Horse Info

Category: Glossary

Equine terms and definitions

  • OTTB: Definition of Off-Track Thoroughbred

    OTTB is an acronym for Off-Track Thoroughbred: a registered Thoroughbred horse that has retired from racing and is being transitioned to a new career or home. The term is widely used in equine rescue, retraining, and competitive circles in North America, the United Kingdom, and Australia, wherever Thoroughbred racing operates at scale.

    The United States retires approximately 25,000 racehorses per year. Most are OTTBs, though the category also includes horses that never raced (failed-to-start, breeding stock) but were raised and trained in a racing environment. OTTBs typically become available between ages three and seven, as the prime racing years end, though some older horses retire after longer careers at smaller tracks.

    Why OTTBs Are Valued

    A sound, well-conformed OTTB between four and eight years old represents substantial athletic value: it is already broke to ride, accustomed to bathing, clipping, shoeing, trailering, and handling, and has logged significant cardiovascular conditioning. Its price at the point of retirement, often $500 to $3,000, reflects the volume of horses entering the market, not their intrinsic worth as athletes. Many OTTBs go on to successful second careers in three-day eventing, show jumping, dressage, fox hunting, polo, and trail riding. The Retired Racehorse Project's Thoroughbred Makeover, held annually at the Kentucky Horse Park, showcases OTTBs competing across 18 disciplines after a 10-month retraining window.

    Retraining Considerations

    The transition from racing to a pleasure or sport horse career requires adjustment. OTTBs have been conditioned to gallop in company and to respond to race-specific cues. They must learn to accept contact and collection, slow gaits for trail or flatwork, and a calmer stable routine. Most experienced OTTB adopters describe a 60-to-90-day settling period before the horse stabilizes in its new environment. Organizations including the Thoroughbred Aftercare Alliance (TAA), CANTER USA, and New Vocations vet, retrain, and place OTTBs. See also the full Thoroughbred breed profile for health considerations specific to retired racehorses.

    Further Reading: Thoroughbred Aftercare Alliance (TAA): accrediting body for OTTB adoption organizations. Retired Racehorse Project.

  • Coggins Test: Definition, Requirements, and What It Detects

    A Coggins test is a serological blood test used in horses to detect the presence of antibodies to Equine Infectious Anemia (EIA), a potentially fatal viral disease caused by a lentivirus in the same family as HIV. The test was developed by Dr. Leroy Coggins in the early 1970s, and his name has become the colloquial term for both the test and the official EIA test certificate it generates.

    EIA has no approved vaccine and no cure. Infected horses may show acute signs (fever, anemia, weakness, edema) or remain as asymptomatic carriers capable of transmitting the virus to other horses via blood-feeding insects, primarily horseflies and deerflies. Because carriers show no clinical signs yet remain infectious for life, blood testing is the only way to identify them.

    Legal Requirements

    A negative Coggins test result is legally required for interstate transport of horses in the United States under USDA regulations, and individually by most states for intrastate movement to shows, competitions, trail rides, sales, or boarding facilities. Most equine events require a negative result dated within 12 months (some within 6 months). The official test uses the agar gel immunodiffusion (AGID) method; a competitive ELISA (cELISA) is approved as a screening test. Testing is performed by accredited veterinarians who collect a blood sample and submit it to a USDA-approved laboratory. Results are documented on a federally-approved certificate issued in the horse’s name and with identifying markings.

    What a Positive Result Means

    A horse that tests positive for EIA antibodies must by law be permanently identified (lip tattoo or microchip), quarantined from other horses, or euthanized. Sale of an EIA-positive horse without disclosure is a federal offense. The horse cannot be moved across state lines. Positive horses are reported to USDA APHIS, which maintains a national EIA database.

    Further Reading: USDA APHIS Equine Infectious Anemia program.

  • Lameness

    Lameness is the clinical term for any alteration in a horse’s normal gait caused by pain, mechanical restriction, or neurological dysfunction originating in the limbs or feet. It is one of the most common reasons horses are removed from work and presented to veterinarians, and it encompasses a wide spectrum of conditions ranging from minor soft-tissue soreness to structural disease of bone and joint. The degree of lameness is graded on standardized scales, the American Association of Equine Practitioners grades from 0 (no detectable lameness) to 5 (non-weight-bearing), which allows consistent communication between clinicians and owners about severity and progression.

    The hoof and pastern region account for the majority of forelimb lameness cases; in hindlimb cases, the hock is among the most commonly affected structures. A trained observer can detect forelimb lameness by watching the horse’s head: the head drops when the sound limb bears weight and rises when the lame limb contacts the ground. Hindlimb lameness is assessed by observing hip asymmetry during the trot. Flexion tests, hoof testers, nerve blocks, and imaging, including radiography, ultrasonography, and scintigraphy, are used in systematic lameness examination to localize the source.

    Common underlying causes include laminitis, a hoof abscess, arthritis of the coffin or fetlock joint, navicular disease, soft-tissue injuries to tendons and ligaments, and fractures. The fetlock and cannon bone area are frequent sites of strain-related lameness in performance horses. Management depends entirely on the diagnosis: rest and anti-inflammatory medication suffice for many soft-tissue conditions, whereas structural joint disease may require intra-articular therapy, corrective shoeing, or surgical intervention. Early detection, guided by regular observation and consistent movement assessment, significantly improves prognosis across most lameness conditions.

    Further Reading

  • Lice

    Lice are small, wingless, dorsoventrally flattened insects of the order Phthiraptera that live their entire life cycle on the body surface of a host animal, feeding on skin debris, secretions, or blood depending on species. In horses, infestation with lice (pediculosis) is most common during winter and early spring when horses are kept in close contact, have longer coats, and reduced grooming. Heavy infestations cause intense pruritus (itching), hair loss, skin irritation, and restlessness, and can lead to weight loss in severe cases due to the metabolic cost of chronic stress and reduced feed intake.

    Two species primarily infest horses: Damalinia equi (also called Werneckiella equi), a biting or chewing louse that feeds on skin scales and debris, and Haematopinus asini, a sucking louse that pierces the skin to feed on blood. The biting louse is more common and is found in the mane, forelock, tail base, and along the topline; the sucking louse favors the head, neck, and inner legs where skin is thinner. Both species attach their eggs (nits) firmly to individual hair shafts, distinguishing an active infestation from simple debris or dandruff. The mane and forelock should be checked during routine grooming by parting the hair and inspecting the skin surface.

    Lice are host-specific and do not infest humans, so the zoonotic risk is negligible, but lice spread readily between horses through direct contact or shared grooming equipment, blankets, and tack. Diagnosis is by direct visualization; lice and nits are visible to the naked eye on close inspection. Treatment involves topical insecticides (pyrethrin, permethrin, or organophosphate-based products), applied twice fourteen days apart to catch eggs that were not killed by the first treatment. All horses in contact should be treated simultaneously. New horse owners should include a lice check in their quarantine protocol alongside a fecal parasite baseline and vaccination review.

    Further Reading

  • Laminitis

    Laminitis is an inflammatory condition of the sensitive laminae, the interdigitating tissue layers that bond the coffin bone to the inner hoof wall inside the hoof capsule. When blood flow to the laminae is disrupted or overwhelmed, the tissue becomes ischemic, inflamed, and structurally weakened. In severe cases the coffin bone loses its lamellar attachment and rotates or sinks within the hoof capsule, a condition called founder. Laminitis is one of the most serious and potentially career-ending conditions in horses and is a leading cause of equine euthanasia when severe rotation occurs.

    The condition most commonly affects the forefeet, which bear approximately 60 percent of the horse’s body weight, though all four feet can be involved. Acute episodes present as intense pain in the feet, the horse adopts a characteristic “sawhorse” stance, shifting weight back onto the hindlimbs to relieve pressure on inflamed forefeet, and is reluctant to move or turn. The digital pulse at the pastern and fetlock region is often bounding and elevated. The frog may feel warm compared to surrounding structures. Diagnosis is confirmed by clinical signs, hoof tester response, and radiographs showing the degree of coffin bone displacement relative to the hoof wall.

    Triggers include excessive carbohydrate intake from lush pasture or grain overload, systemic illness such as colitis or retained placenta, Equine Metabolic Syndrome, Pituitary Pars Intermedia Dysfunction (PPID), prolonged weight-bearing on a contralateral limb due to an existing soundness problem, and administration of certain corticosteroids. Management in the acute phase centers on removing the inciting cause, strict box rest on deep soft bedding, cold therapy applied to the feet, and non-steroidal anti-inflammatory medication. Long-term management involves a skilled therapeutic farrier to realign the coffin bone and redistribute load, dietary restriction of soluble carbohydrates, and regular radiographic monitoring. Horses on pasture prone to laminitis should have body condition assessed regularly, as obesity is a major predisposing factor.

    Further Reading

  • Infection in Horses: Definition, Types, and Recognition

    Infection is the condition in which a pathogenic microorganism has established itself in the tissues of a host, evaded or overwhelmed the initial innate defenses, and begun to replicate and cause measurable tissue damage or systemic physiological disruption. It is distinguished from mere exposure or contamination by the element of establishment: an organism that contacts the skin surface without penetrating it does not constitute infection. Clinically, infection is recognized by the cardinal signs of cardinal signs of local tissue response: heat, swelling, redness, pain, and loss of function, at the affected site, and by systemic signs including elevated temperature (see hyperthermia), elevated heart and respiratory rate, and depression when the infection spreads beyond its initial focus.

    Infections in horses are classified by the causative agent and anatomical location. Bacterial infections range from locally contained abscesses, the most common cause of severe acute lameness (see hoof abscess), to systemic septicemia in neonatal foals lacking adequate passive passive immunity in neonatal septicemia. Viral infections such as equine influenza, equine herpesvirus, and equine arteritis virus spread rapidly through respiratory secretions and can move through an entire barn population within days. Fungal infections (dermatomycosis, guttural pouch mycosis, aspergillosis) tend to affect immunocompromised horses or specific anatomical niches. Internal parasitic infection, while technically an infestation in precise terminology, produces pathological changes indistinguishable in clinical appearance from tissue-invasive bacterial and protozoal infections.

    Diagnosis requires identification of the causative organism through culture and sensitivity testing for bacteria, PCR for viruses, and cytological or histological examination for fungi. Treatment is agent-specific: antibiotics for susceptible bacteria, antifungals for mycotic infections, and supportive care for viral infections where no specific antivirals are licensed for equine use. The route and duration of antibiotic therapy must be guided by culture results to avoid treatment failure and minimize selection pressure for resistance. Hygienic biosecurity measures at the facility level, quarantine, disinfection, foot baths, and equipment isolation, remain the primary tools for preventing infectious disease from entering or spreading within a herd, because prevention is substantially less costly than treatment and the disruption to training or showing schedules from an outbreak can be severe.

    Further Reading

  • Pica

    Pica is a compulsive craving to ingest substances that are not normal feed items, such as soil, sand, wood, feces, or other non-nutritive materials. In horses, pica can reflect nutritional deficiencies (particularly of sodium, phosphorus, or trace minerals), gastrointestinal parasitism, boredom, or underlying systemic disease. Coprophagy (eating feces) is normal in foals during the first few weeks of life as a mechanism to inoculate the hindgut with beneficial microflora, and should not be confused with pathological pica. Wood chewing in mature horses, while sometimes classified under pica, more often reflects inadequate forage intake or stereotypic behavior rather than a mineral hunger. Dirt and sand ingestion can lead to sand accumulation in the large colon, contributing to sand colic, a form of gastrointestinal obstruction; this risk is heightened in horses kept on sandy substrates without adequate forage. Diagnosis involves dietary history, serum biochemistry and mineral analysis, and fecal egg counts to rule out gastrointestinal parasite burden. Management addresses the underlying cause: correcting mineral imbalances through dietary supplementation, increasing forage availability, and enriching the horse’s environment to reduce boredom. Rubber stall mats and raised feeders reduce incidental soil ingestion. For context on correcting mineral gaps through ration balance that minimize nutritional gaps and on sand colic from accumulated ingested soil related to sand accumulation.

    Further Reading

  • Inflammatory Airway Disease in Horses: Causes, Signs, and Treatment

    Inflammatory airway disease (IAD) is a non-infectious condition of the lower respiratory tract characterized by lower airway inflammatory process of the bronchi and bronchioles, excessive mucus accumulation, and bronchoconstriction without systemic signs of illness. It affects horses of all ages, breeds, and disciplines, including racehorses, sport horses, and working horses, and is considered one of the most prevalent performance-limiting respiratory conditions in equine athletes. IAD differs from severe equine asthma (formerly called recurrent airway obstruction or heaves) primarily in severity: horses with IAD do not show signs of respiratory distress at rest, do not have an elevated resting respiratory rate, and do not display the characteristic heave line from hypertrophied external abdominal oblique muscles.

    The causes are multifactorial. Inhaled organic dusts and molds from hay and bedding are major triggers; horses kept in poorly ventilated stalls and fed dry hay have consistently higher airway inflammatory cell counts than horses kept at pasture or fed soaked or haylage. Viral respiratory viral respiratory infections as IAD triggers: equine influenza, equine herpesvirus types 1 and 4, and equine rhinitis viruses, can initiate or exacerbate IAD by damaging airway epithelium and priming a persistent inflammatory response. Air pollutants at competition venues, diesel exhaust from transport, and endotoxin from gram-negative bacterial contamination of feed are recognized environmental contributors. Some horses appear to have an allergic component, with eosinophil-predominant cytology on tracheal wash samples suggesting hypersensitivity to specific antigens rather than generalized particulate irritation.

    Diagnosis requires endoscopic assessment showing excess mucus in the trachea, combined with cytological analysis of a bronchoalveolar lavage (BAL) sample showing elevated neutrophils, mast cells, or eosinophils above reference thresholds. Clinical signs are subtle: intermittent coughing, mild nasal discharge, and reduced performance or early fatigue during exercise. Treatment centers on environmental management first, maximizing ventilation, replacing dry hay with soaked hay or complete feed pellets, and switching to low-dust bedding such as paper, cardboard, or kiln-dried shavings, because pharmacological management without removing the trigger produces only temporary improvement. Corticosteroids (inhaled or systemic) and bronchodilators (clenbuterol, albuterol) reduce lower airway inflammatory process and relieve bronchoconstriction acutely; current protocols favor inhaled corticosteroids for long-term management because systemic administration suppresses adrenal function and may worsen laminitis risk in horses with concurrent metabolic conditions. Vaccination against respiratory viruses reduces the frequency of infection-triggered exacerbations.

    Further Reading

  • Inflammation in Horses: Definition, Signs, and Management

    Inflammation is the localized protective response of vascular connective tissue to injury, infectious trigger driving the response, or irritants. It is a fundamental biological mechanism, not a disease in itself: the five cardinal signs recognized since antiquity, heat (calor), pain (dolor), swelling (tumor), redness (rubor), and loss of function (functio laesa), are the outward expression of increased blood flow, vascular permeability, and the migration of immune cells to the site of insult. In horses these signs appear across a wide spectrum of conditions: a hot, swollen fetlock joint from a minor sprain, a painful abscess in the hoof, an inflamed tendon sheath (tenosynovitis), or the systemic inflammatory cascade of endotoxemia.

    The process unfolds in sequence. Tissue injury releases damage-associated molecular patterns (DAMPs) that activate resident mast cells and macrophages; these cells release vasoactive mediators, histamine, prostaglandins, and bradykinin, that dilate local blood vessels and increase capillary permeability. Protein-rich plasma leaks into the interstitium (producing the swelling), neutrophils emigrate from dilated vessels within minutes to hours and begin phagocytosing bacteria or cellular debris, and monocytes follow over the subsequent twenty-four to forty-eight hours to sustain the response and initiate repair. Prostaglandins, particularly PGE2, sensitize pain receptors at the site and act on the hypothalamus to raise body temperature (see hyperthermia), creating the fever associated with acute systemic inflammatory states.

    In equine clinical practice, management of acute inflammation relies primarily on non-steroidal anti-inflammatory drugs (NSAIDs), phenylbutazone (bute) and flunixin meglumine (Banamine) being the most widely used, which inhibit cyclooxygenase enzymes and reduce prostaglandin synthesis. Cold therapy (icing or cold-hosing) applied in the first twenty-four to forty-eight hours of an acute soft-tissue injury limits the initial vascular response and reduces pain. Rest and controlled loading protect the inflamed tissue from further mechanical damage while repair proceeds. Chronic inflammation in which the resolution phase fails, as in some tendon, joint, and airway conditions, may require corticosteroid treatment, targeted regenerative therapies (PRP, IRAP), or management of the underlying trigger such as airway conditions where resolution fails. The body condition of the horse is a relevant variable because adipose tissue in obese horses secretes pro-inflammatory adipokines that sustain low-grade systemic inflammation and worsen conditions such as insulin dysregulation and laminitis.

    Further Reading

  • Hypocalcemia in Horses: Definition, Causes, and Clinical Signs

    Hypocalcemia is an abnormally low concentration of ionized calcium in the blood. Calcium is the most abundant mineral in the equine body, and its ionized (free) fraction in the bloodstream is maintained within a narrow range by parathyroid hormone, calcitonin, and vitamin D acting on bone, kidney, and intestine. Normal ionized calcium in horses is approximately 1.4 to 1.8 mmol/L; values below 1.2 mmol/L produce measurable clinical signs, and severe hypocalcemia below 1.0 mmol/L constitutes a medical emergency because calcium is essential for normal neuromuscular transmission, cardiac conduction, and smooth muscle contractility.

    The most clinically recognized form is transport tetany (also called transit tetany or transit hypocalcemia), which develops in mares that have been transported for extended periods without adequate feed, water, or rest. Prolonged alkalosis from hyperventilation during transport reduces the ionized fraction of calcium even when total calcium is normal, because alkalotic conditions shift calcium from the free ionized form to protein-bound forms. Lactating lactating mares at peak milk production are at heightened risk because colostrum and milk production impose a sustained calcium drain; the postpartum period in heavy-producing mares is analogous to milk fever (parturient paresis) in dairy cattle. Blister beetles contaminating alfalfa hay cause hypocalcemia as part of cantharidin toxicosis, in which kidney damage impairs calcium regulation.

    Clinical signs reflect failure of the calcium-dependent neuromuscular system: synchronous diaphragmatic flutter (thumps), in which the diaphragm contracts in time with each heartbeat, producing a visible flank flicker, is the hallmark finding in horses. Muscle trembling, stiff gait, sweating, facial twitching, and tetanic spasms of the jaw and neck muscles may accompany or precede thumps. Treatment is intravenous calcium gluconate or calcium borogluconate administered slowly while cardiac rhythm is monitored; rapid infusion can cause cardiac dysrhythmia and arrest. Dietary calcium adequacy, particularly in horses fed grain-heavy rations low in roughage, is assessed against NRC requirements as a preventive measure. Correct dietary calcium-to-phosphorus ratio (at minimum 1:1, ideally 1.5:1 to 2:1) is a standard part of calcium-to-phosphorus ratio in ration planning.

    Further Reading