedlot, and only need the stresses of transportation and the feeding program to result in clinical disease. Refinements in building design and reduced animal density in confinement situations are more effective long-term measures to control pneumonia than antibiotic usage. Experience suggests that flocks which lamb outdoors in the spring tend to have a low incidence of lamb pneumonia.

Diarrhea in young lambs is caused by several kinds of bacteria, viruses, and protozoa. Lambs that do not receive adequate colostrum are at greatest risk of developing diarrhea. However, even animals that received adequate amounts may still develop diarrhea if the colostrum did not contain specific antibodies to these agents. In addition, colostral antibody can be overcome by a severe buildup of infectious agents in the environment. Lambs with diarrhea may shed hundreds of millions of infectious organisms in every teaspoonful of manure. For many infectious organisms, ingestion of only a few is necessary to cause disease. For example, fewer than 10 Cryptosporidium parvum oocysts are needed to cause a productive infection. As if all this weren’t bad enough, some ewes act as inapparent carriers of these infectious agents and seed the environment with low numbers. One might ask why most lambs don’t get sick.

Healthy vigorous lambs, with adequate colostrum, and in a relatively clean, well-ventilated environment, may withstand exposure to low levels of many infectious agents and not get sick. In fact, this is a necessary process in order to insure that their immune system responds to these low level challenges and develops resistance (protection). This exposure process eventually results in replacement animals that successfully make and pass protective antibodies to their own lambs. This is a dynamic situation. It is when things get out of balance that clinical disease becomes evident.

Overcrowding, excessive moisture or humidity, lack of bedding, and poor sanitation all contribute to raising the overall level of contamination by infectious agents to levels that result in disease. Infectious agents in the environment are not only acquired by the lamb nosing about the pens, but also by nursing udders which are contaminated by dirty environments. In addition, once a scours outbreak is in progress, much of the environment rapidly becomes contaminated, and many lambs get exposed. Isolating ewe/lamb pairs when diarrhea occurs in the lamb can help reduce the number of cases that develop. Likewise, good overall sanitation with dry, relatively deep bedding can reduce the amount of exposure lambs get to disease-causing organisms.

Most flocks harbor many of the common infectious agents responsible for the bulk of lamb losses caused by infectious disease. These agents are either in the environment or harbored by the animals themselves. Whether or not clinical disease occurs is usually a function of the interactions between animals with their environment. Our role in minimizing management factors that contribute to disease development is crucial to the health status of our flocks.

Reference

Tonkovich et al. Trends in Reproductive Performance and Condition of White-tailed Deer

in Ohio. Ohio Journal of Science 104 (5):112-122, 2004.

2. The highest concentrations of prussic acid occurs in the leaves of immature plants and the lowest concentrations are in the stalks of mature plants.

3. When the plant tissue is damaged or killed by frost, a reaction occurs that produces cyanide which is lethal to cows (and people). Cyanide is a gas but it takes a while to volatilize and leave the dead plant tissue.

4. For several days after frost damage, animals should not be allowed to graze these forages and these forages should not be green-chopped. They can be chopped for silage or mowed for hay. Hay and silage made from frost damaged plants are safe.

The silage should be allowed to ferment a few weeks before feeding and the hay must be fully cured before feeding.

5. Frost damaged plants can be grazed after waiting several days after the frost. The damaged plant tissue should be dry which means that the cyanide volatilized and left the area. After another frost, the same thing occurs and you have to wait several days

Bill Weiss, Dairy Nutrionist, The Ohio State University

In February of last year, the U.S. Department of Agriculture’s (USDA) Animal and Plant Health Inspection Service (APHIS) officially announced the discovery of a Nor98-like scrapie case in a ewe from a flock in Wyoming. This was the first case of scrapie consistent with Nor98 discovered in the United States.

Since then, four more cases have been discovered that originated from flocks in Colorado, Indiana, Minnesota and California. These cases are not related to either the first one in Wyoming or to each other.

This scrapie type was first found in Norway in 1998 and has since been found in sheep and goats in many countries in Europe.

“It does affect goats,” says Diane Sutton, DVM, national scrapie coordinator for USDA. “So far not here in the United States, but chances are, we might eventually see it in goats here too.”

This type of scrapie affects sheep of all commonly occurring genotypes including those that are resistant to classical scrapie.

According to Sutton, those flocks in the United States that are found to be infected with Nor98-like scrapie will not be able to use the current genetic-base approach to flock clean up. Producers whose flocks have risk factors for classical scrapie are still encouraged to test at codon 171 for classical scrapie resistance, as has been done in the past.

The World Organization for Animal Health (OIE) has formed an ad hoc committee to consider how to address Nor98-like scrapie with respect to trade. It will likely be at least two years before a code change could be made should a consensus be reached.

“Until research provides us with other options for eliminating Nor98-like scrapie and the international community reaches a consensus on guidelines for trade we will continue to use flock depopulation and exposure-based clean up plans for Nor98-like scrapie affected flocks,” says Sutton. “As other viable options are identified, we will evaluate them using pilot projects.”

According to Linda Detwiler, DVM, assistant director, Center for Public and Corporate Veterinary Medicine, it is important to note that it isn’t known if the appearance of non-classical scrapie cases in Europe and the United States are more likely due to the increased ability to test for and detect non-classical scrapie than to increasing rates of infection. Scientists in European countries are beginning to look at archived samples in an attempt to identify non-classical cases that may have occurred earlier than 1998.

“I would caution everyone that it’s premature to be able to say much of anything about these non- classical cases. At this point in time, there are many unknowns such as: 1) is there more than one strain, 2) what is the origin, 3) are there natural modes of transmission, 4) does the genotype affect incubation time and clinical presentation, 5) do codons other than 136, 141, 154 and 171 influence these cases and 6) how long have these cases been occurring?” she questions.

Because of Europe’s increased awareness of non-classical scrapie, there has been quite a bit of research into understanding how and if the disease is transmitted and how it affects sheep.  Research is currently underway in the United States.

“The first U.S. material became available in February, so ARS (Agricultural Research Service) is gearing up to study it. But, because of the nature and long-term aspects of the disease, it will take a while to study, so we will probably be seeing research from Europe published first,” Sutton adds.

In the meantime, it is stressed that officials will continue to handle the disease as it has in the past, and that producers should be aware of Nor98-like scrapie but not alarmed.

“We are going to treat it as scrapie until the international community removes it as a trade barrier or science finds that there is a better way to handle it than the current system,” Sutton says.

Jim Logan’s, DVM, chair of ASI’s Animal Health Committee, best advice to producers to protect their flock from Nor98-like scrapie is to maintain a closed ewe flock. He says that to prevent the introduction of all scrapie types, producers need to be aware of where new purchases are coming from, know the genetics of new purchases and avoid purchasing ewes unless familiar with the scrapie status of the farm of origin or maintain a closed ewe flock.  “Essentially, people need to use common sense and maintain good sanitation and husbandry practices,”he explains.

The Science Behind Nor98 in Sheep

Nor98 is a relatively common prion disease or transmissible spongiform encephalopathy of sheep. The first descriptions of the disorder were in sheep diagnosed in 1998 in Norway, although a retrospective study has revealed a case in England in 1989. Improved methods for diagnostic testing were published in 2002 and surveillance was initiated in many European countries. Most cases are identified in clinically normal sheep tested in routine slaughter surveillance. The disease is experimentally transmissible to sheep and genetically altered mice by inoculation into their brains but no data are yet available on whether the disease is transmitted between sheep in an affected flock.

CLINICAL SIGNS
Most cases have been discovered in clinically normal sheep tested at slaughter. Of the few clinical cases, a common sign is progressive incoordination (ataxia), occurring most likely because the abnormal prions accumulate in the cerebellum, the region of the brain (the cerebellum) that integrates information coming in from the senses with nerve impulses going to the muscles.

DIAGNOSIS
Both classical scrapie and Nor98-like scrapie are characterized by accumulation of abnormal prion proteins. However, the distribution of the prion proteins differ. In classical scrapie, prions are usually found earliest in the lymph nodes and later in the region of the brain associated with innervation of the gut. As discussed above, abnormal prions are found in different areas of the brain in cases of Nor98. Further, prion proteins are not found in the lymph nodes of sheep with Nor98 and the current live animal tests of lymphoid tissues are not suitable. Nor98 is a challenging diagnosis but skilled pathologists, working with a panel of three different diagnostic tests, can accurately diagnose the disease in the brain of affected sheep.

GENETICS
Susceptibility to classical scrapie is associated with naturally occurring differences in the gene for the prion protein, particularly differences at position 136 and 171. Each sheep has two copies of this gene and commercially available genotype tests show the differences at those positions. Sheep with the genotypes 136VV 171QQ and 136AV 171QQ are very susceptible to classical scrapie strains. Sheep with the 136AA 171QQ genotype are susceptible to the most common classical scrapie strain in the United States and represent the most common genotype found in U.S. scrapie cases. Sheep with at least one copy of the gene 136A 171R are generally resistant to the more common type of classical scrapie.

Although no genotype is considered to be resistant to Nor98-like scrapie, the disorder is found most frequently in sheep with changes in positions 141 and/or 154. The genetic signature AFRQ indicates a sheep with 136A and 171Q with the additional change to “F” at 141. The signature AHQ indicates a sheep with 136A and 171Q with a change to “H” at position 154. A large survey of 4,000 sheep in Europe and numerous reports on smaller study populations has demonstrated that sheep with either the AFRQ or the AHQ gene were eight to 15 times more likely to be diagnosed with Nor98-like scrapie than were sheep with the most common genotype ARQ. Sheep with both changes were more than 20 times more likely to be diagnosed with Nor98-like scrapie. Sheep with the 171R form of the gene are generally resistant to classical scrapie but are susceptible to Nor98-like scrapie, particularly in 171QR sheep that have an AFRQ gene.

EPIDEMIOLOGY
Classical scrapie is usually found in more than one sheep in a flock, with prevalence as high as 30 percent with some scrapie strains. In contrast, more than one sheep with Nor98-like scrapie is usually found only in flocks of more than 500 sheep. In addition to genotype, age appears to represent a significant risk factor for Nor98-like scrapie. In the large European study, 80 percent of the cases of classical scrapie were found in sheep ages 3-5, a finding similar to that reported in the US. In contrast, more than 60 percent of the sheep with Nor98-like scrapie were older than five years and more than 25 percent were more than 10 years old. Nor98 is found in most countries performing large-scale surveillance; the disorder occurs at a rate of approximately one in 1,400 mature sheep at slaughter even if the rate of classical scrapie is very low.

The low prevalence of Nor98 within flocks, the wide geographic distribution of the disorder, the range in age of onset or diagnosis, and the genetic factors increasing the risk of Nor98 are strikingly different than those found in classical scrapie. There may be additional genetic factors influencing development of this disorder, in addition to factors such as route of infection or age at which sheep are infected. Alternatively, Nor98 may be a sporadic disease of sheep, appearing primarily but not exclusively in older sheep. Additional findings from experimental studies and large scale surveillance using improved diagnostic methods will be useful in understanding this wide-spread prion disease of sheep.

BACKGROUND INFORMATION
Luhken and others, 2007, Veterinary Research 38: 65-80.
Bruce and others, 2007, Veterinary Record 160: 665-666.
Benestad and others, 2003, Veterinary Record 153: 202-208.

(Originally Published in Sheep Team Newsletter October 2003)

Toxic levels of prussic acid or otherwise known hydrocyanic acid (HCN) form naturally in the leaves of many annual warm season grasses as well as a few other plants.  Johnson grass, sorghum, sudangrasses, sorghum-sudan hybrids and even the leaves of wild cherry trees have this process occurring immediately after a killing frost.  Also the tender new growth that occurs after a drought can have toxic levels of prussic acid.  The young fast growing plants are more likely to be toxic than the older mature plants. Fields with these plants that were mowed or grazed in September will have a higher level of prussic acid after a frost than fields mowed earlier in the summer and allowed to regrow to a more mature stage.  Even herbicides like 2, 4-D can cause prussic acid to form in these plants.

Prussic acid causes death in the animals by interfering with the oxygen transferring ability of the red blood cells.  Symptoms include excessive salivation, rapid breathing and muscle spasms.  The animal will stagger, collapse and eventually die.  These symptoms can occur within ten to fifteen minutes after eating the plants with high levels of prussic acid.

Prussic acid levels will drop in the plants with time.  Standing plants killed by frost are normally save to graze after about a week.  The ensiling and hay curing process will also reduce the prussic acid to safe levels.  Care needs to be taken with scattered frosts.  Portions of the field may be initially killed and later frosts will cause the remaining plants to have high levels of prussic acid.  This will create problems in managing the grazing of the field.  Producers need to be able to identify the plants that have the potential for prussic acid poisoning.

Grazing management decisions need to consider waiting a week after a frost or the rain that breaks a drought to graze or green chop these plants.  Grazing animals should be introduced into the field slowly with their rumens full.