Laminitis is a systemic disease which is manifested as a non infectious condition in the foot. The word "laminitis" means "inflammation of the laminae," (tissue layer) and it can refer to either a short-term (acute) inflammation or the disease caused by chronic attacks of inflammation. Laminitis affects an area within the hoof known as the "sensitive lamina," the connective layer between the hoof and the coffin bone (also called pedal bone) that holds the coffin bone in place. Laminitis occurs when the lamina becomes inflamed and the coffin bone begins o separate from the hoof. With severe laminitis, the coffin bone may actually come out of the bottom of the hoof. Rotation, the separation of the bone from the hoof shows up on the X-rays. Laminitis mostly occurs in mature horses. It is rarely seen in animals less than one year of age.
The pedal bone is equivalent to the last digit of the middle finger or toe of each of our limbs. It is covered with sensitive tissue (laminae) like the quick of our nails and lies suspended within the hoof wall capsule (equivalent to our nail) by means of interlocking with the hoof's lining of insensitive epidermal lining. Both bones and tissues are nourished by a complex system of arteries and capillaries and veins that bracnh around the pedal bone. Laminitis causes inflammation and subsequent tearing the interlocking system that suspends the pedal bone within the hoof. It is caused by a disruption of the normal blood flow and is extremely painful.
Laminitis can develop in the forefeet, in all four feet, or in the hindfeet only. Laminitis is an extremely complex condition with many, often apparently unrelated causes and predisposing factors. It can be caused by pressure on the foot or it can be the result of decreased blood flow to the laminae that leads to tissue death, and swelling of the laminae. The cause of the decreased blood flow is not currently known. The Equine Metabolic Syndrome (EMS) is predisposing for developing laminitis, and it is characterized by obesity, insulin resistance, trauma as a result of galloping on hard ground), ingestion of cold water, hypertension and dyslipidemia (abnormalities in the serum levels of fats, including overproduction or deficiency), systemic infections, uterine infection, chronic diarrhea etc. A genetic predisposition is supposed.
Pasture-induced laminitis in the horse is associated with the overconsumption of fermentable carbohydrate, in the form of simple sugars, fructans, or starch. The fermentation of carbohydrate in the cecum and large intestine results in the production of lactic acid and other toxins or "laminitis trigger factors."
Endotoxemia is an important risk factor for development of acute laminitis in horses during hospitalization for medical or surgical conditions. Early recognition of endotoxemia, or the potential for it to develop in certain disease states, and initiation of treatment directed at endotoxemia or its consequences may help prevent laminitis in horses during hospitalization.
The horse is said to have foundered if the interlaminar system has broken down sufficiently to allow the pedal bone to become displaced within the foot.
Clinical signs depend on the severity of the disease. In mild cases, laminitic horses display consistently altered or abnormal behaviors such as increased forelimb lifting. Lameness may not be evident at a walk, but the horse will have a short stilted gait at a trot. Increased pulse in the leg may be visible. As the condition progresses, horses will be more reluctant to move and will resist lifting a foot. Because of the pain, horses have increased respiratory rate, trembling, and anxiety. Where there has been bone separation, there is an increased risk of infection. The risk is especially high if the bone prolapses through the sole, but this is rare.
Several approaches to treat laminitis are available, including pharmacological and orthopedic strategies as well as the management of the feeding and housing conditions. However, the prophylaxis to prevent laminitis is extremely important. Horses have to be fed with hay and supplemented with minerals and vitamins. Feeding exclusively straw and feed restriction has to be avoided. Any obvious conditions causing laminitis should be treated accordingly. If no underlying conditions can be established, treatment often involves administration of antibiotics and anti-inflammatory medications. External support to take weight-bearing forces off the foot and help normal blood flow may be required. Laminitis tend to recur, causing more damage to the horse's hoof. Many horses become lame for life. Providing proper shoeing and feeding balanced diet can prevent this debilitating disease.
Bacteria have been implicated in a broad range of disorders including Crohn’s disease, chronic diarrhea, inflammatory bowel disease, type I diabetes, obesity, and asthma. The nutrition and health of horses is closely tied to their gastrointestinal microflora. Gut bacteria break down plant structural carbohydrates and produce volatile fatty acids, which are a major source of energy for horses. Bacterial communities are also essential for maintaining gut health and have been linked to contribute to various diseases including laminitis. Excess nonstructural carbohydrates (starches, fructans, or simple sugars) that are not digested in the foregut enter the cecum and colon, where bacterial fermentation produces byproducts including lactic acid and gas, which can cause colic. The same initiators can also lead to the development of laminitis, which often occurs subsequent to overconsumption of grain or after feeding on lush pasture rich with nonstructural carbohydrates. The primary microbes detected consisted of Gram-positive bacteria, many of which were associated with Clostridia, Streptococcus species, and Lactobacillus species.7
How do gut bacteria get to other sites of the body? It has been established that polymers (fructans) in pasture grasses are metabolised in the horse's gut to fructose, a simple sugar present in honey and fruit. When fructans (such as from Jersualem artichokes) are administered to horses, there is the rapid degradation of fructans in the small bowel. Thus, the administration of fructans is expected to result in fructose generation in the gut of horses that have fructan-degrading bacteria. Fructose is unique among foods in its remarkable ability to induce metabolic disease in animals. The administration of fructose to laboratory rats, for example, can induce insulin resistance, elevated blood pressure, increased serum triglycerides, low HDL cholesterol, fatty liver (hepatic steatosis), and obesity. Metabolism of fructose in the intestinal wall might lead to local inflammation and increased intestinal permeability that allows the bacteria to enter the bloodstream.8