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Omega Fatty Acids
Why all the talk about Omega Fatty Acids in horses diet? Unsure of how to supplement your horses diet appropriately? Read on for some insight into why horses are being supplemented to help you make the best educational choice for your individual horse!
What are Omega Fatty Acids?
Omega fatty acids are not produced directly by the horse’s body, which means they are considered “essential fatty acids”. This fact creates the need for a balanced diet to obtain the appropriate ratio. Without getting too scientific and to describe a complex pathway in the simplest of forms, Omega -6’s are originally from Linoleic acid (LA) while Omega-3’s stem from alpha-linoleic acid (ALA). This fact is important because horse’s require a balanced ratio of Omega 6 (LA) and Omega-3 (ALA) fatty acids in their diet to maintain the proper amount of inflammatory modulators. Once ingested, ALA’s (Omega 3’s) can convert to eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are intermediates in the formation of eicosanoids. Eicosanoids are important because they have potential to reduce inflammatory responses, support immune function, and enhance fertility. The proper ratio of ALA (Omega 3) to LA (Omega 6) at this time is not yet perfected and further research is being performed to determine the appropriate ration.
What are the sources of Omega 3 & 6?
Omega 3’s (ALA) are found predominantly in leafy plants, which obviously are the more traditional components of equine diets. Linseed oil (flaxseed), fish oil and canola oil are also a rich source of omega-3 fatty acids. EPA and DHA are a great source of omega 3’s, however they are derived from fish, which we all realize is not the normal equine diet, therefore creating the drive for supplementing Omega 3’s in the equine diet using plant material and or fish oil.
Omega-6 fatty acids originate from the oil of cereal grain and seeds. Examples of feedstuff containing higher omega 6’s are corn oil, safflower oil, rice bran and sunflower oil. Studies have shown that horses are able to absorb fatty acids when they are supplemented in the diet regularly. High performance horses and horses that are hard keepers tend to need more grain/concentrate rations (higher in Omega 6) then forage sources (naturally higher in omega 3). This is important because horses need both sources of Omegas, however a diet with a higher Omega-3 to Omega 6 ratio appears to be more desirable.
Why are Omega Fatty Acids important for the equine diet?
Once ingested, fatty acids are metabolized (broken down) by the body to produce prostaglandins (inflammatory mediators). Prostaglandins are hormones that participate in strong physiologic effects throughout the body. They play a large roll in promoting and inhibiting parts of the inflammatory cascade. Knowing this fact, researchers have evaluated horses that were supplemented with Omega 3/6 to determine if there is a change in the level of inflammation, which eventually leads to osteoarthritis. Research and supplementing has shown that Omega Fatty acids have appeared to improved coat and skin health, hoof quality, boosting immune systems, helps aid in reproduction, helping hard keepers maintain their weight along with protecting horses with EIPH (exercise induced pulmonary hemorrhage), lowering overall heart rates and protecting RBC (red blood cell) membrane fragility. A study performed by Kentucky Equine Research showed that 60 ml/day of fish oil supplementation increases serum and RBC EPA and DHA in horses. (Pagan, Lawrence, Lennox). (Remember that EPA and DHA, which are a source of Omega-3’s help aid as anti-inflammatory modulators).
What’s the future of Omega Fatty Acids?
Researchers are continuing to determine what the best ratio is for Omega 6 to Omega 3 supplementation for horses are. They are also continuing to do research on the best form of supplementation.
What are some drawbacks to supplementing Omega Fatty Acids?
Horses that are easy keepers may not do well on a fat supplement mostly due to obesity. Horse’s that are overweight should be on a high forage diet with minimal concentrates (grain), which will help increase their Omega 3 amounts!
Treatment Options for Kissing Spine
Lori Smolkovich, DVM
Overriding dorsal spinous processes, better known as "kissing spine" is a condition that many horse owners fear, because, until recent years, treatment options were very limited. In this article, the anatomy of the horse’s back, clinical signs, and treatment options will be discussed.
Individual bones called vertebrae fit together to form the spine. The vertebrae are named for their location. Starting at the head and moving toward the tail, the equine spine consists of seven cervical or neck vertebrae (#1 in image), 18 thoracic vertebrae (#2 in image), 6 lumbar vertebrae (#3 in image), 5 sacral vertebrae (#4 in image), and approximately 20 caudal or tail vertebrae (#5 in image). When discussing kissing spine, the area of interest is the thoracic and lumbar vertebrae (#2 and #3).
As you can see in the picture, there are bony "protuberances" that project dorsally (or up) along the spine. These "protuberances" are part of the vertebrae called dorsal spinous processes (DSPs). There are ligaments that are in between each DSP called the interspinous ligament, and a ligament and several muscles that run over the top of the DSPs. These muscles and ligaments make up the top line of the horse and help support the vertebrae to give it strength. Kissing spine occurs most frequently when the dorsal spinous processes come in contact with each other because the back muscles are weak and do not provide the support the spine needs. When the DSPs "kiss", or touch, the repetitive rubbing causes inflammation and bony changes. As a result of inflammation, the horse develops back pain. The bony changes in the DSPs can be easily diagnosed with radiographs.
Radiograph #1 illustrating normal DSPs
Radiograph #2 illustrating kissing spine. Notice the lack of space between the DSPs and the increased bone density where the rubbing and pressure has occurred.
There are two broad categories of treatment for kissing spine; medical management and surgical intervention. Medical management commonly consists of shockwave therapy, bisphosphonates, corticosteroid injections, and physical therapy. Shockwave therapy is utilized to modulate pain and discomfort. Bisphosphonates and corticosteroid injections treat and quiet inflammation. Physical therapy is required to strengthen the back muscles and build the top line so that the DSPs have more support and are less likely to contact each other. If medical treatment is not able to manage the horse's clinical signs, surgical intervention is often the next step.
There are several ways to surgically approach kissing spine. Two of the more common procedures will be discussed in this article. One surgical option is a subtotal ostectomy of the impinging dorsal spinous processes (SODSP). This means that a portion of the DSP is removed to create a wider gap between the DSPs thus preventing them from touching or "kissing". This procedure has been performed under general anesthesia and on horses standing with heavy sedation. The decision to perform the surgery standing or under general anesthesia is often dependent on which DSPs are affected, surgeon's preference, and risk factors specific to the individual horse. The other surgical option is an interspinous ligament desmotomy (ISLD). Unlike the SODSP, which is a surgery that removes a portion of bone, the ISLD approaches “kissing spine” by altering the soft tissue structures around the affected DSPs. As previously discussed, in between each DSP, there is a ligament called the interspinous ligament. In an ISLD, those ligaments are incised or cut, allowing the DSPs to not be held so tightly together. As a result the DSPs can spread apart and therefore do not “kiss”. The ISLD is surgery that is performed standing under heavy sedation so general anesthesia is not required.
Regardless of the surgical procedure that is utilized, physical therapy plays an integral role in the success of the horse following surgery. Once the DSPs are no longer kissing, the back must be strengthened to ensure the DSPs are supported as much as possible so that the condition does not reoccur. Physical therapy often begins after surgery with carrot stretches, later on, the horse is worked on a lunge line in a chambon, Pessoa, or other rig to encourage the horse to use his body and back properly while not adding the weight of a rider. Once the horse is ready, under saddle work that encourages engagement of the back and hind end is necessary to continue to build strength and to maintain the back muscles.
Kissing spine is a painful condition for horses and a frustrating one for riders. Fortunately there are many ways to help your horse achieve relief. If you think your horse may be affected by kissing spine, have your veterinarian evaluate him and discuss which options may be best for you and your horse.
Jacklin, B.D., et al. (2014). A new technique for subtotal (cranial wedge) ostectomy in the treatment of impinging/overriding spinous processes: Description of technique and outcome of 25 cases. Equine Veterinary Journal, 46, 339-344.
Brink, P. (2014). Subtotal Ostectomy of Impinging Dorsal Spinous Processes in 23 Standing Horses. Veterinary Surgery, 43, 95-98.
Coomer, Richard P.C., et al. (2012). A Controlled Study Evaluating a Novel Surgical Treatment for Kissing Spines in Standing Sedated Horses. Veterinary Surgery, 41, 890-897.
Catarina Ruksznis, DVM
Despite its relatively small size, the equine eye is a complex organ which can go very seriously wrong, very quickly when injured. If your horse comes in from the pasture with his eye swollen shut, take no chances- have your vet take a look as soon as possible. These clinical signs could be due to anything from a bump, to a foreign body, to a disease process within the eye. One of the more common problems we see are corneal ulcers. In order to understand this problem, let's first think about the anatomy of the eye.
In its most simple conception, the eye is a round structure divided into two compartments: the anterior ("forward") chamber and the posterior ("behind") chamber. The two compartments are separated from one another by a divider made up of the iris and lens. The anterior chamber lies between the cornea and the iris/lens, while the posterior chamber lies behind the iris/lens and the back of the eye. The cornea is the clear "window" at the front of the eye through which light enters and we can see. It is made up of different layers of cells like layers of a sandwich. The bread is formed by epithelial layers and the contents by the stromal layers, which form the majority of the corneal thickness. In total, the thickness of the equine cornea is only about 1 mm. The cornea is by necessity a very specialized tissue (it's clear!) and contains various mechanisms through which water is excluded from the stroma and transparency is maintained. The remainder of the outside of the eye is covered with a fibrous layer of white tissue (the "whites of the eye"), which is called the sclera.
Corneal ulcers are injuries, abrasions or erosions, to the cornea. While superficial corneal ulcers only involve the outermost epithelial layer (the 'top slice' of bread), deeper ulcers may include loss of the stromal layers and even expose the inner endothelial layer. Any depth of ulcer is painful, and horses may display squinting, tearing or rubbing at the offending eye. You may also see redness, swelling of the eyelids or thick, abnormal discharge from the eye.
When examining an eye, your vet will begin with a careful ocular exam. This will include looking for causes of the ulcer, such as a foreign body stuck in the eye, decreased tear production or the inability to blink. Corneal ulcers can then be definitively diagnosed by staining the eye with a colored dye called fluorescein. Fluorescein stain is not taken up by the normal corneal epithelium, but does stick to the inner stromal layers of the cornea (the filling of the sandwich) in places where the epithelium has been scraped away. While the stain appears yellow/green to the naked eye, it fluoresces green when viewed under a blue light. Ulcers appear as areas of intense green on the cornea. It is important to note that deep corneal ulcers, ones which have gone through all of the stromal layers, will only show a thin ring of stain uptake on the edges of the ulcer. This is because the endothelial layer which forms the bottom of the ulcer does not adhere to the stain but the sides of the ulcer, where the stroma is exposed, do. Other stains may also be used to evaluate the eye, such as rose bengal and lissamine green, to look for viral or fungal infection.
Management of corneal ulcers involves both systemic (oral or intravenous) treatment and treatments applied directly to the eye. Pain from the corneal ulcer is managed with systemic banamine, a non-steroidal anti-inflammatory medication similar to ibuprofen, along with topical atropine. Atropine is an anticholinergic agent which stops the spasmotic contraction of muscles within the eye secondary to pain, allowing the pupil to dilate.
Corneas, like your skin, are constantly exposed to the environment. Once there is a breech in the epithelial barrier, there is an opportunity for infection to occur. Bacterial or fungal infection may cause significant corneal damage and even corneal melting (keratomalacia) as the body tries to respond. Topical antibiotic therapy is therefore an essential part of treatment for corneal ulcers. There are a wide variety of antibiotic choices available, the most common of which is triple antibiotic ointment, composed of three antibiotics (Neomycin, Polymixin B, Bacitracin). This product has a broad spectrum of activity against many of the probable bacterial contaminants and is a good choice for an uncomplicated ulcer. It is essential to remember that this product is composed of only antibiotics and is often referred to as NeoPolyBac. There is a very similar product known as NeoPolyDex, which contains a steroid in addition to antibiotics. Steroids should never be applied to a corneal ulcer, as they inhibit healing. In cases of more complicated or non-healing ulcers, corneal scrapings can be taken to sample the cells and bacteria/fungi within the cornea and to guide antibiotic choice. In addition to an antibiotic, an antifungal is often added to the treatment regime in more complicated cases.
In the case of an uncomplicated corneal ulcer, healing should be complete within 7 to 10 days. If the ulcer does not heal or worsens, more intensive treatments or diagnostics are warranted.
Irby, Nita L. "Ophthamology." Equine Emergencies Treatment and Procedures. Fourth ed. St. Louis: Elsevier Saunders, 2014. 400-07. Print.
Gilger, Brian C., ed. Equine Ophthalmology. Second ed. Maryland Heights: Elsevier Saunders, 2011. Print.
Equine Protozoal Myeloencephalitis: An overview
Equine Protozoal Myeloencephalitis (EPM) is a commonly diagnosed neurologic disease of the horse that has captured the attention of equine veterinarians and horse-owners alike since it was first documented 30 years ago. It is a progressive and degenerative disease of the equine central nervous system, and is caused most commonly by the protozoan species, Sarcocystis neurona. (There have been few documented cases identifying Neospora hughesi as the causative agent, though the two species are clinically indistinguishable from one another.) Recent studies show that approximately 22-65% of horses in the United States are seropositive with antibodies from S. neurona, but only a small portion of these horses will go on to develop clinical disease.
The definitive host of Sarcocystis neurona is the opossum. This is the host in which sexual reproduction of the parasite occurs. Infected opossums shed sporocysts in their feces which are in turn transmitted to the intermediate host when ingested. Intermediate hosts include cats, armadillos, skunks, raccoons, and sea otters, and once infected, they develop sarcocysts in their skeletal muscle. Once this muscle is ingested by the opossum, the life cycle is completed. In the pathogenesis of EPM, horses are considered aberrant, or dead-end hosts, which halt the life cycle of the organism. Horses become infected through ingestion of contaminated feed or water and once infection is established, disease progression ensues.
While the pathogenesis of EPM infection is still widely a mystery, it is postulated that the ingested sporocysts are able to penetrate the intestinal wall and enter the cells that line the horse's arteries. The organism develops within the arterial walls until they rupture into the bloodstream where they can spread to other parts of the body. At this point it is possible for the horse to clear the infection on his own, leaving him seropositive, but without any clinical signs or evidence of disease. It is unknown how S. neurona enters the CNS in horses, though once the protozoa gain access they can establish infection in any area of the brain or spinal cord. Horses infected with S. neurona are unable to transmit the disease to other horses.
EPM can manifest itself through a variety of clinical signs, though the most classic are the three As: Ataxia, Asymmetry, and Atrophy. A common appearance of a horse with EPM is one with severe asymmetrical gluteal muscle atrophy. Since the organism can infect any area of the central nervous system, ataxia, or incoordination, is frequently observed in horses with EPM. Moreover, a variety of neurologic deficits can be seen, ranging from cranial nerve abnormalities in the form of a head tilt or facial paralysis to a dull or depressed mentation. Various gait abnormalities may also be seen and can occasionally be mistaken for lameness. The timeline for disease progression is variable, but if left untreated, in its most severe form, EPM can lead to seizures, coma, and even death.
Obtaining a diagnosis for EPM can be challenging, and it's important to know that a truly definitive diagnosis may not be attainable during a horse's lifetime. That being said, tests for EPM in live horses include the Western blot, indirect fluorescent antibody test (IFAT), and surface antigen-1 ELISA test (SAG-1 ELISA). Simple seropositivity for S. neurona antigen is not sufficient for a diagnosis, as that only relays if there are circulating antibodies within the vasculature. All exposed horses should be seropositive, but it takes the protozoan entering the central nervous system from the systemic circulation for the horse to actually have EPM.
To make a diagnosis of EPM, cerebral spinal fluid (CSF) and blood samples should ideally be submitted together for paired testing and analysis. The Western blot test looks for IgG antibodies against S. neurona within the CSF, though false positives are possible, especially if there is blood contamination of the sample. With a specificity of only 44-60%, it is likely that the immunoblot tests are best to rule out the presence of EPM, rather than provide a diagnosis for the disease. The IFAT test has shown comparable sensitivity, better specificity, and it is less affected by blood contamination. However, this test might give positive results for the protozoa S. fayeri, which might or might not cause disease in the horse. The newest test, the SAG-1 ELISA, looks for the presence of a particular surface protein of S. neurona, but not all strains express this particular protein. Therefore, false negative results are common.
The gold standard for diagnosing EPM in the horse is based on finding characteristic lesions on post-mortem exam within the CNS. However, due to the small number of organisms needed to cause the disease, the diagnosis can be missed even with a full neurologic necropsy. In general for the live animal, a clinical diagnosis is best established in horses with clinical signs of neurological disease consistent with EPM combined with positive CSF testing. Another option for diagnosis of EPM is looking for improvement in clinical signs in response to treatment. Since test results can take days to weeks to come back, horses are often started on treatment for the disease once they begin showing signs of neurologic disease while other possible causes continue to be ruled out.
Treatment for EPM is generally successful with studies indicating clinical improvement in 60-70% of cases. However, a portion of horses that are treated will have some residual neurologic signs that do not completely resolve with treatment. Relapse of disease once treatment is stopped is possible, though uncommon. There are four drugs that have been approved by the FDA for treatment of EPM: pyrimethamine, sulfadiazine, ponazuril and diclazuril. The most common oral medication used for the treatment of EPM is ponazuril (Marquis). It is administered once daily for 28 days or more depending on disease severity. While studies show ponazuril can effectively rid horses of S. neurona, it does not improve the CNS damage that occurs before treatment begins. Regardless of which medication is instituted, early detection and prompt treatment are essential for a positive outcome and a full recovery.
If you have any questions regarding this article or the health of your horse, please contact your veterinarian or the doctors at New EnglandEquineMedical & SurgicalCenter.
Tessa Lumley, DVM
New England Equine Medical & Surgical Center, 15 Members Way, Dover, NH03820
Volunteer Management Survey Kicks Off
It probably comes as no surprise that volunteers are the life blood of the horse industry. Recruiting and retaining volunteers can be challenging, and it can be one of the key obstacles to growth. It can also be difficult to figure out where to start to improve volunteer management.
Blue Ribbon Consulting, LDO, LLC is conducting a volunteer management survey to develop a white paper that will provide a snapshot on where the horse industry stands. The survey results can help nonprofits to determine next steps to strengthen their volunteer management practices. Those that operate an equine oriented nonprofit, or on the board of directors are invited to take a few moments to participate in this survey. Answers are confidential and will only be used in aggregate to produce a white paper that will be posted to the Blue Ribbon Consulting website. If you don't run an equine nonprofit but know someone that does, please send the link along to them.
Find the survey here: https://www.surveymonkey.com/r/FFV9S3Y . Please complete the survey by December 15, 2014. The white paper will be available in early 2015.
Since 1995, Blue Ribbon Consulting has provided evaluation, planning, research, marketing and problem-solving services to clients around the world to take their horse businesses successfully through their business transitions. Lisa Derby Oden, Blue Ribbon Consulting’s founder and principal, has also been a nonprofit founder, board member, and executive officer for state and national organizations. She has worked with nonprofits in strategic planning, program development, corporate development, fundraising, grant writing and grant administration. Lisa has delivered business development, marketing, and leadership seminars throughout the United States. In addition to her horse business books, she has also been a columnist and freelance writer for many equine trade publications. Lisa has received state and national awards for her work in the horse industry.
Contact: Lisa Derby Oden
Blue Ribbon Consulting, LDO, LLC
Synovial infections in adult horses
Elizabeth Taylor, DVM, MS
Septic arthritis and tenosynovitis are orthopedic conditions in horses that develop following penetrating trauma or less commonly following an injection. They can carry serious complications for the horse if left untreated. Potential complications of synovial infections include arthritis, irreversible cartilage damage, adhesions, and severe lameness sometimes requiring humane euthanasia. It is important that these conditions be recognized promptly in order to instill immediate and accurate diagnosis and treatment aimed at eliminating the infection, reducing pain and inflammation and ultimately returning the horse to function.
In adult horses, joint or tendon sheath infection usually results from contamination via wounds. Because the lower leg of horses is poorly covered with soft tissue, joints and tendon sheaths are located very superficially and are prone to contamination following many lacerations, including heel bulb lacerations, and lacerations to the front or back of the pastern or fetlock.
It is important to contact your veterinarian if your horse has a laceration of the lower leg in a location near a synovial structure. Typically, horses with a synovial infection are quite lame (grade 4/5), however if the affected joint or tendon sheath is open and draining, lameness can be less severe. Frequently there is marked effusion (swelling), heat and sensitivity to the touch.
Analysis of synovial fluid is key in diagnosing and treating an infection. A sample should be obtained for both cytology and culture. Culture of the fluid is the “gold standard” for the diagnosis of an infection, however this only occurs in approximately 50% of cases. Therefore, analysis of the fluid’s cell count and protein, as well as examination under a microscope can help with an immediate diagnosis.
Diagnostic imaging can also aid in the diagnosis of a synovial infection. Ultrasonography can be helpful in the acute phase, when effusion is most prominent and accurate aspiration of fluid can be obtained. Radiography is less helpful in the acute phase, as soft tissue swelling is the only evidence of infection, but it can be useful to identify osteomyelitis (infection of the bone) should the infection spread.
The mainstay of treatment is to remove bacteria, devitalized tissue and other debris and reduce pain and inflammation. The goal of treatment is to return the articular cartilage to a normal environment, thus preventing cartilage loss. Cartilage health is imperative in maintaining an athletically sound horse.
Physical removal of bacteria and inflammatory mediators is best accomplished early and with a high volume of fluid. This can be done via needle lavage, arthroscopy or open drainage. Arthroscopy is advantageous because it also allows evaluation of the articular cartilage and removal of debris.
Antimicrobial therapy is directed by culture results, however because results may take days and positive results are not always obtained, therapy should be broad spectrum. In addition to systemic administration of antimicrobials, local administration of antimicrobials results in high concentrations directly at the site, while avoiding untoward systemic effects.
Lastly, synovial infections are very painful and can lead to support limb laminitis if proper analgesia is not maintained. Non-steroidal anti-inflammatory drugs (NSAIDs), such as phenylbutazone or flunixin are used to decrease the pain and inflammation associated with synovial infections. Their use must be judicious as serious side effects (gastric ulcer formation, colitis and renal toxicity) can arise with long-term use.
It is important to monitor synovial infections very closely as they can become life threatening if the horse has continued pain and lameness. Early recognition, accurate diagnosis and aggressive therapy of synovial infections greatly increase the prognosis for a horse to return to full athletic function.