Equine medicine accounts for roughly 14.7% of NAVLE questions—the third-largest species block after canine and feline. That is about 53 questions in a 360-question exam. You cannot afford to skip large animal, but you also do not need to become a specialist. You need to know the high-yield conditions cold: respiratory, metabolic, GI emergencies, and reproduction.
Equine Respiratory Disease
Recurrent Airway Obstruction (RAO / Heaves)
RAO is equine asthma. Exposure to hay dust, mold, and endotoxins triggers airway hyperreactivity in susceptible horses. The classic patient is a stabled horse fed dry hay in a poorly ventilated barn.
Clinical signs progress over time: a dry chronic cough first, then exercise intolerance, then at-rest respiratory effort. The heave line—a visible muscular ridge along the ventral abdomen from hypertrophy of the external abdominal oblique—develops from chronic forced expiration. Horses with severe RAO breathe with nostril flare at rest and use an exaggerated abdominal push to exhale.
Diagnosis: bronchoalveolar lavage (BAL) cytology showing >20% mast cells or >25% neutrophils confirms neutrophilic airway inflammation. Endoscopy shows mucus accumulation in the trachea.
Treatment priorities: (1) environmental management first—hay soaking, pelleted feed, turn-out to pasture; (2) systemic dexamethasone 0.05–0.1 mg/kg SID for acute flares; (3) inhaled bronchodilators (albuterol via equine mask) and inhaled fluticasone for long-term management. Environmental change without medication is often insufficient for established cases.
Strangles (Streptococcus equi subsp. equi)
Strangles is one of the most contagious equine respiratory diseases. The classic presentation: fever >40°C, bilateral mucopurulent nasal discharge, and firm painful enlargement of the submandibular and retropharyngeal lymph nodes that eventually abscess and rupture.
The pathogen, Streptococcus equi subsp. equi, spreads via direct contact and fomites. Infected horses shed the organism nasally for weeks, including during the convalescent phase. The "drip line" effect—areas of pasture contaminated by nasal discharge—persists for weeks.
Treatment: penicillin G is effective; however, timing is controversial—treating during the abscess maturation phase may delay drainage and prolong disease. Most clinicians treat severe cases or those with complications. Vaccination: modified-live intranasal vaccine available; do NOT vaccinate horses with high SeM titers or recent infection (risk of triggering purpura).
Equine Herpesvirus (EHV)
Four clinically important strains:
- EHV-1: abortion storms (no maternal prodrome), respiratory disease in foals and young horses, and myeloencephalopathy (EHM)
- EHV-4: primarily respiratory disease; rarely causes abortion
- EHV-3: coital exanthema—vesicular lesions on genitalia; transmitted venereally
- EHM (EHV-1 neuropathogenic): hindlimb ataxia, urinary incontinence, recumbency; quarantine critical; vaccination does NOT prevent EHM but reduces viral shedding
Equine Metabolic Conditions
Equine Metabolic Syndrome (EMS)
Who: Ponies, Morgans, Paso Finos, easy-keeper breeds
Mechanism: Insulin dysregulation + obesity → hyperinsulinemia → lamellar damage
Signs: Cresty neck, supraorbital fat pads, regional adiposity, recurrent laminitis
Diagnosis: Resting insulin >20 μIU/mL; oral sugar test
Treatment: Low-NSC hay (<10%), weight loss, exercise; levothyroxine short-term
PPID (Equine Cushing’s)
Who: Horses >15 years; all breeds
Mechanism: Loss of dopaminergic inhibition of pars intermedia → ACTH overproduction
Pathognomonic: Hypertrichosis (long curly coat that won’t shed)
Diagnosis: Resting plasma ACTH >35 pg/mL (non-autumn); TRH stimulation test
Treatment: Pergolide mesylate (Prascend) — dopamine agonist; lifelong
Hyperlipemia
Ponies and donkeys are the most susceptible species. Negative energy balance—from illness, pregnancy, stress, or feed restriction—triggers massive fatty acid mobilization. The liver cannot process the lipid load and hepatic lipidosis follows.
Diagnosis: grossly lipemic serum (visible white cloudiness); plasma triglycerides >500 mg/dL. Treatment: glucose supplementation (IV dextrose, nasogastric feeding with simple carbohydrates), insulin, and correction of the primary cause. Prognosis is guarded once overt hyperlipemia is established.
Equine Reproduction
The mare has a 21-day estrous cycle with a 5–7 day estrus period. Ovulation occurs 24–48 hours before the end of estrus. Mares are long-day seasonally polyestrous—cycling during increasing photoperiod (spring/summer), with a winter anestrus.
Caslick’s vulvoplasty: Poor perineal conformation in mares allows air aspiration into the vagina (pneumovagina → ascending contamination → endometritis → subfertility). Caslick’s procedure: suture the dorsal vulvar lips to create a seal. The episiotomy must be performed before foaling.
Dystocia in mares: Normal equine delivery is rapid—active second stage labor should be <30 minutes. Any deviation = emergency. The most common cause is carpal flexion (front limb with flexed knee). Correction: repulsion + extension of the limb.
Endometritis: Most common cause of subfertility in mares. Culture + cytology via uterine swab. Gram-negative organisms (E. coli, Klebsiella, Pseudomonas) and Streptococcus equi subsp. zooepidemicus most common. Treatment: uterine lavage, intrauterine antibiotics, PGF2α for luteal regression if needed.
Equine Infectious Diseases
Equine Protozoal Myeloencephalitis (EPM)
Caused by Sarcocystis neurona. The opossum is the definitive host—horses are dead-end hosts that become infected by ingesting opossum feces-contaminated feed or water. Classic presentation: asymmetric ataxia and weakness (the asymmetry distinguishes it from EHV myelopathy, which tends to be symmetric).
Diagnosis: CSF or serum immunoblot for S. neurona antibodies; serum:CSF titer ratio helps distinguish true CNS infection from seroconversion without disease. Treatment: ponazuril 5 mg/kg PO SID for 28 days or diclazuril.
West Nile Virus
Flavivirus transmitted by Culex mosquitoes. Horses are dead-end hosts (cannot infect mosquitoes). Presents as encephalomyelitis: hindlimb weakness and ataxia, cranial nerve deficits, somnolence, fever. Can be clinically indistinguishable from EPM. Serology (IgM ELISA) is diagnostic. Annual vaccination is highly effective and strongly recommended.
Tetanus
Horses are the most susceptible domestic species to tetanus toxin. Clostridium tetani produces tetanospasmin (blocks inhibitory neurotransmitter release → spastic paralysis). Classic signs: third eyelid prolapse (nictitating membrane elevation), trismus (lockjaw), sawhorse stance, hypersensitivity to stimuli, risus sardonicus. Treatment: penicillin G, tetanus antitoxin, muscle relaxants (acepromazine, methocarbamol), dark quiet stall. Mortality is high even with treatment. Prevention: annual tetanus toxoid vaccination.
Equine Nutrition & GI
Choke (Esophageal Obstruction)
Horses cannot vomit—esophageal obstruction (choke) presents as feed material and saliva draining from the nostrils, neck extension, anxiety, and repeated swallowing attempts. Common triggers: dry hay bolus, sugar beet pulp, pelleted feed given dry. Treatment: sedation (xylazine 0.5 mg/kg IV), gentle lavage via nasogastric tube. Most cases resolve within 2–4 hours. Serious risk: aspiration pneumonia from material entering the trachea.
Selenium: Deficiency vs. Toxicity
Deficiency (White Muscle Disease): Nutritional myodegeneration in foals in selenium-deficient regions. Skeletal and cardiac muscle necrosis → weakness, stiffness, difficulty nursing. Treatment: selenium + vitamin E supplementation.
Toxicity (Alkali Disease / Blind Staggers): Chronic selenium toxicosis from seleniferous soils (Great Plains). Signs: hair loss (mane, tail), hoof abnormalities (coronary band lesions, hoof wall separation), lameness. Acute selenium toxicosis causes "blind staggers" (neurological signs). Selenium has one of the narrowest safe ranges of any mineral.