Veterinary · Clinical · also Equine Practice
The horse in health and disease: colic, lameness, respiratory and infectious diseases, dentistry, reproduction, neonatology, performance and welfare. Taught internationally; not a separate MSVE course.
In the exams: NAVLE equine 14.7%; RCVS SME equine 87 of 367 items; SAVC Paper 1 equine 30; ECFVG / NEB CPE equine section
Equine medicine, surgery and practice is the clinical study of the horse, pony, donkey and mule in health and disease. It is organised the way an equine practitioner meets problems: a horse with abdominal pain at midnight, a lame horse before a competition, a coughing yard, a mare that will not conceive, a weak newborn foal, a buyer who wants an opinion before paying, and a regulator who wants to know whether a horse was medicated or may enter the human food chain.
It is a sport and leisure animal in Europe, North America and Australasia, a working and transport animal for many millions of families in South Asia, Africa and Latin America, and in several countries a food animal. That mix means the same clinical decision can carry different legal weight in different places: a drug that is routine in a US sport horse may make a European horse permanently ineligible for slaughter for food, and a positive glanders test in India or Brazil triggers official action that a clinician cannot override.
This manual follows the curriculum units: colic; lameness; respiratory disease with strangles and equine influenza; the three notifiable infections most examined worldwide (glanders, equine infectious anaemia and African horse sickness) together with general biosecurity; dentistry; reproduction; neonatology; sport and performance medicine including the prepurchase examination and medication control; and welfare. Licensing examinations weight the horse heavily: about 14.7% of NAVLE items are equine, and the RCVS Statutory Membership Examination has a separate equine domain of 87 of 367 items that must be passed on its own.
The only drug dose given is one widely printed in standard texts, and it carries the house warning that it must be confirmed locally.
Colic means abdominal pain. It is a sign, not a diagnosis, and in the horse most colic arises from the gastrointestinal tract, although pain from the uterus, urinary tract, liver or even pleura can look the same. The horse is predisposed by its anatomy. It cannot vomit effectively because of a strong cardiac sphincter and the oblique entry of the oesophagus into the stomach, so gastric distension can end in rupture. The small intestine hangs on a long mesentery, which allows volvulus and entrapment. The large colon is a folded, largely unattached organ with abrupt changes in diameter, especially at the pelvic flexure, where ingesta slows and impactions form, and it can displace or twist around its own mesentery. Sudden feed changes, high-concentrate rations, reduced water intake, restricted turnout, poor dentition and parasites add risk.
Most colic is mild, but a minority are strangulating lesions in which the blood supply to a segment of bowel is cut off. Those horses deteriorate from endotoxaemia and shock within hours. The central task of the first-opinion vet is therefore triage: is this horse medical or does it need referral?
History covers duration, feed, water, management change, pregnancy and any drugs already given, which may mask signs. Severity of pain is one of the most useful single guides to the need for surgery: pain that persists despite adequate analgesia strongly suggests a surgical lesion.
Normal resting values in the adult horse are commonly given as a heart rate of about 28 to 44 beats per minute, a respiratory rate of about 8 to 16 breaths per minute and a rectal temperature of about 37.5 to 38.5 C. A heart rate persistently above about 60 per minute, a prolonged capillary refill time, dark red or purple mucous membranes with a toxic line at the gingival margin, and cold extremities point to cardiovascular compromise. Auscultate all four abdominal quadrants for borborygmi; their absence is a worrying sign.
Nasogastric intubation is both diagnostic and therapeutic. Net reflux of more than about 2 litres is significant and suggests small-intestinal obstruction or proximal enteritis. Rectal palpation identifies distended small intestine, a large colon impaction at the pelvic flexure, tight transverse bands of a displaced or twisted colon, the nephrosplenic space, and a distended caecum.
Packed cell volume, total protein and blood lactate track dehydration and perfusion. Abdominocentesis, usually at the most dependent point of the ventral abdomen, samples peritoneal fluid. Normal fluid is clear and pale yellow with a low protein and low cell count. Serosanguineous fluid with raised protein and a peritoneal lactate higher than blood lactate suggests ischaemic, strangulated bowel. Turbid, brown fluid with plant material means rupture or accidental enterocentesis; the latter is judged by the whole picture.
A rapid protocol of several fixed windows, often called FLASH (fast localised abdominal sonography of horses), looks for distended, turgid, non-motile small-intestinal loops, thickened colon wall, free fluid, gastric distension, and the absence of the spleen-to-kidney view in nephrosplenic entrapment. It is safe in ponies and foals too small for rectal palpation.
Simple obstructions include pelvic flexure impaction, sand accumulation where horses graze sandy pasture, enteroliths, and gastric impaction. Spasmodic or gas colic is the commonest mild form. Displacements include left dorsal displacement of the large colon into the nephrosplenic space. Strangulating lesions include small-intestinal volvulus; pedunculated lipomas, which wrap round small intestine in older horses; epiploic foramen entrapment, which is associated with crib-biting; inguinal hernia in stallions; and large colon volvulus, classically in broodmares around foaling, which is one of the most rapidly fatal colics. Proximal (duodenitis-proximal) jejunitis produces large volumes of reflux, fever and often less pain once the stomach is decompressed, which helps separate it from surgical obstruction.
Equine grass sickness (equine dysautonomia) is a neurodegenerative disease of grazing horses reported mainly in Great Britain and northern Europe; it causes dysphagia, gut stasis and weight loss, and its cause is thought to involve Clostridium botulinum neurotoxin but is not fully settled. Gastric ulceration (equine gastric ulcer syndrome) causes low-grade recurrent colic and poor performance and is diagnosed by gastroscopy.
Non-steroidal anti-inflammatory drugs give analgesia and reduce the effects of endotoxin. Flunixin meglumine is widely printed at about 1.1 mg/kg intravenously — confirm against the product label and your national formulary; because it is so effective it can mask a surgical lesion, so reassess the horse after it acts. Alpha-2 agonists such as xylazine and detomidine, often with the opioid butorphanol, give short, strong sedation and analgesia but lower gut motility. Enteral fluids by nasogastric tube, with or without electrolytes or osmotic laxatives, treat large colon impactions if there is no reflux; intravenous fluids are used when the horse is dehydrated, shocked or cannot take enteral fluids.
Fluid volumes are calculated from bodyweight. Maintenance is commonly given as about 50 to 60 mL/kg/day in the adult; the deficit is estimated as percentage dehydration multiplied by bodyweight, so a 500 kg horse estimated at 8% dehydrated has a deficit of about 40 L, to which maintenance and ongoing losses such as reflux are added.
Refer or operate when there is severe or recurrent pain despite analgesia, persistent tachycardia, significant reflux, distended small intestine on palpation or ultrasound, abnormal peritoneal fluid, or a palpable displacement that does not respond. Discuss cost and prognosis early, because delay costs bowel. Postoperative complications include ileus, incisional infection, adhesions, jugular thrombophlebitis and laminitis. Where surgery is not an option, humane euthanasia is the welfare decision for a horse with a strangulating lesion.
Lameness is an abnormal gait caused by pain or mechanical restriction. The examination starts with history, then a static inspection for conformation, swelling, muscle wastage and hoof balance, followed by palpation of every limb with the limb weight-bearing and raised, and hoof testers applied to the sole and frog.
The horse is then seen moving in a straight line at walk and trot on a firm surface, on the lunge on hard and soft ground in both directions, and if needed under saddle. In forelimb lameness the head rises when the lame limb is on the ground and nods down when the sound limb lands, which is summed up as 'down on sound'. In hindlimb lameness the pelvis shows asymmetric movement, often seen as a greater rise of the tuber coxae on the lame side (a 'hip hike'), and a marked hindlimb lameness can produce a head nod that mimics lameness in the ipsilateral forelimb. Body-mounted inertial sensors now measure these asymmetries objectively.
The American Association of Equine Practitioners (AAEP) scale grades lameness from 0 to 5: grade 0 is not perceptible; grade 1 is difficult to observe and inconsistent; grade 2 is difficult to see at walk or straight trot but consistent under certain conditions such as circling or weight carrying; grade 3 is consistently seen at the trot under all conditions; grade 4 is obvious at the walk; grade 5 shows minimal weight bearing or inability to move. Flexion tests give supporting but non-specific information.
Perineural and intrasynovial analgesia (nerve and joint blocks) are the backbone of lameness localisation. A local anaesthetic such as mepivacaine or lidocaine is injected aseptically and the horse is re-examined. Blocks are done from distal to proximal, because a proximal block desensitises everything below it.
In the forelimb, the palmar digital nerve block, placed on the medial and lateral palmar digital nerves just above the collateral cartilages, desensitises the palmar part of the foot, including the navicular apparatus, much of the sole and the heels, and may also affect the distal interphalangeal joint. The abaxial sesamoid block at the base of the proximal sesamoid bones desensitises the whole foot and much of the pastern. The low four-point (low palmar) block at the distal ends of the splint bones desensitises the fetlock and below. The high four-point block in the proximal metacarpus adds the flexor tendons and most of the suspensory ligament. The hindlimb equivalents are the plantar blocks; the tibial and fibular (peroneal) nerve blocks desensitise the hock and below. Blocks are not perfectly specific: anaesthetic diffuses proximally with time and joint blocks can desensitise nearby nerves, so interpret the pattern of results. Intrasynovial injection risks septic synovitis; use sterile technique.
Radiography is the first-line imaging for bone and joint, ultrasonography the main tool for tendons and ligaments, nuclear scintigraphy finds increased bone turnover where blocks fail or in the upper limb and back, and MRI transformed the diagnosis of soft-tissue foot pain. Imaging findings must be tied to the block results, because many horses carry radiographic changes that are not causing lameness.
The foot is the commonest site of forelimb lameness. A subsolar abscess is the classic cause of acute, severe, single-limb lameness, with increased digital pulses, focal pain to hoof testers, and relief once drained. Palmar foot pain (navicular syndrome or navicular disease) is chronic, often bilateral forelimb lameness improved by palmar digital analgesia. Management combines farriery, controlled exercise and anti-inflammatory therapy.
Laminitis is failure of the attachment between the distal phalanx and the inner hoof wall. Three broad causes are recognised: endocrinopathic laminitis associated with hyperinsulinaemia in equine metabolic syndrome or pituitary pars intermedia dysfunction (PPID), which accounts for most cases in practice; laminitis associated with systemic inflammation, such as grain overload, retained placenta, colitis or endotoxaemia; and supporting-limb laminitis in a limb overloaded because the opposite limb cannot bear weight. Signs include a shifted-back stance, bounding digital pulses, reluctance to turn and toe pain on hoof testers. Lateral radiographs show rotation of the distal phalanx relative to the hoof wall or distal displacement ('sinking'). Treatment addresses the cause, gives analgesia and sole support, uses cryotherapy early in sepsis-associated cases, and controls diet in endocrinopathic cases.
Osteoarthritis of the distal interphalangeal, fetlock, carpal and distal tarsal joints (the last often called bone spavin) is common in older sport horses. Osteochondrosis, including osteochondritis dissecans (OCD), is a developmental disease of young horses with typical sites such as the lateral trochlear ridge of the femur, the distal intermediate ridge of the tibia and the sagittal ridge of the third metacarpal bone.
Superficial digital flexor tendinitis ('bowed tendon') is common in racehorses and eventers; ultrasonography shows a core lesion and guides a long, graded return to work. Proximal suspensory desmitis is common in both fore and hind limbs of sport horses. Racehorses develop stress-related bone injury: dorsal metacarpal disease ('bucked shins') in young Thoroughbreds, condylar fractures of the third metacarpal or metatarsal bone, and sagittal fractures of the proximal phalanx. Septic synovitis from a wound near a joint or tendon sheath is an emergency: confirm by synoviocentesis, lavage early and give systemic and regional antimicrobials.
Strangles is caused by Streptococcus equi subspecies equi. Transmission is by direct contact with nasal discharge or pus and indirectly by shared water, tack, handlers and equipment. Affected horses show fever, depression, a mucopurulent nasal discharge and painful swelling and abscessation of the submandibular and retropharyngeal lymph nodes. Retropharyngeal abscesses drain into the guttural pouches.
Complications include guttural pouch empyema with inspissated pus concretions (chondroids); 'bastard strangles', meaning metastatic abscesses in abdominal or thoracic lymph nodes or other organs; purpura haemorrhagica, an immune-complex vasculitis with limb and head oedema and petechiae, usually two to four weeks after infection or exposure. The critical epidemiological fact is the carrier: a proportion of recovered horses remain persistently infected in the guttural pouches, shed intermittently without signs, and restart outbreaks.
Diagnosis is by culture or PCR of nasal swabs, nasopharyngeal washes or abscess pus. Serology for antibody to the SeM protein helps identify recent exposure and screen new arrivals. Carriers are identified by endoscopy of the guttural pouches with lavage for PCR and culture, and treated by removing chondroids and instilling antimicrobial.
Treatment of uncomplicated cases is supportive: isolation, soft moist food, anti-inflammatory drugs and hot packing to mature abscesses, which are then lanced. The use of penicillin is debated; it is generally reserved for horses with severe illness, dysphagia or airway obstruction, and there is concern that early treatment of a horse with established lymph node infection may delay abscess maturation. Outbreak control uses a 'traffic light' system of red (clinical), amber (in contact) and green (unexposed) groups, separate staff and equipment, temperature monitoring twice daily, and screening of all recovered horses before release. Vaccine availability varies by country.
Equine influenza is caused by influenza A virus, in the family Orthomyxoviridae. The circulating subtype is H3N8; the H7N7 subtype has not been isolated for decades and is thought to be extinct. The virus spreads rapidly by aerosol, with a short incubation of about one to three days, causing high fever, a harsh dry cough, serous nasal discharge, depression and inappetence. Secondary bacterial pneumonia is the main complication, and damage to the ciliated airway takes weeks to repair; the traditional guide is one week of rest for every day of fever.
Diagnosis is by PCR or antigen detection on nasopharyngeal swabs taken early, or by a rise in antibody on paired sera. Vaccination reduces disease and shedding but does not give sterile immunity. Under Fédération Équestre Internationale (FEI) rules, a primary course of two doses 21 to 92 days apart is followed by a first booster within seven months, then boosters at no more than 12-month intervals, and a competing horse must have had a booster within six months and 21 days before arrival at an event and none within seven days of it; racing and national rules differ and change, so check the current rule book.
Equine herpesvirus 1 (EHV-1) and 4 (EHV-4) cause rhinopneumonitis in young horses. EHV-1 also causes late-gestation abortion storms, weak neonatal foals and equine herpesvirus myeloencephalopathy (EHM), in which endothelial infection of spinal cord vessels produces vasculitis and thrombosis, with hindlimb ataxia, urinary incontinence and tail weakness. A single-nucleotide variation in the viral DNA polymerase gene (the D752 genotype) is associated with a higher risk of neurological disease, although the other genotype can also cause it. Latent virus reactivates after stress and starts new outbreaks. Diagnose by PCR on nasal swab and whole blood. EHM outbreaks are managed by stopping movement, isolating and monitoring temperatures of in-contact horses twice daily, and in many countries by reporting to the authorities. Vaccines have not been shown to prevent EHM.
Severe equine asthma (formerly recurrent airway obstruction or 'heaves') affects mature horses, is triggered mainly by inhaled organic dust and moulds in hay and bedding, and causes episodes of laboured breathing at rest with an expiratory push that builds a 'heave line' from hypertrophy of the abdominal muscles. Mild to moderate asthma (formerly inflammatory airway disease) affects horses of any age and causes cough, mucus and poor performance without respiratory effort at rest. Diagnosis rests on endoscopy with tracheal mucus scoring, and on bronchoalveolar lavage cytology, with raised neutrophils, mast cells or eosinophils; severe asthma typically shows a marked neutrophilia, commonly cited as more than 25% of cells.
Environmental management is the foundation of treatment and the one step that must not be skipped: turnout where possible, soaked or steamed hay or haylage instead of dry hay, low-dust bedding and good ventilation. Corticosteroids, systemic or inhaled, and bronchodilators such as inhaled beta-2 agonists control flare-ups but do not replace environmental change.
Rhodococcus equi pneumonia of foals is covered in the neonatal chapter.
Recurrent laryngeal neuropathy ('roaring') is a distal axonopathy of the recurrent laryngeal nerve, mainly of the left side because of its greater length, which paralyses the dorsal cricoarytenoid muscle and prevents full abduction of the left arytenoid cartilage. Tall horses are predisposed. It causes inspiratory noise and exercise intolerance. It is graded at resting endoscopy (the Havemeyer scheme grades I to IV) and confirmed by endoscopy during exercise, and treated by prosthetic laryngoplasty ('tie-back'), often with ventriculocordectomy. Dorsal displacement of the soft palate causes an expiratory gurgling noise during fast exercise. Exercise-induced pulmonary haemorrhage (EIPH) is very common in racehorses and arises from the dorsocaudal lung fields; it is diagnosed by tracheobronchoscopy after exercise, and furosemide is used before racing in some jurisdictions and prohibited on race day in most others. Guttural pouch mycosis, a fungal plaque usually over the internal carotid artery, can cause fatal epistaxis and cranial nerve deficits such as dysphagia; treatment is arterial occlusion.
Glanders is a contagious, usually fatal disease of equids caused by Burkholderia mallei, a Gram-negative, non-motile bacillus that is an obligate mammalian pathogen and does not persist long in the environment. Horses, donkeys and mules are the natural hosts. Donkeys typically develop an acute, rapidly fatal form, mules are intermediate, and horses more often have a chronic course that allows them to shed for long periods. Humans are infected through skin abrasions and mucous membranes or by inhalation, and the disease can be fatal, so glanders is an important occupational zoonosis for veterinarians, farriers, grooms and laboratory staff. Laboratory work needs high containment.
Glanders was eradicated from Western Europe and North America during the twentieth century by test and slaughter, but it persists or re-emerges in parts of South Asia (including India and Pakistan), the Middle East and South America (notably Brazil). It is a WOAH-listed disease, so outbreaks must be reported, and international movement of horses requires testing.
Three overlapping forms are described. In the nasal form, nodules in the nasal mucosa ulcerate into deep, crater-like ulcers that heal as stellate (star-shaped) scars, with a unilateral or bilateral purulent, sometimes blood-stained, nasal discharge and enlarged, firm submandibular lymph nodes that may adhere to the surrounding tissue. In the pulmonary form, nodules and pneumonia develop in the lungs, with cough, dyspnoea and weight loss. In the cutaneous form, called farcy, nodules develop along lymphatic vessels of the limbs and ventral body; they ulcerate and discharge a sticky, honey-like pus, and the thickened lymphatics are described as 'farcy pipes' or cords. Most chronic cases have a mixture of forms.
The differential diagnosis includes strangles, epizootic lymphangitis caused by the fungus Histoplasma capsulatum var. farciminosum, ulcerative lymphangitis caused by Corynebacterium pseudotuberculosis, sporotrichosis and melioidosis (Burkholderia pseudomallei), which shares antigens with B. mallei and can confuse serology.
The mallein test is a delayed hypersensitivity test in which purified mallein is injected into the lower eyelid (the intradermo-palpebral test), and a positive reaction is swelling of the eyelid with purulent conjunctivitis at about 48 hours. It can interfere with later serology. Serology is the basis of trade testing: the complement fixation test has long been the prescribed test for international trade, and ELISAs and immunoblot tests are used to improve specificity and confirm results.
There is no vaccine. Treatment of infected equids is not recommended or is prohibited in most control programmes because treated animals may remain carriers and a source of human infection. Control is by notification, movement restrictions, testing of in-contacts, humane destruction of positive animals with compensation where the law provides it, safe carcass disposal, disinfection and surveillance. In India glanders is a scheduled disease under the Prevention and Control of Infectious and Contagious Diseases in Animals Act, 2009, with a national control approach of testing, culling and compensation. The veterinarian's duties are to recognise the disease, avoid personal exposure, notify, and not treat.
Equine infectious anaemia (EIA), sometimes called swamp fever, is caused by a lentivirus of the family Retroviridae. It integrates into host cells, so an infected horse, donkey or mule is infected for life and is a potential source of virus even when it looks healthy. There is no treatment and no vaccine in general use.
Transmission is mechanical, by blood. Large biting flies, especially horse flies and deer flies (tabanids) and stable flies, carry blood on their mouthparts from one horse to the next when their painful bite is interrupted; the virus does not replicate in the insect, and risk falls sharply with distance between horses. Iatrogenic transmission by reused needles, instruments and plasma has caused serious outbreaks.
The acute phase, one to several weeks after exposure, is often missed: fever, lethargy and thrombocytopenia. Some horses then enter a chronic phase of recurrent fever with anaemia, weight loss, ventral oedema and petechiae, each episode linked to a new antigenic variant of the virus. Most infected horses become inapparent carriers. Transmission risk is greatest during fever, but carriers remain infectious. Anaemia is mainly immune-mediated destruction of red cells coated with virus and complement, plus suppressed erythropoiesis.
Diagnosis rests on detecting antibody. The agar gel immunodiffusion test, known as the Coggins test, is the historical standard and remains the confirmatory test in many programmes. ELISAs are more sensitive and faster, and in many regulatory programmes an ELISA-positive sample is confirmed by agar gel immunodiffusion or immunoblot. Foals of infected mares carry maternal antibody for several months and must be retested later before they are called infected. A negative test within a stated period is required for international movement, sales and competition in many countries.
EIA is WOAH-listed. Control measures, which vary by country, include compulsory testing, notification, and for positive animals either humane destruction or lifelong quarantine at a prescribed distance from other equids with fly control, and permanent identification. In practice, prevention depends on single-use needles and syringes, never pooling medication vials between horses, cleaning dental and surgical instruments of blood between patients, using tested blood and plasma donors, controlling biting flies and testing new arrivals.
Several other infections cause fever, anaemia or oedema and must be considered alongside EIA. Equine piroplasmosis, caused by the tick-borne protozoa Theileria equi and Babesia caballi, causes fever, haemolytic anaemia and icterus; it is endemic across much of the tropics and subtropics, is WOAH-listed and restricts movement to free countries; horses infected with T. equi generally remain carriers. Equine viral arteritis, caused by an arterivirus, causes fever, limb and scrotal oedema, conjunctivitis and abortion, and is maintained by carrier stallions that shed virus in semen. Neurological arboviral infections, including West Nile virus and the eastern, western and Venezuelan equine encephalitis viruses, are important because horses are dead-end or amplifying hosts depending on the virus and because several are zoonotic; vaccines exist for some. Tetanus is a constant risk because horses are very susceptible, and every horse should have vaccine protection; rabies must be considered in any horse with unexplained neurological signs, and handled with personal protection.
African horse sickness (AHS) is a non-contagious, insect-borne viral disease of equids caused by an orbivirus (family Reoviridae in older texts; the orbiviruses are now placed in the family Sedoreoviridae). Nine serotypes are recognised. The virus is transmitted biologically by biting midges of the genus Culicoides, with Culicoides imicola the principal vector in Africa; the virus replicates in the midge. Horses are the most susceptible species, mules less so, donkeys largely resistant, and zebras are infected without signs and are considered the natural reservoir hosts.
AHS is endemic in sub-Saharan Africa. It has caused major epidemics outside Africa, in Spain and Portugal between 1987 and 1990, and in Thailand in 2020. Transmission is seasonal, peaking in warm, wet conditions when midges are abundant, and midges are most active at dusk and dawn. AHS is WOAH-listed, and it is one of the diseases for which WOAH officially recognises country freedom, which directly controls international horse movement.
Four clinical forms are described. The pulmonary (peracute) form causes high fever, severe respiratory distress, spasmodic coughing and frothy fluid from the nostrils, with death often within hours of the onset of dyspnoea; mortality in fully susceptible horses is very high, commonly quoted as above 95%. The cardiac (subacute) form causes fever followed by oedema of the supraorbital fossae, eyelids, head and neck, with haemorrhages under the tongue; mortality is lower but still substantial. The mixed form, with both pulmonary and cardiac signs, is the commonest at necropsy. Horse sickness fever is the mildest form, with fever and little else; it is seen in partially immune horses, donkeys and zebras.
Differential diagnoses include equine encephalosis (another Culicoides-borne orbivirus, usually milder), equine viral arteritis, EIA, piroplasmosis, purpura haemorrhagica and anthrax. Laboratory confirmation is by virus detection with real-time RT-PCR, virus isolation, and serotyping, and by serology.
In endemic areas horses are protected by vaccination and by reducing midge exposure. Live attenuated polyvalent vaccines are used in southern Africa, given in more than one combination so that all serotypes are covered; they are not used in free countries except under official emergency control, because vaccinated animals complicate proof of freedom. Midge exposure is reduced by stabling horses from before dusk until after dawn in insect-proofed stables and by repellents. In an incursion into a free country, control follows the national contingency plan: confirmation, notification to WOAH, a standstill on equid movements, control and surveillance zones, vector control, and emergency vaccination with a serotype-matched vaccine.
Everyday biosecurity prevents infectious agents entering a population and spreading within it. For a yard, stud or clinic the core measures are: know every horse's vaccination and health status; isolate new arrivals, commonly for about three weeks, with temperature monitoring and, where appropriate, strangles serology; keep an isolation area with separate staff or strict order of work; take temperatures twice daily in an outbreak, because fever often precedes other signs; do not share water, tack or transport between groups; control insects and ticks; and clean before disinfecting, because organic matter inactivates most disinfectants. Veterinarians must report notifiable diseases; the list differs by country.
Horses have hypsodont teeth: long-crowned teeth with a large reserve crown embedded in the jaw that erupts continuously throughout life at a rate commonly given as about 2 to 3 mm per year, while the occlusal surface wears at a similar rate. The occlusal surface is a grinding table of enamel folds, dentine and cementum, and the incisors contain an infundibulum (the 'cup'). The permanent dental formula is incisors 3/3, canines 0-1/0-1, premolars 3-4/3 and molars 3/3 on each side, so an adult has 36 to 44 teeth. Canines are usually present in males and absent or small in most mares, and the first premolar, the 'wolf tooth', is a small vestigial tooth present in some horses, mainly in the upper jaw.
The modified Triadan system numbers every tooth with three digits. The first digit is the quadrant: 1 upper right, 2 upper left, 3 lower left, 4 lower right, and 5 to 8 for deciduous teeth in the same order. The next two digits count from the midline: 01 to 03 incisors, 04 the canine, 05 the wolf tooth, and 06 to 11 the cheek teeth (06 to 08 premolars, 09 to 11 molars). So 109 is the upper right first molar.
The upper jaw is wider than the lower (anisognathism), and chewing is a side-to-side grinding stroke, so sharp enamel points develop on the buccal (cheek) edge of the upper cheek teeth and the lingual (tongue) edge of the lower cheek teeth, where they ulcerate the cheek and tongue.
The deciduous central incisors erupt in the first week of life, the intermediates at about four to six weeks and the corners at about six to nine months. The permanent incisors replace them at about 2.5 years (centrals), 3.5 years (intermediates) and 4.5 years (corners), so a horse with a full permanent incisor arcade in wear is at least about five years old. Canines erupt at about four to five years. After that, estimates rely on the disappearance of cups, the appearance of the dental star (secondary dentine filling the pulp cavity), the shape of the occlusal surface changing from oval to round to triangular, the angle of the incisors becoming more sloping, a hook on the upper corner incisor often seen around seven years and again later, and Galvayne's groove on the labial surface of the upper corner incisor, which appears at the gum line at about ten years, reaches halfway at about 15, reaches the table at about 20 and grows out by about 30. All of these signs after five years vary with breed, diet and individual, so age estimates in older horses should be given as a range and not stated as fact in a legal or sale context.
Signs include quidding (dropping partly chewed food), weight loss, long fibre in faeces, bit resistance, halitosis and nasal discharge. The oral examination needs sedation, a full-mouth speculum, good light, a dental mirror or oral endoscope, and rinsing of the mouth. Every tooth is examined and charted using the Triadan numbers, including periodontal pockets and diastemata (gaps between teeth) packed with food.
Routine care corrects sharp points, hooks, ramps, and overgrowths that limit lateral or rostrocaudal jaw movement, by rasping with hand or motorised instruments. Motorised instruments can overheat the tooth and expose pulp if used carelessly, so reduction should be limited and water cooling used. Who may perform dental procedures differs by country: in some, non-veterinary equine dental technicians may do defined routine tasks while extractions and procedures needing sedation remain veterinary acts.
Periodontal disease, usually starting at a diastema where food packs between cheek teeth, is among the most painful dental disorders of the horse and is managed by removing food, widening or treating the diastema, and correcting the underlying overgrowth. Apical (root) infection of the upper cheek teeth whose reserve crowns lie within the maxillary sinuses, mainly 08 or 09 to 11, causes secondary sinusitis with a unilateral foul-smelling nasal discharge; apical infection of lower cheek teeth causes mandibular swelling and draining tracts. Diagnosis combines oral examination, radiography with oblique views, and ideally CT. Infected teeth are extracted, preferably orally in the standing sedated horse.
Equine odontoclastic tooth resorption and hypercementosis (EOTRH) is a painful disease of the incisors and canines of older horses, with gingivitis, draining tracts and bulbous cementum over the roots; affected teeth are extracted, and horses usually eat well afterwards. Poor teeth in old horses and donkeys predispose to weight loss, impaction colic and choke.
The mare is a seasonally polyoestrous long-day breeder. Increasing day length in spring reduces melatonin secretion by the pineal gland, which releases GnRH secretion and restarts cyclicity. The year includes a winter anoestrus, a spring transitional phase with several waves of anovulatory follicles and irregular, often prolonged oestrus behaviour, the ovulatory season, and an autumn transition.
The oestrous cycle averages about 21 days, with oestrus lasting about five to seven days and dioestrus about 14 to 15 days. Ovulation occurs in the last 24 to 48 hours of oestrus, and only through the ovulation fossa, because the equine ovary is inverted. The pre-ovulatory follicle usually reaches about 35 mm or more, with breed variation. During oestrus, oestrogen produces endometrial oedema visible on ultrasound as a 'cartwheel' pattern that fades shortly before ovulation. The corpus luteum becomes responsive to prostaglandin F2-alpha from about five to six days after ovulation; luteolysis at the end of dioestrus is caused by endometrial prostaglandin release.
Artificial lighting advances the breeding season: a total of about 16 hours of light a day, started around 60 to 90 days before the desired first ovulation (commonly from about 1 December in the northern hemisphere), brings mares out of anoestrus earlier. Progestagens such as altrenogest suppress oestrus and are used to synchronise mares and to shorten the transitional phase once follicles are developing. Prostaglandin F2-alpha or its analogues given to a mare with a mature corpus luteum ends dioestrus early ('short-cycling'). Ovulation is induced with human chorionic gonadotrophin or a GnRH agonist such as deslorelin once a suitable follicle and endometrial oedema are present, and ovulation usually follows in about 36 to 48 hours; this allows a single, well-timed cover or insemination. No hormone doses are given here; products differ by country.
Gestation averages about 340 days, with a normal range of roughly 320 to 365 days or more; it is longer for colt foals, in some breeds and for mares foaling early in the year. The equine conceptus stays spherical and mobile, moving through the uterus until about day 16 to 17, and this mobility is part of maternal recognition of pregnancy by preventing luteolysis. It then becomes fixed, usually at the base of a uterine horn. Transrectal ultrasound can detect the conceptus from about day 10 to 12 and is routinely done at about day 14 to 16, when twins are still mobile and can be separated and one crushed manually. Twins are a major cause of abortion.
Endometrial cups, formed by invading trophoblast cells at about days 35 to 40, secrete equine chorionic gonadotrophin (eCG) until about days 100 to 150; if a mare loses a pregnancy after the cups form, she often will not return to normal cycling until they regress. Late pregnancy is monitored for ascending placentitis, which begins at the cervical star and causes premature udder development and vulvar discharge; transrectal ultrasound measurement of the combined thickness of the uterus and placenta against gestational-age reference values helps detect it. Other causes of abortion include EHV-1, equine viral arteritis, twins and umbilical cord torsion.
A rise in mammary secretion calcium helps predict foaling. Stage one (positioning of the foal, restlessness, sweating) lasts about one to four hours. Stage two, from rupture of the chorioallantois to delivery, is rapid and forceful, normally completed in about 20 to 30 minutes; any delay beyond that is an emergency because the foal's placental oxygen supply fails quickly. Stage three, expulsion of the placenta, is normally within about three hours, and a placenta retained longer is treated promptly (commonly with oxytocin) because mares with retained fetal membranes can develop metritis, endotoxaemia and laminitis. Check every placenta for completeness. A 'red bag' delivery, in which the red velvety chorioallantois appears at the vulva without rupturing, means premature placental separation and must be opened immediately.
Dystocia in the mare is less common than in cattle but more urgent. Options run from assisted vaginal delivery to controlled delivery under general anaesthesia, fetotomy and caesarean section. Foal heat, the first postpartum oestrus, occurs at about 5 to 12 days after foaling and may be used for breeding, although pregnancy rates are sometimes lower. Uterine artery haemorrhage in older mares is a postpartum emergency.
Persistent breeding-induced endometritis is the most important cause of subfertility in older mares. All mares have a short inflammatory response to semen, but susceptible mares, often with poor perineal conformation or impaired uterine clearance, fail to clear fluid and inflammation. Diagnosis uses ultrasound to detect intrauterine fluid after breeding, and endometrial cytology and culture; treatment includes uterine lavage and ecbolic drugs such as oxytocin after breeding. Poor vulvar conformation causes pneumovagina and is corrected by vulvoplasty (Caslick's operation), which must be opened before foaling. Endometrial biopsy is graded by the Kenney-Doig system into categories I, IIA, IIB and III with falling expected foaling rates. Contagious equine metritis, caused by Taylorella equigenitalis, is a venereal disease that is notifiable in many countries; carriers are detected by swabbing the clitoral fossa and sinuses of mares and the urethra, urethral fossa and penile sheath of stallions.
Stallion breeding soundness examination covers libido and mating ability, the external genitalia and testes, and semen: volume, gel-free volume, sperm concentration, progressive motility and morphology. Artificial insemination with fresh, cooled or frozen semen is allowed in many breeds, but the Thoroughbred studbooks require natural cover.
The foal is born precocious. A widely taught rule of thumb is 1-2-3: the foal should stand within about one hour, suck within about two hours, and the mare should pass the placenta within about three hours. Meconium is usually passed within the first hours; straining and tail swishing in a foal that has not passed it suggest impaction. A full udder with dried milk on the mare's teats is an early sign that the foal is not nursing. Use neonatal, not adult, reference ranges for vital signs.
The epitheliochorial placenta does not transfer antibody, so the foal depends on colostrum. Specialised enterocytes absorb intact immunoglobulin for only about the first 24 hours ('gut closure'), with efficiency falling from a few hours after birth. Failure of transfer of passive immunity (FTPI) is the commonest predisposing factor for neonatal sepsis. Serum IgG is measured at about 12 to 24 hours; widely used thresholds are below 400 mg/dL (4 g/L) as failure, 400 to 800 mg/dL as partial failure, and above 800 mg/dL (8 g/L) as adequate. Causes include premature lactation, poor colostrum, a weak foal and rejection by the mare. Before about 12 to 18 hours of age good colostrum can be given by bottle or nasogastric tube; after gut closure, equine plasma is given intravenously and IgG rechecked.
Sepsis is the leading cause of death in foals in the first week. Bacteria enter through the gut, umbilicus or respiratory tract, and Gram-negative organisms such as Escherichia coli, Actinobacillus, Klebsiella and Salmonella are common, with Gram-positive organisms also important. Early signs are vague: reduced suck, lethargy, injected mucous membranes, and later fever or hypothermia, diarrhoea, uveitis, joint swelling (septic arthritis) and shock. Treatment is broad-spectrum bactericidal antimicrobials, fluids, nutrition, plasma and nursing care; septic joints need lavage.
Neonatal maladjustment syndrome, also called neonatal encephalopathy or hypoxic-ischaemic encephalopathy, produces the 'dummy foal': a foal that loses its affinity for the mare, wanders, has an abnormal or absent suck, may vocalise abnormally ('barker') and may have seizures. Perinatal hypoxia is one cause; persistence of fetal neurosteroids is another proposed mechanism. Most foals recover with supportive nursing, nutrition and seizure control.
Neonatal isoerythrolysis is haemolytic anaemia caused by maternal alloantibody against foal red-cell antigens, most importantly Aa and Qa, that the mare lacks and the foal inherits from the stallion. The mare is sensitised by previous pregnancies or blood transfusion, so it occurs in multiparous mares, and mule foals are at particular risk because of the donkey red-cell antigen. The foal is normal at birth and becomes weak, jaundiced and tachycardic after nursing, usually within the first one to several days. Prevention in at-risk pairs uses a jaundiced foal agglutination test or crossmatch of mare colostrum or serum against the foal's red cells before the first suck; if positive, the foal is muzzled and fed alternative colostrum for about the first 24 to 36 hours.
Uroperitoneum from a ruptured bladder, more common in colt foals, causes progressive abdominal distension, straining to urinate, and at a few days of age the classic electrolyte pattern of hyponatraemia, hypochloraemia and hyperkalaemia; a peritoneal fluid creatinine of at least twice the serum creatinine confirms it, and the bladder is repaired surgically after the hyperkalaemia is corrected, because hyperkalaemia is dangerous under anaesthesia. Lethal white foal syndrome in foals of two frame overo Paint horses is an inherited absence of enteric ganglia (an endothelin receptor B mutation), fatal from colic in the first days, and prevented by genetic testing of the parents.
Foal heat diarrhoea is mild and self-limiting. Infectious diarrhoea in young foals includes rotavirus, Clostridium perfringens and Clostridioides difficile, Salmonella and Cryptosporidium; weanlings develop Lawsonia intracellularis proliferative enteropathy with hypoproteinaemia and ventral oedema.
Rhodococcus equi pneumonia is a disease of foals roughly one to six months old, acquired from inhaled soil dust on endemic farms. It produces pyogranulomatous bronchopneumonia with pulmonary abscesses, often with surprisingly mild signs until lesions are large. Virulent strains carry the vapA gene on a plasmid. Farms use thoracic ultrasound screening to find subclinical abscesses; confirmation is by culture and PCR of a tracheal aspirate. Treatment is traditionally a macrolide combined with rifampicin, but mass treatment of small subclinical lesions has selected for resistance, and many subclinical lesions resolve without treatment, so current advice is to treat foals with clinical signs or larger lesions.
The common causes are musculoskeletal pain, upper and lower respiratory disease, cardiac disease, muscle disease, and behavioural or management problems, and many horses have more than one. The work-up combines lameness and back examination, resting and exercising endoscopy, bronchoalveolar lavage, resting and exercising electrocardiography and echocardiography, blood tests including muscle enzymes, and a ridden examination.
In the heart, second-degree atrioventricular block at rest is a normal finding in many fit horses because of high vagal tone and disappears with exercise. Atrial fibrillation is the most common clinically important arrhythmia in performance horses; it causes a sudden drop in performance in racehorses while many lower-level horses show little at rest, and it can often be converted to sinus rhythm pharmacologically or by transvenous electrical cardioversion.
Exertional rhabdomyolysis ('tying up') causes stiffness, sweating, reluctance to move and firm, painful muscles, with raised creatine kinase and aspartate aminotransferase, and in severe cases myoglobinuria and acute kidney injury. It may be sporadic, from overexertion, or recurrent. Recurrent exertional rhabdomyolysis is common in nervous young Thoroughbred fillies and relates to abnormal calcium regulation in muscle. Polysaccharide storage myopathy type 1 is caused by a dominant mutation in the glycogen synthase 1 (GYS1) gene and is common in Quarter Horses and related breeds and in some draught breeds; it is managed with regular exercise and a diet low in starch and sugar with fat as the energy source.
Endurance horses risk the exhausted horse syndrome: dehydration, electrolyte loss, heat stress, synchronous diaphragmatic flutter (a 'hiccup' synchronous with the heartbeat, associated with low ionised calcium and alkalosis), colic and rhabdomyolysis.
A prepurchase examination (the 'vetting') is an examination of a horse on behalf of a prospective buyer. Its purpose is to identify clinical findings and give an opinion on whether they are likely to affect the horse's use for the purpose the buyer intends. It is not a guarantee of future soundness, and it cannot detect every condition. In the United Kingdom and Ireland the examination is traditionally done in five stages: a preliminary examination at rest including eyes, heart, lungs, teeth and limbs; walk and trot in hand, including turning, backing and, if agreed, flexion tests; a period of strenuous exercise to assess wind and heart; a period of rest and re-examination; and a second trot-up and examination of the feet. A blood sample is commonly taken and stored so that it can later be tested for substances that might have masked a problem.
In North America the AAEP guidance emphasises that the veterinarian reports findings and their potential significance, and does not 'pass' or 'fail' the horse or give an opinion on value; the buyer makes the decision. Good practice everywhere is to confirm the horse's identity (microchip and markings against the passport or registration papers), avoid a conflict of interest when the vet also acts for the seller, and record everything, because prepurchase examinations are a common source of legal claims.
Medication control protects horse welfare and fair competition. Rules are set by the sport's governing body: the FEI for international equestrian sport, and national racing authorities (whose standards are coordinated internationally through the International Federation of Horseracing Authorities) for racing. The FEI Equine Prohibited Substances List divides substances into Banned Substances, which have no legitimate use in the competition horse and must never be present, and Controlled Medication substances, which have therapeutic uses but must not be present during competition. Racing rules in most jurisdictions work on a similar principle of no prohibited substance on race day, with published screening limits or detection times for common therapeutic drugs.
A detection time is the time after a stated dose at which a drug was no longer detected in a group of experimental horses; it is not a withdrawal time. A practitioner must add a safety margin for individual variation, dose, route, formulation and repeated dosing, and is responsible for advising the owner or trainer accordingly. The person responsible for the horse is liable for a positive sample.
In many countries the horse is legally a food-producing species. In the European Union and the United Kingdom every equid must have a lifetime identification document (passport) linked to a microchip, and the document records whether the animal is intended for slaughter for human consumption. A horse that receives a medicine not permitted in food-producing animals, such as phenylbutazone, must be declared permanently excluded from the food chain in its passport, and a declaration once made cannot be reversed. For horses that remain in the food chain, only authorised substances may be used, with their withdrawal periods; a list of substances considered essential for equine treatment may be used with a statutory withdrawal period (six months under current EU rules), recorded in the passport. Rules differ elsewhere: in the United States horses are not currently slaughtered for food domestically but are exported for slaughter, and many drugs routinely used in horses carry label statements prohibiting use in horses intended for food. The practitioner must know the local rule, check the horse's status before treating, and record treatments as the law requires.
Animal welfare describes the state of the animal as it experiences it. The Five Freedoms (from hunger and thirst; discomfort; pain, injury and disease; fear and distress; and freedom to express normal behaviour) remain the basis of much law and policy. The Five Domains model (nutrition, physical environment, health, behavioural interactions, and the resulting mental state) adds the idea that animals should have positive experiences, not merely an absence of suffering. Welfare protocols combine animal-based indicators (body condition, lameness, wounds, behaviour) with resource-based ones (water, shelter, space).
Body condition is scored on a 1 to 9 scale (the Henneke system) or a 0 to 5 scale (common in the UK and Europe); donkeys have their own scale because they store fat differently, in the neck crest, over the ribs and at the rump. Pain is assessed with composite scales and the Horse Grimace Scale, which scores stiffly backward ears, orbital tightening, tension above the eye, strained chewing muscles, strained mouth and chin, and strained nostrils.
Welfare problems arise when management denies social contact, forage and movement. Stereotypies are repetitive, invariant behaviours with no obvious function, such as crib-biting and wind-sucking, weaving and box-walking. They are associated with restricted forage, early abrupt weaning, social isolation and confinement. Physical prevention, such as anti-crib-biting collars or anti-weave grilles, stops the behaviour without addressing its cause and may increase stress, so the aim is to improve the environment: more forage, turnout, companionship and visual contact.
Obesity and equine metabolic syndrome are now the commonest nutritional welfare problems in leisure horses and ponies in many high-income countries, with laminitis as their painful consequence. Hyperlipaemia in donkeys, ponies and miniature horses follows a period of reduced food intake, stress or illness, especially in obese or pregnant animals, and has a high mortality; any inappetent donkey should have its triglycerides checked.
Most of the world's horses, donkeys and mules work: carrying goods, water and people, pulling carts, ploughing, and in brick kilns and tourism. Their owners are often poor, and the animal's health directly affects household income. Common problems are harness and saddle wounds, lameness, overloading, poor hoof care, dehydration and heat stress, and dental disease, together with endemic infectious diseases such as glanders, trypanosomosis, piroplasmosis and tetanus. Improvement comes from working with owners, farriers and harness makers on water, shade, harness and affordable care, not from condemning owners. The WOAH Terrestrial Animal Health Code includes a chapter on the welfare of working equids.
Euthanasia is a veterinary duty when suffering cannot be relieved. Acceptable methods for horses include an intravenous overdose of a barbiturate, usually after sedation and through a jugular catheter, and in trained hands a free bullet or penetrating captive bolt, followed where needed by pithing or exsanguination; the rules vary by country. Before euthanasia confirm consent and ownership and whether the horse is insured, and plan disposal: carcasses containing barbiturate are toxic to scavenging wildlife and dogs and must not enter the food chain. Death is confirmed by the absence of heartbeat, respiration and corneal reflex.
A student must be able to take a history and perform a safe physical examination of a horse, including heart rate, mucous membranes, gut sounds and digital pulses, and to pass a nasogastric tube. Learn the AAEP lameness grades and the order of the distal limb blocks, the Triadan numbering and the eruption times of the incisors, the 1-2-3 rule of the foal and the IgG thresholds, and the causes, vectors and diagnostic tests of glanders, EIA and AHS. Practise charting teeth and describing a lameness in words on real horses. OSCE stations test restraint, twitching, jugular injection and trot-up handling, so learn safe positioning around the horse.
At five years in equine practice the daily decisions are colic triage by telephone and at the stable, when to refer for surgery and how to explain cost and prognosis; systematic lameness work-ups with blocks, radiographs and ultrasound; routine dentistry and vaccination schedules; stud work including follicle scanning, ovulation induction, twin management and foaling emergencies; the first 24 hours of the foal including IgG testing; and prepurchase examinations written in careful language. The practitioner also handles competition medication advice and passport declarations before giving drugs.
A senior clinician with 25 years' experience leads a practice or hospital: sets biosecurity and isolation protocols, runs strangles and EHV-1 outbreak responses with owners and event organisers, mentors younger vets in lameness and colic decisions, and acts as an expert witness in prepurchase and negligence disputes. Such vets advise sport bodies and racing authorities on medication rules and welfare, work with government services on notifiable disease reporting, and in many regions build services for working equid owners in partnership with non-governmental organisations.
A PhD researcher with long clinical experience asks the unanswered questions: the pathogenesis of laminitis and its endocrine triggers, the immunology of strangles carriage and better vaccines, why EHV-1 becomes neurological, the genetics of recurrent laryngeal neuropathy and osteochondrosis, antimicrobial resistance in Rhodococcus equi, objective gait analysis with wearable sensors, and the epidemiology of racing fatalities. Such a researcher also designs surveillance for glanders, EIA and AHS, validates diagnostic tests for trade, and contributes to WOAH and FEI technical committees.
This manual gives only one drug dose (flunixin meglumine), because approvals, dose rates and withdrawal periods for equine drugs differ by country and by the horse's food-chain status; use the national formulary. It does not give numerical reference ranges for foal vital signs, peritoneal fluid cell counts, bronchoalveolar lavage thresholds for mild asthma, combined thickness of uterus and placenta, or mammary calcium values, since sources differ. Hendra virus (Australia), trypanosomosis (surra and dourine), equine protozoal myeloencephalitis, PPID diagnostics, ophthalmology, dermatology, anaesthesia technique, fracture repair and hoof surgery are mentioned briefly or not at all and belong to other subjects or a later edition. Vaccination and competition rules change often; check the current FEI and racing rule books. Survival and prevalence percentages are omitted because published figures vary widely between hospitals and countries.
Original practice questions written to the syllabus and pattern of the exams named in each question's examTags. They are not past papers and do not reproduce any board's questions.
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