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267 Cards in this Set
- Front
- Back
Etiology of Salmonellosis
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Salmonella typhimurium and others
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How is Salmonellosis spread
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from infected horses through the environment and fomites. Stress has an important role.
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Clinical Signs of Salmonellosis.
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No signs to acute, severe diarrhea. Depresion, fever, anorexia, soft to watery feces, foul smelling.
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Diagnosis of Salmonellosis
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Clinical signs, chem values, isolation of salmonella from feces, blood or tissue.
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Lab findings of Salmonellosis
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Neutropenia, dehydration, metabolic acidosis.
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Treatment for Salmonellosis
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IV fluides, Abx controversial
NSAID: Banamine. Prevent by keeping areas clean. |
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Etiology of Potomac Horse Fever
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Neorikettsia risiticii (Gram -)
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Epdemiology of Potomac Horse Fever
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Horses of all ages. Spring, summer, early fall. Snails infested with trematodes that have the bacteria. Infected from ingestion of aquatic insects.
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Clinical Signs Potomac Horse Fever
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Mild depression and anorexia, fever, moderate to severe diarrhea.
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Potomac Horse Fever: Diagnosis
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Clinical signs, seasonal and geographical evidence. Confirmed through isolation.
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Laboratory findings: Potomac Horse Fever
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Leukopenia, leukocytosis or normal.
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Treatment for Potomac Horse Fever:
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Oxytetracycline. Vaccine is available.
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Clostridial Enterocolitis: Etiology
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Clostridium perfringens or difficile.
From Merck: C perfringens (types A, B, C, and D), C sordellii , C difficile , and C cadaveris |
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Clostridial Enterocolitis: Epidemiology
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Horses and foals that have altered intestinal normal flora.
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Clostridial Enterocolitis: Clinical Signs
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Sudden death, diarrhea with or without blood, colic, reduced feed intake, lethargy.
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Clostridial Enterocolitis: Diagnosis
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Mortality is high (especially with C perfringins type C) Usually made at necropsy by isolation of bacteria.
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Clostridial Enterocolitis: Treatment
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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. |
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Clostridial Enterocolitis: Predisposition
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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). |
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Inflammatory Airway Disease: Etiology
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Proposed: allergic airway, recurrent pulmonary stress, inhalationof dust, pollutants, viral infections.
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Inflammatory Airway Disease: Signs
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Chronic cough, mucoid to mucopurulent nasal discharge.
Endoscopy: mucopurulent exudate in pharynx, trachea, and bronchi |
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Inflammatory Airway Disease: Diagnosis
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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) |
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Inflammatory Airway Disease: Treatment
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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. |
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What does cytologic evaluation of bronchoalveolar fluid reveal in Inflammatory Airway Disese?
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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) |
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Culicoides Hypersensitivity: Etiology
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Culicoides gnats
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Culicoides Hypersensitivity: Epidemiology
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Horses allergic to these gnats. Warm months.
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Culicoides Hypersensitivity: Clinical Signs
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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.
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Culicoides Hypersensitivity: Diagnosis
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History of seasonality, locations of lesions, response to therapy.
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Culicoides Hypersensitivity: Treatment
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Keep horses inside from dusk to dawn, fly spray, prednisone if pruritis is bad.
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Equine Infectious Anemia: Etiology
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Lentivirus in the retroviridae family
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Equine Infectious Anemia: Epidemiology
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Blood feeding insects initiate most infections; tabanids, horseflies, deerflies.
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Equine Infectious Anemia: Clinical Signs
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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 |
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Equine Infectious Anemia: Diagnosis
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Clinical Signs, Coggins test (AGID)
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Equine Infectious Anemia: Lab Findings
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Anemia, low platelet count
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Equine Infectious Anemia: Treatment
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No specific treatment or vaccine.
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Equine Infectious Anemia: Necropsy findings
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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.
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Foal pneumonia: Etiology
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Rhodococcus equi, G+
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Foal pneumonia: Epidemiology
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Foals 1-5 months old.
Ubiquitous in the environment. High temps, sandy soil, dust favors spread. |
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Foal pneumonia: Clinical Signs
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Difficult to detect until pulmonary lesions are present. Lethargic, febrile, tachypnic.
Crackles and wheezes. |
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Foal pneumonia: Diagnosis
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CBC, chem, signs, thoracic rads.
Nodular lung lesions with mediastinal lymphadenopathy. Confirm by bacterial culture. |
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Foal pneumonia: Laboratory Findings
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Bronchopneumonia, pulmonary abscessation, suppurative lymphadenitis.
Neutrophilia, hyperfibrinogenemia. |
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Foal pneumonia: Treatment
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Azithromycin and rifampin.
Prevent by decreasing exposure, early detection, ensure foals get colostrum. |
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Acute Bronchointerstitial Pneumonia:
Etiology |
Unclear
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Acute Bronchointerstitial Pneumonia:
Epidemiology |
Foals 1 wk to 8 mo.
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Acute Bronchointerstitial Pneumonia:
Clinical Signs |
Fever, reluctant to move, cyanosis, respiratory distress.
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Acute Bronchointerstitial Pneumonia:
Diagnosis |
Clinical Signs, PE, thoracic rads.
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Acute Bronchointerstitial Pneumonia:
Lab Findings |
Hypoxemia, hypercapnia, respiratory acidosis, hyperfibrinogenemia,
leukocytosis. |
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Acute Bronchointerstitial Pneumonia:
Treatment |
Symptomatic, NSAIDs, broad-spectrum antibiotics, bronchodilation, oxygen.
Mortality is high. |
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Pleuropneumonia: Etiology
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Step, E. coli, Actinobacillus, Klebsiella, Staph, Pasteurella, Clostridium, Fusobacterium
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Pleuropneumonia: Epidemiology
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Race horses mostly. Viral infection, transport, anesthesia, exercise predisposes.
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Pleuropneumonia: Clinical Signs
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Fever, depression, lethargy, inappetence, pleural pain, short strides, guarding thorax, shallow respiration, reluctant to lie down.
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Pleuropneumonia: Diagnosis
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Thoracic ultrasound, thoracocentisis and fluid analysis, increased cellularity and total protien.
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Pleuropneumonia: Laboratory Findings
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Reflect bacterial sepsis or toxemia: neutropenia with left shift, hemoconcentration, azotemia.
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Pleuropneumonia: Treatment
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Chest tube to drain fluid, daily flushing, antibiotics (pen, gent, metro), and NSAIDs
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Botulism-Shaker Foal Syndrome:
Etiology |
Clostridium botulinum
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Botulism-Shaker Foal Syndrome:
Epidemiolgy |
Grows in decaying animal and plant material. Shaker foals are <4 weeks.
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Botulism-Shaker Foal Syndrome:
Clinical Signs |
Progressive motor paralysisdisturbed vision, difficulty chewing and swallowing
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Botulism-Shaker Foal Syndrome:
Diagnosis |
Eliminate other causes of paralysis
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Botulism-Shaker Foal Syndrome:
Treatment |
fix the diet, eliminate the source.
Guanidine hydrochloride shows some ealry efficacy. |
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Bowed Tendon, Tendonitis,
Desmitis: Etiology |
Inflammation of the tendon
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Bowed Tendon, Tendonitis,
Desmitis: Epidemiology |
Horses used at fast work (race horses).
Superficial flexor tendons in forelimb usually. |
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Bowed Tendon, Tendonitis,
Desmitis: Clinical Signs |
Severe lameness, heat, pain, swelling
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Bowed Tendon, Tendonitis,
Desmitis: Diagnosis |
Ultrasound can visualize defects.
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Bowed Tendon, Tendonitis,
Desmitis: Treatment |
Best treated early, stall rest, cold packs, NSAIDs, support/immobilization
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Chronic Obstructive Pulmonary Disease:
Etiology |
AKA Recurrent Airway Dz.
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Chronic Obstructive Pulmonary Disease:
Epidemiology |
Average age is 9 yrs. All breeds, both sexes, heritable component.
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Chronic Obstructive Pulmonary Disease:
Clinical Signs |
Allergic resp. dz. Flared nostrils, tachypnea, cough, heave line, abd. breathing, wheezes.
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Chronic Obstructive Pulmonary Disease:
Diagnosis |
History and PE.
Flattening of diaphragm on rads. |
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Chronic Obstructive Pulmonary Disease:
Lab Findings |
Overinflated lungs. (flat diaphragm) on rads.
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Chronic Obstructive Pulmonary Disease:
Treatment |
Reduce allergen exposure.
Soak hay with water, bronchodilators, steroids. |
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Contagious Equine Metritis: Etiology
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Taylorella equigenitalis, gram - coccobacillus
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Contagious Equine Metritis: Epidemiology
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Mares and stallions.
Spread during mating or AI or contaminated instruments. Found on and around stallion penis. |
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Contagious Equine Metritis: Signs
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Mares: Copious mucopurulent vaginal discharge 10-14 days after mating.
Stallions are asymptomatic. |
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Contagious Equine Metritis: Diagnosis
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Isolation of the organism.
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Contagious Equine Metritis: Lab Findings
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Edema and hyperemia of endometrium, endocervix, and vaginal mucosa.
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Contagious Equine Metritis: Treatment
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Clean Penis/Clitoral area with chlorihexidine and apply ntrofurazone SID X 5 days. Control through identification of those infected.
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Dermatophilosis: Etiology
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Dermatophlus congolensis
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Dermatophilosis: Epidemiology
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Chronically infected animals are reservoir. Prolonged wetting by rain, high humidity/temp, reduced natural bariers to infection
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Dermatophilosis: Clinical Signs
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Most prevalent in young, immunosuppressed.
Pruritis. |
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Dermatophilosis: Diagnosis
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Appearance of lesions and demonstration of organism.
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Dermatophilosis: Lab Findings
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Crusts of scab formation with yellow-green pus underneath.
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Dermatophilosis: Treatment
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Antibiotics: Chloramphenicol, streptomycin, amoxicillin, tetracyclines.
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Dorsal Displacement of the Soft Palate:
Etiology |
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. |
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Dorsal Displacement of the Soft Palate:
Clinical Signs |
Gurgling respiratory noise during expiration.
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Dorsal Displacement of the Soft Palate:
Diagnosis |
Endoscopy
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Dorsal Displacement of the Soft Palate:
Treatment |
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. |
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Laryngeal Hemiplegia: Etiology
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Progressive loss of myelinated fibers of left recurrent laryngeal nerve.
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Laryngeal Hemiplegia: Epidemiology
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Likely heritable
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Laryngeal Hemiplegia: Clinical Signs
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Inspiratory noise during exercise and exercise intolerance.
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Laryngeal Hemiplegia: Diagnosis
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Endoscopy.
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Laryngeal Hemiplegia: Lab Findings
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Paresis/alysis of left arytenoid cartilage and vocal fold.
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Laryngeal Hemiplegia: Treatment
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Prosthetic laryngoplasty, laryngeal ventriculecotmy.
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Pharyngeal Lymphoid Hyperplasia-Pharyngitis: Etiology
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Lymphoid follicles in pharynx enlarge. Viral agent may be the cause.
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Pharyngeal Lymphoid Hyperplasia-Pharyngitis: Epidemiology
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Young horses. (1-3 years old)
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Pharyngeal Lymphoid Hyperplasia-Pharyngitis: Clinical Signs
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Paryngeal pain, reduced appetite, increased swallowing.
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Pharyngeal Lymphoid Hyperplasia-Pharyngitis: Diagnosis
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PE findings.
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Pharyngeal Lymphoid Hyperplasia-Pharyngitis: Laboratory Findings
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Pharyngeal lymph tissue apears hyperemic with mucoid exudate.
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Pharyngeal Lymphoid Hyperplasia-Pharyngitis: Treatment
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Treatment not necessary. Rest and NSAIDs might help if the horse is painful.
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Horse bots-Botflies: Etiology
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Gasterophilus flies
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Horse bots-Botflies: Epidemiology
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Flies lay eggs on hair and horses eat the eggs.
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Horse bots-Botflies: Clinical signs
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Can cause mild gastritis, but usually no signs.
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Horse bots-Botflies: Diagnosis
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Eggs on hair
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Horse bots-Botflies: Lab Values
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Stomach mucosal ulcerations and erosions.
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Horse bots-Botflies: Treatment
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Ivermectin
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Oxyuris-Pinworms: Etiology
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Oxyuris equi
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Oxyuris-Pinworms: Epidemiology
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Horses less than 18 months old.
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Oxyuris-Pinworms: Clinical Signs
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Intense pruritus at tail base and anus.
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Oxyuris-Pinworms: Diagnosis
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Signs, cellophane tape test
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Oxyuris-Pinworms: Treatment
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Any broad spectrum dewormer.
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Parascaris: Etiology
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Parascaris equorum
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Parascaris: Epidemiology
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Sources are young foals and environment
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Parascaris: Clinical Signs
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Heavy infections may have respiratory signs or intestinal obstruction.
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Parascaris: Diagnosis
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Demonstration of eggs in feces.
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Parascaris: Treatment
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Any borad-spectrum anthelmintic.
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Large Strongyles: Etiology
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Strongylus vulgaris, edentatus, or equinus.
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Large Strongyles: Epidemiolgy
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Infection is by ingestion of larvae.
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Large Strongyles: Clincal Signs
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S. vulgaris migrates to the cranial mesenteric artery. Anemia, weakness, emaciation, diarrhea, colic.
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Large Strongyles: Diagnosis
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Demonstration of eggs in feces.
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Large Strongyles: Treatment
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Any broad-spectrum anthelmintic.
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Enteroliths: Etiology
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Accumulation of ammonium magnesium phosphate crystals.
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Enteroliths: Epidemiology
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10 years or older, Arabs, alfalfa diet.
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Enteroliths: Clinical Signs
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History of recurrent colic. Acute onset of severe colic, distention of abdomen.
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Enteroliths: Diagnosis
|
Radiography
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Enteroliths: Treatment
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Surgery
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Cushings Disease: Etiology
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Hyperplasia or ademoma of the pars intermedia of the pituitary
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Cushings Disease: Epidemiology
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All breeds but ponies are at increased risk.
Mean age is 18-23 years. |
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Cushings Disease: Clinical signs
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Hirsutism. Coat color change, weight loss, lethargy, "cresty", laminitis.
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Cushings Disease: Diagnosis
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Clinical signs, confirmed by overnight dexamethasone suppression test.
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Cushings Disease: Lab Findings
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Mild anemia, neutrophilia, lymphopenia, hyperglycemia, increased cortisol.
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Cushings Disease: Treatment
|
Body clip, treat laminitis, maintain good oral health.
Pergolide is effective: dopamine agonist. |
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Exercise Induced Pulmonary Hemorrhage:
Etiology |
Proposed: high pulmonary vascular pressure during exercise, pulmonary neovascularization, coag. dysfunction.
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Exercise Induced Pulmonary Hemorrhage: Epidemiology
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Occurs in the majority of race horses.
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Exercise Induced Pulmonary Hemorrhage:
Clinical Signs |
Epistaxis
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Exercise Induced Pulmonary Hemorrhage: Lab Findings
|
Endoscopy: blood in airways 30-90 minutes after exercise.
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Exercise Induced Pulmonary Hemorrhage:
Treatment |
Furosemide reduces severity and improves race performance.
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Sporadic Exertional Rhabdomyolysis-Tying up: Etiology
|
Necrosis of skeletal mm. after intense exercise.
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Sporadic Exertional Rhabdomyolysis-Tying up: Epidemiology
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Exercise exceeding the state of training.
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Sporadic Exertional Rhabdomyolysis-Tying up: Clinical Signs
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Excessive sweating, tachypnea, tachycardia, mm fasiculations, painful lumbar and gluteal mm after exercise.
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Sporadic Exertional Rhabdomyolysis-Tying up: Diagnosis
|
Signs of mm cramping, no history of previous episodes, stiffness after exercise, elevated CK and AST.
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Sporadic Exertional Rhabdomyolysis-Tying up: Lab Findings
|
Elevated CK and AST adn lactate dehydrogenase.
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Sporadic Exertional Rhabdomyolysis-Tying up: Treatment
|
Tranquilizers, NSAIDs, opiods, stall rest for a couple days, gradual increase back to training.
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PSSM: etiolopgy
(aka tying up or monday morning dz) |
Chronic Exertional Rhabdomyolysis
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PSSM: Epidemiology
|
Quarter horse, Warmbloods, Draft horses.
Rest for a few days prior to exercise predisposes. |
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PSSM: Clinical Signs
|
Tucked up abdomen, camped-out stance, muscle fasiculations, sweating, hindlimb stiffness.
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PSSM: Diagnosis
|
Signs of muscle cramping, history of previous episodes, stiffness after exercise.
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PSSM: Lab Findings
|
Elevated CK and AST and lactate dehydrogenase.
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PSSM: Treatment
|
Tranquilizers, NSAIDs, opiods, stall rest for a few days, gradual increase back to training.
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Recurrent Exertional Rhabdomyolysis:
Etiology |
Chronic Exertional Rhabdomyolysis
|
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Recurrent Exertional Rhabdomyolysis:
Epidemiology |
Thoroghbreds, Standardbreds, Arabs.
Likely d/t abn regulation of intracellular Ca in skeletal mm. |
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Recurrent Exertional Rhabdomyolysis:
Clinical Signs |
Intermittent disruption of mm contraction.
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Recurrent Exertional Rhabdomyolysis:
Diagnosis |
Hx, Clin Signs, elevated CK and AST,
mm bx. |
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Recurrent Exertional Rhabdomyolysis:
Lab Findings |
Elevated CK and AST and lactate dehydrogenase.
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Recurrent Exertional Rhabdomyolysis:
Treatment |
Decrease trigger factors of nervousness or excitement.
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Gastrointestinal Ulceration Etiology
|
Increased exposure to HCl acid secondary to fasting, not nursing, intense exercise.
|
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Gastrointestinal Ulceration: Epidemiology
|
In 50% of foals, in 90% of race horses.
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Gastrointestinal Ulceration: Clinical Signs
|
Usually none. If it becomes severe, diarrhea, dorsal recumbancy, ptyalism, colic, poor appetite, attitude change.
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Gastrointestinal Ulceration: Diagnosis
|
Gastroscopy.
|
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Gastrointestinal Ulceration: Treatment
|
Often heal by themselves. Can use Cimetidine and rantidine and omeprazole.
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Empyema: Etiology
|
usually d/t Strept. equi infection
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Empyema: Epidemiolgy
|
Just having strangles.
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Empyema: Clinical Signs
|
Intermittent purulent nasal discharge, painful swelling in parotid area.
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Empyema: Diagnosis
|
Scope gutteral pouch
|
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Empyema: Treatment
|
Gutteral pouch lavage is necessary with systemic antibiotics
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Gutteral Pouch Mycosis: Etiology
|
Aspergillus spp.
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Gutteral Pouch Mycosis: Epidemiology
|
Most common cause of severe hemorrhage from gutteral pouch.
|
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Gutteral Pouch Mycosis: Clinical Signs
|
Epistaxis, dysphagis, Horner's, dorsal displcement of the soft palate.
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Gutteral Pouch Mycosis: Diagnosis
|
Endoscopy of gutteral pouch
|
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Gutteral Pouch Mycosis: Lab findings
|
Fungal plaques on the caudodorsal aspect of the medial compartment.
|
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Gutteral Pouch Mycosis: Treatment
|
Topical and systemic antibiotics
|
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Hyperlipemia and Hepatic Lipidosis:
Etiology |
High fat in blood stream or liver
|
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Hyperlipemia and Hepatic Lipidosis:
Epidemiology |
Poor fed quality or decrease in feed intake during high energy requirement. Most common in ponies, mini horses, donkeys.
|
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Hyperlipemia and Hepatic Lipidosis:
Clinical Signs |
Lethargy, weakness, anorexia, decreased water intake
|
|
Hyperlipemia and Hepatic Lipidosis:
Diagnosis |
Signalment, history, clincal signs, white to yellow plasma, serum triglyceride >500mg/dl confirms.
|
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HYPP (Hyperkalemic Periodic Paralysis):
Etiology |
Autosomal dominant trait
|
|
HYPP (Hyperkalemic Periodic Paralysis):
Epidemiology |
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):
Diagnosis |
DNA testing of mane and tail
|
|
HYPP (Hyperkalemic Periodic Paralysis):
Treatment |
Acute death common.
Calcium gluconate or IV dextrose alone or combo with bicarb. |
|
Neonatal Isoerythrolysis: Etiology
|
Absorbed colostral antibodies against foals RBC.
|
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Neonatal Isoerythrolysis: Epidemiology
|
Occurs between 12 hours and 4 days of age.
|
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Neonatal Isoerythrolysis: Clinical Signs
|
Pale MM, icterus, depression, anorexia, tachypnea, hemoglobinuria, collapse.
|
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Neonatal Isoerythrolysis: Diagnosis
|
Incompatible minor agglutination cross match and positive Coombs test.
|
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Neonatal Isoerythrolysis: Lab findings
|
Anemia, hemoglobinuria
|
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Neonatal Isoerythrolysis: Treatment
|
Affected foals should be muzzled to prevent further absorption of immunoglobulins. Screen broodmares to control.
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Severe Combined Immunodeficiency (SCID): Etiology
|
Inheritied autosomal recessive disease.
|
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Severe Combined Immunodeficiency (SCID): Epidemiology
|
Arabs. Foals don't live past 6 months.
|
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Severe Combined Immunodeficiency (SCID): Clinical Signs
|
Normal at birth, and for first few months. Then recurrent infections, and death.
|
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Severe Combined Immunodeficiency (SCID): Diagnosis
|
Demonstrate foal is homozygous for SCID gene.
|
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Severe Combined Immunodeficiency (SCID): Lab Findings
|
Lack T and B cell responses.
|
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Severe Combined Immunodeficiency (SCID): Treatment
|
Disease is always fatal.
|
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Laminitis: Etiology
|
Ischemia that leads to the breakdown of the union between the horny and sensitive laminae.
|
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Laminitis: Epidemiology
|
Carbohydrate/grain overload, grazing on lush pasture, endotoxemia, colic, excessive use of corticosteroids.
|
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Laminitis: Clinical Signs
|
Depression, anorexia, slow, crouching, short-strided gait, bounding digital pulse.
|
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Laminitis: Diagnosis
|
History and clinical signs. rotation of coffin bone on radiographs
|
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Laminitis: Lab Findings
|
May show rotation of coffin bone on rads.
|
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Laminitis: Treatment
|
With Grain Overload: 1 gallon mineral oil PO, hot packs on feet, isoxsurine hydrochloride (vasodilator), banamine, special shoes, hoofcare
|
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Navicular Disease: Etiology
|
Damage to flexor surface of navicular bone and osteophyte formation. Cause is unknown.
|
|
Navicular Disease: Epidemiology
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A disease of mature riding horses, usually in the forelimbs.
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Navicular Disease: Clinical Signs
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Keeps the hela of effected foot off the ground. Short stride, stumble, flexion test shows lameness.
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Navicular Disease: Diagnosis
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HIstory and PE findings
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Navicular Disease: Treatment
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Palmar digital nerve block, rest, proper foot care, NSAIDs, intrabursal corticosteriods, palmar digital neurectomy.
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Stringhalt: Epidemiology
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Any breed, rare in foals. Myoclonic affliction of one or both hindlimbs.
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Stringhalt: Clinical Signs
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Hyperflexion while walking, high-stepping gait. Severe cases, atrophy of thigh muscles.
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Stringhalt: Diagnosis
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Clinical signs, confirmed by electromyography.
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Navicular Disease: Laboraory Findings
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Rads show degenerative changes of navicular bone: osteophytes on lateral and proximal border.
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Stringhalt: Treatment
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Many recover spontaneously.
Chronic: lateral extensor tenectomy. Not all cases respond. |
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Peritonitis: Etiology
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Most common from injury to serosal surface of GI tract and ingesta leaks into abdomen.
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Peritonitis: Epidemiology
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Any Horse
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Peritonitis: Clinical Signs
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Severe colic, ileus, distended intestines, gastric reflux, occasional diarrhea, tachycardia, weak pulse, fever.
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Peritonitis: Diagnosis
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Abnormal feces, intestinal stasis, abdominal pain, abnormal peritoneal fluid.
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Peritonitis: Laboratory Findings
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Neutropenia with left shift.
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Peritonitis: Treatment
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IV fluids, electrolytes, broad-spectrum antibiotics (gent, pen, metro), surgery
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EPM:Etiology
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Sarcocystis neurona-protozoan
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EPM: Epidemiology
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Horse is dead end host, opossum is natural host.
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EPM: Clinical Signs
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Can infect any part of CNS. Spinal cord involvement more common. Weakness or ataxia in one or all limbs.
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EPM: Diagnosis
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Postmortem diagnosis confirmed by demonstration of protozoa in CNS lesions. Antibodies in CSF diagnostic.
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EPM: Lab Findings
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CSF analysis: mononuclear pleocytosis, increased protein
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EPM: Treatment
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Ponazril or nitazoxanide for 6 months. Relapses are common.
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Sepicemia in Foals: Etiology
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Gram -, E. coli, Klebsiella, Enterobacter, Actinobacillus, Pseudomonas
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Sepicemia in Foals: Epidemiology
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Usually foals have failure of passive transfer.
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Sepicemia in Foals: Clinical Signs
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Depend on body system involved. Depression, lethargy, dehydration, tachypnea, muddy mm, poor pulse.
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Sepicemia in Foals: Diagnosis
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History, PE
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Sepicemia in Foals: Lab Findings
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Neutropenia, L shift, toxic neutrophils, hyperfibrinogenemia, azotemia, low IgG level (<200 mg/dL)
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Sepicemia in Foals: Treatment
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Borad-spectrum antibiotics (Pen w/amikacin), plasma to raise IgG levels, banamine
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Strangles: Etiology
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Streptococcus equi, G+ coccus
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Strangles: Epidemiology
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Horses, donkeys, mules. Transmission via fomites and direct contact.
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Strangles: Clinical Signs
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Fever, mucopurulent nasal discharge, depression, submandibular lymphadenopathy, abscess in lymph nodes.
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Strangles: Diagnosis
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Bacterial culture from exudate of abscess or nasal swab samples.
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Strangles: Lab Findings
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3 negative swabs needed, each 4-7 days apart to consider cured.
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Strangles: Treatment
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Keep warm, dry, dust free.
Warm compress to facilitate abscessation. Ruptured abscess should be flushed with betadine. NO ABX!! Vaccine available. |
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Subsolar Abscess: Etiology
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Puncture wounds from poor shoeing or stepping on foreign object.:
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Subsolar Abscess: Clinical Signs
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Lameness is usually severe, will point affected foot when standing, heat, pain, draining at coronary band.
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Subsolar Abscess: Diagnosis
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Confirm with hoof testers, observing abscess when dead tissue is scraped away.
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Subsolar Abscess: Treatment
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Foreign bodies should be removed, necrotic tussue should be removed, boot with cotton pad soaked in magnesium sulfate.
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Uveitis: Etiology
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Apaloosas are predisposed.
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Uveitis: Clinical Signs
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Acute: blepharospasm, epiphora, episcleral injetion, corneal edema, aqueous flare, fibrin clots, miosis.
Chronic: corneal scarring, glaucoma, cataracts. |
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Uveitis: Diagnosis
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Clinical Signs
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Uveitis:Treatment
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Undelying cause should be correctd. Systemic and topical meds, pred, dex, flurbiprofen. Topical atropine.
Banamine. |
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EEE, WEE: Etiology
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Arboviruses
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EEE, WEE: Epidemiology
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Spread by arthropods-mosquitos
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EEE, WEE: Clinical Signs
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Weakness, ataxia, stumbling, staggering, circling, muscle fasciculations, head pressing, blindness, seizures, death.
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EEE, WEE: Diagnosis
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IgM antibody caprure ELISA.
DDx: rabies, equine herpes 1, EPM, toxicity |
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EEE, WEE: Treatment
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Supportive.
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Viral Myeloencephalopathy: Etiology
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Equine herpes virus 1 and 4
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Viral Myeloencephalopathy: Epidemiology
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Ubiquitous in horses worldwide. Respiratory in foals. Abortion in mares. Trans: nasal secretions, fetuses, placenta.
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Viral Myeloencephalopathy: Clinical Signs
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Fever, nasal discharge, pharyngitis, cough, anorexia, submandibular
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Viral Myeloencephalopathy: Lab Findings
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Neutropenia, lymphopenia
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Viral Myeloencephalopathy: Treatment
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No specific treatment.
Horses are immune after natural infections and subsequent births are normal. Vaccines available. |
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Equine Influenza: Etiology
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Influenza Virus
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Equine Influenza: Epidemiology
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Transmitted by inhalation of respiratory secretions.
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Equine Influenza: Clinical Signs
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High fever, serous nasal discharge, submandibular lymphadenopathy, coughing, depression, anorexia, weakness. Resolve in 3 days.
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Equine Influenza: Diagnosis
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Presence of rapid spread of a respiraotyr infection in a group of horses characterized with rapid onset and signs. Confirmed by virus isolation.
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Equine Influenza: Treatment
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Rest and supportive care. Rested 1 week for every day of fever, minimum of 3 weeks. NSAIDs for fever.
Vaccine available. |
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Equine Viral Arteritis: Etiology
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Equine Arteritis Virus
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Equine Viral Arteritis: Epidemiology
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Transmitted via aerosol, discharges, semen. Localizes in vascular endothelium. Highest in Standardbred and Warmbloods.
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Equine Viral Arteritis: Clinical Signs
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Fever, depression, limb edema (hindlimbs), edema of scrotum, conjunctivitis, nasal discharge, abortion.
Abortion in mares from 3-10 months. |
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Equine Viral Arteritis: Diagnosis
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Aborted fetusus partially autolozed and devoid of lesions. Nasopharyngeal or conjunctival swabs or blood for VI or PCR.
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Equine Viral Arteritis: Lab Findings
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Leukopenia
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Equine Viral Arteritis: Treatment
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No known treatment.
Vaccine available. |
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Vesiclular Stomatitis: Etiology
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Vesicular stomatitis virus-New Jersey or Indiana. Vesiculovirus in Rhabdoviridae.
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Vesiclular Stomatitis: Epidemiology
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Sporadic in US in SW. Transmission: direct contact, blood sucking insects-black flies.
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Vesiclular Stomatitis: Clinical Signs
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Ptyalism, ulcers in oral cavity, sloughing of tongue epithelium, lesions at mucocutaneous junctions, erosions of coronary bands. Dz is self limiting.
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Vesiclular Stomatitis: Treatment
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No specific treatment.
Affected animal should be isolated. |
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West Nile Virus: Etiology
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Flaviviridae
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West Nile Virus: Epidemiology
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Maintained in wild birds and Culex mosquitos. Horses of all ages.
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West Nile Virus: Clinical Signs
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Neuro abnormalities (spinal): asymetric multifocal or diffuse ataxia, paresis, colic, lameness, anorexia, fever.
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West Nile Virus: Diagnosis
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ELISA, serology: IgM rises sharply and then falls in first 6-8 weeks.
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West Nile Virus: Treatment
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No specific treatment. Pain and inflammation control (banamine), preventing injuries from ataxia. Prevent with vaccine, mosquito control.
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