Horse Info

Category: Glossary

Equine terms and definitions

  • 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

  • Hyperthermia in Horses: Definition, Causes, and Response

    Hyperthermia is the condition in which the core body temperature rises above the normal physiological range. In horses the normal rectal temperature is 99.0 to 101.5 degrees Fahrenheit (37.2 to 38.6 degrees Celsius); readings above 101.5 degrees Fahrenheit constitute hyperthermia, and readings above 104 degrees Fahrenheit represent a medical emergency. The term encompasses both fever (pyrexia), in which the hypothalamic set-point is raised by pyrogens released during infectious disease or inflammatory stimulus, and non-febrile hyperthermia, in which metabolic heat production or environmental heat load exceeds the body's ability to dissipate warmth.

    Heat exhaustion and heat stroke are the clinically most urgent forms of non-febrile hyperthermia in horses. They occur when a horse performing intense work in hot, humid conditions cannot lose heat fast enough through sweating and convective cooling. Horses dissipate approximately 65 percent of exercise-generated heat through evaporative cooling; high ambient humidity reduces evaporative efficiency dramatically, making temperature-humidity index (THI) a better predictor of heat stress risk than air temperature alone. Clinical signs of severe hyperthermia include elevated heart rate, rapid shallow breathing, profuse sweating giving way to a dry hot coat as dehydration progresses, stumbling, and altered mentation. Rectal temperature above 41 degrees Celsius requires immediate cold-water hosing of the large muscle groups and neck vessels, removal of tack, provision of shade and air movement, and veterinary evaluation because sustained temperatures at this level cause protein denaturation, organ damage, and circulatory collapse.

    Febrile hyperthermia in horses arises from viral respiratory diseases, bacterial infections, pleuritis, colitis, and other systemic conditions. A fever below 104 degrees Fahrenheit in an otherwise stable horse is generally allowed to persist unless it causes marked discomfort, because the elevated temperature impairs pathogen replication and supports immune function. Antipyretic drugs, chiefly flunixin meglumine and phenylbutazone, reduce fever by blocking prostaglandin synthesis but do not treat the underlying cause. Monitoring rectal temperature twice daily during a fever episode, combined with a current vaccination record and veterinary guidance, forms the basis of a responsible febrile management protocol.

    Further Reading

  • Paralysis

    Paralysis is the complete or partial loss of voluntary motor function in one or more muscle groups, resulting from disruption at any level of the motor pathway from the cerebral cortex through the spinal cord to the peripheral nerve and neuromuscular junction. In horses, paralysis is classified by anatomical distribution: monoplegia (one limb), hemiplegia (one side), paraplegia (both hindlimbs), and tetraplegia or quadriplegia (all four limbs). Common equine causes include equine protozoal myeloencephalitis (EPM) caused by Sarcocystis neurona, equine herpesvirus type 1 (EHV-1) myeloencephalopathy, cervical vertebral stenotic myelopathy (Wobbler syndrome), botulism affecting the neuromuscular junction, and peripheral nerve damage following trauma or injection site injury. Laryngeal hemiplegia, the partial paralysis of the left arytenoid cartilage caused by damage to the left recurrent laryngeal nerve, is among the most common neurological conditions in performance horses and produces the characteristic inspiratory noise known as roaring. Facial nerve paralysis can result from ill-fitting halters or head trauma. Diagnosis of the underlying cause requires neurological examination, cerebrospinal fluid analysis, serology, and imaging. Treatment depends on etiology; supportive care, physical therapy, and specific antiprotozoal treatment for EPM may be indicated. See also EHV-1 myeloencephalopathy, a viral cause of spinal cord damage and ataxia, and sudden collapse from sleep dysfunction for a non-paralytic differential with overlapping presentation.

    Further Reading

  • Narcolepsy

    Narcolepsy is a neurological sleep disorder characterized by recurrent episodes of uncontrollable drowsiness and sudden loss of muscle tone (cataplexy) that precipitate collapse into sleep. In horses, narcolepsy is rare and can be idiopathic or secondary to underlying conditions such as liver disease, equine protozoal myeloencephalitis, or hypersomnia associated with sleep deprivation from an inability to achieve recumbent rest. Affected horses exhibit characteristic behavior: they become progressively drowsy, the head drops, the knees buckle, and the horse may collapse partially or fully before partially awakening. Skin abrasions on the knees, fetlocks, and muzzle from repeated partial falls are a common physical finding. Diagnosis requires ruling out other causes of episodic weakness or collapse, including paralysis, hypoglycemia, and cardiac arrhythmia. The orexin (hypocretin) system implicated in human and canine narcolepsy is also relevant in horses; imipramine has been used diagnostically and therapeutically. Environmental assessment is important because horses that cannot lie down comfortably in their stabling may develop secondary sleep deprivation that mimics narcolepsy. See also motor pathway disruption as the primary differential when distinguishing true paralytic episodes from narcoleptic collapse, and fetlock anatomy for understanding the abrasion pattern that accumulates from repeated partial falls.

    Further Reading

  • Equine Infectious Anemia in Horses

    Equine infectious anemia (EIA) is a retroviral disease caused by a lentivirus in the family Retroviridae, closely related to HIV in its mechanism of persistence. The virus infects macrophages and monocytes, integrates permanently into the host genome, and is never cleared, an infected horse carries EIA for life. The disease is sometimes called swamp fever or horse malaria, names that reflect historical descriptions of the intermittent fever that marks acute episodes.

    Transmission occurs primarily via blood transfer: large biting insects (horse flies and deer flies of the family Tabanidae) mechanically carry virus on mouthparts interrupted mid-meal and moved to another horse. Contaminated needles and surgical instruments are the principal iatrogenic route, a particular concern in historical herd vaccination programs where needles were reused. Vertical transmission from mare to foal across the placenta or in milk occurs at low frequency. EIA is not transmitted by casual contact, shared water, or small insects such as mosquitoes.

    Clinical presentation falls into three patterns. Acute EIA produces high fever (up to 41 degrees C), thrombocytopenia, dependent edema, and severe anemia within 30 days of infection; untreated acute cases can be fatal. Chronic EIA follows with recurring febrile episodes every few weeks to months, progressive weight loss, and deteriorating body condition. Inapparent carriers show no clinical signs but remain persistently viremic and are the primary reservoir for transmission in managed herds.

    The Coggins test (agar gel immunodiffusion, AGID) detects antibodies against EIA p26 antigen and is the regulatory standard for diagnosis. A positive Coggins result is a reportable finding in all US states and most countries; regulations require either lifelong quarantine at least 200 yards from all other equids, euthanasia, or export under USDA permit. Negative Coggins tests are required for interstate transport, competition entry, and most boarding facilities. A current negative test is a standard document in any horse purchase. There is no vaccine and no cure; control is entirely through testing and movement restriction. See also pre-purchase documentation requirements for why a current negative Coggins test is a non-negotiable item in any sale, and body condition scoring for monitoring the progressive deterioration seen in chronic EIA carriers.

    Further Reading: The virology, Coggins test protocol, and regulatory requirements for EIA are detailed on Wikipedia’s Equine infectious anemia entry. Utah State University Extension’s equine health program publishes a practical overview of testing requirements at USU Extension: Equine Infectious Anemia.

  • Equine Herpes Virus in Horses

    Equine herpesvirus (EHV) is a family of DNA viruses belonging to the Herpesviridae, with five characterized subtypes in horses. EHV-4 causes primarily respiratory illness, rhinopneumonitis, most severe in young horses and resembling moderate influenza. EHV-1 causes respiratory disease but is distinguished by its capacity to produce two additional and more serious syndromes: abortion in pregnant mares and equine herpesvirus myeloencephalopathy (EHM), a neurological form that can cause ataxia, paralysis, and death.

    Both EHV-1 and EHV-4 establish lifelong latency in the trigeminal ganglia and lymphocytes after primary infection. A horse that has recovered from EHV illness carries latent virus indefinitely and may reactivate shedding under stress, weaning, competition, transport, or concurrent illness. This means herd immunity is never complete and outbreak control depends on biosecurity and stress management rather than elimination of the virus from exposed populations.

    EHM outbreaks at competition venues have become a recognized event-management concern. Affected horses display progressive hindlimb ataxia, bladder dysfunction, and in severe cases quadriplegia within days of fever onset. Case fatality in neurological EHV-1 infections ranges from 20 to 40 percent in outbreak settings, making prompt quarantine and reporting to regulatory authorities essential. The index of suspicion should rise for any horse that develops fever and neurological signs within 14 days of attending a competition or event.

    Vaccination for EHV-1 and EHV-4 is available and recommended in the core vaccination schedule for horses with any exposure to other horses. Current vaccines reduce respiratory shedding and provide partial protection against abortion but do not reliably prevent EHM. Biosecurity during transport: checking temperatures during travel, limiting nose-to-nose contact, is the primary mitigation for horses moving between facilities. See also the core vaccination schedule for EHV-1 and EHV-4 timing and the limitation of current vaccines against neurological disease, and the Equus genus entry for the host-specificity context that gives all five EHV subtypes their name.

    Further Reading: The five EHV subtypes, their clinical syndromes, and the EHM neurological form are covered on Wikipedia’s Equine herpesvirus article. Utah State University Extension provides a practical guide to EHV biosecurity and outbreak management at USU Extension: Equine Herpesvirus.