VIN Class 3 - Equine Info

Question 1

Define the term Colic. What are the most common clinical signs of colic recognized by an owner. Is colic always GI in origin?

Answer 1

Colic is a generic term used to describe abdominal pain in horses. It’s most often
attributed to true gastrointestinal pain but horses can also act “colicky” due to non-GI causes. The most common colic signs recognized by an owner are frequent pawing, kicking at abdomen with hind legs, stretching out as if to urinate, laying down, rolling, anorexia, sweating, muscle fasciculations, and Flehman response.

Question 2

Topic: Colic - Small Intestinal Disease

1. Describe the pathogenesis of small intestinal disease.
2. List the different causes of the above pathogenesis.

Answer 2

1. There are several different ways the SI can be affected. Most cause strangulation, cutting off blood supply of affected intestine, and quickly devitalizing tissue.
2. A - Mesenteric lipoma: Typically seen in older horses (20+), twists around one or more pieces of SI –> strangulation.
   B. Volvulus: twist within the SI –> strangulation.
   C. Intussusception: Typically seen in younger horses @ ileocecal junction most commonly. Occurs due to diet changes, parasites (tapeworms).
   D. Herniation: Inguinal, umbilical, or incisional.
   E. Mesenteric defect: piece of SI entrapped through a rent in mesentery causing strangulation. Rarely epiploic foramen entrapment.
   F. Anterior/proximal enteritis: will mimic SI obstruction. Pain usually less severe but significant GI reflux, medical management.

Question 3

Topic: Colic - Small Intestinal Disease cont.
1. What are the clinical signs?
2. How is this disease diagnosed?
3. What is the treatment?
4. Prognosis?

Answer 3

1 & 2. Severe pain, poorly responsive to analgesics.
- Gastric reflux.
- Transabdominal ultrasound will show dilated/non-motile loops of SI.
- As it progresses, abdominal fluid will become serosanguinous with elevated proteins/WBC.
- Rectal exam: rarely palpable distended loops of SI depending on duration.
3. Surgical; resection and anastomosis if bowel devitalized already, surgical reduction only if caught early (rare)
4. Guarded; Poor prognosis if longer duration before surgery or large amount dead bowel (i.e., >15 feet), frequent post-op ileus if resection required

Question 4

Topic: Colic - Large Intestinal Volvulus/Torsion
1. This form of colic happens in horses of what age?
2. Describe the pathogenesis.
3. What are the major clinical signs/diagnostics?
4. How is this treated?
5. Prognosis?
6. List the risk factors

Answer 4

1. This form of colic can happen in horses of any age.
2. A portion of colon twists and rapidly becomes ischemic and begins to necrose
3. Severe pain, poorly responsive to analgesics. Elevated HR; systemic shock. NO gastric reflux, Peritoneal fluid may be normal initially.Rectal exam: palpable diffuse gas distension in LI.
4. surgical correction, nearly impossible to resect LI.
5. good/fair if early surgical correction, poor if more than a few hours
6. older broodmares, just before parturition or up to 4 months postpartum; larger horses (more room for LI to twist), any age.

Question 5

Why is there no gastric reflux seen in horses with LI volvulus/torsion?

Answer 5

B/c the lesion is too caudal to allow fluid to back up to the stomach.

Question 6

What is a major risk of correcting a LI volvolus in a horse?

Answer 6

Risk of endotoxic shock when volvulus is corrected

Question 7

Topic: Colic - Colonic Impaction
1. Etiology
2. Risk factors
3. Describe the clinical signs/diagnostics
4. Treatment
5. Prognosis

Answer 7

1. This type of colic results from backup of fecal material.
2. Older horses w/ poor dentition, fed hay or coarse feed; decreased water intake, stress; Mini horses - small colon impaction common; frequently grooming self/others OR feed material OR poor dentition
3. Mild/intermittent colic signs initially and worsen with prolonged duration w/o treatment. May seem “normal” with analgesics. Decreased appetite.
   ○ Decreased manure production.
   ○ Palpable firm feed impaction on rectal exam.
   ○ Increased HR, pain, dehydration, etc. only if progresses without being treated
4. analgesics; oral fluids with laxatives via intermittent or indwelling nasogastric tube (mineral oil, psyllium, Epsom salts), main goal is to hydrate impaction; IV fluids.
5. good. Surgical intervention only if severe pain or several days duration.

Question 8

Topic: Colic - Colonic Tympany aka Gas Colic

1. What is the traditional cause of colonic tympany?
2. What are the risk factors?
3. What are the C/S and diagnosis?
4. Treatment?
5. Prognosis

Answer 8

1. Traditionally caused by a diet change or diet upset but can happen anytime in any age animal.
2. Diet change or grain overload
3. Spasmodic pain; Go from being normal to being very painful as they pass gas.
4. Analgesics, sedation, IV, and oral fluids. Usually medical unless gas distension becomes severe and causes circulatory issues.
5. Good!

Question 9

Topic: Colic - Colon Displacement
1. Name the different types of colon displacement.
2. Name the risk factors for developing this disease.
3. Describe the pathogenesis.
4. What are the clinical signs?
5. How is it diagnosed?
6. How is this treated?
7. What is the prognosis?

Answer 9

1. A. Right dorsal displacement = colon between cecum and right body wall.
   B. Left dorsal displacement = nephrosplenic entrapment. Colon goes into deep space between the left kidney and spleen, and becomes distended with gas.
   C. Pelvic flexure and “other” colon displacement.
2. large breeds (i.e., warmbloods) as there is more room for colon to displace.
3. Usually thought that colon displaces first then becomes distended with gas and limits ability to move back into the correct position.
4. pain is variable and can be intermittent; increased systemic signs as duration increases.
5. A. Rectal exam: palpable tight ‘bands’,
   gas-distended large colon.
   B. Nephrosplenic entrapment: rectal palpation
   of entrapment; unable to identify left kidney
   on transabdominal ultrasound.
6. Medical initially, surgical if no improvement.
   A. Nephrosplenic entrapment: give phenylephrine IV to shrink spleen and decrease nephrosplenic space. Often give phenylephrine then trot horse around or, rarely, anesthetize and roll horse to encourage colon to return to normal space.
7. good, higher chance of repeat colics.

Question 10

Topic: Colic - Enteroliths/Sand Colic
1. List the risk factors.
2. Describe the pathogenesis?
3. What are the c/s?
4. How is this disease diagnosed?
5. How is it treated?
6. What is the prognosis?

Answer 10

1. Geographic areas with sandy soil (especially California, Florida, Arizona) but can happen anywhere:
   A. Horses fed on dirt ground
   B. Horses fed diets with insufficient roughage or
   thin/malnourished animals
   C. Arabians
   D. Alfalfa hay risk for enteroliths due to mineral composition
2. A. Enteroliths: precipitation of struvite salts (magnesium ammonium phosphate), often around a foreign body nidus. Usually get stuck in small colon or transverse colon due to small size.
   B. Sand: chronic low-grade ingestion of sand or dirt; doesn’t pass in manure well and will settle
   on ventral aspects of colon.
3. Mild/moderate intermittent pain.
   A. Sand: may be able to auscult fluid ‘wave’ on sand in ventral abdomen.
   B. Enteroliths: gas distention on rectal exam if large enterolith because gas will be unable to pass by
4. Positive fecal sand float; sometimes radiopaque sand or stone visible on abdominal radiographs.
5. Enteroliths - enterotomy. Sand colics - sometimes medically treated with frequent nasogastric tubing with water, mineral oil, psyllium, laxatives; surgical enterotomy if medical treatment unsuccessful.
6. Good

Question 11

Topic: Colic - Gastric Ulcers

1. What type of colic pain do gastric ulcers cause?
2. List the risk factors.
3. Describe the pathogenesis
4. What are the clinical signs?
5. How is this disease diagnosed?
6. How is it treated?
7. How is it prevented?

Answer 11

1. A nonobstructive pain.
   2.
   A. Highly stressed horses: showing, racing, traveling
   B. Prolonged time with an empty stomach: no turnout, decreased roughage, nervous horses
   C. NSAID usage
2. ulcers are at squamous region of stomach (i.e., non-glandular dorsal stomach).
3. A. Mild/moderate pain, mild anorexia, cranky/irritable behavior
   B. NO bleeding into GI; often responds well to initial dose of analgesics (i.e., Banamine) but repeated use will worsen ulcers.
   C. No abnormalities on rectal or ultrasound exam, physical exam normal.
4. Fasted gastroscopy
   6.
   A. Omeprazole for several weeks to months
   (gastric hydrogen potassium ATPase inhibitor)
   B. Ranitidine (H2 blocker)
   C. Sucralfate
5. Feeding alfalfa reduces stomach acid,
   maximizing roughage and turnout time, reducing stress

Question 12

Topic: Colic - Parasite Associated Colic
1. Etiology
2. Age range affected
3. Pathogenesis
4. Clinical signs
5. Treat
6. Onward is a different etiology

Answer 12

1. Ascarid Impaction: Parascaris equorum (roundworms)
2. Horses usually < 1-year old
3. Horse hadn’t previously been dewormed and then recently given large dose of anthelmintics. Massive parasite die-off causes physical intestinal blockage.
4. May get ascarids in GI reflux; mild to severe pain.
5. Surgery
6. Verminous arteritis a.k.a. thromboembolic colic: Strongylus vulgaris parasite.
7. Horses of any age with poor parasite control or problems with parasite resistance, especially
   younger horses.
8. S. vulgaris migrates to cranial mesenteric artery; damage and immune response can form thrombus that cuts off blood supply to bowel and causes infarction; cecum most common

Question 13

Topic: Acute Colitis
1. List the different forms
2. What are the c/s?
3. How is it treated?

Answer 13

1. Infectious: Salmonella, Clostridium perfringens or difficile, Potomac Horse Fever (Neorickettsia risticii), Equine coronavirus.
   A. Noninfectious: diet change, right dorsal colitis (secondary to NSAID use), intestinal neoplasia.
   B. Unknown: Colitis X
2. Mild to moderate pain, frequently intermittent or spasmodic; systemic shock.
3. analgesics, supportive medical management, IV fluids, probiotics, Biosponge.
   A. Antibiotics mainly only for Potomac Horse Fever (tetracycline)

Question 14

Topic: Urolithiasis
1. Risk factors
2. Pathogenesis
3. Clinical signs
4. Diagnosis
5. Treatment
6. Prognosis

Answer 14

1. stallions and geldings, horses fed alfalfa or high-protein diets.
2. usually calcium carbonate stones.
3. often acutely severely painful, stretching out as if to urinate repeatedly and straining without producing significant quantities of urine.
4. distended bladder on rectal exam, palpable calculi on rectal or with ultrasound.
5. Emergency surgical removal.
6. Recurrence possible, especially if diet not addressed.

Question 15

Topic: Uterine Torsion
1. Risk factors
2. Clinical signs
3. Treatment
4. Prognosis

Answer 15

1. mares in last trimester of gestation (7 months+).
2. mild to moderate colic signs, frequently anorexic or laying down. Signs persist despite appropriate treatment for GI colic. Broad ligament pulled tight over uterus palpable on rectal exam.
3. Place mare under general anesthesia and roll her with a plank over abdomen to stabilize fetus, essentially rolling mare around the fetus. If unsuccessful, surgery required.
4. good for fetus and mare, especially if treated early.

Question 16

Equine Infectious Anemia
1. What is the etiologic agent of this disease? How is it transmitted?
2. What are the classic clinical signs?
3. How is this disease diagnosed?
4. How is this disease treated?
5. What is important to remember about this disease?

Answer 16

1. Lentivirus; transmitted via biting flies - horse flies, stable flies, deer flies
2. A. Acute: pyrexia, lethargy, thrombocytopenia
   B. Chronic: Petechiation of oral mucosa, recurrent pyrexia, anemia, weight loss, ventral edema
3. All testing must be done at a USDA approved lab
   A. Gold standard = Coggin’s Test
   - The Coggin’s test is a test for an antibody; therefore, it carries several drawbacks/ limitations. In acute episodes of equine infectious anemia (EIA), there is often not yet adequate production of antibody to detect by this test. In foals, false positives can occur due to acquisition of the antibody in colostrum. Persistently infected horses constitute the majority of cases, and because they are under constant antigenic stimulation, they maintain antibody production and can be very accurately diagnosed with the condition by the Coggin’s test.
   B. c-ELISA (false +)
4. No treatment
   A. Seropositive horses must either be in lifelong quarantine at least 200 yards from other horses for life OR euthanized
5. A. This disease is a life-long infection
   B. All horses being moved interstate or sold within a state must test - for EIA at least within the last 12 months.e

Question 17

Topic: Tent Caterpillar Toxicity

Associated with mare reproductive loss syndrome

Question 18

Topic: Ionophore toxicity

1. What is the etiology?
2. What is the pathogenesis?
3. What are the c/s?
4. How is this diagnosed?
5. How is this treated?
6. What is the prognosis?

Answer 18

1. Ionophores such as monensin, salinomycin, and lasalocid are added to cattle and poultry feed to improve feed efficiency + are coccidiostats. Horses are exposed when they get into cattle or poultry feed.
2. ionophores disrupt ion gradients across cell
   membranes, affect energy production in cells.
3. Usually develop c/s within 24 hrs:
   A. Sweating
   B. Refuse feed
   C. Muscle tremors
   D. Tachycardia –> high risk of heart failure.
4. A. BW: Increase CK/AST, cardiac troponin enzyme, Azotemic, hyperglycemic, hyo-cal, kal, myoglobinuria
   B. Echo: decreased cardiac contractility
   C. Test feed for ionophores
5. A. Decontamination
   B. IVF, antiarrythmics
   C. Recheck ecg in 3 months
6. Over 60% mortality rate

Question 19

Topic: Moldy Corn
1. What is the etiology?
2. What is the pathogenesis?
3. What are the c/s?
4. How is this diagnosed?
5. How is this treated?
6. What is the prognosis?

Answer 19

1. Fumonisin spp. grown on corn
2. Disrupts sphingolipid biosynthesis
3. Death within 48-72 hrs
   - Pharyngeal paralysis
   - Blindness, circling, head-pressing
4. A. BW: elevated sphinganine–to–sphingosine ratio (SA/SO ratio) in serum, urine, or tissues
   B. Necropsy: grossly visible leukoencephalomalacia/liquefactive necrosis: white matter of one or both cerebral hemisphere
5. None
6. Poor once neuro signs develop

Question 20

Topic: Blister beetle

1. What is the etiology of this disease?
2. Describe the pathogenesis
3. What are the c/s?
4. How do you diagnose this disease?
5. How is this disease treated?
6. What is the prognosis?

Answer 20

1. Epicauta spp. beetles in hay
2. These beetles secrete an irritant called cantharidan –> ulceration.
3. Oral ulcerations, hematuria, colic, diarrhea, synchronous diaphragmatic flutter aka thumps from the hypocalcemia –> shock, death.
4. A. ID beetles in the hay
   B. BW: Severe hypocalcemia, hypomagnasemia, hypoproteinemia
   C. Increased cardiac troponin enzyme
   D. Urine, GI content cantharidin analysis
5. IVF + Calcium, omeprazole, sucralfate
6. Guarded

Question 21

Topic: Rhodoccocus equii pneumonia in foals

1. What age range is typically affected?
2. Describe the pathogenesis of this disease.
3. What are the clinical signs of the disease?
4. How is this disease diagnosed?
5. How is this condition treated?

Answer 21

1. 1-6 mo of age
2. Rhodococcus equi is a Gram positive facultative intracellular coccobacillus that is not a normal inhabitant of equine respiratory tract but common environmental pathogen,
   especially in large equine breeding operations. Can be readily aerosolized during dry and dusty periods. Organism is inhaled, especially in dusty environments, and subsequently invades alveolar macrophages of infected foals where it replicates, producing pyogranulomatous pneumonia and pulmonary abscessation (Figure 1).
3. R. equi is inhaled early in life and has a slow and insidious onset. Thus affected foals may have significant pneumonia before clinically recognized.
   - Intermittent Fever
   - Inappetance and weight loss/failure to gain weight
   - Cough, tachypnea and increased respiratory effort (e.g. nostril flaring)
   - Abnormal thoracic auscultation (wheezes and/or crackles)
   - Occasionally will see nasal discharge
4. A. BW: Neutrophilic leukocytosis, Hyperfibrinogenemia
   B. Rads/US: Ultrasonographic evidence of pulmonary abscesses are highly suggestive or characteristic radiographic findings of pulmonary abscesses
   C. Confirmation of disease is based on transtracheal wash and positive culture of the organism.
5. Macrolide antimicrobial such as Erythromycin, Clarithromycin, or Azithromycin combined with Rifampin. In addition, supportive care can include:
   a. Anti- inflammatory drugs (NSAIDS)
   b. Cool temperature- controlled environment
   c. Intranasal oxygen supplementation (if necessary)
   d. Maintenance of hydration (if necessary)

Question 22

Topic: Rhodoccocus equii pneumonia in foals - 2
1. Describe the complications of Rhodoccocus equii pneumonia infection in foals

2. What is the prognosis? How can this disease be prevented? Describe the screening measures used.

Answer 22

1. Some of the more common complications include:
   a. Internal Abscessation
   - Ulcerative colitis and/or mesenteric
   lymphadenitis as previously mentioned
   resulting in signs of intermittent colic,
   diarrhea and weight loss (Figure 4).
   - Intervertebral abscess resulting in
   neurologic deficits caudal to the lesion
   such as weakness and ataxia.
   b. Septic Arthritis
   - Organism can occasionally cause septic
   arthritis resulting in an inflamed joint
   associated with pain and lameness.
   c. Osteomyelitis
   d. Joint effusion (non-septic)
2. R. equi pneumonia in foals is fair to good as long as appropriate therapy is
   instituted as soon as the disease is recognized. Occasionally foals are found acutely dead from respiratory distress

• R. equi pneumonia can present as a sporadic disease affecting individual foals. It can also be a devastating endemic problem, especially at breeding facilities.

Prevention:
i. Administration of hyperimmunized plasma against R. equi, early in life
ii. Prophylactic administration of macrolide antimicrobials no longer recommended due to potential for antibiotic resistance and questionable efficacy.
iii. Maintain strict environmental cleanliness and reduce dusty environments as much as possible.

Early Detection:
i. Routine measurement of body temperature and respiratory rate in age susceptible foals. Elevations in either parameter may suggest infection.
ii. Routine screening of a complete blood count observing for leukocytosis, Serum
Amyloid A (SAA) and/or hyperfibrinogenemia.
iii. Routine diagnostic screening of the lung field via ultrasonography or radiography.

Question 23

Topic: Equine herpesvirus 1 & 4, Equine Rhinopneumonitis
1. List the risk factors of this disease.
2. Describe the pathogenesis.
3. What are the major clinical signs?
4. How is it diagnosed?
5. How is it treated?
6. What is the prognosis?
7. How is it prevented?

Answer 23

1. Horses that show or travel with frequent exposure to other horses,
   especially young horses.
2. EHV is latent in individuals until times of stress, at which time they may cause clinical or
   subclinical disease and allow for spread via respiratory secretions.
   - EHV-1 can also mutate to an EHV-1 “wild-type” or “neurogenic” strain to cause neurologic
   disease known as Equine Herpes Myeloencephalopathy (EHM).
3. C/S are worse in naive, young horses ( < 5 yrs)
   - Fever, cough, mucopurulent nasal discharge
   - Abortions in pregnant mares
   - NOTE: rarely EHV-1 may infect endometrium and fetal tissues; abortions can be several months after initial infection.
4. PCR of nasal discharge
   5.
   A. Anti-inflammatories: Phenylbutazone, Flunixin, Pirocoxib
   B. Supportive care
   C. Antiviral drugs - Acyclovir
   D. +/- Rarely, antibiotic use for secondary pneumonia
5. Excellent, rarely secondary serious complications (pneumonia, etc.).
6. A. Isolating new horses or infected horses with strict biosecurity measures.
   B. Vaccine: modified-life intranasal vaccine or killed intramuscular vaccine. Biannual vaccine in
   high-risk horses and mares during pregnancy (5,7,9 mo of gestation) to prevent abortion.

Question 24

Topic: African Horse Sickness

1. What is important to remember about this disease?
2. What is the etiologic agent of this disease?
3. How is this disease transmitted?
4. What are the major clinical signs?
5. How is this disease diagnosed?
6. How is this disease treated?
7. How is this disease prevented and controlled?

Answer 24

1. This is a reportable disease that is not contagious, not zoonotic, and arthropod-borne.
2. Genus: Orbivirus, Family: Reoviridae
3. This disease is transmitted via Culicoides spp. arthropods. during late summer rainfall followed by hot, dry weather in sub-saharan Africa.
4. A. Pyrexia
   B. Supraorbital swelling
   C. Large amounts of frothy serofibrinous fluid coming from the nostrils
   D. Petechia
   E. Pulmonary edema
5. A. Clinical signs
   B. Definitive diagnosis: agent identification
   C. Confirmative diagnosis: RT-PCR
6. There is no specific curative tx. Only supportive care.
7. A. Vaccination
   B. Equine movement control
   C. Vector control

Question 25

Hoof Abscess

Question 26

Topic: CEM
1. Etiology:
2. Considered what type of disease?
3. Is it found in the U.S? Canada?
4. With mares, you would see what grossly?
4. Are there any C/S in stallions typically?
5. Is this disease reportable?

Answer 26

1. Taylorella equigenitalis
2. Considered an exotic disease, CEM did not appear in the U.S. until 1978.
   - An outbreak occurred in multiple states in 2008.
   - Several cases diagnosed since 2010 by USDA.
   - CEM has not yet been detected in Canada.
3. Mares: mucopurulent vaginal discharge in up to 40%, abortion, infertility.
4. Stallions: NO clinical signs, typically.
5. CEM is a REPORTABLE disease!

Question 27

Topic: Laminitis
1. Etiology/Risk factors
2. Pathogenesis
3. C/S

Answer 27

1. • Metabolic disease: obese or overweight horses, metabolic-prone breeds (Morgans, ponies,
     miniatures, etc.), Equine Cushing’s disease, excess grass intake (especially in springtime).
   • Endotoxemic diseases: grain overload, colitis, retained fetal membranes.
   • Support limb laminitis.
   • Iatrogenic steroid-induced
2. Regardless of initial cause, an inflammatory cascade is set off –> laminar projections
   (lamellae, i.e., “velcro”) in hoof capsule become inflamed and weaken.
   ○ Deep digital flexor tendon attaches to coffin bone at palmar aspect. Pull of the flexor tendon
   on weak laminae causes the coffin bone to rotate toe palmar towards ground. Alternatively, coffin bone may “sink” lower in hoof due to weight-bearing force on weak laminae
3. All feet can be affected but usually just fronts or fronts significantly worse.
   - Increased digital pulse
   - Rocked back stance, “walking on eggshells”
   - Total or significantly increased recumbency.
   - Hoof testers: positive to pressure at toe

Question 28

Topic: Laminitis cont.
4. Diagnostics
5. Treatment

Answer 28

1.
- Hoof testers: positive to pressure at toe.
- Radiographs: coffin bone rotated towards
ground and decreased sole depth under point of
coffin bone. Chronic cases may have osteophyte
“ski-tip” at point of coffin bone due to chronic
trauma
- Nerve blocks: rarely necessary and
contraindicated due to increased temporary
weight bearing; if performed won’t fully block
out but will improve with abaxial nerve block.

2. A. Initial stages: icing or cooling feet, anti-inflammatories.
   - Traditionally horses were given phenoxybenzamine to cause vasodilation and improve circulation to hooves; true benefit unknown, not used as frequently now.
   B. Deeply bedded stall, sand bedding.
   C. Cushioned boots or styrofoam on hooves for extra cushion.
   D. Trimming over time to “derotate”: bring back toe and square off, decrease heel angle.
   E. Chronic cases not responding well to traditional treatment: deep digital flexor tendon tenotomy to relieve pull of tendon on coffin bone.
   F. Long term: weight loss, diet changes for low sugar and low starch hay and grain, soaking hay in water to remove sugars before feeding

Question 29

Topic: Navicular Disease

1. What are the risk factors?
2. What is the definition and pathogenesis?
3. What are the clinical signs?
4. How is this condition diagnosed?
5. How is it treated?

Answer 29

1. A. Quarter horses and paint horses - overrepresented
   B. Small feet
2. Navicular disease refers to any sort of pain coming from the navicular bone. Secondary osteophytes off of the navicular bone can lead to secondary pain due to a grating action on the deep digital flexor tendon which attaches to the coffin bone.
3. Typically seen in the forelimbs, bilaterally.
   A. Will see switching lameness; when use palmar digital block, one foot the horse will be lame in the other foot.

4.
A. Hoof tester: positive when apply pressure to the heel
B. Radiographs: Normally the medullary cavity is darker than the outer cortices and there are 3-4 small nutrient foramen. In the case of navicular disease, the medullary cavity is increased in opacity and the outer cortices are thickened. Additionally, there are enlarged and increase nutrient foramen as well as osteophytes.

5. A. Reduce the toe to improve breakover
   B. Add a wedge, heel pad, or eggbar shoe to increase the heel angle to take pressure of the heel
   C. Bisphosphonate injection to decrease osteoclast activity and increase osteoblast activity.
   D. Anti-inflammatories

Question 30

Topic: Tendonitis and Desmitis

1. Which tendons are most commonly affected?
2. Describe the pathogenesis
3. What are the clinical signs?
4. How is this disease diagnosed?
5. How is it treated?

Answer 30

1. Suspensory ligament, DDFT, and SDFT
2. Acute trauma, chronic weakening due to overuse.
   - Degenerative Suspensory Ligament Desmitis/Disease is most common in Peruvian Paso Finos but occurs in most breeds. Occurs due to progressive failure of collagen fiber repair in suspensory ligament apparatus. Over time, the suspensory ligament becomes enlarge –> fetlock drop, positive on flexion, bilateral or in all legs.
3. A. Swollen tendon or tendon sheath, painful to palpation.
   B. Mild to moderate lameness at a trot.
4. Clinical signs and ultrasonography.
5. A. Initial rest followed by long rehabilitation program (6-12 months).
   B. Fasciotomy, neurectomy.
   C. Additional therapies to speed healing such as platelet-rich plasma injection (PRP), shockwave therapy, etc.

Question 31

Topic: Osteoarthritis
1. What are the risk factors?
2. What is the pathogenesis?
3. What are some of the common names for OA and their associated body parts?
4. What are the clinical signs?
5. How is it diagnosed?
6. How is it treated?

Answer 31

1. Older horses with history of heavy workload
2. Repetitive trauma and synovitis –>
   A. Articular cartilage degeneration
   B. Decreased joint fluid viscosity
   C. Remodeling and osteophyte formation
   D. +/- Osteophytes breakoff –> fragments
3. A. Pastern joint OA = High ring bone
   B. Coffin joint OA = Low ringbone
   C. Hock joint (esp intertarsasl) OA = Bone spavin
   D. Tibiotarsal joint effusion = Bog spavin
4. A. Initially mild/subtle lameness at the trot, can progress to significantly lame even at the walk
   B. Positive to flexion of affected joint
5. A. Radiographs: osteophytes, joint narrowing or briding
6. A. Pain medications and anti-inflammatories: phenylbutazone, Equioxx®
   B. Oral joint supplements: MSM and glucosamine-based
   C. Systemic injectable joint supplements: Adequan® i.e., PSGAGs
   D. Targeted intra-articular injections: corticosteroid +/- hyaluronic acid
   D. Intra-articular IRAP
   E. Surgical fusion of joint as salvage procedure; surgical removal of chip fractures

Question 32

Topic: Hoof Abscess (Subsolar Abscess)
1. What are the risk factors?
2. What is the pathogenesis?
3. What are the clinical signs?
4. How is it diagnosed?
5. How is it treated?

Answer 32

1. weak hooves, moist environment, poor hoof hygiene
2. weak or soft spot in hoof allows bacteria to travel into foot and proliferate deep
   in hoof.
3. Lameness, increased digital pulse, heat in hoof
4. Clinical signs; large abscesses will show up as gas pocket on radiograph but usually
   unnecessary for routine abscesses
5. A. Opening abscess and draining material. Most abscesses take a path out the bottom of foot, some will burst out at coronet band instead
   B. Soaking or softening hoof to allow for better drainage. Often soaked in water with
   betadine, epsom salts, etc.
   C. Bandaging +/- poultice to draw abscess material out, keep foot clean, provide support
   D. Systemic antibiotics are rarely indicated because limited blood supply to superficial
   hoof means poor antimicrobial penetration.
   E. Anti-inflammatories, tetanus toxoid booster.

Question 33

Topic: Laceration (Septic Joint or Tendon)
1. What are the joints and tendons affected?
2. What is the pathogenesis?
3. What are the clinical signs?
4. How is it diagnosed?
5. How is it treated?
6. What is the prognosis?

Answer 33

1. A. Tendon: deep and superficial tendon sheath infection or complete severing of a flexor tendon.
   B. any joint, although distal limb most common.
2. any size laceration or puncture into a joint or tendon can introduce bacteria and cause
   sepsis. Initial lameness due to pain of joint capsule; may become more lame over several days due to distension and pressure on joint capsule as WBC and inflammatory markers increase effusion.
3. A. Laceration or puncture into joint or tendon structure, sometimes joint fluid can be seen leaking from wound (joint fluid straw-colored and “stringy” between fingers).
   B. Lameness: usually severely lame, may be non weight bearing; more painful on flexion
   of affected joint.
   C. Joint or tendon sheath effusion.
4. A. If the wound is near a structure but involvement unclear can perform sterile
   arthrocentesis and distend joint while looking to see if fluid comes out of the wound.
   B. Analysis of fluid from joint. Septic joint will have increased protein and cellularity
   (Arthrocentesis: WBC >30,000 with 80% neutrophils; total protein >4 g/dl), rarely
   grossly abnormal.
   C. Radiographs +/- probe into wound tract.
5. Early aggressive treatment critical for long term success and soundness.
   ■ Systemic antibiotics based on culture, regional limb perfusions with antibiotic.
   ■ Gold standard: high-volume sterile lavage, often best under general anesthesia
6. if left untreated initially prognosis is poor for long term soundness because of
   secondary osteoarthritis. Prognosis good with aggressive early treatment.

Question 34

Topic: Foals: Septic Joint
1. What are the risk factors?
2. What is the pathogenesis?
3. What are the clinical signs?
4. How is it diagnosed?
5. How is it treated?

Answer 34

1. Omphalophlebitis, failure of passive transfer (IgG <800 mg/dl)
2. hematogenous seeding of synovium with bacteria
3. Joint effusion, lameness, pyrexia, frequent recumbency, multiple systems often septic
4. A. Elevated or depressed WBC
   B. Hyperfibrinogenemia
   C. Arthrocentesis: WBC >30,000 with 80% neutrophils; total protein >4 g/dL
5. A. Systemic and intra-articular antibiotics based on bacterial culture and sensitivity from arthrocentesis. Amikacin and gentamicin are common along with a beta-lactam.
   B. Sterile joint lavage.
   C. Anti-inflammatories

Question 35

Topic: Foals: Congenital Flexural Limb Deformity
1. What is the pathogenesis?
2. What are the clinical signs?
3. How is it treated?

Answer 35

1. unknown, intrauterine malpositioning and genetic predisposition, dysmaturity
2. A. Carpus and fetlock most common, often
   bilateral or multiple limbs affected
   B. Contraction: physically unable to extend limb, may knuckle over
   C. Extension: mostly fetlock extension, may walk on heels with toe in air and abrade palmar/plantar fetlock on ground
3. A. Judicious use of splints and bandages to support and protect limbs, corrective glue-on shoes
   B. Contraction: IV oxytetracycline (1-3 g IV q 24 hours for 1-3 treatments), recommended to monitor renal values before and after administration
   C. Desmotomy rarely needed, only if severe and unresponsive to medical treatment

Question 36

Topics: Osteochondritis Dissecans (OCD)
1. What are the risk factors?
2. What is the pathogenesis?
3. What are the clinical signs?
4. How is it diagnosed?
5. How is it treated?

Answer 36

1. Young horses (average age 1-2 years old), especially large or fast growing breeds, rich or improperly balanced diet (especially Ca:P ratio).
2. Failure of normal endochondral ossification. When cartilage at articular surface fails to ossify properly OCD forms
3. Joint effusion, lameness usually at trot
4. Joints affected: tarsus, stifle
   A. Radiographs: subschondral lucencey at articular surface
5. A. Young horses (<1 year): conservative rest, diet changes, exercise restrictions
   B. Arthroscopic removal of OCD lesions and fragments in 1-2 year olds, especially if no improvement with conservative management

Question 37

In a salivating, tooth-grinding foal, rule out what first?

Answer 37

Ulcers (the common disease)

Poorly understood pathogenesis
* NSAID use has been associated with development of ulcers.
* Treatment is to reduce/neutralize gastric acid:
- Omeprazole, a proton pump inhibitor, is most effective
- Histamine receptor antagonists ( cimetidine) are also useful.

Question 38

Topic: Right Dorsal Colitis

Question 39

Topic: Failure of Passive Transfer in Foals

1. Define failure of passive transfer.
2. What is the etiology?
3. List the clinical signs
4. What diagnostics do you run for cases like this?
5. Treatment?

Answer 39

1. FPT occurs when foals do not drink their mother’s colostrum rich in immunoglobulins. Foals are only capable of absorbing these molecules within the first 24 hrs after birth
2. There are several etiologies:
   A. Mom - low AB concentration in colostrum, colostrum leaking out before foal is born, not enough AB in colostrum, poor quality colostrum, rejection of the foal.
   B. Foal - Cleft palate, being orphaned, etc.
3. A. Lethargy, pyrexia, anorexia, inability to stand, diarrhea, swollen joints
   B. Check IgG concentrations: IgG Concentrations must be > 800 mg/dL to be considered adequate.
   - Partial FPT diagnosis is if IgG concentration is 400-800 mg/dL. Complete FPT diagnosis is if IgG is less than 400 mg/dL.
4. A. If less than 12 hrs:
   - 1-2 L of good quality equine colostrum over 8 hrs
   - Can use bovine colostrum if desperate but has a shorter half life.
   - Donor mare must be vaccinated and have no Aa or Qa alloantigens.
   B. If greater than 12 hrs:
   - Sedate foal
   - Hyperimmune plasma (1-2L per 50kg foal).

Question 40

Foals are born without circulating immunoglobulins (IgG) and depend on colostral IgG for immunocompetency. Adequate colostral intake must happen as soon as possible after birth.

Ideally, ~ 1 liter of colostrum within the first 90 min of life.

Serum IgG concentrations in the foal should be 800 mg/dI.

• Gut “closure” virtually complete by 24 hours
• After 24 hours, must give plasma IV. (Frozen equine plasma is readily available.)

Question 41

Topic: Neonoatal Isoerythrolysis

1. Signalment
2. Pathogenesis?
3. Treatment

Answer 41

1. Most common in horses, pigs, cattle, and cats.
2. Happens only in foals of mares that have developed anti-RBC antibodies during a previous pregnancy. Foal swallows colostrum containing maternal antibodies to the neonate’s erythrocyte antigens.
   - Type II hypersensitivity reaction causes neonate RBC lysis
   - Normal neonates become weak & icteric 2-3 days after birth.
3. Rx:
   - STOP ingestion of colostrum and
   - Give blood transfusions (often washed maternal RBCs).
   * In large animals, Ni does not occur in maiden dams.
   * But cats can have anti-RBC antibodies without prior exposure, and first litters may be affected by NI.

Question 42

Is a continuous murmur normal in a neonatal foal?

Answer 42

• A continuous murmur on left side is normal in
  newborn foals.
• Due to a slight opening of the ductus arteriosus,
• Usually closes within a week

Question 43

What is the most common cause of equine pregnancy loss? When do these losses occur? When does the mare com back into heat?

Answer 43

Twinning is the most common cause of equine pregnancy loss.

Most losses occur too early to be classified as abortion.

If pregnancy ends before
day 38, the mare will come into heat on the next cycle and may be rebred.

Question 44

Topic: EHV-1
1. This is the most common cause of?
2. This, along with what other herpes virus cause?
3. Weeks to months later, you may see what?
4. Clinical signs?
5. With some EHV-1 strains you can see what C/S after what particular incidiences?
6. What is the cause of coital xanthema?

Answer 44

• Equine herpes: most common cause of equine infectious abortion.
• EHV-1 & EHV-4 both cause acute, febrile, upper respiratory disease and both may result in latent infection.
• With EHV-4 see respiratory disease more in weanlings.
• Weeks to months later, you may see 3rd trimester abortions in mares.
• Aborting mares seldom show premonitory signs.
• With some EHV-1 strains, you can see neurological symptoms in mares after abortion storms or in other horses.
• FYI: EHV-3 causes coital exanthema.

Question 45

Topic: EHV-1
1. EHV-1 and what other herpesvirus can recrudesce during times of stress? What are the C/S?
2. How can this be prevented?
3. Is infection with EHV common? Which strains are horses most commonly exposed to?
4. What is a major DDx for EHV-1?

Answer 45

• EHV-1 and EHV-4 infections can recrudesce in times of stress
• Affected horses cough, are febrile, lymphopenic, and neutropenic +/- retropharyngeal/submandibular lymphadenopathy
• Vaccination at 5, 7, and 9 months of gestation helps prevent abortion.
• EHV-1 and EHV-4 are ubiquitous:
• > 85% of adult horses thought to be exposed to, or latently infected with EHV-1, so…
• Even with regular vaccination,
• No horse is absolutely protected.
• Equine viral arteritis (EVA): not common but can cause abortion and should be a DDx for abortion due to EHV-1

Question 46

Topic: Viral resp disease
1. What is a major clue that avirus is responsible?
2. Key diagnostics?
3. Equine viral rhinopneumonitis is caused by?
4. EVA is transmitted via?
5. Equine influenza is or is not contagious?
6. Major clinical signs?
7. Is there a carrier state for EVA?
8. Consequences

Answer 46

• Leukopenia is a clue that a virus may be responsible.
• Real-time polymerase chain reaction (PCR) testing of nasopharyngeal (NP) swabs
• Equine viral respiratory pathogens are NOT distinguishable based on clinical signs.
• Equine viral rhinopneumonitis is usually caused by EHV-4.
• Equine viral arteritis (EVA) transmitted resp. & venereal routes
• Equine influenza is very contagious.
• Rapid onset of high fever, depression, and cough.
• No carrier state is known.
• Influenza virus destroys tracheal & bronchial epithelium.
• During epithelial regeneration (3 wks), horse susceptible to secondary bacterial infection cause norm. mucociliary defense mech. are not functioning well.`

Question 47

Topic: Strangles
1. What is the etiology of strangles?
2. What are the major clinical signs? When do c/s appear?
3. Does it require a primary viral infection to cause disease?
4. Is this disease contagious?
5. What is the source of infection? How is it transmitted?
6. Bacteria can survive for how long outside host?
7. How is this disease diagnosed?
8. Treatment?
9. Prognosis
10. Prevention

Answer 47

1. Streptococcus equi equi, a Gram-positive bacteria.
2. Clinical signs appear 2 days to 2 weeks post exposure:
   Fever, mucopurulent nasal discharge, dramatic neutrophilia
   - Enlarged head and neck lymph nodes; submandibular most common abscessation & drainage of can occur.
   —- RARELY —-
   - Strangles disseminates to internal organs and forms abscesses known as “bastard strangles.”
   - Purpura hemorrhagica: aseptic vasculitis (severe edema, petechiae, septicemia) immune
   reaction from repeated exposures to natural infection or vaccination, can be fatal.
   - Chondroids: solidified caseous material (small “stones”) in guttural pouches, can persist for
   years and be a source of bacterial shed if not removed.
3. Does NOT require a primary viral infection to cause disease.
4. Highly contagious; trans. by direct contact and fomites.
5. Carrier animals a source of infection; It is transmitted via the respiratory secretions of infected animals and inhaled or ingested.
6. Bacteria may survive 9 weeks outside the host.
7. A. Acute Disease: PCR from nasal swab, nasopharyngeal lavage fluid, or guttural pouch lavage fluid; bacterial culture.
   B. Chronic Disease: serology for SeM-specific antibody, high titers suggest Purpura
   hemorrhagica or bastard strangles; guttural pouch endoscopy.
8. Most infections are cleared naturally. Antibiotics are contraindicated because they can prolong recovery.
   - Rarely: Lymph node abscess cut off airway and require emergency tracheotomy.
9. Good
10. A. Isolate new or infected horses with strict biosecurity measures.
    B. Vaccine: modified-life intranasal vaccine or killed intramuscular vaccine.
    - Vaccination, especially if recent natural exposure or infection, or frequent vaccination, increases risk of Purpura hemorrhagica immune reaction, thus is contraindicated in an outbreak.

Question 49

Topic: Equine Pneumonia & Pleuropneumonia

1. Name the risk factors that can predispose horses to develop pneumonia.
2. What clinical signs are highly suggestive of pneumonia?
3. What happens as a result of pleuropneumonia?
4. Describe the pathogenesis of this disease?

Answer 49

1. History of extended transportation or exposure to large number of horses.
2. Clinical signs, particularly cough, fever and increased respiratory rate/effort, are
   highly suggestive of pneumonia.
3. Pleuropneumonia occurs in conjunction with pneumonia and may result in significant accumulation
   of fluid within the thoracic cavity.
4. Bacterial pneumonia commonly follows viral respiratory infection or another stressful event such as prolonged transport, general anesthesia, intense training or overcrowding. Viral infection may damage respiratory epithelial cells, decrease mucociliary clearance and impair immune function.

Question 50

Topic: Equine Pneumonia & Pleuropneumonia - 2

1. List the causes of equine pneumonia.

Answer 50

1. Bacterial: Mixed bacterial infections occur frequently and can include:
   a. Gram Positive Bacteria: Streptococcus zooepidemicus
   b. Gram Negative Bacteria: E. coli, Pasteurella, Klebsiella
   c. Anaerobic Bacteria: Bacteroides fragilis, Clostridium sp.
   ● Viral: Viruses may set the stage for bacteria to invade the lung, thus leading to bacterial pneumonia. Potential viruses that attack the respiratory system include:
   a. Equine Herpes Virus
   b. Equine Influenza
   c. Equine Viral Arteritis Virus
   ● Fungal: Primary fungal pneumonia is rare but may occur, especially in immune-compromised horses. Potential fungi include:
   d. Coccidiodes, Cryptococcus, Histoplasma, and Aspergillus

Question 51

Topic: Equine Pneumonia & Pleuropneumonia - 3

1. Name the clinical signs seen in horses with pneumonia.
2. List the clinicopathologic abnormalities.
3. What other diagnostic tests should be done?

Answer 51

1. Intermittent fever/lethargy/depression
   b. Tachypnea
   c. Nasal discharge
   d. Cough
   e. Anorexia/inappetance
   f. Weight loss (chronic; Figure 1)
   g. Pleurodynia
   h. Exercise intolerance
   i. Abnormal thoracic auscultation (crackles, wheezes)
2. Clinicopathologic Abnormalities
   a. Leukopenia (acute) to leukocytosis (chronic)
   b. Hyperfibrinogenemia
   c. Hyperglobulinemia
   d. Hypoproteinemia/Hypoalbuminemia
   e. Anemia

3.
A. Xrays of cranio-ventral and caudo-ventral thorax; +/- fluid line, abscesses.
B. Ultrasound: +/- free fluid within pleural space, pleural thickening, fibrin deposition, lung consolidation.
C. TTW + bacterial culture
D. +/- Collection of pleural fluid if present
E. CBC/Chem/Arterial blood gas

Question 52

Topic: Equine Pneumonia & Pleuropneumonia - 4

1. How is this condition treated?
2. What is the prognosis of this disease?

Answer 52

1. A. Antimicrobial therapy: ideally based on culture and sensitivity testing.
   - May include penicillin or a cephalosporin coupled with an aminoglycoside; consider metronidazole for anaerobes.
   B. Anti-inflammatory drugs: judicious use of flunixin meglumine may help with fever, pain, inflammation and general attitude and appetite.
   C. General supportive care such as maintaining hydration and oxygenation and providing a high calorie, palatable diet are necessary.
   D. Laminitis can occur as a result of endotoxemia; measures to “prevent” laminitis should be considered.
   E. Thoracocentesis and indwelling chest tube may be indicated when large amounts of pleural fluid are noted (Figure 4).
2. Fair to good if appropriate therapy is instituted immediately
   - Anaerobic infections tend to be worse than aerobic infections) and development
   of complications (laminitis, coagulopathy, hypoproteinemia) may impact prognosis.
   - Prognosis for pleuropneumonia may be guarded to fair; expect long-term therapy and recovery with these cases and be prepared for complications such as laminitis.

Question 53

What is a threat the mother of a R. equi foal takes ? How is the mother treated? How is this controlled on a farm?

Answer 53

• Clostridium difficile enterocolitis: a threat to dams of treated foals.
• Foal’s antibiotics given for lengthy periods: 4 to 9 weeks.
• Dam ingests antibiotics when cleaning foal: affects her gut flora.
• Case fatality rate without treatment ~ 80%.
• Rhodococcus equi control
• On farms with endemic R. equi, control strategies include:
• Isolation of pneumonic foals,
• Avoidance of dust and overcrowding,
• Close monitoring of foals <5 months old, including,
• Monthly checks of fibrinogen concentration and CBC.
• Hyperimmune plasma administration to young foals may reduce the incidence of disease in endemic situations.

Question 54

Topic: Equine Asthma
1. List the risk factors of this disease.
2. Describe the pathogenesis.
3. What are the major clinical signs?
4. How is it diagnosed?
5. How is it treated?
6. What is the prognosis?
7. How is it prevented?

Answer 54

1. Warm dry climates, horses kept inside with less turnout, barns with poor ventilation and
   dusty or dirty environments
2. Inflammation of lower airways causes bronchospasm, excess mucus, and airway
   remodeling, leading to partially obstructed airways.
3. Tachypnea, dyspnea, dry cough, Auscultation of a wheezing noise during respiration (especially during end exhalation), “heave line” - chronically affected horses may have a hypertrophied external abdominal
   oblique muscle from chronic muscle effort to exhale.
4. clinical signs, cytology of bronchoalveolar lavage with increased neutrophils for definitive diagnosis.
5. A. Environmental modifications are critical: reduce dust in bedding, feed, etc.; turn out in
   pasture; stabled only with good ventilation.
   B. Corticosteroids, inhaled or systemic.
   C. Bronchodilators (albuterol, ventipulmin), inhaled or oral.
   – Note: Oral antihistamines’ effectiveness unknown.
   – Allergen testing and desensitization.
6. Management and treatment to decrease and control disease flares but it’s a chronic
   disease that is rarely “cured.”

Question 55

Topic: Lungworms
1. Etiology
2. C/S
3. Diagnostics
4. Tx

Answer 55

1. Dictyocaulus arnfieldi
   * Donkeys are often the source of that infect horses.
   - Donkeys have patent infections.
   - So testing donkeys is a higher-yield approach.
   - Most adult horses DO NOT have patent infections (a few can but not all).
   * Coughing is common in adult horses.
   * Donkeys usually asymptomatic.
   * Prepatent period is 2 to 3 months.
   * Treatment is moxidectin or ivermectin.

Question 56

Six yearlings on a breeding farm have experienced a sudden onset of severe diarrhea and weight loss.
On exam, the affected horses are thin with ventral edema.

Bright red larvae are evident in the feces of some affected horses.

Which choice is the most likely diagnosis?
A. Stomach worms (Habronema spp.)
B. Ascarids (Parascaris equorum)
C. Cyathostomes (small strongyles)
D. Strongyloides westeri
E. Cryptosporidiosis (Cryptosporidium parvum)

Question 57

Topic: Cyathostomiasis
Missed first slide on this ~ 1 hr inx
1. Etiology
2. C/S
3. Dx
4. Tx
5. Prevention

Answer 57

Dx: Eggs may not be apparent on fecal exams;
- Rectal palpation is normal BUT at necropsy, large intestinal wall may feel gritty, due to the presence of encysted larvae
- Passage of adult cyathostomes does not necessarily indicate illness
- Symptoms are due to the emergence of hypobiotic larvae into the intestinal lumen.

Major Gl parasite of concern in U.S. horses.
- 3rd-stage larvae can undergo hypobiosis (arrested development) and encyst in gut wall.
- Hypobiotic larvae can emerge en masse from intestinal wall in late winter and spring.
- They cause severe weight loss and diarrhea.
- Prognosis is guarded if this occurs.

• Rx: Hypobiotic larvae harder to eradicate than adult worms.
• Moxidectin or high dose fenbendazole are the most effective way to control hypobiotic larvae.
• Ivermectin NOT reliably effective.
• Resistance increasingly an issue
• Adults susceptible to common dewormers: benzimidazoles, avermectins, pyrantel salts.
• Prevention
• Regular deworming of all horses on premises
• Removing fecal material regularly from living spaces helps.

Question 58

Topic: Ethmoid Hematoma
1. What is an ethmoid hematoma? What are the major clinical signs?
2. What age range is typically affected?
2. What is the etiology?
3. What diagnostics do you typically run?
4. How is it treated?
5. What happens in refractory cases?

Answer 58

1.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.
2. Older horses
2. Etiology unknown
3.
A. Endoscopy: Usually visible in nasal passages on endoscopy
4.
A. Initial Rx: formalin injection directly into hematoma mass, using endoscopy to guide placement.
B. Electrocautery is indiscriminate and damages surrounding anatomic structures
5. Recurrence is common; Manage recurrence surgically

Question 59

Topic: EIPH
1. What is the signalment for this disease process?
2. What is the main clinical sign?
3. Describe the pathophysiology of this disease.
4. Diagnostics
5. Tx

Answer 59

1. Common in Thoroughbred, Quarter Horses, and Standardbred racehorses
2. The main clinical sign is epistaxis after exercise. This DOES NOT OCCUR IN ALL HORSES WITH EIPH.
   - Other supporting c/s include: decreased performance, labored breathing, loss of speed during
   exercise or competition and/or coughing.
3. The pathophysiology is debatable, but one theory suggests that EIPH results from rupture of pulmonary
   capillaries that are weakened by inflammatory disease, while another hypothesis suggests stress failure of
   pulmonary capillaries.
   - Note: The prevalence of EIPH is related to intensity of exercise rather than duration of exercise, and on necropsy, the caudodorsal lung fields are most commonly involved.
4. A. Blood in one or both nostrils after exercise is an indicator of EIPH.
   B. Endoscopy and cytologic examination of BAL fluid.

5.
A. Furosemide is the most commonly utilized therapy for EIPH AND PERMITTED BY RACING OFFICIALS IF ADMINISTERED 4 HOURS PRIOR TO RACING.
B. Other therapies include: pro-coagulants, Vit K, hormone therapy, nutraceuticals.

Question 60

Topic: Dorsal Displacement of Soft Palate
1. Describe this disease process.
2. Etiology
3. C/S
4. Diagnostics
5. Tx

Answer 60

Epligottis is completely hidden. Normally triangular shaped epiglottis would be visible but in these horses the dorsally displaced soft palate is getting in the way. Makes it hard for horse to breathe properly.

• Common
• Gurgling expiratory sound during exercise
• Caudal border of soft palate DORSAL to epiglottis and the epiglottis not visible on endoscopy
• Often caused by problem with the pharyngeal branch of cranial nerve 10, the vagus
• May be secondary to upper respiratory infections in young horses
• In chronic cases the treatment of choice is the “tie-forward” surgery with about an 80% success rate.

Question 61

Topic: Laryngeal Hemiplegia
1. AKA?
2. What is the signalment?
3. Describe the pathogenesis.
4. What are the major clinical signs?
5. How is it diagnosed?
6. How is it treated?
7. What is the prognosis?

Answer 61

1. Recurrent Laryngeal Nerve Paralysis, Roaring
2. Thoroughbreds, warmbloods, or other large-breed athletic horses.
3. Idiopathic neuropathy of the left recurrent laryngeal nerve causes the left arytenoid
   cartilage to either partially or completely fail to abduct during inspiration, resulting in partial airway
   obstruction.
   – NOTE: Left recurrent laryngeal nerve is the longest equine nerve therefore it is usually the
   affected one. –
4. A. Upper respiratory noise at inspiration during exercise.
   B. Exercise intolerance, poor performance
5. Upper airway endoscopy, most diagnostic while horse is exercising and un-sedated
6. Laryngoplasty (“tie-back”) surgery with or without cordectomy, essentially ties open the left arytenoid cartilage. There is a risk of chronic cough or potential pneumonia if not well-placed.
7. good. Mild cases unlikely to affect performance in low-intensity events.

Question 62

Topic: Eplglottic Entrapment
1.

Answer 62

• Less common.
• Epiglottic mucosa covers the lateral margin and apex of the epiglottis,
• Reduced performance with inspiratory and expiratory noise.
• Endoscopy is diagnostic:
• Outline of epiglottis is visible; but mucosa covers epiglottis, so normal crenated margin is hidden.
• Surgical correction is effective.

Question 63

Myopathy Types To Know:

1. Exertional rhabdomyolysis (“Tying up”), COMMON
   * If sporadic, may be due to simple overexertion
   * Chronically may be polysaccharide storage myopathy [PSSM] or
   abnormal regulation of calcium in skeletal muscle
2. Toxicities, and various other etiologies.
3. Hyperkalemic periodic paralysis (HYPP, inherited mutation)

Question 64

Topic: Exertional Rhabdomyolysis
1. AKA?
2. Define this condition.
3. Describe the pathogenesis of this condition.
4. What are the clinical signs of disease?
5. What diagnostics should you run? What test is provides confirmatory diagnosis? What does this test also do?
6. How is this condition treated?

Answer 64

1. “Tying up”
2. Exertional myopathy in horses is a syndrome of muscle fatigue, pain, or cramping associated with exercise
   Signs after intense exercise
3. Exertional myopathies produce necrosis of striated skeletal muscle. There are two different forms: sporadic and chronic exertional rhabdomyolysis.
   - Sporadic: The most common cause is exercise that exceeds the horse’s state of training.
   - Chronic: There are several forms of chronic exertional rhabdomyolysis including:
   - Type 1 & Type 2 polysaccharide storage myopathy (PSSM) = seen in Quarterhorses, Warmbloods, or Draft horses with abnormal glycogen storage
   - Malignant hyperthermia
   - Recurrent exertional rhabdomyolysis = seen in Thoroughbreds or Standardbreds with abnormal intracellular calcium metabolism.
4. Clinical signs include: Profuse sweating, hard painful muscles with a reluctance to move, Tachypnea, Tachycardia, dark urine –> myoglobinuria.
5. BW: Elevated CK & AST.
   - To confirm diagnosis, perform muscle biopsies (semimembranosus, usually) both confirm and differentiate recurrent exertional rhabdomyolysis from polysaccharide storage myopathy (PSSM).
   - For PSSM (type I) – genetic test
6. Treatment varies depending on the form of exertional rhabdomyolysis:
   A. Acute – analgesics (NSAIDs), vasodilators (acepromazine), +/- IV fluids
   B. Long-term – low starch/high fat diet, daily exercise
   C. For RER – minimize stress, pre-treat with dantrolene (calcium-channel blocker)

Question 65

Topic: Hyperkalemic Periodic Paralysis (HyPP)
1. Categorized as?
2. Onset is?
3. Etiology
4. Signalment
5. C/S
6. Diagnostics
7. Treatment

Answer 65

1. Technically, NOT an exertional myopathy (genetic mutation)
2. Onset is unpredictable
3. Not induced by exercise - Heritable
4. Affected horses are commonly descended from the quarterhorse stallion “Impressive.” Usually diagnosed in young horses (<3 years old).
5. Muscle fasciculations, weakness (sometimes leading to recumbency).
   - Horses appear normal after episodes
   - Diet changes can trigger episodes (especially high-potassium foods) and other stressors.
6. Diagnosis by DNA testing of hair.
7. Management varies:
   - Mild episodes controlled by exercise or ingestion of grain or corn syrup.
   - IV dextrose is preferred therapy for severely affected animals.
   - Avoid high-potassium feeds (alfalfa, molasses).
   - High-fat, low-carbohydrate diets seem to help control symptoms.

Question 66

Topic: Nosocomial Salmonellosis

Answer 66

Nosocomial Salmonellosis:
Severe Acute Colitis
* Nosocomial infection=patient was infected in a clinic or hospital.
- Lots of horses are inapparent carriers of
Salmonella
- Because stressed animals are more susceptible to infection, horses hospitalized for other reasons are at risk for salmonellosis.
* Most common types: Salmonella enterica serovar
Typhimurium and S. enterica Agona.
* ZOONOTIC

• Signs: Some adult horses develop acute colitis
• High fever and watery diarrhea.
• Rapid dehydration, +/- hypovolemic shock
• Horse can die within 24 hours.
• СВС (complete blood count) shows neutropenia. ***
• Acidosis and hyponatremia
• Horses need intensive fluid therapy and correction of acidosis.
• Laminitis can be a sequela to Salmonella septicemia.
• Rx is mainly supportive
• IV fluids and electrolytes.
• Gl protectants (e.g., biosponge, bismuth subsalicylate, activated charcoal) may help to bind bacterial toxins.
• NSAIDs like flunixin meglumine (Banamine) help counteract endotoxin effects, control pain, may help prevent laminitis.
• Low-dose polymyxin B (3,000 units/kg, BID) has been advocated to bind circulating endotoxin.
• Systemic antimicrobial Rx is controversial
• Antibiotics do NOT appear to alter course of colitis or to decrease shedding of Salmonellae.
• In horses with extremely low WBC, broad-spectrum IM antibiotics may be given to prevent secondary infections.

Question 67

Topic: Potomac Horse Fever Enterocolitis
1. Etiology
2. Transmission
3. C/S
4. Diagnostics
5. Tx

Answer 67

• Caused by Neorickettsia risticii
• Carried by trematodes in a snail vector
• Horses pastured near water at risk.
• Related to Neorickettsia helminthoeca, agent of salmon poisoning in dogs.
• Acute enterocolitis syndrome
• Mild colic, fever, and diarrhea
• Horses of all ages
• Laminitis and abortion may follow.
• Diagnosed by PCR of blood or feces
• Rx = oxytetracycline,
• If given early in disease, response usually w/in 12 hr
• Overall case fatality rate 5%-30%.

Question 68

Topic: Equine Tetanus
1. Etiology
2. Transmission
3. C/S
4. Diagnostics
5. Treatment
6. Prevention

Answer 68

• Caused by a neurotoxin produced by Clostridium tetani.
• Anaerobic inhabitant of the soil and of animal intestinal tracts.
• Horses are very sensitive to the neurotoxin.
• C. tetani grows in necrotic tissue.
• Disease is usually preceded by a puncture wound.
• Tetanus signs
• Prolapse of the third eyelid
• Erect tail and ears
• Dilation of the nares
• “Sawhorse” stance
• Diagnose by clinical signs and history
• Treatment
• Tranquilization/sedation
• 5,000-50,000 IU tetanus antitoxin bid
• Wound drained, penicillin
• Tetanus immunization and booster annually
• Mortality is high (80%)
• Prevention: Immunize broodmares with tetanus toxoid 4 to 6
  weeks PRE-partum.

Question 69

Topic: Theiler’s Disease:
Acute Equine Hepatitis
1. Caused by?
2. C/S
3. Dx
4. Tx

Answer 69

• Most common cause of acute equine liver disease.
• Associated with biologics, e.g. tetanus antitoxin
• Mares that receive tetanus antitoxin at foaling at risk of acute hepatitis.
• See icterus, anorexia, hepatic encephalopathy.
• Dx: Hepatic biopsy
• Mortality is high (up to 88%).
• Routine administration of tetanus antitoxin to recently foaled mares is NOT a good idea.
• Recent research indicates a parvovirus is a possible cause.

Question 70

Mortality in horses showing clinical signs from eastern equine encephalitis virus (EEEV) is ?

Answer 70

50%- 90% .

Question 71

Topic: Arboviruses
1. Arboviruses is a portmanteau for?
2. Spread via?
3. List the enzootic arboviruses affecting horses
4. Diagnostics

Answer 71

1. Arbovirus is a portmanteau word (arthropod-borne virus)
2. Spread by mosquitoes or other hematophagous arthropods (e.g., sandflies, ticks)
3. Enzootic arboviruses affecting horses:
   - Eastern Equine Encephalitis
   - Western Equine Encephalitis
   - Venezuelan Equine Encephalitis
   - West Nile Virus

• By the time horses are neurologic, they are no longer viremic. So the blood of febrile stable mates is best way to isolate EEE virus at this point.
• You could do a CSF tap (difficult in a neurologic horse), BUT Diagnosis requires virus isolation, not just cytology. CSF cytology and protein levels might suggest severe CNS inflammation.

Question 72

Which togaviruses can you not differentiate between based on clinical signs alone?
What is the definitive diagnostics method?

Answer 72

1. CANNOT differentiate these togaviruses based on clinical Sx.
   - Eastern equine encephalitis (EEE)
   - Western equine encephalitis (WEE)
   - Venezuelan equine encephalitis (VEE)
2. Definitive diagnosis requires virus isolation.

Question 73

List the regions in which EEE, WEE, and VEE occur

Answer 73

EEE, WEE, & VEE usually occur in specific geographic regions.
- EEE: all states EAST of Mississippi river and a few states west of it.
- WEE: WEST of Mississippi river.
- VEE: enzootic in Florida, the Rockies, and northern plain. (rarely causes disease in horses or people in the U.S.).

Question 74

• EEE and WEE have a bird-mosquito cycle:
• People and horses are dead-end hosts.
• People and horses have low levels of viremia.
• No direct spread among infected horses, people, birds.
• EEE is the most dangerous to people
• WEE & VEE usually cause only mild human disease.
• VEE usually has a rodent-mosquito cycle;
• Horses and people are incidental hosts.
• UN-like EEE and WEE,
  horses infected with VEE can amplify virus; i.e., they can transmit the virus to biting mosquitoes.

Question 75

Topic: West Nile Virus
1. WNV is one of the most recent leading causes of ?
2. How is this disease transmitted to horses?
3. Describe the c/s seen in infected horses.
4. How is this disease diagnosed? How is the diagnosis confirmed?
5. How is this disease treated?
6. What is the prognosis?

Answer 75

1. Human and Equine viral encephalitis since the 1999 U.S. outbreak.
2. WNV-infected mosquito; the virus is transmitted between birds and infected mosquitos –> horses.
3. NOTE: Not all horses infected with WNV develop clinical signs of disease.
   - Horses that are vaccinated against WNV demonstrate reduced, if any, clinical manifestations.
   - If subject does develop c/s, it would look like the following: depressed mental state, ataxia,
   weakness, muscle fasciculations, fever and recumbency.
4. C/S, CSF: elevated protein and mononuclear pleocytosis
   - Confirm diagnosis via:
   A. Antigen (IgM) capture ELISA
   B. Virus isolation
   C. Plaque reduction neutralization.
5. Supportive care including anti-inflammatory medications and fluid therapy
6. Variable, with many horses recovering from WNV infection
   ● One investigation reported a mortality rate of 33%

Question 76

Topic: Togavirus Encephalitis

1. How is this disease transmitted?
2. What are the c/s?
3. How is this disease diagnosed?
4. How is it treated?
5. What is the prognosis?

Answer 76

1. Togaviridae persist in infected, but asymptomatic, wild animals such as birds and small mammals. Different species of biting insects (i.e. mosquitoes) serve as vectors and may, in part, be related to the viral 3distribution. Vector transmission is the most important route that infection spreads.
2. Most profound in non-vaccinated horses and include fever, anorexia, depression, somnolence (sleeping sickness) to hyperesthesia, proprioceptive deficits, recumbency and cerebral/cranial nerve signs (head pressing, propulsive walking,circling, head tilt).
3. A. Clinical signs
   B. Abnormal CSF findings (elevated CSF protein and cell count)
   C. Definitive diagnosis based on serology or necropsy evaluation
4. Primarily supportive and includes anti-inflammatory medications and fluid therapy.
5. EEE has a high mortality rate (75-100%) whereas WEE (20-50%) and VEE (40- 80%) are lower
   - Residual neurologic deficits may be present in horses that do recover.

Question 77

Which of the equine viral encephalitis viruses fall under the Flaviviridae family?

Answer 77

WNV

Question 78

Which of the equine viral encephalitis viruses fall under the Togaviridae family?

Answer 78

EEE, WEE, VEE

Question 79

Topic: Angular Limb Deformities in Foals
1. What valgus deviation is normal in foals? How can it be treated?
2.
3. Tx options

Answer 79

• Valgus deviation up to 6 degrees is normal in foals
• Does not require treatment.
• Stall rest allows mild valgus deformity to correct on its own.
• Corrective hoof trimming also therapeutic
• More severe valgus deformities may be corrected by surgery
• Periosteal transection SPEEDS growth on side where you do it.
• Transphyseal bridging SLOWS growth on side where you do it..

Surgical options:
- Hemi-circumferential periosteal transection on lateral (concave) aspect of radius
-Or-
- Transphyseal bridging of medial (convex) side of radius
-Or-
- Some combination of both techniques.

Question 80

Topic: Septicemia in the Neonatal Foal

1. What is the biggest risk factor leading to septicemia?
2. Etiology
3. Clinical signs
4. Treatment

Answer 80

• Failure of passive transfer of maternal antibodies is biggest risk factor.
• Gram-negative infections are common.
• But gram-positive bacteria are often contributing factors.
• Endotoxin release from gram-negative bacteria contributes to septic shock.
• Clinical signs: initially depression, but progress to septic shock.
• Recumbency
• Muddy mucous membranes
• Hypotension
• Dehydration
• Tachycardia
• Treatment
• Broad-spectrum antibiotics, usu. penicillin and amikacin
• IV fluids and plasma transfusions are routine
• Hyperimmune plasma administration should be considered
• Nutritional support is very important
• Intensive care of up to one month is typical
• Survival rates >50% are expected at referral hospitals

Question 81

Topic: Tyzzer’s Disease
1. Etiology & transmission
2. Signalment
3. C/S
4. Diagnostics
- What is seen on necropsy?
5. Treatment

Answer 81

1. Clostridium piliforme (gram-negative, spore-forming, intracellular organism), Route of infection is assumed to be by ingestion.
2. Neonatal foals ~1 - 6 weeks of age most often affected.
3. A. Acute necrotizing hepatitis with multisystemic consequences
   - Convulsions caused by profound hypoglycemia.
   - Affected foals usually become comatose and die rapidly.
4. Hyperfibrinogenemia, hypoglycemia, elevated liver enzymes
   - On necropsy: Colitis, lymphoid and focal myocardial necrosis.
5. Supportive care
   - IV dextrose, sodium bicarbonate, potassium chloride, penicillin, and sulfamethoxazole-trimethoprim.

Question 82

Topic: Equine Corneal Ulcers and atropine

Answer 82

• Corneal ulcers very common in horses.
  Image courtesy of Dr. Den
• Often Rx ulcers with topical antibiotic and atropine.
• Atropine causes mydriasis, inhibits ciliary muscle spasm, and minimizes synechiae formation.
• Colic is a possible adverse effect of topical atropine.
• Atropine affects intestinal motility, even to the point of causing cecal impaction.
• Monitor all horses treated w/ topical atropine for colic.
• STOP atropine if:
• Intestinal sounds diminish -or-
• Intestinal transit time is prolonged.

Question 83

Topic: Foaling Related Perineal Laceration

DEscribe grades of perinela lac

Answer 83

Foaling-Related Perineal Laceration
* Common foaling-related injury.
* 1st, 2nd, or 3rd degree.
- 1st-degree tears=mildest: involve only skin and mucous membrane of the dorsal commissure of vulva.
- 2nd-degree lacerations extend to muscle of perineal body but not to anal sphincter or wall of the rectum.
- 3rd-degree tears=worst: extend through rectovestibular shelf and penetrate rectum (rectovestibular fistulas).

Question 84

• 1st- and 2nd-degree lacerations predispose mare to pneumovagina, due to disruption of the vulvar lips.
• 2nd- and some 1st-degree tears need Caslick’s to prevent pneumovagina and urine pooling.
• 3rd-degree lacerations always require surgical
  repair,
• Should delay repair from 3 weeks post-foaling to weaning.
• Allows maximal healing before surgery.

Question 85

Bonus Q

Three weaner pigs in a group of 30 died yesterday. Four more pigs were found dead this morning. A few animals are down and paddling. Some are blind, others are uncoordinated. These pigs have been off-feed for 3 days.
Cultures from necropsy tissue of dead pigs:
* Lungs: Hemophilus parasuis, Streptococcus suis,
Pasteurella multocida;
* Pharynx: Hemophilus parasuis, Streptococcus suis,
Pasteurella multocida;
* Brain: Streptococcus suis;
* Heart: Streptococcus suis; and
* Pleura: Mixed growth, including Proteus spp.

Which choice is the most likely cause of illness in
these pigs?

A. Actinobacillus suis

B. Hemophilus parasuis

C. Pasteurella multocida

D. Proteus spp.

E. Streptococcus suis

Answer 85

C ??? answer on dashboard

Question 86

Topic: Equine Influenza A

1. List the risk factors of this disease.
2. Describe the pathogenesis.
3. What are the major clinical signs?
4. How is it diagnosed?
5. How is it treated?
6. What is the prognosis?
7. How is it prevented?

Answer 86

1. A. This is endemic in the equine population
   B. Outbreaks occur from horses that show or travel with frequent exposure to other horses, especially young horses and racehorses.
2. Inhalation of aerosolized virus from respiratory secretions.
3. Fever, dry cough, mucoid nasal discharge, lethargy, anorexia.
4. Nasal swab PCR
5. A. Anti-inflammatories - Phenylbutazone, Flunixin, Firocoxib
   B. Supportive care.
   - NOTE: Antibiotics used rarely, only for
   secondary pneumonia.
6. Excellent
7. A. Isolating new horses or infected horses with strict biosecurity measures.
   B. Vaccine: modified-live intranasal vaccine or killed intramuscular vaccine. Biannual vaccine in high-risk horses.

Question 87

Topic: Sinusitis

1. Describe the pathogenesis.
2. What are the major clinical signs?
3. How is it diagnosed?
4. How is it treated?
5. What is the prognosis?

Answer 87

1. True sinusitis in horses is almost always secondary to a dental problem. Teeth may be
   clinically normal or abnormal at initial exam. Teeth involved are usually 08-11, with 09 the most
   common; sinus affected is dependent on which tooth is involved.
2. Chronic unilateral mucopurulent nasal discharge, often foul-smelling. Discharge may
   resolve with antibiotics but return when discontinued. Affected animals usually afebrile, BAR otherwise
3. A. Culture and/or PCR of discharge to rule out other viral or bacterial causes of nasal discharge.
   B. Nasal endoscopy to identify neoplasia, masses, etc.
   C. Head and dental radiography, CT; especially to identify dental involvement.
4. A. Extract affected teeth.
   B. Repeated sinus lavage
   C. Culture with appropriate antibiotics, may be extended duration.
5. Good; treatment is intensive

Question 88

Topic: Gastro-Esophageal Obstruction [Choke]

1. List the risk factors of this disease.
2. Describe the pathogenesis.
3. What are the major clinical signs?
4. How is it diagnosed?
5. How is it treated?
6. What is the prognosis?
7. How is it prevented?

Answer 88

1. Older horses with poor dentition or poor dental care, horses that eat rapidly especially in a herd environment, horses fed large quantities of dry grain or pellets.
2. Food bolus not properly chewed into small enough particles and becomes lodged in esophagus. Feed and saliva back up.
3. A. Copious bilateral nasal discharge, usually initially green tinged
   B. Coughing, gagging, retching, ptyalism
   C. If obstruction is not quickly resolved (within 6-12 hours), horses are at risk for true aspiration pneumonia.
4. Clinical signs and inability to pass nasogastric tube into stomach.
5. A. Gentle lavage with water via nasogastric tube, lubricating agents contraindicated due to risk of aspiration.
   B. Sedation: lowers head to reduce risk of aspiration and allows passage of NG tube.
   C. Esophageal muscle relaxants: oxytocin, buscopan.
   D. Antibiotics, anti-inflammatories
6. good if treated early, fair to guarded if treatment is delayed and horse already has pneumonia.

Question 89

Topic: Neonatal Isoerythrolysis

1. Describe the pathophysiology of this disease.
2. How should the foal be treated?
3. What advice should you give the owners if they want to breed again?

Answer 89

1. A Qa or Aa alloantigen + stallion breeds with a Qa or Aa - mare –> mare produces AB against antigens that now her baby possess –> when foal is born and begins nursing, mom’s AB in milk will attack foal’s RBC –> lysis of RBC.

In most cases, the first time a mare has a foal with the antigen, she will not produce sufficient antibodies to cause severe damage to the foal. Therefore, this condition is usually seen in multiparous dams or in mares that have previously had a blood transfusion that exposed them to the red blood cell antigens.

2. Supportive care: ↓ stress, fluids, Abs * Blood transfusion
   * Washed mare RBC (3x washed, suspended in saline)
   * Compatible donor: major & minor crossmatch (Aa-/Qa- donor)
   * Gelding of same breed that never received transfusion

Mare: Screen the mare around 2 weeks before foaling to check for AB. Perform jaundice foal agglutination test (mare colostrum + blood). Can also empty mare with Domperidone + milk out.

Foal: Muzzle foal to prevent nursing from mare, “empty mare”, provide alternative source of colostrum.

Stallion: Breed only Qa and AA negative stallion.

Question 90

Topic: PPID/Equine Cushing’s

1. This is most common in horses of what age group?
2. Describe the etiology and pathogenesis of this condition.
3. What are the clinical signs?
4. How is this diagnosed?What will be seen on bloodwork?
5. How is this condition treated?
6. Younger horses with regional adiposity, laminitis, and insulin dysregulation considered to have?

Answer 90

1. Ages 15 and older.
2. Pars intermedia have melanotropes; only need a little ACTH. In horses, these melanotropes are under negative inhibition from dopamine from hypothalamus. In PPID, hypo does not send dopamine down so either get hyperplasia, adenoma, or microadenoma of melanotropes - make too much of pro-hormone and ACTH.
3. A. Chronic laminitis
   B. Hypertrichosis (long curly haircoat)
   C. Recurrent infections (hoof abscesses, sinusitis)
   D. Loss of topline musculature
   E. Lethargy
   F. Abnormal fat deposition (e.g., supraorbital fat pads)
   G. Polyuria/polydipsia/ polyphagia
4. ACTH stim
   - Stress leukogram, hyperglycemia, low USG.
5. Daily pergolide, a dopamine agonist, to induce the negative feedback from the hypothalamus.
6. equine metabolic syndrome

Question 91

Topic: EPM

1. What type of disease is EPM?
2. Is there an age or breed predilection?
3. Name the etiologic agent.
4. Name the definitive host of this disease.
5. Name the aberrant/dead-end host.
6. Describe the life cycle.
7. What are the key clinical signs ? What are these due to?
8. How is this disease diagnosed?
9. How is this condition treated?
10. What is the prognosis?

Answer 91

1. Neurological disease
2. None
3. Sarcosystic neurona
4. Opossum
5. Horse
6. Opossum releases infective sporocysts into environment –> cat/skunk/raccoon ingests –> opossum ingests sporocyst infested tissue of intermediate host –> horse exposed to opossum.
7. Asymmetric ataxia, weakness, and muscle atrophy due to the organism’s ability to cause multifocal areas of necrosis in random areas of the spinal cord and brain.
8. Difficult to confirm. Can run a western blot analysis of CSF (+), IFA testing. These tests are difficult to interpret.
9. Ponazuril (anti-protozoal). TMS - blocks folate metabolism in protozoa, Nitazoxinade
10. Varies. Some horses can completely recover from EPM with appropriate therapy and have gone on to
    perform normally. Others may have little to no improvement or have residual neurologic deficits

Question 92

Topic: Equine Viral Arteritis

1. How is EVA transmitted?
2. What type of virus is EVA?
3. What does EVA cause in infected horses?
4. How is this diagnosed?
5. How is this treated?
6. How can this be prevented?

Answer 92

1. Venereally - Carrier stallions can infect mares.
   - It can also be spread by aerosol.
2. Equine viral arteritis (EVA) is in the genus Arterivirus, family Arteriviridae
3. It causes vasculitis leading to limb edema, conjunctivitis, rhinitis, and abortion.
   - it is one of the most common causes of upper respiratory tract disease (along with EHV1,4, equine influenza virus, & equine rhinitis virus) as well as abortion.
4. A. Necropsy + histopath of the fetus - usually autolyzed
   B. Culture - fetus and fetal membranes
   C. PCR - fetus and fetal membranes
5. None!
6. Vaccinate!

Question 93

Topic: Cervical vertebral stenotic myelopathy

make on 03/18

Question 94

Topic: Equine degenerative myeloencephalopathy

1. Signalment
2. C/S
3. Dx
4. Tx
5. Prognosis

Answer 94

1. 6 mo - 1 yr old foals
2. Slowly progressive, symmetrical ataxia, hypometria, weakness, etc.
3. A. Low serum vitamin E
   B. C/S, history, response to therapy
   4.Vit E supplementation; Proposed etiology is lack of access to fresh green forage
4. Guarded; tx helps but not curative.

Question 95

Topic: EMND

1. Signalment
2. C/S
3. Dx
4. Tx
5. Prognosis

Answer 95

1. Adult onset (peak ~ 16 yrs of age)
2. Elephant on ball stance, NO ataxia, low head carriage, progressive weakness, etc.
3. A. Low serum Vit E
   B. Sacrocaudalis dorsalis muscle and spinal accessory nerve biopsies
4. Vit E supplementation; Proposed etiology is lack of access to fresh green forage
5. Guarded; tx helps but not curative.

Question 96

Topic: Polyneuritis equi
1. AKA?
2. Signalment & Etiology
3. C/S
4. Dx
5. Tx
6. Prognosis

Answer 96

1. Cauda equine neuritis
2. Any breed or age EXCEPT young foals and very aged horses; Ab against P2-myeline protein
3. A. Urinary incontinence
   B. Fecal impaction
   C. Urine scald
   D. Tail head rubbing
   E. Analgesia and areflexia of tail, anus, perineum, rectum, and penis
4. Based on C/S since ELISA gives many false +
   A. CSF: mononuclear pleocytosis, xanthochromia, elevated protein
   B. EMG
5. Nursing care
6. Poor for functional recovery

Question 97

Topic: Uroperitoneum

make on 03/18

Question 98

Topic: Mare Reproductive Loss Syndrome

make on 03/18

Question 99

Topic: Stringhalt

make on 03/18

Question 100

Topic: Vesicular Stomatitis

1. Vesicular stomatitis is caused by what type of virus?
2. How is this disease transmitted?
3. What are the clinical signs?
4. How is this disease diagnosed?
5. How is it treated?
6. How is it prevented?

Answer 100

1. Rhabdovirus
2. A. Direct contact with infected animals with clinical signs of disease (lesions)
   B. Biting insects:
   - Black flies (Simuliidae)
   - Sand flies (Lutzomyia)
   - Biting midges (Culicoides spp)
3. A. Ulcers and erosions of the oral mucosa
   B. Sloughing of the epithelium of the tongue
   C. Lesions at the mucocutaneous junctions of the lips
4. C/S, ELISA
5. Supportive care
6. Vector mitigation, isolating sick animals

Question 101

Topic: Brucellosis in Equids

1. What is the etiologic agent?
2. What are the clinical signs?
3. How is it treated?

Answer 101

1. Brucella abortus
2. Suppurative bursitis, a pus-filled inflammation of connective tissue over the shoulders or poll.
3. A. Complete dissection and removal of the infected bursae, nuchal ligament, and associated necrotic tissues.
   B. Ventral drainage should be established.
   C. Surgery for fistulous withers can be done using local anesthesia in the standing horse. D. Culture of the drained fluid and selection of antimicrobial drugs based on susceptibility patterns of isolated microorganisms can be useful.

Question 102

Topic: Guttural Pouch Anatomic Considerations

1. What does the GP communicate with?
2. In the avg size horse, the GP can hold how many mls of fluid?
3. How many divisions/sections does the GP contain?
4. What structures does the GP contain?

Answer 102

1. The pharynx
2. 300-500 mls
3. The GP is divided into the medial and lateral pouches by the stylohyoid bone. The medial pouch is larger than the lateral pouch.
4. A. CN VII, IX, X,XI, XII (7,9,10,11,12)
   B. Sympathetic trunk
   C. Vascular structures: Internal and external carotid, Maxillary arteries

Question 103

Topic: Guttural Pouch Tympany
1. What is the etiology of this disease?
2. What is the pathogenesis?
3. List the c/s
4. How is this disease diagnosed?
5. How is it treated?
6. What is the prognosis?

Answer 103

1. Congenital; Typically seen in foals. Characterized by nonpainful distension of the GP with air –> noticeable external swelling of the throat-latch region.
2. Unknown. Potentially related to abnormal or excessive mucosal flap at the pharyngeal orifice. The flap may serve as a one-way valve allowing air to get trapped in the GP.
3. Unilateral or bilateral
   A. Soft, non-painful swelling in the throat-latch region of a foal
   B. +/- Respiratory stertor, dysphagia, aspiration pnuemonia
4. Signalment, C/S, radiographic evidence of an air-filled GP
5. Surgical

A. For unilateral tympany: fenestration of the median septum
that separates the two GP compartments.

B. For bilateral: resection or modification of the
pharyngeal orifice may be necessary.

6. Uncomplicated cases have a good prognosis. Horses with dysphagia or aspiration pneumonia have a fair to guarded prognosis

Question 104

Topic: Guttural Pouch Empyema
1. What is the etiology of this disease?
2. What is the pathogenesis?
3. List the c/s
4. How is this disease diagnosed?
5. How is it treated?
6. What is the prognosis?

Answer 104

1. GP Empyema refers to the accumulation of purulent exudate in the GP.
2. GP Empyema occurs secondary to URI. The etiologic agent that typically causes this is Streptococcus equi or zooepidemicus. Another cause could be due to the rupture of the retro-pharyngeal lymph node into the pouch.
3. Nasal dc, regional LN enlargement, +/- dysphagia
4. Confirmatory diagnostic test: endoscopy (exudate seen in GP) or xray (fluid line in GP).
5. A. Aggressive GP lavage
   B. Local and systemic AB
   C. +/- surgical lavage
6. Good to excellent

Question 105

Topic: Guttural Pouch Mycosis
1. What is the etiology of this disease?
2. What is the pathogenesis?
3. List the c/s
4. How is this disease diagnosed?
5. How is it treated?
6. What is the prognosis?

Answer 105

1. GP mycosis is characterized by the development of fungal plaques in the GP that result in clinical signs due to the involvement of vascular and/or neural structures. The plaques are typically present on the dorsal aspect of the guttural pouch.
2. Unknown. Aspergillus is the commonly associated pathogen.
   A. Erosion of the wall of one of the arteries by fungal plaques within the GP results in epistaxis.
   B. Dysphagia results from damage to the cranial nerves within the GP.
3. A. If artery involved = hemorrhage, epistaxis
   B. IF neural structure involved = dyphagia, horner’s syndrome, or facial nerve paralysis
4. Confirmatory diagnostic test = endoscopy
5. Surgical occlusion of affected arteries, antifungal medications (less efficacious). Can also spontaneously resolve.

Question 106

Topic: GI Parasites

1. List the etiologies.
2. What are the c/s?
3. How is this disease diagnosed?
4. How is this treated?
5. Predilection sites for each?

Answer 106

1. • 2. A. Cyathostomes/Small strongyles = diarrhea, weight loss, colic
        B. Large Strongyles: Strongylus vulgaris = colic
        C. Tapeworms - Anoplocephala perfoliata = colic
        D. Roundworms/Ascarids - Parascaris equorum = weight loss, colic, and—in foals—pneumonia
2. Fecal egg count
3. A. Cyathostomes/Small strongyles = Fenbendazole or Moxidectin
   B. Large Strongyles: Strongylus vulgaris = Adults - most antihelminthics, larvae = macrocytic lactones
   C. Tapeworms - Anoplocephala perfoliata = Praziquantel or 2x pyrantel
   D. Roundworms/Ascarids = most antihelminthics work
4. A. Cyathostomes = Cause damage to large intestinal wall and colitis; big parasite of concern
   B. Large strongyles = Larvae migrate through cranial mesenteric artery causing arteritis & loss of blood supply to large intestine
   C. Tapeworms = Attach at ileocecal junction
   D. Roundworms = Large adult worm burden in small intestine leads to impaction

Question 107

Topic: Infectious Abortion

1. List the etiologies of infectious abortion in equids.
2. What are the classic clinical signs for each cause?
3. How is it diagnosed?
4. How is it treated?
5. How can this be prevented?

Answer 107

1. A. EHV-1
   B. EVA
   C. Leptospirosis
   D. Other ascending bacteria, fungal
2. A. EHV-1: Late-term abortion, minimal fetal autolysis, placenta grossly normal; can be an outbreak
   B. EVA: AUTOLYZED fetus
   C. Leptospirosis: AUTOLYZED fetus, icteric
   D. Other ascending bacteria: placenta grossly normal; brown in color, fibrinonecrotic exudate
   E. Fungal: thickened placenta, minimal fetal autolysis
3. Necropsy, fetal and placental PCR, culture, Histopath
4. None
5. A. Vaccinate - lepto, EHV-1, EVA
   B. EHV-1, EVA, Lepto = contagious; Lepto = zoonotic

Question 108

Topic: Foal Diarrhea

List the etiologies, clinical signs, diagnostics, and tx for the most common causes of foal diarrhea.

Answer 108

Question 109

Topic: Sarcoid
1. Etiology
2. Signalment
3. C/S
4. Diagnostics
5. Treatment
6. Prognosis

Answer 109

1. Bovine papillomavirus 1,2
2. NA
3. Can be several forms:
   A. Nodular: raised spherical bumps
   B. Occult: hairless, thinned skin
   C. Verrucuous: warty, scaly
   D. Fibroblastic: hemorrhagic, ulcerated
   E. Malignant/Malevolent
   F. Mixed = MOST COMMON
4. Excisional biopsy
   - If do not completely remove, can trigger aggressive lesion behavior
5. Surgical excision +/- cryoptherapy
   - immunotherapy
6. Guarded due to recurrence

Question 110

Topic: SCC
1. Etiology
2. Signalment
3. C/S
4. Diagnostics
5. Treatment
6. Prognosis

Answer 110

1. Chronic irritation or US exposure
2. NA
3. Thickened, reddened, & ulcerated areas
   - On non-pigmented skin of the face and eyes, penis, and perineal area
   4/5. excisional biopsy + radiation therapy
4. Often recurrs but rarely metastasizes

Question 111

Topic: Melanoma
1. Etiology
2. Signalment
3. C/S
4. Diagnostics
5. Treatment
6. Prognosis

Answer 111

1. NA
2. Gray horse over 10 yrs of age
3. Black nodules under tail, at perineum, lips, prepuce, eyelids, parotid salivary glands, & guttural pouches
4. clinical appearance or fine needle aspirate
5. Cimetidine
6. May become locally aggressive or [uncommonly] metastasize

Question 112

Topic: Habronema
1. Etiology
2. Signalment
3. C/S
4. Diagnostics
5. Treatment
6. Prognosis

Answer 112

1. Larvae of the stomach worm migrate and emerge creating granulomatous lesions, usually around the eye, male genitalia, or lower extremities. Inside granulomas you can find dead larvae.
2. NA
3. AKA summer sores
4. Sulfur granules, biopsy
5. Local steroids, antihelminthics, removal/cryotherapy
6. Chronic, difficult to eliminate, can reoccur

Question 113

Topic: Onchocerca
1. Etiology
2. Signalment
3. C/S
4. Diagnostics
5. Treatment
6. Prognosis

Answer 113

Onchocerca. Onchocerca can cause dermatitis in the horse due to hypersensitivity to dying microfilariae.

Lesions include alopecia and scaling of the ventral midline, face, and pectoral region. Often lesions are diamond shaped and there may be a “bull’s eye” lesion on top of the head.

Onchocerca is nonseasonal, in contrast to culicoides hypersensitivity and variably pruritic.

Ocular lesions can also occur with onchocerca including uveitis, conjunctivitis, and keratitis.

Tx: Ivermectin

Question 114

Topic: Red maple toxicosis

Answer 114

Question 115

Topic: Black walnut toxicosis

Answer 115