BOARD REVIEW: EQUINE MEDICINE

Allison Stewart BVSc(hons), Eduard Jose-Cunilleras DVM and Richard Pearcy BVSc, MACVS 2001

Below is a list of clinical presentations, if you have undergone the equine medicine rotation already, try to list the most likely differentials for each clinical sign. If you have not gone through our rotation, make the list as you read through the rest of the handout. Don’t forget the things that you may have seen on the ambulatory rotation, or in any of the other rotations or classes you have taken during the last four years. Medicine is medicine! Don’t get put off by the species! When you have reached the final page compare your list with mine.

Remember that we tend to see rare diseases here in the hospital - don’t forget that common things occur commonly when in practice and that you are more likely to be asked about one of these diseases than something unusual that often gets presented at OSU!

• coughing • chronic weight loss • spinal • dysphagia • jaundice • recumbent ‘flat’ neonatal foal • polydipsia • diarrhea • stiffness

When you have made your list and studied the rest of the handout, make sure in your own mind that you would be able to separate the diseases based on 1) signalment, 2) history, 3) clinical signs, 4) further diagnostic tests. Make sure that you know the appropriate action / treatment / owner advice for each of your differentials.

Feel free to contact me if you have any questions.

1 BOARD REVIEW: EQUINE MEDICINE Allison Stewart BVSc(hons) 2001

I. RESPIRATORY:

A. Viral: Most viral disease in is associated with high morbidity and low mortality. It is therefore of major economic importance to the racing and horse show industry.

1. Equine Influenza: Young horses, crowded conditions, incubation 1-3 days. Two different subtypes: A/Equi 1 and A/Equi 2; antigenic drift. Pyrexia (104F plus), depression, anorexia, serous nasal discharge, cough. Secondary bacterial infections.

Dx: Virus isolation via protected nasopharyngeal swabs; serology - acute and convalescent samples Vaccination: modified live intranasal vaccine has good efficacy. Killed intramuscular vaccine has very poor efficacy and requires vaccination every 3 to 4 months. Rx: antipyretic, stall rest +/- antibiotics to prevent secondary bacterial infection. Remember: severe major epizootics occur when a new subtype/strain enters new region / country (strict movement and vaccination regulations).

2. Equine Herpes Virus: EHV-1 (subtype 1): Abortigenic form, abortion occurs several weeks post-exposure; 9 to 11 months into gestation, mares often don't show clinical signs. Fetus is jaundiced, hepatic necrosis and pulmonary edema. For diagnosis need fetal liver and lung; see intranuclear inclusion bodies. Keep pregnant mares away from young horses, dispose (burn) placenta and bedding. Vaccination with killed vaccine at 3, 5, 7, 9 months gestation. Immunity short-lived. May also have a weak foal born, which dies with respiratory disease in a few days. Virus can also produce neurological disease (immune mediated vasculitis - virus has been found within the endothelium of blood vessels in the spinal cord (epitheliotropic, but recent reports suggest that it is also neurotropic), resulting in an ascending paralysis, urinary incontinence and decreased tail tone (see neuro section) +/- respiratory disease?

EHV-4 (subtype 2) Respiratory form: fever, anorexia, depression, cough, enlargement of submandibular / parotid lymph nodes. Young horses, incubation period 2 to 10 days, subclinical carriers and latent infections (trigeminal ganglion - recrudescence at times of stress?). Secondary bacterial infection possible. Vaccinate with modified live vaccine every 3 to 4 months, however most horses are carriers or are exposed from a very early age.

EHV-2 Equine cytomegalovirus: ubiquitous within the horse population, minimal clinical signs, chronic pharyngitis with lymphoid hyperplasia.

EHV-3 Coital exanthema, does not affect the reproductive capability of stallion or mare

3. Adenovirus:

2 Respiratory infection in foals with combined immunodeficiency syndrome (CID), (Arabian foals), otherwise thought to be a normal inhabitant of upper respiratory tract

4.Rhinovirus: Mild / subclinical infection - rest - probably not that important unless immunosuppressed.

5. Equine Viral Arteritis: A Toga virus, produces a vasculitis, damage to tunica media of small arteries and venules leading to thrombus formation and ischemic necrosis. Clinical signs include: pyrexia (104-106F) after an incubation period of 3 to 14 days, depression, anorexia, leukopenia, limb edema, conjunctivitis, rhinitis, periorbital and supraorbital edema. EVA can also cause abortion storms, mares may or may not show clinical signs, see abortions 3 to 10 months of gestation during or after febrile episode.

Stallions can be chronic carriers of EVA in semen rich portion of ejaculate, and then infect mares. The two most important routes of transmission are via respiratory route, and venereally. Diagnosis is made via virus isolation or serum-neutralizing antibody. All breeding TB stallions tested for EVA antibody if negative receive yearly vaccination.

B. Bacterial:

1. Streptococcus equi subspecies zooepidemicus Most common pathogen in equine respiratory disease. Gram positive cocci, sensitive to penicillin, resistant to aminoglycosides. Pneumonia, pleuropneumonia, neonatal septicemia. Can be a normal inhabitant of nasopharynx.

2. Actinobacillus equuli, A. suis Gram negative rod, variable sensitivity pattern. Pneumonia, peritonitis, pleuritis, abscessation in adult; neonatal septicemia in foals.

3. Streptococcus equi subspecies equi: Upper respiratory infection, Bastard strangles, Purpura hemorrhagica. “Strangles” refers to upper airway obstruction, generally high morbidity, low mortality. Gram positive cocci, sensitive to penicillin. Highly contagious, generally young horses, incubation period 6 to 21 days, abscessation of submandibular lymph & retropharyngeal lymph nodes; guttural pouch empyema (may have cranial nerve dysfunction e.g. dysphagia) from ruptured retropharyngeal lymph node. Chronic cases of empyema may lead to chondroid formation (inspisated pus) in which case surgery is often required.

Clinical signs: fever, cough, mucopurulent nasal discharge, swollen, painful lymph nodes, leukocytosis, hyperfibrinogenemia, hyperglobulinemia. May see dysphagia, dyspnea Treatment: hot pack, drainage, NSAIDs, penicillin, tracheotomy (if necessary). May remain infectious generally for 4 to 8 weeks following recovery. Long-term carrier state - months to up to a year. Culture of nasopharangeal swab or guttural pouch to determine carrier status. Vaccination yearly (best to use M - protein vaccine or intranasal vaccine), variable response, injection reactions.

Bastard strangles: abscessation throughout body lymph nodes, abdomen, lung, . Long-term penicillin (+/- rifampin)

Purpura hemorrhagica: an immune-mediated disease, Ag-Ab deposition in vessels, edema, skin sloughing, laminitis, death.

3 Diagnosis - clinical signs, petechiae/ ecchymoses, history of previous strangles. Treatment steroids, penicillin.

4. Rhodococcus equi Gram positive, pleomorphic rod, (intracellular). Variable pathogenicity associated with “Virulence Factor” (Vap-A plasmid). Organism is ubiquitous in the environment, but generally does not have the Vap-A plasmid. Foals 3 to 4 months of age, may see sudden onset. Bronchopneumonia, pulmonary abscessation, diarrhea, and abdominal abscessation. Diagnosis: history, clinical exam, radiographs, tracheal wash and ultrasound. Serology techniques have limited use in individual animals. Hyperfibrinogenemia is a good on-farm screening test. Treatment: (expensive) erythromycin & rifampin (lipid soluble, penetrate intracellular) until chest rads and fibrinogen normal. May take 3 to 4 months. Erythromycin can cause fatal colitis in adults and occasionally hyperthermia in foals treated in hot weather.

Prophylaxis - hyperimmune serum to foals at birth Remember: Farm problem, therefore outbreaks; organism survives in soil, spread in dust.

5. Pleuropneumonia Adult horses; associated with: 1. Stress, e.g. long distance transport 2. Inhalation pneumonia-esophageal obstruction (choke), pharyngeal paralysis/ dysphagia. 3. Bacteremia (esp. foals) 4. Penetrating chest wound Organisms: Streptococcus sp., Staphylococcus sp., Actinobacillus sp., Enterobacteriaceae (E.coli, Klebsiella, Proteus),Pseudomonas sp., Bordetella sp., Anaerobes (Bacteroides sp., Clostridia sp., Eubacterium and Fusobacterium sp.) and Mycoplasma felis. Clinical signs: fever, cough, dyspnea, fetid breath (anaerobes), reluctance to move, pectoral / sternal edema, laminitis. Chronic cases pleural friction rubs, extensive adhesion formation.

Diagnosis: clinical signs, lung auscultation and percussion, ultrasound, radiography, thoracocentesis, tracheal wash, hematology. Treatment: Penicillin, gentamicin, metronidazole (if bacteroides), thoracic drainage. Prognosis: guarded to good, treatment very expensive. Given time, many will do well.

C. Allergic:

Chronic Obstructive Pulmonary Disease (COPD): Heaves Pulmonary hypersensitivity (Types 1, 3, 4) to dust, fungal spores, pollens. Wide range of clinical signs, (mild to "crippling"), nasal discharge, cough, severe exercise intolerance, dyspnea, hypoxemia, cyanosis, heave line. Chronic disease often with acute exacerbations. Primary lesion is bronchiolitis, mucus plugging of airways, peribronchiolar fibrosis, alveolar emphysema with destruction of alveolar walls.

Diagnosis: auscultation may reveal expiratory wheezes, tracheal wash neutrophilic exudate (Remember - usually no or low numbers of eosinophils, otherwise very similar to feline asthma) +/- bacterial infection, (often Strep. zoo.) endoscopy yellow viscous exudate in trachea, radiographs peribronchial infiltrates, over- expanded lung fields, interstitial pattern. Bronchoalveolar lavage (BAL) may also be done, however good for cytology only (again mostly neutrophils), not for culture (pharyngeal contaminants). Skin test to identify allergens (don’t diagnose with serum testing). About half respond to hyposensitization vaccinations.

4 Treatment: change environment, get horse outside, wet down hay, feed from floor to encourage drainage; corticosteroids (dexamethasone, prednisone, prednisolone, beclomethasone, fluticasone), bronchodilators (B2-specific agonists [clenbuterol {Ventipulin}, albuterol, terbutaline {Brethine}, anticholinergics - antagonists of acetylcholine [atropine, glycopyrilate, ipatropium bromide{Atrovent}), methylxanthines – inhibitors of phosphodiesterase activity {theophylline}; antibiotics - SMZ/TMP. Inhalants – Ipatropium bromide {Atrovent} Albuterol and beclomethasone Sodium cromoglycate {Intal} (mast cell membrane stabilizer) –prophylaxis Great efficacy without systemic side-effects

D. Exercise Induced Pulmonary Hemorrhage:

Blood in the tracheobronchial tree following exercise / epistaxis. Scope horses 60 minutes after race or training (44 to 75% of horses bleed at some time in their career). Transtracheal wash several days later, hemosiderin-laden macrophages. Radiographs reveal interstitial pattern in caudodorsal lung fields. Recurrent problem for certain horses.

Pathogenesis: most of the evidence suggests that stress failure of pulmonary capillaries secondary to exercise-induced pulmonary hypertension is the reason for EIPH. Other theories include: small airway disease, upper airway obstruction, hemostatic abnormalities, intrathoracic sheer forces generated during running, bronchial artery angiogenesis.

Bleeding will affect race performance, but controversial if furosemide reduces the incidence of bleeding. Recently proven that Lasix (furosemide) improves race performance (possibly independent of effect on EIPH), so advantageous for horses to get pre-race furosemide.

II. GASTROINTESTINAL

A. Enterocolitis: 50% acute diarrhea cases remain undiagnosed, therefore often better to invest client’s money in treatment rather than diagnosis if finances are limited or at least warn them that you may not determine the etiology. Do consider the legal implications for your hospital or the barn in regards to not testing for Salmonella. (CYA)

1. Salmonella: Peracute; acute, & chronic diarrhea. Subclinical carriers, (shedders) 5-30% of horses (however shedders rarely excrete enough salmonella to infect another healthy adults, but problems with stressed, immunocompromised and foals). Over 2200 different serotypes, virulence varies (e.g. Salmonella typhimurium is very pathogenic)

Clinical signs range from severe endotoxemia, fever, depression, colic, tachycardia, severe neutropenia (< 2,500/l) with left shift, metabolic acidosis, hypoproteinemia, hyponatremia, hypokalemia, hypochloremia, cardiovascular collapse and coagulopathies (DIC). Diagnosis: cultures obtained 24 hours apart, Selenite green. PCR (too sensitive)

Treatment: supportive (IV or oral fluids and electrolytes), anti-endotoxin plasma ("Endoserum") or polymyxin B (binds endotoxin), flunixin meglumine (Banamine), +/- antibiotics (indicated if septicemic, neutropenic, dysentry or foal). If severe guarded prognosis shock, laminitis, necrotizing colitis, DIC, death). On occasions so severe that death occurs before onset of diarrhea (colitis on post mortem; ddx clostridia or “colitis X” (severe colitis of undetermined etiology)

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2. Potomac Horse Fever: Ehrlichia risticii (Equine Monocytic Erlichiosis) (USA only): Clinical signs: fever, anorexia, profuse watery diarrhea, laminitis, leukopenia in acute stages then leukocytosis. Intracellular organism resides in monocytes. Seasonal incidence (summer), transmitted by trematodes in water snails that infect mayflies that are subsequently ingested inadvertently by the horse). Diagnosis: Serology: IFA, classical rise in titer, buffy coat PCR or isolation from culture Treatment: supportive, I.V. oxytetracycline, Banamine. Often rapid response to antibiotics. Vaccination: killed vaccine, questionable efficacy only one of ~ ten serotypes, does not prevent disease, but may decrease clinical signs. Many horses successfully cured of colitis, but subsequently develop laminitis. Depression, fever, white blood cell abnormalities and subsequent laminitis can occur without signs of colitis – consider IFA serology if above signs are observed with no other explanation in endemic areas –esp. in vaccinated horse.

3. Antibiotic-Induced Diarrhea: Drugs: Trimethoprim-sulfa, I.V. Naxcel (ceftiofur), oxytetracycline, erythromycin, clindamycin, lincomycin (the last 3 should not be given to adult horses) Can be life threatening (Colitis X syndrome): have been reported associations with Salmonellosis and Clostridium difficile, but doesn't happen all of the time. Changes between antibiotics may be more important than any certain antibiotic. Diagnosis: fecal culture for Salmonella, C. difficile ELISA for toxin A Consider metronidazole for anaerobic overgrowth.

4. Clostridium perfringens / C. difficile (“one cause of Colitis X”) Severe life threatening peracute diarrhea. Treatment as for acute salmonellosis. ?metronidazole

5. Rotavirus Diarrhea: Signalment: Foal, newborn to a few months old. Clinical signs: watery to pasty diarrhea, decreased nursing, colic, high morbidity, low mortality. Fecal oral route of transmission, adults harbor infection. Stunting of villi decreases surface area, decreased absorption and digestion of disaccharides, leads to an osmotic diarrhea (supplemental lactade may be useful) Diagnosis: Latex agglutination tests for virus in feces, ELISA also available (Rotazyme II) Treatment: supportive, anti-ulcer meds (H2 blockers or proton pump inhibitors)

6. Chronic diarrhea Remember for diarrhea must have large intestine involvement. e.g. Chronic salmonellosis, lymphosarcoma, infiltrative bowel diseases, cyathostomiasis (can be acute when hypobiotic larvae erupt in spring). Also remember other less common causes e.g. liver disease, peritonitis.

7. Anterior enteritis Often acute onset. Moderate to severe colic or depression with small intestinal distension. Often slight fever at outset and variable leukopenia / endotoxemia. Colic and tachycardia are relieved following nasogastric decompression by refluxing the horse. (reflux may be brown or red tinged and often foul smelling). May be caused by salmonella or clostridia - ?culture reflux

DDX: small intestinal obstruction / strangulation Peritoneal tap variable results (elevated protein and/or high white cell count)

Treatment: frequent decompression of stomach (which would otherwise rupture); IV fluids; Banamine; endoserum? Antibiotics? Sometimes surgical decompression necessary.

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B. Ulcerative diseases:

1. Vesicular Stomatitis: Lyssa virus, (family Rhabdoviridae), three main strains; all three infect horses. Viral disease of horses, , swine, occasionally humans. In livestock see: vesicles and ulceration of teats, oral mucosa, tongue and coronary bands. In humans: influenza-like symptoms. High morbidity, low mortality. Virus transmitted by blackflies and sandflies. Outbreaks in the US have occurred in western states. Reportable disease: quarantine until clinical signs resolve. Only vesicular disease to effect horses.

2. Gastroduodenal ulcers: Suckling foals < 4 months of age, associated with stress & NSAID administration. Very common in racehorses (may be assymptomatic). Ulcers along margo plicatus, glandular mucosa, & proximal duodenum. Clinical signs in foals: bruxism, ptyalism, colic (dorsal recumbency), depression, anorexia occasionally diarrhea, sudden death with peritonitis in the case of perforating ulcer. In adults: mild intermittent colic, irritability, weight loss.

Sequela: Gastric rupture, fibrosis of pylorus or duodenum may cause gastric outflow obstruction & reflux. Diagnosis: Clinical signs, endoscopic exam. Treatment: H2 blockers, (cimetidine ranitidine), proton pump inhibitors (omeprazole), protectants (sucralfate)??? Decrease stress, turn out, constant roughage availability

3. NSAID toxicity: (especially phenylbutazone) Adult horses with history of high dose or prolonged NSAID therapy. Oral, gastric, colonic ulcers (right dorsal colon). Clinical signs: colic, hypoproteinemia, melena, +/- diarrhea, edema, renal failure (papillary necrosis) Diagnosis: History, clinical signs Treatment: anti-ulcers, +/- surgery large colon resection, low residue diet, omega 6 FA promote GI blood supply. Prevention better than cure. Be careful of appropriate dose that you prescribe, and inform clients of the dangers. Some horses

4. Granulomatous Enteritis: Malabsorption syndrome resulting from granulomatous infiltration of small intestine. Signalment: 2 to 3-year-old, often Standardbreds. Clinical signs: chronic weight loss, good/increased appetite, panhypoproteinemia, edema, rare to see diarrhea. Diagnosis: glucose or D-xylose absorption test, intestinal biopsy, rectal mucosal biopsy. Treatment: most of time none, small intestinal resection, medical therapy generally unsuccessful (steroids).

C. Colic: Remember that colic simply refers to abdominal pain, which may be mild to severe, acute or chronic. Generally in horses it relates to an abnormality of the GI tract, however other abdominal organs may be involved (kidneys, reproductive tract)

Remember basic principles when dealing with a case of colic: • 9/10 cases can be managed medically • parasitism, teeth problems, abrupt changes in management, feed, water may predispose • colic may be infectious (e.g. salmonella) - a CBC may be useful • always pass a nasogastric tube (horses with small intestinal distension often die from gastric rupture)

7 • if it is safe try to rectal horses with colic, unless the horse is too small. Use adequate restraint and plenty of lube. Sedate if necessary. Use ultrasound on small horses or foals. • rectal findings generally will fit into one of several categories: 1) normal 2) small intestinal distension (usually fluid) 3). large colon gas distension with or without displacement or torsion, which may be suggested by tight bands 4). large or small colon impactions (doughy mass). • increased gut sounds may indicate gas / spasmodic colic; decreased gut sounds may suggest ileus, strangulation, impaction. • relief of pain after gastric decompression is more indicative of anterior enteritis than a small intestinal strangulating lesion. • abdominocentesis can be useful to determine the integrity of the bowel, (but if you are going to refer the horse, please do not perform on the farm). • pelvic flexure impactions are seen commonly in practice and can frequently be treated with limited analgesics, laxatives and intravenous or ideally oral fluids. Gas colics can usually be treated with analgesics and withholding food for 12 hours. • continued or frequent analgesic drugs required to keep a horse pain free, or deteriorating vital signs are poor prognostic indicators and may suggest the need for referral and possible surgery. • IF IN DOUBT REFER THE CASE EARLY Don’t let the sun set on your colic. Two or more doses of Banamine is often one dose too many.

III. Liver Disease

Remember horse liver enzymes: GGT & ALP = cholestasis, GGT specific for biliary system, ALP biliary, bone, gastrointestinal ; AST (muscle and liver) & SDH specific for hepatocellular necrosis, but SDH short half life, difficult assay. Remember….ALT is not useful in large animals! Also remember tests of liver function - primarily bile acids (no pre and post as in small animals) and ammonia Bilirubin - breakdown product of hemoglobin; unconjugated (INDIRECT) bilirubin is transported bound to albumin and then taken up and conjugated by the liver (DIRECT). Note that horses are peculiar in that they respond to fasting by having an unconjugated hyperbilirubinemia (INDIRECT). Liver biopsy & ultrasound - perform clotting profiles first.

1. Theiler's Disease: "Acute hepatic failure" Causes: serum hepatitis 4 to 10 weeks after administration of biologic of equine origin (e.g. tetanus antitoxin) or can occur in other horses in the same location as those given equine origin biologics… current theory is that it is caused by a virus!

Clinical signs: depressed, CNS signs (head pressing, hepatoencephalopathy, circling, seizures, coma) spontaneous bleeding (poor prognostic sign), hypoglycemia, low BUN, elevated bilirubin, elevated AST, SDH, GGT, elevated clotting times (OSPT, APTT), acidosis, increased NH3, bile acids, hemoglobinuria (terminal). Treatment: supportive, dextrose, anti-seizure meds (diazepam, phenobarbital) can use neomycin & lactulose to acidify colon and decrease uptake of ammonia, low protein/high energy diet (beet pulp- high in branch chain amino acids- and cracked corn), antibiotics, fresh plasma. Prognosis: generally poor with hepatoencephalopathy.

2. Pyrrolizidine Alkaloids: Chronic Liver Failure

8 Plants: Crotolaria, Heliotropium, Amsinckia, & Senecio (Ragwort): prolonged ingestion Horses present with weight loss (chronic) or sometimes acute liver failure. Pyrrolizidine alkaloids are antimitotic and therefore cause hepatocellular swelling (hepatomegalocytes), death and fibrosis Clinical signs: anorexia, icterus, behavioral changes, hepatoencephalopathy, soft stool, colic, photosensitization of nonpigmented skin (phyloerythrin accumulation from chlorophyll, which is photoactive), rarely bilateral laryngeal paralysis increased GGT, AST, & SDH but may have no changes in chronic fibrotic disease.

3. Hyperlipemia: Signalment: ponies, donkeys, & minis (especially if fat & third trimester pregnancy, or parasitism) poor prognosis. Careful when limiting feed intake from fat ponies with laminitis or with-holding feed due to colic.

Clinical signs: anorexia triggered adipose mobilization leads to lipid accumulation in the blood liver & kidney, exacerbated by azotemia, depression, icterus, weakness, edema, muscle fasciculations, fetid breath, bleeding disorders, acidosis, & hypoglycemia, hyperlipemia (TRIG >500mg/dl) characteristic milky serum - easy instant test in practice; diarrhea. Can be life threatening: hepatic or renal failure This is in contrast to ketosis in ruminants (in horses triglycerides accumulate in negative energy balance instead of ketones)

Treatment: improve food intake (NG intubation) offer fresh grass, IV dextrose, IM insulin & oral glucose / galactose to decrease lipid mobilization, induction of abortion may be necessary. Administration of pharmaceuticals is controversial: nursing care and feeding is most important.

4. Tyzzer's Disease: Bacillus piliformis Signalment: foals up to 2 months. Clinical signs: sudden death, peracute icterus, toxemia, hepatoencephalopathy. Gram negative, spore-forming organism, does not grow in culture, but can be seen with silver stain within hepatic tissue. Rarely survive even with intensive therapy.

IV. NEUROLOGIC DISEASE:

A. Encephalitis: Eastern, Western & Venezuelan Etiologic agent: Alphavirus in the Togavirus family, horses & man dead end host (except Venezuelan). Horses more susceptible than man. Viral life style is sylvatic: waterfowl & rodents are reservoirs, mosquito is the vector. Clinical signs: fever, depression, circling, multiple cranial nerve signs, (cerebrum & brainstem signs), dementia, respiratory arrest. Rapid progression in 24 to 72 hours EEE is more severe and fatal, survivors have residual neurological deficits and are often "dummies". Therapy: supportive; Prevention: vaccination twice yearly before onset of mosquito season, vector control, Venezuelan is reportable. Vaccinate horses on the Mexico border.

West Nile Virus: See Preventive Med website for the latest info. New vaccine is recommended. Likey to be efficacious.

B. Rabies: Etiological agent: Rhabdovirus, transmitted by bite or wound contamination with infected saliva. Incubation period variable: 3 to 6 weeks. Death: usually 5 to 7 days once showing neurologic signs. Pathophysiology: migration through peripheral nerve to brain and spinal cord with migration from brain to cranial nerves then to salivary glands.

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Clinical signs: wide variety, can look like anything (may present as a , colic or choke!) most common is rear limb lameness & hypersthesia, skin mutilation & hyperexcitability, ataxia, paresis, hypersalivation, dysphagia, colic, paraphymosis, flaccid tail and anus, urinary incontinence. Diagnosis: IFA on brain tissue (gold standard), histopath Negri bodies (intracytoplasmic inclusion bodies in neurons). Prevention: vaccination (not 100%), quarantine bite victim for 6 months. Human health risk: remember to refer in contact humans to physicians for post-exposure vaccination, and keep your own titers high!!

C. Tetanus: Etiologic agent: Clostridium tetani, gram positive spore forming anaerobe replicating in a deep wound, incubation period 3 to 30 days. Pathophysiology: Exotoxin produced by bacteria: tetanospasmin prevents release of inhibitory neurotransmitter glycine in the spinal cord internuncial neurons of the ventral horn (Renshaw cells), brain/ sympathetic nervous system (stimulation). Recovered animals aren't immune because the amount of toxin needed to produce clinical signs in the horse isn't enough to produce antigenic stimulation. Horses are the most susceptible species.

Clinical signs: stiff gait, sawhorse stance, prolapsed nictitans, erect ear carriage, pump-handle tail, hyperreactivity. DDX: hypocalcemia (“hypocalcemic tetani”)

Treatment: wound debridement (anaerobic to aerobic environment), penicillin to prevent further bacterial growth, anti-toxin (massive doses, therefore expensive) to bind circulating toxin but won't bind toxin in CNS so intrathecal administration has been tried (questionable), tetanus toxoid, tranquilizers (valium, dantrolene) quiet and dark environment. Prevention: vaccinate annually, if wound occurs vaccinate again, unvaccinated horses should receive antitoxin and toxoid simultaneously. Ensure that every horse you examine is up to date for tetanus: cheap insurance. Treatment is usually unsuccessful)

D. Botulism: Etiologic agent: Clostridium botulinum gram positive spore forming anaerobic bacteria, produces a variety of neurotoxins depending on the type, name given to toxin i.e. type B vs. type C Type B most common in KY, OH, PEN, then type C. Type B antitoxin costs ~$400, while the multivalent costs ~$2000

Pathophysiology: toxin binds to the presynaptic neuron at the neuromuscular junction and prevents the release of acetylcholine, does not cross blood brain barrier. Horses extremely sensitive to toxin. Three forms described: wound botulism - relatively rare, forage poisoning (ingestion of preformed toxin, wilted grass silage, dead animal baled in hay or ground up in pelleted feed), and toxicoinfectious (ingestion of bacteria with proliferation of bacteria in GI tract and local production and absorption of toxin) Shaker foals: toxicoinfectious form most likely, weeks to months of age.

Clinical signs: weakness with muscle fasciculations, dysphagia, decreased tail, tongue and eyelid tone, decreased PLRs, respiratory difficulty, ileus & constipation (often present as a colic as they have progessive recumbency and may have mild SI distension on rectal palpation). Death from dehydration, apnea or complications (aspiration pneumonia, bladder rupture, or iatrogenic cystitis from bladder catheterization, exposure keratitis resulting in corneal ulceration). Diagnosis- from clinical signs, feeding history etc. - mouse assays / fecal examination for spores (unreliable and takes months for results). No characteristic postmortem signs therefore exclude other diseases. Therapy: anti-toxin very expensive binds circulating toxin (therefore will not bind toxin already producing clinical signs… must be given early- preferably before permanent recumbency), penicillin (procaine,

10 aminoglycosides, tetracycline are contraindicated) supportive care, (mechanical ventilation). Nursing care and rest are crucial in the recovery period while new synapses are formed.

Prevention: Vaccinate mares in areas of disease, Type B toxoid, foals are most at risk.

E. Cerebellar Abiotrophy: Signalment: Arabian foal 2 to 6 months of age Clinical signs: Base wide stance, intention tremors, ataxia, Clinical signs progress or plateau is not grossly reduced in size, cerebellar cortical degeneration, (Purkinje cell loss) No treatment

SPINAL ATAXIA

F. Cervical Stenotic Myelopathy / Cervical vertebral malformation (CVM) (True Wobbler) Signalment: usually 1 to 3 year old horses, higher incidence in TB & well developed males.

Etiology: developmental abnormalities (related to osteochondrosis syndrome) of the cervical vertebrae which results in spinal cord compression. Hereditary, nutritional component, trauma. Dynamic: compression occurs during ventroflexion or extension of the neck, instability between adjacent vertebrae C3-C4 most common site Static: compression occurs regardless of neck position occurs most often C5 to C6 or C6 to C7.

Clinical signs: symmetric spinal ataxia, rearlimbs>forelimbs Diagnosis: standing lateral projections (saggital ratio of vertebral canal to vertebral body <50-52%), but myelogram is necessary for a definitive diagnosis. Treatment: cervical vertebral ventral stabilization (with metal basket), also conservative- limit feed intake (energy and protein 50% of NRC requirement) & restricted exercise. Consider use of NSAID.

G. Equine Protozoal Myelitis (USA only): Signalment: Horses 2 months and up, any horse, any breed, higher incidence in Ohio vs. west coast. Etiological agent: Sarcocystis neurona migrating through spinal cord and/or brainstem and/or brain. Opossum feces Clinical signs: Varriable, asymmetric spinal ataxia, +/- cranial nerve involvement, muscle atrophy, multifocal. Diagnosis: Western blot for antibodies to sarcocystis (Note that it is possible to have false positives {low specificity “SpIN”} in CSF as well as serum) and PCR for DNA (many false negatives {low sensitivity “SnOUT”}), clinical signs, CSF cytology usually normal, response to treatment. Remember to also perform a red blood cell count on the CSF, as clear looking CSF can have up to 1200 RBC/L, and as few as > 8 RBC/L can be enough make a negative CSF sample positive if the serum titer is high. In short: 1) Never test or treat non-neurologic horses. 2) Rule out cervical spine compression with plain radiographs, 3) A negative serum or CSF result is useful in saving the client the cost of treatment, 4) a positive result in an uncontaminated CSF sample, in a horse with neurological deficits than has normal cervical radiographs is worth treating with a presumptive (NOT definitive diagnosis of EPM). About 70% of horses improve, but not all return to athletic soundness. Neurological damage may be permanent in some cases, but you can only “treat the treatable”, and most other differentials have an even poorer response to therapy. Treatment: Marquis (ponazuril) for 30 days has replaced the experimental, off-lable drugs - diclazuril (Baycox) and toltrazuril. Trimethoprim-sulfa or sulphadiazine & pyrimethamine (Daraprim) for 90-150 days may be cheaper. Steroids in severe acute cases ( of severe laminitis) do not seem to cause deterioration experimentally, therefore immune component of disease probably exists.

H. Equine Degenerative Myeloencephalopathy: A progressive degenerative disease of the CNS, several breeds reported. Etiology: Felt to be an inherited trait, reduced ability to use vitamin E, disease incidence decreases in certain familial lines with vitamin E supplementation

11 Clinical signs: symmetric spinal ataxia, rearlimb = or > forelimb deficits, onset from 6 months to 2 years of age, CSF, radiographs, myelogram normal. Diagnosis: exclusion of all other diseases, histopath neuraxonal degeneration & spheroid formation in brainstem and spinal cord (fasciculus cuneatus & gracilis).

I. Herpes Myelitis: (EHV1) An ascending paralysis/ataxia of rear limbs to fore limbs, urine dribbling, may see cranial nerve involvement. Mild to severe, acute. Frequently seen in older mares at stud farms in outbreaks. Etiology: vasculitis (EHV-1) and endothelial damage of vessels in spinal cord. Diagnosis: CSF abnormal (increased protein, xanthochromia, normal wbc), serology (4 fold rise in titer after 10-14 days), clinical signs, history of respiratory infection on farm. Treatment: steroids (consider risks of laminitis), vaccination in face of neurological outbreak generally recommended but is controversial Bladder catheterization (~TID) often required, at risk for iatrogenic cystitis (prophylactic antibiotics recommended, especially with concurrent corticosteroids) Poor prognosis if horse is down. Vaccination not protective

J. Equine Lower Motor Neuron Disease Progressive symmetrical muscle wastage (esp. triceps and quadriceps) and weight loss, muscle fasciculations and prolonged recumbency. Excellent appetite. Characteristic stance with all 4 legs close together under body and tail head elevated). Teeth may be black, and characteristic retinal lipofuschin accumulation (looks like chicken fencing wire) often visible on retinal examination. May relate to low Vit. E levels combined with some other toxic or inherited trait. Diagnosis: clinical signs, EMG (fibrillation potentials and positive sharp waves), muscle / nerve biopsy, retinal examination. CBC and profile generally unremarkable (may see slight elevation in CK) Post Mortem reveals degeneration in ventral horn cell bodies of spinal cord, Wallerian degeneration of motor nerves. A few horses improve on Vit E supplementation but won’t return to athletic function. Generally euthanized due to progressive recumbency. Many of the affected horses have not had access to green pasture and have been fed a pelleted diet.

V. FOAL DISEASES:

A. Septicemia Most important predisposing factor is failure of passive transfer. Frequently pneumonia, septic joints, patent urachus, etc. Diagnosis: depression, loss of suckle, petechiae, fever or hypothermia, CBC, fibrinogen, post suckle CITE (Less then 400 mg/dl IgG, partial failure 400 to 800 mg/dl), chest radiographs. Treatment: Colostrum if foal less then 12 hours old, I.V. plasma if older, broad-spectrum antibiotics, IV fluids, +/- endoserum, anti-ulcer medications (controversial), inotropes (dobutamine,nore-epinephrine or vassopressin) if hypotensive, nursing care, nutrition (10-25% of body weight in mare’s milk per day, ideally divided between hourly to two hourly feedings (normal foals nurse ~ 5 times per hour c/f a calf that may nurse 5-6 times per day!). Prognosis guarded without intensive therapy, and even then ~40% mortality for foals presented and treated at referral institutions). Treat every sick neonatal foal as septicemic until proven otherwise. Aseptically collected blood cultures are worth obtaining (ideally) prior to antibiotic therapy EVEN in the field. PLEASE refer early. Penicillin and amikacin (intravenous) are ideal. SMZ-TMP is generally not satisfactory.

12 Train your clients to examine the placenta or to collect it for veterinary examination. Suggest that all your breeding clients (all large animal species) keep their own colostrums bank. Collect half the colostrum from one side of the udder, and strip out all mares who loose their foals. COLOSTRUM IS GOLD!!!: it contains immunoglobulins, white blood cells, complement and CD14. IgG and CD14 concentration is much higher in colostrums than in serum, and IV plasma will not provide any local protection for the gut. If enough of your clients save colostrums, then you can often arrange trades between farms within your practice (not ruminants due to bovine leucosis etc)

B. Neonatal Maladjustment syndrome (hypoxic ischemic encephalopathy) Foals born neurologic or become neurologic within 24 hours. May have history of dystocia or placentitis. Pathophysiology relates to brain ischemia and reperfusion injury causing edema formation. Clinical signs: depression, lack of suckle, protruding tongue, wandering, bark like vocalizations, seizures. Diagnosis: clinical signs (rule out septicemia with examination and blood work) Treatment: nursing care, maybe steroids, DMSO, mannitol?, magnesium? And antibiotics due to risk of concurrent septicemia. Ischemia can effect the kidneys and intestine in addition to the brain, therefore fluid therapy is often also required.

C. Hypoglycemia/Hypothermia: Check mare for milk. Be aware of possible failure of passive transfer. Invest in a glucometer or at least blood glucose sticks. DON’T GUESS. Blood glucose is difficult to predict, and many veterinarians end up making foals hyperglycemic. (5% dextrose infused as a drip per second is usually, but not always safe). NG tube or IV dextrose. Keep the foal dry and warm (use a heat lamp, warm saline bags (careful not to burn the foal). If referring the foal in cold ambient temperatures suggest transporting the foal inside the vehicle rather than in the trailer with the mare.

D. Neonatal Isoerythrolysis Intra and extravascular hemolytic anemia in newborn foals due to absorption of alloantibodies produced by the mare as a result of alloimmunization by erythrocyte antigens foreign to her in a previous year (hence multiparous mares), but possessed by the stallion and inherited by the foal. Antigens Aa and Qa are most commonly involved. Clinical signs - icterus, unconjugated (INDIRECT) bilirubin, hemoglobinuria, weakness, tachycardia, tachypnea, severe anemia, death. Diagnosis - clinical signs, serodiagnostic test - agglutination or hemolysis of sensitized foal erythrocytes. Hemolysins are common. Treatment - prevent further ingestion of antibodies until foal is 24 hours old (muzzle foal). RBC replacement - washed mare RBC (ideal since not destroyed by the colostral antibodies already absorbed by the foal, but must be washed of all the plasma!) Alternative: well vaccinated, blood-typed gelding. A and Q negative (which is quite rare) Prevention - mare serum tested for A or Q antigens in late pregnancy, withhold colostrum from foals (strip out onto ground prior to and after parturition) in mares with previous history of A/Q antigens or previous NI foal.

E. Ruptured bladder Usually present as medical emergencies (hyperkalemia) rather than surgical ones. Clinical signs: depression, abdominal distension, colic. Diagnosis: hyperkalemia, hyponatremia, hypochloremia. Abdominal fluid has higher creatinine concentration than serum (2:1 ratio). Abdominal ultrasound / contrast studies. Low sodium and chloride caused by the large third space. Treatment: stabilize with IV sodium chloride and abdominal drainage. Then surgery.

F. Combined Immunodeficiency (CID): (rare)

13 Seen in Arabians, genetic disorder, due to autosomal recessive trait, positive foal incriminates both dam & sire. B (humoral) and T (cell mediated) immunity impaired. Diagnosis: lymphopenia < 1,000; absence of IgM pre-suckle; hypoplasia of lymphoid tissue (spleen & thymus). Clinical signs begin to appear at 2-3 months of age as passive immunity wanes. Adenovirus, Pneumocystis carnii pneumonia.

VI. Hemolymphatic

A. Equine Infectious Anemia (related to HIV) 1. Recurrent febrile episodes, ventral edema, enlarged spleen on rectal exam. Acute onset of extravascular hemolytic anemia, with depression, fever, weight loss. 2. Retrovirus infected leukocytes may circulate indefinitely. 3. Diagnosis - Coggins (AGID). Reportable. 4. Treatment - euthanasia or quarantine for life.

B. Lymphosarcoma (a common neoplasm of any aged horse) 1. Any age horse. 2. Alimentary form (generally 2 to 7 years) - malabsorption with hypoproteinemia and weight loss, occasionally chronic colic and diarrhea. 3. Mediastinal form - pleural effusion, fever, peripheral lymphadenopathy, weight loss, ventral edema. 4. Generalized (multicentric form) - lymph nodes, liver, kidney, spleen, intestine, lung; fever, weight loss. 5. Cutaneous form - single or multiple non-painful subcutaneous nodules; good prognosis if no other organs affected. 6. Paraneoplastic syndromes - hypercalcemia, thrombocytopenia and IgM deficiency. 7. Treatment - pred., cytoxan (cyclophosphamide), cytosar (cytosine arabinoside), vincristine. Poor response.

C. Purpura Hemorrhagica 1. Immune-mediated vasculitis initiated by bacterial, fungal, or viral pathogens. Most commonly a sequella to Strep. equi infection. 2. Clinical signs - edema of head, legs (often marked cut off) and abdomen; petechiae, colic, respiratory distress, organ failure. Skin may slough. 3. Treatment - penicillin, steroids and supportive care.

VII. ENDOCRINE / METABOLIC

A. Pituitary Adenoma (pars intermedia) “Cushings Disease” very common in older horses and ponies 1. PU/PD, hirsutism, increased appetite, hyperhidrosis, pot-bellied, laminitis, loss of condition, recurrent infections (foot abscess), bulging supra orbital fat, “cresty” neck, sometimes hyperglycemia 200 - 300 mg/dl, neutrophilia, lymphopenia. 2. Inappropriate secretion of ACTH, melanocyte-stimulating hormone, POMC, compression of the hypothalamus, lack of normal glucocorticoid feedback on ACTH secretion. 3. Diagnosis: clinical signs. Overnight dexamethasone suppression test. 4. Treatment (palliative only)- cyproheptadine (serotonin antagonist); pergolide (dopamine agonist) Note that some horses do OK without treatment (which is for life and expensive), some don’t respond to treatment, and some relapse following successful treatment

Monitor blood glucose or repeat dex suppression test to determine response to drugs.

14 B. Anhidrosis 1. Inability to sweat, thermoregulate in heat or during exercise. May be degeneration of sweat glands or down regulation of beta receptors due to chronically elevated epinephrine levels or hypothyroidism. 2. Occurs in hot, humid climates, tachypnea, exercise intolerance, alopecia, collapse, loss of body condition. 3. Diagnosis - intradermal epinephrine challenge, lack of sweat is poor prognostic sign. 4. Treatment - change environment, provide fans, water, electrolyte supplementation.

C. Synchronous Diaphragmatic Flutter “thumps” Diaphragm contracts in synchrony with heart associated with disruption of normal membrane potential of phrenic nerve as it passes close to atria. Generally associated with electrolyte abnormalities especially hypocalcemia.

Clinical signs: Characteristic twitching of flank in time with heartbeat Treatment: Electrolyte correction therapy, administer calcium.

VIII. CARDIOLOGY

A. Atrial fibrillation occurs most commonly in racehorses. 1. Most common arrhythmia of clinical significance in horses (sinus arrhythmia and 2° AV block most common - not clinically significant). Associated with high vagal tone and large atrial mass. 2. Primary - mild exercise intolerance, low resting HR, better prognosis. 3. Secondary to heart disease - exercise intolerance, high (> 60 bpm) resting HR, murmur, signs of CHF, poor prognosis, poor chance for conversion. If chronic condition conversion is more difficult and relapse is more likely. 4. ECG - no p wave, irregularly irregular spacing of QRS complex and f (fibrillation) waves. Rx – Quinidine.

IX. RENAL

A. Glomerulonephritis (rare) 1. proteinuria, weight loss, azotemia, ventral edema, hypercholesterolemia. 2. immune-mediated disease caused by circulating Ag/Ab complexes or direct basement membrane Ab (similar to humans). 3. Coggins test (for EIA) or source of chronic infection. 4. Poor prognosis.

B. Renal Tubular Disease 1. Aminoglycoside toxicity, exacerbated by dehydration, trough levels of <2 mg/dl are most important, increase the dosing interval in compromised patients. 2. NSAIDs - renal papillary necrosis, exacerbated by dehydration, blood flow to kidney is PG mediated.

C. Chronic Renal failure Tubular- interstitial diseases 1. Progression of vascular, septic or toxic acute renal failure 2. Urinary Obstruction 3. Pyelonephritis 4. Neoplasia Clinical signs: weight loss, depression, fever, PU/PD, oral ulceration, excessive dental tartar. Diagnosis: serum creatinine and urea (note that urea can be influenced by diet). Serum calcium usually elevated unlike other species (therefore don’t see “rubber jaw” or secondary renal hyperPTHism) Remember: horses normally excrete calcium carbonate crystals in the urine, which makes it cloudy Urinalysis, Culture, Fractional excretion ratios, renal ultrasound, biopsy.

15 Treatment: Low protein diet, access to water and electrolytes. Prognosis poor.

X. MUSCULOSKELETAL

A. Hyperkalemic Periodic Paralysis (Quarter Horses ‘Impressive’ blood line) 1. Usually less than 4 years old; episodes of weakness, flaccid paralysis, tremors, protruding nictitans, associated with hyperkalemia, arrhythmias, resp arrest, death. Dominant inherited trait causing a defect in the sarcolemmal Na channel. 2. Diagnosis – PCR from blood or hair samples, EMG abnormalities (myotonic discharges), potassium challenge (controversial), serum K during episode vitreous fluid K level post-mortem. 3. Treatment - a) episodic - calcium gluconate, bicarbonate, fluids, terbutaline b) long-term- acetazolamide (carbonic anhydrase diuretic), dietary management - limit alfalfa hay (high K), regular exercise (turn-out)

B. Exertional Rhabdomyolysis (Azoturia, tying up, Monday morning disease) Probably multiple causes, therefore a syndrome. Generalized myopathy occurring during or following exercise. Either an isolated event, or frequently intermittent bouts that may vary from mild to severe, life threatening disease in predisposed animals.

Unknown etiology: 1. Dietary CHO intake maintained through period of rest followed by exercise 2. Vit E / selenium 3. Hypothyroidism (does this really exist in horses???) 4. Electrolyte deficiencies (perform fractional excretion ratios) 5. Increased risk in fillies. (therefore sex / genetic predisposition?) ?hormonal influence 6. Deficient Ca ion uptake back into Sarcoplasmic reticulum?

Pathophysiology: Primarily fast twitch fiber hypoxia leading to lactate accumulation (this was an old theory and may not be true. More recent theories due to abnormal calcium release into muscle cells), and myodegeneration. Myoglobin release leads to myoglobinuria and nephrotoxicity (tubule obstruction and vasoconstrictive effects of the pigments) in severe cases.

Clinical signs: Stiffness, cramps, firm muscles (particularly back, lumbar and gluteals), sweating.

Diagnosis: elevated CPK (peak 6 hours may reach 100,000’s iu/l, declines within days); elevated AST (peak 24 hours >1000 iu/l for days to weeks)

Treatment: Limit exercise, NSAID (analgesia), steroids? (stabilize muscle membranes), muscle relaxants (e.g. methocarbamol), vasodilators (ACE) if not in shock, vitamin E, FLUID THERAPY to prevent acute renal failure from myoglobin.

Prophylaxis: Diet/ electrolyes; Correct training regime; Phenytoin, dantrolene sodium, Vit E / Sel; thyroxine.

C. Polysaccharide Storage Myopathy Mild to severe muscle stiffness/rhabdomyolysis in frequently calm / docile Quarter horses and Warmbloods, draft breeds. Abnormal accumulations of a polysaccharide within muscle fibers. Diagnosis: muscle biopsy. Treatment: symptomatic during disease episode, high fat /low starch diet, regular exercise.

D. Nutritional Myopathy (white muscle disease)

16 Young rapidly growing foals (birth - 7 months): Vitamin E / selenium deficiency in utero or during growth Clinical signs: Stiff gait, incoordination, dysphagia. Diagnosis: elevated CPK, AST. Decreased glutathione peroxidase activity, low serum Vit E, Muscle biopsy Treatment : Vit E and Selenium. Prophylaxis in deficient areas. (OHIO is deficient in selenium!!!! We recommend vitamin E/selenium injection to all foals in the first day of life. Any young horse fed on pasture and local Ohio hay may be selenium deficient, therefore pelleted feed or oral supplement recommended. At recommended dosages as selenium toxicity can easily occur!) Guarded prognosis.

E. Malignant Edema: Etiological agent: Clostridium septicum,, perfringens, & chauvei infection through laceration or injection (ivermectin, xylazine, bute, Banamine). Incubation period 12 to 48 hours. Clinical signs: local reaction, swelling pain, fever, crepitus, shock & death. Diagnosis: clinical signs & history, detection of Gram-positive rods on fine needle aspirate. Treatment: wound debridement, fillet area, I.V. penicillin or oxytetracycline and metronidazole, local infiltration with penicillin, NSAID, fluids.

F. Laminitis (founder) very common Sinking and / or rotation of pedal bone associated with disruption and instability of sensitive / insensitive laminar bond in hoof. Multiple etiologies 1. (road founder) 2. Grain / grass overload - esp. Ponies (? relative insulin resistance) - high dietary CHO intake causes pH change in gut which allows massive absorption of Gram negative bacteria and endotoxemia. 3. Endotoxemia e.g. Salmonellosis, PHF, pleuropneumonia, endometritis (after retained placenta) etc. 4. Pituitary Adenoma - hormonal effects (cortisol?) 5. Drug induced - steroid administration 6. Toxicity - Black Walnut 7. Supporting limb (e.g. post surgery etc)

Clinical signs: stance, gait, digital pulse amplitude, depression at coronary band, prolapsed P3 through sole. Diagnosis: History and clinical signs. chronic vs. acute Radiography -rotation, sinking, gas shadows, sepsis, boney changes Treatment: NSAIDs, vasodilators, aspirin, heparin, DMSO, fluids, endoserum. SUPPORT, CORRECTIVE SHOEING, NURSING CARE IF DOWN. Prognosis guarded at best

XI. TOXICOLOGY

A. Red Maple Leaf 1. Anorexia, depression, methemoglobinemia, tachypnea, weakness, intra and extravascular hemolysis, Heinz body anemia, hemoglobinuria, icterus, cyanosis. Poor prognosis. 2. Treatment: New Methylene Blue is not effective. Vitamin C at high doses, RBC replacement (transfusion of fresh blood), Mineral oil or cathartics.

B. Black Walnut l. toxicity seen when black walnut shavings (dark in color) are used as bedding, 12 - 18 hours after exposure. 2. laminitis, limb edema, colic, tachypnea. 3. remove from shavings, mineral oil.

C. Blister Beetle (Cantharidin) 1. Clinical signs - GI and urinary irritation, renal insufficiency, myocardial failure, hypocalcemia, shock. Oral ulceration, thumps, colic, melena, frequent drinking, excessively strong heartbeat.

17 2. Remove source, supportive treatment, mineral oil.

D. Moldy Corn 1. Leukoencephalomalacia (cerebral signs: amarosis, head pressing, dementure, depression 2. Fusarium moniliforme

E. Slaframine 1. mycotoxin produced by fungus Rhizoctonia leguminicola that grows on red clover. 2. paraympathomimetic toxicosis, slobbering is the only clinical sign 3. Seen in summer. Resolves when animals are removed from pasture with red clover.

Important subjects not covered by this review include dermatology, parasitology and oncology. Please refer to your notes or a textbook.

Differential Diagnoses 1. Coughing Horse - remember horses generally cough from the lungs, determine quality and nature of nasal discharge. Unilateral discharge suggests URT problem • COPD • viral resp disease (Herpes, influenza etc) • bacterial bronchopneumonia (Streps, Actinobacillus, Rhodococcus) • foreign body • lungworm

2. Chronic weight loss - remember the common problems, determine if the horse has significant underlying disease, check serum albumin • teeth problems • parasitism • poor diet, social hierarchy • chronic infection / abscesses • heart failure • renal failure • protein losing enteropathy • neoplasia • EMND

3. Spinal ataxia - determine neuroanatomic localization, is it symmetric or not? History of respiratory disease? • EPM • CVM • EDM • Herpesvirus-1 • West Nile • Rabies

4. Dysphagia - recently eaten? vaccination status. Scope horse / pass NG tube • choke - esophageal obstruction • strangles • botulism • rabies • EPM • fractured stylohyoid bone

5. Jaundice - vaccination status. Do UA . Direct and indirect bilirubin levels, Coombs and Coggins tests. • fasting • IHA • EIA • liver disease • Piroplasmosis (Babesia equi is exotic to USA) • NI foal • DMSO administration • Red maple toxicity

18 6. Flat foal - many diseases look very similar in foals - always check IgG with a SNAP or CITE test. Best clinical impression based on history, PE and blood work. • hypoglycemia • hypothermia • septicemia • NMS • NI • ruptured bladder

7. Polydipsia • Pituitary adenoma • CRF • Pyschogenic • Diabetes insipidus (central or nephrogenic)

8. Diarrhea- often treat empirically • dietary • antibiotic induced • salmonella • PHF • cyathostomiasis • rotavirus • clostridia

9. Stiffness - history, breed, recent wound, occurring following exercise etc. • laminitis • Rhabdomyolysis • Polysaccharide storage myopathy • Tetanus • White muscle disease Good luck!

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