Equine Diseases Flashcards

Chronic obstructive pulmonary disease
Terms Definitions
Etiology of Salmonellosis
Salmonella typhimurium and others
How is Salmonellosis spread
from infected horses through the environment and fomites. Stress has an important role.
Clinical Signs of Salmonellosis.
No signs to acute, severe diarrhea. Depresion, fever, anorexia, soft to watery feces, foul smelling.
Diagnosis of Salmonellosis
Clinical signs, chem values, isolation of salmonella from feces, blood or tissue.
Lab findings of Salmonellosis
Neutropenia, dehydration, metabolic acidosis.
Treatment for Salmonellosis
IV fluides, Abx controversial
NSAID: Banamine. Prevent by keeping areas clean.
Etiology of Potomac Horse Fever
Neorikettsia risiticii (Gram -)
Epdemiology of Potomac Horse Fever
Horses of all ages. Spring, summer, early fall. Snails infested with trematodes that have the bacteria. Infected from ingestion of aquatic insects.
Clinical Signs Potomac Horse Fever
Mild depression and anorexia, fever, moderate to severe diarrhea.
Potomac Horse Fever: Diagnosis
Clinical signs, seasonal and geographical evidence. Confirmed through isolation.
Laboratory findings: Potomac Horse Fever
Leukopenia, leukocytosis or normal.
Treatment for Potomac Horse Fever:
Oxytetracycline. Vaccine is available.
Clostridial Enterocolitis: Etiology
Clostridium perfringens or difficile.
From Merck: C perfringens (types A, B, C, and D), C sordellii , C difficile , and C cadaveris
Clostridial Enterocolitis: Epidemiology
Horses and foals that have altered intestinal normal flora.
Clostridial Enterocolitis: Clinical Signs
Sudden death, diarrhea with or without blood, colic, reduced feed intake, lethargy.
Clostridial Enterocolitis: Diagnosis
Mortality is high (especially with C perfringins type C) Usually made at necropsy by isolation of bacteria.
Clostridial Enterocolitis: Treatment
IV fluids, NSAIDs
Also From Merck: Neonates may need gastric protectants, and Broad-spectrum systemic antibiotics are indicated if the horse is suspected of being septic or is severely leukopenic.
Metronidazole has been used in foals with some success however side effects are not known.
Clostridial Enterocolitis: Predisposition
Stress, food deprivation, antimicrobials.
Erythromycin treatment of foals has been associated with fatal clostridial enteritis in mares. (Remember, this is an overgrowth of a bacteria that is normally present).
Inflammatory Airway Disease: Etiology
Proposed: allergic airway, recurrent pulmonary stress, inhalationof dust, pollutants, viral infections.
Inflammatory Airway Disease: Signs
Chronic cough, mucoid to mucopurulent nasal discharge.
Endoscopy: mucopurulent exudate in pharynx, trachea, and bronchi
Inflammatory Airway Disease: Diagnosis
Poor performance and clinical signs.
Bronchoalveolar lavage is used to characterize the type of inflammation. There are 3 recognized types. (mixed inflammatory, eosinophilic and mast cells)
Inflammatory Airway Disease: Treatment
Aerosolized bronchodilator therapy prior to exercise. Corticosteroid for type 1 hypersensitivity.
1-inflammatory: low-dose, interferon-a is recommended for immunomodulation and antiviral activity
2-eosinophilic: consider parasitic pulmonary disease in addition to hypersensitivity pneumonitis. Systemic corticosteroid therapy is recommended to reduce pulmonary inflammation in horses with eosinophilic IAD
3-mast cell: likely represents a local pulmonary hypersensitivity response and may represent an early form of recurrent airway obstruction. aerosol administration of nedocromil sodium (a mast cell-stabilizing drug) improves the clinical signs of respiratory disease and prevents histamine release.
What does cytologic evaluation of bronchoalveolar fluid reveal in Inflammatory Airway Disese?
One of 3 possiblities: (Tx varies accoringly)
1. mixed inflammation with high total nucleated cells, mild neutrophilia (15% of total cells), lymphocytosis, and monocytosis (usually d/t previous dz or irritation)
2. increased metachromatic cells (mast cells >2% of total cells)
3. eosinophilic inflammation (5-40% of total cells)
Culicoides Hypersensitivity: Etiology
Culicoides gnats
Culicoides Hypersensitivity: Epidemiology
Horses allergic to these gnats. Warm months.
Culicoides Hypersensitivity: Clinical Signs
Gnats feed along the topline and ventral midline in the evening. Intense pruritiis, Excoriations, crusts, scaling, alopecia of forehead, neck, withers, shoulders, rump, ventral midline, tail.
Culicoides Hypersensitivity: Diagnosis
History of seasonality, locations of lesions, response to therapy.
Culicoides Hypersensitivity: Treatment
Keep horses inside from dusk to dawn, fly spray, prednisone if pruritis is bad.
Equine Infectious Anemia: Etiology
Lentivirus in the retroviridae family
Equine Infectious Anemia: Epidemiology
Blood feeding insects initiate most infections; tabanids, horseflies, deerflies.
Equine Infectious Anemia: Clinical Signs
Can be inapparent, acute or chronic.
Recurring clinical bouts of fever accompanied by marked platelet reductions, petechial hemorrhages, anemia, depression, weight loss, cachexia, and dependent edema
Equine Infectious Anemia: Diagnosis
Clinical Signs, Coggins test (AGID)
Equine Infectious Anemia: Lab Findings
Anemia, low platelet count
Equine Infectious Anemia: Treatment
No specific treatment or vaccine.
Equine Infectious Anemia: Necropsy findings
In acute cases, the spleen and splenic lymph nodes are enlarged. In chronic cases, necropsy reveals emaciation, pale mucous membranes, subcutaneous dependent edema, splenomegaly, and enlarged abdominal lymph nodes.
Foal pneumonia: Etiology
Rhodococcus equi, G+
Foal pneumonia: Epidemiology
Foals 1-5 months old.
Ubiquitous in the environment.
High temps, sandy soil, dust favors spread.
Foal pneumonia: Clinical Signs
Difficult to detect until pulmonary lesions are present. Lethargic, febrile, tachypnic.
Crackles and wheezes.
Foal pneumonia: Diagnosis
CBC, chem, signs, thoracic rads.
Nodular lung lesions with mediastinal lymphadenopathy.
Confirm by bacterial culture.
Foal pneumonia: Laboratory Findings
Bronchopneumonia, pulmonary abscessation, suppurative lymphadenitis.
Neutrophilia, hyperfibrinogenemia.
Foal pneumonia: Treatment
Azithromycin and rifampin.
Prevent by decreasing exposure, early detection, ensure foals get colostrum.
Acute Bronchointerstitial Pneumonia:
Acute Bronchointerstitial Pneumonia:
Foals 1 wk to 8 mo.
Acute Bronchointerstitial Pneumonia:
Clinical Signs
Fever, reluctant to move, cyanosis, respiratory distress.
Acute Bronchointerstitial Pneumonia:
Clinical Signs, PE, thoracic rads.
Acute Bronchointerstitial Pneumonia:
Lab Findings
Hypoxemia, hypercapnia, respiratory acidosis, hyperfibrinogenemia,
Acute Bronchointerstitial Pneumonia:
Symptomatic, NSAIDs, broad-spectrum antibiotics, bronchodilation, oxygen.
Mortality is high.
Pleuropneumonia: Etiology
Step, E. coli, Actinobacillus, Klebsiella, Staph, Pasteurella, Clostridium, Fusobacterium
Pleuropneumonia: Epidemiology
Race horses mostly. Viral infection, transport, anesthesia, exercise predisposes.
Pleuropneumonia: Clinical Signs
Fever, depression, lethargy, inappetence, pleural pain, short strides, guarding thorax, shallow respiration, reluctant to lie down.
Pleuropneumonia: Diagnosis
Thoracic ultrasound, thoracocentisis and fluid analysis, increased cellularity and total protien.
Pleuropneumonia: Laboratory Findings
Reflect bacterial sepsis or toxemia: neutropenia with left shift, hemoconcentration, azotemia.
Pleuropneumonia: Treatment
Chest tube to drain fluid, daily flushing, antibiotics (pen, gent, metro), and NSAIDs
Botulism-Shaker Foal Syndrome:
Clostridium botulinum
Botulism-Shaker Foal Syndrome:
Grows in decaying animal and plant material. Shaker foals are <4 weeks.
Botulism-Shaker Foal Syndrome:
Clinical Signs
Progressive motor paralysisdisturbed vision, difficulty chewing and swallowing
Botulism-Shaker Foal Syndrome:
Eliminate other causes of paralysis
Botulism-Shaker Foal Syndrome:
fix the diet, eliminate the source.
Guanidine hydrochloride shows some ealry efficacy.
Bowed Tendon, Tendonitis,
Desmitis: Etiology
Inflammation of the tendon
Bowed Tendon, Tendonitis,
Desmitis: Epidemiology
Horses used at fast work (race horses).
Superficial flexor tendons in forelimb usually.
Bowed Tendon, Tendonitis,
Desmitis: Clinical Signs
Severe lameness, heat, pain, swelling
Bowed Tendon, Tendonitis,
Desmitis: Diagnosis
Ultrasound can visualize defects.
Bowed Tendon, Tendonitis,
Desmitis: Treatment
Best treated early, stall rest, cold packs, NSAIDs, support/immobilization
Chronic Obstructive Pulmonary Disease:
AKA Recurrent Airway Dz.
Chronic Obstructive Pulmonary Disease:
Average age is 9 yrs. All breeds, both sexes, heritable component.
Chronic Obstructive Pulmonary Disease:
Clinical Signs
Allergic resp. dz. Flared nostrils, tachypnea, cough, heave line, abd. breathing, wheezes.
Chronic Obstructive Pulmonary Disease:
History and PE.
Flattening of diaphragm on rads.
Chronic Obstructive Pulmonary Disease:
Lab Findings
Overinflated lungs. (flat diaphragm) on rads.
Chronic Obstructive Pulmonary Disease:
Reduce allergen exposure.
Soak hay with water, bronchodilators, steroids.
Contagious Equine Metritis: Etiology
Taylorella equigenitalis, gram - coccobacillus
Contagious Equine Metritis: Epidemiology
Mares and stallions.
Spread during mating or AI or contaminated instruments.
Found on and around stallion penis.
Contagious Equine Metritis: Signs
Mares: Copious mucopurulent vaginal discharge 10-14 days after mating.
Stallions are asymptomatic.
Contagious Equine Metritis: Diagnosis
Isolation of the organism.
Contagious Equine Metritis: Lab Findings
Edema and hyperemia of endometrium, endocervix, and vaginal mucosa.
Contagious Equine Metritis: Treatment
Clean Penis/Clitoral area with chlorihexidine and apply ntrofurazone SID X 5 days. Control through identification of those infected.
Dermatophilosis: Etiology
Dermatophlus congolensis
Dermatophilosis: Epidemiology
Chronically infected animals are reservoir. Prolonged wetting by rain, high humidity/temp, reduced natural bariers to infection
Dermatophilosis: Clinical Signs
Most prevalent in young, immunosuppressed.
Dermatophilosis: Diagnosis
Appearance of lesions and demonstration of organism.
Dermatophilosis: Lab Findings
Crusts of scab formation with yellow-green pus underneath.
Dermatophilosis: Treatment
Antibiotics: Chloramphenicol, streptomycin, amoxicillin, tetracyclines.
Dorsal Displacement of the Soft Palate:
Inflammation of the upper resp. tract may cause neuropathy of pharyngeal branch of vagus nerve as it traverses the floor of the medial compartment of the guttural pouch, resulting in neuromuscular dysfunction of the pharyngeal muscles that control the soft palate.
The retropharyngeal lymph nodes are in direct contact with the pharyngeal branch of the vagus nerve, and retropharyngeal lymphadenopathy may result in compression and irritation.
Hypoplasia of the epiglottis.
Dorsal Displacement of the Soft Palate:
Clinical Signs
Gurgling respiratory noise during expiration.
Dorsal Displacement of the Soft Palate:
Dorsal Displacement of the Soft Palate:
2 year olds: Rest and anti-inflammatories.
Caudal retraction of the tongue elevates the soft palate and pushes the larynx caudally, both of which may predispose a horse to DDSP. Placing a tongue tie during exercise reduces caudal retraction of the tongue.

Sternothyrohyoideus myectomy performed in horses prone to DDSP to alter the anatomy of the upper respiratory tract is successful in ~50% of horses.
Soft palate resection (staphylectomy) is frequently performed in horses with DDSP and also has a success rate of ~50%; however, the mechanism of improvement after surgery is unclear. Success has been attributed to reduction in the mass of soft palate obstructing the airway, easier replacement of the shorter soft palate to the subepiglottic position, and firming of the caudal edge of the soft palate to keep it ventral to the epiglottis.
Laryngeal Hemiplegia: Etiology
Progressive loss of myelinated fibers of left recurrent laryngeal nerve.
Laryngeal Hemiplegia: Epidemiology
Likely heritable
Laryngeal Hemiplegia: Clinical Signs
Inspiratory noise during exercise and exercise intolerance.
Laryngeal Hemiplegia: Diagnosis
Laryngeal Hemiplegia: Lab Findings
Paresis/alysis of left arytenoid cartilage and vocal fold.
Laryngeal Hemiplegia: Treatment
Prosthetic laryngoplasty, laryngeal ventriculecotmy.
Pharyngeal Lymphoid Hyperplasia-Pharyngitis: Etiology
Lymphoid follicles in pharynx enlarge. Viral agent may be the cause.
Pharyngeal Lymphoid Hyperplasia-Pharyngitis: Epidemiology
Young horses. (1-3 years old)
Pharyngeal Lymphoid Hyperplasia-Pharyngitis: Clinical Signs
Paryngeal pain, reduced appetite, increased swallowing.
Pharyngeal Lymphoid Hyperplasia-Pharyngitis: Diagnosis
PE findings.
Pharyngeal Lymphoid Hyperplasia-Pharyngitis: Laboratory Findings
Pharyngeal lymph tissue apears hyperemic with mucoid exudate.
Pharyngeal Lymphoid Hyperplasia-Pharyngitis: Treatment
Treatment not necessary. Rest and NSAIDs might help if the horse is painful.
Horse bots-Botflies: Etiology
Gasterophilus flies
Horse bots-Botflies: Epidemiology
Flies lay eggs on hair and horses eat the eggs.
Horse bots-Botflies: Clinical signs
Can cause mild gastritis, but usually no signs.
Horse bots-Botflies: Diagnosis
Eggs on hair
Horse bots-Botflies: Lab Values
Stomach mucosal ulcerations and erosions.
Horse bots-Botflies: Treatment
Oxyuris-Pinworms: Etiology
Oxyuris equi
Oxyuris-Pinworms: Epidemiology
Horses less than 18 months old.
Oxyuris-Pinworms: Clinical Signs
Intense pruritus at tail base and anus.
Oxyuris-Pinworms: Diagnosis
Signs, cellophane tape test
Oxyuris-Pinworms: Treatment
Any broad spectrum dewormer.
Parascaris: Etiology
Parascaris equorum
Parascaris: Epidemiology
Sources are young foals and environment
Parascaris: Clinical Signs
Heavy infections may have respiratory signs or intestinal obstruction.
Parascaris: Diagnosis
Demonstration of eggs in feces.
Parascaris: Treatment
Any borad-spectrum anthelmintic.
Large Strongyles: Etiology
Strongylus vulgaris, edentatus, or equinus.
Large Strongyles: Epidemiolgy
Infection is by ingestion of larvae.
Large Strongyles: Clincal Signs
S. vulgaris migrates to the cranial mesenteric artery. Anemia, weakness, emaciation, diarrhea, colic.
Large Strongyles: Diagnosis
Demonstration of eggs in feces.
Large Strongyles: Treatment
Any broad-spectrum anthelmintic.
Enteroliths: Etiology
Accumulation of ammonium magnesium phosphate crystals.
Enteroliths: Epidemiology
10 years or older, Arabs, alfalfa diet.
Enteroliths: Clinical Signs
History of recurrent colic. Acute onset of severe colic, distention of abdomen.
Enteroliths: Diagnosis
Enteroliths: Treatment
Cushings Disease: Etiology
Hyperplasia or ademoma of the pars intermedia of the pituitary
Cushings Disease: Epidemiology
All breeds but ponies are at increased risk.
Mean age is 18-23 years.
Cushings Disease: Clinical signs
Hirsutism. Coat color change, weight loss, lethargy, "cresty", laminitis.
Cushings Disease: Diagnosis
Clinical signs, confirmed by overnight dexamethasone suppression test.
Cushings Disease: Lab Findings
Mild anemia, neutrophilia, lymphopenia, hyperglycemia, increased cortisol.
Cushings Disease: Treatment
Body clip, treat laminitis, maintain good oral health.
Pergolide is effective: dopamine agonist.
Exercise Induced Pulmonary Hemorrhage:
Proposed: high pulmonary vascular pressure during exercise, pulmonary neovascularization, coag. dysfunction.
Exercise Induced Pulmonary Hemorrhage: Epidemiology
Occurs in the majority of race horses.
Exercise Induced Pulmonary Hemorrhage:
Clinical Signs
Exercise Induced Pulmonary Hemorrhage: Lab Findings
Endoscopy: blood in airways 30-90 minutes after exercise.
Exercise Induced Pulmonary Hemorrhage:
Furosemide reduces severity and improves race performance.
Sporadic Exertional Rhabdomyolysis-Tying up: Etiology
Necrosis of skeletal mm. after intense exercise.
Sporadic Exertional Rhabdomyolysis-Tying up: Epidemiology
Exercise exceeding the state of training.
Sporadic Exertional Rhabdomyolysis-Tying up: Clinical Signs
Excessive sweating, tachypnea, tachycardia, mm fasiculations, painful lumbar and gluteal mm after exercise.
Sporadic Exertional Rhabdomyolysis-Tying up: Diagnosis
Signs of mm cramping, no history of previous episodes, stiffness after exercise, elevated CK and AST.
Sporadic Exertional Rhabdomyolysis-Tying up: Lab Findings
Elevated CK and AST adn lactate dehydrogenase.
Sporadic Exertional Rhabdomyolysis-Tying up: Treatment
Tranquilizers, NSAIDs, opiods, stall rest for a couple days, gradual increase back to training.
PSSM: etiolopgy
(aka tying up or monday morning dz)
Chronic Exertional Rhabdomyolysis
PSSM: Epidemiology
Quarter horse, Warmbloods, Draft horses.
Rest for a few days prior to exercise predisposes.
PSSM: Clinical Signs
Tucked up abdomen, camped-out stance, muscle fasiculations, sweating, hindlimb stiffness.
PSSM: Diagnosis
Signs of muscle cramping, history of previous episodes, stiffness after exercise.
PSSM: Lab Findings
Elevated CK and AST and lactate dehydrogenase.
PSSM: Treatment
Tranquilizers, NSAIDs, opiods, stall rest for a few days, gradual increase back to training.
Recurrent Exertional Rhabdomyolysis:
Chronic Exertional Rhabdomyolysis
Recurrent Exertional Rhabdomyolysis:
Thoroghbreds, Standardbreds, Arabs.
Likely d/t abn regulation of intracellular Ca in skeletal mm.
Recurrent Exertional Rhabdomyolysis:
Clinical Signs
Intermittent disruption of mm contraction.
Recurrent Exertional Rhabdomyolysis:
Hx, Clin Signs, elevated CK and AST,
mm bx.
Recurrent Exertional Rhabdomyolysis:
Lab Findings
Elevated CK and AST and lactate dehydrogenase.
Recurrent Exertional Rhabdomyolysis:
Decrease trigger factors of nervousness or excitement.
Gastrointestinal Ulceration Etiology
Increased exposure to HCl acid secondary to fasting, not nursing, intense exercise.
Gastrointestinal Ulceration: Epidemiology
In 50% of foals, in 90% of race horses.
Gastrointestinal Ulceration: Clinical Signs
Usually none. If it becomes severe, diarrhea, dorsal recumbancy, ptyalism, colic, poor appetite, attitude change.
Gastrointestinal Ulceration: Diagnosis
Gastrointestinal Ulceration: Treatment
Often heal by themselves. Can use Cimetidine and rantidine and omeprazole.
Empyema: Etiology
usually d/t Strept. equi infection
Empyema: Epidemiolgy
Just having strangles.
Empyema: Clinical Signs
Intermittent purulent nasal discharge, painful swelling in parotid area.
Empyema: Diagnosis
Scope gutteral pouch
Empyema: Treatment
Gutteral pouch lavage is necessary with systemic antibiotics
Gutteral Pouch Mycosis: Etiology
Aspergillus spp.
Gutteral Pouch Mycosis: Epidemiology
Most common cause of severe hemorrhage from gutteral pouch.
Gutteral Pouch Mycosis: Clinical Signs
Epistaxis, dysphagis, Horner's, dorsal displcement of the soft palate.
Gutteral Pouch Mycosis: Diagnosis
Endoscopy of gutteral pouch
Gutteral Pouch Mycosis: Lab findings
Fungal plaques on the caudodorsal aspect of the medial compartment.
Gutteral Pouch Mycosis: Treatment
Topical and systemic antibiotics
Hyperlipemia and Hepatic Lipidosis:
High fat in blood stream or liver
Hyperlipemia and Hepatic Lipidosis:
Poor fed quality or decrease in feed intake during high energy requirement. Most common in ponies, mini horses, donkeys.
Hyperlipemia and Hepatic Lipidosis:
Clinical Signs
Lethargy, weakness, anorexia, decreased water intake
Hyperlipemia and Hepatic Lipidosis:
Signalment, history, clincal signs, white to yellow plasma, serum triglyceride >500mg/dl confirms.
HYPP (Hyperkalemic Periodic Paralysis):
Autosomal dominant trait
HYPP (Hyperkalemic Periodic Paralysis):
Descent from the stallion Impressive. Quarterhorses, Paints, Appaloosas. Foals to 3 yrs. Triggered by high potassium in diet (alfalfa, molasses)
HYPP (Hyperkalemic Periodic Paralysis):
Clinical Signs
Asymptomatic to intermittent muscle fasciculations and weakness. Begins in flank, neck, and shoulders-becomes generalized. Become weak, ataxic, stagger during attacks.
HYPP (Hyperkalemic Periodic Paralysis):
DNA testing of mane and tail
HYPP (Hyperkalemic Periodic Paralysis):
Acute death common.
Calcium gluconate or IV dextrose alone or combo with bicarb.
Neonatal Isoerythrolysis: Etiology
Absorbed colostral antibodies against foals RBC.
Neonatal Isoerythrolysis: Epidemiology
Occurs between 12 hours and 4 days of age.
Neonatal Isoerythrolysis: Clinical Signs
Pale MM, icterus, depression, anorexia, tachypnea, hemoglobinuria, collapse.
Neonatal Isoerythrolysis: Diagnosis
Incompatible minor agglutination cross match and positive Coombs test.
Neonatal Isoerythrolysis: Lab findings
Anemia, hemoglobinuria
Neonatal Isoerythrolysis: Treatment
Affected foals should be muzzled to prevent further absorption of immunoglobulins. Screen broodmares to control.
Severe Combined Immunodeficiency (SCID): Etiology
Inheritied autosomal recessive disease.
Severe Combined Immunodeficiency (SCID): Epidemiology
Arabs. Foals don't live past 6 months.
Severe Combined Immunodeficiency (SCID): Clinical Signs
Normal at birth, and for first few months. Then recurrent infections, and death.
Severe Combined Immunodeficiency (SCID): Diagnosis
Demonstrate foal is homozygous for SCID gene.
Severe Combined Immunodeficiency (SCID): Lab Findings
Lack T and B cell responses.
Severe Combined Immunodeficiency (SCID): Treatment
Disease is always fatal.
Laminitis: Etiology
Ischemia that leads to the breakdown of the union between the horny and sensitive laminae.
Laminitis: Epidemiology
Carbohydrate/grain overload, grazing on lush pasture, endotoxemia, colic, excessive use of corticosteroids.
Laminitis: Clinical Signs
Depression, anorexia, slow, crouching, short-strided gait, bounding digital pulse.
Laminitis: Diagnosis
History and clinical signs. rotation of coffin bone on radiographs
Laminitis: Lab Findings
May show rotation of coffin bone on rads.
Laminitis: Treatment
With Grain Overload: 1 gallon mineral oil PO, hot packs on feet, isoxsurine hydrochloride (vasodilator), banamine, special shoes, hoofcare
Navicular Disease: Etiology
Damage to flexor surface of navicular bone and osteophyte formation. Cause is unknown.
Navicular Disease: Epidemiology
A disease of mature riding horses, usually in the forelimbs.
Navicular Disease: Clinical Signs
Keeps the hela of effected foot off the ground. Short stride, stumble, flexion test shows lameness.
Navicular Disease: Diagnosis
HIstory and PE findings
Navicular Disease: Treatment
Palmar digital nerve block, rest, proper foot care, NSAIDs, intrabursal corticosteriods, palmar digital neurectomy.
Stringhalt: Epidemiology
Any breed, rare in foals. Myoclonic affliction of one or both hindlimbs.
Stringhalt: Clinical Signs
Hyperflexion while walking, high-stepping gait. Severe cases, atrophy of thigh muscles.
Stringhalt: Diagnosis
Clinical signs, confirmed by electromyography.
Navicular Disease: Laboraory Findings
Rads show degenerative changes of navicular bone: osteophytes on lateral and proximal border.
Stringhalt: Treatment
Many recover spontaneously.
Chronic: lateral extensor tenectomy.
Not all cases respond.
Peritonitis: Etiology
Most common from injury to serosal surface of GI tract and ingesta leaks into abdomen.
Peritonitis: Epidemiology
Any Horse
Peritonitis: Clinical Signs
Severe colic, ileus, distended intestines, gastric reflux, occasional diarrhea, tachycardia, weak pulse, fever.
Peritonitis: Diagnosis
Abnormal feces, intestinal stasis, abdominal pain, abnormal peritoneal fluid.
Peritonitis: Laboratory Findings
Neutropenia with left shift.
Peritonitis: Treatment
IV fluids, electrolytes, broad-spectrum antibiotics (gent, pen, metro), surgery
Sarcocystis neurona-protozoan
EPM: Epidemiology
Horse is dead end host, opossum is natural host.
EPM: Clinical Signs
Can infect any part of CNS. Spinal cord involvement more common. Weakness or ataxia in one or all limbs.
EPM: Diagnosis
Postmortem diagnosis confirmed by demonstration of protozoa in CNS lesions. Antibodies in CSF diagnostic.
EPM: Lab Findings
CSF analysis: mononuclear pleocytosis, increased protein
EPM: Treatment
Ponazril or nitazoxanide for 6 months. Relapses are common.
Sepicemia in Foals: Etiology
Gram -, E. coli, Klebsiella, Enterobacter, Actinobacillus, Pseudomonas
Sepicemia in Foals: Epidemiology
Usually foals have failure of passive transfer.
Sepicemia in Foals: Clinical Signs
Depend on body system involved. Depression, lethargy, dehydration, tachypnea, muddy mm, poor pulse.
Sepicemia in Foals: Diagnosis
History, PE
Sepicemia in Foals: Lab Findings
Neutropenia, L shift, toxic neutrophils, hyperfibrinogenemia, azotemia, low IgG level (<200 mg/dL)
Sepicemia in Foals: Treatment
Borad-spectrum antibiotics (Pen w/amikacin), plasma to raise IgG levels, banamine
Strangles: Etiology
Streptococcus equi, G+ coccus
Strangles: Epidemiology
Horses, donkeys, mules. Transmission via fomites and direct contact.
Strangles: Clinical Signs
Fever, mucopurulent nasal discharge, depression, submandibular lymphadenopathy, abscess in lymph nodes.
Strangles: Diagnosis
Bacterial culture from exudate of abscess or nasal swab samples.
Strangles: Lab Findings
3 negative swabs needed, each 4-7 days apart to consider cured.
Strangles: Treatment
Keep warm, dry, dust free.
Warm compress to facilitate abscessation.
Ruptured abscess should be flushed with betadine. NO ABX!! Vaccine available.
Subsolar Abscess: Etiology
Puncture wounds from poor shoeing or stepping on foreign object.:
Subsolar Abscess: Clinical Signs
Lameness is usually severe, will point affected foot when standing, heat, pain, draining at coronary band.
Subsolar Abscess: Diagnosis
Confirm with hoof testers, observing abscess when dead tissue is scraped away.
Subsolar Abscess: Treatment
Foreign bodies should be removed, necrotic tussue should be removed, boot with cotton pad soaked in magnesium sulfate.
Uveitis: Etiology
Apaloosas are predisposed.
Uveitis: Clinical Signs
Acute: blepharospasm, epiphora, episcleral injetion, corneal edema, aqueous flare, fibrin clots, miosis.
Chronic: corneal scarring, glaucoma, cataracts.
Uveitis: Diagnosis
Clinical Signs
Undelying cause should be correctd. Systemic and topical meds, pred, dex, flurbiprofen. Topical atropine.
EEE, WEE: Etiology
EEE, WEE: Epidemiology
Spread by arthropods-mosquitos
EEE, WEE: Clinical Signs
Weakness, ataxia, stumbling, staggering, circling, muscle fasciculations, head pressing, blindness, seizures, death.
EEE, WEE: Diagnosis
IgM antibody caprure ELISA.
DDx: rabies, equine herpes 1, EPM, toxicity
EEE, WEE: Treatment
Viral Myeloencephalopathy: Etiology
Equine herpes virus 1 and 4
Viral Myeloencephalopathy: Epidemiology
Ubiquitous in horses worldwide. Respiratory in foals. Abortion in mares. Trans: nasal secretions, fetuses, placenta.
Viral Myeloencephalopathy: Clinical Signs
Fever, nasal discharge, pharyngitis, cough, anorexia, submandibular
Viral Myeloencephalopathy: Lab Findings
Neutropenia, lymphopenia
Viral Myeloencephalopathy: Treatment
No specific treatment.
Horses are immune after natural infections and subsequent births are normal. Vaccines available.
Equine Influenza: Etiology
Influenza Virus
Equine Influenza: Epidemiology
Transmitted by inhalation of respiratory secretions.
Equine Influenza: Clinical Signs
High fever, serous nasal discharge, submandibular lymphadenopathy, coughing, depression, anorexia, weakness. Resolve in 3 days.
Equine Influenza: Diagnosis
Presence of rapid spread of a respiraotyr infection in a group of horses characterized with rapid onset and signs. Confirmed by virus isolation.
Equine Influenza: Treatment
Rest and supportive care. Rested 1 week for every day of fever, minimum of 3 weeks. NSAIDs for fever.
Vaccine available.
Equine Viral Arteritis: Etiology
Equine Arteritis Virus
Equine Viral Arteritis: Epidemiology
Transmitted via aerosol, discharges, semen. Localizes in vascular endothelium. Highest in Standardbred and Warmbloods.
Equine Viral Arteritis: Clinical Signs
Fever, depression, limb edema (hindlimbs), edema of scrotum, conjunctivitis, nasal discharge, abortion.
Abortion in mares from 3-10 months.
Equine Viral Arteritis: Diagnosis
Aborted fetusus partially autolozed and devoid of lesions. Nasopharyngeal or conjunctival swabs or blood for VI or PCR.
Equine Viral Arteritis: Lab Findings
Equine Viral Arteritis: Treatment
No known treatment.
Vaccine available.
Vesiclular Stomatitis: Etiology
Vesicular stomatitis virus-New Jersey or Indiana. Vesiculovirus in Rhabdoviridae.
Vesiclular Stomatitis: Epidemiology
Sporadic in US in SW. Transmission: direct contact, blood sucking insects-black flies.
Vesiclular Stomatitis: Clinical Signs
Ptyalism, ulcers in oral cavity, sloughing of tongue epithelium, lesions at mucocutaneous junctions, erosions of coronary bands. Dz is self limiting.
Vesiclular Stomatitis: Treatment
No specific treatment.
Affected animal should be isolated.
West Nile Virus: Etiology
West Nile Virus: Epidemiology
Maintained in wild birds and Culex mosquitos. Horses of all ages.
West Nile Virus: Clinical Signs
Neuro abnormalities (spinal): asymetric multifocal or diffuse ataxia, paresis, colic, lameness, anorexia, fever.
West Nile Virus: Diagnosis
ELISA, serology: IgM rises sharply and then falls in first 6-8 weeks.
West Nile Virus: Treatment
No specific treatment. Pain and inflammation control (banamine), preventing injuries from ataxia. Prevent with vaccine, mosquito control.
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