Horses Flashcards

Question

**What is the treatment for persistent epistaxis from guttural pouch mycosis?** - Systemic itraconazole - Occlusion of appropriate artery or arteries - Ligation of the external carotid artery - Ligation of the external jugular vein

Answer 1

Answer: **Occlusion of appropriate artery or arteries** Explanation The correct answer is occlusion of appropriate artery or arteries. This closes off the artery over the guttural pouch, which has been destroyed by the fungal infection. Systemic itraconazole will not stop the bleeding. *The treatment for persistent epistaxis due to guttural pouch mycosis is the occlusion of the appropriate artery or arteries. This procedure stops the bleeding by closing off the artery that has been damaged by the fungal infection. Systemic itraconazole is ineffective in stopping the bleeding.* **Guttural Pouch Mycosis in Horses - Comprehensive Veterinary Information** Definitions and Terminology: • Guttural Pouch Mycosis: A fungal infection of the guttural pouch, often life-threatening. Causative Agents: • Primary Fungus: Aspergillus spp. Physiopathology: • Location: Fungal plaques form on the caudodorsal aspect of the medial guttural pouch over the internal carotid artery. • Complications: Damage to cranial nerves and arteries, leading to hemorrhage and nerve dysfunction. Clinical Signs: • Epistaxis: Spontaneous, severe nasal bleeding, possibly recurrent. • Neurologic Signs: Dysphagia, Horner syndrome, dorsal displacement of the soft palate, facial paralysis. Diagnosis: • Endoscopy: Visualization of fungal plaques. • Clinical Signs: Observation of epistaxis and neurologic deficits. Treatment: • Antifungal Therapy: Prolonged topical and systemic antifungal treatment. • Surgical Intervention: Occlusion of affected arteries (ligation, balloon catheter, or transarterial coil embolism) to prevent fatal hemorrhage and arrest fungal growth. Prognosis: • Varies: Based on severity of hemorrhage and neurological involvement.

Answer 2

Answer: **Hypoventilation， respiratory acidosis** Explanation The correct answer is hypoventilation, respiratory acidosis. Hypoventilation is defined by the PaCO2. Normal is about 40 (35-45). This horse has an elevated PaCO2 indicating he is under-ventilating and not blowing off sufficient CO2. This increase in CO2 causes a respiratory acidosis because CO2 is an acid that interacts with carbonic anhydrase to form carbonic acid. This is why the horse's pH is low (normal pH is about 7.4). The relatively normal base excess indicates there is minimal metabolic component to this horse's acidosis. *The horse’s status is hypoventilation with respiratory acidosis. The elevated PaCO2 (60 mmHg) indicates inadequate ventilation, leading to CO2 retention, which causes respiratory acidosis by forming carbonic acid. The low pH (7.255) confirms acidosis, and the normal base excess suggests minimal metabolic involvement.*

Answer 3

Answer: **7th rib space at costochondral junction** Explanation Thoracocentesis can be performed at different locations; however, the 7th rib space at the level of the costochondral junction is the most appropriate answer available. The 4th rib space is near the heart, whereas the 10th or 13th rib space involves the caudal aspect of the thorax. This 7th rib space is a good choice because it is one of the more dependant regions where fluid will tend to accumulate; it is also caudal to where the heart should sit and well cranial to the diaphragm. When available, ultrasound guidance should be used to guide placement. *** PowerPage: Pneumonia and Pleuropneumonia *The proper site for thoracocentesis in a horse suspected of pleuropneumonia with pleural effusion, when ultrasound is not available, is the 7th rib space at the costochondral junction. This location is optimal because it is a dependent region where fluid accumulates and is safely positioned away from the heart and diaphragm.* **Comprehensive NAVLE Study Guide: Equine Pleuropneumonia** Definitions and Etiology: • Pleuropneumonia: A severe, often polymicrobial lung infection affecting the pleura. • Causative Agents: Primarily Streptococcus equi subsp. zooepidemicus, Pasteurellaceae, anaerobes like Bacteroides, Fusobacterium spp. • Predisposing Factors: Long-distance transportation, strenuous exercise, anesthesia, viral infections, and aspiration. Pathophysiology: • Initial Stage: Aspiration of oropharyngeal organisms leading to lung infection. • Disease Progression: The infection extends from the pulmonary parenchyma to the pleura. • Stages: • Subacute: Early bacterial proliferation, primarily facultative anaerobes. • Acute: Pneumonia and pleuritis with severe inflammation. • Chronic: Anaerobic bacteria dominate, leading to abscesses, necrosis, and poor prognosis. • End-Stage: Irreversible damage with bronchopleural fistulae and fibrosis. Clinical Signs: • Acute Signs: Lethargy, fever, pleurodynia (pleural pain), dyspnea, malodorous breath. • Chronic Signs: Weight loss, ventral edema, persistent coughing. Diagnosis: • Physical Exam: Thoracic auscultation, percussion, and observation of clinical signs. • Laboratory Tests: • Haematology: Leukocytosis or neutropenia with toxic neutrophils. • Bacteriology: Transtracheal aspiration, thoracocentesis for culture. • Imaging: Thoracic radiography and ultrasonography for pleural effusion and lung abscesses. Medications: • Antibiotics: • Penicillin: Effective against Streptococcus and many anaerobes. • Gentamicin: Targets Gram-negative aerobes but less effective in chronic cases. • Metronidazole: For penicillin-resistant anaerobes. • Ceftiofur: A broad-spectrum cephalosporin for Gram-negative coverage. • Dosages: Dependent on the stage and severity; typically administered intravenously. • Adjunct Therapies: • NSAIDs (e.g., Flunixin Meglumine): For inflammation and endotoxemia. • Bronchodilators: Limited use; examples include Clenbuterol and Isoproterenol. • Mucolytics: Limited data; Bromhexine and Dembrexine suggested. • Drainage: Essential for pleural effusion management. Treatment Protocols: • Early Stage: Aggressive antibiotic therapy with thoracic drainage. • Chronic Disease: Involves more intensive treatments, including potential thoracotomy and long-term antibiotic use. • Prognosis: Best with early intervention; worsens significantly with chronic or anaerobic infections. Important Considerations: • Anaerobic Infections: Anaerobes often signify poor prognosis; managing these requires specific antibiotics like metronidazole. • Supportive Care: Includes fluids, nutritional support, and potentially corticosteroids for inflammation.

Answer 4

Answer: **Streptococcus spp.** Explanation The most correct answer is Streptococcus spp. Streptococcus is a common cause of pneumonia in both foals and in adult horses; however, polymicrobial infections are also common. Other common bacterial isolates associated with pneumonia include E. coli, Klebsiella sp, and various anaerobic bacteria. Rhodococcus (Corynebacterium) equi is also a common cause of pneumonia in foals 2-6 months of age. Actinobacillus can be associated with pneumonia, but the other two answers are not commonly isolated from equine pneumonia. ***PowerPage: Top 9 Equine Respiratory Diseases

Answer 5

Answer: Equine adenovirus Explanation The correct answer is equine adenovirus. Adenovirus is normal in the upper respiratory tract but can cause a lower respiratory tract infection in immunocompromised individuals, particularly foals with failure of passive transfer or combined immunodeficiency. In fact, adenovirus is the most common cause of death in foals with those two conditions, leading to an often fatal pneumonia.

Answer 6

Answer: Aspergillus Explanation Aspergillus is the most commonly identified fungal pathogen in guttural pouch mycosis. While this disease can present with epistaxis, dysphagia is sometimes a presenting complaint. Remember, cranial nerves IX, X, XI, and XII travel through the pouch and may be damaged from mycotic lesions, thus resulting in dysphagia. If you are unfamiliar with endoscopic images of the equine guttural pouch, the mycotic lesion is seen from approximately 1 to 7 o'clock while the stylohyoid bone is evident in the left side of the image. ***PowerPage: Guttural Pouch Disease ***PowerLecture: Neurologic Disorders

Answer 7

Answer: **Exercise-induced pulmonary hemorrhage** Explanation The correct answer is exercise-induced pulmonary hemorrhage. This has multiple other names, and horses with this condition are sometimes referred to as bleeders or as bobbling, chocking, or gurgling. It is thought to be extremely common in Thoroughbreds. In this condition, following exercise at speed and large efforts from the lungs, pulmonary damage occurs and bleeding starts, usually in the caudal dorsal lung lobes. Common clinical signs are excessive swallowing after exercise because the horse is swallowing blood that was brought up. They may also cough to clear blood from their airways. Epistaxis is actually only seen in about 10% of horses with exercise-induced pulmonary hemorrhage. The other options in this question such as airway disease and heart failure would not be consistent with this horse's excessive swallowing after racing. ***PowerLecture: Respiratory Diseases *The most likely diagnosis for a Thoroughbred racehorse with poor performance, labored breathing, excessive swallowing, and occasional coughing after races is exercise-induced pulmonary hemorrhage (EIPH). EIPH, common in Thoroughbreds, involves pulmonary damage and bleeding, typically in the caudal dorsal lung lobes, following intense exercise. Clinical signs include excessive swallowing due to blood in the airways, though epistaxis is seen in only about 10% of cases.* **Exercise-Induced Pulmonary Hemorrhage (EIPH) in Horses: NAVLE Study Guide** Definitions and Causative Agents • EIPH: The presence of blood in the airways of horses after strenuous exercise, commonly detected by tracheobronchoscopy or bronchoalveolar lavage (BAL). Pathophysiology • Mechanism: High intravascular pressures during exercise lead to capillary stress failure in the lungs, causing hemorrhage. Lesions predominantly occur in the caudodorsal lung fields. • Progression: EIPH is progressive, with repeated episodes leading to pulmonary fibrosis, vascular remodeling, and potentially chronic lung damage. Clinical Findings • Signs: Visible epistaxis, poor performance, and subtle signs like coughing or increased respiratory rate. • Lesions: Hemosiderin deposition, fibrosis, and venous remodeling in affected lung regions. Diagnosis • Primary Tests: Endoscopic examination post-exercise is the gold standard. BAL can identify red blood cells and hemosiderophages. • Imaging: Ultrasonography and radiography can detect lung changes, though with variable sensitivity. Treatment and Prevention • Furosemide: Administered IV 4 hours before exercise; it reduces pulmonary pressures, decreasing the severity and incidence of EIPH. • Management: Includes the use of nasal strips and minimizing exposure to dust and irritants. Horses with severe EIPH may require rest and modification of training regimens. Prognosis • Impact on Performance: Severe EIPH (Grade 4) is associated with shorter racing careers and poorer race outcomes. Horses with less severe EIPH (Grades 1-3) can still perform well with proper management. • Long-Term Effects: Repeated episodes may lead to significant lung damage and reduced athletic capacity. Key Points for Veterinary Professionals • Early Detection: Regular monitoring using endoscopy or BAL in at-risk horses. • Prophylaxis: Furosemide remains the primary intervention, though its use is controversial due to potential performance-enhancing effects. • Ongoing Research: Understanding of EIPH is still evolving, with continued research into its pathogenesis and management. [Link](https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/jvim.12593?download=true&campaigns=[{"position":"ereader-last-page","uri":"uri:707b1a3c-73e6-4188-b21f-2b05b70307d8"},{"position":"ereader-first-page","uri":"uri:7691ea89-90f5-4086-9241-486673caed61"}]b)

Answer 8

Answer: **Take nasopharyngeal swabs for viral isolation** Explanation The correct answer is to acquire *nasopharyngeal swab for viral isolation*. Given the history of a rapidly-spreading infection with fever and cough, the most likely differential is **equine influenza**. This is caused by an orthomyxovirus. Other less likely rule-outs include equine viral rhinopneumonitis and equine viral arteritis. The way to definitively diagnose this is with viral isolation; a nasopharyngeal swab is the best sample. Growth in a bacterial culture would be more likely to indicate a secondary infection than a primary pathogen. Serology could be useful, but because influenza is so ubiquitous, paired titers are really needed to yield a diagnosis. Gross necropsy findings with influenza are fairly minimal and variable. Thoracic radiographs would not give you a diagnosis. ***PowerPage: Top 9 Equine Respiratory Diseases *The best step to definitively diagnose a rapidly spreading respiratory infection with fever and cough in a large group of horses is to take nasopharyngeal swabs for viral isolation. The most likely cause is equine influenza, caused by an orthomyxovirus. Viral isolation from a nasopharyngeal swab is more reliable than bacterial culture, serology, necropsy, or thoracic radiographs.* **Comprehensive Information on Equine Influenza for BCSE Test** 1. Definitions: • Equine Influenza (EIV): A highly infectious respiratory disease caused by the influenza A virus. 2. Causative Agents: • Orthomyxovirus: Specifically A/equine type-2 (H3N8), first recognized in 1963. 3. Epidemiology: • Transmission: Direct inhalation of respiratory secretions, fomites. Epidemics arise from newly introduced infected horses. • Hosts: Primarily affects horses aged 1-5 years. 4. Clinical Findings: • Symptoms: High fever (up to 106°F), depression, anorexia, serous nasal discharge, dry harsh cough, submandibular lymphadenopathy. • Course: Symptoms appear within 1-3 days post-exposure, lasting under 3 days in uncomplicated cases. Severe cases may take up to 6 months to recover. 5. Pathophysiology: • Viral Replication: Occurs within respiratory epithelial cells, leading to destruction of tracheal and bronchial epithelium. • Complications: Secondary bacterial infections like pneumonia, chronic bronchitis, and pleuropneumonia due to compromised respiratory defenses. 6. Diagnosis: • Definitive Tests: RT-PCR, viral isolation from nasopharyngeal swabs, stall-side immunoassays, antigen-capture ELISA, serology. • Sampling: Nasopharyngeal swabs early in illness (1-2 days post-onset). 7. Treatment: • Supportive Care: Rest, NSAIDs for fever control, antibiotics for secondary bacterial infections. • Rest Period: 1 week of rest for every day of fever, minimum 3 weeks. 8. Prevention: • Biosecurity: Isolation of new or sick horses, hygiene practices. • Vaccination: Inactivated and modified-live vaccines; biannual boosters for high-risk horses. Intranasal vaccines provide rapid protection. 9. Medications: • NSAIDs: Control fever and inflammation. • Examples: Flunixin meglumine, phenylbutazone. • Antibiotics: For secondary bacterial infections. • Examples: Trimethoprim-sulfamethoxazole, penicillin. 10. Key Points: • Vaccination and Biosecurity: Crucial for prevention and control of outbreaks. • EIV vs. Other Respiratory Diseases: Rapid spread, high fever, and severe cough help differentiate from other viral infections like EHV-1 and EHV-4. https://www.merckvetmanual.com/respiratory-system/respiratory-diseases-of-horses/equine-influenza

Answer 9

Answer: Scents are moved to the vomeronasal organ Explanation The flehmen response, as described in the question, helps animals trap pheromone scents in the vomeronasal organs (VNOs) so they can be analyzed more closely. Pheromones are the chemical signals emanating from other animals. When a horse draws in an organic odor, he curls up his lip to temporarily close the nasal passages and hold the particles inside. The upward head tilt seems to help the airborne molecules linger in the VNOs, which are located under the floor of the horse's nasal cavity. While sex pheromones are the most common flehmen trigger, they are not the only ones, and the response itself does not indicate sexual interest.

Answer 10

Answer: Furosemide Explanation In this instance, the discharge is blood, with the most likely diagnosis being exercise-induced pulmonary hemorrhage (EIPH). One of the most commonly administered medications for EIPH is furosemide, which seems to decrease the incidence or lessen the severity of bleeding. The exact mechanism by which this occurs is not completely known but may be associated with reduced pulmonary capillary pressure. ***PowerPage: Exercise Induced Pulmonary Hemorrhage

Answer 11

Answer: Neutrophilic inflammation Explanation In health, BAL fluid primarily consists of macrophages. However, in RAO, neutrophils are the predominant cellular finding. RAO typically affects older horses and is a response to environmental allergens. The classic case is the horse that is stalled in the winter and possibly housed in the vicinity of the hay storage. When the horse is exposed to hay allergens (via inhalation), bronchoconstriction and neutrophilic inflammation occur resulting in clinical signs. *** PowerPage: Recurrent Airway Obstruction *** PowerLecture: Respiratory Diseases The presence of neutrophilic inflammation in bronchoalveolar lavage (BAL) fluid is supportive of recurrent airway obstruction (RAO) in horses. RAO, often triggered by environmental allergens like hay dust, primarily affects older horses and leads to bronchoconstriction and neutrophilic inflammation, resulting in increased respiratory effort and expiratory wheezes. Comprehensive NAVLE Study Guide: Recurrent Airway Obstruction (RAO) in Horses Definitions and Etiology • Recurrent Airway Obstruction (RAO): Also known as heaves, previously termed chronic obstructive pulmonary disease (COPD), a hypersensitivity-mediated, chronic respiratory condition in horses characterized by airway inflammation and obstruction. • Causative Agents: Organic dust, including bacterial endotoxins, molds (Aspergillus fumigatus, Faenia rectivirgula), peptidoglycans, microbial toxins, forage mites, and other airborne particles commonly found in stables. • Predisposing Factors: Age (≥4 years), breed (Thoroughbreds), winter and spring seasons, poor ventilation, and hay or straw exposure. Pathophysiology • Inflammatory Response: Inhaled antigens trigger a delayed hypersensitivity reaction, leading to an influx of neutrophils, mucus accumulation, bronchospasm, and airway hyper-reactivity. • Chronic Changes: Persistent exposure results in airway remodeling, including smooth muscle hyperplasia, thickening of the airway walls, mucus hypersecretion, and airway obstruction. Clinical Signs • Acute Exacerbations: Increased expiratory effort, coughing, nasal discharge, exercise intolerance, and labored breathing with flared nostrils. • Chronic Cases: Persistent cough, weight loss, and decreased performance. Some horses may develop a “heave line” due to hypertrophy of the abdominal muscles used for forced expiration. Diagnosis • History and Clinical Signs: Chronic cough, dyspnea, and history of exposure to dusty environments. • Endoscopy: Visual confirmation of mucus accumulation in the trachea. • Bronchoalveolar Lavage Fluid (BALF) Cytology: Increased neutrophils (>25%), reduced macrophages and lymphocytes. • Lung Function Tests: Measurement of lung resistance, dynamic compliance, and work of breathing. Impulse oscillometry is the most commonly used method. Treatment • Environmental Management: Essential for controlling RAO; includes minimizing dust exposure by using low-dust bedding, feeding soaked or pelleted hay, and improving stable ventilation. • Medications: • Corticosteroids: First-line treatment to reduce airway inflammation. • Oral Prednisolone: Bioavailability-dependent, used to reduce airway neutrophilia. • Dexamethasone: Administered orally or intravenously, effective in severe cases. • Inhaled Corticosteroids: Beclomethasone, budesonide, fluticasone; used to deliver high concentrations locally with fewer systemic side effects. • Bronchodilators: • Beta-2 Agonists: Clenbuterol (oral), albuterol (inhaled) for short-term relief of bronchospasm. • Anticholinergics: Ipratropium, glycopyrrolate, and atropine for acute bronchodilation. • Adjunct Therapies: Antioxidants like ascorbic acid and mucolytics for supportive care. Prevention and Management • Stable Management: Maintaining a dust-free environment is crucial. Horses should be kept outdoors when possible, or in well-ventilated stables with minimal exposure to organic dust. • Monitoring and Follow-Up: Regular assessment of lung function, airway inflammation, and response to treatment through BALF cytology and lung function tests. Complications • Chronic Airway Remodeling: Prolonged inflammation can lead to irreversible changes, making management more challenging and increasing the risk of recurrent episodes. • Secondary Infections: Due to compromised airway defenses, horses may be more susceptible to bacterial infections. Prognosis • With Early Intervention: Good prognosis with appropriate environmental management and treatment. However, horses with chronic or severe RAO may have a poorer prognosis and require ongoing management.

Answer 12

Answer: Rhodococcus equi pneumonia Explanation R. equi is the most likely cause resulting in pulmonary abscess formation that may be noticed on thoracic ultrasound. In the ultrasound image, you should note the capsular structure with an anechoic center which represents a fluid-filled abscess. R. equi is typically observed in older foals (2-6 months age) and demonstrates a slow insidious onset characterized by some or all the following findings: weight loss, fever, cough, nasal discharge, increased respiratory effort, and ill-thrift. Ultrasonography of the chest can provide a quick screening test for foals with R. equi pneumonia. All the other pathogens can cause pneumonia but are not classically associated with abscess formation. *** PowerPage: Rhodococcus equi *** PowerLecture: Rhodococcus equi

Answer 13

Answer: **Facial** Explanation The correct answer is facial. The facial nerve is responsible for providing motor innervation to the muscles of facial expression. Damage to this nerve may result in an inability to blink, muzzle deviation, ear droop, lack of nostril flare, and a loss of the menace and palpebral response. The oculomotor nerve is involved in motor innervation to the dorsal, medial, and ventral rectus muscles. Additionally, this nerve innervates the palpebral levator, which is responsible for raising the upper eyelid. The trochlear nerve innervates the dorsal oblique muscle of the eyeball. Injury to this nerve will yield a dorsomedial strabismus. The trigeminal nerve provides sensation to most of the face and also motor innervation to the muscle of mastication. The abducens nerve provides motor innervation to the lateral rectus and part of the retractor bulbi muscles. *Inability to blink and corneal ulceration in a mare indicates a lesion in the facial nerve. The facial nerve controls the muscles of facial expression, including those responsible for blinking. Damage to this nerve can lead to loss of blink reflex, muzzle deviation, ear droop, and corneal ulceration due to impaired eyelid function.* **Facial Paralysis in Animals** • Facial Paralysis: Involves paralysis of muscles of facial expression due to lesions of the facial nerve (cranial nerve VII). • Causes: Trauma, otitis media, guttural pouch infections, hypothyroidism, neoplasia, idiopathic. 2. Physiopathology: • Lesions affecting the facial nerve or its nucleus in the brainstem cause dysfunction in facial muscle movement, tear and saliva production. 3. Symptoms and Clinical Changes: • Inability to blink, drooping lips, ear droop, reduced tear production, deviation of the nose, drooling, food accumulation in the mouth. 4. Diagnosis: • Based on clinical signs, neurologic examination, otoscopic examination, thyroid testing, imaging (CT/MRI), and possibly CSF analysis for infections. 5. Treatment and Medications: • Underlying Cause: Address primary condition (e.g., antibiotics for infections, surgery for neoplasia). • Supportive Care: Artificial tears, manage corneal ulcers, corrective surgery for nostril collapse. • Medications: Antibiotics for infections (based on culture), thyroid supplements for hypothyroidism, corticosteroids for inflammation. 6. Prognosis: • Variable, depending on etiology. Early treatment increases recovery chances. Idiopathic cases may partially recover.

Answer 14

Answer: Onchocerca cervicalis Explanation The correct answer is Onchocerca cervicalis. Uveitis is caused by aberrant migration of the microfilariae; when they die, an inflammatory response is generated. Thelazia lacrymalis does cause ocular disease in the horse but mainly causes conjunctivitis rather than uveitis. Neospora and Toxoplasma can cause uveitis in dogs and cats but this is not frequently recognized in horses. Sarcocystis neurona is the cause of equine protozoal myelitis but is not a cause of uveitis. The most common parasitic cause of uveitis in horses is Onchocerca cervicalis. Uveitis occurs due to the inflammatory response triggered by the death of migrating microfilariae. While Thelazia lacrymalis can cause ocular disease in horses, it primarily leads to conjunctivitis rather than uveitis. Comprehensive NAVLE Study Guide: Onchocerciasis in Animals Definitions and Etiology • Onchocerciasis: A parasitic dermatitis caused by Onchocerca species, primarily affecting equines and ruminants. • Causative Agents: Onchocerca cervicalis in horses, found in the ligamentum nuchae; transmitted by Culicoides spp. in equines, and Simulium spp. in ruminants. Pathophysiology • Adult Worms: Located in connective tissues such as the ligamentum nuchae in horses, causing inflammation ranging from acute necrosis to chronic granulomatous changes, resulting in fibrosis and mineralization. • Microfilariae: Found in the dermis and occasionally in peripheral blood, accumulating in the ventral midline, face, neck, chest, withers, forelegs, and abdomen. They may trigger immunologic reactions leading to dermatitis. Clinical Signs • Dermatitis: Pruritic lesions on the ventral midline and other regions, including scaling, crusting, ulceration, alopecia, and depigmentation. • Ocular Involvement: Microfilariae may also accumulate in the eyes, though their direct association with uveitis remains debated. Diagnosis • Histology and Skin Scraping: Identification of microfilariae is done through full-thickness skin biopsy (>6 mm), with tissue being minced, macerated, and stained with methylene blue for microscopic differentiation. • PCR Testing: Can be performed on tissue sections to confirm the species of Onchocerca. Treatment • Macrocyclic Lactones: Effective against microfilariae but not adult worms. • Ivermectin: 200 mcg/kg dosage, >99% efficacy. • Moxidectin: 400 mcg/kg dosage, similarly efficacious. • Post-Treatment Reactions: Some horses may develop marked ventral midline swelling post-treatment, which usually resolves spontaneously but may require symptomatic management. Prevention • Vector Control: Application of topical repellents to prevent bites from Culicoides spp. and other vectors. https://www.merckvetmanual.com/integumentary-system/helminths-of-the-skin/onchocerciasis-in-animals?query=Onchocerca cervicalis equine Thelazia lacrymalis in Horses - NAVLE Test Prep Definition and Etiology: • Thelazia lacrymalis is a nematode that parasitizes the conjunctival sac and lacrimal ducts of horses, causing ocular irritation. Pathophysiology: • The lifecycle involves transmission by Musca spp. flies, which deposit larvae in the horse’s eyes during feeding. Clinical Signs: • Symptoms include conjunctivitis, excessive tearing, and potential corneal opacity or ulceration. Diagnosis: • Identification of the worms in the conjunctiva or lacrimal ducts. Treatment: • Anthelmintics like ivermectin, along with mechanical removal if necessary. https://www.merckvetmanual.com/eye-diseases-and-disorders/eyeworm-disease/eyeworms-of-large-animals?query=thelazia spp Equine Protozoal Myeloencephalitis (EPM) Definitions and Terminology • Equine Protozoal Myeloencephalitis (EPM): A neurologic disease in horses caused by protozoan parasites, primarily Sarcocystis neurona and occasionally Neospora hughesi. Causative Agents • Sarcocystis neurona: The primary protozoan responsible for EPM. • Neospora hughesi: Less common cause of EPM. Pathophysiology • Life Cycle of Sarcocystis neurona: • Definitive Host: Opossums (release sporocysts in feces). • Intermediate Hosts: Various mammals (develop sarcocysts in tissues). • Accidental Hosts: Horses ingest sporocysts from contaminated feed or water. • Neurological Infection: Sporocysts migrate to the CNS, causing inflammation and damage to neural tissues. Clinical Changes and Symptoms • Neurological Signs: Often asymmetric and progressive. • Ataxia: Uncoordinated movements, stumbling. • Muscle Atrophy: Focal muscle loss, particularly noticeable on the gluteal muscles. • Weakness: Generalized or focal weakness, leading to difficulty rising. • Spinal Cord Dysfunction: Paresis, proprioceptive deficits. • Cranial Nerve Deficits: Head tilt, facial paralysis, dysphagia (difficulty swallowing). • Behavioral Changes: Depression, lethargy. • Gait Abnormalities: Swaying, dragging hooves, crossing legs while walking. Diagnosis 1. Clinical Examination: • Neurologic Assessment: Evaluating gait, reflexes, and cranial nerve function. • Symmetry and Atrophy: Checking for muscle atrophy and asymmetry. 2. Laboratory Tests: • Serology: Detecting antibodies against Sarcocystis neurona or Neospora hughesi in serum or cerebrospinal fluid (CSF). • Indirect Fluorescent Antibody Test (IFAT): Commonly used serologic test. • Enzyme-Linked Immunosorbent Assay (ELISA): Measures antibody levels. • CSF Analysis: Elevated protein levels, increased white blood cells, presence of antibodies. • PCR: Detecting protozoan DNA in CSF. 3. Imaging Studies: • Radiography: To rule out other causes of neurological signs. • MRI/CT: Detailed imaging of the CNS if available. Management Strategies 1. Antiprotozoal Therapy: • Ponazuril: 5 mg/kg orally once daily for at least 28 days. • Diclazuril: 1 mg/kg orally once daily for at least 28 days. • Sulfadiazine/Pyrimethamine: Combination therapy to inhibit folic acid synthesis in protozoa. • Dosage: Sulfadiazine 20 mg/kg and pyrimethamine 1 mg/kg orally once daily for at least 28 days. 2. Anti-inflammatory Therapy: • NSAIDs: To reduce inflammation and manage pain. • Examples: Flunixin meglumine, 1.1 mg/kg intravenously once daily. • Corticosteroids: Used cautiously to reduce severe inflammation. • Examples: Prednisolone, based on veterinary discretion. 3. Supportive Care: • Physical Therapy: To improve muscle strength and coordination. • Nutritional Support: Ensuring adequate nutrition to support recovery. • Environmental Management: Keeping the horse in a safe, accessible environment to prevent injury. Prognosis • Variable: Dependent on the severity of the disease, the timeliness of diagnosis, and response to treatment. • Early Detection: Improves the chances of a favorable outcome. • Chronic Cases: May result in permanent neurological deficits despite treatment. Prevention • Environmental Management: Reducing exposure to opossums and their feces. • Feed and Water: Ensuring clean, uncontaminated feed and water sources. • Vaccination: Currently, no effective vaccine is available for EPM. Summary for Veterinary Professionals • EPM is a serious neurological disease in horses caused by Sarcocystis neurona and occasionally Neospora hughesi. • Clinical signs include ataxia, muscle atrophy, weakness, spinal cord dysfunction, and cranial nerve deficits. • Diagnosis involves clinical examination, serology, CSF analysis, and potentially imaging studies. • Management includes antiprotozoal therapy, anti-inflammatory drugs, and supportive care. • Prognosis varies, with early treatment improving outcomes, but chronic cases may have lasting neurological deficits. https://www.merckvetmanual.com/horse-owners/brain-spinal-cord-and-nerve-disorders-of-horses/equine-protozoal-myeloencephalitis

Answer 15

Answer: **Disrupts motor innervation to the orbicularis oculi** Explanation The auriculopalpebral nerve, a branch of the facial nerve, is motor only. The auriculopalpebral block is useful in providing eyelid akinesis by blocking motor innervation primarily to the orbicularis oculi, thereby allowing manipulation of the eyelids without putting pressure on an already painful eye. This block is motor only and does not provide any desensitization. The supraorbital/frontal nerve block can be used to block a branch of the ophthalmic division of the trigeminal nerve, desensitizing the middle two-thirds of the upper eyelid and forehead skin. It may also provide some motor block of the levator palpebrae superioris due to a branch of the oculomotor nerve which runs adjacent.

Answer 16

Answer: Infection Explanation The correct answer is infection. When a corneal ulcer takes on a melting appearance, this indicates that the ulcer is deepening into the stroma of the cornea due to infection. A melting ulcer can exist without having a descemetocele or globe rupture. If this is the case, you should consider swabbing the ulcer for cytology and culture to treat the ulcer most effectively. In horses, melting ulcers are most commonly due to infection with Pseudomonas.

Answer 17

Answer: No treatment is necessary Explanation The correct answer is no treatment is necessary. Entropion in foals is fairly common and will usually resolve spontaneously. Surgical correction is reserved for cases that do not resolve, because over correction in a young animal could result in further eyelid defects as the foal grows. If clinical signs are severe enough, a procedure where local anesthetic is infused and the eyelid is everted and stapled can be performed as a temporary fix until the problem resolves. Enucleation or patching of the eye are not indicated. No treatment is necessary for entropion in foals, as it commonly resolves on its own. Surgical correction is typically avoided due to the risk of overcorrection, which could lead to further eyelid defects as the foal grows. Severe cases may temporarily be treated by everting and stapling the eyelid after local anesthesia, but enucleation or eye patching are not recommended. Comprehensive NAVLE Study Guide: Entropion in Newborn Foals Definition and Etiology • Entropion: A condition where one or both eyelid margins roll inward, causing corneal irritation. • Prevalence: Commonly seen in newborn foals, with the lower eyelid being more frequently affected. Pathophysiology • Inward Rolling of Eyelids: Leads to mechanical irritation of the cornea by the eyelashes or eyelid hair. • Potential Causes: Often associated with dehydration or other underlying systemic conditions. Clinical Signs • Blepharospasm: Involuntary tight closure of the eyelids. • Epiphora: Excessive tearing. • Corneal Ulceration: Secondary to prolonged irritation, potentially leading to further ophthalmic complications. Diagnosis • Ophthalmologic Examination: Involves a thorough assessment of the eyelids and cornea, often utilizing fluorescein staining to check for corneal ulcers. Treatment • Initial Interventions: • Manual Eversion: Temporary manual correction of the eyelid. • Ophthalmic Lubricants: Applied to protect the cornea from irritation. • Medical Management: • Procaine Penicillin G Injection: Subcutaneous injection under the lower eyelid to evert it. • Suture Techniques: Placement of vertical mattress sutures to maintain the eyelid in a proper position. Sutures are generally 4-0 non-absorbable monofilament. • Topical Antibiotics: Applied post-procedure to prevent infection. • Surgical Correction: Reserved for cases where the eyelid fails to correct with less invasive measures. Surgery involves the removal of excess skin to permanently correct the eyelid position. Post-Treatment Care • Monitoring: For signs of suture dehiscence, rubbing, or continued ocular irritation. • Suture Management: Ensuring sutures do not irritate the cornea and do not impair eyelid closure. Sutures should be removed within 10-14 days. • Rehydration: Addressing any underlying dehydration that may have contributed to the condition. Prognosis • Good with Early Intervention: Early diagnosis and treatment generally result in a favorable outcome with resolution of entropion and prevention of corneal damage. https://sci-hub.se/downloads/2021-05-27/91/dascanio2021.pdf?download=true

Answer 18

Answer: **Equine recurrent uveitis** Explanation Although all of the listed answers could potentially result in blindness (directly or as a result of enucleation), the most common cause of blindness in horses is equine recurrent uveitis (ERU). This disease is also known as moon blindness or periodic ophthalmia. Recurrent episodes may result from dysregulated immune responses within the eye; typical clinical signs include blepharospasm, photophobia, lacrimation, miosis and aqueous flare. *Equine recurrent uveitis (ERU) is the most common cause of blindness in horses, also known as moon blindness or periodic ophthalmia. ERU results from recurrent immune-mediated episodes within the eye, leading to clinical signs such as blepharospasm, photophobia, lacrimation, miosis, and aqueous flare. Other listed causes can also lead to blindness, but ERU is the most frequent.* **Comprehensive NAVLE Study Guide: Equine Recurrent Uveitis (ERU)** Definitions and Etiology • Equine Recurrent Uveitis (ERU): A chronic, immune-mediated panuveitis also known as moon blindness or periodic ophthalmia. It is the leading cause of blindness in horses. • Prevalence: Approximately 8% of horses in the United States are affected, with Appaloosas being particularly predisposed. Pathophysiology • Immune-Mediated Process: ERU involves recurrent inflammation of the uveal tract, which includes the iris, ciliary body, and choroid. • Inflammation: Triggered by various factors, including infections, trauma, or systemic diseases, leading to a breakdown in the blood-aqueous barrier and infiltration of inflammatory cells. • Types: • Classic ERU: Characterized by episodes of acute inflammation with periods of minimal ocular signs in between. • Insidious ERU: Low-grade, persistent inflammation often unnoticed until significant damage occurs, most common in Appaloosas. • Posterior ERU: Predominantly affects the vitreous, retina, and choroid, leading to vitreal degeneration and retinal detachments. Clinical Signs • Acute Uveitis: Redness, photophobia, blepharospasm, corneal edema, aqueous flare, miosis, and hypopyon. • Chronic Changes: Cataracts, posterior synechiae, corpora nigra atrophy, retinal degeneration, and phthisis bulbi. Diagnosis • Clinical Examination: Based on characteristic signs, recurrent episodes, and differentiation from other causes of uveitis. • Laboratory Tests: Complete blood count, biochemistry, and serology for infectious agents may be conducted to identify potential causes. Treatment • Primary Goals: Preserve vision, reduce inflammation, and control pain. • Medical Therapy: • Topical Corticosteroids: Prednisolone acetate 1%, dexamethasone 0.5%-1% for potent anti-inflammatory effects. Caution is needed due to the risk of corneal fungal infection. • NSAIDs: Flurbiprofen for anti-inflammatory purposes, reducing pain without potentiating infection. • Mydriatics/Cycloplegics: Atropine 1% to relieve pain, prevent synechiae, and maintain pupil dilation. • Systemic NSAIDs: Flunixin meglumine or phenylbutazone to manage severe cases, though long-term use may predispose to gastric and renal toxicity. • Systemic Corticosteroids: Prednisolone or dexamethasone for potent anti-inflammatory effects, with careful monitoring for laminitis. • Adjunctive Treatments: Doxycycline and intravitreal gentamicin are sometimes used for cases suspected to be associated with Leptospira infections. • Surgical Therapy: • Intravitreal Cyclosporine A Implants: Used to prevent recurrent episodes by providing sustained immunosuppression directly to the eye. Indicated for horses with controlled active inflammation and without significant cataract formation. • Core Vitrectomy: Involves removing the vitreous to decrease the initiation of recurrent episodes. However, it is associated with a high risk of cataract formation and potential loss of vision. Prevention and Management • Environmental Management: Reducing exposure to allergens, improving fly control, and minimizing ocular trauma are essential strategies. • Regular Monitoring: Early intervention at the first signs of uveitis is crucial to prevent permanent ocular damage. Prognosis • Variable: While many horses can be managed effectively, some may experience progressive vision loss despite treatment. Chronic management is often required to control recurrent episodes and maintain ocular health.

Answer 19

Answer: Uveitis Explanation The correct answer is uveitis. Equine recurrent uveitis (also referred to as periodic ophthalmia, recurrent iridocyclitis, and moon blindness) is common in horses. There are many proposed causes for this condition, but it is thought to usually be from infection (Onchocerca, Leptospira, or Borrelia) or immune-mediated processes. Because recurrent bouts of uveitis can lead to serious problems including cataracts, lens luxation, and glaucoma, it should be treated aggressively with topical and systemic anti-inflammatory drugs and topical atropine to prevent synechiae and ciliary spasm. Systemic antibiotics are usually not indicated unless the horse is febrile or an infectious cause is identified.

Answer 20

Answer: **Topical tobramycin** Explanation The correct answer is topical tobramycin. Tobramycin is an aminoglycoside and would be effective against most gram negative organisms, including Pseudomonas, which are the most common cause of bacterial keratitis. Cefazolin would be useful topically for a gram + infection. Systemic antibiotics would not penetrate to the site at levels that would be effective. Natamycin is an antifungal drug and would not be useful in this case of bacterial keratitis. [Ophthalmic Emergencies in Horses](https://www.merckvetmanual.com/emergency-medicine-and-critical-care/emergency-medicine-in-horses/ophthalmic-emergencies-in-horses#Corneal-Ulceration-or-Laceration_v95698698)

Answer 21

Answer: **Hypercalcemia, hypophosphatemia** Explanation *Hypercalcemia and hypophosphatemia* would be the best answer of those provided. The classic findings of renal failure include **hyponatremia, hypochloremia, hyperkalemia, and azotemia**. Somewhat unique to the horse, hypercalcemia is noted because of the high amounts of calcium present in the diet. Serum phosphorus levels may be low because of the high calcium. Hypercalcemia and hypophosphatemia are typical electrolyte changes in horses with chronic renal failure (CRF). While renal failure generally presents with hyponatremia, hypochloremia, hyperkalemia, and azotemia, horses uniquely show hypercalcemia due to their calcium-rich diet. Serum phosphorus levels may be low due to the elevated calcium. These findings help differentiate CRF in horses from other species. **Comprehensive NAVLE Preparation: Chronic Renal Failure (CRF) in Horses** Definition & Pathophysiology: • CRF: Progressive renal dysfunction causing loss of urinary concentrating ability, nitrogen retention, electrolyte imbalance, and hormonal dysfunction, ultimately leading to uremia. This syndrome develops when more than 75% of nephron function is lost. CRF leads to progressive multi-organ dysfunction, including cardiovascular, gastrointestinal, and hematological complications. Pathophysiological Mechanisms: • Compensatory Mechanisms: Surviving nephrons increase in size and filtration capacity, resulting in increased glomerular capillary pressure and activation of the renin-angiotensin-aldosterone system (RAAS), leading to hypertension and glomerular damage. The progression of CRF is marked by chronic inflammation and fibrosis in renal tissues, leading to irreversible damage. • Nephron Loss: As nephrons are lost due to either congenital anomalies, immune-mediated diseases (e.g., glomerulonephritis), or chronic interstitial nephritis (CIN), surviving nephrons undergo hypertrophy and increased filtration pressure. However, this compensation ultimately results in glomerulosclerosis, furthering renal decline. • RAAS Activation: Increased glomerular capillary pressure stimulates the RAAS, leading to sodium retention, hypertension, and further renal damage. Causes: • Congenital Anomalies: Includes renal agenesis, hypoplasia, dysplasia, and polycystic kidney disease. These are often diagnosed in young horses and are linked to breed predispositions (e.g., Thoroughbreds, Standardbreds, Clydesdales). • Glomerulonephritis (GN): Immune-mediated glomerular injury, often triggered by chronic infections (e.g., Streptococcus equi, Leptospira spp., Equine Infectious Anemia virus). GN leads to proteinuria, hematuria, and ultimately renal failure. • Chronic Interstitial Nephritis (CIN): A catch-all term for chronic tubular and interstitial damage, often secondary to acute tubular necrosis (ATN) caused by ischemia, sepsis, or nephrotoxins (e.g., aminoglycosides, NSAIDs, heavy metals). • Pyelonephritis: Ascending urinary tract infections, often complicated by obstructive nephrolithiasis or ureterolithiasis, can also lead to CRF. Symptoms: • Early Signs: Chronic weight loss, lethargy, polyuria-polydipsia, ventral edema, and decreased performance are common early signs. Horses may also present with anorexia, rough hair coat, and mild anemia (due to decreased erythropoietin production). • Advanced Signs: Uremic signs, such as a “fishy” odor from increased urea excretion in sweat, oral ulcers, gingivitis, and protein-losing enteropathy, may develop as the disease progresses. Diagnostic Evaluation: • Clinical Signs: Chronic weight loss, ventral edema, and polyuria-polydipsia are commonly noted. Lethargy, poor coat condition, and decreased performance are also indicators. • Laboratory Findings: The combination of azotemia (increased BUN and creatinine), hypercalcemia, isosthenuria (urine specific gravity of 1.008-1.012), and anemia are hallmark findings of CRF in horses. Hyperkalemia, hyponatremia, and hypophosphatemia may also be observed. • Imaging: Ultrasonography can reveal small, irregular kidneys with increased echogenicity, nephrolithiasis, or hydronephrosis. • Biopsy: Renal biopsy can confirm glomerulonephritis or CIN, though its utility decreases in advanced disease stages. Treatment & Management: • Diet: Transition to low-calcium, low-protein diets (e.g., grass hay over alfalfa) is recommended. Ensure adequate energy intake through palatable feeds, and consider supplementation with omega-3 fatty acids to reduce inflammation. • Supportive Care: Fluid therapy should be administered cautiously to avoid volume overload, with close monitoring for edema. Discontinue nephrotoxic medications. • Medications: • ACE Inhibitors: May help manage proteinuria by reducing glomerular pressure through RAAS inhibition. • Corticosteroids: Used selectively for glomerulonephritis with substantial proteinuria. • Antioxidants: Vitamins C and E may theoretically benefit by reducing oxidative stress, though data is limited. Prognosis: • Variable Outcomes: Horses with creatinine levels <5 mg/dL may be managed for months to years, while those with levels >10 mg/dL generally have a poor prognosis, often surviving only a few weeks. Regular monitoring of renal function and supportive care can prolong survival and improve the quality of life. Important Points for NAVLE: • Understand the progression and compensatory mechanisms of CRF in horses. • Be familiar with diagnostic markers, including azotemia, hypercalcemia, and isosthenuria. • Recognize the clinical signs and manage CRF with appropriate dietary modifications, fluid therapy, and medical management. • Differentiate between the causes of CRF, including congenital, immune-mediated, and tubulointerstitial diseases. Electrolyte Changes in Chronic Renal Failure (CRF) in Horses Key Electrolyte Changes: • Hypercalcemia: A hallmark of CRF in horses, not due to increased parathyroid hormone (PTH) but related to reduced urinary calcium excretion. Horses absorb dietary calcium excessively, and as renal function declines, urinary calcium excretion diminishes, leading to hypercalcemia. High-calcium diets like alfalfa exacerbate this, while switching to grass hay can normalize calcium levels. • Hypophosphatemia: Often accompanies hypercalcemia, associated with Williams-Smith syndrome in CRF. Reduced renal excretion of phosphate can lead to its decline in serum levels. • Hyponatremia and Hypochloremia: These are frequently observed in horses with CRF, reflecting the kidneys’ inability to reabsorb sodium and chloride efficiently. • Hyperkalemia: Present in over half of the cases, resulting from the kidneys’ reduced ability to excrete potassium. Mechanisms: • RAAS Activation: Chronic renal hypoperfusion stimulates the renin-angiotensin-aldosterone system (RAAS), leading to sodium retention and contributing to hypertension, edema, and altered electrolyte balance. • Polyuria-Polydipsia: Horses with CRF often develop polyuria due to increased tubular flow rates and impaired renal concentrating ability, further disrupting sodium, potassium, and chloride balance. • Acid-Base Balance: Metabolic acidosis can develop in terminal stages due to the kidneys’ reduced ability to excrete hydrogen ions and conserve bicarbonate. Management of Electrolyte Imbalances: • Dietary Modifications: Switching from high-calcium feeds (alfalfa) to grass hay can help control hypercalcemia and reduce BUN levels. Electrolyte monitoring and adjustments are crucial in managing CRF long-term. • Fluid Therapy: Administer cautiously to prevent overhydration, which can exacerbate electrolyte imbalances, particularly in advanced cases. Clinical Implications: • Prognosis: Horses with moderate azotemia and controlled electrolyte imbalances may maintain acceptable quality of life for extended periods, whereas severe electrolyte disturbances often correlate with poor prognosis.

Answer 22

Answer: **Shunting of blood from the right atrium to the left atrium** Explanation The correct answer is shunting of blood from the right atrium to the left atrium. The foramen ovale is a small slit that allows shunting between the right atrium and left atrium in the fetus. Once the foal is born, the lungs expand (right atrial pressure decreases) and the left atrium becomes a higher pressure system than the right. This higher pressure in the left atrium at birth forces the closure of the foramen ovale flap against the septum secundum and, in health, typically fusion of these tissues occurs to permanently close the foramen ovale. However, if the foramen ovale flap does not fuse, this leads to patency. In this case, the flap acts somewhat akin to a one-way valve so when the LA pressure is higher the flap is closed, but when the RA pressure is higher, blood can flow right to left. This occurrence (RA pressure > LA pressure) may happen when the patient coughs, takes a deep breath or sneezes which increases the return of venous blood to the RA. *Failure of foramen ovale closure in a healthy foal results in right-to-left atrial shunting due to higher left atrial pressure post-birth, preventing the foramen ovale flap from fusing, potentially causing blood flow from the right atrium to the left atrium during increased venous return events like coughing or deep breathing.* **Congenital Cardiac Defects in Neonatal Foals: NAVLE Study Guide** Definitions and Causative Agents • Congenital Cardiac Defects: Developmental anomalies in the heart present at birth in foals. • Common Defects: Ventricular septal defect (VSD), tetralogy of Fallot (TOF), tricuspid valve atresia (TVA), and others. Pathophysiology • Ventricular Septal Defect (VSD): A hole between the ventricles, causing abnormal blood flow. • Tetralogy of Fallot (TOF): Combination of four defects leading to cyanosis and decreased oxygenation. • Tricuspid Valve Atresia (TVA): Absence or underdevelopment of the tricuspid valve, leading to heart failure. Clinical Findings • Symptoms: Heart murmurs (≥3/6), tachycardia, tachypnea, cyanosis, poor growth, and exercise intolerance. • Breed Predilection: Higher incidence in Arabian foals. • Other Signs: Concurrent congenital defects (e.g., craniofacial anomalies, renal dysplasia). Diagnosis • Clinical Examination: Auscultation of heart murmurs, cyanotic mucous membranes. • Echocardiography: Identifies structural defects, assesses blood flow. • Necropsy: Confirms diagnosis post-mortem. Treatment • Medical Management: Supportive care, oxygen therapy, and management of concurrent infections or complications. • Surgical Interventions: Rare in foals due to complexity and cost. Prognosis • General: Poor prognosis with high mortality, especially for defects involving right-to-left shunting. • Long-Term Survivors: Some foals with isolated VSD may survive and perform athletically. Key Points • Early Detection: Important for management and determining prognosis. • Close Monitoring: Necessary for foals with murmurs, cyanosis, or known breed predispositions. https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/j.1939-1676.2009.0445.x?download=true&campaigns=[{"position":"ereader-last-page","uri":"uri:707b1a3c-73e6-4188-b21f-2b05b70307d8"},{"position":"ereader-first-page","uri":"uri:7691ea89-90f5-4086-9241-486673caed61"}]

Answer 23

Answer: **This conduction finding is common in racehorses and is unlikely to contribute to poor performance** Explanation Second-degree atrioventricular block is commonly seen in athletic horses. First-degree and second-degree blocks are considered variations of normal in the horse and are usually associated with high vagal tone. Horses with second-degree atrioventricular block are NOT predisposed to electrical-mechanical disassociation. This is not a cause of poor performance or a concern in horses because high vagal tone is overcome by sympathetic tone during exercise. *A 6-year-old racehorse with decreased performance and a slow heart rate of 16 beats per minute with irregular rhythm, confirmed by ECG as a second-degree atrioventricular block, exhibits a common finding in athletic horses due to high vagal tone, which is not a cause of poor performance and is resolved during exercise by increased sympathetic tone.*

Answer 24

Answer: **Cardiotoxicity** Explanation The correct answer is cardiotoxicity. Monensin is a coccidiostat used to increase productivity in cattle. Horses are much more susceptible to toxic effects of monensin than cattle and mistakes in feeding or accidental access to cattle feed can lead to toxicity. Monensin toxicity results in myocardial necrosis and development of dilated cardiomyopathy in horses. Clinical signs include progressive respiratory distress, heart murmur, weakness, and hypovolemic shock. Acutely, mild colic and diarrhea can occur as well but is less of a concern than the cardiovascular effects. *A horse ingesting cow feed containing monensin is at risk for cardiotoxicity, leading to myocardial necrosis and dilated cardiomyopathy; clinical signs include progressive respiratory distress, heart murmur, weakness, and hypovolemic shock, with mild colic and diarrhea occurring acutely but being less concerning than the cardiovascular effects.* **Monensin Toxicosis in Horses: NAVLE Study Guide** Definitions and Causative Agents • Monensin Toxicosis: A toxic condition in horses caused by ingestion of monensin, an ionophore antibiotic produced by Streptomyces cinnamonensis. • Causative Agent: Monensin, used as a feed additive to improve feed efficiency in cattle and prevent coccidiosis in poultry. Pathogenesis • Mechanism: Monensin disrupts ion gradients across cell membranes, affecting cellular function, particularly in cardiac and skeletal muscles. • Sensitivity: Horses are highly sensitive to monensin compared to other livestock. The estimated lethal dose (LD50) is approximately 1.38 mg/kg of body weight. Clinical Findings • Symptoms: Partial to complete anorexia, colicky pain, sweating, tachycardia, uneasiness, polyuria, progressive ataxia, recumbency, frequent attempts to rise, and thrashing of limbs, followed by death. • Lesions: Hemorrhage and pale areas in the heart, transudation into body cavities, degenerative cardiomyopathy, congestive heart failure, increased activities of muscle origin enzymes. Diagnosis • History and Clinical Signs: Sudden onset of colic and ataxia after exposure to monensin-containing feed or supplements. • Laboratory Tests: Elevated muscle enzymes (SGOT, LDH) and necropsy findings of cardiac lesions. Treatment • Supportive Care: Immediate removal from monensin source, activated charcoal to reduce absorption, IV fluids, and electrolytes. • Medications: No specific antidote; supportive treatments are aimed at managing symptoms and preventing complications. Prognosis • General: Poor prognosis, especially with high doses; horses surviving initial exposure may have long-term cardiac damage affecting performance. Prevention • Feed Management: Avoid mixing errors, ensure monensin-containing feeds are not accessible to horses. • Monitoring: Regularly check feed and supplements for monensin contamination, educate farm personnel about the risks. Detailed Information • Initial Exposure: Greatest risk of intoxication, evidenced by colicky pain, sweating, and rapid progression to severe symptoms. • Post-Exposure: Horses surviving initial exposure tend to avoid further ingestion of monensin-containing feed.

Answer 25

Answer: **Ventricular septal defect** Explanation The correct answer is ventricular septal defect. There is echo dropout immediately below the aortic valve and extending into the right ventricle. The auscultatory findings also fit with a VSD as the murmur is typically louder on the right. A PDA would cause a continuous heart murmur. There is no narrowing in the LV outflow tract so subaortic stenosis is not evident. There is no evidence of a vegetation or mass on the tricuspid valve so endocarditis is not correct. *A 2-year-old Standardbred gelding with a grade IV/VI systolic murmur on the right thorax and an echocardiogram showing echo dropout below the aortic valve into the right ventricle is diagnosed with a ventricular septal defect, characterized by louder murmurs on the right and distinct from PDA, subaortic stenosis, or tricuspid valve endocarditis.*

Answer 26

Answer: **This is a second-degree atroventricular block, which is commonly seen in athletic horses.** Explanation The correct answer is this is a second-degree atrioventricular block, which is commonly seen in athletic horses. First-degree and second-degree blocks are considered variations of normal in the horse and are usually associated with high vagal tone. They are not predisposed to electrical-mechanical disassociation. An electrical rhythm is an ineffective method in trying to determine if there is a ventricular septal defect. If such a defect is suspected, the best way to evaluate the horse is by performing a cardiac ultrasound. For the PowerLecture™ on this topic, view Cardiology (3:15) * This is a second-degree atrioventricular block, which is commonly seen in athletic horses. First- and second-degree AV blocks are normal variations in horses, typically associated with high vagal tone. These findings do not indicate a predisposition to electrical-mechanical disassociation, nor are they related to ventricular septal defects. No immediate treatment is required, and the condition is generally not a concern for purchase decisions. If a structural defect is suspected, a cardiac ultrasound would be more appropriate for evaluation.*

Answer 27

Answer: **Ventricular septal defect (VSD)** Explanation The image demonstrates a VSD or a hole in the intraventricular septum (identified by two markers). This is one of the more common congenital defects of the heart in horses. The murmur occurs as blood is shunted from the left side of the heart to the right during systole. Some horses can perform normally with a VSD while others, with large defects, can demonstrate heart failure. In this case, it was an incidental finding, as the horse was bright and alert at the time of exam. The remainder of the answers (ASD, PDA, and truncus arteriosus) can occur but are less common and would appear differently on echocardiography. It is unlikely but possible that you will be asked to interpret an echocardiogram on your board exam. If you are, this is likely to be one of the diseases you could be shown. *Ventricular septal defect (VSD) is the diagnosis based on auscultation and echocardiographic findings. VSD is a common congenital heart defect in horses, characterized by a holosystolic murmur on the right side due to blood shunting from the left to the right ventricle during systole. While some horses with VSD can perform normally, larger defects can lead to heart failure. In this case, the defect was an incidental finding, as the colt appeared healthy. Other congenital defects like ASD, PDA, and truncus arteriosus are less common and present differently on echocardiography.*

Answer 28

Answer: **Atrial fibrillation** Explanation Atrial fibrillation is most commonly associated with exercise intolerance in horses. There is no underlying rhythm to the heart beats. The ECG reveals absence of P waves and widely variant Q-Q intervals. There may or may not be a serious underlying heart disease. ***PowerLecture: Cardiology *Atrial fibrillation is the most likely diagnosis. Atrial fibrillation is commonly associated with exercise intolerance in horses and presents with an irregularly irregular heart rhythm, often without a discernible pattern. The ECG typically shows an absence of P waves and widely variable Q-Q intervals. While it may not always indicate serious underlying heart disease, it significantly affects performance in athletic horses like racehorses.* **Detailed Information on Cardiac Arrhythmias in Horses for NAVLE Preparation** General Overview • Cardiac Arrhythmias: Deviations from the normal heart rhythm that can impact performance and potentially pose risks to both horses and riders. Arrhythmias are classified based on their origin (atrial vs. ventricular) and the type of rhythm disturbance (bradyarrhythmia, tachyarrhythmia, premature depolarizations, fibrillation). Etiology • Physiologic Arrhythmias: Typically related to high vagal tone, such as sinus arrhythmia and second-degree atrioventricular (AV) block. These usually disappear with exercise or stress and are not clinically significant. • Pathologic Arrhythmias: May result from underlying cardiac diseases like valvular disease, congenital defects, myocardial damage, or non-cardiac conditions such as electrolyte imbalances, hypoxemia, or endotoxemia. Pathophysiology • Abnormal Impulse Formation: Enhanced automaticity or triggered activity leads to premature depolarizations or tachyarrhythmias. • Abnormal Impulse Conduction: Includes blocks (e.g., AV block) and reentry circuits, leading to sustained arrhythmias such as atrial fibrillation (AF). Clinical Signs • Asymptomatic: Many horses with physiologic arrhythmias show no clinical signs. • Poor Performance: Pathologic arrhythmias, especially AF and ventricular arrhythmias, can lead to exercise intolerance, reduced performance, and fatigue. • Syncope or Collapse: Severe arrhythmias, particularly ventricular tachycardia (VT) or third-degree AV block, can cause episodes of fainting or collapse. Diagnostics 1. Electrocardiography (ECG): • Resting ECG: Identifies arrhythmias like AF, premature depolarizations, and AV block. • Exercise ECG: Useful for detecting exercise-induced arrhythmias that may not be present at rest. • 24-hour Holter Monitoring: Provides continuous ECG recording to capture intermittent arrhythmias. 2. Echocardiography: Assesses underlying structural heart disease, chamber enlargement, or myocardial lesions. 3. Blood Tests: Evaluate electrolyte levels, cardiac biomarkers (e.g., troponins), and acid-base status. Specific Arrhythmias 1. Atrial Fibrillation (AF) • Definition: The most common clinically significant arrhythmia in horses, characterized by chaotic atrial electrical activity and loss of effective atrial contraction. • Causes: May occur in horses with underlying heart disease (e.g., mitral valve regurgitation) or in otherwise healthy horses due to atrial dilation or favorable electrophysiologic conditions. • Clinical Signs: Irregular heart rhythm, poor performance, and exercise intolerance. Some horses may have paroxysmal AF that resolves spontaneously, while others develop persistent AF. • Diagnosis: ECG showing absence of P waves, presence of fibrillation waves (f-waves), and irregular RR intervals. • Treatment: • Medical Treatment: Quinidine sulfate (22 mg/kg via nasogastric tube every 2 hours) for conversion to sinus rhythm, but with significant risks of toxicity (e.g., hypotension, tachycardia, QT prolongation). • Transvenous Electrical Cardioversion (TVEC): High success rate (>95%) for converting chronic AF, requiring general anesthesia and specialized equipment. • Post-treatment Monitoring: Echocardiography and 24-hour ECG monitoring are recommended to assess for recurrence and atrial function recovery. • Prognosis: Varies depending on the presence of underlying heart disease. Recurrence of AF is common, especially in horses with structural heart disease. 2. Atrial Premature Depolarizations (APD) • Definition: Premature atrial contractions that can predispose horses to AF. • Clinical Impact: Often asymptomatic, but may lead to atrial tachycardia (AT) or AF in some cases. • Management: Antiarrhythmic drugs like sotalol (2-3 mg/kg PO twice daily) may reduce the risk of recurrence in horses with a history of AF. 3. Ventricular Arrhythmias • Ventricular Premature Depolarizations (VPD): Isolated early beats originating from the ventricles, which may be benign or indicate underlying myocardial disease. • Ventricular Tachycardia (VT): Three or more consecutive VPDs, associated with a high risk of sudden death. • Management: Lidocaine (0.25-0.5 mg/kg IV bolus, followed by a continuous infusion) is the first-line treatment for VT. Rest and corticosteroids may be used for less severe cases. 4. Atrioventricular Block (AV Block) • First- and Second-Degree AV Block: Often physiologic in horses due to high vagal tone and resolve with exercise. • Third-Degree AV Block: Complete dissociation between atrial and ventricular activity, leading to severe bradycardia and collapse. Pacemaker implantation is the definitive treatment. Medications • Quinidine Sulfate: Class IA antiarrhythmic for AF conversion, with significant risks of toxicity. • Sotalol: Class III antiarrhythmic for reducing recurrence of AF. • Lidocaine: Class IB antiarrhythmic for treating VT, with careful monitoring for adverse effects. • Amiodarone: Used for refractory arrhythmias, with both intravenous and oral formulations available, though it requires careful monitoring due to potential side effects. Prognosis • AF: Horses with AF and no underlying heart disease may return to athletic function after successful cardioversion, though recurrence rates are high. Horses with structural heart disease or persistent AF have a guarded prognosis. • Ventricular Arrhythmias: Prognosis depends on the severity of the arrhythmia and the presence of underlying disease. Horses with structural heart disease and VT have an increased risk of sudden death.

Answer 29

Answer: **Ventricular septal defect** Explanation The correct answer is ventricular septal defect. Clinically, you will hear a murmur bilaterally with the point of maximum intensity on the right side. A patent ductsus arteriosus will create a characteristic continuous machinery or washing machine murmur. This will be audible throughout systole and diastole. Additionally, the point of maximum intensity is usually on the left side between the 3rd and 4th intercostal space. When listening to a tetralogy of Fallot, one can expect a loud holosystolic murmur on the left 4th-6th intercostal space. This congenital anomaly is rather rare and will automatically be lower on your differential list. Just to review, the tetralogy of Fallot consists of an overriding aorta, ventricular septal defect, pulmonic stenosis, and right ventricular hypertrophy. *Ventricular septal defect is the most common congenital cardiac abnormality in horses. It typically presents with a murmur heard bilaterally, with the point of maximum intensity on the right side. In contrast, a patent ductus arteriosus produces a continuous “machinery” murmur, most audible on the left side. Tetralogy of Fallot, which is rarer, involves a loud holosystolic murmur on the left side and includes an overriding aorta, VSD, pulmonic stenosis, and right ventricular hypertrophy. Pulmonic stenosis alone is less commonly seen in horses.*

Answer 30

Answer: **Ventricular septal defect** Explanation The correct answer is ventricular septal defect. This is the most commonly occurring congenital defect, and the physical exam findings are consistent with this diagnosis. A patent ductus arteriosus will create a characteristic continuous machinery or washing machine murmur. This will be audible throughout systole and diastole. Additionally, the point of maximum intensity is usually on the left side between the 3rd and 4th intercostal space. When listening to a tetralogy of Fallot, one can expect a loud holosystolic murmur on the left 4th-6th intercostal space. This congenital anomaly is rather rare and will automatically be lower on your differential list. Just to review, the tetralogy of Fallot consists of an overriding aorta, ventricular septal defect, pulmonic stenosis, and right ventricular hypertrophy. Bacterial endocarditis is an acquired infection of older horses and will not present as an incidental murmur in a foal.

Answer 31

Answer: **An increase in the P-R interval** Explanation The correct answer is an increase in the P-R interval. First-degree, second-degree, and third-degree blocks are associated with delays in conduction at the level of the atrioventricular conduction system. In a first-degree block, the impulse is still able to transmit through the atrioventricular conduction system; however, it takes longer. Therefore, you will see an increased P-R interval. Second-degree AV block is associated with intermittent AV block in which some but not all P waves are conducted to the ventricles. In third-degree block, there is complete dissociation between the P waves and the QRS complexes. Frequently in third-degree block, the heart rate is slower than normal (20 beats/min) because a subservient pacemaker (i.e. in the AV node or ventricle) has to fire to cause ventricular contraction. *An increase in the P-R interval characterizes a first-degree atrioventricular conduction block. This block delays conduction through the AV node, but the impulse still reaches the ventricles, leading to a prolonged P-R interval on the ECG. In contrast, second-degree blocks involve intermittent failure to conduct some P waves, and third-degree blocks show complete dissociation between P waves and QRS complexes, often with a slower heart rate due to reliance on a secondary pacemaker.*

Answer 32

Answer: **Quinidine** Explanation The correct answer is quinidine. The physical exam findings are consistent with the most common equine arrhythmia encountered, atrial fibrillation. Ideally, you would begin oral dosing of quinidine via a nasogastric tube at 2 hour intervals until there is conversion or toxicosis. An increase in the QRS duration of greater than 25% as compared to before initiation of treatment is considered a sign of toxicity. Clinical signs of toxicosis include colic, ataxia, hypotension, diarrhea, and edema. Digoxin will not convert an atrial fibrillation to a normal rhythm. However, it is indicated as adjunctive therapy when the vagolytic effect of quinidine causes a significant acceleration in ventricular response rate, the resting heart rate is in excess of 90 beats per minute, if the horse is exhibiting a low vagal tone, or if conversion has not been achieved within 24 hours of initiating quinidine therapy. This horse is probably not in congestive heart failure given the exam findings and will not benefit from the use of diuretics. A precordial thump is ineffective, and defibrillation is only indicated during ventricular fibrillation, not atrial. Usually, there is an excellent prognosis for conversion if the horse has a heart rate of less than 60 beats per minute, atrial fibrillation of less than four months duration, and if there is a murmur less than or equal to a grade 3/6. Recently, novel therapies that have been used for atrial fibrillation in horses include amiodarone, flecainide, and transvenous electrical cardioversion. However, quinidine still remains the most commonly used drug, despite its potential toxic side effects. ***PowerLecture: Cardiology *Quinidine is the treatment of choice for atrial fibrillation in horses, as indicated by the physical exam findings of an irregularly irregular rhythm and a heart rate of 40 beats per minute. Quinidine is administered orally via a nasogastric tube, typically every 2 hours, until conversion to normal rhythm or signs of toxicity appear. Toxicity signs include colic, ataxia, hypotension, diarrhea, and edema. While digoxin can be used as adjunctive therapy in certain situations, it does not convert atrial fibrillation to a normal rhythm. Diuretics like furosemide, precordial thump, and defibrillation are not indicated in this case, as they are used for other conditions.*

Answer 33

Answer: **Quinidine** Explanation Oral quinidine can be used for therapy. It is a class lA sodium channel blocker that has vagolytic properties which prolong the refractory period of the myocardium. This is not a perfect solution, as it does not work in all cases and can be associated with side effects including oral ulcers, hypotension, and allergic reactions. For these reasons, other treatments such as electrical cardioversion and alternative drugs such as flecainide are sometimes tried. When evaluating an ECG strip for atrial fibrillation, look for irregular R-R intervals and the classic fibrillation wave of the base line. Lidocaine is a sodium channel blocker used primarily for ventricular arrhythmias. Furosemide is a loop diuretic used to treat congestive heart failure rather than a rhythm abnormality. Atropine is an anticholinergic used primarily for supraventricular bradyarrhythmias.

Answer 34

Answer: **This conduction finding is common in racehorses and is unlikely to contribute to poor performance** Explanation Second-degree atrioventricular block is commonly seen in athletic horses. First-degree and second-degree blocks are considered variations of normal in the horse and are usually associated with high vagal tone. Horses with second-degree atrioventricular block are NOT predisposed to electrical-mechanical disassociation. This is not a cause of poor performance or a concern in horses because high vagal tone is overcome by sympathetic tone during exercise.

Answer 35

Answer: **Monensin** Explanation The correct answer is monensin. Monensin is a commonly used coccidiostat in feedstuff of cattle. This ionophore is highly toxic to horses (the toxic dose for hoses is 10 to 15 times less than for cattle) and will result in cardiomyopathy and myocardial necrosis. Unfortunately, there is no quick and easy antidote, and treatment usually consists of trying to empty the intestinal tract by using mineral oil, activated charcoal, and fluid therapy. Lasalocid and salinomycin are also ionophores that you might worry about, but monensin is much more toxic to horses. Selenium and copper are usually added to feedstuffs as a result of being deficient in the soil. Lack of supplementation with these minerals may result in cardiovascular disease, such as white muscle disease with selenium deficiency, and excessive bleeding in aged parturient mares with copper deficiency. One way of determining prognosis is to evaluate the horse's fractional shortening via echocardiography. Normally the fractional shortening is 30-40%; if you calculate fractional shortening to less than 20%, the prognosis is poor. *Monensin is the feed additive known to be highly toxic to horses and can cause cardiomyopathy if consumed in sufficient quantities. Monensin is an ionophore commonly used in cattle feed as a coccidiostat, but it is extremely dangerous to horses, with a toxic dose much lower than that for cattle. Ingesting monensin leads to myocardial necrosis and cardiomyopathy, and treatment typically involves supportive care, such as administering mineral oil, activated charcoal, and fluids to reduce absorption. While other ionophores like lasalocid and salinomycin are also toxic, monensin is the most dangerous for horses. Selenium and copper are essential minerals, but deficiencies, not toxicities, in these can lead to cardiovascular issues in horses.*

Answer 36

Answer: **Atrial Fibrillation** Explanation These changes are typical of atrial fibrillation. Note that the horse tracing (top) also shows fibrillation waves.

Answer 37

Answer: **Myocardial toxicity** Explanation The correct answer is myocardial toxicity. Although the clinical signs associated with ionophore toxicity are wide, the main postmortem finding is myocardial necrosis. lonophore toxicity usually occurs accidentally when livestock feeds containing ionophores get mixed up with that of a horse. The main ionophore that results in toxicity is monensin. Horses are very susceptible to monensin toxicity.

Answer 38

Answer: **Ventricular tachycardia** Explanation The rhythm noted is ventricular tachycardia. You can tell that the horse has tachycardia when you compare the rate to the lower strip (~40 beats/min). Characteristics of ventricular tachycardia include QRS complexes that are wide, bizarre, and have no association with P-waves. However, you may see underlying P-waves occasionally within the rhythm (top strip) as the small positive deflections. The cause of the ventricular tachycardia in this horse was vegetative endocarditis; administration of lidocaine abolished the arrhythmia. *The arrhythmia observed on the ECG is ventricular tachycardia. This condition is characterized by wide, bizarre QRS complexes that lack association with P-waves, although occasional P-waves may be seen. The rapid heart rate of ~90 beats/min, compared to a normal rate (~40 beats/min), supports this diagnosis. In this case, the underlying cause was vegetative endocarditis, and lidocaine was the medication used to treat the arrhythmia by abolishing the ventricular tachycardia.*

Answer 39

Answer: **This horse most likely has aortic regurgitation due to degeneration of the aortic valve and should have no impact on performance** Explanation The correct answer is this horse most likely has aortic regurgitation due to degeneration of the aortic valve and should have no impact on performance. Given the location of the murmur and signalment, this should be the logical answer to choose. The thing you need to know is that aortic regurgitation in the horse is usually a degenerative change and there isn't much that can be done about it. Horses are rarely impaired by development of the murmur. In a true pre-purchase exam, you would be wise to recommend a full cardiac work-up to definitively diagnosis the source of the heart murmur. The potential buyer may decline further diagnostics, but at least you will have offered the choice and have provided the proper information to the client. *The horse most likely has aortic regurgitation due to degeneration of the aortic valve, which typically has no impact on performance. The harsh, decrescendo holodiastolic murmur heard at the left base is characteristic of this condition. Aortic regurgitation in horses is usually a degenerative change and rarely impairs their ability to perform. During a pre-purchase exam, it would be prudent to recommend a full cardiac work-up for a definitive diagnosis, though the buyer may decline further diagnostics.*

Answer 40

Answer: **Alfalfa hay** Explanation The correct answer is alfalfa hay. Alfalfa hay in California is thought to be particularly high in magnesium. This may be a predisposing factor which results in magnesium ammonium phosphate enteroliths.

Answer 41

Answer: **Hypoventilation, respiratory acidosis** Explanation The correct answer is hypoventilation, respiratory acidosis. Hypoventilation is defined by the PaCO2. Normal is about 40 (35-45). This horse has an elevated PaCO2 indicating he is under-ventilating and not blowing off sufficient CO2. This increase in CO2 causes a respiratory acidosis because CO2 is an acid that interacts with carbonic anhydrase to form carbonic acid. This is why the horse's pH is low (normal pH is about 7.4). The relatively normal base excess indicates there is minimal metabolic component to this horse's acidosis.

Answer 42

Answer: **Bone Marrow Aspirate** Explanation The horse does not release reticulocytes into the peripheral circulation; therefore you must look at a bone marrow sample to identify if the horse has a regenerative anemia. If this were the case, you would see hypercellular bone marrow with a low myloid/erythroid ratio (<0.5). Increased peripheral reticulocyte count and increased MCV are indicators of regeneration in other species. An increased MCV is inconsistent in horses with regenerative anemia. Therefore, the most definitive diagnostic test to determine if you have a regenerative anemia is to evaluate a bone marrow aspirate.

Answer 43

Answer: **Neomycin and polymyxin B and dexamethasone (Neo-Poly-Dex)** Explanation The correct answer is Neo-Poly-Dex. This is an illustration of a melting ulcer. Any corneal ulcer, whether it is superficial or deep, can be perpetuated by steroid use such as the dexamethasone in this medication. Steroids increase protease activity causing the "melting" pathology, whereas, one of the primary goals in managing corneal ulcers is to decrease protease activity by using EDTA and serum. Aggressive topical antibiotic use is also essential. Tobramycin, gentamicin, and neomycin-polymyxin B-bacitracin, among others are appropriate. Intravenous banamine is the drug of choice for ocular pain and inflammation in horses. Tropicamide is used for its mydriatic and cycloplegic effect because all animals with corneal ulcers have uveitis. Atropine is an alternative to tropicamide. It is important to note, even though atropine has a longer duration of action than tropicamide, atropine must be used with extreme caution in horses as it may potentiate colic.

Answer 44

Answer: **Ectopic ureter** Explanation Urine scalding, as pictured, along with the age and gender of this patient, would lead to a high suspicion of an ectopic ureter. While this is a comparatively rare problem, it is the most common congenital anomaly of the equine urinary tract. Nearly 90% of the cases reported are fillies, with the primary complaint of urinary incontinence and urine scalding (dermatitis). Surgical correction has been successful. The chronic history in a young animal makes primary urinary tract infection less likely.

Answer 45

Answer: **Achilles tendon** Explanation The correct answer is Achilles tendon. A complete laceration of the Achilles tendon involves rupture of the gastrocnemius and superficial flexor tendons. A gastrocnemius rupture alone may cause a dropped hock, but horses with this injury will still bear weight on the affected limb. Prognosis for this injury is grave.

Answer 46

Answer: **This is a second-degree atrioventricular block, which is commonly seen in athletic horses.** Explanation The correct answer is this is a second-degree atrioventricular block, which is commonly seen in athletic horses. First-degree and second-degree blocks are considered variations of normal in the horse and are usually associated with high vagal tone. They are not predisposed to electrical-mechanical disassociation. An electrical rhythm is an ineffective method in trying to determine if there is a ventricular septal defect. If such a defect is suspected, the best way to evaluate the horse is by performing a cardiac ultrasound. ***PowerLecture: Cardiology

Answer 47

Answer: **Excessive time spent on very hard surfaces such as concrete** Explanation Carriage horses spend hours at a time on hard asphalt or concrete, which increases the incidence of hoof and leg conditions.

Answer 48

Answer: **Cerebellar abiotrophy** Explanation The correct answer is cerebellar abiotrophy. The cerebellum is responsible for the coordination and regulation of range, rate, and strength of movement along with balance and posture. Clinical signs associated with cerebellar disease include intention tremors, hypermetria, hypometria, and ataxia. In addition, weakness is not observed with cerebellar abiotrophy. Mentation will be normal if the disease is strictly confined to the cerebellum. The key clinical sign not observed in this question is intention tremors. The clinical signs and presentation are definitely compatible with equine degenerative myeloencephalopathy, cervical vertebral myelopathy, and occipito-atlanto-axial malformation (OAAM). Computerized tomography (or radiography) is needed to rule in or rule out cervical vertebral myelopathy and OAAM. OAAM is relatively rare, but is most frequently observed in Arabian foals. These foals may be born dead, or may develop ataxia at several months of age. Histopathologic examination is the only way to definitively diagnose equine degenerative myeloencephalopathy (lesions in caudal brainstem nuclei and spinal cord).

Answer 49

Answer: **Provide artificial light for 16 hours per day 60 days prior to the start of breeding** Explanation The correct answer is to provide 16 hours of artificial light 60 days prior to the start of breeding. To get a horse to transition out of seasonal anestrus, you can gradually increase the amount of light to 15-16 hours per day to initiate ovarian activity. It usually takes at least 60 days until physiologic breeding will occur. There are hormonal methods to promote cycling, but they are less consistent than altering light. ***PowerLecture: Estrous Cycle

Answer 50

Answer: **Exposure or ingestion of eastern tent caterpillars** Explanation The correct answer is exposure or ingestion of eastern tent caterpillars. The exact pathogenesis of MRLS is still unknown, but the presence of eastern tent caterpillars was strongly associated with the disease. Later, experimental studies in which pregnant mares were exposed to or fed eastern tent caterpillars resulted in early and late fetal loss.

Answer 51

Answer: **Right side - peripheral vestibular dysfunction C** Explanation The correct answer is right side, peripheral vestibular dysfunction. Peripheral vestibular dysfunction causes signs of head tilt, nystagmus, circling and asymmetric ataxia with preservation of strength. The head tilt is toward the affected side as is circling towards the lesion. Comparatively, central vestibular disease has similar clinical signs but general conscious proprioceptive deficits, weakness and cranial nerve deficits may also be present along with depression.

Answer 52

Answer: **Ventricular septal defect** Explanation The correct answer is ventricular septal defect. This is the most commonly occurring congenital defect, and the physical exam findings are consistent with this diagnosis. A patent ductus arteriosus will create a characteristic continuous machinery or washing machine murmur. This will be audible throughout systole and diastole. Additionally, the point of maximum intensity is usually on the left side between the 3rd and 4th intercostal space. When listening to a tetralogy of Fallot, one can expect a loud holosystolic murmur on the left 4th-6th intercostal space. This congenital anomaly is rather rare and will automatically be lower on your differential list. Just to review, the tetralogy of Fallot consists of an overriding aorta, ventricular septal defect, pulmonic stenosis, and right ventricular hypertrophy. Bacterial endocarditis is an acquired infection of older horses and will not present as an incidental murmur in a foal.

Answer 53

Answer: **Osteolysis** Explanation The correct answer is osteolysis. Navicular syndrome is a chronic degenerative condition of the navicular bursa and navicular bone. The precise etiology is unknown and is likely multifactorial involving the navicular bone, the suspensory ligament, the coffin joint, the navicular bursa, and the deep digital flexor tendon. Osteophyte formation, bony remodeling, and enlarged vascular channels are the hallmark radiographic findings in horses with navicular syndrome. Osteolysis is generally not a component of this condition. **Navicular Syndrome in Horses: NAVLE Study Guide** Definition and Etiology • Navicular Syndrome: A degenerative condition affecting the navicular bone and associated structures (navicular bursa, collateral sesamoid ligaments, deep digital flexor tendon). • Causes: Poor hoof conformation (narrow feet, long toes, low heels), genetic predisposition, poor shoeing, and heavy body mass on small feet. Pathophysiology • Degeneration: Chronic mechanical stress leads to bone remodeling, vascular channel enlargement, and damage to soft tissues. • Bilateral Condition: Often involves both forelimbs, causing chronic, progressive lameness. Clinical Signs • Lameness: Gradual onset, shortened stride, shuffling gait, stumbling. Sensitivity to hoof testers in the heel, with improvement after a palmar digital nerve block. • Imaging: Radiographs, MRI, or CT show osseous cyst-like lesions, medullary sclerosis, or soft tissue injury. Diagnosis • Radiography: Enlarged vascular channels, sclerosis, and fragments on the navicular bone. • Advanced Imaging: MRI provides detailed visualization of both bone and soft tissue structures. Treatment • Conservative: Corrective shoeing, NSAIDs (e.g., phenylbutazone, firocoxib), bisphosphonates, intra-articular corticosteroids (triamcinolone, betamethasone), and biologic therapies (platelet-rich plasma). • Surgical: Navicular bursoscopy or palmar digital neurectomy in advanced cases. Prognosis • Lifelong Management: Often requires ongoing treatment, and lameness may return over time, especially after neurectomy.

Answer 54

Answer: **Granulosa-thecal cell tumor** Explanation The correct answer is granulosa-thecal cell tumor. The clinical signs and palpation findings are both consistent with this diagnosis. The other choices listed may create a palpable ovarian mass but would not cause atrophy of the contralateral ovary and should not cause infertility. **Granulosa Cell Tumors (GCTs) in Mares: NAVLE Study Guide** #### Definitions and Etiology - **Granulosa Cell Tumor (GCT)**: The most common ovarian tumor in mares, comprising over 85% of equine reproductive tract tumors. GCTs are typically benign but can rarely be malignant. #### Pathophysiology - **Hormonal Activity**: GCTs may secrete hormones like inhibin, testosterone, and estradiol, leading to abnormal reproductive behaviors such as prolonged anestrus, continuous or intermittent estrus, and stallion-like behavior. The contralateral ovary is often small and inactive due to the suppression of FSH secretion by inhibin. #### Clinical Signs - **Behavioral Changes**: Mares with GCTs may exhibit prolonged anestrus, continuous estrus, or aggressive stallion-like behavior. - **Physical Signs**: The presence of a unilaterally enlarged ovary with a small, inactive contralateral ovary during the breeding season is suggestive of GCT. #### Diagnosis - **Ultrasonography**: GCTs may appear as a multicystic (honeycomb-like) or solid mass on ultrasound, often with a thick capsule surrounding the mass. - **Endocrine Testing**: Elevated levels of inhibin and testosterone are common in affected mares. Measurement of these hormones, along with progesterone levels, is used to confirm the diagnosis. Inhibin is considered a more reliable marker than testosterone. #### Treatment - **Surgical Removal**: The recommended treatment for GCTs is surgical removal of the affected ovary. Techniques include colpotomy, flank, ventral midline, paramedian laparotomy, or laparoscopy. - **Post-Surgical Prognosis**: After removal, the contralateral ovary typically resumes normal function, with many mares returning to regular estrous cycles and fertility within a few months. #### Potential Complications - **Complications**: While most GCTs are benign, they can cause complications such as colic, abdominal adhesions, or, rarely, metastasis. Intra-abdominal hemorrhage due to tumor rupture has also been reported. #### Differential Diagnosis - **Other Ovarian Tumors**: Differential diagnoses include teratomas, serous cystadenomas, dysgerminomas, and other rare ovarian neoplasms. Non-neoplastic causes of ovarian enlargement, such as persistent anovulatory follicles or multiple corpora lutea of pregnancy, should also be considered. #### Summary for Veterinary Professionals - **Key Points**: GCTs are the most common ovarian tumors in mares and can be diagnosed based on clinical signs, ultrasonographic appearance, and endocrine testing. Surgical removal is the primary treatment, with a generally favorable prognosis for returning to reproductive function. This guide provides a comprehensive overview of granulosa cell tumors in mares, essential for NAVLE preparation.

Answer 55

Answer: **Peroneus tertius rupture** Explanation The correct answer is peroneus tertius rupture. Damage to the peroneus tertius muscle disrupts the stay apparatus of the hind limb. The characteristic diagnostic feature is the ability to extend the hock and flex the stifle simultaneously because an intact peroneus tertius prevents this. ***PowerPage: Top 9 Equine Lameness **Rupture of the Fibularis (Peroneus) Tertius in Horses** The fibularis (peroneus) tertius is a tendinous structure that originates from the extensor fossa of the femur and runs over the craniolateral aspect of the tibia to insert on the dorsoproximal aspect of the third metatarsal bone, the calcaneus, and the third and fourth tarsal bones. It is part of the reciprocal apparatus of the hindlimb, which means there is concurrent flexion and extension of the hock and stifle. Rupture of the fibularis tertius may occur as a result of hyperextension of the limb and usually occurs in the middle of the crus, or laceration may occur on the dorsal aspect of the tarsus. Avulsion of the origin on the fibularis tertius is rare in mature horses but may occur in young animals. Clinical signs are pathognomonic, because rupture of the fibularis tertius means horses are able to extend the hock while the stifle is flexed. Horses are able to bear weight on the affected limb. At walk, the gastrocnemius and superficial digital flexor muscles appear rather flaccid, and there is a characteristic dimple on the caudodistal aspect of the soft tissues of the crus. At trot, an obvious lameness is usually evident, with delayed protraction of the limb due to overextension of the hock. Diagnosis is usually based on clinical signs and can be confirmed with ultrasonography. Conservative treatment with 3-4 mo of stall rest followed by slow and careful reintroduction to exercise usually results in complete resolution of signs and return to athletic soundness. (Merck Manual: Peritoneus T Rupture) [https://www.merckvetmanual.com/musculoskeletal-system/lameness-in-horses/rupture-of-the-fibularis-peroneus-tertius-in-horses?query=Peroneus%20tertius%20rupture]

Answer 56

Answer: **Skin scraping and microscopic examination of affected areas to detect Chorioptes** Explanation The correct answer is skin scraping to identify the Chorioptes mite on microscopic examination. Chorioptic mange is caused by infestation with Chorioptes equi; this mite typically affects the distal limb region but can also extend to the ventral abdomen. Draft horses are particularly susceptible because of their long feathered hair coat of the distal limbs. Chorioptes is more common in the winter months and causes intense pruritus. In regard to the other answers, intradermal skin testing is sometimes used to detect insect hypersensitivity, but insect hypersensitivity typically affects the trunk or ventral abdomen. Food allergies are not a major cause of dermatologic diseases in the horse and pemphigus is a generalized disease. Onchocerca can cause pruritus, but is diagnosed via skin biopsy or response to ivermectin therapy.

Answer 57

Answer: **lleocolonic agangliosis** Explanation The correct answer is ileocolonic agangliosis. The other name for this condition is lethal white foal syndrome. This is an autosomal recessive trait seen in Overo horses. The foals are white with blue irises. Diagnosis is confirmed by histopathology showing a lack of ganglia in the colon. Most develop colic and die by 2 days of age. **PowerLecture: Foal Neuromuscular Disorders

Answer 58

Answer: **Penetrating wound** Explanation The correct answer is penetrating wound. To answer this question, you should realize that the clinical signs being described are classic for tetanus. Tetanus is caused by Clostridium tetani. Infection usually occurs via deep puncture wounds. Clostridium tetani releases a toxin which is capable of ascending up the nerves and into the spinal cord resulting in an ascending paralysis. The toxin blocks post synaptic inhibition to motor nerves, causing hypertonia and spasticity.

Answer 59

Answer: **Feed a pelleted ration rather than hay** Explanation The correct answer is to feed pelleted ration rather than hay. Environmental factors and dust are thought to play a major role in the pathogenesis of COPD. An alternative to feeding pellets is to soak hay prior to feeding to reduce the dust taken in when eating. Stabled horses are much more likely to develop signs. Atropine can be given to bronchodilate in emergencies for acute attacks but should not be given routinely, as it can predispose to development of colic. Antibiotics would not be an effective recommendation because the disease is not infectious (there is no bacterial component to treat in most cases). ***PowerPage: Recurrent Airway Obstruction

Answer 60

Answer: **Red maple leaves (Acer rubrum)** Explanation The sclera appears icteric. In combination with the clinical signs, ingestion of Red maple leaves would result in these signs due to hemolysis and low oxygen content of the blood. Oak is toxic but causes diarrhea and abdominal pain, whereas Black walnut is associated with laminitis. Yellow star thistle causes nigropallidal encephalomalacia resulting in CNS signs.

Answer 61

Answer: **Quinidine** Explanation Oral quinidine can be used for therapy. It is a class IA sodium channel blocker that has vagolytic properties which prolong the refractory period of the myocardium. This is not a perfect solution, as it does not work in all cases and can be associated with side effects including oral ulcers, hypotension, and allergic reactions. For these reasons, other treatments such as electrical cardioversion and alternative drugs such as flecainide are sometimes tried. When evaluating an ECG strip for atrial fibrillation, look for irregular R-R intervals and the classic fibrillation wave of the base line. Lidocaine is a sodium channel blocker used primarily for ventricular arrhythmias. Furosemide is a loop diuretic used to treat congestive heart failure rather than a rhythm abnormality. Atropine is an anticholinergic used primarily for supraventricular bradyarrhythmias. ***PowerLecture: Cardiology

Answer 62

Answer: **Clostridium botulinum** Explanation The correct answer is Clostridium botulinum (also known as Shaker Foal Syndrome). Foals (2 weeks-6 months) are susceptible to the toxicoinfectious form of botulism, where they ingest the spores which grow in their intestines and make the toxin. The toxin blocks the release of acetylcholine from the neuromuscular junction, thus resulting in flaccid paresis or paralysis. Adults usually will only show clinical signs if they ingest the preformed toxin. Clinical signs are shaking, flaccid paralysis, drooling, decreased muscle tone, weakness, and dyspnea. The weak tongue tone is considered a cardinal sign. With medical treatment, prognosis is favorable; however prognosis is poor if treatment is not instituted, as many die of respiratory paralysis or pneumonia within days. ***PowerPage: Top 12 Equine Neurologic Diseases

Answer 63

Answer: **Neorickettsii risticii, Supportive test- a PCR of blood or feces** Explanation The correct answer is Neorickettsii risticii, the causative agent of Potomac Horse Fever (PHF). The clues that best indicate PHF are the time of year (disease usually occurs in the summer in the northern states), the high fever and diarrhea, and the presence of laminitis. The horse is also dehydrated and has a profound leukopenia, both consistent with PHF. Salmonella also causes diarrhea and leukopenia, and could be a viable choice, but Salmonella can occur at any time of the year; moreover, laminitis is not as often seen with Salmonella. This question has a practical aspect to it as horses often present with the described history and physical examination findings, and the veterinarian has to decide if he or she wants to treat specifically for PHF; the drug of choice is oxytetracycline. In this clinical situation, you as a veterinarian would have to start treatment empirically as your PCR test will take several days to get results. The good news is that PHF is very susceptible to oxytetracycline. **Comprehensive List of Important Information on Potomac Horse Fever** #### Etiology and Transmission 1. **Causative Agent:** - *Neorickettsia risticii* (gram-negative obligate intracellular bacterium). - Associated with aquatic insects and freshwater snails. 2. **Transmission:** - Ingestion of insects (caddisflies, mayflies) carrying N. risticii. #### Pathogenesis 1. **Infection Process:** - Invades enterocytes of the small and large intestine. - Causes acute enterocolitis. #### Clinical Findings 1. **Symptoms:** - Early: Depression, anorexia, fever (38.9°–41.7°C). - Later: Diarrhea, mild colic, dehydration, sepsis. - Complications: Laminitis (20%-30% cases), abortion in pregnant mares. #### Diagnosis 1. **Diagnostic Methods:** - PCR assay for N. risticii DNA in blood/feces. - Rising paired titers (serology). - Cell culture (time-consuming). #### Treatment 1. **Medications:** - Oxytetracycline (6.6 mg/kg IV every 12 hours). - Supportive care: Fluids, NSAIDs, cryotherapy for laminitis. #### Prevention 1. **Vaccination:** - Inactivated whole-cell vaccines (variable efficacy). 2. **Management Practices:** - Reduce insect ingestion by turning off barn lights. For detailed information, refer to the original [Merck Veterinary Manual article](https://www.merckvetmanual.com/digestive-system/infectious-diarrheal-diseases-in-horses/potomac-horse-fever?autoredirectid=19925).

Answer 64

Answer: **Dermatophilus congolensis** Explanation The correct answer is Dermatophilus congolensis infection. The description and distribution of these lesions makes Dermatophilus most likely. Dermatophilus congolensis is a gram positive branching bacteria. It typically enters skin that is damaged by wetness during rainy seasons and causes suppurative crusts, usually along the dorsum of horses. Staphylococcal cellulitis is uncommon and usually causes severe acute swelling dissecting along fascial planes and devitalizing the overlying skin. Trichophyton equinum, or ringworm infection, usually causes multifocal lesions with alopecia and some crusting, usually around the head, neck, and shoulders. Culicoides hypersensitivity can cause pruritus and excoriations and can be distributed dorsally or ventrally. Pemphigus foliaceus is an autoimmune skin disease and results is vesicles, erosions and ulcerations, especially around mucocutaneous junctions.

Answer 65

Answer: **Nigropallidal encephalomalacia** Explanation The correct answer is *nigropallidal encephalomalacia*. Consumption of yellow star thistle destroys the globus pallidus and the substantia nigra. These lesions will result in a characteristic dysphagia.

Answer 66

Answer: **Immunodiffusion** Explanation The correct answer is immunodiffusion. This is more commonly known as the *Coggin's test*. There are ELISA tests available but if the result is positive, you always need to confirm this with a Coggin's test, as there is the possibility of a false positive. ElA is caused by a virus that is related to the human immunodeficiency virus, and there is no way to visualize it in the blood on a smear. Treatment of ElA usually involves isolation and supportive care. The main modes of transmission are via blood-sucking flies that act as vectors and contaminated instruments.

Answer 67

Answer: **Neurologic signs associated with hyperammonemia and intestinal disease** Explanation Ok, admittedly this is a tough question, but we do not want to make them too easy. Hyperammonemia has been associated with intestinal disease in horses. The exact cause of the neurologic signs and disease process is unknown, but it is presumed to result from excessive ammonia production within the intestinal tract. This overwhelms the ability of the liver to metabolize ammonia, and subsequently causes the development of encephalopathic signs, such as those reported in this question. Diarrhea is a common concurrent problem suggesting a possibility that overgrowth of ammonia producing bacteria causes an elevated blood ammonia. In regards to the other possible answers, hyponatremia can cause neurologic deficits if the sodium is very low (100-105 mE/L), so the sodium of 124 mEg/L in this question rules that option out. The mild azotemia and hyperglycemia are unlikely to cause neurologic deficits and there is no other evidence to support hepatic disease.

Answer 68

Answer: **Deep digital flexor tenotomy** Explanation The case descriptions and radiographs are consistent with chronic laminitis. The dorsal hoof wall is much thicker distally due to P3 rotation. Gas tracks under the dorsal hoof wall are evident and there is a round lucent defect in the cranial medial aspect of the sole. There is P3 osteopenia and remodeling of the distal aspect of P3. Although the optimal treatment for chronic laminitis remains controversial, the best answer is clearly deep digital flexor tenotomy. Deep digital flexor tenotomy is reported in several studies to be useful in the management of chronic laminitis, particularly when the distal phalanx is rotated or pedal bone penetration is present. Unfortunately, chronic laminitis is sometimes refractory to this therapy as well. Other reported options include dorsal hoof wall resection, curettage of regions of septic osteitis, and many types of corrective shoes. Again, all of these options may be ineffective. The options of arthrodesis and surgical exploration of the joint are poor choices as this is not a joint disease. Palmar digital neurectomy is a procedure used to manage navicular disease and results in desensitization of the heel.

Answer 69

Answer: **Ventricular tachycardia** Explanation The rhythm noted is ventricular tachycardia. You can tell that the horse has tachycardia when you compare the rate to the lower strip (-40 beats/min). Characteristics of ventricular tachycardia include QRS complexes that are wide, bizarre, and have no association with P-waves. However, you may see underlying P-waves occasionally within the rhythm (top strip) as the small positive deflections. The cause of the ventricular tachycardia in this horse was vegetative endocarditis; administration of lidocaine abolished the arrhythmia.

Answer 70

Answer: **Cervical vertebral stenotic myelopathy** Explanation Also known as Wobbler Syndrome or cervical vertebral instability, this condition results in symmetrical spinal ataxia. ***PowerPage: Equine Cervical Vertebral Malformation For the ***PowerLecture: Neurologic Disorders

Answer 71

Answer: **Horse bot eggs** Explanation The correct answer is horse bot eggs. Horse bots (Gasterophilus spp.) can lay their eggs anywhere. However, Gasterophilus intestinalis, which is the common bot, typically will lay their yellowish eggs on the medial aspect of the forelimb cannon bones. Stomach worm (Habronema spp.) eggs are actually ingested by houseflies which are then ingested by horses. Sometimes the infective larvae leave the fly as it is feeding around the lips of the horse and goes on to infect the horse. Pinworm (Oxyuris spp.) eggs are laid by gravid females around the perineum by cementing the eggs around the anus. Flea infestations are not typical in horses.

Answer 72

Answer: **Synergistic hemolysis inhibition test** Explanation The correct answer is the synergistic hemolysis inhibition test. Other clinicopathologic data that would support an internal abscess would include leukocytosis, hyperfibrinogenemia and hyperglobulinemia. A KOH test is used to diagnose dermatophytes. The zinc sulfate turbidity test evaluates for failure of passive transfer. The Coggin's test is for equine infectious anemia. Remember, goats get C. pseudotuberculosis as well.

Answer 73

Answer: **Rouleaux, lymphocyte, platelets** Explanation The correct answer is rouleaux, lymphocyte, and platelets. This is an image of an equine blood smear. The reason this is not agglutinated red blood cells is because a) rouleaux have a more uniform linear arrangement while agglutinated red blood cells are all bunched together and b) the white blood cell in this image is a lymphocyte making the other answers incorrect. A way to differentiate between rouleaux and agglutinated red blood cells diagnostically, is to mix blood with normal saline. Rouleaux blood will dissipate where agglutinated red blood cells will not.

Answer 74

Answer: **Hepatic failure with secondary hemolysis** Explanation When the liver fails in the horse, it often results in a hemolytic crisis as RBCs become more fragile due to toxic metabolites in the blood. This crisis is usually fatal and indicates terminal stages of liver failure in the horse. ***PowerLecture: Hepatobiliary Disorders

Answer 75

Answer: **Place a subpalpebral lavage system** Explanation The system allows for a continuous drip of the topical meds without having to handle the horse frequently, and the reservoir can be filled without touching the horse. Treatment of fungal keratitis is optimal via direct ophthalmic administration, so you do not want to change your route of administration.

Answer 76

Answer: **Neutrophilic inflammation** Explanation In health, BAL fluid primarily consists of macrophages. However, in RAO, neutrophils are the predominant cellular finding. RAO typically affects older horses and is a response to environmental allergens. The classic case is the horse that is stalled in the winter and possibly housed in the vicinity of the hay storage. When the horse is exposed to hay allergens (via inhalation), bronchoconstriction and neutrophilic inflammation occur resulting in clinical signs. ***PowerPage: Recurrent Airway Obstruction ***PowerLecture: Respiratory Diseases

Answer 77

Answer: **Respiratory and reproductive** Explanation The correct answer is respiratory and reproductive. The main signs seen with equine herpesvirus (EHV-1) or equine viral rhinopneumonitis are copious nasal discharge in foals and abortion in mares. It can also cause central nervous system signs and occasionally can cause neonatal death from pneumonia. The nasal discharge in foals is sometimes referred to as "Snots" in horses and may be serous or purulent if there is secondary bacterial infection.

Answer 78

Answer: **Respiratory and reproductive** Explanation The correct answer is respiratory and reproductive. The main signs seen with equine herpesvirus (EHV-1) or equine viral rhinopneumonitis are copious nasal discharge in foals and abortion in mares. It can also cause central nervous system signs and occasionally can cause neonatal death from pneumonia. The nasal discharge in foals is sometimes referred to as "Snots" in horses and may be serous or purulent if there is secondary bacterial infection.

Answer 79

Answer: **Trimethoprim-sulfa and pyrimethamine** Explanation The correct answer is trimethoprim-sulfa and pyrimethamine. Equine protozoal myeloencephalitis is caused by Sarcocystis. This combination of drugs blocks folate metabolism by the protozoan at multiple steps and is generally agreed to be the most effective treatment for this condition. Recently, ponazuril has been approved and labeled for the treatment of EPM in horses and works by the same general mechanism. ***PowerPage: Equine Protozoal Myeloencephalitis ***PowerLecture: Neurologic Disorders

Answer 80

Answer: **Carpus vagus** Explanation This is one of the most common angular limb deformities that occurs in foals, usually as the result of asynchronous growth of the metaphyseal and epiphyseal growth plates.

Answer 81

Answer: **Navicular disease** Explanation Palmar foot pain can be the result of pain from any number of structures including the navicular bone, navicular suspensory or deep digital flexor tendon, navicular bursa, or several other heel areas. Navicular disease is a term used for pain associated with any of these structures. ***PowerPages: Nerve blocks

Answer 82

Answer: **Thelazia** Explanation Thelazia is a genus of **nematode worms (eyeworms)** which are found in the ocular tissues. Adults are usually found in the eyelids, tear glands, tear ducts, or the nictitating membrane. They may be found in the eyeball itself under the conjunctiva or in the vitreous. Thelazia are transmitted by Diptera (flies) which do not bite but feed on tears. Toxocara, which causes ocular larval migrans, usually causes granulomas which may be seen in the retina and appear more circular.

Answer 83

Answer: **Long chains of branching cocci** Explanation The correct answer is long chains of cocci. Dermatophilus has a classic "railroad track" appearance on cytology due to the long branching chains of gram positive cocci. [Dermatophilosis in Animals](https://www.merckvetmanual.com/integumentary-system/dermatophilosis/dermatophilosis-in-animals?query=dermatophilus%20congolensis%20horse)

Answer 84

Answer: **II, VII, IX, X** Explanation The correct answer is II, VII, IX, X. These are the vitamin K-dependent coagulation factors. Warfarin is an inhibitor of vitamin K and interferes with hepatic synthesis of these factors. ***PowerPage: Hemostasis

Answer 85

Answer: **The horse had a positive Coombs test and Coggin's test** Explanation The correct answer is the horse had a positive Coombs and Coggin's test. In this case, the probable cause of the immune-mediated hemolytic anemia is the equine infectious anemia retrovirus. It is known that corticosteroids tend to cause recrudescence of viremia and worsen anemia in infected animals. If a horse is receiving an antibiotic prior to development of immune-mediated hemolytic anemia, the drug should be discontinued, because it may be the cause of the anemia due to a drug reaction. In such an instance, a completely different class of antibiotic should be chosen in its place.

Answer 86

Answer: **Abbreviated (shortened) activated partial thromboplastin time (aPTT)** Explanation Disseminated intravascular coagulation is a complex disorder that can be described as widespread activation of the coagulation system, resulting in a pro-coagulant state with systemic thromboses and secondary diffuse hemorrhage throughout the body. DIC is secondary to pathologic conditions such as sepsis, localized infections, colitis, neoplasia, trauma, hepatic or renal failure, vasculitis, and various other disorders. DIC is associated with thrombocytopenia (from platelet consumption), prolongation of coagulation times such as PT and aPTT (from consumption of coagulation factors), elevations in D dimers (from degradation of fibrin), and low antithrombin III (from consumption). Thus the correct answer to this question is shortened aPTT. These criteria for DIC apply to all species, not just horses.

Answer 87

Answer: **Haemotobia irritans** Explanation The correct answer is Haematobia irritans. This fly is commonly known as the horn fly. It causes ventral midline dermatitis, as described in the question, on horses housed near cattle. They are often found around the horns, back, and sides of cattle on cooler days, and will affect the ventral abdomen on hot sunny days. Horn flies feed on blood and cause great economic losses in cattle. It can also serve as an intermediate host to Stephanofilaria stilesi, a filarial parasite that causes plaque lesions on the ventrum of cattle. Treatment and control of the flies is relatively easy with insecticide sprays, dust bags, or insecticide feed additives. Sarcoptes scabei infections and Culicoides hypersensitivity are extremely pruritic. Dermatophytosis is a good differential also, but Haematobia is a better choice, since the horses are affected by flies and are housed near cattle.

Answer 88

Answer: **Equine adenovirus** Explanation The correct answer is equine adenovirus. Adenovirus is normal in the upper respiratory tract but can cause a lower respiratory tract infection in immunocompromised individuals, particularly foals with failure of passive transfer or combined immunodeficiency. In fact, adenovirus is the most common cause of death in foals with those two conditions, leading to an often fatal pneumonia.

Answer 89

Answer: **Mesenteric rent** Explanation The correct answer is a mesenteric rent. A mesenteric rent can result in a strangulating intestinal obstruction. Other causes of strangulating intestinal obstructions include intussusceptions, hernias, epiploic foramen incarceration, volvulus, and strangulating lipomas. Left dorsal colon displacement is the same thing as splenic entrapment and will typically not result in a colic presentation this severe. ***PowerPage: Top 8 Equine Acute Colics ***PowerLecture: Gastrointestinal Disorders

Answer 90

Answer: **Lateralization of signs and concurrent neurogenic muscle atrophy of the quadriceps and gluteal regions** Explanation With EPM, the important signs to remember are asymmetry, ataxia, and atrophy. Lateralization of the signs (asymmetry) and quadriceps and/or gluteal muscle atrophy are most consistent with EPM. Herpes myeloencephalitis is caused by EHV1 and often has an acute onset following an episode of fever, cough and nasal discharge or following abortions on a farm. This condition often affects more than one horse on a farm. The ataxia and weakness is usually symmetric. Cervical vertebral stenotic myelopathy (VM) and equine degenerative myeloencephalopathy typically cause symmetric signs with the hindlimbs usually a grade worse than the forelimbs. The signs of CVM may be worsened by flexing or hyperextending the neck. Polyneuritis equi is more common in mature horses and usually starts with hyperesthesia progressing to anesthesia. There is progressive paralysis of the tail, rectum, bladder and urethra leading to urine dribbling. Verminous myeloencephalitis is less common and the onset is usually sudden with rapid deterioration and death. ***PowerPage: Equine Protozoal Myeloencephalitis

Answer 91

Answer: **Strongylus edentatus and Strongylus equinus** Explanation The correct answer is Strongylus edentatus and Strongylus equinus. The L3 larvae migrate through the portal vein and into the liver, through the peritoneum and retroperitoneal space. After a few months, the larvae will then return into the lumen of the gut. Strongylus vulgaris will migrate through small vessels and into the cranial mesenteric artery. Anoplocephala perfoliata is a tapeworm and does not migrate through blood vessels.

Answer 92

Answer: **The horse has a metabolic acidemia with respiratory compensation** Explanation You should really know approximate normal reference intervals for the test., pH = 7.35-7.45; PO2 is variable in venous blood; PCO2 = 40 mmHg, HCO3 = 24-30 mEq/L, iCa++ = 1.4-1.8 mmol/L. This is a general range, with each species having slight changes to this range. Explanation: The correct answer is metabolic acidemia with respiratory compensation. The pH is low which suggests acidemia, the HCO3 is low which suggests the cause of acidemia; the PCO2 is low and respiratory rate is high which suggests respiratory compensation. If you did not know the normal reference intervals and they were not provided, you should still be able to make an educated guess that a horse (or any other species) with notable diarrhea has a good chance of having a metabolic acidemia because of the loss of bicarbonate in the feces and the fact that the patient typically rehydrates by consuming electrolyte bicarbonate-free water orally.

Answer 93

Answer: **Most horses improve with treatment but relatively few make a complete recovery** Explanation This is a case of *Equine protozoal myeloencephalitis*. EPM can be tricky to diagnose because the clinical signs can be quite variable but the key findings are the "3 A's", namely asymmetry, ataxia, and atrophy. The onset of clinical signs are frequently gradual but rapid progression is seen in some cases. Ditterential diagnoses can include cervical vertebral malformation, equine degenerative myeloencephalopathy, equine herpes myeloencephalitis, polyneuritis equi, and verminous myeloencephalitis. However, the asymmetric and multifocal signs as well as the horse's age and gradual onset of signs make EPM the most likely diagnosis. The prognosis for horses with EPM is often described as variable. Studies show that about 70% of treated horses will improve but only up to 25% recover completely and perform normally. In addition, a subset (5-20%) of horses may improve while undergoing treatment but then relapse when treatment is discontinued. It is unclear whether relapse represents reemergence or persistence of resistant parasite or re-exposure. Based on these features of EPM, the best answer choice of those listed is that most horses improve with treatment but relatively few make a complete recovery. **PowerPage: Top 12 Equine Neurologic Diseases

Answer 94

Answer: **Tetanus antitoxin** Explanation The correct answer is tetanus antitoxin. Theiler's disease, or serum hepatitis, is an acute, diffuse, necrotizing hepatitis that occurs most commonly in association with introduction of an equine origin compound. The most commonly implicated product is tetanus antitoxin, which is an antiserum of equine origin. The disease usually occurs 4-10 weeks after administration and presents as malaise and weight loss, progressing to acute hepatoencephalopathy and icterus, and can be rapidly progressive and fatal. Pyrrolizidine alkaloids can also cause similar clinical signs but are distinguishable pathologically by the presence of the histologic triad of megalocytosis, fibrosis, and bile duct proliferation. Bacillus or Clostridium piliformis is the cause of Tyzzer's disease; this is a hepatopathy seen usually in foals. Aflatoxins can also be hepatotoxic. Tetanus toxoid is not an equine origin compound and is not associated with Theiler's disease. ***PowerLecture: Hepatobiliary Disorders

Answer 95

Answer: **Winter** Explanation The correct answer is winter. It is normal for horses to be in anestrus in the winter season. They will not respond to teaser stallions and have inactive ovaries and uterus. As the length of day increases at the end of the winter, the horses should return to normal cycling. This can be brought on with artificially increasing the length of light exposure. At the end of this period, it is normal for mares to have an inconsistent transitional period as they return to breeding. This is referred to as the vernal transition. PowerLecture: Estrous Cycle

Answer 96

Answer: **Equine recurrent uveitis** Explanation Although all of the listed answers could potentially result in blindness (directly or as a result of enucleation), the most common cause of blindness in horses is equine recurrent uveitis (ERU). This disease is also known as moon blindness or periodic ophthalmia. Recurrent episodes may result from dysregulated immune responses within the eye; typical clinical signs include blepharospasm, photophobia, lacrimation, miosis and aqueous flare.

Answer 97

Answer: **Disrupts motor innervation to the orbicularis oculi** Explanation The auriculopalpebral nerve, a branch of the facial nerve, is motor only. The auriculopalpebral block is useful in providing eyelid akinesis by blocking motor innervation primarily to the orbicularis oculi, thereby allowing manipulation of the eyelids without putting pressure on an already painful eye. This block is motor only and does not provide any desensitization. The supraorbital/frontal nerve block can be used to block a branch of the ophthalmic division of the trigeminal nerve, desensitizing the middle two-thirds of the upper eyelid and forehead skin. It may also provide some motor block of the levator palpebrae superioris due to a branch of the oculomotor nerve which runs adjacent.

Answer 98

Answer: **Systemic penicillin** Explanation The correct answer is systemic penicillin. Streptococcus equi ssp. equi is the agent causing strangles in horses. When they have lymph node abscessation, antibiotics are contraindicated because they will prolong the course of the disease but will not eliminate it. Because this disease is spread by direct contact, isolation of the horse is important. To obtain a definitive diagnosis, the lymph nodes could be aspirated. The treatment is to lance abscesses ventrally and dispose of all the material from the abscess to prevent spread of the organism. ***PowerPage: Strangles (Streptococcus equi) ***PowerLecture: Streptococcus equi

Answer 99

Answer: **Inhalation** Explanation The correct answer is inhalation. Equine herpesvirus-1 or equine viral rhinopneumonitis is a rapidly-spreading disease that is spread by inhalation directly or indirectly from infected nasal discharge, aborted fetuses or placenta. EHV-3, the cause of equine coital exanthema is spread venereally. Both EHV-1 and EHV-4 are a cause of rhinopneumonitis, but they are very important because they also result in abortions. EHV-1 is also associated with myeloencephalitis and has resulted in various outbreaks in the U.S. and abroad. EHV-1 is the main cause of paresis, abortions, and neonatal foal deaths, according to a recent article by Patel and Heldens. ***PowerPage: Top 9 Equine Respiratory Diseases

Answer 100

Answer: **Yellow star thistle toxicity** Explanation Centaurea solstitialis, aka yellow star thistle, grows in dry fields in California. Centaurea repens, or Russian knapweed, can also cause the same disorder. Some horses appear to avoid it; others appear to eat it with impunity, while some eat it and develop nigropallidal encephalomalacia. The loss of these upper motor ganglia results in loss of inhibition and dystonia, making it impossible for the animal to eat. Slow starvation results.

Answer 101

Answer: **Laminitis with rotation of the third phalanx** Explanation Laminitis, or founder, is severe and has progressed to the point of rotation of the third phalanx. The angle of the hoof wall surface and the dorsal third phalanx are no longer parallel. These radiographic findings along with the clinical signs are diagnostic for laminitis. ***PowerPage: Top 9 Equine Lameness ***PowerLecture: Laminitis

Answer 102

Answer: **Neomycin** Explanation The correct answer is neomycin. This is followed by gentamicin and then amikacin. Streptomycin is the least nephrotoxic aminoglycoside. Amphotericin B is an anti-fungal and not an aminoglycoside.

Answer 103

Answer: **Intravenous administration of 0.9% sodium chloride (NaCl) and 5% dextrose** Explanation The hereditary disease you should suspect is hyperkalemic periodic paralysis. In acute episodes of HYPP, the clinician should try and drive down the serum potassium. This can be accomplished by administering potassium-free IV fluids (such as 0.9% NaCl) and medications (such as dextrose) to drive potassium into the cell. While LRS could be used when no other IV fluid is available, it does contain potassium. Additionally, enalapril is an ACE inhibitor used for hypertension. One would clearly want to avoid IV solutions that contain high concentrations of potassium (KCI) or are extremely hypertonic (50% dextrose). Finally, while furosemide may sometimes be used to induce diuresis in some cases of HYPP, spironolactone is a potassium-sparing diuretic that would not decrease the serum potassium concentration. ***PowerLecture: Musculoskeletal Disorders

Answer 104

Answer: **Cyanide toxicity** Explanation The correct answer is cyanide toxicity. The bright red-colored blood and mucous membranes with signs of respiratory distress are typical findings for cyanide toxicity. There are many plants that can accumulate cyanide to levels that are toxic to horses. Treatment is with sodium nitrate or sodium thiosulfate IV.

Answer 105

Answer: **Streptococcus equi ssp. equi** Explanation The correct answer is Streptococcus equi ssp. equi. The exact reason why some horses develop purpura is unknown, but this is a relevant complication of equine strangles. Purpura hemorrhagica occurs weeks after infection or can occur after a bacterin is given. ***PowerPage: Strangles (Streptococcus equi) ***PowerLecture: Streptococcus equi

Answer 106

Answer: **Weekly application of topical (anti-pruritic) shampoo** Explanation Multiple therapies are commonly needed to control this problem. Certainly steroids (oral or parenteral) will alleviate the hives and decrease the pruritus, and fly spray will help cut down the frequency that the horse is exposed to fly bites. Hyposensitization injections may help for long-term control but are not always efficacious. However, topical shampoos are not likely to do anything.

Answer 107

Answer: **African Horse Sickness** Explanation *African horse sickness (AHS)* is a viral disease of equids that is transmitted by insects, primarily Culicoides. Clinical signs of AHS typically develop 5-7 days after infection and begin with fever and conjunctivitis. Some animals may recover but many go on to develop the pulmonary and/or cardiac form of AHS. The pulmonary form consists of acute respiratory distress, coughing, sweating, and foaming from the nostrils; this form is usually fatal. The cardiac form consists of edema of the head and neck as well as abdominal pain and depression. A characteristic sign is swelling in the indentation above the eyes (also referred to as swelling of the supraorbital fossa). About 50% of animals with the cardiac form die from heart failure while the rest gradually recover after about one week. Glanders is a bacterial disease caused by Burkholderia mallei (previously known as Pseudomonas mallei). Burkholderia mallei causes 3 different forms of disease: nasal glanders, pulmonary glanders, and cutaneous glanders. The nasal form presents with high fever, loss of appetite, and labored breathing with cough. The pulmonary form often develops over several months, beginning as a fever with dyspnea and cough. The cutaneous form develops over several months as nodules develop in subcutaneous tissue along the course of the lymphatics of the legs, costal areas, and ventrum. Surra is a trypanosomal disease causing primarily fever, weakness, and lethargy. Rift Valley Fever is a viral disease primarily of ruminants causing influenza-like signs and hepatic lesions.

Answer 108

Answer: **St. John's wort** Explanation This image shows a horse with skin sloughing due to cutaneous photosensitization. St. John's wort acts as a primary photosensitizer and can lead to photophobia, conjunctivitis, sloughed skin, and icterus. Blue-green algae cause sudden death. Slaframine causes hypersalivation and cantharidin causes colic.

Answer 109

Answer: **Long term furosemide administration** Explanation The correct answer is long term furosemide administration. Horses with glomerulonephritis are usually polyuric. Furosemide is only indicated for oliguric renal failure. The other choices are commonly used in the treatment and management of glomerulonephritis. A low protein diet will help decrease the amount of proteinuria and blood urea nitrogen circulating at any given time, therefore helping reduce the degree of azotemia.

Answer 110

Answer: **Cranial nerves VII and VIII (left side); fracture of the basisphenoid bone** Explanation The correct answer is damage to cranial nerves VII (facial nerve) and VIII (vestibular nerve) on the left side caused by fracture of the basisphenoid bone. This is a common injury when a fractious young foal rears up and falls backward on the poll. The basisphenoid bone becomes injured resulting in injury to cranial nerves VII and VIII. Damage to the facial nerve results in the muzzle deviation (opposite direction of the side of injury, in this case deviated to the right), ptosis of the left eye and drooping of the left ear. Damage to the vestibular nerve results in the head tilt.

Answer 111

Answer: **Short, low arc stride, landing toe first** Explanation Bone spavin is osteoarthritis of the distal intertarsal joint and/or the tarsometatarsal joint. Horses with bone spavin tend to have a shortened forward flight of the hoof with decreased hock action and they tend to drag the toe. A gait with the hindleg in rigid extension, pulling forward dragging the toe is seen with upward fixation of the patella Minimal weight bearing and marked foot sensitivity is seen with conditions of the feet such as subsolar abscesses and septic navicular bursitis (also known as "street nail") A leaning forward stance is seen with navicular disease. Horses with navicular disease also tend to have short strides and place the toe first. ***PowerPage: Top 9 Equine Lameness

Answer 112

Answer: **About 5%** Explanation You do not need to know anything about the disease in this question in order to get the correct answer. You are told that the disease is recessive. Because the trait is recessive, homozygotes will be the only individuals affected. In order for a foal to be born homozygous for the trait, BOTH parents MUST be carriers. The chances of both parents being carriers is 90% x 20% (or 0.9 × 0.2) = 0.18 or 18%. For any autosomal recessive trait, if both parents are carriers, the offspring will have a 25% chance of being homozygous and affected by the disease. In this example, there is an 18% chance that both parents are heterozygous carriers for the disease. Applying the 25% rate of passage of both diseased alleles, (0.18 x 0.25) = 0.045, or there is 4.5% chance that the foal will be affected.

Answer 113

Answer: **Balanoposthitis** Explanation The correct answer is balanoposthitis. EHV-3 causes papules, pustules, and ulcers on the vestibular mucosa, and vulvar skin, as well as the penis and prepuce (balanoposthitis). Less frequently, it can affect the skin of the face. There are no systemic signs or consequences of the infection, although secondary bacterial infections are possible. EHV-3 is transmitted by sexual contact and fomites such as contaminated equipment and rectal sleeves. Therefore, sexual rest and appropriate sanitation of equipment are required to allow affected areas to heal and to prevent transmission of the virus. Spontaneous recovery usually occurs over about 2 weeks, although a topical antibiotic may be warranted in the case of a secondary bacterial infection.

Answer 114

Answer: **Psyllium** Explanation The correct answer is psyllium. Psyllium is a hemicellulose laxative that has the ability to bind with sand and help remove it from the gastrointestinal tract. Feeding the horse in a stall and/or utilizing hay racks will also help the inadvertent consumption of sand that may be ingested if a horse is eating on sandy ground. None of the other answer choices are as effective as psyllium. ***PowerPage: Top 8 Equine Acute Colics

Answer 115

Answer: **Answer** Explanation The correct answer is winter. It is normal for horses to be in anestrus in the winter season. They will not respond to teaser stallions and have inactive ovaries and uterus. As the length of day increases at the end of the winter, the horses should return to normal cycling. This can be brought on with artificially increasing the length of light exposure. At the end of this period, it is normal for mares to have an inconsistent transitional period as they return to breeding. This is referred to as the vernal transition. ***PowerLecture: Estrous Cycle

Answer 116

Answer: **Perineum and tail base** Explanation The correct answer is perineum and tail base. Melanomas occur in up to 80% of gray horses. They occur most commonly on the perineum and tail base but can arise anywhere on the body. Most melanomas of gray horses are benign with varying degrees of invasiveness. They have the potential to develop into malignant tumors. Treatment includes surgery or cryosurgery. Horses that develop one melanoma are predisposed to developing others in the future.

Answer 117

Answer: **Entropion** Explanation The correct answer is entropion. This is a common condition in foals where the lower eyelid is inverted and can cause conjunctivitis or keratitis. The condition will usually correct spontaneously but sometimes will require treatment to evert the lid. One method for this is to use a local anesthetic, mechanically evert the lid, and staple it. Alternatively, surgical correction can be performed but is rarely indicated. Ectropion is the opposite condition where the eyelid everts out and can lead to exposure keratitis, but this is uncommon in horses. Ocular onchocerciasis is caused by microfilariae and is seen in about 50% of horses with cutaneous onchocerciasis.

Answer 118

Answer: **Venereally** Explanation The correct answer is venereally. Carrier stallions can infect mares. It can also be spread by aerosol. Equine viral arteritis (EVA) is in the genus Arterivirus, family Arteriviridae and causes vasculitis leading to edema, conjunctivitis, rhinitis, and abortion.

Answer 119

Answer: **Patent urachus, as described in the case here, requires systemic antimicrobial therapy and possibly surgical** Explanation These symptoms are indicative of a foal with a patent urachus; some neonatal foals have a patent urachus for a few days and leak clear, yellow urine. However, in this case, the history describes a purulent discharge which would suggest an infection of the urachal structures and a more serious condition. Thus systemic antimicrobials are indicated to eliminate infectious agents. In some instances (large urachal abscess, urachal necrosis, uroabodmen), surgical removal and repair are indicated. Cases of acquired patent urachus associated with navel infection should not be treated with cauterizing agents as this will potentially seal the urachus but prevent drainage of the infection. In the absence of infection, many cases of patent urachus will close on their own. However, if the problem persists, an ultrasound examination should be performed to reveal any abnormalities associated with the internal structure of the umbilicus. Patent urachus is not known to be due to a genetic mutation in foals

Answer 120

Answer: **Abaxial Sesamoid Nerve Block** Explanation First, you must determine that there is osteoarthritis of the pastern joint (proximal interphalangeal joint). Observe the periosteal bone proliferation and sclerosis along the medial side of the joint along with collapse of the medial joint space. Next, it is important to know what locations are blocked by the various perineural injections. You are likely to see at least one question on the board exam in regard to nerve blocks. The palmar digital nerve block typically blocks the palmar part of the foot; the abaxial block desensitizes the foot and proximal interphalangeal (pastern) joint; the low four point block desensitizes the foot, pastern and fetlock joint; and the subcarpal block desensitizes the metacarpal region and below. Thus, the lowest block that would likely desensitize the area in question is the abaxial sesamoid block. ***PowerPage: Nerve Blocks ***PowerLecture: Musculoskeletal Disorders

Answer 121

Answer: **Supportive care** Explanation Sacroiliac luxations in horses are generally considered untreatable. The condition will often stabilize with time and supportive care with rest and NSAIDs. Some horses may return to their previous level of activity or competitiveness but most have residual limitation. Reduction is not typically an option. Total hip arthroplasty has been reported in horses but is typically reserved for severely injured horses that do not improve with supportive care.

Answer 122

Answer: **Dohle Bodies indicating toxic change to the neutrophil** Explanation Dohle bodies are bluish-gray inclusions within the neutrophil that are retained aggregates of rough endoplasmic reticulum. Dohle bodies are one manifestation of toxic (i.e. endotoxemia) morphologic change to the leukocytes. Other changes in neutrophil morphology that occur with toxemia include cytoplasmic basophilia, vacuolation, and toxic granulation. These changes are commonly found in septic foals and may be considered "defects" in the neutrophil during intense cell production and maturation. In this image, there are numerous dark blue aggregates suggestive of Dohle bodies. ***PowerPage: Neonatal Sepsis ***PowerLecture Failure Of Passive Transfer And Foal Septicemia

Answer 123

Answer: **Arabian** Explanation The correct answer is Arabian. Arabian foals can develop combined immunodeficiency (CID) characterized by a lack of production of functional lymphocytes. No curative treatment exists, and foals will succumb to infection. In a CID foal, the foal typically has immunity from maternal antibodies for the first few months of life. However, as maternal antibodies begin to wane after 2-3 months, foals with CID will begin to develop recurrent infections that are responsive to antimicrobials. Once antimicrobials are discontinued, infection returns. Owners should be advised on the heritable nature of this disease. A genetic blood test is available to determine if a horse is a carrier of the CID trait.

Answer 124

Answer: **Cerebellar abiotrophy** Explanation The correct answer is cerebellar abiotrophy. Cerebellar abiotrophy is usually observed in foals which are less than one year of age, particularly 1-6 months of age. Cerebellar abiotrophy is the most common cerebellar disease found in horses. It is mostly seen in Arabian, Oldenburg, and Gotland breeds. There is no treatment, and signs may be progressive. Diagnosis is based on a good history and clinical signs such as intention tremors, lack of a menace, hypermetria, and ataxia.

Answer 125

Answer: **Less than 2.5 mmol/L** Explanation The correct answer is less than 2.5 mmol/L. It is important to remember a general reference range for all diagnostic laboratory data; lactate is commonly performed on hand-held lactometers that do not provide a reference range. As you may recall, lactate is produced from pyruvate in anaerobic environments to keep the process of glycolysis running. When a horse/foal is hypovolemic, blood lactate may increase because of poor blood perfusion to the body. Several studies have investigated blood and peritoneal lactate as a means of predicting survival in neonatal sepsis and equine colic. It may be necessary to look up these studies if you want exact findings (different reports provide different findings), but not surprisingly, the higher the lactate, the poorer the prognosis. ***PowerLecture: Failure Of Passive Transfer And Foal Septicemia

Answer 126

Answer: **Disseminated intravascular coagulation (DIC)** Explanation The correct answer is disseminated intravascular coagulation (DIC). DIC can be defined by having elevated PT/PTT, thrombocytopenia, and positive D dimer (a type of fibrin degradation product). Another parameter to evaluate is the fibrinogen concentration. Fibrinogen may be low in other species during DIC but is not commonly observed in horses. Usually two of these findings are enough to diagnose DIC. Antithrombin Ill activity is often decreased. Coagulopathies are not uncommon in horses with infections, diseases such as severe colitis, pleuropneumonia, or strangulating intestinal lesions. DIC is a more severe coagulopathy in which both thrombosis and hemorrhage are occurring.

Answer 127

Answer: **Surgical exploration and drain placement** Explanation The correct answer is surgical exploration and drain placement. A hygroma is a fluid filled swelling at the carpus, usually seen from repeated trauma leading to local bursitis. Horses are usually not lame from this condition but have restricted range of motion of the joint. Simply aspirating the fluid and/or injecting corticosteroids is rarely effective and the swelling usually recurs. Surgical excision of the bursal lining may be indicated when recurrence is a problem.

Answer 128

Answer: **Strangles** Explanation Historically, an intramuscularly administered Strangles vaccine has been available and has been associated with soft tissue reaction. More recently, an intranasal vaccine has become available, which is associated with local protection without any injection reaction.

Answer 129

Answer: **Anaplasma phagocytophilum infection** Explanation Based on the clinical signs (fever, lethargy, tachycardia and limb edema), CBC results (leukopenia, neutropenia, thrombocytopenia) and microscopic observation of a morula within the neutrophil, the correct answer and diagnosis is Anaplasma phagocytophilum infection. Diagnosis can be supported via PCR assays. Anaplasmosis (formerly Ehrlichi equi) infects primarily neutrophils and form inclusion bodies which consists of one or more coccobacillary organisms within these cells, known as morula. The complete pathogenesis of this disease is not fully elucidated but the organism is spread via tick bites. Other clinical signs that may be associated with this disease include petechiation, icterus and ataxia. The drug of choice for this disease is...(think about it for a second...you got it...oxytetracycline.

Answer 130

Answer: **Dermatophilosis** Explanation The answer is dermatophilosis. Dermatophilus congolensis is a gram positive, non-acid fast, facultative anaerobic actinomycete. It causes a crusting dermatitis in large animals when there is high moisture on the skin as well as mechanical irritation. Horses with long, wet haircoats are often affected. Lesions are commonly on the dorsum and pasterns of horses and are classically described as paintbrush lesions. It can be diagnosed with a direct smear preparation. Treatment includes keeping the haircoat clean and dry and penicillins if the lesions are severe. Lesions typically heal rapidly.

Answer 131

Answer: **Surgical occlusion of involved arteries (i.e. internal or external carotid artery) under general anesthesia** Explanation Guttural pouch mycosis has several different clinical presentations. In some horses, epistaxis is observed, while in others, cranial nerve deficits such as dysphagia may be observed. When hemorrhage is present, the disease is advanced and more aggressive therapy must be pursued. In this case, surgical occlusion of the involved arteries is necessary (i.e. embolization coils or balloons). If you lavaged the guttural pouch in this case, you may exacerbate the bleeding. Passage of the endoscope may also disrupt the clot and cause further hemorrhage. Furthermore, cauterization of the vessels involved using an endoscope is not possible. Tying off the left common carotid artery seems like a good idea, but because of the circular blood flow in the brain, hemorrhage will continue.

Answer 132

Answer: **Surgical occlusion of involved arteries (i.e. internal or external carotid artery) under general anesthesia** Explanation Guttural pouch mycosis has several different clinical presentations. In some horses, epistaxis is observed, while in others, cranial nerve deficits such as dysphagia may be observed. When hemorrhage is present, the disease is advanced and more aggressive therapy must be pursued. In this case, surgical occlusion of the involved arteries is necessary (i.e. embolization coils or balloons). If you lavaged the guttural pouch in this case, you may exacerbate the bleeding. Passage of the endoscope may also disrupt the clot and cause further hemorrhage. Furthermore, cauterization of the vessels involved using an endoscope is not possible. Tying off the left common carotid artery seems like a good idea, but because of the circular blood flow in the brain, hemorrhage will continue.

Answer 133

Answer: **Osteolysis** Explanation The correct answer is osteolysis. Navicular syndrome is a chronic degenerative condition of the navicular bursa and navicular bone. The precise etiology is unknown and is likely multifactorial involving the navicular bone, the suspensory ligament, the coffin joint, the navicular bursa, and the deep digital flexor tendon. Osteophyte formation, bony remodeling, and enlarged vascular channels are the hallmark radiographic findings in horses with navicular syndrome. Osteolysis is generally not a component of this condition.

Answer 134

Answer: **Upward patellar fixation** Explanation Upward patellar fixation causes the gait described above. Any horse that has the hind limb in rigid extension and is unable to flex it should be suspected of having this problem. One condition that can mimic this gait is luxation of the coxofemoral joint which can lead to an inability to flex the hind limb but this can be distinguished clinically because the limb will not be extended Normally, when horses are standing and resting their hindlimbs, the patella elevates to the top of the femoral trochlea, and the medial patellar ligament hooks over the medial ridge of the trochlea, locking the joint and allowing the horse to rest the limbs. To flex the stifle again, the quadriceps femoris muscle contracts, lifting the medial patellar ligament free of the medial trochlear ridge allowing the patella to return to its working position. When something prevents the horse's ability to release the stifle, the condition is known as upward patellar fixation (also called "upward fixation of the patella" or "locked stifle"). Most cases of upward patellar fixation can be managed conservatively (exercise (physical therapy), improved body condition). In severe and unresponsive cases, surgery to cut the medial patellar ligament is an option. Stringhalt is involuntary flexion of the hindlimb and is usually bilateral. The problem in this case is rigid extension. Stringhalt is treated with lateral digital extensor tenectomy. Gonitis is a term indicating stifle arthritis. It is nonspecific to the underlying cause and could be due to osteochondrosis, ligament injury, or some other problem. Upward patellar fixation and its consequences could be referred to as gonitis but this is a less specific diagnosis in this case. Jack spavin is a lay term for cunean bursitis or irritation of the cunean tendon as a result of bone growth on the medial hock. Thoroughpin is the term for effusion of the tarsal sheath (sheath of the deep digital flexor). ***PowerPage: Top 9 Equine Lameness

Answer 135

Answer: **Pituitary pars intermedia dysfunction** Explanation This disorder used to be called equine Cushing's. This condition is a result of hypertrophy, hyperplasia, and micro- or macroadenoma of the pituitary pars intermedia that secretes increased amounts of propiomelanocortin peptides. Adjacent pituitary tissues are compressed and secrete less of some other peptides. Data suggest that horses with this disease have hypothalamic dysfunction and decreased amounts of dopamine.

Answer 136

Answer: **>800 mg/dL** Explanation Foals are born immunocompetent but lack antibodies when born; therefore they must ingest maternal antibodies through colostrum. Veterinarians commonly evaluate passive transfer by performing a semi-quantitative ELISA test. For adequate passive transfer, antibodies should be greater than 800 mg/dL.

Answer 137

Answer: **30 liters of water** Explanation The correct answer is 30 liters of water. Horses consume about 50-70 ml water/kg/day, this will vary somewhat based on temperature, diet, and other factors. However, of these choices, 30 liters is the best choice. Normal urine production in the horse is about 15-30 ml/kg/day.

Answer 138

Answer: **Defect in voltage-dependent sodium channels** Explanation In horses with HYPP, the defect is in the sodium channel. In this disease, a population of sodium channels fail to inactivate and remain open. This, in turn, results in depolarization of the muscle membrane (closer to threshold) and hyperexcitability of the muscle. With further depolarization, the muscle cell membrane becomes unexcitable and paralysis may occur. The reason for the hyperkalemia is partially because of the movement of potassium out of the muscle cell as the myocyte repolarizes.

Answer 139

Answer: **Ponazuril** Explanation EPM can be tricky to diagnose because the clinical signs can be quite variable but the key findings are the "3 A's", namely asymmetry, ataxia, and atrophy. The onset of clinical signs are frequently gradual but rapid progression is seen in some cases. Differential diagnoses can include cervical vertebral malformation, equine degenerative myeloencephalopathy, equine herpes myeloencephalitis, polyneuritis equi, and verminous myeloencephalitis. However, the asymmetric and multifocal signs as well as the horse's age and gradual onset of signs make EPM the most likely diagnosis. Treatment options for EPM include: 1) Ponazuril (Marquis) antiprotozoal paste 2) Diclazuril (Protazil) antiprotozoal pellets 3) Nitazoxanide (Navigator) antiprotozoal paste 4) Sulfadiazine-pyrimethamine combination Surgical vertebral stabilization would be a treatment option for cervical vertebral malformation but this is less likely based on the asymmetric signs, temporal muscle atrophy, and normal cervical radiographs. Stall rest and phenylbutazone could be appropriate for certain orthopedic injuries. Ivermectin with praziquanel and pyrantel pamoate are dewormers but are not effective for EPM. Verminous myeloencephalitis is uncommon and typically has sudden onset with rapid deterioration and death.

Answer 140

Answer: **Tenectomy of the lateral digital extensor** Explanation The correct answer is tenectomy of the lateral digital extensor. Stringhalt is a myoclonic disease affecting one or both pelvic limbs. It causes spasmodic hyperflexion of the leg. The etiology is unknown but sweet pea poisoning is thought to be associated with the condition. Diagnosis is based on clinical signs, but electromyography can be used to confirm the diagnosis. Treatment involves tenectomy of the lateral digital extensor; however, not all cases respond to the treatment.

Answer 141

Answer: **Right side - peripheral vestibular dysfunction** Explanation The correct answer is right side, peripheral vestibular dysfunction. Peripheral vestibular dysfunction causes signs of head tilt, nystagmus, circling and asymmetric ataxia with preservation of strength. The head tilt is toward the affected side as is circling towards the lesion. Comparatively, central vestibular disease has similar clinical signs but general conscious proprioceptive deficits, weakness and cranial nerve deficits may also be present along with depression.

Answer 142

Answer: **Bone Spavin: osteoarthritis of the distal intertarsal joint and/or tarsometatarsal joint** Explanation The correct answer is bone spavin: osteoarthritis of the distal intertarsal joint and/or tarsometatarsal joint. Bog spavin is synovial distention of the tarsocrural joint, which you cannot see or appreciate with the given image. The only true answer with the information given is osteoarthritis of the distal tarsal and tarsometatarsal joint. All you have to do is memorize which spavin correlates with the appropriate anatomy. This question is designed to help you use the information given and not to get caught up in over analyzing the question.

Answer 143

Answer: **Baermann** Explanation The correct answer is Baermann. Dictyocaulus is the lungworm of horses/donkeys. The life cycle of the worm is that an infective larva is ingested and migrates through the mesenteric lymph nodes through lymphatics to the lung where it develops into an adult, producing eggs that are coughed up, swallowed, and passed in the feces. 1st stage larvae hatch in the feces and are most likely to be detected with a Baermann. Other useful diagnostic techniques include a transtracheal wash, which may show eosinophils and possibly parasites, ova, or larvae. It is rare for horses to have patent infections. You will observe them more often in foals than in adult horses. Donkeys are considered the reservoir.

Answer 144

Answer: **Myotonia** Explanation The correct answer is myotonia. These clinical signs and findings are consistent with a horse with myotonia. Etiology is not completely understood, but a genetic component is suspected. The 'dive bomber' sound heard on EMG is produced by repetitive firing after contraction of affected muscle fibers and is essentially pathognomonic for myotonia. Hyperkalemic periodic paralysis would be seen in Quarter Horses, Paint horses, and Appaloosa horses rather than Thoroughbreds.

Answer 145

Answer: **Aminocaproic acid** Explanation Aminocaproic acid is the best choice of those listed. This medication is believed to facilitate clot stabilization by blocking the activation of plasminogen to plasmin. As you may recall, plasmin is the active enzyme that dissolves clots; therefore, aminocaproic acid inhibits fibrinolysis. The other medications listed would have an anticoagulant effect and would be contraindicated in this mare.

Answer 146

Answer: **Upward patellar fixation** Explanation Upward patellar fixation causes the gait described above. Any horse that has the hind limb in rigid extension and is unable to flex it should be suspected of having this problem. One condition that can mimic this gait is luxation of the coxofemoral joint which can lead to an inability to flex the hind limb but this can be distinguished clinically because the limb will not be extended. Normally, when horses are standing and resting their hindlimbs, the patella elevates to the top of the femoral trochlea, and the medial patellar ligament hooks over the medial ridge of the trochlea, locking the joint and allowing the horse to rest the limbs. To flex the stifle again, the quadriceps femoris muscle contracts, lifting the medial patellar ligament free of the medial trochlear ridge allowing the patella to return to its working position. When something prevents the horse's ability to release the stifle, the condition is known as upward patellar fixation (also called "upward fixation of the patella" or "locked stifle"). Most cases of upward patellar fixation can be managed conservatively (exercise (physical therapy), improved body condition). In severe and unresponsive cases, surgery to cut the medial patellar ligament is an option. Stringhalt is involuntary flexion of the hindlimb and is usually bilateral. The problem in this case is rigid extension. Stringhalt is treated with lateral digital extensor tenectomy. Gonitis is a term indicating stifle arthritis. It is nonspecific to the underlying cause and could be due to osteochondrosis, ligament injury, or some other problem. Upward patellar fixation and its consequences could be referred to as gonitis but this is a less specific diagnosis in this case. Jack spavin is a lay term for cunean bursitis or irritation of the cunean tendon as a result of bone growth on the medial hock. Thoroughpin is the term for effusion of the tarsal sheath (sheath of the deep digital flexor).

Answer 147

Answer: **Bog spavin** Explanation The correct answer is bog spavin. Bog spavin, also known as tarsal hydrarthrosis, is often due to poor conformation and can result in increased synovial fluid formation. Both hindlimbs are usually affected. The horse is usually not lame from this condition. Distension may spontaneously appear and disappear in young horses. Bone spavin is osteoarthritis of the hock. Curb is thickening of the plantar tarsal ligament due to strain. Sweeney is supraspinatous contracture.

Answer 148

Answer: **Respiratory and reproductive** Explanation The correct answer is respiratory and reproductive. The main signs seen with equine herpesvirus (EHV-1) or equine viral rhinopneumonitis are copious nasal discharge in foals and abortion in mares. It can also cause central nervous system signs and occasionally can cause neonatal death from pneumonia. The nasal discharge in foals is sometimes referred to as "Snots" in horses and may be serous or purulent if there is secondary bacterial infection.

Answer 149

Answer: **Papillomavirus is believed to play a role in the pathogenesis.** Explanation Sarcoids are one of the most common tumors in horses. They are considered non-metastatic tumors in virtually all cases. For this reason, small lesions are sometimes treated with benign neglect, but they are not expected to regress. More advanced lesions or tumors in certain sites do need to be treated more aggressively. Unfortunately, no single treatment is universally effective. Recurrence rates after surgical excision are approximately 50%. Although there is still controversy surrounding this issue, either bovine papillomavirus or an equine variant is thought by many to play a role in development of these tumors.

Answer 150

Answer: **Cerebellar abiotrophy** Explanation The correct answer is cerebellar abiotrophy. Cerebellar abiotrophy is usually observed in foals which are less than one year of age, particularly 1-6 months of age. Cerebellar abiotrophy is the most common cerebellar disease found in horses. It is mostly seen in Arabian, Oldenburg, and Gotland breeds. There is no treatment, and signs may be progressive. Diagnosis is based on a good history and clinical signs such as intention tremors, lack of a menace, hypermetria, and ataxia.

Answer 151

Answer: **Application of horse shoes** Explanation The correct answer is application of horse shoes. Laminitis is an inflammatory condition of the lamina in one or more feet of a horse. It is often a manifestation of systemic disturbances such as endometritis and salmonellosis. A high carbohydrate diet (carbohydrate overload), excessive weight bearing on an individual leg, and corticosteroid administration also predispose a horse to laminitis. Application of horse shoes has no association with development of laminitis.

Answer 152

Answer: **Duodenitis-proximal jejunitis** Explanation Duodenitis-proximal jejunitis, also known as either anterior enteritis, or proximal enteritis best fits this case because of the characteristic reflux, fever, peritoneal fluid characteristics, rectal findings, the depression and relatively less pain than would be expected with an obstruction. The cause is still uncertain, but a relationship of this disease to positive cultures of reflux for Clostridioides difficile has been found. Typically these cases are treated medically, which would include repeated decompression of the stomach, IV fluids, replacement of electrolyte deficiencies, analgesics and correction of any acid-base abnormalities. ***PowerPage: Top 8 Equine Acute Colics ***PowerLecture: Gastrointestinal Disorders

Answer 153

Answer: **7th rib space at costochondral junction** Explanation Thoracocentesis can be performed at different locations; however, the 7th rib space at the level of the costochondral junction is the most appropriate answer available. The 4th rib space is near the heart, whereas the 10th or 13th rib space involves the caudal aspect of the thorax. This 7th rib space is a good choice because it is one of the more dependant regions where fluid will tend to accumulate; it is also caudal to where the heart should sit and well cranial to the diaphragm. When available, ultrasound guidance should be used to guide placement.

Answer 154

Answer: **Neonatal Isoerythrolysis** Explanation Neonatal Isoerythrolysis (NI) would be a possible cause of the icterus noted in the sclera. NI is common in multiparous mares and usually affects foals between 24-72 hours of age. Ni results in hemolysis, hyperbilirubinemia, and icterus. A low packed cell volume would further support NI. NI develops because the newborn foal expresses alloantigens on its red blood cells inherited from the sire that the mare does not have. If the mare becomes sensitized to the sire's specific antigen, maternal antibodies are produced and absorbed by the foal soon after birth. This subsequently results in lysis of the red blood cells.

Answer 155

Answer: **Equine metabolic syndrome** Explanation EMS is characterized by gross or severe regional obesity and clinical or subclinical laminitis. These animals are insulin-resistant and often have higher than normal insulin levels in blood. ***PowerPage: Top 9 Equine Lameness

Answer 156

Answer: **Parascaris equorum** Explanation The correct answer is Parascaris equorum. This is a roundworm that undergoes migration through the lung. It is common in foals, and during its migration, it can damage the lower respiratory tract and carry in bacteria. Dictyocaulus is the equine lungworm, but it generally does not cause clinical signs in foals; however it can cause cough and respiratory signs in adults. Strongylus and Strongyloides are gastrointestinal parasites and do not migrate through the lungs.

Answer 157

Answer: **Persistent corpus luteum** Explanation The correct answer is persistent corpus luteum. Progesterone made by the corpus luteum prevents estrus. There will be follicles in the ovaries, and the horse may still ovulate but is non-receptive to stallions. The corpus luteum is usually not palpable. A granulosa cell tumor is less likely because usually the involved ovary is large and the other small, unless there are bilateral tumors, which is uncommon. Gonadal dysgenesis is a chromosomal abnormality, and the mare would not have been able to have had a normal pregnancy previously. Pituitary tumor in a 5 year old would be very unusual, and she appears normal (no failure to shed out). Pituitary tumor is a possible cause but very unlikely. Pregnancy has been ruled out by your rectal palpation, since it has been months.

Answer 158

Answer: **Dipylidium spp** Explanation The correct answer is Dipylidium spp. Dipylidium tapeworms are found in cats and dogs. The other three tapeworm species can occur in horses. Clinical signs include unthriftiness, anemia, and colic. Infections can be treated with praziquantel. Pyrantel salts are only effective against Anoplocephala spp., but not P. mamillana.

Answer 159

Answer: **Acepromazine** Explanation The correct answer is acepromazine. Phenothiazine tranquilizers can cause relaxation of smooth muscles and engorgement of the corpus cavernosum with blood, leading to an inability to withdraw the penis into the sheath or paraphimosis. While this drug side effect is very rare, veterinarians should be cautious in the use of acepromazine in stallions and should consider another sedative such as xylazine or detomidine when sedation is necessary.

Answer 160

Answer: **Evaluation of creatine kinase (CK) and aspartate aminotransferase (AST) to rule-out myopathy** Explanation Based on the clinical signs, the most likely cause is recurrent exertional rhabdomyolysis, commonly observed in racing Thoroughbreds. Typical clinical signs include muscle cramping of the major muscle groups; the cramping is painful and consequently causes the tachycardia, tachypnea, and profuse swelling. The muscle pain can be exacerbated upon physical examination by firm palpation of the larger muscle groups. The most sensitive serum enzyme to evaluate myositis is creatine kinase, a muscle specific enzyme with a short half-life. AST is not muscle specific but does become elevated at a slower pace, as compared to CK. Thus CK will rise and fall quickly whereas AST will increase and decrease slower once the myositis has resolved.

Answer 161

Answer: **West Nile Encephalitis (WNV); Serum Immunoglobulin M (IgM) capture ELISA** Explanation The correct answer is WNV. This is a mosquito born flavivirus that affects horses in multiple areas of the United States. Clinical signs are variable and can be mild (muscle fasiculations, slight ataxia) to severe (recumbency). Of note, muscle fasiculations is somewhat characteristic of WNV but fever may be detected in all patients. A readily available diagnostic test is the serum IgM capture ELISA which will detect infection, even in the face of vaccination. There is a vaccine available for WNV, making the clinical presentation less common. ***PowerPage: Top 12 Equine Neurologic Diseases

Answer 162

Answer: **Osteolysis** Explanation The correct answer is osteolysis. Navicular syndrome is a chronic degenerative condition of the navicular bursa and navicular bone. The precise etiology is unknown and is likely multifactorial involving the navicular bone, the suspensory ligament, the coffin joint, the navicular bursa, and the deep digital flexor tendon. Osteophyte formation, bony remodeling, and enlarged vascular channels are the hallmark radiographic findings in horses with navicular syndrome. Osteolysis is generally not a component of this condition.

Answer 163

Answer: **The horse had a positive Coombs test and Coggin's test** Explanation The correct answer is the horse had a positive Coombs and Coggin's test. In this case, the probable cause of the immune-mediated hemolytic anemia is the equine infectious anemia retrovirus. It is known that corticosteroids tend to cause recrudescence of viremia and worsen anemia in infected animals. If a horse is receiving an antibiotic prior to development of immune-mediated hemolytic anemia, the drug should be discontinued, because it may be the cause of the anemia due to a drug reaction. In such an instance, a completely different class of antibiotic should be chosen in its place.

Answer 164

Answer: **Maxilla buccal and mandible lingual** Explanation The correct answer is maxilla buccal and mandible lingual. This is because the mandible is narrower than the maxilla thus predisposing points and hooks to form at the buccal surface of the maxilla and the lingual surface of the mandible. If these become sharp they can irritate tissues, cause difficulty in mastication, lacerate the tongue in cheek, and result in weight loss.

Answer 165

Answer: **Maxilla buccal and mandible lingual** Explanation The correct answer is maxilla buccal and mandible lingual. This is because the mandible is narrower than the maxilla thus predisposing points and hooks to form at the buccal surface of the maxilla and the lingual surface of the mandible. If these become sharp they can irritate tissues, cause difficulty in mastication, lacerate the tongue in cheek, and result in weight loss.

Answer 166

Answer: **Guttural pouch tympany** Explanation The correct answer is guttural pouch tympany. Guttural pouch tympany is a condition where the pouch becomes distended with air. It is thought to be due to a defect in the Eustachian tube or pharyngeal tissues. It leads to a characteristic non-painful, air-filled swelling and is treated by fenestrating the membrane between the normal and affected pouch. In an animal this young, guttural pouch mycosis is unlikely, and the most common clinical sign of mycosis is epistaxis or dysphagia. A ruptured longus capitis occurs from trauma and causes severe hemorrhage from the guttural pouch rather than the swelling described. Streptococcus equi ssp. equi usually affects animals of 1 year of age or older, and usually causes swelling of lymph nodes. It can lead to guttural pouch empyema, but that is less likely given the signalment and presentation of this animal. ***PowerPage: Guttural Pouch Disease

Answer 167

Answer: **Chorioptes equi** Explanation The correct answer is Chorioptes equi. Chorioptes is a mange mite that is usually found around the foot and fetlock. It causes a pruritic dermatitis that can cause the formation of papules, crusts, thickened skin, as well as alopecia. The mites are often found in the feathered hair around the fetlocks of draft horses. As with other mites, ivermectin is the treatment of choice. Culicoides, Haematobia irritans (the Horn fly) and onchocerciasis often cause dermatitis at the ventral midline of horses.

Answer 168

Answer: **Chorioptes equi** Explanation The correct answer is Chorioptes equi. Chorioptes is a mange mite that is usually found around the foot and fetlock. It causes a pruritic dermatitis that can cause the formation of papules, crusts, thickened skin, as well as alopecia. The mites are often found in the feathered hair around the fetlocks of draft horses. As with other mites, ivermectin is the treatment of choice. Culicoides, Haematobia irritans (the Horn fly) and onchocerciasis often cause dermatitis at the ventral midline of horses.

Answer 169

Answer: **Purulent inflammation and gram positive cocci with large capsules** Explanation The correct answer is purulent inflammation and gram positive cocci with large capsules. The causative agent of strangles is streptococcus equi ssp. equi, a gram positive cocci with a large capsule. It causes enlargement and suppurative abscessation of the mandibular and retropharyngeal lymph nodes. ***PowerPage: Strangles (Streptococcus equi)

Answer 170

Answer: **Mosquito** Explanation The correct answer is the mosquito. There have been over 27 different species of mosquitoes known to transmit EEE. After inoculation, it spreads via the lymphatics, and you don't usually see neurologic signs until approximately 5 days post infection. Both cortical and thalamic lesions result and they don't necessarily have to be symmetrical. Clinical signs may include head pressing, altered mentation, paresis, paralysis, convulsions, circling, ataxia, and death. Death may occur 2-3 days after the onset of clinical signs. These clinical signs apply to any of the forms of equine encephalomyelitis (VEE and WEE).

Answer 171

Answer: **Onchocerca cervicalis** Explanation The correct answer is Onchocerca cervicalis. Clinical signs result from hypersensitivity to dying microfilariae. However, most infected horses will remain asymptomatic. Lesions include patchy to diffuse alopecia, erythema, and scaling. The lesions are usually not pruritic, although there are a few reports of horses experiencing severe pruritis. A "bull's eye" or circular lesion in the center of the forehead is highly suggestive of onchocerciasis. Ventral midline dermatitis is also commonly associated with the disease.

Answer 172

Answer: **Cyanide toxicity** Explanation The correct answer is cyanide toxicity. Cyanide does not allow hemoglobin to release oxygen, thus causing the cherry red lips. It is found in cherries, chokecherries, arrow grass, and Sudan grass. Large amounts must be consumed. There is a bitter odor of almonds to the GI tract with this toxicity. Treatment is sodium nitrate and sodium thiosulfate. Prognosis is poor due to the rapid onset. Carbon monoxide can cause cherry red mucous membranes but would not cause the almond smell.

Answer 173

Answer: **Prolonged gestation and decreased milk production** Explanation Common clinical signs associated with fescue toxicosis include prolonged gestation and/or decreased milk production (agalactia). Ergopeptine alkaloids are ingested by the mare, which act as dopamine agonists. Dopamine serves to inhibit prolactin, thus inhibiting lactation. Placental thickening and weak or stillborn foals may also occur.

Answer 174

Answer: **Erythromycin (or other macolide antimicrobial such as clarithromycin or azithromycin) and rifampin** Explanation The correct answer is Erythromycin and rifampin. This is a must-know fact, as this disease is very commonly encountered. Treatment is usually for about 2 months but should be based on resolution of clinical signs, radiographic signs, and bloodwork. More recently, newer macrolide antimicrobials such as Clarithromycin and Azithromycin have been used in foals with R. equi pneumonia. One clinical study demonstrated better outcome with Clarithromycin and rifampin; additionally, Clarithromycin is typically administered twice daily, whereas erythromycin may have to be administered four times a day. ***PowerPage: Rhodococcus equi ***PowerLecture: Rhodococcus equi

Answer 175

Answer: **Polysaccharide Storage Myopathy (PSSM)** Explanation Based on the breed and clinical signs, PSSM should be a top consideration. A subset of horses have a storage disorder in which there is an accumulation of glycogen and abnormal polysaccharide within the skeletal muscle. PSSM has been linked to an autosomal dominant mutation of the glycogen synthase gene in Quarter Horses. However, other breeds, such as Paint, Appaloosas, Warmbloods and draft horses can also be affected. Horses with PSSM often have elevations in creatine kinase and aspartate aminotransferase; rhabdomyolysis in PSSM likely results from an energy deficiency within the contracting muscles.

Answer 176

Answer: **Splints** Explanation Explanation - This is a description of splints or metacarpal exostosis which involves periostitis of the interosseous ligament between the third and second metacarpal (or metatarsal) bone. Treatment usually involves rest and anti-inflammatory medications, although if the bony exostoses impinge on the suspensory ligament, surgical removal of the proliferative tissue may be indicated. Sidebone refers to ossification of the alar cartilage of the coffin bone. High ringbone refers to osteoarthritis of the proximal interphalangeal (pastern) joint. Osselets are inflammation of the periosteum on the dorsal distal epiphyseal surface of the third metacarpal bone and fetlock joint. Thoroughpin is the term for effusion of the tarsal sheath (sheath of the deep digital flexor).

Answer 177

Answer: **Otitis media-externa** Explanation Mycoplasma is a common cause of otitis media-externa. Usually, the infection is a result of consuming contaminated milk. A congenital brain tumor is highly unlikely. Otobius (soft tick with predilection for ears) is unlikely because the clinical signs are not consistent; however, it is a good differential. With Otobius the calf would probably not show such extreme clinical signs and would probably be scratching and rubbing at the ear. Polioencephalomalacia is more likely to present with stargazing, head pressing, depression, and blindness. Polioencephalomalacia is caused by a thiamine deficiency. An excellent differential for the clinical signs described would be listeriosis and thromboembolic meningoencephalitis.

Horses Flashcards

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