Horses Flashcards
what does urine scalding (+incontinence) indicate?
ectopic ureter
90% cases are fillys (young)
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?
Red maple intoxication Castor bean intoxication Black walnut intoxication Sweet pea intoxication Senecio or groundsel intoxication
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.
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
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.
duration mare estrus? 1d 12h 20d 6d 14d
6 days
Many times, horses require additional muscle relaxation during anesthesia. Which of the following is commonly used for its property of being a centrally acting muscle relaxant?
Guaifenesin
Ketamine
Atracurium
Succinylcholine
The correct answer is guaifenesin. Unfortunately, the exact mechanism is unknown; however, we do know that guaifenesin acts centrally by blocking nerve impulse transmission at the internuncial neuron level in the subcortical brain, brain stem, and spinal cord. Veterinarians should be careful not to give too much guaifenesin because early signs of toxicity are in the form of increased rigidity. So what does the vet do? Give more guaifenesin, causing respiratory and cardiac arrest. Ketamine is a dissociative agent and is known for its ability to cause hypertonia. Atracurium is a non-depolarizing neuromuscular blocking agent that acts by competitively binding to cholinergic receptors at the motor endplate. Succinylcholine is a depolarizing neuromuscular blocking agent.
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?
a. Exposure or ingestion of red maple leaves
b. Exposure or ingestion of Japanese yew
c. Exposure or ingestion of black walnut
d. Exposure or ingestion of blister beetles
e. Exposure or ingestion of eastern tent caterpillars
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.
Most equine uroliths are composed of which of the following substances?
Magnesium ammonium phosphate Calcium oxalate Calcium carbonate Cysteine Phosphate
The correct answer is calcium carbonate. Equine urine contains high amounts of calcium carbonate. Magnesium ammonium phosphate (aka struvite crystals) is also occasionally noted in horse urine.
You are examining a 2-year old pony with lameness that worsens after activity or work. The pony displays mild lameness on your exam and is sensitive to deep palpation of the third metacarpal bone of the left front limb. Radiographs reveal periostitis and new bone formation along the second metacarpal bone. No fracture is present. What term describes this condition?
Splints Thoroughpin Osselets High ringbone Sidebone
This is a description of splints or metacarpal exostosis which involves periostitis of the interosseous ligament between the third and second metacarpal (or metatarsal) bone. Treatment usually involves rest and anti-inflammatory medications, although if the bony exostoses impinge on the suspensory ligament, surgical removal of the proliferative tissue may be indicated.
Sidebone refers to ossification of the alar cartilage of the coffin bone. High ringbone refers to osteoarthritis of the proximal
interphalangeal (pastern) joint. Osselets are inflammation of the periosteum on the dorsal distal epiphyseal surface of the third metacarpal bone and fetlock joint. Thoroughpin is the term for effusion of the tarsal sheath (sheath of the deep digital flexor).
Horses are predisposed to developing enteroliths in California. What food item is considered to be playing a role in the formation of enteroliths?
Sweet feed
Alfalfa hay
Grass hay
Oat hay
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.
What is the most common cause of colic in a newborn foal?
Salmonella Meconium impaction Correct Answer Strongylus vulgaris Parascaris equorum Nephrosplenic entrapment
The correct answer is meconium impaction. Meconium impaction occurs in the rectum or small colon. Clinical signs include straining, swishing of the tail, and restlessness. Rectal examination reveals numerous hard fecal balls. Treatment consists of an enema with water and a mild soap. Meconium is the first intestinal discharges of the newborn foal, consisting of epithelial cells, mucus, and bile.
A 12-year old mare presents for a sudden onset of ptyalism and an inability to prehend food. Where is the lesion?
a. Corpus callosum and amygdala
b. Substantia nigra and globus pallidus
c. Caudal cerebellar peduncle and medial longitudinal fasciculus
d. Lateral lemniscus and rostral olivary nucleus
b. The correct answer is substantia nigra and globus pallidus. A lesion to these basal ganglia will result in movement disorders. Particularly, yellow star thistle poisoning will lead to an inability to prehend food in horses. The corpus callosum connects the two cerebral hemispheres together, and the amygdala is involved with fear and memory. The caudal cerebellar peduncle connects the medulla to the cerebellum and is involved in transmission of signals pertaining to movement. The medial longitudinal fasciculus is involved in conjugate gaze. The rostral olivary nucleus and lateral lemniscus are both involved in auditory pathways.
The 3-year old stallion in the photo was recently treated by you for Strangles. He is now in isolation and the owner would like to know when he can safely reintroduce the horse to his stable. Which of the following should you tell the owner?
a. It is best to wait for 30 days after resolution of signs and then perform 3 consecutive weekly negative nasopharyngeal cultures
b. It is never safe to reintroduce the horse because most horses become lifelong carriers and shed the organism
c. He should vaccinate all of the horses at his stable and then reintroduce the horse 3 weeks later
d. It is best to wait until the horse has negative serology to antibodies against the SeM virulence factor
e. Fortunately, Strangles is not contagious to other horses
a. Strangles can be a difficult disease to control and vigilant preventative measures are necessary to minimize transmission as a small percentage of horses develop persistent infection of the guttural pouches associated with purulent inflammation or the presence of chondroids. These carriers can be detected either by culture or by detection of S. equi DNA using the polymerase chain reaction (PCR) test. PCR is a more sensitive test but also more expensive and may have false positives in recently infected horses due to residual DNA from dead bacteria.
Investigation of carriers should be done either before a new animal is introduced into a stable or herd, or at least 30 days following recovery of a horse from strangles. Animals should be isolated until there have been 3 consecutive weekly negative cultures and/or PCR reactions.
If an animal is positive, endoscopic evaluation of the guttural pouch is recommended, chondroids removed, and guttural pouches treated by flushing and infusing 5 million units of penicillin G in 3% gelatin. In addition, these horses should be treated with penicillin G intramuscularly for 7 days, isolated for 30 days, and then retested with the 3 consecutive series of nasopharyngeal swabs and culture.
You should note that even this diligent recommendation is not 100% fail-safe. However, this is still the best answer choice. It is not true that most horses become lifelong carriers as this applies to <10% of horses. Waiting 90 days after resolution without testing or retreating is not recommended.
Vaccines against S. equi are available; there are intramuscular and intranasal vaccines available. The intramuscular vaccine is associated with pain and abcessation at the vaccine site as well as purpura hemorrhagica. The killed vaccine does not provide complete protection but it does reduce the severity of clinical illness. A live, attenuated S. equi vaccine has been introduced as an intranasal vaccine for the prevention of strangles. It is strongly recommended that other vaccines or injections not be administered at the same time as the intranasal vaccine. Since the live organism may persist in the nose, control measures that involve detection of carriers may not be effective in horses immunized with this vaccine.
Serology is best for determining the exposure status of a horse and is mainly used to aid in the diagnosis of purpura hemorrhagica and bastard strangles.
Guttural pouch infections in the horse may result in pharyngeal paresis and food may reflux from the nose because:
a. The epiglottis does not close normally against the rima glottidis.
b. The soft palate no longer seals normally against the roof of the nasopharynx.
c. The upper esophageal sphincter remains open.
d. The tongue fails to engage the hard palate.
e. The arytenoid cartilages fail to seal the glottis.
b. In normal swallowing, the soft palate moves dorsally to contact the roof of the nasopharynx and occlude the nasal passages such that food cannot reflux. This reflex is lost when cranial nerves 9 through 12 are inflamed or damaged in the guttural pouch due to infection. Mycotic infection is most frequently the cause.
All of the other answers except for the choice about the upper esophageal sphincter are also things that happen with pharyngeal paresis, but they are not responsible for feed refluxing from the nose. The epiglottis and arytenoids abnormalities result in coughing and aspiration of food into the larynx. Tongue problems result in food being dropped from the mouth during chewing and/or difficulty moving the food bolus to the pharynx for swallowing. If the upper esophageal sphincter remains open, there would be few clinical signs; that alone would not result in food refluxing from the nose.
A 3 month old Arabian foal presents for a progressive onset of intention head tremors, ataxia, dysmetria, and spasticity. On physical exam, the foal is noted to have proper mentation and is not weak. Heart rate, respiratory rate, and temperature are within normal limits. Given the signalment and presentation, what is the most likely diagnosis?
Inner ear disease
Cerebellar abiotrophy
Sarcocystis neurona
Cerebellar dysplasia
b. The correct answer is cerebellar abiotrophy. Cerebellar abiotrophy is usually observed in foals which are less than one year of age, particularly 1-6 months of age. Cerebellar abiotrophy is the most common cerebellar disease found in horses. It is mostly seen in Arabian, Oldenburg, and Gotland breeds. There is no treatment, and signs may be progressive. Diagnosis is based on a good history and clinical signs such as intention tremors, lack of a menace, hypermetria, and ataxia.
Which of these conditions is associated with excess dietary calcium and vitamin D in young horses?
Osteochondrosis
Nutritional secondary hyperparathyroidism
Goiter
Rickets
The correct answer is osteochondrosis. Rickets and nutritional secondary hyperparathyroidism are caused by calcium deficiency or excess phosphorus. Goiter is caused by insufficient or excess iodine.
causes of dysphagia in horses
tetanus
guttaral pouch mycosis
rabies
what does auriculopalpebral block?
motor innervation to orbicularis oculi
horse cant prehend, lips pulled back, tongue tremors
yellow star thistle
normal finding in (race)horses with bradycardia as result of high vagal tone
1st or 2nd degree AV block
PPID
pituitary adenoma
horses >15yrs
plasma ACTH high (or TRH stim)
tx: pergolide(suppresses pituitary secretion)
(*hirsutism, PU/PD, laminitis, lethargy, sweating/lactation, loss of muscle, infertility, infection -tooth root abscess)
Equine infectious anemia
- test with coggins - IMMUNODIFFUSION
- immunodeficiency virus transmitted by bloodsucking flies and contaminated instruments
Where do they lay eggs?
- horse bot
- flea
- pinworm
- stomach worm
- horse bot - ANYWHERE, gasterophilus usually have yellow eggs CANNON BONE
- flea - not in horses
- pinworm- PERINEUM
- stomach worm (habronema) eggs in feces
Which of these viruses are normally found in the upper respiratory tract of the horse?
Equine viral arteritis virus
Equine influenza
Equine adenovirus
Equine herpesvirus
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 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?
Application of horse shoes
Prednisone
Phenoxybenzamine
Trimethoprim sulfa
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 2-year old Arabian gelding presents for acute cutaneous lesions and restlessness after coming in from the pasture. The cutaneous lesions are elevated, flat-topped, and range in size from 2cm to 8cm in diameter. The lesions are scattered multifocally all over the horse. What is the most appropriate treatment at this time?
Cephalexin
Parenteral dexamethasone
Oral diphenhydramine
Procaine penicillin
The correct answer is parenteral dexamethasone. The horse is suffering from urticaria or hives. Urticaria in horses is commonly caused by an allergic reaction. Toxins, plants, insect bites, medications, chemicals, heat, sunlight, stress, and genetic abnormalities are just a few of the factors that can cause an outbreak of urticaria. The lesions are caused by localized edema in the dermis. Treatment for an allergic reaction with urticaria includes parenteral fast-acting steroids such as dexamethasone. Diphenhydramine can be given as well, but oral administration is slower acting and the efficacy is much less (if at all) when compared to steroids. There is no indication for antibiotics.
Carpal fractures in horses occur most commonly in which carpal bones?
3rd and 4th carpal bones
Ulnar and accessory carpal bones
Accessory, 2nd and 3rd carpal bones
Radial and 3rd carpal bones
The correct answer is radial and 3rd carpal bones. Most carpal fractures in horses occur at the dorsal aspect of the carpal joint, particularly at the radial and 3rd carpal bones. Both chip and slab fractures may occur. These fractures usually result in immediate swelling and severe lameness. Diagnosis is based on radiographs and arthroscopic surgical repair is frequently the treatment of choice.
Which of these tests is used to diagnose a Corynebacterium pseudotuberculosis infection with internal abscesses in horses?
KOH test
Coggin’s test
Zinc sulfate turbidity test
Synergistic hemolysis inhibition test
The correct answer is hemaglutination inhibition test. Other clinicopathologic data that would support an internal abscess would include leukocytosis, hyperfibrinogenemia and hyperglobulinemia. A KOH test is to look for dermatophytes. The zinc sulfate turbidity test is for failure of passive transfer. The Coggin’s test is for equine infectious anemia. Remember, goats get C. pseudotuberculosis as well.
Which of these drugs should be used with great caution in stallions due to the risk of causing paraphimosis or priapism?
Ketamine
Atropine
Trimethoprim-sulfa
Acepromazine
The correct answer is acepromazine. Phenothiazine tranquilizers can cause relaxation of smooth muscles and engorgement of the corpus cavernosum with blood, leading to an inability to withdraw the penis into the sheath or paraphimosis. While this drug side effect is very rare, veterinarians should be cautious in the use of acepromazine in stallions and should consider another sedative such as xylazine or detomidine when sedation is necessary.
What is the treatment of choice for a carpal hygroma in a horse?
Local injection of corticosteroids Surgical exploration and drain placement Carpal arthrodesis Systemic antibiotics Aspiration of fluid from the hygroma
The correct answer is surgical exploration and drain placement. A hygroma is a fluid filled swelling at the carpus, usually seen from repeated trauma leading to local bursitis. Horses are usually not lame from this condition but have restricted range of motion of the joint. Simply aspirating the fluid and/or injecting corticosteroids is rarely effective and the swelling usually recurs. Surgical excision of the bursal lining may be indicated when recurrence is a problem.
Which of the drugs below is used to treat horses with atrial fibrillation?
Lidocaine Furosemide Quinidine Atenolol Atropine
Oral quinidine can be used for therapy. It is a class IA sodium channel blocker that has vagolytic properties which prolong the refractory period of the myocardium. This is not a perfect solution, as it does not work in all cases and can be associated with side effects including oral ulcers, hypotension, and allergic reactions. For these reasons, other treatments such as electrical cardioversion and alternative drugs such as flecainide are sometimes tried. When evaluating an ECG strip for atrial fibrillation, look for irregular R-R intervals and the classic fibrillation wave of the base line.
Lidocaine is a sodium channel blocker used primarily for ventricular arrhythmias. Furosemide is a loop diuretic used to treat congestive heart failure rather than a rhythm abnormality. Atropine is an anticholinergic used primarily for supraventricular bradyarrhythmias.
You are examining a well-muscled 3-year old Quarter Horse stallion for muscle stiffness, difficulty walking, and prolapse of the third eyelid, followed by recumbency. The trainer informed you that the stallion has demonstrated similar clinical signs of lesser severity in the past. Based on this information, you suspect inherited disorder. What is the most appropriate therapy for this acute episode?
Intravenous administration of 0.9% sodium chloride (NaCl) and 5% dextrose
Intravenous administration of 0.9% potassium chloride and 50% dextrose
Intravenous administration of spironolactone (diuretic)
Intravenous administration of lactated ringer’s solution (LRS) and enalapril
The hereditary disease you should suspect is hyperkalemic periodic paralysis. In acute episodes of HYPP, the clinician should try and drive down the serum potassium. This can be accomplished by administering potassium-free IV fluids (such as 0.9% NaCl) and medications (such as dextrose) to drive potassium into the cell. While LRS could be used when no other IV fluid is available, it does contain potassium. Additionally, enalapril is an ACE inhibitor used for hypertension. One would clearly want to avoid IV solutions that contain high concentrations of potassium (KCl) or are extremely hypertonic (50% dextrose). Finally, while furosemide may sometimes be used to induce diuresis in some cases of HYPP, spironolactone is a potassium-sparing diuretic that would not decrease the serum potassium concentration.
A horse owner in Louisiana calls you frantically concerned that he has heard reports of African Horse Sickness in adjacent states and he wants to know what he can do to protect his horses. Which of the following is the best recommendation for preventing transmission of this disease?
a. The owner should not travel to any of the states where the disease is present because the virus is transmitted by fomites and can survive for extended periods
b. Institute strict arthropod control measures because the disease is transmitted primarily by Ixodes ticks
c. Treat all horses with oxytetracycline because the etiologic agent is exquisitely sensitive to this antibiotic
d. Stable all horses in insect-proof housing, particularly at night because the disease is transmitted primarily by Culicoides flies
e. Separate all horses from each other and all other animals because horses are most commonly infected by direct contact with infected animals
African horse sickness (AHS) is a viral disease of equids that is transmitted by insects, primarily Culicoides.
African horse sickness is endemic in sub-Saharan Africa and outbreaks have periodically extended to the Middle East and southern Spain. The primary and biological vector is Culicoides but the virus may also be transmitted by mosquitoes. The virus has been isolated from certain ticks but arthropod transmission is not believed to play a significant role.
Clinical signs of AHS typically develop 5-7 days after infection and begin with fever and conjunctivitis. Some animals may recover but many go on to develop the pulmonary and/or cardiac forms of AHS. The pulmonary form consists of acute respiratory distress, coughing, sweating, and foaming from the nostrils; this form is usually fatal. The cardiac form consists of edema of the head and neck as well as abdominal pain and depression. A characteristic sign is swelling in the indentation above the eyes (also referred to as swelling of the supraorbital fossa). About 50% of animals with the cardiac form die from heart failure while the rest gradually recover after about one week.
Diagnosis can often be made based on history of exposure to endemic areas, clinical signs and lesions but must be confirmed by viral isolation and/or serology. There is no effective treatment and prevention/control can be accomplished by vector control and vaccination. There are multiple serotypes of virus and animals immunized against certain serotypes are still susceptible to others. In an outbreak situation, affected horses should be removed/euthanized and remaining horses should be vaccinated with a polyvalent vaccine until the specific serotype can be determined and then animals should be revaccinated with the corresponding vaccine.
For importing equids from Africa, a 2 month quarantine is required and then horses must test free of virus. Presence of antibodies does not disqualify a horse from importation. Because of the vector-borne nature of the disease, it is recommended that planes flying from endemic areas be sprayed with insecticides on arrival to disease-free countries.
Consumption of yellow star thistle results in this lesion.
Destruction of the pons
Nigropallidal encephalomalacia
Leukoencephalomalacia of the reticular system
Destruction of the lateral and medial geniculate nucleus
The correct answer is nigropallidal encephalomalacia. Consumption of yellow star thistle destroys the globus pallidus and the substantia nigra. These lesions will result in a characteristic dysphagia.
Which of the following would not be seen on a navicular bone radiograph in a horse with navicular syndrome?
Enlarged vascular channels
Osteophyte formation
Osteolysis
Bone remodeling
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.
In the Spring of 2001, a syndrome later termed Mare Reproductive Loss Syndrome, also known as MRLS, occurred in central Kentucky. This resulted in the abortion of 20-30% pregnant mares. Which of the following was NOT a manifestation of MRLS?
Neonatal foal deaths Fetal or neonatal hemoabdomen Late-term abortion Early fetal loss Fibrinous pericarditis
The correct answer is fetal or neonatal hemoabdomen. All other choices listed were potential disease manifestations of MRLS. 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, via NG tube, eastern tent caterpillars resulted in early and late fetal loss.
RBC changes in anemic horses?
The correct answer is normocytic, normochromic anemia. In the horse, it is very uncommon to see morphologic changes to red blood cells, even if there is a strong regenerative response. Therefore, most types of anemia in the horse will be normocytic, normochromic.
A 4-year old Standardbred stallion presents to you in the afternoon with a recent onset of lameness. The owner reports that in the early morning, feed was delivered and the horse apparently got into a bag of grain. On exam, you note heat over the hoof wall and coronary band in the front feet and a very strong digital pulse. The horse is tremoring and sweating. A hoof tester reveals pain over the sole at the toe and the horse is sensitive to tapping on the hoof wall. What treatment is most appropriate?
a. Administer intravenous fluids, penicillin, and gentamycin
b. Attempt to empty any grain out of the stomach via NG lavage of the stomach, administer NSAIDs and start IV fluids
c. Induce vomiting with xylazine and then administer activated charcoal by stomach tube
d. Administer neomycin and lactulose by stomach tube and cold pack the feet
e. Administer 1 gallon of saline by stomach tube and give an injection of dexamethasone
The clinical presentation is consistent with a case of acute laminitis secondary to grain overload. Acute laminitis is frequently associated with excessive ingestion of carbohydrates, grazing of lush pastures, and/or excessive exercise.
Acute laminitis more commonly affects the front feet but can affect all four. Local heat and pain are usually detected as well as bounding digital pulses. Pain may also manifest as tachycardia, muscle tremors, or sweating.
The goals of treatment are to prevent further development of laminitis, reduce pain, and reduce other complications from laminitis. Acute laminitis is considered a medical emergency and treatment should be initiated as soon as possible. When a horse is suspected of grain overload, administration of mineral oil by stomach tube acts as a laxative and decreases absorption of toxic material from the gastrointestinal tract. Other recommended treatments include intravenous fluids, parenteral antimicrobials, anti-inflammatory drugs (such as flunixin meglumine or phenylbutazone), and hyperimmune serum or plasma. It is also recommended to place the horse in a stall with soft flooring. Other treatment considerations include heparin, phenoxybenzamine, and heart-bar shoeing. There are some practitioners who recommend cold packs but there is conflicting evidence that hot packs may be more beneficial. Corticosteroids are contraindicated.
This 15-year old gelding in the picture presents for acute lameness of the right thoracic limb. Pain is elicited in the foot with hoof testers. After close examination, you notice a draining tract at the coronary band. Based on the most likely diagnosis, what is your best treatment option?
a. Surgical exploration
b. Adequate drainage and poultices
c. Systemic antibiotics
d. Corticosteroids
The most common cause of acute toe-touching, lameness in horses would be a foot abscess but other causes would include a fracture of one of the bones of the distal limb. Based on the fact that a draining tract is present, an abscess would be more likely and providing adequate drainage would be appropriate. Alternatively, if you still suspected a fracture, radiographs would be the next step to confirm this.
A windswept foal will have which combination of angular deformity?
Varus deformity of either both front or rear limbs
Valgus deformity of one front and one rear limb Your Answer
Valgus deformity of one front limb and varus deformity of one rear limb
Valgus deformity of either both front or both rear limbs
Valgus deformity of one limb and varus deformity of the contralateral limb
The correct answer is valgus deformity of one limb and varus deformity of the contralateral limb. Incomplete ossification is an important cause of this type of deformity and occurs most frequently in the carpus or tarsus. Congenital angular deformities are frequently attributable to intrauterine malpositioning and laxity of periarticular supporting structures.
Pregnant Mare showing signs of colic. anorexic, frequently attempting to urinate. On rectal, the broad ligament is pulled tight over the uterus from right to left.
diagnosis?
uterine torsion.
The correct answer is uterine torsion. These are the typical clinical signs seen in uterine torsions (colic and frequent urination in a late-term mare) and the key finding is the rectal palpation of the tight broad ligament coursing over the uterus. Speculum exam is not diagnostic in horses because torsions typically do not involve the cervix as they do in cows. Medical treatment may be attempted by placing the mare under short-acting anesthesia and rolling her (plank-in-the-flank), or surgical correction may be necessary.
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 regurgitation due to degeneration of the pulmonic valve and should have no impact on performance
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 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
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.
ossification of carpal bones in newborn foals?
partially ossified/incompletely ossified indicated premature parturition.
they will ossify with age but can collapse with foal’s weight pressing on soft cartilage -> misshapen bones and chronic lameness
which toxin acts as photosensitizer in horses
St. Johns wort
leads to photophobia, conjunctivitis, sloughed skin, icterus
Ear plaques, coalescing depigmentation, hyperkeratotic on concave surface bilaterally.
Cause?
vector?
tx?
papillomavirus
insect (black fly)
imiquimod cream (Aldara)
(just insect control won’t cause lesion regression)
Which of the following is true about the horse?
Enamel pillars are not held together by cementum
The maxilla is narrower than the mandible
The mandible is narrower than the maxilla
Teeth stop growing after twenty years of age
The correct answer is the mandible is narrower than the maxilla. All other answer choices are not true. Teeth erupt throughout the entire life of the horse. Cementum does hold enamel pillars together, and the maxilla is wider than the mandible.
Is patent urachus normal in foals?
yes, for a few days.
if infected needs abx and possibly surgery.
A horse presents to you in respiratory distress. He has dilated pupils and bright red mucous membranes. You pull blood which is also bright red in color. What is your diagnosis?
Chronic obstructive pulmonary disease
Cyanide toxicity
Nitrate toxicity
Pleuropneumonia
The correct answer is cyanide toxicity. The bright red-colored blood and mucous membranes with signs of respiratory distress are typical findings for cyanide toxicity. There are many plants that can accumulate cyanide to levels that are toxic to horses. Treatment is with sodium nitrate or sodium thiosulfate IV.
A mare in the last month of gestation develops ventral edema from the udder to the xiphoid. She then becomes acutely painful and tachypneic and does not want to ambulate. What condition did the mare experience?
Vaginal cystocele
Colonic torsion
Uterine torsion
Ruptured prepubic tendon
The correct answer is ruptured prepubic tendon. This tendon courses along the ventrum and provides the major support for all the structures in the equine abdomen. It can rupture in late pregnancy, especially in obese draft mares. This is usually preceded by ventral swelling. If such swelling is noted, preventative measures should be taken such as restricting activity and possibly slinging the abdomen to provide support. This condition is very painful to the mare and may affect the ability to increase intra-abdominal pressure during parturition. Assisted parturition by a veterinarian should be strongly considered. A body wall hernia may also result in similar signs as a ruptured prepubic tendon.
Navicular Disease etiology? rads? CS? tx?
etiology unknown
rads - osteophyte, remodelling, enlarged vascualar channels
- affects navicular bone/sespensory/ddf tendon/nav bursa/other heel areas
CS:
- shortstrided, stilted gait in forelimbs, more painful on hard surface, hoof tester elicits pain on posterior third on both forefeet
- hoof appears normal except narrow heels
- palmar digital n block causes loss of sensitivity and improved gait
tx = shoe that elevates the heel
epistaxis ddf?
tx?
EIPH
ethmoid hematoma
guttural pouch mycosis
aminocaproic acid - only fibrinolytic med (binds plasminogen) to promote hemostasis
Upward fixation patella
vs. coxofemoral luxation
hind rigid extension, toe drag
vs. limb not extended
Gonitis Jack spavin Thorough pin Bone Spavin Bog Spavin Street Nail Navicular ds Stringhalt Osslets tenosynovitis seedy toe scratches buttress foot
GONITIS - stifle OA
JACK SPAVIN - cunean bursitis (bone growth medial hock)
THOROUGH PIN - effusion ddf (hock)
BONE SPAVIN - OA distal IT (hock)
BOG SPAVIN - Fluid in TT joint (No lameness)
STREET NAIL - Navicular bursitis or subsolar abscess
NAVICULAR DISEASE - cd heel pain, narrow heel, short stride
STRINGHALT - spasmotic hyperflexion
OSSLETS - inflam dorsal MC3, fetlock, bilateral , short choppy gait
TENOSYNOVITIS - bowed tendon, tear sdf from racing stress
SEEDY TOE - hollowing of hoof wall, secondary to laminitis
SCRATCHES - dermatitis of palmar/plantar pastern
BUTTRESS FOOT - pyramidal disease, thick coronet, strain on p3 and cde
club foot
flexural deformity of distal IP joint. ddf contracture
causes: rapid bone growth, excessive feed, lack of exercise
Sx: desmotomy of accesory of ddf
Sweeny
supra and infra-spinatous contraction
P3 fracture
stabalize with shoe bar and rest
if articular and chronic old horse prob needs internal fixation
OCD horse
DIRT (cr distal intermedial ridge tibia)
cause: Cu deficiency, excessive Zn, rapid growth, high E diet, articular trauma
tx: restrict exercise, dec feed, sx if advanced
equine nerve blocks
1) Palmar dig n. (palmar foot)
2) abaxial sesamoid n (pastern and foot)
3) Palmar MC OR low 4 pt (fetlock and foot)
4) Subcarpal n OR high 4 pt (MC -> foot)
HyPP
- quarter horses!!
- CS: Spasmotic Grin sporatic weakness and collapse, protrusion third eyelid, muscle fasiculations
- many triggers, onset is unpredictable - high K diet, fasting, anesthesia, sedation, stress are some
- Autosomal dominant - Impressive
- tx:
acute - NaCl, dextrose, CaGluconate, bicarb (drive K intracellular)
longterm - Acetazolamide
Pigment Nephropathy
- result of myositis/tying up
- myoglobin -> nephrosis
analasma /equine granulocytic ehrlichiosis
- Ixodes tick
- CS: icteric, petechia, undulating fever
- dx: inclusion bodies in neuts
- California
tx: Oxytet
Equine Infectious Anemia
blood borne flies
fever, petechia, dependent edema
- keep positive animals 200m from other equids/euthanize
- Coggins /AGID
Equine Viral Arteritis
fever, dependent edema, conjunctivitis, rhinitis
- endothelial swelling, neut infiltration -> edema, hemorrhage
- abortion(partly autolyzed)
- vaccine if at risk
Equine Metabolic Syndrome
- insulin dysregulation
- test: resting insulin
- CS: obesity, laminitis
tx: exercise, low carb low cal diet, thyroxine metformin
Equine Cushings
PPID
- Adenoma Pars intermedia
- DEC DOPAMINE, excess POML, excess cortisol
- CS: muscle wasting, recurrent infection, laminitis, SWEATING
tx: peroglide (dopamine agonist)
Tyzzers Disease
clostridium piliforme
6d-6w old
Sudden death! (dead foal disease)
inc liver enzymes, dec. glucose, acidosis
Transient hypogamma globulinemia
delayed Ig production for up to 3 months
CS: recurrent bacterial/viral infection (usually respiratory)
Theilers
ADULT horses
widespread hepatic necrosis
idiopathic IIAHD) but may have etiologies including tetanus antitoxin, flavivirus
hepatic failure (anorexia, hepatic encephalopathy, and icterus)
Shaker foal syndrome
C. botulinum, progressive motor paralysis, tremors
Equine Denerative Myelopathy
4m-3y
dec. Vit E or Idiopathic
ataxia, CP def
Lethal White syndrome
foals
aganglionosis of intestines (dec. motility, megacolon, colic, death)
OAAM
occipito atlanto-axial malformation
ataxia, weakness, CP def
Neonatal maladjustment syndrome
aka dummy foals
- peripartum asphyxia, wanderer
+/- premature placental separation
tx: abx,supportive 80% survive with tx
SCID
def in B&T lymphocytes
arabians
repeat infections after loss of maternal Ab
herpes virus in horses
abortion - foal has necrotic foci on liver,bronchiolitis
vaccinate mares 5,7 9m
no premonitory sings, but “snots” in younger horses 4-5m before abortion storms
Equine viral arteritis
abortion - fetus partially autolyzed, and Mare WILL show clinical signs
Equine Estrous, estrus, gestation lengths?
estrus = 5-7 days estrous= 21 days (19-26) gestation= 11m
Caslicks procedure
for pneumovagina…
Stages of equine labor
1- onset of contractions, ends with sac bursting, fluid (1-2hr)
2- expulsion fetus/active labor, 20-30 min
3- pass placenta, 1-3 hrs (retained >3h)
Aural plaques equine
- spread by black flies
- papillomavirus
tx: topical imiquimod cream, and insect control
Urticaria
allergy (toxin, plant, insect, chems, chemical, heat, sun, stress)
tx: parenteral steroid (dexmethasone) oral diphenhydramide is slower and less efficacious
Wobblers in horses
young, <5y
no CSF changes
SYMMETRIC ATAXIA, wide stance, CP def
Equine Herpes
hindlimb paralysis, dribbling urine, ataxia
yellow CSF
EPM
AAA - asymmetric atrophy(gluteal) and ataxia
sarcocystis neurona
tx: ponazuril
Equine Encephalitis arboviruses
- Progressive CNS signs, head tilt, ataxia. HYPERESTHESIA, propulsive walking
- mosquito!
VEE - high viremia
WEE - mononuclear pleocytosis
EEE - neutrophilic pleocytosis (75-90%mortality)
blind, head pressing, delerium?
moldy corn - fusarium
uncoordinated, twitching tremors, seizures
dec. thiamin (braken fern)
EDM
vit E deficiency foals 4m-3y
symmetric ataxia
Dandy walker syndrome
arabians
midline cerebellum
cauda equina syndrome
inflam nerve roots
LMN signs - paresis/paralysis
chewing tail, hypotonic anus, fecal retention, incontinence, hindlimb ataxia
West nile encephalitis
sep-oct
mosquito
fever, anorexia, SUDDEN ataxia, weakness, muscle fasciculations
polyneuritis equi
mature horses, hyperesthesia (like WEE) progressive paralysis of tail, rectum, bldder
Heaves
recurrent airway obstruction
Allergic ds in OLDER horses
DRY hay, STRAW bedding, mold, dust
dx: spirals of mucus (curshmanns spirals); atropine response test, neutrophils on BAL is normal
- part of equine asthma complex
- inc. RR at REST
tx: dexmethasone , house outside, bronchodilators,
heaves vs. inflam airway sydrome
heaves is inc RR at rest and older horses
IAD is younger exercise intolerant with cough
both have inc mucus and neuts on BAL(IAD can have more inflam cells present)
Strangles
strep equi equi = G+ cocci with large capsule
as exudate accumulates, dec. drainage creates CHONDROID
tx: flush infuse pen G in 3% gelletin, Pen G IM x7d, isolate 30d
retest 3 series of nasopharyngeal swabs and culture
duodenitis/ proximal jejunitis/ anterior enteritis
- inc reflux, hemorrhagic, orange/brown, foul smell
- dilated loops on rectal
- cause unknownn +/- C. dif
tx: decompress, fluids, replace electrolytes, analgesia, fix a/b
mesenteric rent
Strangulating intestinal obstruction
- acute colic, pawing, red MM, absent GI sounds
- inc reflux, yellow
LD displacement - nephrosplenic entrapment
does not cause severe colic
can’t image L kidney
tx: phenylephrine and exercise; rolling; sx
foal diarrhea
- most common cause?
- Proliferative enteritis?
- rotavirus
2. lawsonia, thickened intestine weanling age horses, VENTRAL EDEMA
sentinel animal for west nile
chicken
Common causes of bacterial folliculitis in horses?
tx?
- staph aureus
- staph intermedius
- Corynebacterium
topical abx; systemic abx(if needed)
Horse treated for strangles 2 weeks ago now presents for urticarial wheals x2d that progressed to well demarcated edema of the muzzle,eyes, belly, limbs, that is painful. dyspnea, diarrhea, petechia and eccymoses on MM.
diagnosis?
Purpura Hemorrhagica
classic history is a mixed clinical picture (painful edema, purpura, dyspnea, diarhea, or colic) two weeks after strangles.
most common cause is sensitization to s. equi or from s. equi vaccines.
immune complexes damaging vasculature
horse dental formula
3/3 1/1 3or4/3 3/3
Horners syndrome
"My 3rd Sunken Toe" - Miosis - 3rd eyelid protrusion - sunken eye (enophthalmos) - ptosis \+/- anisocoria \+/- sweaty horses (vs. anhydrosis in not horses)
Tying up
aka rhabdomyolysis
inc. CK
pigmenturia, sweating, muscle fasiculations and stiffness (workout after a few days without exercise
Causes of inc CK in horses?
rhabdomyolysis (tying up)
monensin toxicity
abx labeled for intrauterine use in horses in USA
amikacin
ceftiofur, penicillin, ampicillin are frequently used to treat endometritis but are extralabel
horse blood volume (%)
8% of body weight
eCG in horses?
just means she was successfully bred, not that fetus is viable
between 30-150 days endometrial cups product eCG to stim formation of secondary CL to produce progesterone
*cups dont regress until 150days regardless of fetal viability
recurrent uveitis
CS: aqueous flare, corpora nigra atrophy, fibropupillary membranes, posterior synechia
- most will develop cataracts
cataracts
foals - congenital
older - secondary to recurrent uveitis
A fib in horses
not uncommon in horses, usually asymptomatic except when exercising at high speeds
prognosis is GOOD
- eval K, Mg
- tx: QUINIDINE sulfate via NG q2h unti arrythmia converts or signs improve
vs. Grave prognosis if with primary heart disease/severe signs/CHF
4week foal with icterus and severe hypoglycemia and high bilirubin
primary differential?
Tyzzers
12 hr old foal is straining, swishing tail from side to side with arched back and is rolling on stall floor.
diagnosis?
how to test?
meconium impaction, do a rectal exam.
*most common cause of colic in newborn foal (within 24h)
colts>fillies (bc smaller pelvis)
types perineal lacerations post foaling?
1st degree - only involve mucosa of vestibule and skin of dorsal commissure of vulva
2nd degree - involve mucosa and submucosa and some of musculature. may need episioplasty depending on extent.
3rd degree - RECTOVAGINAL FISTULA more common in maiden mares. *delay repair 4-8 weeks (bc inflammation) if repaired, breeding soundness should be normal
purpura hemorrhagica
history of strangles or strangles vaccine followed (2w later) by mixed clinical signs (afebrile, purpura, painful edema, respiratory difficulty, diarrhea, colic)
- less commonly after equine flu or chronic suppurating wounds.
- due to immune complexes damaging vasculature
Edema in horses (big 3?)
purpura
EIA
EVA
potomac horse fever
neorickettsia risticii
febrile colitis/diarrhea, with laminitis 3-5d after diarrhea
- NE USA river valley in JULY/AUGUST
Salmonella
septicemia, fever, diarrhea
lyme disease
arthritic joints, low fever, reluctant to move (more common in dogs/humans)
primary hyperammonemia in horses
enteric disease(colic, diarrhea) - overgrowth of urease producing bacteria CS: blindness, severe neuro signs, severe metabolic acidosis, hyperglycemia (normal liver enzymes)
