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Equine

Fescue Toxicosis

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With foaling season upon us it is important to discuss fescue grass and the negative impact it can have on late term gestation in broodmares. Fescue is commonly found in Oklahoma pastures and is known for being a durable, drought-resistant grass due to a symbiotic relationship with an endophytic fungus called Acremonium coenophialum (or Neotyphdium coenophialum). Research has found that over 85% of Oklahoma’s fescue grass has been infected by this endophyte. Unfortunately, there are no visual differences between regular fescue and infected fescue so horse owners cannot know if their mares are safe to continue grazing their pastures without further testing. Furthermore, there are no treatment regimens that will successfully remove the endophyte from the infected grass, so mare owners are best off if they remove the mares from infected pastures during the late stage of gestation.

            The endophyte, Acremonium coenophialum, survives by living inside intercellular spaces on blades of fescue grass. Since it does not actually enter the host plant’s cells, it is unable to detect the ongoing infection and continues to grow and reproduce seeds that are also infected by endophytes. These infectious endophytes are responsible for producing various alkaloid toxins that benefit the grass in many ways. For example, peramine is an alklaoid toxin that has been proven to prevent the grass from insect damage. Experimental removal of these endophytes has produced “non-infectious” fescue that was shown to be more susceptible to root disease, insects and drought. The primary alkaloid toxin that horse owners should be concerned with is called ergovaline. Studies have shown that ergovaline can be found in every part of infected fescue grass but concentrates most in the seed heads.  

            When late term broodmares graze on infected fescue, they inevitably consume the ergovaline toxin, which can have negatives effects on hormone production and the progression of their pregnancy. Ergovaline will affect the mare’s anterior pituitary gland and cause a decrease in the secretion of prolactin, a hormone that is necessary for mammary gland development and milk production. Often, the only clinical sign of fescue toxicosis is the lack of an udder as the birthing date approaches. Researchers are also studying the effects ergovaline has on pituitary gland development in the fetus. It is possible this toxin also inhibits developments of the fetal anterior pituitary gland, which may help explain why foals from affected mares are stillborn or suffer from neonatal maladjustment syndrome (“dummy foal” syndrome).

            Unfortunately, broodmares affected by fescue toxicity do not show many clinical signs before parturition begins so it is important that mare owners are carefully monitoring their udder development, particularly in the last 21 days of gestation. These mares will also commonly carry past their due dates because the toxin impacts the normal hormone signaling between the mare and the foal, which slows down the progression of the pregnancy. Some of these mares will abort or have stillborn foals, while others will struggle with dystocia because the longer gestational time will lead to foals that are enlarged or malpositioned and cannot pass through the birthing canal without assistance. These mares can also be more likely to a have thickened, edematous placenta and a higher rate of placental retention.  

            The best treatment for fescue toxicosis in mares is to avoid consumption of infected fescue during the late stages of her pregnancy. It is recommended that owners remove their mares from possible sources of infected fescue 90-120 days before their due dates. However, if the mare is allowed to graze on fescue, there are things that can be done to try and minimize the effects of the toxicity. Agalactia is the most common clinical sign of fescue toxicosis in mares so if owners notice that the mare is not developing an udder within the last two-three weeks before the due date, it is recommended that they start her on domperidone. Domperidone will counteract the effects ergovaline has on the pituitary gland and allow for serum prolactin levels to increase, which stimulates udder development and milk production. Mares that are not caught in time or not treated with domperidone will have no milk supply for their foal once it is born. Also, these mares will fail to produce any colostrum, which means the foals will be unable to obtain any antibodies from their mother and will need to be supplemented with colostrum from another mare or be administered intravenous plasma from a donor horse in order to have any immune function for the first several months of their life.

It is also very important these mares be monitored for prolonged gestation, which can be a warning sign for a possible dystocia. In these cases, mare owners should be prepared for the mare to have difficulties with parturition due to increased fetal size or fetal malpositioning. Any owner concerned about fescue toxicosis should speak with their veterinarian and have an emergency plan in place for foaling. It is often best these mares foal out in a hospital where immediate intervention can be provided if a dystocia does occur. Affected mares can also have thick, edematous fetal membranes, which can lead to abortion or stillborn foals due to placental insufficiencies at the end of the pregnancy. However, foals born alive can offer suffer from neonatal maladjustment syndrome, which can have varying degrees of severity. Some of these foals may be unable to stand while others may not have a strong suckle reflex or the ability to find and latch on to the mare’s teat.  These foals will require a significant amount of intervention and supportive care in order to survive and begin to function normally.

Owners should be aware of fescue and the many negative impacts it can have on their mare’s pregnancies and foals. They are encouraged to seek veterinary advice as soon as possible if there are any questions or concerns about possible fescue toxicity in their mares. Early intervention can be the key to saving the mare and foal as well as a lot of money and potential heartache during foaling season. 

Read more in the June 2020 issue of Oklahoma Farm & Ranch.

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Equine

Equine Flexural Limb Deformities

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By Dr. Garrett Metcalf

Flexural limb issues can occur in different age groups of horses, starting with newborns up to two- to three-year-olds. These issues occur somewhat predictably in age groups and can be addressed rather quickly when needed. There are various treatments and methods that can be used to address flexural issues. This article will discuss the most common flexural abnormalities and treatment methods.

Foal Flexural Issues

Foal flexural issues are often considered congenital flexural limb abnormalities because they are born with them. We don’t fully understand why this occurs but there is some evidence in the human literature that lack of fetal activity in the womb causes club feet in babies. In foals, it is thought that uterine positioning is to blame for part of the contracted tendons. Other causes can be exposure of the mare to toxic plants or substances that may be toxic to the fetus.

The most common area that a foal will have contracture of limb is at the carpus or knee. These foals will not be able to fully extend the knee and often will affect both at the same time. These foals can have difficulty standing to nurse or will get fatigued quickly and will not be able to stand for longer periods of time. There can also be damage to the extensor tendons or even rupture of extensor tendons caused by the high strain placed on them when the foal tries to stay standing. The rupturing of these tendons is not overly concerning but the lack of extensor function can make the flexural limb deformity worsen.

Other common locations of flexural limb deformities can be at the fetlock or coffin joint level. These deformities are not usually as detrimental to allowing the foal to stand and nurse properly compared to carpal flexural deformities. These deformities can be addressed similar to carpal deformities with some exceptions.

Treatment of Flexural Deformities

Splints or casts can be used to stretch and support the effected limbs of foals. Splints are often preferred by most veterinarians because they can be repositioned or reset as needed. Splints are easier to place on the limbs of foals but they do need resetting every 24 to 48 hours. Casting of the limbs is more rigid but is not adjustable once placed. Casting is often needed in more severe cases and requires changing frequently. Whenever placing these devices, care must be taken to prevent splint or cast sores because foal skin is rather delicate.

Surgical intervention is needed in some cases of carpal flexural deformities. A study out of Australia found that cutting of two muscle/tendon groups on the back of the carpus greatly improved the ability to extend the carpus with splinting methods. Cutting of these tendons do not have consequence to future athletic function. The two muscles are called flexor carpi ulnaris and ulnaris lateralis.

An antibiotic called Oxytetracycline is helpful to treat flexural limb deformities because of its side effect of causing tendon laxity. The laxity is created by chelating calcium within the tendons and allows the relaxation of tendons. This method does have some risk because of the high dose required and renal injury that it can cause when not administered with IV fluids.

Toe extension shoes are used when it comes to dealing with lower limb flexural limb deformities. These shoes are often applied with adhesives and after the splinting or casting is no longer needed. The toe extension shoe allow foal to continue to stretch those tendons every time they take a step and prevent from becoming contracted again.

Older horses (six months or older) with contracted tendons often get acquired limb deformities and the horses need surgical intervention to correct these deformities. These surgeries cut or release check ligaments that allows the musculotendinous unit of the deep digital or superficial digital flexor tendon to elongate. The deep digital flexor tendon is responsible for causing club feet or a flexural limb deformity at the coffin joint. The superficial digital flexor tendon is responsible flexor tendon that causes a flexural limb deformity at the fetlock joint. The check ligaments attach the tendon to bone and do not allow the tendon to elongate past a certain point. By eliminating these ligaments the flexural limb deformity can be corrected by allowing the muscle to stretch since the tendon is much more rigid.

Flexural limb deformities can be caused by excessive laxity or weakness of the tendons. These deformities are often seen in premature foals or foals that are born at a much smaller birth weight. The excessive laxity will cause the toes of there feet to flip up in the air and the fetlocks to be touching the ground. The areas where the skin is contacting the ground will cause sores and abrasions. If these areas are note protected the wounds can get into deep structures causing serious infection and injury the flexor tendons.

Treatment for tendon laxity is to add heel extension shoes to keep the toes flat to the ground. The extension behind the foot forces the toe down under the foals own weight. As the foal becomes stronger from normal activity the muscle attached to the tendons can support the foal and the limb laxity will correct itself. Abrasions still can occur even with heel extension shoes are in place so bandages need to be applied to protect these areas.

Flexural limb issues are a common issue that horses and owners will face. It is best to have your horse evaluated by a veterinarian whenever these problems are suspected. Foal flexural limb deformities can be life threatening because of the limitation of standing on time to nurse colostrum. Without colostrum within the first hours of life the foal is a much higher risk of sepsis and death.

Read more in the August 2023 issue of Oklahoma Farm & Ranch.

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Equine

Equine Foot Abcesses

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What a pain!

By Dr. Garrett Metcalf, DVM

A foot abscess is a common occurrence in horses throughout the year. Often wet weather can play a factor in the increase number of foot abscesses that horses will experience. A foot abscess can cause a great deal of pain, lameness, swelling and misery to the horse that often needs to be addressed quickly and provide pain management to keep them comfortable. There are many methods of addressing a foot abscess that people use. This article will discuss techniques to evaluate and treat the abscess as quickly as possible.

Foot abscess is a focal or sometimes diffuse infection that is trapped between the sensitive and non-sensitive lamina of the foot capsule. A foot abscess can form randomly from the normal stresses and environmental changes that cause the foot to allow bacteria to enter down to the sensitive tissues. Other causes are penetrating injuries to the bottom of the foot that allows bacteria to enter the through the outer lamina, such as nails, sharp rocks or even thorns. Poor foot care and misplaced shoeing nails can also lead to foot abscesses. A common area for abscesses to form is at the white line (area where the sole and hoof wall meet) and at the bars of the heels.

Foot abscess can cause a horse to have variable amounts of lameness, but generally they will be lame at a walk or even be non-weight bearing from the severity of the pain. Swelling starting at the foot and working its way up the limb can be noted when the abscess is trying to migrate out at the coronary band. These types of abscess are often referred to as “gravel” abscesses. “Gravel” is no more than just a regular foot abscess that has found the path of least resistance to the coronary band, where it ruptures out and causes a draining tract. An abscess in the hind foot can make the horse move rather abnormal to the point that it makes owners and veterinaries perceive the horse as acting neurologic.

Examination of the horse for lameness is the first step in diagnosing a foot abscess. The horse will often be lame at walk but some need to be watched at a trot to determine the lame limb. Lameness localization with regional nerve blocks can help make sure the pain is coming from the foot and not other parts of the limb. The foot will often have an increase digital pulse with occasional notable heat in the foot. The pulse is from inflammation causing a bounding of the digital arteries most notably behind the ankle region. The foot examination often needs to be performed with the shoe removed from the foot if the horse is shod. Hoof testers help pinpoint the area of most concern on the foot and often horses will be rather painful in response to the pressure created by the hoof testers. Knifing the foot out to clean up and remove any old sole or frog material is imperative to be able to locate the abscess with as much accuracy as possible. Often there will be a defect in the hoof or a dark focal tract that will lead to the abscess.

Treatment of the foot abscess can be done multiple ways and many people have lots of opinions on this topic. My treatment of choice is to open that abscess as soon as possible to give the horse nearly immediate relief and to quickly resolve the abscess infection. There are many methods to doing this but a good sharp hoof knife or loop knife one of the easiest ways to get the abscess drainage through the bottom of the foot. Whenever drainage of the abscess is achieved at the bottom this can eliminate the formation of a “gravel” and keep it from migrating out at the coronary band. Also drainage at the bottom allows a more effective treatment of the abscess with topically applied poultice agents. After the abscess has been opened to drain, bandaging the foot with a poultice agent is effective at eliminate the abscess and preventing foreign material from packing to the abscess area.

A great method of bandaging the foot is with the use of a large baby diaper. The diaper is very absorbent and foots the foot rather well. The diaper can be covered with layers of Vetrap, Duck Tape and Elaskiton to keep it protected or the foot can be placed in a medicine boot to keep the diaper protected.

Poultice choices are rather personal experience or availability, but also depend on the nature of the abscess. Epsom salt based foot poultice agent called Magna Paste or similar products are rather good at drawing out the remaining part of the abscess once it is opened. A homemade poultice of sugar combined with Betadine solution can make a really good poultice. There are various other topical agents that can be used effectively. The main thing when choosing a topical product is to make sure it is safe and that it has some antimicrobial properties.

Some foot abscess cases can be difficult to pinpoint and to drain. In these situations often time, pain management and soaking of the foot in Epsom salt water baths can help to allow the abscess rupture or make it easier to identify. In rather difficult abscess or when abscesses keep reoccurring in the same location, X-ray imaging of the foot is helpful to examine the structures of the foot. The abscess itself cannot be seen often with X-ray because the abscess fluid is the same density as the hoof wall. The only way to identify an abscess on X-ray is if there is gas present in the abscess making it visible on the film. Whenever there is a penetrating injury to the foot, X-ray is a must to make sure that the injury is not going into the deeper structures of the foot like the coffin joint or navicular bursa. These injuries are much more serious and need to be examined as quickly as possible. It is also recommended whenever possible to leave the penetrating object in the foot until the X-ray is taken. This will help the veterinarian understand what structures may have been injured.

Prevention of foot abscess is not always possible but a great start to this is really good hoof care. Routine trimming on a timely schedule is key part of good hoof care. The longer the feet go without a trim can affect the lamina and cause stretching of the white line, opening it up to allow bacteria to enter the foot. The use of special shoeing nails and other methods of good shoeing practices also limit the risk of abscessation.

Read more in the June issue of Oklahoma Farm & Ranch.

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Equine

Guttural Pouch Diseases of Horses

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The guttural pouches of horses may not be very well known to most horse owners. These bilaterally paired pouches are located below the base of the skull, below the ears and extend into the throat latch region. The pouches purpose is not fully understood, but some theories is that they reduce the weight of the skull or have a blood cooling function to reduce the temperature of the arterial blood going to the brain. The guttural pouches can be plagued with a multitude of issues that are difficult to treat or can be life threatening to the horse. Other species contain guttural pouches such as some bats, American Forest mouse and Hyraxe.

The anatomy of the guttural pouches is complex and houses various important anatomic structures. The guttural pouches are an auditory tube diverticulum that is analogous to human Eustachian tubes but much larger. The volume of the guttural pouches can be up to 400-600 milliliters of air. The guttural pouches contain large arteries, nerves, the bones of the inner ear, muscle tissue and part of the hyoid apparatus that connects the skull to the larynx. The opening of the guttural pouches is deep in the nasopharynx through the slights call the pharyngeal ostium, which can only be accessed with an endoscope passed up the nose. The difficulty of accessing this area makes treatment of these diseases challenging at best. The guttural pouch is the only location in the horse that allows direct visualization of the arteries and nerves. The main arteries that are present in the guttural pouch are the maxillary artery and the internal and external carotid arteries that provide all the blood to the skull. The nerves in the guttural pouch are cranial nerves that exit directly from the brain or brain stem that innervate critical structures that control breathing, swallowing, chewing and ocular functions of the skull.

Read more in the April issue of Oklahoma Farm & Ranch.

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