Connect with us

Equine

Fescue Toxicosis

Published

on

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.

Continue Reading

Equine

Here’s to the Great Horses

Published

on

By Summer McMillen

Everyone that knows anything about horses knows that there are bad ones, good ones, and great ones.

The bad ones are good for nothing. You can’t catch them, you can’t saddle them, and you can’t get on them without feeling like you need a helmet, some kind of padded vest and, an instruction manual. Once you do mount up the whole ride is a battle and heaven forbid, you actually have a job to do because they are little to no help in holding the herd. We all find ourselves owning a bad one or two throughout our lives. Best case scenario is they find a more tolerable home to go to through via a horse sale or the classifieds. Worst case scenario all you can do is say “Vaya con Dios,” put a sign on them that reads “Do Not Attempt,” and turn them out to pasture. Hoping they are decent enough to stay within the borders and make a beautiful yard ornament.

Good horses are usually much more tolerable. They’re pretty easy to catch, saddle, and hop up on. Sometimes they might have a bad habit or two like setting back when they’re tied to a fence or, getting cold backed on early mornings that you tolerate because they are so skilled in a specific field. A good horse is usually only good for one thing. They have a niche talent m, if you will. They can be a good heel horse. A good head horse. The horse you want to gather pastures on because you know he won’t knicker or rare up when you get dropped off in the jig line. A good kid horse. Your rodeo horse. The horse you put your wife on when she’s being a little wimpy that day. Good horses usually get sold because they are proficient in their given field and they find good homes making both parties happy. We will all own many good horses in our lives and be happy to do so.

Great horses are a rare and treasured possession. They are simultaneously easy and hard to own. Easy because you can do anything on them. Hard because everyone is always trying to buy them from you. A great horse stands still while your kid pulls their head down all the way to the ground so they can halter them. A great horse is never cold backed and always ready to cinch tight and take off. A great horse can be ridden in the pasture and the rodeo arena on the same day. A great horse doesn’t need practice. A great horse is always willing to do anything you ask of them at any given moment. Great horses find their homes as horse colts and usually live out the rest of their days at the same home because great horses are irreplaceable.

People and horses are not all that different. There are bad, good, and great ones. The more time I spend around horses the more I am convinced of the kind of person I want to be. “Bad” will absolutely not do. “Good“ is much too common  and just doesn’t quite cut it more often than not. “Great” is what I aspire to be.

Great can be defined in so many ways when we let human standards get involved but, I want to be great as defined in the qualities of a great horses.

I want to be kind and patient while my children are learning. I want to be ready to help anyone who asks me. I want to go the extra mile. I want to make my home a beautiful place to come to after a full day’s work outside. I want to not be thrown off by life’s twists and turns but, firm in my faith.

So, basically what I’m saying is I want to be a great horse. And honestly there are worse things we could all aspire to be.

Here’s to great horses. May we know them, love them, and if we’re lucky be great just like them.

Continue Reading

Equine

Degenerative Suspensory Ligament Desmitis of the Horse

Published

on

By Dr. Garrett Metcalf

The suspensory ligament is a vital component of the limb of a horse to produce normal locomotion and support. The suspensory ligament is a common area of concern in performance horses of various disciplines and can be single handedly the cause of lameness or performance issues. This article is going to look at a specific degenerative disease of the suspensory ligament and what horses are at risk for this disease.

DSLD or degenerative suspensory ligament desmitis was first discovered in the early 1980’s in Peruvian Paso horses. The name has been changed because the suspensory ligament is not the only organ affected from the disease but the suspensory is ultimately the biggest issue. The newer name, ESPA or equine systemic proteoglycan accumulation, is more correct because other ligaments and tissues are affected by this disease. In this article we will only focus on the suspensory ligament. The most commonly affected breeds are Peruvian Paso, Paso Fino, Morgan, Saddlebred, Warmblood, Paints, American Quarter Horse, and Thoroughbred breeds. The age of onset of the disease is variable among breeds but it is more common to be seen in middle age to older horses.  However it has been documented in horses as young as one year of age. The disease generally will have a slow insidious onset that can go undiagnosed for months or years depending on the horses work and discipline.

A horse that begins to show early signs of DSLD may have a vague lameness issue that is difficult to isolate and they most likely will resolve with a period of rest. As the horse returns to moderate level of work the lameness will return. This scenario may go on for several months or more before the discovery of the DSLD is made. The first indication of DSLD is often pain isolated in the suspensory branches or fetlock region when a flexion test is performed. Horses with DSLD will also have a “dropped” fetlock appearance because the suspensory is the main supporting structure of the fetlock joint.  DSLD can affect the hind limbs, forelimbs or all limbs at the same time. A unique sign of DSLD is that not just one limb is affected but rather bilaterally affecting the limbs, meaning it will either affect either both forelimbs or hind limbs at the same time. It is my experience that the hind limbs are more commonly affected compared to the forelimbs. Horses will often have enlargement of the fetlock region and increased joint fluid or wind puffs. Horses will often have a straight hock or post legged hind limb appearance. Horses will often shift weight frequently in an effort to get relief from the discomfort and this can be confused with other lameness issues or foot related pain.

Diagnosis of DSLD is often made by clinical signs, breed and ultrasound findings. Ultrasound imaging of the suspensory ligaments will often show diffuse enlargement of the suspensory body and branches. The suspensory ligament will have a poor heterogeneous fiber pattern with periligamentious soft issue thickening from scar tissue deposition and edema or fluid within the tissue.  Radiographs of the lower limb may reveal abnormal bone changes in the sesamoid bones behind the fetlock joints and even osteoarthritis of the pastern and or fetlock joints. A definitive diagnosis can be made from a biopsy of a ligament in the neck called the nuchal ligament, but is not often performed because of the invasiveness of the biopsy.

Treatment is very limited and it is mostly geared towards protection of further damage by prolonged rest. Pain management is also important to attempt to keep the horse as comfortable as possible. Different shoeing techniques can be used with marginal success. In early cases of DSLD, a suspensory shoe that helps engage more work from the deep digital flexor tendon can help elevate the fetlock and offer more protection to the suspensory ligament. The devastating thing about this disease is that there is no cure and there are hardly any good options to slow the progression of the disease. DSLD carries a poor prognosis when the diagnosis is made in any breed of horse or any discipline. Although some cases can be managed better than others, it often progresses to the point of debilitating pain and discomfort to the point of humane euthanasia especially in the Peruvian Paso breed.

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

Continue Reading

Equine

Gastric Ulcers

Published

on

By Dr. Devan England DVM

Does your horse have gastric ulcers? Gastric or stomach ulcers are frequently blamed for a variety of things including poor performance, acting ‘cinchy’, weight loss, not eating, poor coat condition, diarrhea and colic. However, gastric ulcers are not always the culprit and the only way to know for sure if your horse has gastric ulcers is to look at the stomach on camera, using an endoscope. Poor appetite and poor body condition are the mostly widely observed clinical signs with gastric ulcers, however, these are non-specific. If you think your horse might have gastric ulcers, the best place to start is to talk to your veterinarian and consider scheduling a gastroscopy. Gastroscopy requires the horse be held off feed for at least 16-18 hours and held off water for at least 6-8 hours. Fasting off feed and water is necessary to allow the veterinarian to see the whole stomach. If restricting feed or water is difficult in your management situation, many veterinarians will allow you to hospitalize your horse the night before gastroscopy for proper fasting.

Gastric ulcers are split into two types, classified by the location of the ulcer in the stomach. Squamous ulcers are ulcers that occur in the squamous or skin like portion of the stomach. This is the top part of the horse’s stomach, is closest to the esophagus, and has squamous tissue to protect this portion of the stomach from stomach acids. The other ulcer type are glandular ulcers. Glandular ulcers occur in the bottom portion of the stomach, which is closest to the small intestine. This portion of the stomach has glandular mucosa with cells responsible for producing stomach acids for digestion as well as cells that produce mucus and buffers to protect the lining from stomach acid. Gastroscopy is important not only for diagnosing whether ulcers are present but also determining the severity and the type of ulcer, because these two ulcer types require different treatments.

Squamous gastric ulcers are common in racehorses both in and out of training, with higher prevalence in racehorses under training. Prevalence in Thoroughbred racehorses in training has been reported to be up to 100% (Sykes 2015). Squamous ulcers are also prevalent in Western pleasure horses, Thoroughbred stallions on breeding farms, and Italian donkeys (Sykes 2015). Glandular gastric ulcer prevalence has not been as well described as squamous ulcers. Glandular ulcers are reported to be most common in Thoroughbred and Standardbred racehorses, Canadian showjumpers and polo ponies, and American Quarter Horses (Sykes 2015).

Risk factors for ulcers vary by ulcer type. Anti-inflammatories (Bute, Banamine) can increase the risk of glandular ulcers in some horses by affecting normal defense mechanisms but are not a high risk in most horses. Horses that display stereotypic behaviors, such as cribbing, have an increased risk of squamous ulcers. Grain fed before hay in non-exercising horses, feeding larger amounts of grain, and increased time between meals increases the risk of squamous ulcers. Increased time with high intensity exercise and housing in single pens is associated with increased risk of glandular ulcers. A straw only diet, lack of water access and lack of direct contact with other horses increases the general risk of gastric ulcers.

If your horse is diagnosed with ulcers, the mainstay of treatment is a buffered formulation of omeprazole (Gastrogard, Ulcergard). Over the counter Omeprazole and compounded Omeprazole are not effective because without buffering, the acidic stomach quickly breaks down the drug before absorption. Most horses with squamous ulcers will have healing of these ulcers after a 4-week course of Gastrogard or Ulcergard at treatment dose (whole tube for the average horse). Some horses may be healed by 3 weeks of treatment, but all horses should undergo a recheck gastroscopy before stopping treatment. Horses diagnosed with glandular ulcers need combination therapy with Gastrogard/Ulcergard and Sucralfate for 4 weeks. About 2/3 of horses with glandular ulcers will heal in this time, but some horses may require longer treatment times so a recheck is always recommended before discontinuing treatment.

Horses at higher risk of gastric ulcers may benefit from preventative (low) doses of Ulcergard (1/4 tube in average sized horse) given for a few days before and during high stress situations like long distance travel and competitions. Sea buckthorn berry supplement may be protective against formation of glandular ulcers. Dietary management to decrease the risk of ulcers includes providing more frequent small hay meals if pasture access is not available, limiting high sugar grains as much as possible and adding vegetable oil to the feed.

Sykes BW, Hewetson M, Hepburn RJ, Luthersson N, Tamzali Y. European college of equine internal medicine consensus statement – equine gastric ulcer syndrome in adult horses. J Vet Internal Med 2015; 29:1288-1299.

Continue Reading
Ad
Ad
Ad

Trending