Horses Flashcards
A horse presents to your clinic after ingesting a large amount of grain. What is your major concern?
A. Choke
B. Torsion
C. Impaction
D. Laminitis
E. Acidosis
Answer: Laminitis.
The correct answer is laminitis secondary to endotoxemia. Laminitis, endotoxemia, and diarrhea are commonly associated with grain overload and appropriate therapy to evacuate any remaining stomach contents, ameliorate endotoxin and prevent laminitis should be instituted immediately. Laxatives such as mineral oil are commonly administered.
Which of the following is not known to classically cause crusting dermal lesions on horses?
Pemphigus foliaceus
Generalized granulomatous disease
Corynebacterum pseudouberculoss
Dermatophilosis
Dermatophytosis
Answer: Corynebacterium pseudotuberculosis
Explanation
The correct answer is Corynebacterium pseudotuberculosis. Corynebacterium pseudotuberculosis is also known as pigeon fever. It causes an ulcerative lymphangitis and abscesses in the pectoral region of horses. Treatment is aimed at hot packing the swellings and draining the abscesses. Antibiotics can be administered but have been known to prolong the disease by delaying abscess formation. The other four answer choices classically present as crusting dermal lesions on horses.
A 4-year old male Thoroughbred horse presents to you for colic. During your work up, you note a painful enlargement at the root of the mesentery on rectal palpation. You suspect that the cause of the horse’s colic are adults from the egg shown in the
picture below. Which of the following drugs effectively kills the adult organisms that can cause this condition?
A. Rifampin
B. Metronidazole
C. Praziquantel
D. Piperonyl butoxide
E. Ivermectin
Answer: Ivermectin
Colic with an associated painful mass at the root of the mesenery is suspicious for verminous arteritis caused by damage to the cranial mesenteric artery and its branches by Strongylus vulgaris. The strongyle egg shown in the picture confirms the cause in this question. A number of anthelmintics are effective including benzimidazoles, pyrantel and ivermectin.
Praziquantel is effective against tapeworms. Rifampin and metronidazole are antibacterial drugs. Piperonyl butoxide is a pesticide synergist used in insecticide mixtures in horses.
A client notices that her 8-year old Paint Horse gelding is lethargic, inappetant and looks to be in pain when forced to walk. Additionally, your client collected a urine sample for you to examine (see image). You collect a plasma sample to help determine the cause and it appears clear and normal. Which of the answer choices accurately describes a likely clinical scenario?
Extravascular hemolysis based on urine color and normal-appearing plasma
Normal urine based on the fact that horse urine has ample calcium carbonate crystals
Hemoglobinuria based on urine color and a normal-appearing plasma sample
Myoglobinuria based on urine color and a normal appearing plasma sample
Answer: Myoglobinuria based on urine color and normal appearing plasma sample.
Explanation
Myoglobinuria is characterized by brownish urine that does not clear on centrifugation along with normal-colored plasma. Myoglobin does not bind to serum proteins and is quickly excreted before reaching levels that would discolor the plasma. Also, the painful gait suggests a myopathy that may be related to the myoglobinuria.
Conversely, hemoglobinuria is associated with a reddish discoloration of the plasma because hemoglobin is maintained in the plasma longer and is lost in the urine more slowly.
A 9-month old foal presents with difficulty walking. You immediately note that the foal appears to have a flexural deformity of the right forelimb consisting of an increased dorsal hoof wall angle of 80 degrees such that the heel does not contact the ground. The coronary band is prominent. You take radiographs which confirm a broken forward hoof-pastern angle. What is the most appropriate treatment for this type of flexural limb deformity?
- Superior check ligament desmotomy
- Lateral digital extensor tenectomy
- Desmotomy of the accessory ligament of the deep digital flexor tendon
- Transection of the insertion of the semitendinosus
Answer: Desmotomy of the accessory ligament of the deep digital flexor tendon
Explanation
This case describes a severe flexural deformity of the distal interphalangeal joint, also known as “clubfoot”. This is typically a congenital condition in young horses although it can be acquired. A genetic component is suspected. Mild cases can sometimes be managed conservatively with NSAIDs, farriery, exercise and nutritional changes. Severe cases often require surgery; the surgical procedure of choice is desmotomy of the accessory ligament of the deep digital flexor tendon (also known as inferior check ligament desmotomy). The accessory ligament of the deep digital flexor tendon (inferior check ligament) runs from the palmar surface of the proximal metacarpus to the deep flexor tendon in the mid-metacarpal region.
The superior check ligament originates above the knee and attaches to the superficial flexor tendon, and its primary purpose is to support the tendon. Superior check ligament surgery is used to treat a bowed tendon.
Lateral digital extensor tenectomy is a procedure used to treat stringhalt. Transection of the insertion of the semitendinosus is used to treat fibrotic myopathy.
It is a rainy April and you are visiting a horse farm to evaluate a horse with itchy and flaky skin lesions on the pastern and mild lameness. On examination, you see an exudative seborrheic dermatitis of the plantar aspect of the pastern that is slightly malodorous. Which of the following is a term used to describe this condition in horses?
Sweeney
Summer sores
Sweet itch
Scratches
Ringbone
Answer: Scratches
Explanation
Scratches is a condition of chronic seborrheic dermatitis of the palmar/plantar aspect of the pastern. The condition is sometimes referred to by several other names including “grease heel”, “dermatitis verrucosa”, “dew poisoning” and “mud fever”. It is not specific to the underlying infectious cause but the condition is generally associated with horses kept in wet or muddy environments.
Summer sores are caused by Habronema spp. and Draschia spp. stomach worms of the horse. The larvae in feces are ingested by the maggots of flies, and the flies can deposit them at susceptible moist skin areas, damaged skin areas, or mucous membranes where the larvae cause an eosinophilic granuloma as a reaction to their migration.
Sweet itch results from a Type 1 allergic reaction to Culicoides spp. Clinical signs of sweet itch are usually in the form of self-trauma due to pruritus.
Sweeney is the common name for shoulder atrophy in the horse. The muscle atrophy is caused by damage to the suprascapular nerve which innervates to the infraspinatus and supraspinatus muscles.
Ringbone refers to osteoarthritis or bony exostosis in the pastern (high ringbone) or coffin (low ringbone) joints.
A 9-year old Standardbred stallion comes to see you for evaluation of muscle atrophy. You examine the horse and note atrophy of the lateral thigh and gluteal muscles. When the horse is backed up, spasmodic hyperflexion of either hindlimb occurs resulting in a high-stepping gait. Which of the following is most likely responsible for the observed signs?
Black walnut intoxication
Sweet pea intoxication
Senecio or groundsel intoxication
Castor bean intoxication
Red maple intoxication
Answer: Sweet pea intoxication
Explanation
This case describes a horse with stringhalt or sudden flexion (contraction of the lateral extensor tendons) of one or both hind legs. It is most evident when the horse is backing up slowly or turning. It can involve one or both hind legs. The etiology in some cases is unknown but the condition can be associated with chronic intoxication of sweet peas (Lathyrus spp.). Australian stringhalt has been associated with flatweed ingestion (Hypochoeris radicata). The precise pathogenesis is not understood, but a mycotoxin affecting the long myelinated nerves in the hind limbs has been suggested based on the types of nerve damage seen in affected horses.
Black walnut intoxication is associated with laminitis and colic after exposure to wood shavings of black walnuts.
Red maple intoxication is associated with acute hemolytic anemia. Senecio or groundsel intoxication is associated with liver disease after chronic exposure. Castor bean intoxication is associated with severe gastrointestinal irritation and hemorrhagic diarrhea.
You are assessing welfare of horses at a lesson barn. Most captive horse welfare concerns develop due to which of the following?
Social hierarchy issues
Colic
Lack of exercise
Escape
Neglect
Answer: Neglect
Explanation
The majority of animal welfare concerns in captive horses are due to neglect.
Which of the following is true regarding equine rabies vaccination in the United States?
It is not required by law but recommended
It is mandated by state law in all 50 states
It is mandated by federal law
It is required by state law only in endemic areas
Answer: It is not required by law but recommended
Explanation
Rabies vaccination in horses is only recommended in endemic areas and is not required by law. In endemic areas, boosters are usually performed annually.
The American Association of Equine Practitioners (AAEP) recommends rabies as a core vaccine in horses.
You wish to sedate a horse to re-check a lesion on the hind leg. Which of the following choices will provide the shortest duration of action?
- Xylazine
- Romifidine
- Medetomidine
- Detomidine
Answer: Xylazine
Explanation
The correct answer is xylazine. Xylazine has the lowest receptor affinity, duration of action, and has the largest dose requirement of the alpha 2 agonists. Although xylazine will provide the shortest duration of action, clinicians are told to be careful when using xylazine and working with the hind limbs because these horses can have a sudden rapid limb movement known as a phantom kick. Sedative effects of xylazine last for about 20 minutes. Sedative effects of detomidine typically last approximately 90 minutes; however, peak sedation is achieved for 10-20 minutes.
Romifidine is similar to detomidine; however, the side effects are believed to be decreased.
Which of these would be appropriate for a horse with hyperkalemic periodic paralysis (HYPP)?
Timothy hay
Alfalfa hay
Beet molasses
Brome hay
Answer: Timothy hay
Explanation
The correct answer is timothy hay. Of these choices, the only feed with low potassium is timothy hay. A low potassium diet is the most important nutritional modification in the treatment of HYPP. Regular exercise and feeding smaller, frequent meals can also reduce clinical signs. This disease is inherited in an autosomal dominant fashion, and owners should be discouraged from breeding affected animals.
***PowerLecture: Musculoskeletal Disorders
For a horse with hyperkalemic periodic paralysis (HYPP), timothy hay is the appropriate feed because it is low in potassium, which is crucial in managing HYPP. A low potassium diet, along with regular exercise and smaller, frequent meals, helps reduce clinical signs. HYPP is an autosomal dominant inherited condition, and breeding affected animals should be discouraged.
Hyperkalemic Periodic Paralysis
Hyperkalemic periodic paralysis (HYPP) is marked by sudden attacks of paralysis which, in severe cases, may lead to collapse and sudden death. It is an inherited mis-sense mutation in the gene encoding the alpha chain of the adult skeletal muscle sodium channel, resulting in increased sodium permeability across the skeletal muscle cell membrane. Quarter horse, Paint horse, and Appaloosa progeny tracing back to the Quarter horse sire “Impressive” can be affected with this disease and must be eliminated from any reproductive program. Most affected horses are heterozygotes. A sequela of HYPP in horses that undergo general anesthesia is malignant hyperthermia syndrome.
Which nerve block would be most specific for alleviating pain associated with laminitis?
Suspensory ligament block
Abaxial sesamoid block
Palmar digital block
High 4 point block
Answer: Abaxial sesamoid block
Explanation
The correct answer is the abaxial sesamoid block. The four basic blocks used by equine clinicians are the palmar digital, abaxial sesamoid, low four point and high four point block, each desensitizing more of the limb as your blocks move more proximal on the limb. The palmar digital desensitizes the palmar third of the foot whereas the abaxial sesamoid desensitizes the entire foot. As laminitis is associated with separation of the dorsal lamina, the abaxial sesamoid block would be most likely help with laminitis. Of note, desensitizing the foot during acute laminitis is not typically employed as a standard treatment but is rather used to help alleviate pain so that the clinician can perform radiographs of the feet or trim the feet. The low 4 point block desensitizes the palmar aspect distal to the distal end of the second and fourth metacarpals. The high 4 point block desensitizes the leg distal to the carpus or tarsus. The suspensory ligament block desensitizes the deep branch of the lateral palmar nerve at the level of the carpometacarpal joint.
***PowerPage: Nerve Blocks
You diagnose this 15-year old mare in the picture with a mild, acute laminitis. Which of the following can be used as treatment for this horse?
Trimethoprim sulfa
Phenoxybenzamine
Application of horse shoes
Prednisone
Answer: Phenoxybenzamine
Explanation
The correct answer is phenoxybenzamine. Phenoxybenzamine is an alpha-adrenergic antagonist promoting vasodilation and restoration of blood flow to the digits. Prednisone is contraindicated in laminitis because corticosteroids are believed to induce the condition. Antibiotics are not indicated unless a secondary bacterial infection develops. Application of a horse shoe would not help and would be very painful in an already sensitive and painful condition. Other medications used to restore blood flow to the digits include acepromazine, isoxsuprine hydrochloride, dimethylsulfoxide (DMSO), heparin, and nitroglycerine.
A Thoroughbred race horse has been moved from California to Florida in July and is experiencing poor performance, exercise intolerance and tachypnea. You observe the horse working out one hot afternoon and see these signs, but you also note that the horse is not sweating. You check the rectal temperature and note that it is 104F (40 C). What is the diagnosis?
Equine Cushing’s
Hypothyroidism
Influenza
Anhidrosis
Diabetes insipidus
Answer: Anhidrosis
Explanation
Anhidrosis is the inability to sweat, which can be fatal if not addressed. The cause is unknown. It tends to occur in hot humid climates, and may occur in horses raised in the climate, or more commonly, horses brought into the climate. The most successful treatment is to move the horse back to a more favorable climate.
What body systems are most affected in an anaphylactic reaction in a horse?
- Lungs and colon
- Liver and lungs
- Kidney and colon
- Liver and kidneys
- Heart and small intestine
Answer: Lungs and colon
Explanation
The correct answer is lungs and colon. These are referred to sometimes as the shock organs in the horse. When a horse undergoes an anaphylactic reaction from an allergen or chemical stimulus, the primary signs will be respiratory and lower Gl and will include dyspnea or severe respiratory distress and diarrhea. Other common signs include anxiety, tachycardia, piloerection, and sweating. Treatment of anaphylactic shock usually includes injection with some combination of epinephrine, corticosteroids, and an antihistamine.
Measurement of blood lactate is commonly used in foals and adult horses as an overall reflection of cardiovascular status. What is the normal blood lactate in a healthy foal or horse?
Less than 2.5 mmol/L
Less than 5 mmol/L
Less than 10 mmol/L
Less than 7.5 mmol/L
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
You suspect disseminated intravascular coagulation (DIC) in a 16-year old Arab mare presented for colic and epistaxis (see image). Which of the following parameters is NOT associated with a diagnosis of DIC?
- Prolongation of Prothrombin Time (PT)
- Elevation in D-dimers
- Decreased antithrombin Ill activity
- Thrombocytopenia
- Abbreviated (shortened) activated partial thromboplastin time (aPTT)
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 Ill (from consumption). Thus the correct answer to this question is shortened aPTT. These criteria for DIC apply to all species, not just horses.
Disseminated Intravascular Coagulation (DIC) in Veterinary Medicine: NAVLE Study Guide
Definitions and Etiology
• DIC: A secondary, life-threatening condition characterized by widespread intravascular coagulation leading to microthrombi formation and subsequent multiorgan failure, accompanied by paradoxical bleeding due to the consumption of platelets and clotting factors. • Causes: DIC can arise from numerous conditions, including sepsis, severe infections (e.g., canine parvovirus, FIP), neoplasia (e.g., hemangiosarcoma), trauma (e.g., heatstroke, burns), and immune-mediated diseases (e.g., IMHA).
Pathophysiology
• Mechanisms: Excessive thrombin generation leads to systemic fibrin formation and microthromboses. The consumption of clotting factors and platelets results in thrombocytopenia and hypocoagulability, causing hemorrhagic diathesis. • Fibrinolysis: Impaired fibrinolysis due to increased plasminogen activator inhibitor (PAI-1) leads to an accumulation of fibrin and reduced clearance of microthrombi.
Clinical Signs
• Phases of DIC: • Peracute/Hypercoagulable: Rapid onset with microvascular thrombosis, shock, and multiorgan failure. • Acute Consumptive: Characterized by widespread hemorrhage, petechiae, and ecchymoses. • Chronic Silent: May present with subtle signs such as intermittent bleeding or thrombosis, often seen in malignancies. • Specific Signs: Spontaneous bleeding (e.g., hematuria, melena), shock, organ dysfunction (e.g., renal failure), and neurological deficits.
Diagnosis
• Laboratory Tests: • Coagulation Tests: Prolonged PT, aPTT, elevated D-dimers, reduced fibrinogen, and low antithrombin (AT) levels. • Blood Smear: Presence of schistocytes. • Advanced Diagnostics: Thromboelastography (TEG) for monitoring coagulation status, D-dimer assays for fibrin degradation products.
Treatment
• Primary Goal: Treat the underlying cause (e.g., antibiotics for sepsis, surgery for tumors) and manage coagulopathy. • Supportive Care: • Blood Products: Fresh frozen plasma (FFP) or fresh whole blood to replace consumed clotting factors. • Anticoagulants: Heparin or low-molecular-weight heparin (LMWH) during the hypercoagulable phase, particularly if AT activity is sufficient. • Novel Therapies: Experimental treatments in human medicine, such as recombinant activated protein C (APC) and antithrombin concentrates, may have potential in veterinary practice.
Prognosis
• Outcome: Varies based on the underlying cause, stage of DIC, and response to treatment. The prognosis is generally guarded to poor, with early detection and intervention being critical to improving outcomes.
Key Points for Veterinary Professionals
• Monitoring: Regularly assess coagulation status in patients at risk for DIC using a combination of clinical signs and laboratory tests. • Intervention: Early, aggressive treatment of the underlying cause and careful management of coagulopathy are essential. • Emerging Therapies: Stay updated on advancements in DIC management, particularly those translating from human to veterinary medicine.
Which antibiotic is contraindicated in foals?
Cefazolin
Enrofloxacin
Ampicillin
Amikacin
Gentamicin
Answer: Enrofloxacin
Explanation
The correct answer is enrofloxacin. Enrofloxacin is a fluoroquinolone and thus, its mechanism of action involves the inhibition of DNA gyrase. The reason you don’t want to use it in foal is because it can result in arthrotoxicity and subsequent erosion of cartilage. Ampicillin, gentamicin, and amikacin are commonly used to provide broad-spectrum coverage against potential septicemia. Ampicillin is a penicillin; gentamicin and amikacin are both aminoglycosides. Cefazolin is a first-generation cephalosporin that is occasionally used in the face of septicemia if a penicillin is not available.
Which of these vaccines administered intramuscularly is most likely to cause a local reaction at the injection site of a horse?
Rabies
Tetanus antitoxin
Rhinopneumonitis
Strangles
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.
Which of the following is one of the biggest welfare concerns for wild horses and burros?
Fighting
Lack of veterinary care
Exposure to weather
Rough terrain
Overpopulation
Answer: Overpopulation
Explanation
Overpopulation is a major welfare concern and can lead to starvation and death without proper herd management.
Horses that are used to pull carriages in tourist destinations, so-called “carriage horses”” commonly experience leg and hoof issues that impact their long-term welfare. These issues stem from:
Excessive time spent on very hard surfaces such as concrete
Inappropriate training
Injuries caused by neglect
Lack of insufficient nutrients to support bone health
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.
A 4-year old Arabian mare is shipped from the United Arab Emirates to New York where you examine the horse. You note that the horse has a mucopurulent discharge from the nares and has labored breathing and cough. Heart rate is 24 bpm, respiratory rate is 40 breaths per minute and temperature is 104.9 F (40.5 C). You make a smear of the discharge and see large numbers of extracellular straight Gram-negative rods with rounded ends. Which diagnostic test is most likely to confirm your clinical suspicion?
- PCR of the exudate for SeM protein of Streptococcus equi subsp. equi
- Biopsy of the mandibular lymph node
- Mallein test
- PCR of the exudate for Rhodococcus equi virulence associated plasmid
- Viral culture of a guttural pouch wash
Answer: Mallein test
Explanation
The horse’s history of arrival from the United Arab Emirates along with the clinical and cytologic findings are consistent with the nasal form of glanders.
Burkholderia mallei causes 3 different forms of disease; nasal glanders, pulmonary glanders, and cutaneous glanders (also referred to as Farcy).
The nasal form presents with high fever, loss of appetite and labored breathing with cough. Viscous mucopurulent discharge or crusting may be present around the nares. There may be ulceration of the upper respiratory passages that resolve in the form of star-shaped cicatrices (“stellate scars”). Regional lymph nodes may be enlarged and indurated and may rupture or adhere to deeper tissues.
The pulmonary form often develops over several months, beginning as a fever with dyspnea and cough. Lung lesions commence as light colored nodules surrounded by hemorrhage or as diffuse pneumonia. The nodules may become caseous or calcified and discharge contents to the upper respiratory tract. Nodules may also be found in other organs.
The cutaneous form develops over several months, beginning with cough and dyspnea as well. Eventually, nodules develop in subcutaneous tissue along the course of the lymphatics of the legs, costal areas, and ventrum. They can rupture and excrete infectious purulent exudate. Infected lymphatics may form thickened cord-like lesions that sometimes coalesce into a string of beads appearance known as “farcy pipes”. Nodular lesions of other organs may also be found.
Burkholderia mallei can be identified in smears made from fresh lesions as mainly extracellular straight Gram-negative rods with rounded ends. Several diagnostic tests exist including PCR, ELISA, and Western Blot but the two that you actually need to know about because they are used in international trade are complement fixation (CF) serology and the mallein test. The mallein test is considered the most reliable, sensitive, and specific test; it involves injection of mallein purified protein derivative intradermally into the lower eyelid. The test is read at 24 and 48 hours and a positive reaction is characterized by edematous swelling or purulent discharge.
Horses should not be treated; local authorities should be notified if a case is suspect and if disease is confirmed, horses must be humanely destroyed and affected carcasses should be burned and buried.
The most likely test to confirm glanders in a horse with a history of arrival from the UAE, mucopurulent nasal discharge, labored breathing, and Gram-negative rods in the discharge, is the mallein test. Glanders, caused by Burkholderia mallei, can present in nasal, pulmonary, or cutaneous forms. The mallein test involves injecting purified protein derivative into the lower eyelid and checking for a reaction. If glanders is confirmed, the horse must be humanely destroyed, and the carcass appropriately disposed of.
Glanders: Overview
Causative Agent
• Bacteria: Burkholderia mallei.
Pathophysiology
• Transmission: Direct contact with infected animals, ingestion of contaminated food/water, inhalation.
• Invasion: Bacteria enter through mucous membranes, spreading via lymphatics and bloodstream, leading to multiple organ involvement.
Clinical Signs
• Acute Form: High fever, nasal discharge, nodules, ulcers.
• Chronic Form: Progressive weight loss, nodular lesions in lungs and spleen, cutaneous form (“farcy”) with nodules along lymphatics.
• Latent Form: Inapparent infections, may reactivate under stress.
Diagnosis
• Tests: Mallein test, culture, PCR, serology (e.g., CFT, ELISA).
• Necropsy Findings: Granulomatous nodules, caseous material in organs.
Treatment and Prevention
• No Effective Treatment: Euthanasia recommended.
• Prevention: Quarantine, strict biosecurity, disinfection, and controlling animal movements.
Zoonotic Potential
• Humans: Can contract glanders through direct contact, presenting with pneumonia, septicemia, and skin infections. Fatal if untreated.
A 4-year old Arabian mare is shipped from the United Arab Emirates to New York where you examine the horse. You note that the horse has a mucopurulent discharge from the nares and has labored breathing and cough. Heart rate is 24 bpm, respiratory rate is 40 breaths per minute and temperature is 104.9 F (40.5 C). You make a smear of the discharge and see large numbers of extracellular straight Gram-negative rods with rounded ends. Which diagnostic test is most likely to confirm your clinical suspicion?
- PCR of the exudate for SeM protein of Streptococcus equi subsp. equi
- Biopsy of the mandibular lymph node
- Mallein test
- PCR of the exudate for Rhodococcus equi virulence associated plasmid
- Viral culture of a guttural pouch wash
Answer: Mallein test
Explanation
The horse’s history of arrival from the United Arab Emirates along with the clinical and cytologic findings are consistent with the nasal form of glanders.
Burkholderia mallei causes 3 different forms of disease; nasal glanders, pulmonary glanders, and cutaneous glanders (also referred to as Farcy).
The nasal form presents with high fever, loss of appetite and labored breathing with cough.
Viscous mucopurulent discharge or crusting may be present around the nares. There may be ulceration of the upper respiratory passages that resolve in the form of star-shaped cicatrices (“stellate scars”). Regional lymph nodes may be enlarged and indurated and may rupture or adhere to deeper tissues.
The pulmonary form often develops over several months, beginning as a fever with dyspnea and cough. Lung lesions commence as light colored nodules surrounded by hemorrhage or as diffuse pneumonia. The nodules may become caseous or calcified and discharge contents to the upper respiratory tract. Nodules may also be found in other organs.
The cutaneous form develops over several months, beginning with cough and dyspnea as well. Eventually, nodules develop in subcutaneous tissue along the course of the lymphatics of the legs, costal areas, and ventrum. They can rupture and excrete infectious purulent exudate. Infected lymphatics may form thickened cord-like lesions that sometimes coalesce into a string of beads appearance known as “farcy pipes”. Nodular lesions of other organs may also be found.
Burkholderia mallei can be identified in smears made from fresh lesions as mainly extracellular straight Gram-negative rods with rounded ends. Several diagnostic tests exist including PCR, ELISA, and Western Blot but the two that you actually need to know about because they are used in international trade are complement fixation (CF) serology and the mallein test. The mallein test is considered the most reliable, sensitive, and specific test; it involves injection of mallein purified protein derivative intradermally into the lower eyelid. The test is read at 24 and 48 hours and a positive reaction is characterized by edematous swelling or purulent discharge.
Horses should not be treated; local authorities should be notified if a case is suspect and if disease is confirmed, horses must be humanely destroyed and affected carcasses should be burned and buried.
The most likely test to confirm glanders in a horse with a history of arrival from the UAE, mucopurulent nasal discharge, labored breathing, and Gram-negative rods in the discharge, is the mallein test. Glanders, caused by Burkholderia mallei, can present in nasal, pulmonary, or cutaneous forms. The mallein test involves injecting purified protein derivative into the lower eyelid and checking for a reaction. If glanders is confirmed, the horse must be humanely destroyed, and the carcass appropriately disposed of.
CGPT: Glanders in Horses and Other Animals - Comprehensive Veterinary Information
Glanders: Overview
Causative Agent
• Bacteria: Burkholderia mallei.
Pathophysiology
• Transmission: Direct contact with infected animals, ingestion of contaminated food/water, inhalation.
• Invasion: Bacteria enter through mucous membranes, spreading via lymphatics and bloodstream, leading to multiple organ involvement.
Clinical Signs
• Acute Form: High fever, nasal discharge, nodules, ulcers.
• Chronic Form: Progressive weight loss, nodular lesions in lungs and spleen, cutaneous form (“farcy”) with nodules along lymphatics.
• Latent Form: Inapparent infections, may reactivate under stress.
Diagnosis
• Tests: Mallein test, culture, PCR, serology (e.g., CFT, ELISA).
• Necropsy Findings: Granulomatous nodules, caseous material in organs.
Treatment and Prevention
• No Effective Treatment: Euthanasia recommended.
• Prevention: Quarantine, strict biosecurity, disinfection, and controlling animal movements.
Zoonotic Potential
• Humans: Can contract glanders through direct contact, presenting with pneumonia, septicemia, and skin infections. Fatal if untreated.
A 9 year old Thoroughbred mare presents for intermittent left-sided epistaxis over several months. There is no history of trauma. The horse has mildly increased respiratory effort on your physical exam. Which of these is the most likely cause of recurrent, intermittent, unilateral epistaxis in this animal?
- Exercise induced pulmonary hemorrhage
- Ethmoid hematoma
- Purpura hemorrhagica
- Warfarin toxicity
Answer: Ethmoid hematoma
Explanation
The correct answer is ethmoid hematoma. An ethmoid hematoma is a progressive and locally destructive mass that resembles a tumor but is not truly neoplastic. The most common clinical sign is mild, persistent, spontaneous, intermittent epistaxis that can be unilateral or bilateral.
Warfarin is not as likely in this horse due to the recurrent nature of the condition and the fact that it is unilateral.
Exercise-induced pulmonary hemorrhage actually causes epistaxis only about 10% of the time. Also, since the bleeding is pulmonary in origin, the epistaxis would likely be bilateral. Epistaxis with this condition also occurs immediately after exercise, which was not reported in this horse.
Purpura hemorrhagica is a vasculitis that results from a type Ill immune complex hypersensitivity after a streptococcus equi infection. This leads to vasculitis, and the main clinical signs are petechia and ecchymoses of mucous membranes.
The most likely cause of recurrent, intermittent, unilateral epistaxis in a 9-year-old Thoroughbred mare is an ethmoid hematoma. This is a locally destructive mass that causes mild, spontaneous, and intermittent nosebleeds, which can be unilateral or bilateral.
Other conditions like warfarin toxicity, exercise-induced pulmonary hemorrhage, and purpura hemorrhagica are less likely due to the specific nature of the symptoms and their typical presentations.
Progressive Ethmoid Hematoma in Horses: NAVLE Study Guide
Definitions and Etiology
• Progressive Ethmoid Hematoma (PEH): A non-neoplastic mass in the nasal passages or paranasal sinuses of horses, characterized by recurrent submucosal hemorrhage and subsequent encapsulation. The exact cause remains unknown.
Pathophysiology
• Expansion: PEH grows by repeated hemorrhage within the submucosa, leading to a well-encapsulated mass that can distort surrounding tissues and bone.
• Location: Originates from the ethmoidal labyrinth, potentially extending into nasal cavities or sinuses, causing local destruction and distortion.
Clinical Signs
• Common Symptoms:
• Epistaxis: Mild, intermittent, unilateral nosebleed, often the first sign.
• Respiratory Noise: Stridor due to airflow obstruction.
• Facial Deformities: Distortion of facial bones or swelling over the maxillary sinus.
• Advanced Signs: Head shaking, coughing, or dysphagia if the mass extends into the nasopharynx.
Diagnosis
• Initial Assessment:
• Endoscopy: Visualization of a greenish-yellow to purplish-red mass in the nasal cavity.
• Radiography: Lateral projections showing a soft tissue opacity in the ethmoidal labyrinth area, often with fluid lines.
• Histopathology: Definitive diagnosis through biopsy revealing submucosal fibrous tissue, hemorrhage, and inflammatory infiltrates.
• Advanced Imaging: CT or MRI can assess the extent of the mass and potential bone involvement.
Treatment
• Surgical Excision: Traditional method via frontonasal bone flap, often associated with significant hemorrhage.
• Complications: Hemorrhage, respiratory distress, recurrence (30-60%).
• Cryosurgery: Sequential freezing and surgical removal, potentially reducing hemorrhage but with risks like brain damage if improperly applied.
• Laser Surgery (Nd:YAG Laser): Precision excision with reduced morbidity, but risk of complications like respiratory distress and meningoencephalitis.
• Intralesional Formalin Injection: Minimally invasive, leading to mass regression but risks include nasal discharge and severe complications like neurological signs if the cribriform plate is compromised.
Prognosis
• Long-Term Outcome: Guarded to poor due to high recurrence rates despite treatment; regular follow-up and re-evaluation are necessary.
Key Points for Veterinary Professionals
• Early Detection: Crucial for better outcomes; regular endoscopic evaluations are recommended.
• Comprehensive Management: Treatment choice depends on mass size, location, and available resources.
• Multimodal Approach: Combining surgical and conservative treatments may offer the best outcomes.
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: 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.
A horse presents to you in respiratory distress. You perform blood gas analysis and get the following results: PaCO2-60 mmHg, Pa02- 75 mmHg, pH 7.255, Base excess= -1.8. How would you describe this horse’s status?
- Hypoventilation, respiratory alkalosis
- Hyperventilation, respiratory acidosis
- Hyperventilation, respiratory alkalosis
- Hypoventlaton， respiratory acidosis
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.
You suspect pleuropneumonia with pleural effusion in a horse. What is the proper site for thoracocentesis for pleural effusion removal in the horse if ultrasound is not available?
- 7th rib space at costochondral junction
- 10th rib space in the dorsal third of the chest
- 10th rib space at costochondral junction
- 13th rib space at costochondral junction
- 4th rib space at costochondral junction
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.
Which of the following is the most common etiologic agent causing pneumonia in foals?
- Streptococcus spp.
- Actinobacillus equuli
- Bordetella bronchiseptica
- Mycoplasma spp.
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
Which of these viruses are normally found in the upper respiratory tract of the horse?
Equine influenza
Equine viral arteritis virus
Equine adenovirus
Equine herpesvirus
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.
You are performing endoscopy of the guttural pouch of a 6 year old Quarter Horse gelding presented for dysphagia. What is the most likely causative organism?
Histoplasma
Aspergillus
Coccidioides
Cryptococcus
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
A Thoroughbred racehorse presents to you for having poor performance, stopping at the ends of races, and having labored breathing. After races, the horse swallows excessively and will sometimes cough. What is your most likely diagnosis?
- Dynamic airway collapse
- Exercise-induced pulmonary hemorrhage
- Congestive heart failure
- Large airway obstruction
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.
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”}]
Many horses in a large group develop a rapid-onset high fever, weakness, depression, and cough. What step is most likely to lead you to a definitive diagnosis?
- Perform a transtracheal wash for bacterial culture
- Take thoracic radiographs of several affected horses
- Perform serologic testing for antibodies to common respiratory pathogens
- Euthanize several affected horses and perform gross necropsies
- Take nasopharyngeal swabs for viral isolation
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.
- Causative Agents:
• Orthomyxovirus: Specifically A/equine type-2 (H3N8), first recognized in 1963. - Epidemiology:
• Transmission: Direct inhalation of respiratory secretions, fomites. Epidemics arise from newly introduced infected horses.
• Hosts: Primarily affects horses aged 1-5 years. - 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. - 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. - 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). - 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. - 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. - Medications:
• NSAIDs: Control fever and inflammation.
• Examples: Flunixin meglumine, phenylbutazone.
• Antibiotics: For secondary bacterial infections.
• Examples: Trimethoprim-sulfamethoxazole, penicillin. - 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
You are out in the field and you notice a horse tilt his head up and curl back his lips in a manner that makes it appear to be “grimacing”. You identify this as a flehmen response. What is thought to be happening when this response occurs?
This is a sign of sexual interest or arousal and you need to be careful if the horse is nearby
This is a sign of colic
This is a pathognomonic sign of yellow star thistle toxicity
Scents are moved to the vomeronasal organ
This is a display of aggression or dominance that a horse will display when it detects the presence of other stallions
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.
You are examining a 3 year old Thoroughbred gelding that just completed a race and notice discharge from the nostrils. What would be an appropriate treatment for this horse prior to the next race?
Furosemide
Plasma transfusion to replace clotting factors
Vitamin K
Vasopressin
Whole blood transfusion
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
You suspect that an 18-year-old Quarter Horse mare has recurrent airway obstruction (RAO, also known as chronic obstructive pulmonary disease) based on clinical signs of increased respiratory rate and effort, expiratory wheezes on auscultation, and the age of the horse. What cytologic finding of bronchoalveolar lavage (BAL) fluid would be supportive of RAO?
Neutrophilic inflammation
Mononuclear inflammation
Eosinophilic inflammation
Mixed inflammatory response (neutrophils, macrophages, and eosinophils)
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.
You are examining a 4 month old Thoroughbred colt with a 2 week history of weight loss, fever, and increased respiratory rate. You suspect pneumonia and notice the pictured lesion on thoracic ultrasonography. What is the most likely cause?
Streptococcus zooepidemicus pneumonia
E. coli pneumonia
Rhodococcus equi pneumonia
Equine Herpes Virus pneumonia
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
A mare with an inability to blink and corneal ulceration indicates a lesion to this cranial nerve.
Facial
Trigeminal
Abducens
Trochlear
Oculomotor
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.
What is the most common parasitic cause of uveitis is the horse?
Sarcocystis neurona
Neospora caninum
Toxoplasma gondii
Onchocerca cervicalis
Thelazia lacrymalis
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
A 6-year old Morgan horse presents for an ocular evaluation. The owner is concerned that the horse has a corneal ulcer. You notice that the horse has marked blepharospasm. Which of the following best describes the effects of an auriculopalpebral nerve block in this horse?
Blocks sensory innervation of the cornea
Disrupts motor innervation to the orbicularis oculi
Disrupts motor and sensory innervation to the eyelids
Blocks sensory innervation of the upper two-thirds of the eyelids
Disrupts motor innervation to the levator palpebrae superioris
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.
A horse presents to you with a melting corneal ulcer. What does the fact that the ulcer is melting indicate?
Trauma
Globe rupture
Infection
Indolent ulcer
Descemetocele
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.
You examine a one-week old female foal for eye problems. She has mild blepharospasm and epiphora. On ocular exam, you note that the lower eyelid margin is inverted inward. What is the usual treatment for this condition?
Place a patch over the eye
Surgical correction of the defect
Enucleation
No treatment is necessary
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
What is the most common cause of blindness in horses?
- Fungal ulcerative keratitis
- Equine recurrent uveitis
- Cataract(s)
- Trauma
- Bacterial ulcerative keratitis
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.
What is the most common cause of cataracts in horses?
Diabetes mellitus
Inherited cataracts
Uveitis
Lens trauma
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.
A horse presents to you with a corneal ulcer. You are concerned because it appears to be infected. You perform cytology and find gram negative rods. What is the most appropriate treatment for this infection?
Systemic penicillin
Topical tobramycin
Topical natamycin
Topical cefazolin
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.
Chronic renal failure (CRF) in horses commonly results in clinical signs such as weight loss, inappetence, polydipsia and polyuria. Besides azotemia, what electrolyte changes would you likely see on serum biochemistry evaluation of a horse with CRF?
Hypernatremia, hypochloremia
Hypercalcemia, hypernatremia
Hyperkalemia, hyperchloremia
Hypercalemia, hypophosphatemia
Answer: Hypercalemia, 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.
Failure of closure of the foramen ovale within the first 48 hours of life in a healthy foal will result in
Shunting of blood from the right atrium to the ductus arteriosus
Shunting of blood from the left ventricle to the right ventricle
Shunting of blood from the right atrium to the left atrium
Shunting of blood from the left atrium to the right atrium
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”}]
You are examining a 6-year old race horse that has been experiencing decreased performance. On auscultation you note, a slow heart rate of 16 beats per minute with an irregular rhythm consisting of occasional dropped beats. An ECG confirms the presence of a second degree atrioventricular block. Which of the following should you tell the owner?
This conduction finding is a life-threatening abnormality and placement of a pacemaker is indicated
This conduction finding is common in racehorses and is unlikely to contribute to poor performance
This conduction finding is a common cause of poor performance and is usually effectively treated by quinidine
This conduction finding likely indicates serious underlying pathology in the heart and further diagnostic tests are needed
This conduction finding is a common cause of poor performance and is not treatable; the horse should be retired
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.
A horse gets into cow feed that contains the ionophore, monensin. What is your biggest concern?
Hepatotoxicity
Nephrotoxicity
Neurotoxicity
Cardiotoxicity
Gastrointestinal toxicity
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.
A 2-year old Standardbred gelding presents for a prepurchase exam. On auscultation you hear a loud grade IV/VI systolic murmur on the right thorax. An echocardiogram is performed, which is shown below. The cardiac chambers are labeled LV (left ventricle), RV (right ventricle), Ao (Aorta). What is your diagnosis?
Ventricular septal defect
Tricuspid valve endocarditis
Unremarkable echocardiogram
Patent ductus arteriosus
Subaortic stenosis
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.
In addition to a routine pre-purchase exam of a 12 year old Thoroughbred mare, an ECG was performed which showed an increase in the P-R interval followed by occasional P waves that are not followed by a QRS-T complex. What does the owner need to know about this finding?
This horse is predisposed to developing an electrical-mechanical disassociation and needs further diagnostics before purchasing
This mare most likely has a ventricular septal defect and should not be purchased.
This is a second-degree atroventricular block, which is commonly seen in athletic horses.
This is a first-degree atrioventricular block and should be treated immediately with quinidine.
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.*
The owner of a weanling colt has asked for a pre-purchase examination to be performed on her 4 month old colt. The colt appears in good health based on physical examination with the only abnormality noted being a holosystolic murmur heard best on the right side of the thorax. What is your diagnosis based on auscultation and echocardiographic findings (see image; long-axis view from left side)?
Patent ductus arteriosus (PDA)
Truncus arteriosus
Ventricular septal defect (VSD)
Atrial septal defect (ASD)
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.
A Thoroughbred racehorse has been brought to you for examination because the trainer has noted exercise intolerance. The only abnormality your exam reveals is an irregularly (randomly) irregular heart rhythm when the horse is at rest, with a heart rate of 45 beats/minute. Given this finding and the complaint of exercise intolerance, which of the following is the most likely diagnosis?
Ventricular fibrillation
Sinoatrial block
Sinus arrhythmia
Atrial fibrillation
Sinus bradycardia
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.
The most common congenital cardiac abnormality in the horse is depicted below, what is it?
Ventricular septal defect
Tetralogy of Fallot
Patent ductus arteriosus
Pulmonic stenosis
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.
During a routine physical exam of a 15 day old female Arabian foal, a holosystolic murmur can be clearly heard. The murmur is graded as being 4/6. This murmur is heard bilaterally, and the point of maximum intensity is on the right side. What is the most likely diagnosis?
Ventricular septal defect
Bacterial endocarditis
Patent ductus arteriosus
Tetralogy of Fallot
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.
A first-degree atrioventricular conduction block is characterized by _________
An increase in the S-T interval
An increase in the P-R interval
A lack of P waves
A widening of the QRS complex
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.
A 14 year old Warmblood presents for an acute onset of exercise intolerance. On physical exam, an irregularly irregular rhythm with variable heart sounds is present. The heart rate is 40 beats per minute. There are no other abnormal physical exam findings. Given this, what is the treatment of choice assuming that the findings are confirmed via an ECG?
Digoxin
Quinidine
Defibrillation
Precordial thump
Furosemide
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.
Which of the drugs below is used to treat horses with atrial fibrillation?
Quinidine
Atenolol
Lidocaine
Furosemide
Atropine
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.
You are examining a 6-year old race horse that has been experiencing decreased performance. On auscultation you note, a slow heart rate of 16 beats per minute with an irregular rhythm consisting of occasional dropped beats. An ECG confirms the presence of a second degree atrioventricular block. Which of the following should you tell the owner?
This conduction finding likely indicates serious underlying pathology in the heart and further diagnostic tests are needed
This conduction finding is a common cause of poor performance and is not treatable; the horse should be retired
This conduction finding is common in racehorses and is unlikely to contribute to poor performance
This conduction finding is a common cause of poor performance and is usually effectively treated by quinidine
This conduction finding is a life-threatening abnormality and placement of a pacemaker is indicated
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 19 year old Saddlebred gelding presents with a history of staggering and respiratory distress. On physical exam, it is noted the horse is sweating, has a heart rate of 52, and a respiratory rate of 44. Hemoglobinuria is identified on urinalysis. This horse lives in close proximity to cattle, and it is suspected that he may have been eating cow feed. What feedstuff additive is known to be very toxic to horses and result in cardiomyopathy if consumed at high enough doses?
Lasalocid
Selenium
Copper
Monensin
Salinomycin
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.
The two tracings show a horse (top) and a cow (lower) ECG with irregular QT intervals and absence of P waves. What cardiac disorder is this indicative of?
Atrial Fibrillation
Ventricular tachycardia
Ventricular fibrillation
Myocarditis
Pericarditis
Answer: Atrial Fibrillation
Explanation
These changes are typical of atrial fibrillation. Note that the horse tracing (top) also shows fibrillation waves.
Consumption of an ionophore in a horse classically results in
Nephrotoxicity
Gastrointestinal ulceration
Myocardial toxicity
Myelosuppression
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.
A 6 year old Saddlebred is presented for lethargy, anorexia and fever. Upon physical exam, you determine that the heart rate is approximately 90 beats/min. You quickly perform an ECG using the base-apex lead (see top image). What is the arrhythmia that you observe on the ECG (also consider what medication you would use to treat this arrhythmia)? (The bottom ECG strip is a normal rhythm for reference.)
Ventricular bigeminy
Ventricular fibrillation
Atrial fibrillation
Ventricular tachycardia
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.
During a routine pre-purchase exam of a 24 year old Peruvian Paso, a harsh and decrescendo holodiastolic 3/6 murmur is auscultated with a point of maximum intensity at the left base of the heart. There were no other abnormal physical exam findings. What is the most likely diagnosis based on clinical exam and prognosis of this horse?
This horse most likely has pulmonic stenosis due to turbulent flow resulting in severe stenosis, which will limit the ability to perform
This horse most likely has aortic regurgitation due to degeneration of the aortic valve and should have no impact on performance
This horse most likely has pulmonic regurgitation due to degeneration of the pulmonic valve and should have no impact on performance
This horse most likely has aortic stenosis due to turbulent flow resulting in severe stenosis, which will limit the ability to perform
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.
Horses are predisposed to developing enteroliths in California. What food item is considered to be playing a role in the formation of enteroliths?
- Grass hay
- Sweet feed
- Alfalfa hay
- Oat hay
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.
A horse presents to you in respiratory distress. You perform blood gas analysis and get the following results: PaCO2-60 mmHg, Pa02-75 mmHg, pH 7.255, Base excess= -1.8. How would you describe this horse’s status?
- Hyperventilation, respiratory acidosis
- Hypoventilation, respiratory alkalosis
- Hypoventilation, respiratory acidosis.
- Hyperventilation, respiratory alkalosis
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.
You are presented with a 4-year old Thoroughbred gelding for lethargy and weight loss. Hematology reveals a hematocrit of 16% (28-42%); in order to identify if this is a regenerative anemia, what would you further examine?
- Reticulocyte Count
- Mean corpuscular volume (MCV) and mean corpuscular hemoglobin concentration (MCHC)
- Bone Marrow Aspirate
- Concentration of indirect bilirubin
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.
A 3-year-old Standardbred gelding presents with epiphora, blepharospasm, and severe pain of the right eye (see image). There are numerous treatment options. Which medication would be contraindicated for this case?
- Tropicamide
- Tobramycin
- Serum
- Banamine
- Neomycin and polymyxin B and dexamethasone (Neo-Poly-Dex)
- EDTA
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.
You are presented with an 8-month old Quarter horse filly with a chronic history of urinary incontinence. The image provides one of the findings on physical examination. The remainder of the physical exam, along with a CBC and chemistry profile, is normal. What is the most likely cause of these signs in this filly?
- Equine herpes virus myeloencephalopathy
- Equine protozoal myelitis (EPM)
- Severe urinary tract infection
- Ectopic ureter
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.
A horse presents to you with a laceration across the caudal aspect of the hock; the horse is not weight-bearing, and the hock completely dropped to the ground. What structure has likely been ruptured to cause these clinical signs?
- Achilles tendon
- Suspensory ligament
- Gastrocnemius
- Superficial digital flexor
- Proximal check ligament
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.
In addition to a routine pre-purchase exam of a 12 year old Thoroughbred mare, an ECG was performed which showed an increase in the P-R interval followed by occasional P waves that are not followed by a QRS-T complex. What does the owner need to know about this finding?
- This is a second-degree atrioventricular block, which is commonly seen in athletic horses.
- This horse is predisposed to developing an electrical-mechanical disassociation and needs further diagnostics before purchasing
- This is a first-degree atrioventricular block and should be treated immediately with quinidine.
- This mare most likely has a ventricular septal defect and should not be purchased.
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
Horses that are used to pull carriages in tourist destinations, so-called “carriage horses”, commonly experience leg and hoof issues that impact their long-term welfare. These issues stem from:
- Excessive time spent on very hard surfaces such as concrete
- Lack of insufficient nutrients to support bone health
- Injuries caused by neglect
- Inappropriate training
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.
A 4 month old male Arabian presents with a one-week history of ataxia, hypometria, conscious proprioceptive deficits, and generalized weakness. On physical exam, there is no muscle atrophy or cranial nerve deficits and normal mentation. Additionally, the temperature is 100.2F (37.9 C). Which of the following is not a likely differential based on the clinical signs?
- Equine degenerative myeloencephalopathy
- Cerebellar abiotrophy
- Cervical vertebral stenotic myelopathy
- Occipito-atlanto-axial malformation (OAAM)
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).
If a horse is in seasonal anestrus, which of these is the most effective means of hastening the start of the breeding season?
- Provide artificial light for 12 hours per day 30
days prior to the start of breeding - Provide artificial light for 12 hours per day 60
days prior to the start of breeding - Provide artificial light for 16 hours per day 30
days prior to the start of breeding - Provide artificial light for 16 hours per day 60 days prior to the start of breeding
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
In the Spring of 2001, a syndrome later termed Mare Reproductive Loss Syndrome, MRLS, occurred in central Kentucky. This syndrome was characterized by early and late-term fetal loss, fibrinous pericarditis, neonatal foal death and unilateral uveitis. Which of the following was incriminated as a likely potential cause of MRLS?
- Exposure or ingestion of red maple leaves
- Exposure or ingestion of eastern tent caterpillars
- Exposure or ingestion of Japanese yew
- Exposure or ingestion of blister beetles
- Exposure or ingestion of black walnut
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.
If a patient exhibits a head tilt to the right, circling to the right, and has normal strength, what type of lesion does it have
- Left side - central vestibular dysfunction
- Right side - central vestibular dysfunction
- Left side - peripheral vestibular dysfunction
- Right side - peripheral vestibular dysfunction C
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.
During a routine physical exam of a 15 day old female Arabian foal, a holosystolic murmur can be clearly heard. The murmur is graded as being 4/6. This murmur is heard bilaterally, and the point of maximum intensity is on the right side. What is the most likely diagnosis?
- Tetralogy of Fallot
- Patent ductus arteriosus
- Ventricular septal defect
- Bacterial endocarditis
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.
Which of the following would not be seen on a navicular bone radiograph in a horse with navicular syndrome?
- Bone remodeling
- Osteolysis
- Enlarged vascular channels
- Osteophyte formation
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.
A 12-year old mare presents for infertility and abnormal sexual behavior. On rectal palpation, you feel a large multicystic ovary and the other ovary feels very small. What is the most likely diagnosis?
- Granulosa-thecal cell tumor
- Cystic ovarian follicles
- Ovaritis
- Ovarian hematoma
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
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
- 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.
This 5 year old Standardbred mare in the picture presents for lameness in the right hind limb. There is a jerking motion as she moves the leg forward. On physical exam, you are able to extend the hock and flex the stifle simultaneously. What is your diagnosis?
- Achilles tendon rupture
- Bog spavin
- Stringhalt
- Gastrocnemius rupture
- Peroneus tertius rupture
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]
An 8-year old Clydesdale gelding presented to you for a 7 day history of pruritus of the distal limbs, particularly the feathered areas of the leg (see image). Upon further examination, you observe irritation, scabbing, and alopecia of the fetlock region likely due to self-induced trauma secondary to pruritus. The horse is restless and bites at the distal limbs frequently. What is the most likely diagnostic test to lend a diagnosis in this case?
- Intradermal skin testing to detect insect hypersensitivity
- Elimination diet to detect food allergy
- Skin scraping and microscopic examination of affected areas to detect Chorioptes
- Skin punch biopsy to detect pemphigus foliaceus
- Intradermal skin testing to detect Onchocerca hypersensitivity
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.
You are examining a 5-year old pony for lethargy, anorexia, and mild intermittent colic. Upon physical examination, you notice the abnormal finding in the image. Consumption of which of the following can produce these clinical signs and physical examination findings?
- Red maple leaves (Acer rubrum)
- Black walnut (Juglans nigra)
- Yellow star thistle (Centaurea solstitialis)
- Oak leaves and acorns (Quercus sp)
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.
A 6 year old Saddlebred is presented for lethargy, anorexia and fever. Upon physical exam, you determine that the heart rate is approximately 90 beats/min. You quickly perform an ECG using the base-apex lead (see top image). What is the arrhythmia that you observe on the ECG (also consider what medication you would use to treat this arrhythmia)? (The bottom ECG strip is a normal rhythm for reference.)
- Ventricular bigeminy
- Ventricular tachycardia
- Atrial fibrillation
- Ventricular fibrillation
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 radiograph illustrates an equine neurologic disorder. The neck is flexed to demonstrate a narrowing of the intervertebral canal at the junction of C5 and C6. What is this condition?
- Canary grass staggers
- Equine degenerative myeloencephalopathy
- Cervical vertebral stenotic myelopathy
- Ankylosing spondylitis
- Shaker foal syndrome
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
With the given microscopic image (see image), identify all of the structures.
- Rouleaux, neutrophil, platelets
- Rouleaux, lymphocyte, platelets
- Agglutinated red blood cells, basophil, stained debris (artifact)
- Agglutinated red blood cells, platelets, neutrophil
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.
You examine an 8-year old pleasure horse because the owner has noted weight loss, poor appetite and a loss of energy over the last few weeks, and today saw dark urine. The horse’s temperature is 101F (38.3 C), HR is 56, and RR is 40. You catch a stream of urine from the mare and it is dark red (see photo). The sclera is slightly yellow. You submit blood to the lab for a CBC and chemistry panel and find that SDH, GGT, ALP, AST, total bilirubin, direct and indirect bilirubin are all markedly elevated, and the PCV is 23%. What do you tell the owner the mare has?
- Immune mediated thrombocytopenia
- Equine infectious anemia
- Tyzzer’s disease
- West Nile virus
- Hepatic failure with secondary hemolysis
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
The image shows a 2 month old Thoroughbred foal with a limb abnormality. What is the name of this abnormality?
- Subchondral bone cyst
- Carpus varus
- Osteoarthritis
- Carpus vagus
- Septic arthritis
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.
You are doing a summer externship in South America and performing physical exams on a variety of animals. You are performing a fundic exam on the eye of a horse and note what appears to be a worm migrating through the conjunctiva (see image). Because of the location and appearance of this parasite, you suspect this is which of the following?
- Oxyuris
- Toxocara
- Dirofilaria
- Thelazia
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.
You suspect disseminated intravascular coagulation (DIC) in a 16-year old Arab mare presented for colic and epistaxis (see image). Which of the following parameters is NOT associated with a diagnosis of DIC?
- Elevation in D-dimers
- Decreased antithrombin Ill activity
- Abbreviated (shortened) activated partial thromboplastin time (aPTT)
- Thrombocytopenia
- Prolongation of Prothrombin Time (PT)
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.
You are called one day in August to examine a 7 year old mare that is kept pastured in a weedy field in California. She is thin and dull, has a normal TPR, and is neither pregnant nor lactating. In an effort to assess her appetite, you hold out some oats and she tries to eat them but cannot; her lips are pulled back and her tongue seems to tremor as she attempts to eat (see image). You believe this is some type of neurologic dystonia. What diagnosis should be strongly considered here?
- Protozoal myeloencephalitis
- Rabies
- Yellow star thistle toxicity
- Brain abscess
- Lead poisoning
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.
You examine a horse for lameness and find that the 8-year old gelding is lame on both forelimbs. The stride is short and choppy, and the horse is reluctant to move. There is an increased digital pulse in both forelimbs, and the horse is sensitive to tapping on the hoof wall. At rest he leans back and puts more weight on his rear limbs. The horse appears improved and moves much better following a nerve block of the foot using local anesthesia. You take radiographs (see image). What is the diagnosis?
- Fracture of the third phalanx
- Coffin joint sepsis
- Laminitis with rotation of the third phalanx
- Navicular disease
- Sole abscesses
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
An 8-year old Thoroughbred horse presents to you for evaluation of skin lesions. On exam, you see the lesions shown in the photo. Which of the following toxins is most likely responsible for these lesions?
- Blue-green alga
- Cantharidin
- St. John’s wort
- Slaframine
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.
A 15-year old Quarter Horse gelding is presented for a chronic history of right forelimb lameness. Upon examination of the radiograph (see image), what is the most distal diagnostic nerve block necessary to desensitize the source of lameness?
- Palmar Digital Nerve Block
- Subcarpal Nerve Block (high four point)
- Palmar Metacarpal Nerve Block (low four point)
Abaxial Sesamoid Nerve Block
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
You are examining a 3-day old neonatal foal for suspected sepsis. Upon review of a blood smear, you notice the blue aggregates in many of the neutrophils (see image). What are these called and what do they suggest?
- Neutrophil hypersegmentation suggestive of bacterial phagocytosis
- Dohle Bodies indicating toxic change to the neutrophil
- Weible-Palade bodies suggestive of systemic inflammation
- Barr Bodies suggestive of endotoxemia
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
An 8 year-old, 1223 lb, Quarter Horse gelding is presented to you with a 4-day history of lethargy, inappetance, intermittent fever (ranging from 101.2-104.5F, 38.4-40.3 C), and peripheral limb edema. Upon physical examination, you note the following abnormalities: lethargy, tachycardia (60 beats/min), limb edema and fever (103.2F, 39.6 C).
The serum biochemistry analysis is within relatively normal reference intervals but the CBC yields the following abnormalities:
WBC: 1.50 x 10,000/mcL (reference 5.0-11 x 10,000/mcL)
HCT: 32% (reference 34-45%)
Platelet: 71 × 10,000/mcL (reference 130-300 × 10,000/mcL)
Neutrophil: 1.20 x 10,000/mcL (reference 2.2-6.5 × 10,000/mcL)
Lymphocyte: 0.23 x 10,000/mcL (reference 1.3-4.5 x 10,000/mcL)
Fibrinogen: 500 mg/dL (reference 100-400 mg/dL)
In addition, the following was observed on microscopic examination of the blood smear (see image). The most likely diagnosis, based on the history, clinical findings, and CBC results in this case, is which of the following?
- Anaplasma phagocytophilum infection
- Endotoxemia/septicemia (toxic changes within cell)
- Streptococcus equi infection
- Heinz body anemia
- Equine infectious anemia (EIA) infection
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.
You are examining a 7 year old Thoroughbred gelding for severe bilateral epistaxis. After the epistaxis has decreased, endoscopy of the pharynx reveals blood from the left guttural pouch opening (see image). What is the most appropriate treatment for hemorrhage from guttural pouch mycosis?
- Lavage guttural pouch with antifungals
- Surgical occlusion of involved arteries (i.e. internal or external carotid artery) under general anesthesia
- Pass endoscope into affected guttural pouch and cauterize involved vasculature
- Tie off the left common carotid artery
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.
You are examining a 7 year old Thoroughbred gelding for severe bilateral epistaxis. After the epistaxis has decreased, endoscopy of the pharynx reveals blood from the left guttural pouch opening (see image). What is the most appropriate treatment for hemorrhage from guttural pouch mycosis?
- Lavage guttural pouch with antifungals
- Surgical occlusion of involved arteries (i.e. internal or external carotid artery) under general anesthesia
- Pass endoscope into affected guttural pouch and cauterize involved vasculature
- Tie off the left common carotid artery
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.
A 5-year old brood mare presents with a history of intermittent hind limb lameness. The onset of the lameness has been gradual. The mare is an active cutting horse. With your initial hands-off examination, you compare the structural integrity of both hocks (see image). Without using any further diagnostics, what disease process and corresponding anatomical structures do you suspect is causing the lameness?
- Bog Spavin: osteoarthritis of the distal intertarsal joint and/or tarsometatarsal joint
- Bone Spavin: osteoarthritis of the distal intertarsal joint and/or tarsometatarsal joint
- Bone Spavin: synovial distention of the tarsocrural joint
- Bog Spavin: synovial distention of the tarsocrural joint
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.
A 6-year old Quarter Horse presents with the lesion seen in the photograph. Which of the following is true regarding equine sarcoids?
- Metastasis is common with advanced lesions
- Surgical excision is nearly always curative
- Papillomavirus is believed to play a role in the pathogenesis.
- They usually regress spontaneously without treatment
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.
You are treating a colicky 8-year old horse and pass a stomach tube to assess gastric reflux. The 20 liters of reflux is hemorrhagic, orange-brown in color, and foul-smelling. On physical exam, you find T=101.5F (38.6 C), HR=70, and RR=35 and overall depressed attitude. There are few auscultable gut sounds. Oral mucous membranes are injected. On rectal exam, there are multiple dilated fluid-filled loops of bowel palpated. Peritoneal fluid is serosanguinous with a 3.5 gm/dl protein and a WBC count of 7000. After decompressing the stomach, the horse appears less painful, but remains depressed. Based on these findings, what is the best tentative diagnosis?
- Verminous arteritis caused by strongylus vulgaris
- Large bowel torsion
- Duodenitis-proximal jejunitis
- Acute small intestinal obstruction
- Impaction colic (large bowel impaction)
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
A 36 hour foal born from a multiparous mare presents for weakness, decreased appetite, and tachycardia. On physical exam, you examine the sclera as seen in the photo. Based on the signalment and findings, what is a likely cause?
- Failure of passive transfer
- Congenital iron toxicity
- Neonatal Isoerythrolysis
- Immune mediated thrombocytopenia
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.
