LAMENESS SYNDROMES IN CATTLE, SHEEP, PIGS AND HORSES

Class Notes 4/4/06
http://www.uwyo.edu/vetsci/undergraduates/courses/patb_4110/2009_lectures/27_lameness/html/class_notes.htm#Foot_rot[01-Oct-16 8:25:38 PM]
LAMENESS SYNDROMES IN CATTLE,
SHEEP, PIGS AND HORSES
Lecturer: Dr. Donal O'Toole
Lameness in Cattle Foot Rot
in cattle Foot rot in sheep
Lameness in Sheep Footwarts in cattle Chlamydial arthritis in sheep
Lameness in Horses Sole ulcers in cattle Founder in horses
Lameness in Pigs Toe abscesses in cattle Tying up in horses
Lameness in Goats Broken bones in cattle Navicular disease
Muscle injuries in cattle Sole bruises in horses
Septic arthritis in cattle Hoof cracks in horses
Polyarthritis due to M bovis Alkali disease
Laminitis in cattle Athletic injuries in horses
CAE in goats
Lameness in dairy cows is second only to mastitis in terms of its detrimental effect on herd productivity, and is
an important source of reduced production and culling decisions. It is also important in feedlots, since it is
relatively common. In a recent study of western US feedlots, the price received for salvaged lame animals was
53% of the original purchase price. When lame cattle in the study were sold on average 85 days after arrival,
they weighed on average only 10 lb more than their in-weight.
Diseases of digits account for approximately 70% of all cases of lameness. If you want to figure out what is
going on, you have to pick up the foot to make a proper examination. Never medicate the animal before
making a proper diagnosis. Other causes of lameness include injuries to upper skeleton or major muscles
(15%), septic joints (12%) and injection site lesions (3%).
There is a good web site by an international group of veterinarians, including some well known for their
interest in lameness.
CATTLE
1. Foot rot (infectious pododermatitis)
Nationally, approximately 20% of all diagnosed lameness in
cattle are due to foot rot, a bacterial infection caused by specific
strains of Fusobacterium necrophorum. It is not common in
Wyoming due to aridity, but is seen wherever cattle get to
stand in water or mud for extended periods. The causative
organism is associated with calf diphtheria, and with hepatitis
that occurs as a sequel to ruminal acidosis. F. necrophorum-
induced hepatitis due to grain diets is common in some feedlots
(up to 40% of some animals affected when they come to
slaughter). The organism is found in the rumen, passed out
with the stool, and is common on the sole of the foot of healthy
cattle. Problems occur when it invades skin. Other bacteria

Class Notes 4/4/06
"cooperate" with F. necrophorum to establish infection. The first
signs of foot rot are lameness, acute swelling of interdigital
tissue, and swelling around the hairline of both hooves.
Eventually interdigital skin cracks open, revealing foul smelling,
necrotic, core-like material (image at left).   Untreated foot rot
may progress up the foot to the fetlock or higher. More
importantly, it can invade the deeper structures of the foot such
as the navicular bone, coffin joint, coffin bone, and tendons.
   Clinical signs consist of a sudden onset, mild to severe
lameness of one limb, with swelling of the coronet and
interdigital space. The interdigital space is often necrotic and fissured, with a characteristic horrible smell.
Typically the disease affects 1 - 2% animals, but occasionally it can be as high as 10 - 15%. Foot rot in
feedlots is probably overdiagnosed - other causes, such as sole ulcers, may present like foot rot.
     Control: Preventive measures are centered on the prevention of mechanical damage to the foot caused by
frozen or dried mud, stones, brush, and stubble, and by minimizing time that cattle spend standing in wet
areas. The risk of foot rot can minimized by thoroughly cleaning pens after cattle are removed and
liberally spreading lime over the pen surface. Leaving the pen vacant for at least a week after liming will
contribute to the control of foot rot organisms. Good drainage is an essential to any feedlot arrangement
and aids in preventing constant contact with manure-laden mud or water. Footbaths used once or twice a
week, consisting of 10% zinc or copper sulfate may be helpful, particularly for confinement beef or dairy
operations. Novartis makes a vaccine approved for use in cattle as a control for foot rot. Reported results by
producers and veterinarians have been mixed from their use of this product. A recent study from western
Canada reported that the product reduced both foot rot and liver abscesses due to F. necrophorum.
     Treatment: This is usually successful, provided it is instituted early.   Treatment should begin with cleaning
and examining the foot to confirm that lameness is due to foot rot. At this time a topical treatment of choice
should be applied since mild cases respond to topical therapy alone. Most cases require the use of systemic
antimicrobial therapy, although it may require the use of restricted antibiotics such as Naxcel
TM
or Micotil
TM
.
Affected animals should be kept in dry areas until healing occurs.    If improvement is not evident within 3 - 4
days, it may mean the infection has invaded the deeper tissues of the foot.    Infections that do not respond to
initial treatments need to be re-evaluated by a veterinarian. He or she will want to determine if re-cleaning,
removing infected tissue, application of a topical antimicrobial, and bandaging are appropriate along with an
antimicrobial change.   In the more severe cases, the choices may be salvage for slaughter (following drug
withdrawal), claw amputation, or in valuable animals, claw salvaging surgical procedures.   If it appears a
substantial number of animals in a pen is affected, mass medication of remaining animals in the pen with sulfa
and tetracycline in feed for five days may be needed. Medicating all the animals through the feed often stops
an outbreak of foot rot within 24 hours.
Popular article on foot rot from Iowa Beef Center.
2. Footwarts
(papillomatous digital dermatitis)
In the past 10 years, footwarts emerged as a serious problem in North
America, particularly in the dairy cattle. In a recent survey, 43% of
1,182 U.S. dairy herds reported seeing a case.

It causes lameness,

Class Notes 4/4/06
decreased milk yield, body weight loss, and decreased reproductive
performance. Although the disease may have been around in the past, it
appears to have increased in importance recently. As Wyoming has
essentially no dairy industry, we have not recognized the disease here.
But it is important in California, other dairy states in the US, and Europe.
In spite of the accepted name (papillomatous digital dermatitis), which
seems to imply that this is an infection due to papillomaviruses, no
viruses have been associated with the disease. It is currently thought to
be bacterial in origin.
Typically this is form of lameness affects first calf heifers. Lameness
usually affects the interdigital part of the hooves of the pelvic limbs.
Some common names for the disease are descriptive of what lesions look
like ("hairy footwarts"; heel warts; "strawberry foot disease" etc).
Lesions are probably due to a family of spiral anaerobic bacteria
(spirochetes; most likely Treponema phagedenis or something closely related to it), since they occur in large
numbers in affected skin. The lesions usually start at back of foot near the interdigital cleft/heel bulb, and
"mature" to form discreet moist round moist masses that resemble a hairy strawberry (see image at left).
Lesions are chronic, painful and tend to bleed. It is worth noting that similar organisms have been seen in
canker in horses; their role is unclear.
Control: Manage corrals/free stalls so that feet are not continually wet. Avoid conditions that result in
caking of lower legs with manure-rich slurry. Biosecurity: quarantine, examine and treat new arrivals,
especially heifers.
Treatment: Cleansing plus topical application of antibiotics under a wrap are usually highly effective.
Recurrent or new lesions may develop within 7-12 weeks of successful treatment in 50% of cows. There are
various vaccines on the market, but these are not considered curative.
3. Sole ulcers
Sole 'ulcers' are areas of damage and hemorrhage in the
sole of the foot, typically the lateral claw of the pelvic limb
and medial claw of the thoracic limb. They are often
hidden under overgrown horn which has to be pared away.
When this is done you see a discreet area where young
scar ("granulation") tissue protrudes through the damaged
sole. This has to pared down in such a way that as much
weight can be shifted to the healthy digit. Since the
equivalent of the nail bed is destroyed, these are slow
lesions to heal. Such cattle often remain permanently
lame. The only way to manage it is to do corrective
trimming several times a year.
4. Toe abscesses
Young cattle coming from lush and/or irrigated pastures are prone to toe
'abscesses,' which affect the front part of the digit. The cause is not clear,
but it is assumed to be due to excitable calves with soft hooves coming off
grass and abrading horn from their toes on concrete surfaces. There is
disagreement whether the problem is strictly traumatic, or whether some
nutritional factor associated with lush pastures (laminitis?) is involved. Dried
manure provide a cushion to the hoof so some feedlots only have a problem
with toe abscesses after rains wash that cushion away.
To confirm the diagnosis, pick up the hoof and see if you can palpate a soft

Class Notes 4/4/06
area at the front part of the hoof. You may see a crack between the hoof wall
and the sole, but this is not always present. There should be no swelling
between the toes - this is a cardinal sign of foot rot, unrelated to toe
abscesses. Feedlot operators often make the mistake of treating all lame
cattle for foot rot or upper leg injuries, when toe abscesses may be part or all of the problem. If toe abscesses
are not treated in time, the toe may have to be amputated or the animal sold for salvage. Toe abscesses are
treated by trimming the end of the hoof just enough to relieve the pressure inside the hoof caused by injury. If
the animal bleeds when you trim the end of the hoof, you trimmed too much. In addition to trimming, animals
should be treated with a long-acting tetracycline. Antibiotics alone will not benefit the animal -- the hoof must
be trimmed.
5. Broken bones
If the animal is not under medication withdrawal time restrictions, it is best to salvage cattle with broken bones
as soon as possible. If time restrictions exist, and the fracture does not break the skin, cattle with fractures can
get along quite well if kept in a small pen. The fracture will not heal, but it allows the animal to clear the
medication before marketing.
6. Muscle injury
Severe muscle damage is common in feedlots among newly arrived cattle, and in bullers. Newly arrived cattle
should be allowed to rest before processing (6 - 72 hours). Muscle damage can often be traced to handling
techniques. It is important to handle only small numbers of cattle at a time and handle them gently. Muscle
damage in bullers can be severe. It is important to be looking for bullers constantly and to remove them from
riding cattle as soon as they are noticed. When bullers are removed from a pen it is common for the animals to
be re-tagged, have implants removed and placed in a "buller pen." There is no information to support the
removal of the implants, but the implants should be checked and replaced if the implant is crushed or
abscessed. Finishing bullers in a buller pen seems to be an effective management tool. Antibiotic therapy is
usually not required in the treatment of bullers. Your veterinarian can prescribe medications to minimize the
effects from muscle damage and help with effective buller management.
7. Septic arthritis
Swollen joints account for 12% of lameness in feedlots. Common causes are
Haemophilus somnus (the cause of TEME - see Dr. Montgomery's CNS
lectures), Pasteurella multocida, and E. coli. While the bacteria are sensitive to
tetracyclines and penicillin, treatment with antibiotics is often rewarding since
many antibiotics do not penetrate well into joints, particularly when there is a
lot of pus present. Sale for salvage is often the best option for animals with
swollen joints. If the swollen joint appears before the animal has cleared its
drug withdrawal time from the medications and vaccines used at processing,
treatment with antibiotics should be considered. An antibiotic with a short
withdrawal time is recommended so that the animal can be marketed as soon
as possible. Swollen joints are painful, and the animal may not eat enough for
minimum body maintenance. If the animal is under a long withdrawal time for
a medication when the swollen joint is diagnosed, humane euthanasia should
be considered.
8. Combined infection of tendons, tendon sheaths and joints due to M. bovis

Class Notes 4/4/06
We have begun to recognize a "new" disease which has a typical
presentation in Wyoming feedlots. It is due to the bacterial agent,
Mycoplasma bovis, which is also a cause of pneumonia. A feature of
the Mycoplasma group is that they lack a cell wall which makes
antibiotic therapy and vaccination. Many antibiotics work by disrupting
cell walls. Long duration of expensive therapy maybe required.
Resistance is becoming more common. Lameness caused by M. bovis
typically causes swelling of multiple joints (polyarthritis) and tendon
sheaths (tenosynovitis). You can see the swelling running up the leg,
due to spread along tendon sheaths - it is more extensive than just a
joint swelling. This can be a hard bug to grow, so if you think you are
dealing with M. bovis, work with your veterinarian and diagnostic laboratory so that you can get an accurate
diagnosis. There are no fully approved vaccines for Mycoplasma spp. in the USA at present.
DEALING WITH LAMENESS IN CATTLE - THE BOTTOM LINE
1. Make sure you have the problem diagnosed BEFORE you treat the animal.
2. Most cases of lameness in cattle are in the feet. The only way to diagnose the cause is to pick them up
and examine them (the feet, not the cattle).
3. Check the toes for abscesses. If abscesses are present, trim enough hoof to relieve the pressure.
Trimming too much can make the problem worse.
4. Foot rot is a disease of the soft tissue between the toes and responds well to medication. If you do not
get a good response, question your diagnosis.
5. Consider salvage of animals with swollen joints or broken bones before you treat them.
6. Bullers can have severe muscle damage - consider separation in a buller pen.
7. Think twice before trying to salvage a downer - this is a welfare issue. The best approach may be
humane euthanasia on site and eat the loss.

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SHEEP
Foot rot (infectious pododermatitis)
Foot rot is a common and serious disease in sheep. Once it is in a flock, it is a major nuisance to get rid of - it
may years of determined effort and culling of affected animals. For a small flock of grade ewes, selling out and
starting over may the wisest decision. The principal cause in sheep is not the same as in cattle, but it is also a
bacterium, Dichelobacter nodosus, which exists as multiple strains (17 - 19). The large number of stains
creates a problem from a vaccine standpoint - protection against one strain may not result in protection
against another. B. nodosus lives only on sheep hooves and dies in soil in ~2 weeks. It grows slowly, so
incubation periods can be long. Moist soil conditions contribute to the cause and spread of foot rot. A
determined eradication effort in New South Wales was successful in limiting the disease there, but it
underscores that a combination of culling, checking hoofs, time, biosecurity and antibiotics are needed to do
this.
To avoid
foot rot:
Be careful buying in new sheep, since this is how it enters herds. Examine incoming sheep to make sure
they are free of infection.
Buy only from flocks you know are free of foot rot.
Be careful about using other people's trailers or facilities. The organism lives in muck. Using
contaminated equipment or facilities may allow it get into your flock

Class Notes 4/4/06
You may consider vaccination. Several products are on the American market, but none is 100% in part
because there are multiple strains of the primary infecting organism.
To treat
foot rot and clean up a flock
Set up every sheep and examine every foot to find any with foot rot lesions.
If you decide to treat, trim affected hoof walls to the quick in all sheep. The organism is an anaerobe
(needs oxygen-free environment to survive). Exposing it to air helps kill it.
Soak affected hooves for five minutes in a foot bath containing 90% water and 10% formalin (37%
formaldehyde) or 10% zinc sulfate. Zinc sulfate is as effective as formalin, and safer to use (formalin is
the solution used by pathologists to fix tissues after a post-mortem - it is a harsh disinfectant).
Proprietary solutions are also available commercially.
Turn apparently cured sheep into an uncontaminated area. Doing so can create a problem, because some
sheep thought to be clean remain infected. With time and moist conditions, they can re-infect other
sheep.
Reexamine all sheep and remove any limpers initially thought to be clean. Force sheep to move through
a 10% zinc sulfate solution daily for 30 days. This has become the most successful treatment scheme.
Sell persistent limpers.
Repeat hoof examination and culling process every 3ï¿½ 4 weeks until none are found for two
consecutive examinations. After that, be on the lookout for lame sheep - if you find any, and they have
foot rot, return to Go.
If you sell all sheep, wait three weeks before bringing in new sheep.
Extension
article from University of Utah on foot rot in sheep
Chlamydial polyarthritis
Polyarthritis means arthritis involving one or more leg joints (poly: many; arthritis: inflammation of joints). It
may or may not produce pus in the joint space. A common cause is Chlamydophila pecorum. This is related
to, but distinct from, the agent that causes abortion in sheep; the anti-abortion vaccine will not protect against
this agent, which also is a major cause of pink eye in sheep and goats. Polyarthritis is typically seen in lambs.
They are reluctant to get up and move around, and often act stiff. If you force one to move, it will gradually
become less lame and stiff. If you watch it closely, it will seem to limp on one leg and then another - this is
because multiple joints are affected. Its temperature may be elevated. Producers in southern Wyoming and
Utah have complained of a "summer lameness" that occurs in flocks at high elevations. It is antibiotic
responsive. When we've investigated this, we've found Chlamydia in the lesions. It is mostly a problem for
those producers who want to produce "organic" lambs, and who therefore must stay away from antibiotics. It
responds well to long acting oxytetracyline. If sale time is within the month, however, another drug with a
shorter withdrawal time (e.g., Tylan) should be chosen. There are other causes of infectious lameness in
sheep. Often these enters the body through the umbilicus or docking or castration wounds. To prevent
polyarthritis, disinfect the navel cord and docking and castrating wounds. Treatment with antibiotics is only
moderately successful.
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HORSES

Class Notes 4/4/06
One-half of U.S. horse operations report having at least one horse with lameness in the previous year, with
13% reporting a horse with laminitis. Laminitis, navicular disease, and sole bruises or abscesses were the
most common causes of foot problems, and together explained 70ï¿½80% of the foot problems reported in any
season.
1.
Laminitis ("founder"; "hoof wall rings")
Laminitis is inflammation of the "quick" of the hoof,
the soft blood-filled tissue that interdigitates with the
hoof. Swelling leads to destruction of the cellular
bond between the sensitive and insensitive laminae of
the hoof. These structures normally attach the hoof
wall to the coffin bone. This condition covered in the
enteric diseases lecture in horses, since a common
cause is dramatic feed changes. Grazing lush pasture
and grain overload are the perceived causes for more
than half of all laminitis cases. Other causes are a
major work change and systemic illness, such as
salmonellosis or PHF (and you remember what that is,
right?). Acute laminitis results in a typical gait -
horses stand with an obvious heel-toe stance as they
try to get weight off their thoracic limbs, and off the
sensitive laminae inside the hoof wall. Chronic
laminitis results in abnormal growth of the hoof with
excessive growth and ring formation.
Treatment: Careful farriery is needed to correct the underlying disorder and the foot/hoof problem. Often this
is a slow and costly process.
2. Tying up syndrome (exertional rhabdomyolysis)
Tying-up is a generic term used to describe the symptoms of several muscle diseases. Tying-up can be career-
threatening for horses. Tying-up show signs of a stiff gait, reluctance to move, firm painful cramping muscles,
sweating, increased heart and respiratory rates. In addition to clinical signs, horses that tie-up will have
biochemical evidence of muscle damage (muscle enzymes are found in blood; myoglobin passed via the
kidneys into urine, causing coffee -brown discoloration(. Currently it is split out into several types. Sporadic
tying up usually involves a specific muscle group and should be considered a veterinary emergency if the
horse sweats profusely, is reluctant to move or has dark urine. Treatment involves giving the horse relief for
muscle pain. In addition, fluids and electrolytes may be given to ensure that myoglobin passed via the kidney
does result in renal damage. Further treatment includes stall rest followed by hand walking and turnout once
initial muscle stiffness is gone. Grain intake is drastically reduced or eliminated since these horses are likely to
be on a reduced exercise program. When horses have repeated episodes of tying-up, the disease is considered
chronic; there are two recognized forms of chronic tying up.
One is recurrent exertional rhabdomyolysis, which may be inherited as a dominant trait, at least in
Thoroughbreds. RER is thought to be an abnormality in how muscle contraction is regulated in the horse - it
may involve calcium metabolism in muscle cells. Muscle samples (biopsies) from affected horses have an
increased sensitivity to contraction when exposed to caffeine and the anesthetic halothane - in the case of the
former, I suspect I may have RER. Reduction in the amount of carbohydrate (grain) and increases in the
amount of fat (e.g., vegetable oil) and fiber in the diet reduce excitability and enhance tractability in horses
with RER. It is recommended that <20% of the calories are supplied from carbohydrates and >20% come from
fat.
The other chronic form of typing up for which a specific biochemical syndrome is recognized is polysaccharide
storage myopathy. This is a glycogen (= muscle sugar) storage disease in which an abnormal polysaccharide
builds up inside muscle cells. Horses with PSSM are able to quickly clear sugar from their blood and store 1.5
to 4 times the normal amount of muscle glycogen (in an abnormal form). It can be seen microscopically in
muscle from affected horses. PSSM has been identified in draft,
Quarter Horses, Paints, Appaloosas,

Class Notes 4/4/06
warmbloods, and some Thoroughbreds. It is remarkably common in draft breeds - up to 86% have microscopic
evidence of the disease. Unlike RER, PSSM horses tend to have a calm, rather than nervous, demeanor.
Preventing horses with PSSM, RER and other forms of tying up from developing clinical signs include:
Diets low in starch/sugar (grain), high in fiber/fat.
Regular daily activity, riding or lunging, along with pasture turnout.
We occasionally see fatal rhabdomyolysis in Wyoming horses exposed to cold, damp conditions in winter. This
is given various unhelpful names in the veterinary literature, such as "atypical rhabdomyolysis" and "seasonal
pasture myopathy." Horses left out in the wind with no shelter in winter may be found weak, stiff, shivering
and depressed. Even horses in good nutritional condition are susceptible. If they go down they have difficulty
getting up. If they are standing they may refuse to move. Clinically horses have breakdown of skeletal
muscles and muscles of respiration. Some can be saved with aggressive supportive and nursing care, but a
surprisingly high proportion can die - cardiac lesions are reported in the literature. A diagnosis can be made on
the basis of clinical signs and evidence of extensive muscle breakdown (serum chemistry).
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3. Navicular disease:
This is a disease or syndrome is associated with degenerative changes in the navicular region, which includes
the bone that lies behind the middle and distal phalanx. The disease is common and presents as intermittent
progressive lameness of the forelimbs of horses aged 4 - 15 years. It renders many unfit for use. By one
estimate, it is responsible for one third of all chronic forelimb lameness in horses, particularly Quarter Horses
and Thoroughbreds. Some owners and equine veterinarians can hold forth at extraordinary length about the
cause and best treatment for the disease - these can be pointless conversations, since the cause is not known,
and effectiveness of treatment is a function of stage of the disease, use of the horse, and its conformation .
Affected horses generally have an asymmetrical bilateral lameness, with disuse atrophy of specific muscles that
extend the forelimb. There is a large number of ways to establish that a horse has navicular disease. The
simplest is to flex the digit and see if it immediately exacerbates lameness. Other methods are to block the
nerves to the digit, which results in immediate temporary relief from lameness, as well as radiography of the
navicular bone to look for degenerative changes in the bone. Treatment is by using good farriery, with
attention to maintaining a proper hoof angle and proper medial-to-lateral balance, combined with long-term
nonsteroidal anti-inflammatory drug (NSAID) therapy in early cases. Some cases do respond favorably to
intraarticular medications, e.g., sodium hyaluronate and corticosteroid combinations, injected into the distal
interphalangeal joint. When these treatments fail to keep the horse sound enough for use, a fallback is to
surgically cut the two nerves that innervate the caudal one third of the foot and sole (palmar digital
neurectomy). This can salvage the horse for use for several years.
4. Sole bruises/corns:
This is a common, avoidable form of lameness. It is trauma of the sole of the digit, resulting in hemorrhage.
They are most easy to see when they are superficial and the sole is unpigmented. A "corn" is a bruise that
occurs at the angel of the wall of the hoof and the bar, often due to poor shoeing technique or a wedged
stone. Bruises and corns tend to occur in horses with flat feet, thin soles, are barefoot, or have their hoof walls
too short. If a horse is lame and you can't see the bruise, you may need hoof testers to localize the pain.
Many bruises resolve if the horse is allowed rest from heavy work, the material over the bruise is lightly pared
to relieve some of the pressure, the sole is protected with a pad, and anti-inflammatory drugs used as needed.
Some bruises can become infected and develop into an abscess - these need to be drained, the area treated
daily with disinfectant solution and dressed, and protected until fresh scar tissue grows in.
5. Vertical (toe cracks, quarter cracks, heel cracks) and horizontal cracks in hoof
These are cracks in the hoof wall that extend either vertically or horizontally. Vertical ones may start at the
bearing surface (= grass crack), or at the coronet (= sand crack). The name depends on the location: toe if in
front, quarter on the side, heel if at the back. The most common cause of vertical cracks is excessive growth
of the hoof due to lack of trimming. Wet conditions leading to softening of the hoof, following by sand or

Class Notes 4/4/06
gravel damage, can also start a grass crack. Not all horses with vertical cracks become lame. Horizontal
(blowout) cracks are usually due to damage to the growth area (coronet) or mechanical damage. Since hoof is
not alive, it cannot heal - cracks have to grow out, and be replaced by new growth, just as in a torn fingernail.
Treatment involves stabilizing the crack so it does not get worse and, if the horse is lame, shifting weight off
that part of the hoof. Grass cracks can be fixed by a good trimming of the over-long hoof. Other cracks can
be treated by applying a variety of stabilizing devices such as screwed on plates or acrylic materials
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6. Alkali disease:
This is a form of chronic selenium toxicity of horses and cattle. The name is a misnomer since it is not due
to alkali - it is due to eating forages high in selenium. It is characterized by hair loss from the mane and tail
(bobtail), sloughing of hooves, and lameness. Areas with high selenium soils are west of the Mississippi River
and Wyoming has several such areas. During a recent three-year study in
Wyoming, Dr. Merl Raisbeck in our
department found only four substantiated cases of selenium toxicity of horses due to the ingestion of high
selenium forage. The older literature claimed the disease was common in Wyoming, but that has not been
our
experience. Cases are seen South Dakota, western Nebraska, and Colorado The hooves may be sloughed
with full blown alkali disease - the most humane thing to do for these animals may be euthanasia. Earlier
studies have associated Se toxicity with a host of mysterious maladies including "blind staggers". However, a
recent
study that Dr. Raisbeck and I conducted did not reproduce these signs of Se toxicity, suggesting that
some of the early work done on selenium poisoning is unreliable.
There is no treatment for alkali disease, but if you have seleniferous land you can minimize the risks:
Know your land - identify seleniferous areas . There are specific Se-accumulator plants, like two
grooved milk vetch, which tell you where seleniferous shales exist. If you have a problem you may need
to do soil and plant sampling to measure Se levels. This will help identify safe routes for trailing
livestock from one range to another. Plants and soils with >1.0 and >2.0 ppm selenium respectively are
potentially toxic.

Fence livestock and horses out of worst areas. The most effective way to counteract Se toxicity is
to remove animals from the areas where high Se levels occur in soil or water. Close seleniferous areas to
livestock production. Areas covered with dense stands of highly seleniferous native range plants should
be withdrawn from grazing if possible. Fencing livestock out of seleniferous areas may not be practical
when the area makes up a large portion of a ranch. However, fencing off small sections of the most
seleniferous soil on the property, though expensive, can prevent considerable livestock injury.
Landscape managers should take precautions when grazing livestock on reclaimed mine and disturbance
sites, since four-wing saltbush and milk vetch are often planted on such sites because of their soil-
stabilizing and nitrogen-fixing characteristics. These plants accumulate Se that can be hazardous to
livestock.

Avoid overgrazing. Since scarcity of good forage forces livestock to feed on seleniferous vegetation,
avoid overstocking. Maintain a strong grass community so animals donï¿½t have to consume unpalatable
plants high in Se. If given a choice, animals will not eat high Se plants since they are unpalatable.
Moderate to light stocking rates allow animals to select higher quality forages. Even at conservative
stocking rates, extended grazing periods on areas with high Se contents may cause chronic Se poisoning,
either because scarce forage forces animals to eat accumulator plants, or because animals eat enough
non-accumulator plants with marginal Se concentrations to trigger toxicity. Conservative stocking rates,
combined with frequent moves to fresh pasture, help animals avoid ingestion of toxic Se levels. It is
critical to allow sufficient forage regrowth and recovery time before moving animals back into a pasture.

Weed management. Manage weeds to enhance grass forages. Destruction of seleniferous native range
plants and revegetation with non-accumulator forages may be desirable in some situations. Since many
of the Se-accumulating plants are broad-leafed (not grasses), selective herbicide (e.g., Grazon P+D,
Tordon, Escort, or 2,4-D) is a management option when plants reach high densities. Closely monitor

Class Notes 4/4/06
fence lines for accumulator plants. Herbicides may be required for several years to achieve effective
weed control, although intensive control may not be practical or economical.
7. Athletic injuries in performance horses:
A large number of disorders can occur in performance horses - the bible of
lameness in horses, which is in the UW library, addresses these at consider
length (Adams' Lameness in Horses - 4th edition -ed. Dr. Ted S. Stashak).
Important ones are degenerative joint disease (DJD) of specific joints
(depending on the sport), tenosynovitis, fatigue fractures of bones,
and thoraco-lumbar and sacro-iliac pain. The disorders follows the
sport: fractures of the middle phalanx of the hind limb is seen almost
exclusively in rodeo horses, associated with abrupt, forceful stops and
severe torque in sharp turns. Degenerative joint disease frequently
develops in the interphalangeal joints of older horses that have been used
hard, particularly in those with pigeon-toed conformation. Some are
managed reasonably well with medical therapy. In refractory cases with
advanced DJD of the proximal interphalangeal joint, surgical fusion of the
joint (arthrodesis) is a viable option for treatment. Treatment of these
athletic injuries involves some combination of rest, nonsteroidal anti-
inflammatory drugs, polysulfated glycosaminoglycans, intravenous sodium
hyaluronate, and intra-articular injections (sodium hyaluronate and
corticosteroids). Surgical repair of long bones in horse is possible, but
requires specialized facilities, an experienced surgeon and no shortage of
the crinkly green stuff you buy pigs with.
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PIGS
Please see pig lecture
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GOATS
Caprine arthritis-encephalitis
CAE is a common viral disease of goats. The agent is in the same group as
the AIDS virus (i.e., it is a lentivirus;
lenti- meaning slow, due to the slow
clinical course). The disease can be insidious and chronic. As the name
suggests, two major manifestations are arthritis (in adult goats) and
encephalitis (in kid goats). Most goats infected with CAE virus are show no
clinical signs. The arthritic form of CAE vis the most common manifestation
of the disease and is generally seen in sexually mature goats (>6 months).
Arthritis tends to be chronic and progressive. Early arthritic signs may be
subtle or severe. Subtle signs include stiffness, shifting leg lameness,
decreased ambulation, weight loss, reluctance to rise, and abnormal posture
after rising. More severe arthritic signs can include acute swellings without
pain upon palpation. Joints that are drained of fluid simply refill. There is no
effective treatment, no vaccine is available, and the best approach is to stop
it getting it into herds, and if it does to cull affected animals.
If you see lameness affecting multiple joins in many
animals, either with or without other signs typical of the
syndrome (encephalitis, among others), think CAE and get
the herd blood tested. The best way to avoid it is to keep

Class Notes 4/4/06
a closed herd. Some owners of large commercial goat herd
test for CAE every 6 months, beginning at 6 months of
age. Seropositive individuals should be segregated and
culled. If culling is not an option, a variety of measures
can be taken to minimize CAE viral transmission. One is to
remove kids from does immediately after birth to prevent
contact (including sniffing and licking) that may promote
transmission. Seropositive and seronegative does should
be held in separate pastures.

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1. Describe what you would do if you found you had footrot in your flock of sheep
2. What are the principal differences between footrot in sheep and polyarthritis due
to Chlamydophila sp.?
3. "Laminitis is common in horses but irrelevant in dairy cattle." Discuss in one
paragraph.
4. Why is alkali disease associated with Wyoming and surrounding states. What can
be done to prevent this disease?
5. You are the proud owner of a herd of goats, and you find that some have soft
swellings of their knee joints. What is most likely to cause it. What will you do to
establish the cause and the best way to control it?
6. What is the difference between alkali disease and laminitis due to grain overload
in horses?
7. It is now clear that "tying-up" consists of more than one disease syndrome. Given
that fact, how are these disease syndromes controlled?
Dr. Donal O'Toole
Updated:
05/07/2009

LAMENESS SYNDROMES IN CATTLE, SHEEP, PIGS AND HORSES

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LAMENESS SYNDROMES IN CATTLE, SHEEP, PIGS AND HORSES