Diseases of Dietary Origin
The axiom, "You are what you eat" does have relevance to horses with regard to health and well-being. Although horses have evolved to eat plant material, not all plants are safe to eat. Some food substances directly exert toxic effects, while others grow fungi that do so. Availability and type of food are important issues to intestinal health and nutritional balance. In addition, imbalances of nutritional compounds such as microminerals, energy, carbohydrates, and protein can have adverse effects on equine health. Let's review some of the more common dietary problems that affect various organ systems.
Developmental orthopedic disease (DOD) results from a variety of multi-factorial issues, but nutritional imbalances are known to predispose a young, growing horse to this malady. DOD is linked to an imbalance of calcium and phosphorus, and/or a deficiency in microminerals such as copper, zinc, and manganese. Physitis (formerly called epiphysitis) is one manifestation of DOD. Other problems that develop due to nutritional inconsistencies during growth include osteochondrosis and wobbler syndrome. DOD can have significant consequences for future performance.
Physitis is a term that describes defects in the ossification (process of cartilage hardening into bone) of the growth plate (physis) at the end of a long bone. The syndrome should be more correctly called physeal dysplasia since it is both the growth plate and metaphysis (a section of bone between the epiphysis and the long part of the bone) that are affected. (The growth plate is responsible for lengthening of the long bones.) A young horse four to six months of age typically exhibits problems in the fetlocks, while a yearling up to two years of age is susceptible to physitis around the knees. Affected knees or ankles exhibit an hourglass-shaped, firm swelling just above the joints. The joints appear "knobby" and enlarged. Only one limb might be affected, but usually there will be signs of change in similar joints on two or more limbs. A horse with physitis might be lame, but not always.
Dietary imbalances of copper, zinc, calcium, and/or phosphorus are linked to physitis. Overfeeding is just as likely a cause as imbalanced nutrition in stimulating this disease. Rapid growth due to excess energy intake is implicated in causing physitis, which also can occur from "crushing" of the physeal plate by trauma due to excessive loading of the limb (too much exercise) or by a growing horse being too heavy for his young bones. Additionally, abnormal conformation can overload one side of a growth plate to create this condition, and trauma from a kick or fall can cause damage. Although seemingly innocuous, physitis is often the tip of the iceberg for DOD.
Osteochondrosis is another component of the DOD syndrome. A defect in the endochondral ossification process at the joint surface causes displacement of an area of abnormal cartilage as a fragment or flap (this condition is termed osteochondritis dissecans), or as a cyst that remains just beneath the surface of the joint. Eventually, osteochondrosis in any of these forms can cause lameness and arthritis. More than 60% of horses diagnosed with osteochondrosis show clinical signs prior to their first birthday. Signs include varying degrees of lameness, distention (swelling) of the affected joint, and reluctance to flex the limb, especially when osteochondrosis develops in the hocks and/or stifles. Some horses might have difficulty getting up or down. In more than half of the cases, osteochondrosis is present in bilateral (both front or hind) joints, although obvious signs might only show up in one.
Osteochondrosis is considered a multifactorial problem, although diet is highly implicated. Excess energy intake (120% of National Research Council--NRC--requirements) has been correlated with osteochondrosis. Too many calories enables a growing horse to become fat, with subsequent overload of developing joints. Hormonal changes associated with a rich diet also can affect joint metabolism.
Mineral imbalances have deleterious effects on joint cartilage development. It is known that high phosphorus (and relatively low calcium) levels will cause cartilage defects. A diet that is low in copper also increases the development of osteochondrosis. High zinc levels can suppress copper absorption and result in a diet that is relatively deficient in copper. Thus, microminerals in the feed should be analyzed to determine if the diet is properly balanced.
Adverse effects of an imbalanced diet are amplified by other high-risk factors. The potential for rapid musculoskeletal development is dependent on genetics as well as on nutrition. Rapid growth adds stress to a growing skeletal system, bones, and joints when they can least withstand the added body mass. Osteochondrosis as a developmental problem occurs by virtue of joints being more susceptible to damage during specific times in their development. The stifles and hocks are most at risk in horses six to eight months of age. Risk increases if the youngster overly stresses the limbs with excessive exercise, causing damage to bone and to the blood supply within the joints.
Conformation also has a role to play in osteochondrosis development. Crooked limbs and less-than-perfect conformation traits can overload susceptible joints, potentially leading to cartilage damage. One controversial, yet significant, stressor to joint development is confinement. Youngsters limited in their daily exercise might not have sufficient development of the subchondral (beneath the cartilage) bone to support their body weight. Then, when the youngster is turned out, he might abruptly overload under-challenged joint cartilage.
Cervical vertebral malformation (CVM) is another manifestation of DOD. This occurs when the joint surfaces of spinal vertebrae develop osteochondrosis lesions. Instability in affected cervical vertebrae can compress the spinal cord, eliciting subsequent neurologic disease that is known as wobbler syndrome (more on this later).
Nutritional Secondary Hyperparathyroidism
Also called "big head disease" or "bran disease," this syndrome results from a diet that is too high in phosphorus, or too low in calcium (calcium intake should always exceed that of phosphorus). Feeding excess amounts of bran (rice or wheat) or grain provides abundant phosphorus in the diet. With a relative deficiency of dietary calcium, parathyroid hormone stimulates mobilization of calcium from the bones as well as increasing reabsorption of calcium from the kidneys and excreting excess phosphorus from the kidneys. The overall result is skeletal depletion of calcium.
Signs of this problem include shifting leg lameness, a stilted gait, distortion of facial bones, broadening of the face across the bridge of the nose, and loosening teeth. Supplementing with legume hays (which tend to be high in calcium) along with removing grain and bran from the diet can resolve this disease if it's caught early before permanent skeletal damage occurs.
White Muscle Disease
A diet deficient in selenium can create muscle problems. The NRC lists the required amount at 0.1 mg/kg of the diet. Foals might exhibit stiff and painful muscle disease and cardiac problems, while older horses have recurrent episodes of tying-up. Selenium deficiency occurs in certain geographic areas such as the Northwest and the northeastern United States. However, caution must be taken not to supplement with too much selenium as toxicity can occur. The maximum tolerable level is 2 mg per kg of the diet, according to the NRC. Supplementing selenium to toxic levels could trigger several adverse effects, including colic, diarrhea, hair loss, and separation of the hooves from the coronary band.
Moldy corn poisoning, also known as encephalomalacia or blind staggers, is associated with consumption of corn that has been contaminated with the fungus Fusarium moniliforme. This fungus thrives on corn plants that have been stressed by drought, disease, or insects prior to harvest. High humidity and moisture encourage proliferation of the mold. Exposure to high doses of this fungus over a short period of time results in liver toxicity, while low doses ingested over a longer time result in brain damage or moldy corn poisoning. Clinical signs include decreased appetite; behavioral changes such as depression, anxiety, or hyper-excitability; and neurologic signs such as circling, blindness, difficulty chewing or swallowing, muscle tremors, ataxia, recumbency, and eventually coma. Depending on the amount of toxin ingested, moldy corn poisoning takes seven to 75 days before the horse demonstrates clinical signs; once signs are seen, death can occur within two to three days.
Botulism in a dietary form occurs in horses which have ingested feed contaminated with this toxin (produced by the bacterium Clostridium botulinum. The toxin forms when a decomposing animal or bird is accidentally baled with the hay or is processed with pelleted or cubed feed. Haylage or silage that is improperly prepared without sufficient heating allows for continued decay of organic material and production of the toxin. Moist or rotten hay, especially legume hay, can also spawn growth of anaerobic bacteria responsible for generating the toxin. Botulinum toxin is extremely potent and lethal, resulting in flaccid paralysis and dysphagia (difficulty swallowing) preceding death.
Botulism affects young foals as shaker foal syndrome. The causative organism, Clostridium botulinum, is eaten, and once in the gastrointestinal tract can proliferate in an ulcerated area and secrete a toxin that affects nerve and muscle tissues. Mares on breeding farms of known incidence should be vaccinated before foaling to develop antibodies to pass to the foal in the colostrum.
Gastric ulcers can affect adults and foals. Even when horses are not eating, the stomach continues to secrete digestive acid. Two different tissue types in the stomach--the glandular and non-glandular squamous cell epithelium--depend on different protective devices against stomach acid. In adult horses, most (80%) of the problems seen with equine gastric ulcer syndrome (EGUS) develop in the upper area of the non-glandular squamous mucosa as a result of excess acid secretion.
Intermittent feed deprivation is known to cause EGUS. It has been demonstrated that horses on a diet of free-choice grass hay or pasture have less gastric acidity than horses fed at fixed intervals, as occurs with set multiple daily feedings. Food in the stomach retains acid within the lower areas where the glandular epithelium is more resistant to stomach acid. It is also known that roughage has a buffering (acid-neutralizing) effect. Small amounts of alfalfa hay seem to buffer stomach acid for up to five hours.
Grain supplementation elicits greater acid secretions in the stomach and thereby compounds problems related to a diet with low roughage intake. Horses on unrestricted access to fiber are less commonly afflicted with gastric ulcers. Thus, owners should provide free choice access to grass hay or pasture when possible and limit concentrate intake as much as possible.
Enteroliths--In certain geographic areas, especially in California, horses fed high amounts of calcium- and magnesium-rich hay such as alfalfa might develop an intestinal "stone" known as an enterolith. Layers of salts develop around a small object, such as a tiny pebble. Enteroliths can grow to obstructive sizes within the large colon, causing recurrent colic pain. Abdominal radiographs can identify these for surgical removal.
Malnutrition is not just about dietary imbalances. It also relates to caloric intake and body condition. Obesity is a nutritional disease with great impact on performance and quality of life.
Lipomas--An intestinal lipoma is a fatty tumor that develops in the mesenteric fat cloaking the small intestines. The stalk of such a tumor can wrap around the intestines, resulting in strangulation of a loop of bowel. The horse presents with severe and unrelenting colic pain that requires surgery. Lipomas occur most commonly in Arabian horses, particularly those which are overweight.
Laminitis is inflammation within the sensitive laminae of the feet. It can occur for many reasons, but as a nutritional problem it is commonly linked to grain-rich diets, ingestion of too much rich pasture, and obesity. Grain overload or a diet rich in high-carbohydrate feed (grain or lush pasture) initiates a series of metabolic and endocrine (hormone) disturbances in the body. A diet abundant in carbohydrates upsets normal intestinal bacteria, allowing more endotoxins from harmful bacteria to be absorbed into the bloodstream than can be neutralized by the liver. Additionally, the endocrine system might run amuck because of excess body fat stores and persistent feeding of carbohydrate-rich food. Blood flow in the feet is particularly sensitive to toxins in the bloodstream, and to hormonal disturbances associated with too many groceries.
Peripheral Cushingoid syndrome is also known as equine metabolic syndrome or peripheral Cushing's disease. An horse with recurrent laminitis might have Cushing's disease, but instead of being a primary problem within the pituitary gland as is seen with Cushing's, the excessively high levels of circulating corticosteroids originate from enzyme activity in intestinal sources. These sources include the liver or fat cells of the mesentery (membrane) that covers the bowel. Fat cells are responsive to endocrine signals; the more fat cells present (as occurs with obesity), the greater the risk of hormonal irregularities. Many affected horses are erroneously diagnosed as hypothyroid (having a deficiency in thyroid hormone); although there might be some degree of diminished thyroid hormone levels, the problem is not within the thyroid gland but rather is due to irregular hormonal feedback in the entire body as a result of high circulating levels of corticosteroids.
Despite dietary restriction, it is difficult to reduce the weight on horses afflicted with equine metabolic syndrome. Fat deposits are distributed in the crest of the neck, in the rump areas, and within the prepuce of male horses. Affected horses often have fertility issues. At the current time, there is no approved medical treatment of this condition other than strict dietary management. A dietary strategy relies on feeding only grass hay at amounts less than two percent of body weight per day. It is important to entirely eliminate grain products and other high-carbohydrate feeds that exacerbate the problem of insulin resistance. For more on this, see "Cutting Down on Carbs for Your Horse" on page 116.
Photosensitivity can be caused by plant ingestion. Certain plants contain photo-reactive pigments that are absorbed into the blood when a horse eats the plant. In the presence of ultraviolet light from the sun, these then react in areas of non-pigmented skin, and the horse's skin sunburns. Two main plants are culprits in this situation: St. John's wort (Hypericum perforatum) and buckwheat (Fagopyrum esculentum). Other plants create a photosensitivity response secondary to damage in the liver caused by alkaloids in the plants. Examples of these include Tansy ragwort or groundsels (Senecio spp.), hound's tongue (Cynoglossum spp.), horsebrush (Tetradymia spp.), and alsike clover (Trifolium hybridum). Legume hays have also been implicated in setting up these conditions for skin problems.
Generally, a horse has to consume these plants for a few months before the liver effects are severe enough to allow accumulation of a by-product of plant chlorophyll breakdown in the blood. This compound is called phylloerythrin, and its accumulation in areas of non-pigmented skin causes photosensitivity. Affected areas on the lower limbs are often referred to as scratches, but the process is more correctly known as photoactivated vasculitis.
Chronic obstructive pulmonary disease (COPD) can be caused by various allergens. Like an asthmatic person, a horse can be afflicted by respiratory allergies that are often attributable to mold and mold spores in hay. Poor-quality roughage or hay that has a high moisture content is prone to mold growth. When a susceptible horse is exposed to these molds, a cascade of inflammatory events begins in the lungs. The end result is an emphysematous-like condition known as COPD or inflammatory airway disease (IAD), historically called heaves.
Inflammation in the lower airways triggers spasms and constriction of the bronchioles (tiny airways of the lungs) and bronchi (larger airways of the lungs). As the diameter of these air tubes closes down, resistance to airflow increases. Irritated lung tissue becomes coated in mucus and fibrin (an insoluble protein that forms blood clots) in response to the inflammation. Eventually, adhesions and scar tissue "glue" together localized areas of the tiny saccules of alveoli (small cells containing air in the lungs) so they no longer expand to fill with air, nor are they able to completely empty of residual air. Bronchospasms (muscle spasms of the smooth muscle of the bronchi) and inflammatory debris limit the extent of air capacity in the lungs. These conditions stimulate nerve receptors in the lungs, eliciting a cough reflex.
What might start as an intermittent and infrequent cough can become more persistent as more lung tissue is affected and the lower airway becomes more sensitive to the effects of environmental allergens. It is not just the presence of dust or mold that elicits the COPD syndrome; respiratory viruses or chronic respiratory infections also create similar damage.
Any situation that results in damage to the lower airways and alveoli reduces the amount of lung tissue available for transferring of oxygen to the blood. The result is that the horse's tolerance for exercise diminishes and performance suffers.
Fescue toxicosis occurs when tall fescue, a common pasture and hay forage for horses throughout the United States and Canada, is infected with a fungal endophyte (a plant parasite living within another organism). This fungus produces ergot alkaloids that exert detrimental effects on the pregnant mare and fetus. Common signs of fescue endophyte toxicity include prolonged gestation, lack of udder development, absence of milk production, abortion, thickened placentas, retained placentas, stillbirths, and foal mortality. In fescue areas known to be infected with endophyte, pregnant mares should be removed from the fescue in the latter months of pregnancy, at least by Day 300 of gestation. Daily doses of domperidone can be given orally to mares in late gestation to counteract adverse responses to the fungus.
Knowing the risks that these and other feeds pose to your horse's health is the first step to avoiding problems. You should discuss local plant/hay/feed risks with your veterinarian so that you can formulate a plan of action to remove any dietary obstacles from your horse's diet.
About the Author
Nancy S. Loving, DVM, owns Loving Equine Clinic in Boulder, Colorado, and has a special interest in managing the care of sport horses. Her book, All Horse Systems Go, is a comprehensive veterinary care and conditioning resource in full color that covers all facets of horse care. She has also authored the books Go the Distance as a resource for endurance horse owners, Conformation and Performance, and First Aid for Horse and Rider in addition to many veterinary articles for both horse owner and professional audiences.
POLL: Laminitis Experience