Horses

Question 1

Corneal Ulcers

Answer 1

Classic case:Acute onset of unilateral blepharospasm, photophobia, miosis, epiphora, corneal edema

Dx:Thorough ophthalmic exam with ophthalmoscope, fluorescein stain positive

Rx:

Topical antimicrobials, atropine (mydriatic to decrease iridocyclospasm and improve drainage), and anticollagenases (e.g., serum, EDTA), +/- antifungals

Systemic nonsteroidal anti-inflammatories

Use subpalpebral lavage system if patient is difficult or ulcer is severe

Surgical - conjunctival grafts for severe cases

Pearls:

NEVER use steroids when an ulcer is present

Main differential is recurrent uveitis – has similar clinical signs butNOfluorescein uptake. Rx is topical steroids

Desmetoceles and stromal abscessesare sequelae to corneal ulcers that are CRITICAL but havenostain uptake because all endothelium is gone or covered over, respectively

Question 2

Sinusitis

Answer 2

Classic case:Mucopurulent unilateral nasal discharge +/- facial swelling and epiphora; often malodorous

Dx:

Radiographs to identify sinus or tooth pathology

Upper airway endoscopy to evaluate drainage angles and rule out other causes of discharge

Thorough dental examination

Rx:Sinus trephination/flap and lavage +/- removal of mass or offending infected tooth; long-term antibiotics

Pearls:

Primary - due to upper respiratory infection

Secondary (more common) – due to dental disease, sinus cyst, ethmoid hematoma, or neoplasia

Chronic has guarded prognosis for resolution

Question 3

Pituitary pars intermedia dysfunction (PPID, a.k.a. Cushing’s disease)

Answer 3

Classic case: Horse or pony over 15 years old with chronic laminitis, hypertrichosis (long curly haircoat), recurrent infections (hoof abscesses, sinusitis), loss of topline musculature, lethargy, abnormal fat deposition (e.g., supraorbital fat pads), and polyuria/polydipsia/ polyphagia
Dx:
Increased resting plasma ACTH level
Positive thyrotropin-releasing hormone stimulation test (more sensitive)
Measure fasting insulin or do insulin sensitivity testing because most horses with PPID also have insulin dysregulation
Rx: Daily pergolide (a dopamine agonist); have to increase dose over time as disease progresses
Pearls:
Lack of dopaminergic inhibition of the pituitary pars intermedia by hypothalamus leads to development of functional adenoma in pituitary pars intermedia. See increased ACTH, alpha-MSH, beta-endorphin, and cortisol
Younger horses with regional adiposity, laminitis, and insulin dysregulation considered to have “equine metabolic syndrome”

Question 4

Colitis

Answer 4

Classic case: Depression, inappetance, variable colic, decreased or hypermotile GI sounds, fever, variable degrees of shock/hypoperfusion, +/- watery or hemorrhagic diarrhea
Dx:
Fecal PCR panel (for Salmonella, Clostridium perfringens, C. difficile, Potomac horse fever [PHF], coronavirus), fecal egg count (for cyathastomiasis)
Abdominal ultrasound to assess colon wall thickness (esp. right dorsal colon for NSAID-associated)
+/- Abdominal radiographs to look for sand
Routine labwork shows dehydration, abnormal electrolytes, WBC count (usually neutropenic), protein levels (usually hypoalbuminemic)
Rx: Biosecurity and …
Supportive care – IV fluids and electrolytes and colloids
Anti-endotoxics/anti-inflammatories (e.g., flunixin meglumine, pentoxifylline, polymyxin B, hyperimmune plasma)
Antidiarrheals (e.g., bismuth subsalicylate, Biosponge)
+/- Antibiotics (metronidazole for clostridiosis, oxytetracycline for PHF, otherwise controversial)
Put feet in ice-water slurry to prevent laminitis

Pearls:
Can be mild or severe and life-threatening with huge costs
Salmonellosis and clostridiosis can be zoonotic
For over 50% of cases, there is no definitive diagnosis
“Colitis X” is idiopathic colitis (sometimes antibiotic- or stress-associated)

Question 5

Sepsis in foals

Answer 5

Classic case: Foal less than 14 days old with lethargy, decreased nursing, +/- obvious septic foci (joint effusion, omphalophlebitis, diarrhea, or pneumonia)
Dx:
Blood culture is gold standard but takes 4-7 days
Increased or decreased neutrophils with bands
Increased lactate
Check blood IgG to assess for failure of passive transfer (less than 400 mg/dl)
Ultrasonography/radiography
Rx: Broad spectrum antimicrobials, IV fluids & plasma, anti-endotoxin therapies, nutritional support; treat specific infections (e.g., lavage joint for septic joint, anti-diarrheals for diarrhea, nebulization for pneumonia)
Pearls:
Good prognosis at referral centers with aggressive treatment
CHECK ALL FOALS for adequate passive transfer at 12-24 hours of age to help decrease risk of sepsis
Gram-negative pathogens most common
Foals’ conditions deteriorate rapidly so any decrease in nursing or lethargy in a young foal is an emergency!

Question 6

Infectious Abortion

Answer 6

Classic case: Pregnancy loss after placental development (about 40–45 days)
Equine herpesvirus-1 (EHV-1) – late-term, minimal fetal autolysis, placenta grossly normal; can be an outbreak
Equine viral arteritis (EVA) – fetus autolyzed
Leptospirosis - icteric, autolyzed fetus
Other bacteria/ascending placentitis – grossly edematous, brown, placenta with fibrinonecrotic exudate
Fungal – thickened placenta, minimal fetal autolysis
Dx: Necropsy of fetus & fetal membranes with culture, histopathology, PCR
Rx: None
Pearls:
Prevent viral and leptospiral abortion by vaccination
Poor perineal conformation is risk factor for ascending placentitis
Most common cause of noninfectious abortion is twinning
EHV, EVA, and lepto are contagious and lepto is zoonotic!

Question 7

Exertional rhabdomyolysis(“tying up”)

Answer 7

Classic case:

Hard and painful muscles

Reluctance to move

Weakness

Recumbency

Dark urine due to myoglobinuria

Two most common chronic types affect skeletal muscle:

Polysaccharide storage myopathy (PSSM) – Quarterhorse, Warmblood, or Draft horse with abnormal glycogen storage

Recurrent exertional myopathy (RER) – Thoroughbred or Standardbred with abnormal intracellular calcium metabolism

Dx:

Increased serum muscle enzymes (CK, AST, LDH), +/- azotemia if myoglobinuria

For PSSM (type I) – genetic test

For RER and others – muscle biopsy

Rx:

Acute – analgesics (NSAIDs), vasodilators (acepromazine), +/- IV fluids

Long-term – low starch/high fat diet, daily exercise

For RER – minimize stress, pre-treat with dantrolene (calcium-channel blocker)

Pearls:

Acute renal failure associated with myoglobinuria is not uncommon in these cases

Many other types of myopathies, e.g.: immune-mediated myositis, pasture-associated/atypical myopathy, nutritional myodegeneration, malignant hyperthermia

Question 8

Strangles

Answer 8

Streptococcus equisubsp.equiinfection)

Classic case:

Typically young horse with fever, then…

Mucoid to mucopurulent nasal discharge

Lethargy

Submandibular/retropharyngeal lymphadenopathy

Difficulty swallowing & inspiratory respiratory noise

Dx:PCR or culture on nasopharyngeal or guttural pouch wash or abscessed lymph node exudate

Rx:

Drain & lavage abscess

Antimicrobials (procaine penicillin = Rx of choice) for horses with dyspnea & severe lethargy; otherwise controversial

Supportive care/tracheotomy in horses having difficulty breathing

Pearls:

Transmission via fomites & direct contact

HIGHLY CONTAGIOUS & host adapted

Treat all suspect cases as possible strangles until proven otherwise (i.e., strict biosecurity!)

Complications worsen prognosis – purpura hemorrhagica, guttural pouch infection, bastard strangles

Question 9

Viral Upper Respiratory Tract Disease

Answer 9

Classic case: Typically an outbreak with…
Increased severity in younger horses
Fever, lethargy, & anorexia
Serous nasal discharge
Submandibular lymphadenopathy
Cough
Dx:
Most common causes include: equine herpesvirus-1 (EHV-1) and -4, equine influenza virus, equine rhinitis virus, equine viral arteritis
PCR on nasal swab for viral antigens – rapid turnaround
Paired titers take too long (3-4 weeks)
Rx: Nonsteroidal anti-inflammatories, supportive care; antibiotics only if worried about secondary bacterial infection
Pearls:
Excellent prognosis in uncomplicated cases
EHV-1 can also cause neurologic disease and abortion

Question 10

Laminitis

Answer 10

Classic case:
Horse walks with hind feet under & forefeet extended (due to forelimb pain); appears to “walk on eggshells” & is reluctant to move
Weight shifting (treading)
Recumbency in severe cases
Prominent arterial digital pulses, warm feet

Dx:
4 Main etiologies – systemic inflammatory response syndrome-associated, endocrinopathic, support-limb, and traumatic
Physical exam findings - positive response to hoof testers over the toes
Radiographic changes - (absent in acute or mild cases)
Thickening of hoof-lamellar interface
Rotation/sinking of 3rd phalanx
Gas lines up dorsal hoof wall
Periosteal proliferation of dorsodistal 3rd phalanx (when chronic)

Rx:
Distal limb cryotherapy (esp. in acute phases)
Sole support & stall rest in acute phases
Pain relief (NSAIDs, opioids)
Corrective trimming & shoeing during chronic phase
Address underlying cause!!

Pearls:
Prognosis guarded
Chronic cases have external divergent hoof rings

Question 11

Gastrointestinal Parasitism

Answer 11

Classic case:Depends on type of parasite, but often weight loss, ill thrift, poor coat

Cyathostomes (small strongyles) – diarrhea, weight loss, colic

Large strongyles (Strongylus vulgaris) & tapeworms (Anoplocephala perfoliata) – colic

Roundworms (Parascaris equorum) – weight loss, colic, and—in foals—pneumonia

Dx:Fecal egg count

Rx:Use manure removal and pasture rotation!

Encysted cyathostome larvae – fenbendazole (2x dose for 5 d) or moxidectin

Large strongyles – adults susceptible to most anthelmintics; larvae to macrocyclic lactones

Tapeworms – praziquantel or 2x pyrantel

Roundworms – most anthelmintics work

Pearls:

Cyathostomes

Emerge in favorable climate conditions (wet and not too hot or too cold)

Cause damage to large intestinal wall and colitis

Currently biggest parasite of concern

Large strongyles

Larvae migrate through cranial mesenteric artery causing arteritis & loss of blood supply to large intestine

Cause nonstrangulating infarctive colic

Tapeworms

Attach at ileocecal junction

Cause damage, perforation, & motility disturbances

Roundworms

Large adult worm burden in small intestine leads to impaction

See clinical signs after deworming!

Question 12

Skin Tumors

Answer 12

Classic case: 3 most common are:
Sarcoid
Raised spherical lumps (“nodular”)
Hairless areas w/ thinned skin (“occult”)
Warty & scaly (“verrucous”); hemorrhagic & ulcerated (“fibroblastic”)
Malevolent/malignant
Mixed (most common!)
Squamous cell carcinoma (SCC)
Thickened, reddened, & ulcerated areas
On non-pigmented skin of the face and eyes, penis, and perineal area
Melanoma
Gray horse over 10 years old
Black nodules under tail, at perineum, lips, prepuce, eyelids, parotid salivary glands, & guttural pouches

Dx:
Sarcoid – excisional biopsy (incomplete surgical removal can trigger more aggressive behavior of the lesion!)
SCC – excisional biopsy
Melanoma – clinical appearance or fine needle aspirate

Rx:
Surgical excision +/- cryotherapy, local chemotherapy (cisplatin, 5-fluorouracil), laser therapy
Immunotherapy for sarcoids
Radiation therapy for SCC
Cimetidine for melanomas

Pearls:
Sarcoid suspected due to bovine papillomavirus and spread by flies; guarded prognosis due to recurrence
SCC due to chronic irritation or UV exposure; often recurs but rarely metastasizes
Melanomas may become locally aggressive or [uncommonly] metastasize in grays; malignant melanoma more common in non-gray horses

Question 13

Equine Viral Encephalitis

Answer 13

Classic case:Altered mentation, cranial nerve signs, ataxia, paresis/paralysis

West Nile virus (WNV) – also has fever, fasciculations of face & neck, hyperesthesia, colic

Dx:

4 Main etiologies:

WNV – throughout US and Canada

Eastern encephalitis virus – mortality 50-90%

Western encephalitis virus – less pathogenic and currently less active than others

Venezuelan encephalitis virus – mortality 50-75% and horses are NOT dead-end hosts (vs. they ARE for the other 3)

Cerebrospinal fluid analysis (for all)

IgM capture ELISA (for WNV)

Rx:

Supportive care

Prevent – vaccinate and minimize mosquito exposure

Pearls:

Poor prognosis if animal is recumbent

Rabies always on the list! – so handle all horses with encephalitic signs as if they have zoonotic disease

Question 14

Equine Infectious Anemia

Answer 14

Classic case:Inapparent carrier is most common; also…

Acute – fever, lethargy, thrombocytopenia

Chronic – recurrent fever with anemia, weight loss, ventral edema, petechia

Dx:

Etiology: Lentivirus

Coggins test – AGID (gold standard, takes 24 h)

-or-

c-ELISA (takes 1 h, but more false positives)

Testing must be performed at US Department of Agriculture (USDA)-approved lab & submitted by licensed & federally accredited veterinarian

Rx:None; seropositive horses must either be:

In lifelong quarantine at least 200 yards from other horses

-or-

Euthanized

Pearls:

Lentivirus causes life-long infection

In the US, all horses moved interstate or sold within a state must have been tested negative for EIA at least within the last 12 months

Question 15

Severe Lameness

Answer 15

Classic acute case:

Lame at a walk or nonweight-bearing (4/5 to 5/5 lame onAAEP lameness scale) in 1 limb

4 most common causes are –

Foot abscess – increased digital pulse, sensitive to hoof testers

Septic joint or tendon sheath – effusion of joint or tendon sheath

Cellulitis/lymphangitis – entire limb is swollen & hot, + fever

Fracture/suspensory apparatus breakdown injury – more focally swollen limb, no fever

Dx:

Foot abscess – hoof tester positive, maybe can locate abscess pocket with hoof knife

Septic synovial structure - synovial fluid has increased protein, neutrophils, and lactate

Cellulitis/lymphangitis - ultrasound, Dx of exclusion

Fracture – radiographs

Breakdown injury – ultrasound shows soft tissue injury

Rx:

Foot abscess – paring, poultice, +/- NSAIDs

Septic synovial structure – lavage, systemic and intrasynovial antimicrobials, NSAIDs

Cellulitis/lymphangitis - antimicrobials, anti-inflammatories (NSAIDs and/or steroids), bandaging, cryotherapy

Fracture/breakdown injury – emergency stabilization with splint/bandage; surgical repair for fracture

Pearls:

Prognosis for foot abscess is good

Prognosis for septic synovial structure depends on what structure is affected and how quickly and aggressively Rx’d

Prognosis for cellulitis/lymphangitis is guarded depending on whether acute or chronic, and how quickly and aggressively Rx’d

Prognosis for fracture/breakdown injury depends on location of injury, whether open or closed, degree of soft tissue injury & displacement

Question 16

Atrial Fibrillation (AF)

Answer 16

Classic case:
Athletic horses: exercise intolerance, exercise-induced epistaxis
Pleasure or idle horses: incidental finding
Dx:
Irregularly irregular heartbeat ausculted
Electrocardiogram (ECG) confirms diagnosis
No P waves; instead fibrillation (f) waves with relatively normal-appearing QRS complexes
Irregular R–R interval
Rx:
Don’t treat arrhythmia if underlying cardiac disease (it won’t work and increased risk of fatal arrhythmia) or horse is retired
Do treat if no underlying cardiac disease (“lone” AF) & desire athletic performance
Medical cardioversion: quinidine IV or PO
Transvenous electrical cardioversion: requires general anesthesia
Pearls:
Prognosis good if “lone” AF, poor for athletic performance if AF is secondary to underlying cardiac disease
Large atrial size & high vagal tone predisposes normal horses

Question 17

Equine Gastric Ulcer Syndrome

Answer 17

Classic case:
Can be inapparent
Colic, inappetence
Weight loss
Ill thrift
“Grumpiness,” especially during girthing
Dx: Only definitive diagnostic is fasting gastroscopy
Grading systems based on number and severity of ulcers
Squamous ulceration: most common site is squamous mucosa of lesser curvature just proximal to margo plicatus
Glandular ulceration: most common site is pylorus
Rx:
Proton pump inhibitors (omeprazole) = gold standard
H2-receptor antagonists (ranitidine)
Frequent feeding (turnout) & decrease stress
Pearls:
Prognosis: excellent with appropriate Rx and management changes
Glandular ulcers more difficult to treat than squamous
Very common! At least 60% performance horses have EGUS
Performance horses under constant transport & training stress may require prophylactic Rx

Question 18

Esophageal Obstruction

Answer 18

Classic case:

Ptyalism

Feed material /saliva out of nostrils

Retching, coughing

Palpable lump in esophageal area

Dx:

Clinical signs usually diagnostic

Unable to gently pass nasogastric tube

Advanced cases: esophageal endoscopy, ultrasound

Rx:

Withhold feed & water

Sedation, spasmolytic agents (e.g., Buscopan®), NSAIDs

Pass nasogastric tube & lavage esophagus (make sure head low) if not resolved in 4–6 h

Prophylactic antimicrobials against aspiration pneumonia

Severe, prolonged cases may require IV fluids, anesthesia, or surgical intervention (esophagotomy)

Pearls:

Prognosis excellent for 1st-time/uncomplicated cases

Older horses with dental issues prone to this problem

Complications: aspiration pneumonia; esophageal stricture, diverticulum, or rupture

Improper layperson’s term is “choke”

Question 19

Lower Airway Inflammatory Disease

Answer 19

Classic case:

2 most common types have similar clinical signs: chronic cough, mucoid/mucopurulent nasal discharge, exercise intolerance

Recurrent airway obstruction (RAO, heaves):

Older horse with a “heave line” (muscle definition from abdominal expiration)

Wheezing

Tachypnea at rest during episodes

Inflammatory airway disease (IAD):

Any age horse but usually younger performance horse

NO tachypnea at rest

Dx:

Bronchoalveolar lavage (BAL): increased percentage of inflammatory cells (neutrophils for RAO, neutrophils/mast cells/eosinophils for IAD)

Endoscopy is supportive: shows increased tracheal mucus

Rx:

Environmental management = most important!

Decrease dust and allergens

Medications: systemic or inhaled, 2-pronged:

Corticosteroids: antiinflammatory

Bronchodilators: open airways

Pearls:

Prognosis good with environmental modification

Guarded prognosis if chronic, poorly managed RAO

RAO is similar to human asthma

3 components of RAO: mucus production, bronchospasm, and neutrophil accumulation

Question 20

Colic

Answer 20

Classic case:

Abdominal pain: rolling, pawing, looking at side, stretching, kicking at abdomen, recumbency, groaning

Tachycardia & tachypnea

Decreased appetite & fecal passage

Shock in severe cases

Dx:Goal = ID part of the GI tract involved & type of colic

Physical exam: pain level, HR, RR, GI sounds, mucous membrane color & hydration

Abdominal palpation per rectum: location and dilation of GI tract

Pass nasogastric tube (NGT): abnormal if > 2 L net reflux

Abdominal ultrasound: location, motility, and dilation of GI tract; peritoneal fluid evaluation

Abdominocentesis: increased total protein, serosanguineous color, and high lactate suggest need for surgery

Rx:

Sedatives and analgesics: alpha-2 agonists and opioids, NSAIDs

Parasympatholytics (Buscopan®): for spasmodic colic

NGT: decompression +/- enteral fluids (+/- electrolytes, laxatives) if no significant reflux

IV fluids

Surgery: exploratory laparotomy if pain repeatedly refractory to analgesics and/or exam suggests strangulating lesion

Pearls:

Prognosis variable depending on lesion: e.g., good for basic medical colic vs. guarded for strangulating lesion in shocky horse with large amount of small intestine resected

Colic types divided into:

Medical vs. surgical

Small intestinal vs. large intestinal

Strangulating vs. nonstrangulating

3 most common types encountered in practice:

Spasmodic/gas colic

Impaction colic

Strangulating obstruction (e.g., large colon volvulus, strangulating lipoma)

Specific types common in certain horses:

Large colon volvulus in broodmares

Fecaliths in miniature horses

Lipomas in old horses

Enteroliths in Arabians

Question 21

Equine Protozooal Myelocephalitis (EPM)

Answer 21

Classic case:
More common in younger horses (
Wide spectrum of neurologic signs depending on affected area within the central nervous system
Usually multifocal lesions of the spinal cord and/or brainstem
Asymmetric ataxia
Mayhew’s grading system for ataxia (p. 3):
Grade 0: Normal strength and coordination
Grade 1: Subtle to mild neurologic deficits only noted under special circumstances (e.g. while walking in circles)
Grade 2: Mild neurologic deficits but apparent at all times/gaits
Grade 3: Moderate deficits at all times/gaits that are obvious to all observers regardless of expertise
Grade 4: Severe deficits with tendency to buckle, stumble spontaneously, and trip and fall
Grade 5: Recumbent, unable to stand
Asymmetric muscle atrophy
Random, well-demarcated, focal areas of sweating
Tetraparesis or paraparesis
Dx:
Etiology: Usually Sarcocystis neurona ; occasionally Neospora hughesi
Diagnosis based on COMBINATION OF history, clinical findings, geography, prevalence, elimination of other diseases, and labwork
Ante-mortem gold standard: Serum:CSF ratio of titers highly sensitive and specific
SAG2,4/3 titer (ELISA) for S. neurona ; IFAT for N. hughesi
Serum titers:
Positive serum titers mean nothing b/c many horses exposed
Negative serum titers imply absence of disease except in acute cases (retest in 2 weeks)
Bloodwork and radiography to rule out other diseases
CSF analysis: Mononuclear pleocytosis and increased protein
Check out the UC Davis CVM Diagnostic Flow Chart for EPM
Rx:
Long-term antiprotozoal therapy:
Ponazuril or diclazuril VERY safe
Sulfadiazine and pyrimethamine combo is less effective and has more side effects
Short-term anti-inflammatory drugs
Supportive care
Prevention:
Keep opossums off of property
Minimize stress
Pearls:
Prognosis: Guarded to fair; horses with less severe signs tend to do better
“SAG” in SAG2,4/3 titer stands for surface antigens
Life cycle of S. neurona :
Opossum is definitive host
Horse (aberrant dead-end host) ingests sporocysts
Merozoites found in CNS lesions
Life cycle of N. hughesi is poorly understood

Question 22

Cervical Vertebral Malformation & Malarticulation

Answer 22

Classic case:(aka “wobblers”)

Signalment:

Type I CVM (developmental):

Thoroughbreds, warmbloods, and light breeds most common

Usually a few mos to 4 y of age

Males > females

Type II CVM (acquired): Usually seen in middle-aged horses

History of over-conditioning or rapid growth

Progressive ataxia in pelvic limbs or all four limbs (see circumduction)

Weakness of pelvic limbs or all four limbs (see toe dragging)

Thoracic limb hypometria

Thoracolaryngeal reflex or laryngeal adductory reflex (“slap test”) absent

Dx:

Etiology:

Type I CVM:

Developmental, dynamic

Mid-cervical

Type II CVM:

Acquired due to osteoarthritis or trauma

Caudal cervical

Spinal radiography and myelography:

Vertebral canal stenosis

Abnormal articular processes

Angular deformities

Rx:

Surgical decompression and fusion (aka”basket surgery”)

Young horses: Significant calorie and exercise restriction

Older horses: NSAIDs; +/- vertebral facet injections

Pearls:

Prognosis:

Good:

Young horses

Mild clinical signs

Single site involved

Guarded:

Young horses requiring surgery may not return to athletic function

Older horses

Chronic signs

Poor: Multiple site involvement

Question 23

Central Nervious System Injury

Answer 23

Classic case:

Signalment and history:

Young, fractious, athletic horse

Acute onset

History of fall or thunderstorm

History of flipping over backwards:

Basilar bone fracture due to pull from rectus capitus ventralis muscles

Bleeding from ear, nose, or mouth

Pain, sweating

Forebrain trauma:

Coma, semicoma, somnolence

Dementia

Wandering in circles

Seizures

Cortical blindness

Brainstem trauma:

Strabismus

Nystagmus

Ataxia

Facial nerve deficits

Spinal trauma

Ataxia

Para- or tetraparesis

Paraplegia (“dog-sitting”)

Urinary and/or fecal incontinence

Fractures involving middle/inner ear:

Cranial nerve VII deficits: Ipsilateral facial paralysis (drooping ear, lip)

Cranial nerve VIII deficits: Ipsilateral vestibular deficits (nystagmus - fast phase away from lesion, ataxia)

Paraplegia (“dog-sitting”)

Urinary and/or fecal incontinence

Dx:

Skull/spinal radiographs

MRI/CT

+/- CSF analysis if unsure injury occurred

Rx:

Check airway, stop bleeding, treat shock

Sedation if needed for thrashing (α-2 agonists)

Diazepam for seizures

Antibiotics and tetanus prophylaxis if open wounds or bleeding from orifices

Mannitol for coma or semicoma if duration > 10 minutes

NSAIDs for pain

Surgical debridement

Decompressive surgery and stabilization

AVOID STEROIDS in head trauma (controversial in spinal trauma)

IV DMSO often used but no clear benefit and not licensed for use

Perform serial neurologic exams to determine progress and prognosis

Time is often the best treatment

Pearls:

Prognosis:

Brain injury: Guarded (40-60% survival depending on type and location of injury)

Spinal injury: Guarded (depends on location and severity for return to function)

Grave: If bilateral pupil dilation with coma

Most spinal injuries occur between C1 and T2

Question 24

Clostridial Neurotoxin - botulism & tetanus

Answer 24

Classic case:

Acute onset

Botulism:

Any age affected; in foals called “shaker foal syndrome”

History of food change, especially round bales

Flaccid tetraparesis to tetraplegia

Dysphagia

Hypersalivation

Liquid in nares after drinking

Muscle tremors (fasciculations), especially in foals

Remember: Tongue, tail, and eyelids (poor tone):

Wet, slippery, flaccid tongue

Flaccid tail

Lack of audible click of palpebral reflex

+/- Dyspnea, cyanosis, ileus, dilated pupils

Tetanus:

History of omphalitis, recent injury, recent surgery

Stiff, hypometric gait, tailhead elevated

Bloat

Dysphagia

Erect and pulled back ears

Recumbency

Opisthotonus

Prominent (sometimes flickering) nictitating membranes

Flared nostrils

Hypersensitivity to sound and touch

Dx:

Botulism:

Etiology:Clostridium botulinumtoxin

Toxin blocks exocytosis of acetylcholine at presynaptic membrane

Toxin ingested in feed -OR-

Toxicoinfectious: Organism can grow in wound or abscess and produce toxin

Several different neurotoxins: Most common culprits in horses are B, C, and D

Testing:

PCR (best) or mouse bioassay

Grain test: Suspect botulism if horse unable to eat 1 cup of grain within 2 min

Electromyography (EMG)

Isolation ofC. botulinumfrom feed, feces, or wounds

Tetanus:

Etiology:Clostridium tetanitoxin

Toxin blocks neurotransmitter release frominhibitoryinterneurons in the spinal cord and brainstem

Excess firing of neurons due to lack of inhibition

Testing:

History and classic clinical findings

+/- CSF tap to rule out meningitis

Rx:

Botulism:

Antibiotics (but for toxicoinfectious botulism may cause release of more toxin!)

Nursing care (hydration, alimentation, padded bedding, +/-ventilation)

Antiserum if suspected/known type (expensive!)

Prevention:

C. botulinumtype B toxoid vaccination of mares twice in last trimester in areas where common

Keep water and feed sources clean of dead animals

Tetanus:

Darkened, quiet environment

Sedation – phenothiazine, α2 agonist, benzodiazepine, barbiturate

Tetanus antitoxin (unclear if beneficial)

Clean and debride wounds

Antibiotics: penicillin or metronidazole

Prevention:Core annual vaccine guidelines by AAEP

Pearls:

Botulism:

“Shaker foal syndrome” in 1- to 3-month-old foals usually botulinum type B toxin

Prognosis can range from poor to excellent, but adults that are recumbent for more than 24h usually have poor prognosis

Tetanus:

Giving antitoxin to horses vaccinated against tetanus puts at risk forTheiler’s disease

Prognosis:
Good if animal can drink

Fair to good if not recumbent

Poor if recumbent

Question 25

Equine degenerative myelopathy (EDM)/equine motor neuron disease (EMND)

Answer 25

Classic case:
Northeast U.S.
Lack of access to fresh green forage
EDM: (aka neuroaxonal dystrophy)
Signalment:
6- to 12-month-old foals
Familial in Appaloosa, Standardbred, and Paso Fino
Possibly familial in Norwegian Fjord, Arabian, Quarter horse, Welsh pony, and Haflinger
Signs:
Insidious onset
Slowly progressive ataxia
Hypometria
Weakness
Poor thoracolaryngeal reflex (“slap test”)
Poor cutaneous trunci reflex
EMND:
Signalment:
Adult onset (peak of 16 y)
Quarter horses, Thoroughbreds, and similar
Signs:
Standing with all four limbs close together (“elephant on a ball” stance)
Progressive weakness
Increased recumbency
NO ataxia
Muscle and weight loss
Trembling
Low head carriage
Unable to lock stifles
Weight-shifting
Hypometria
Dx:
Etiology: Both are likely a result of vitamin E deficiency
Low serum vitamin E concentration: Not specific, but suggestive
EDM: Diagnosis based on history, clinical signs, serum vitamin E, and response to therapy
EMND:
Sacrocaudalis dorsalis medialis muscle and spinal accessory nerve biopsies
Electromyography (EMG)
Necropsy
Rx:
Vitamin E supplementation
Prevention: Adequate access to vitamin E-rich forage
Pearls:
Prognosis: Guarded; treatment helps, but not curative
EDM: Strong evidence for a familial predisposing component
EMND: Affected horses move better than they stand

Question 26

Herpes Myeloencephalopathy

Answer 26

Classic case:
Usually adult horses
Single horse or epizootic
Acute onset ataxia or recumbency
Urinary incontinence
Ascending paralysis
Stabilize after 24 h
+/- Stupor or cranial neuropathies
Other horses in herd:
Distal limb edema in pregnant mares
Scrotal edema in stallions
Abortions
Respiratory infections
Fever
Dx:
Etiology: Equine herpesvirus 1 (EHV-1):
Typically the D752 strain causes neurologic disease and N752 strain causes non-neurologic disease
Strain-specific disease is not always clear cut and crossover does occur
Diagnosis based on a combination of clinical suspicion and clinical testing (below)
PCR (on nasopharyngeal swab, buffy coat)
CSF from lumbar puncture:
Xanthochromia (yellow-tinged)
Elevated protein
Usually no increase in cell count
Fourfold rise in EHV-1 serum titer over 2 wks (not practical in acute cases)
Rx:
Glucocorticoids for up to 3 d
Nursing care:
Urinary bladder catheterization
Safe environment
Segregation and isolation of affected animals for 21-28 d after clinical signs and new cases stop
Anti-virals (Valacyclovir) and heparin are used on a case-by-case basis
Prevention:
Vaccination may decrease respiratory signs and abortion but does NOT prevent infection nor prevent neurologic disease
Isolate new arrivals for 2-3 wks
Pearls:
Prognosis:
Good for horses that can walk well
Guarded to poor for recumbent horses

Question 27

Neonatal encephalopathy “aka perinatal asphyxia syndrome (PAS) and hypoxic and ischemic encephalomyelopathy (HIE)”

Answer 27

Classic case:
Signalment:
Newborn up to 1 wk of age
Thoroughbreds are over-represented
+/- History of premature placental separation or dystocia
Typical scenario:
First: Normal newborn for mins to hrs
Then: Loses interest in nursing, inability to suckle (dysphagia)
Lethargic, stuporous, comatose
Aimlessly wandering
Central blindness
Opisthotonus
Seizures
Hypotonia
Abnormal vocalization (hence the nickname “barkers”)
Typically afebrile in cases without concurrent sepsis or meningitis
Dx:
Etiology: Thought to be due to unrecognized in utero or peripartum hypoxia, neuronal hypoxia, oxidative stress, or upregulation of the fetal inflammatory response
Diagnosis based on exclusion of sepsis, premature birth, trauma, or meningitis
CSF may be xanthochromic
Rx:
Anticonvulsants
24 h nursing care
Antibiotics due to risk of sepsis and/or hospitalization
Pearls:
Prognosis: Up to 80% survivial and good quality of life if not septic
Previously referred to as neonatal maladjustment syndrome
Madigan squeeze: New technique that shows great promise! Affected foals are squeezed to mimic the birth canal transition. Check out this video, courtesy of Performance Equine Vets

Question 28

Vestibulopathy

Answer 28

Classic case:
Head tilt (ipsilateral) exacerbated when blindfolded
Nystagmus (fast phase opposite lesion)
Ipsilateral ventral strabismus when head is raised
Ataxia:
Staggering
Truncal swaying
Leaning or falling toward side of lesion
Drifting sideways during ambulation
Examiner unable to predict where feet will land during ambulation
Lifts only one foot at a time
Hypometria
Violent thrashing
Rolling
Wide base stance and gait
Circling (toward affected side)
If central disease (brainstem):
Nystagmus may be in any direction, but vertical nystagmus is only seen with central disease
Somnolence
Weakness
Hemiparesis (ipsilateral)
If peripheral disease (anywhere the vestibular nerve passes from the skull to the inner ear):
Typically horizontal nystagmus with fast phase away from lesion; may be rotary or angular, but never vertical
Facial nerve paralysis may be concurrent in some cases of peripheral disease (otitis, guttural pouch disease, temporohyoid osteoarthropathy, trauma) due to close anatomic proximity of facial and vestibular nerves
Bilateral disease will cause wide swaying movements of the head
Dx:
Multiple etiologies:
Central:
Head trauma
EPM
Migrating parasites
Neoplasia
Peripheral:
Temporohyoid osteoarthropathy
Suppurative otitis media/interna
Guttural pouch disorders
Idiopathic
Skull radiography, CT, MRI
Upper airway, guttural pouch endoscopy
CSF analysis if central
Culture and sensitivity of CSF or exudates
+/- Brainstem auditory evoked response
Rx:
Treat infections aggressively with antibiotics or antifungals (at least 2-4 wks)
Treat for head trauma if indicated (see Equine Neuro Part 1)
Ceratohyoidectomy for temporohyoid osteoarthropathy
Pearls:
Prognosis:
Depends on underlying cause
Fair to good with otitis interna/media
Chronic cases don’t do as well
May have residual head tilt
Head trauma is guarded, depending on extent of injury
The most common causes are temporohyoid osteoarthropathy and head trauma
Paradoxical vestibular syndrome occurs in central lesions that involve specific areas of the cerebellum, resulting in a head tilt and circling away from side of lesion

Question 29

Polyneuritis equi

Answer 29

Classic case: (aka cauda equina neuritis)
Any breed or age (except young foals or aged horses)
Urinary incontinence and fecal impaction
Urine scald
Tail head rubbing (see broken tail head hairs)
Analgesia and areflexia of tail, anus, perineum, rectum, and penis (but not prepuce)
Cranial neuropathies (head tilt, facial nerve paralysis, tongue paralysis)
Impotence in stallions
+/- Recent history of vaccination or respiratory illness
Dx:
Etiology: Likely autoimmune
Can measure circulating antibodies to P2-myelin protein via ELISA (many false positives)
Highly based on clinical suspicion - presence of cauda equina +/- cranial nerve involvement
CSF:
Xanthochromia
Mononuclear pleocytosis
Elevated protein
May be normal in some cases
Electromyography (EMG)
Rx:
Nursing care
Frequent bowel and bladder evacuation
Pearls:
Prognosis: Poor for functional recovery

Question 30

Meningitis

Answer 30

Classic case:

Usually neonatal or weanling foals; sometimes adults

Hyperesthesia (tactile and auditory)

Stiff, extended neck

Muscle tremors

Somnolence

Concurrent omphalitis, ophthalmitis in neonates

Lack of suckling reflex in neonates

+/- Fever

If brain involvement (meningoencephalitis):

Seizures

Central blindness

Wandering

Head pressing

Star gazing

Abnormal vocalization

Dx:

Bacteria: Most commonly …

Actinobacillus equuli

Rhodococcus equi

Streptococcus equi equi

CSF:

Neutrophilic pleocytosis (acute): May not occur in neonates or foals if neutropenic from sepsis

Monocytic pleocytosis (chronic)

Increased protein

Negative glucose (can use urine strip to test)

Blood and CSF culture

Rx:

Antimicrobial therapy:

Based on culture and sensitivity

Treat for 2-6 wks

Notes on the blood brain barrier (BBB):

Meningitis compromises the BBB which allows penetration of most antibiotics early on

However, should always try to start with antibiotics that penetrate the BBB as it will heal before treatment is complete

NSAIDs

+/- Plasma for neonates

Pearls:

Prognosis: Guarded to poor (25% survival in foals)

Failure of passive transfer is a huge risk factor in neonates

Question 31

Rabies

Answer 31

Classic case:

Sudden behavoir changes

Agitation

Aggression

Progressive paralysis

Rapid respirations

+/- Rolling (often misinterpreted as colic)

Dx:

Etiology:Lyssavirusin family Rhabdoviridae

Fresh brain tissue sent to a designated laboratory:

Medulla oblongata

Cerebellum

Immunofluorescent microscopy diagnoses 98-100% of cases

Viral isolation via mouse innoculation or tissue culture if immunofluorescent microscopy results are inconclusive

Rx:

No treatment, always fatal

Prevention: Vaccination

Pearls:

Common reserviors/vectors are cats, dogs, skunks, raccoons, foxes, and bats

Zoonotic risk with fatal outcomes

Question 32

Neuroborreliosis (Borrelia burgdorferisensu stricto)

Answer 32

Classic case:
Ataxia
Uveitis
Cranial nerve deficits
Lethargy
Poor tongue tone
Tremors of the muzzle
Spinal pain
Inappetence, weight loss
Blank staring
Spooking
Muscle atrophy
Occasionally:
Lameness
Peripheral neuropathy
Seizures
Cardiac arrhythmias
Dx:
Etiology: Borrelia burgdorferi sensu stricto
CSF-to-serum ratio using Lyme multiplex (detects 3 different antibodies)
Serology:
C6 ELISA antibody test is most often used
Serology alone (positive or negative) is not diagnostic (may indicate infection or exposure)
Prevention: Vaccination is controversial
Rx:
Doxycycline or minocycline
Pearls:
Prognosis: Poor, even with aggressive therapy
Life cycle:
Vector: Ixodes spp. ticks
Tick host: Odocoileus virginianus (whitetail deer)
B. burgdorferi reservoir hosts: Small mammals (esp. Peromyscus leucopus , the white-footed mouse), birds, reptiles
Many horses in the mid-Atlantic region have been exposed and most do not show clinical signs

Question 33

Alphavirus Encephalomyelitides (EEE, WEE, VEE)

Answer 33

Classic case:
Eastern equine (EEE) and Western equine encephalomyelitides (WEE): (5-14 d incubation)
Fever, depression
Altered mentation
Hypersensitivity
Visual impairment
Head droop
Dysphagia
Ataxia
Paresis or paralysis
Seizures
Lateral recumbency with paddling
+/- pruritus
Rapid progression, especially EEE
Venezuelan equine encephalomyelitis (VEE)
May be asymptomatic or mild
Similar neurologic signs as EEE and WEE
Tachycardia
Diarrhea
Colic
Sudden death
Dx:
Etiology: Alphaviruses are arboviruses (ARthropod-BOrne viruses) in the Togaviridae family
EEEV:
Reservoir hosts: Primarily passerines (perching songbirds), +/- rodents
Horses are dead-end hosts
The Culiseta melanura mosquito is the vector
WEEV:
Reservoir hosts: Passerines +/- blacktail jackrabbits
Horses are dead-end hosts
The Culex tarsalis mosquito is the primary vector
VEEV:
Reservoir hosts: Wild rodents
Horses are important amplifiers for epidemic VEE
Many species of mosquitos can be vectors, but also blackflies, mites, and ticks
Serology:
IgM antibody-capture ELISA (EEE, WEE)
4-fold titer elevation in plaque reduction neutralization (PRN) or high titer in an unvaccinated horse
Vaccination may complicate serology results
Viral isolation:
Can only be done during the early febrile stage for antemortem diagnosis
Brain tissue (EEE)
Pancreatic tissue (VEE)
Immunohistochemistry or PCR (EEE)
Lymphopenia (EEE)
Azotemia from decreased water consumption is common
CSF: Neutrophilic or mononuclear pleocytosis (EEE)
Rx:
Supportive care:
Pain control
Tranquilizers and/or anticonvulsants
Fluids, nutritional support
Sling and hoist
Broad spectrum antibiotics for bacterial infections due to injuries or pneumonia
Prevention:
Vaccination
Mosquito repellants (permethrins)
Clear weeds, feces, and stagnant water from barns, paddocks, and pastures
Pearls:
Mortality:
EEE: 50-90%; sudden death may occur; survivors usually have residual neurologic deficits
WEE: 20-50%
VEE: 50-75%
REPORTABLE!
VEE has not been reported in the U.S. since 1971
Human disease is uncommon, but usually occurs approximately 2 wks after equine cases reported

Question 34

West Nile Virus

Answer 34

Classic case:

Many horses are asymptomatic

Mild fever and depression

Asymmetric ataxia or paresis involving one or more limbs

Cranial nerve deficits (facial (CN 7) or tongue (CN 12) paralysis)

Behavioral changes

Hyperesthesia

Hyperexcitable responses to various stimuli

Coarse head and neck tremors

Head droop with secondary facial edema

Sudden death may occur

Dx:

Etiology: An arbovirus,Flavivirus, in the Flaviviridae family

Lineage 1a causes WNV in North America

Vector: TypicallyCulex pipiensin east and midwest, andC. tarsalisin western U.S. (other arthropods are possible)

Reservoir hosts: Predominantly passerines, but also shorebirds, raptors, and owls

Serology:

Elevated IgM antibodies (IgM-capture ELISA)

4-fold PRN IgG titer elevation

Vaccination may complicate serology results (for IgG, but not IgM)

RT-PCR can be useful

Viral isolation: Best detected in thalamus, hypothalamus, rostral colliculus, pons, medulla, spinal cord

Difficult due to low viral load and short viremic period

Requiresbiosafety level 3containment

CSF: Normal to mononuclear pleocytosis with increased protein

Lymphopenia

Azotemia from decreased water consumption is common

Rx:

Supportive care:

Pain control

Flunixin meglumine can help with tremors and fasciculations

Tranquilizers and/or anticonvulsants

Fluids, nutritional support

Sling and hoist

Broad-spectrum antibiotics for bacterial infections due to injuries or pneumonia

Prevention:

Vaccination

Mosquito repellants (permethrins)

Clear weeds, feces, and stagnant water from barns, paddocks, and pastures

Pearls:

Mortality for symptomatic horses is 35-45%

First identified in U.S. in 1999

Fatal illness occurs in corvids (crows, ravens, jays)

ZOONOTIC (birds to humans) but horses and humans are dead-end hosts

Reportable to state vet, then US reports it to World Health Organization

Question 35

Neurotoxins (fumonisin , hemlock, locoweed, yellow star thistle)

Answer 35

Classic case:
Fumonisin:
Apathy, drowsiness
Pharyngeal paralysis
Central blindness
Circling
Ataxia
Lateral recumbency
Icterus
Death
Hemlock:
Poison hemlock:
Weakness
Ataxia
Ptyalism
Colic
Bradycardia
Irregular respirations and respiratory failure
Death
Water hemlock:
Ptyalism
Muscle twitching of lips, ears, and nose
Dilated pupils
Agitation
Bruxism
Seizures
Coma
Death in less than an hour
Locoweed:
Depression
Emaciation
Ataxia
Infertility and abortion
Circling
Heart failure
Yellow star thistle:
Involuntary chewing
Lip twitching
Tongue flicking
Submerging head into deep water
Mouth held open (or tightly closed)
Death from dehydration/starvation due to inability to eat
Dx:
Fumonisin:
Etiology: Mycotoxin produced by Fusarium verticillioides and F. proliferatum growing on moldy corn/maize
History of moldy corn in feed
Necropsy:
Unilateral or asymmetric malacia (liquefactive necrosis) of cerebral white matter (leukoencephalomalacia)
+/- Hepatic necrosis
Hemlock:
Poison hemlock:
Etiology: Alkaloids produced byConium maculatum
Diagnosed by history and clinical signs
Water hemlock:
Etiology: Cicutoxin and cicutol produced by Cicuta spp.
Diagnosed by history and clinical signs
Locoweed:
Etiology:
Certain species of Astragalus or Oxytropis spp. produce swainsonine which inhibits Golgi alpha-mannosidase II
Chronic ingestion causes excess build-up of glycoproteins which damage CNS neurons (metabolic storage disease)
Diagnosed by history and clinical signs
Yellow star thistle:
Etiology: Toxin produced by Centaurea solstitialis inhibits brain’s dopamine transporter system
Diagnosed by history and clinical signs
Necropsy: Malacia of substantia nigra and globus pallidus (nigropallidal encephalomalacia)
Rx:
Fumonisin:
Supportive care
No effective treatment
Prevent by avoiding moldy corn
Hemlock:
Poison hemlock:
Activated charcoal
Saline cathartics
Atropine
Gastric lavage
Stimulants
Tannic acid
Prevention: Herbicidal treatment of plants (2,4-D plus dicamba)
Water hemlock:
Sedatives
Prevention: Herbicidal treatment of plants (2,4-D plus dicamba) or digging up and burning plants
Locoweed:
No treatment
Prevention via various herbicides
Yellow star thistle
No treatment
Euthanasia
Prevention: Various herbicides
Pearls:
Fumonisin: Horses are very sensitive to this toxin and can develop signs after chronic ingestion of only 8-10 ppm
Hemlock:
Poison hemlock: The hemlock moth defoliates the plant and may help in its control
Water hemlock: Herbicidal treatment appears to enhance the plant’s palatability before it dies off
Locoweed: There are more than 300 species of Astragalus and Oxytropis in the U.S., but only 20 or so are toxic locoweeds
Yellow star thistle: This is only ingested when other forage unavailable

Question 36

Clostridiosis

Answer 36

Classic case: Less than 5-d-old (and definitely less than 10 d) foal
Acute
Hemorrhagic diarrhea
Colic
Severe obtundation
Hypovolemic/septic shock
Often rapidly fatal
Dx:
Etiology:
C. perfringens type C (less commonly, type A)
C. difficile can also be found in intestine/feces of healthy foals and adults
Fecal toxin analysis
PCR for C. perfringens
ELISA for C. perfringens and C. difficile
Fecal culture +/- blood culture
Abdominal ultrasound: see necrotizing enterocolitis - thickened bowel wall with gas in the wall
Necropsy: intraluminal hemorrhage and mucosal necrosis of small intestine (+/- colon)
Rx:
Metronidazole PO or per rectum
Supportive care (applies to all these foal diarrheas):
Broad-spectrum antimicrobials to decrease risk of bacterial translocation and sepsis
IV fluids with electrolyte replacement
Correct failure of passive transfer, if present
NSAIDs
Anti-endotoxemics: polymyxin B, hyperimmune plasma
Intestinal adsorbents: kaolin, pectin, bismuth subsalicylate, di-tri-octahedral (DTO) smectite (Biosponge®)
Nutrition: enteral feeding or parenteral nutrition
+/- Lactase administration PO
Prevention:
Improve farm hygiene
Vaccine?
Pearls:
Prognosis is guarded
Can occur in outbreaks or sporadically

Question 37

Salmonellosis

Answer 37

Classic case: Usually foals less than 1 mo old
Diarrhea
Lethargy, poor nursing
Sepsis
Progresses to hypovolemic shock - cool limbs, thready pulses, recumbent
Dx:
Etiology: Most often Salmonella enterica
CBC shows severe neutropenia
Fecal PCR or culture
Rx:
See supportive care guidelines under clostridiosis
Pearls:
ZOONOTIC
Salmonella can be present in healthy horses’ feces
Stress can increase fecal shedding

Question 38

Rotovirus/coronavirus

Answer 38

Classic case:Foals less than 2 mos old

Depression, anorexia

Profuse, watery, malodorous diarrhea

More severe in younger foals

Self-limiting, usually lasts 4-7 d

Dx:

Fecal immunoassay kit

Fecal electron microscopy

Rx:See supportive care guidelines under clostridiosis

Pearls:

Rotavirus more common than coronavirus

Rotavirus destroys enterocytes at tips of small intestinal villi, leading to malabsorption

Often secondary lactase deficiency

Use rotavirus vaccine in pregnant mares

Highly contagious

Question 39

Lawsonia intracellularis (a.k.a. “proliferative enteropathy”)

Answer 39

Classic case: 4-6-mo-old foal
Poor doer, failure to thrive, weight loss
Diarrhea
Pot-belly
Colic
Ventral abdominal subcutaneous edema
Dx:
Usually do both:
Fecal PCR
Serology - IFAT (can be hard to differentiate exposure from disease with 1-time sample)
Abdominal ultrasound: thickened small intestine
Bloodwork: marked hypoproteinemia
Necropsy: silver stain shows characteristic intracellular bacteria in small intestinal tissue
Rx:
Antimicrobials: tetracyclines, erythromycin, or chloramphenicol
Plasma transfusion if severely hypoproteinemic
Pearls:
L. intracellularis is an intracellular bacteria
Does not grow in culture without permissive cell lines
Lipophilic or amphoteric antimicrobials required
Excellent prognosis with recovery
Takes 4-8 wks for full recovery
Causes a protein-losing enteropathy

Question 40

Foal Heat

Answer 40

Classic case: 4-10-d-old foal
Mild diarrhea, NOT malodorous
No other clinical signs
Dx: Usually none
Rule out other causes if necessary
Rx: Usually none
Apply protectant (e.g. zinc oxide or vasoline) around perineum, on hind limbs
Pearls:
Not actually related to mare’s heat cycle because also seen in orphan foals
Most likely due to changes in foal’s GI flora - as foals start eating grain and hay in addition to milk, and as they perform coprophagy to inoculate their GI tracts
Often concerning to owners