By David A. Rustebakke, DVM
Verterinary Medicine and Animal Nutrition are separate specialties in the animal care industry; however in my career I have found that in order to give good health care advice I need to know something about nutrition. As primary care health providers to these animals, the veterinarian is the one who actually has eyes on the animals or on the herd, and we are in the best position to diagnose a nutritional problem, and recommend specific products to help solve a problem. Many of us in practice are not familiar with all of the products available, and few of us actually have extensive training in nutrition. Because of this, our best option is often to refer the owners to a local feed store where a staff member with a nutritional background can give information on what product will best suit your animal's needs.
Nutritional based diseases seen in a typical veterinary practice
Malnutrition or under nutrition is by far the most common problem I see. This is often a result of ignorance (as opposed to willful neglect) on the part of the owner. These horses are often presented to look for a reason for weight loss. Most of these horses have dental problems, which we correct as well as possible. However the dental problems are often not severe enough to be the entire reason for the weight loss. To fully work up these horses we do a thorough physical examination including taking the vital signs (temperature, pulse, and respiration, listening to the heart and lungs, assessing body condition, hydration, capillary refill time, look for chronic pain issues, see if the stated age corresponds with the age estimated by the teeth, etc..). If no obvious problems are noted, we recommend a blood test (serum chemistry and CBC) to look for any chronic infections or organ system failure. If we identify a specific disease condition, the recommendations are based on whatever disease we see. Otherwise, the next step is to assess the diet and recommend changes.
From here, this is not rocket science. We know that a horse requires a certain number of calories per day for maintenance, and a few more calories for work or production. This can vary from 15 Mcal per day for an average sized horse at maintenance to over 30 Mcal per day for a horse working hard, or in maximum lactation. The problem with most of these horses is not a lack of vitamins or minerals or other micronutrients or probiotics; the problem is a shortage of calories. They may be lacking vitamins, minerals, etc. but that is not why they are thin; they are thin because they are not getting enough to eat. They may or may not be getting enough pounds of feed (2% of body weight per day is the common recommendation). But many of the forages do not have the energy density to provide the required caloric intake at the 2% level. So the solution is to increase the energy density. That is when I refer them to the feed store to provide them with products that will increase the energy density without causing secondary problems. There are a myriad of products out there designed to do just that. It is important to use a product that is safe, which means combining soluble carbohydrates such as found in grain products, with digestible fiber and fat. Most of the commercial products out there, if fed as per the manufacturers label instructions, also include the required vitamins and minerals and often other products to make the entire diet more digestible as well.
Over nutrition and obesity is the next most common problem that I see in practice. This is also often due to a misguided sense of what is good for the horse. A few of these in my practice area are due to the breed standards required by halter classes in horse shows. There is nothing I can do to solve the obesity required by the AQHA halter horses, but I can make dietary recommendations on obese horses, and it is up to the owner to either take or reject my advice.
We used to think that obesity in horses was not a significant health issue. Horses do not get coronary artery disease as do people, so from that standpoint it is not a big deal. However, over my practice career I have become convinced that it is a huge issue affecting the long term quality of life as well as longevity. Overweight horses like overweight people put more stress on their joints, and are much more susceptible to lameness problems especially as they get older. Laminitis or founder is a multi factorial disease, but regardless of the inciting cause it is much more difficult to manage in overweight animals due to the increased pressures involved because of the excess weight. When I see a grossly obese horse, I explain to the owner the risks associated with obesity, and often refer them a feed store to provide products to deal with it. My recommendation is to reduce the quantity of feed (I usually start out recommending they feed half of what they are presently feeding) of a mediocre quality grass hay, and balance that with an appropriate protein, vitamin, and mineral supplement. What we want to do is reduce the total caloric intake while maintaining an adequate intake of protein, vitamins, and minerals.
Laminitis or Founder is another frequently seen problem in equine practice. Although this is a very complex disease with a myriad of causes, nutrition has a huge role in its cause and in its treatment.
Without getting over technical, this is a disease that is generally caused by ingesting a high carbohydrate meal. In horses the disease results from carbohydrates being fed at a rate that allows them to pass into the fermentation vat (large colon and cecum). The sugars and carbohydrates are supposed to be broken down and absorbed out of the stomach and small intestine prior to entering the large colon; large amounts of sugars in the large intestine results in the organisms living there having a massive overgrowth. The overgrowth of gram negative bacteria in either the rumen of ruminant animals or the large colon of horses results in an increase of bacterial byproducts and an increased acidity. This causes large scale death of the bacteria, resulting in decomposition of the bacterial cell wall, and the release of a product known as endotoxin; a component of the bacterial cell wall. The endotoxin causes many adverse events; primarily it increases the permeability of the cell walls of the capillaries in the hoof. This results in swelling of the soft tissues of the hoof. The soft tissues of the foot are encased in a rigid structure known as the hoof capsule that is a perfectly fitting but tight boot. When swelling occurs inside something that can’t accommodate swelling, you get increased pressure. When the pressure gets near to or exceeds the blood pressure the blood flow diminishes inside the hoof, resulting in weakness or death of tissues inside the hoof. In an extreme case the hoof will actually fall off. Milder cases may recover completely, or have varying degrees of chronic lameness depending on the amount of damage and whether or not the damage is irreversible.
The first sign of laminitis is usually reluctance to move. When they do walk, they have a stilted gait. When this is seen it is important to get a veterinarian on your team to help manage the problem. The first step is to get a diagnosis; this is done through history, clinical examination, observation of the typical laminitic gait, the presence of heat and inflammation in the feet, and possibly other systemic signs related to carbohydrate overload. Treatment is aimed at mechanical support of the structures in the hoof, and reduction of the inflammation by the judicious use of drugs, such as non steroidal anti inflammatory drugs, and ice water baths.
Many of these horses are susceptible to recurring attacks of laminitis even if they recover completely. Nutritional management becomes an important part of their care for the rest of their life.
Nutritional management consists of providing a diet that provides them with all of their basic nutritional requirements while minimizing the amount of soluble carbohydrates. The portion of the diet that provides energy should be low in soluble carbohydrates; the energy is made up by providing higher than normal amounts of digestible fiber, and fat
Equine Exertional Rhabdomyolysis is another fairly common disease seen that has a nutritional component in treatment and prevention. When I attended veterinary school in the 1970’s it had several names, Monday Morning Disease, Azotemia, Myoglobinuria, Tying Up Syndrome, among others. It was typically seen in heavy muscled horses that were on a high plane of nutrition, and the treatment at the time was anti inflammatory medication, muscle relaxants, rest, fluid therapy, and decreasing the grain and concentrates in the ration. Forty years later, we have a new name for it, and a much better understanding of what causes it and why, but the treatment has not changed much. We now know that many of these horses have a genetic predisposition for this, and we have learned how to identify these horses through genetic testing, which until recently wasn’t an option. What happens is that these horses have the ability to store large amounts of the polysaccharide “glycogen” in their muscle tissue, which when it breaks down during exercise produces metabolites that can injure the muscle causing it to release the muscle pigment myoglobin into the blood stream. It turns out that the myoglobin is toxic to the kidney, so in a severe case this can cause kidney failure. When a horse has an acute case, it generally requires aggressive veterinary treatment with the aforementioned therapies to have a successful recovery. The important thing is to manage at risk horses nutritionally so that acute episodes do not occur. That is where feed manufacturers come in; there are many commercial feeds on the market today specifically designed to prevent episodes; they all involve feeding high digestible fiber rations with low soluble carbohydrates; animals at work requiring high energy diets get the majority of their calories from fat and digestible fiber rather than sugar and starch. For those of you interested, a detailed paper is available on the AAEP Website at the following address: http://www.aaep.org/info/horse-health?publication=782 The following is a copy of the summary of the paper By Stephanie Valberg, DVM, PhD, Associate Professor, University of Minnesota, College of Veterinary Medicine
“Exertional rhabdomyolysis (ER) has been recognized in horses for more than 100 years as a syndrome of muscle pain and cramping associated with exercise. Recently it has been recognized that this syndrome has numerous possible causes. Sporadic forms of ER are due to over-training and muscle strain, dietary deficiencies of electrolytes, vitamin E and selenium or exercise in conjunction with herpes or influenza virus infections. Chronic forms are due to specific inherited abnormalities such as polysaccharide storage myopathy (PSSM) in Quarter Horses, Warmbloods and Draft breeds or recurrent exertional rhabdomyolysis (RER) in Thoroughbreds, Standardbreds and Arabians.
PSSM, a glycogen storage disorder, can effectively be managed by providing regular daily exercise and a high fiber diet with minimal starch and sugar and provision of a fat supplement. RER appears to be a disorder of intracellular calcium regulation that is triggered by excitement. Changing management to provide horses with a calm environment and training schedule and substitution of fat for grains in high caloric rations are helpful means to manage this condition. Exertional rhabdomyolysis continues to be a performance-limiting or career-ending disorder for many equine athletes.
In the last 15 years, research advances have provided greater insight into this syndrome. Of greatest importance is the realization that exertional rhabdomyolysis comprises several myopathies that, despite similarities in clinical presentation, differ considerably in regards to pathogenesis (cellular events, reactions, and other pathologic mechanisms occurring in the development of disease). In addition, new knowledge regarding effective management of horses with exertional rhabdomyolysis, particularly with regard to diet, has significantly reduced the severity ER in many horses. Most recently the genetic defect for one common form of PSSM has been discovered and a DNA based test is now available.”
Developmental Orthopedic Disease is a catch all phrase for a number of bone related diseases commonly seen in young growing horses. Developmental Orthopedic Disease (DOD is commonly seen in young fast growing horses between 3-4 months up to near 2 years old. These young horses are presented with various degrees of lameness, or hard bony and sometimes painful swellings at the fetlocks, hocks, or knees. The cause has been speculated to be nutritional imbalances involving Calcium, Phosphorous, Zinc, and other trace minerals; trauma, overfeeding, and various genetic factors. I think that most of these horses have a combination of factors involved. In fact I consider some degree of DOD to be normal in most young growing horses, and most survive it just fine. The important thing is recognizing when it is getting out of hand, and taking steps to treat it before it causes permanent damage
Bone in young animals increases in length at the growth plates; there is a thin plate of cartilage at the end of the long bone that is actively laying down new bone. The new bone is relatively soft, and is subject to damage from compressive forces during weight bearing, especially when young horses are engaged in vigorous exercise. This trauma from exercise causes small cracks and fractures in the soft bone at the physis, and often some mushrooming out of the bone which can be seen visually. An owner will often see this bony swelling and possibly also notice that the foal or yearling appears sore or lame. These swellings are often sore when squeezed with finger pressure, and radiographs often show extensive bone remodeling. This type of bone disease is known as “physitis”; commonly called “epiphysitis”. The proper name is “physitis” as the pathology is actually in the growth plate, the physis, and not the epiphysis, which is the segment of bone between the bone end and the growth plate.
Another developmental orthopedic disease is collapse of the soft bone underneath the joint cartilage of the large joints resulting in a defect in the overlying articular cartilage; a disease called osteochondritis dissicans (OCD). Mild cases of OCD can heal with conservative treatment, but many require surgery to clean up the affected cartilage and underlying bone. Our goal is to catch these prior to getting a serious problem, and with simple nutritional adjustments try to reverse the changes.
We think that the problem is that these young horses are growing faster than the bone is able to accommodate the added weight. The next question is why are these horses growing this fast? I think there are two answers to this question, genetics and nutrition. The genetics was already determined at the moment of conception, we can’t do anything about the genetics at this point, so our treatment needs to address what we can control, and that is nutrition.
Studies have shown that the mature size of a horse is determined primarily by genetics. However, we can make an animal grow faster sooner by increasing the energy in the ration. A yearling that has been pushed nutritionally will be taller and heavier than a genetically similar yearling that has been on a lower but adequate plane of nutrition; however the mature height and weight will be the same. This is of special importance in young show animals; by pushing them early we are putting them at increased risk of developmental orthopedic disease; this is true of all species, but particularly in horses because they are expected to be athletes.
The first thing is to make sure the ration is as low in energy as the colt can stand, while still being reasonably balanced with the proper minerals and high quality protein. For me as a veterinarian that generally involves my recommending the owner use a commercial feed that is already balanced. It is also important to reduce the trauma on the damaged bone by confining the animal to a small area, and in some cases we use an anti inflammatory medication to reduce the pain so the animal is able to move reasonably normally to prevent secondary tendon problems.
The final point I would like to make about nutrition is that for animals to survive and thrive, nutrition does not need to be perfect. There is a difference between “optimum nutrition” which is what we need in production livestock and high level equine athletes, and in “adequate nutrition” which is suitable for the hobbyist or backyard horse owner. Our livestock have an amazing ability to do well on a wide variety of feed products, and even do well in the face of deficiencies of some nutrients and an excess of others. Animals lived on whatever forages were available in nature for millions of years before we domesticated them, and the genetics that enabled them to survive then still are with them today. As long as the deficiencies or excesses are not too severe, the internal mechanisms that control the metabolism, such as the liver and kidneys, will make the necessary adjustments. Excess minerals and nutrients will be excreted, and deficient nutrients will be conserved to allow animals to survive and thrive even on sub optimal feeds.
Dr. David A. Rustebakke
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