Equine Flashcards
Bone Spavin
DJD of the hock (tibiotarsal joint) terminating in the formation of exostoses (cartilaginous outgrowths on bone) and akylosis (abnormal stiffening) of the joint
Bucked shins
Front limb lameness in young (2-3y) thoroughbred or racing QH.
Aka metacarpal periostitis
Metacarpal bone painful on manual compression
Likely due to microfractures in bone from compression due to intense exercise
Bog Spavin
Chronic synovitis in the hock (tibiotarsal jiont) causing obvious distension of joint capsule.
what clin path things do you look for on bloodwork that indicates a muscle injury?
creatinine kinase (CK) aspartate aminotransferase (AST)
Exertional rhabdomyolysis
CS
tx
"tying up" muscle necrosis related to exertion high Crt, CK, AST myoglobinuria Tx: rest, NSAIDs, fluids, dantrolene sodium and methocarbamol
post anesthesic myopathy
CS
tx
localized painful, swollen muscle non-weight bearing on affected limbs increased HR and RR increased CK and AST and myoglobinuria tx: same as exertional rhabdomyolysis
how many joint spaces are in the carpus, stifle and hock
carpus and stifle: 3
hock: 4
which joint spaces communicate in the stifle ?
bottom two: the intermediate carpal joint and carpal-metacarpal joint
which joints comunicate in the hock?
top two: tarsocrual joint and proximal intertarsal joint
polysaccharide storage myopathy seen in what breeds? pathophys CS Dx management
quarterhorses, warmbloods and draft breeds
muscle cannot generate enough energy so they uptake glucose and insulin creating enzyme imbalance and increased synthesis of less branched glycogen
dx: muscle biopsy - (+) for PAS (polysaccharide storage myopathy)
management: consistent exrcise, diet low in carbs and sugar, decrease grass hay
what joint spaces communicate in the stifle?
the femorpatellar joint and hte medial femuro-tibial jiont
recurrent exertional rhabdo
seen in what breeds?
Dx
management
seen in thoroughbreds
dx: muscle biopsy - increased # of central nuclei
management: like polysaccharide storage myopathy - consistent exercise; diet low in carbs and sugar and low in grass hay
where does the DDF insert?
palmar side of P3
where does the suspensory ligament originate and insert?
O: from mid cannon (MC3)
I: onto the dorsal digital extensor ligament at the level of P2
where does the SDF insert?
into the DDF at the level of the pastern joint (P1 & P2)
annular ligament - where the heck is it?
runs laterally like a bracelet just proximal to the fetlock (metacarpal-phalangeal joint)
proximal digital annular joint - where is it?
crosses like an “X” on the palmar side of the fetlock joint
hyperkalemic periodic paralysis seen in what breed? CS Dx Tx and management
quarterhorses - autosomal DOMINANT
mutation of Na channels –> hyperexcitable muscles
CS: muscle fasciulations, prolapse of third eyelid, facial muscle spasm
dx: DNA blood or hair test (HH - definitely have it, NH - carriers)
Tx: decrease K levels in plasma. mild: give karyo syrup and grain. severe: give IV bicarb, dextrose, Ca gluconate and insulin
management: diet low in K (no alfalfa, bran or molasses), regular exercise, acetazolamide (increases K excretion in urine)
white muscle disease - nutritional myodegeneration - nutritional muscular dystrophy
CS
non-inflammaotry degenerative disease of skeletal muscle and cardiac m.
caused by deficiency in Vit. E & Selenium
CS has 3 forms:
cardiac form: seen in foals - acute onset of cardiac decompnesation (heart murmurs, pulmonary edema, dyspnea)
subacute skeletal form: foals - weakness, stiff and spastic gait, tense and painful muscles, dysphagia
chronic myopathy: ADULT horses - masseter atrophy and degeneration - dysphagia, inability to eat, etc.
white muscle disease - dx and tx
Dx: incrased CK, AS, low Se and glutathione
Tx: Vit E/Se injections, oral supplementation
clostridial myonecrosis
agent
pathophys
how to tell the difference between clostridial myonecrosis vs injection site abscess
agent: C. perfringens Type A
occurs most commonly due to injections
will see gram (+) rods and will have anaerobic culture
clostridial myonecrosis
CS
Tx
CS: rapid onset of severe local swelling, heat, pain and crepitus, high fever and tachycardia –> severe toxemia, shock and death
tx: penicillin - double dose every 4 - 6 hours, supportive care, debridement and fasciotomy
how do you diagnose septic arthritis?
if TP > 2.5 and WBC > 20,000
what are the 4 most common locations for osteochondrosis in horses?
“DIRT” - distal intermediate ridge of tibia - in hock
lateral trochlear ridge of femur (cartilage flap)
medial condyle of femur (bone cyst)
fetlock - medial condylar ridge
a flexural deformity of the fetlock and pastern involves what tendon and how is it treated?
SDF only
tx: immoblize by splinting to allow tendons to relax can give oxytetracycline if foal <1 week
a flexural deformity of the coffin joint leads to what? what is it caused by and how is it treated?
deformity of coffin joint leads to club foot.
treated by keeping toe long and adding extensions
sx: cut inferior check ligament
in severe cases can cut DDF but this is considered a salvage procedure only done in young foals <1 year
valgus is a what deformity? how is it treated?
lateral deformity
shorten lateral wall and place medial extensions (place extension on side you want foot to grow!)
varus is a what deformity? how is it treated?
medial deformity
shorten medial wall and place lateral extensions
what is sweeny?
inflammation of suprascapular nerve secondary to trauma of shoulder. common in driving horses
tx = surgical release
fistulous withers - 3 causes
brucella abortis
fractured spinous process of thoracic vertebra
penetrating trauma
what is a slab fracture?
fracture of the 3rd carpal bone
bucked shins
inflammation/stress re-modeling of dorsal MC3 (cannon bone)
splints
tx
bony exostosis (growth) of MC 2 & 4; traumatic may have secondary suspensory desmitis
tx: NSAIDs, rest, neglect
breakdown injury
tx
disruption of suspensory apparatus (suspensory ligament, sesamoid bone, distal sesamoid ligament)
tx w/ arthrodesis of fetlock
navicular disease
CS
tx
degenerative disease
CS: switching leg lameness after palmar digital n. block
dx = MRI gold standard
Tx: rest, NSAIDs shoeing (egg bar shoe)
canker
tx
proliferative pododermatitis
hypertrophy of horn-producing tissues of foot; most common in hindlimbs
- looks like hairy growth around frog
tx = debride and topical abx
sidebones
ossification of collateral cartilages of P3
quittor
tx
necrosis of collateral cartilages - most common in forelimb
often happens due to injury near caudal coronary band
tx: surgical excision
keratoma
tumor that develops in deep aspect of hoof wal
foot abscess
subsolar abscess
most common cause of non-weight bearing illness
dx = hoof testers, +/- blocks, rads
tx = pare out with hoof knife, daily soaking and bandaging (no systemic abx!)
street nail
dx
tx
px
can cause septic pedal osteitis and septic bursitis, non-weight baring, can be serious
dx: rads, arthrocentesis (bursal fluid = increased protein & WBC)
tx: arthroscopy, hospital plate
px: guarded
seedy toe
tx
change in character of the horn such that the inner surface is crumbly and there may be a cavity due to lack of substance. will hear a hollow sound when tapped
tx like absces
sheared heels
tx
asymmetry of heels due to imbalance resulting in one part of hte heel to hit the ground before the other. results in asymmetrical growth.
tx w/ repeated trimmings
ringbone
tx
OA of the phalanges.
tx w/ arthrodesis
stringhalt
tx
involuntary FLEXION of the hindlimb, usually bilateral.
tx w/ lateral digital etensor tenectomy
jack spavin
cunean bursitis, irritation of cunean tendon as a result of bone growth on medial hock
thoroughpin
effusion of tarsal sheath (sheath of DDF)
suspensory desmitis - forelimb vs hindlimb
forelimb - Tx = medical; good px
hindlimb - tx = surgical; poor px
septic navicular bursa - common cause?
usually nail puncture - ALWAYS an emergency!!
peroneus tertius rupture
disrupts stay apparatus.
dx feature is ability to EXTEND hock while FLEXING the stifle simultaneously
abaxial sesamoid block: what does it block, where does needle go?
blocks: palmar digital nerves at fetlock, entire foot and pastern joint
needle: between MC 3 and sesamoid bones
palmar/plantar pastern block
blocks: heel region and navicular
needle: caudal aspect of distal P1 just proximal to bony protuberance of P2
4-point block
needle
block
blocks: palmar metacarpal/tarsal n.; entire fetlock and branches of suspensory ligament
needle: distal aspect of splint bones, DDF and suspensory ligament
MUM block
block
needle
blocks: mid-forearm down (prox. radius and ulna)
needle: musculocutaneous n. + ulnar n. + median n.
fractures of stylohyoid bone (the bone that cuts the guttoral pouch in half) can lead to CN signs from what nerves?
7; 9 - 12
what causes primary sinusitis?
streptococcus species
causes fluid/bacteria bulid up and blocks the nasomaxillary opening (which drains sinuses)
strangles CS Dx tx management
step equi - gram (+)
CS: resp distress, CN deficits (dysphagia, facial paralysis)
dx: culture or PCR, serology available
Tx: if not showing clinical signs, dont give abx. only when showing clinical signs do you give penicillin
management: must have 3 negative cultures before release from isolation. monitor spread with temps.
3 causes of episatxis
- ethmoid hematoma - mass originates on ethmoids
- GP mycosis - fungal invasion of GP that erodes vessels - this is what can lead to fatal hemorrhage - be VERY careful.
- exercise induced pulmonary hemorrhage - common in thoroughbreds after strenuous exercise. dx by seeing blood in trachea
TTW vs BAL
BAL - gets more cells, unsterile, less traumatic
TTW - sterile sample! better for culture
what does heave line indicate?
chronic LOWER airway inflammation
inspiratory trouble =
upper airway issue
expiratory trouble =
lower airway issue
equine infleunza age transmission CS dx tx
younger animals (no carrier) transmission: inhalation CS: high fever, cough dx: PCR nasal swab tx: no therapy - supportive
equine herpesvirus age transmission CS dx tx
herpes 1 and 4
younger animals; latent carriers shed when stressed
transmission: inhalation of nasal discharge, aborted fetuses or placenta
CS: fever, nasal discharge
dx: PCR nasal swab
tx: self - limiting
what is the classic story of equine herpes in a herd?
foals get nasal discharge and get better. then 4 months later, mares that are 7 - 11 months pregnant will have an abortion storm
rhodococcus equi
age
transmission
tx
foals 1 - 6m old
transmission: inhalation; forms abscesses in lungs
tx: macrolide (azithromycin or clarithromycin) + rifampin
*remember macrolides kill adults so wipe foal’s mouth after
recurrent airway obstruction and inflammatory airway disease (non-infectious causes of pneumonia) leads to what clinical sign?
explain the pathophys
end expiratory wheezes
as lung volume decreases during expiration, the narrowed bronchioles collapse shut. this traps air distal to the closure and creates the wheezes heard as airways narrow toward the end of expiration.
what is RAO?
what is a common sign?
how is recurrent airway obstruction managed?
its seen in which horse most?
its an allergic disease like asthma
heave line
manage by reducing inflammation - use STEROIDS (systemic: dexamethasone or prednisolone and inhaled: fluticasone)
manage by reducing bronchospasm: oral - aminophylline/pentoxyfylline. inhaled - albuterol. in emergency - atropine
seen in adult horses (mature)
equine viral arteritis
transmission
CS
dx
arteritis
transmission: venereal w/ resp secretions
CS: fever, conjunctvitis, eyelid swelling, abortion, photophobia
dx: serology
reportable!!!
equine lungworm
dx
tx
Dictyocaulus arnfeldi horses pastured with donkeys!!! will look like heaves case L3 = infective stage primary sign = cough dx: baermann tx: ivermectin, moxidectin, fenbendazole
equine adenovirus
upper resp tract virus normally
can cause lower rest tract in immunocompromised horses - especially foals
most common cause of death in foals with failure of passive transfer
what CN is responsible for menace?
CN 2 & 3
what CN is responsible for palpebral?
CN 5 & 7
what CN is repsonsible for PLRs?
2 and 3
what CN is responsible for dazzle?
CN 2 & 7
CN for eye position
4 & 6
which nerve blocks sensation to upper lid?
frontal nerve block
what nerve block blocks motor to orbicularis oculi?
auriculopalpebral nerve block
equine recurrent uveitis common disease name common in what horse? autoimmune disease related to what? what is a common sign of chronic inflammation in this disease? dx therapy
moon blindness
appaloosas predisposed
autoimmune disease in which lepto may play a role
common sign of chronic inflammation = corpora nigra atrophy
dx: uveitis w/ no ulcer that recurs
therapy: reduce inflammation, if lepto give doxycycline. on eye - topical NSAIDs, topical corticosteroids, atropine
musca autumnalis
vector for what disease?
face fly of horses and transmits larvae from one horse to anotherr.
is the most common vector for tehlazia lacrymalis in horses
what are the clinical signs of horner’s in the horse?
- sweating (ipsilateral head and neck)
- enophthalmos (sinking of eyeball)
- ptosis (drooping)
- miosis (constricted pupil)
- prolapsed 3rd eyelid
(the only CS that is different from small animal is sweating)
most common causes (2) of colic in the foal?
- meconium impaction
2. gastric ulcers
lethal white foal syndrome
overo x overo
intestinal aganlionosis = colic
what does bloodwork look like for Fe deficiency?
microcytic, hypochromic non-regenerative anemia
equine infectious anemia transmission CS dx tx
REPORTABLE
retrovirus transmitted by horse flies or deer flies
CS: acute (hemolytic anemia, petechiae), chronic (mild anemia and thrombocytopenia), lifelong infection - no signs unless stressed
Dx: Coggins test!!
Tx: none - euthanasia
Theileria equi
what is it?
what does it cause?
how is the dz treated?
intra-RBC parasite that ruptures RBCs as they multiply
transmitted by infected ticks to horses
vector for equine piroplasmosis - REPORTABLE!
dx: serology
tx: imdiocarb
red maple leaf toxicosis
gallic acid - strong oxidant
causes hemoyiss and enhanced methemoglobin formation
no tx
moldy sweet clover
blocks vitamin K dependent factors just like warfarin
when you see moldy sweet clover, just think of warfarin bc they have the same treatment
equine granulocytic ehrlichiosis agent transmission CS clin path changes dx tx
agent: anaplasma phagocytophilum (formerly Ehrlichia equi)
transmission: tick borne
CS: fever, anorexia, vasculitis, icteris, petechia, ataxia
clin path changes: neutropenia, thrombocytopenia, hyperfibrinogen, mild anemia
intra-cytoplasmic granular inclusion bodies
dx: PCR on blood
tx: oxytet
Pigeon fever agent transmission CS dx tx
corynebacterium pseudotuberculosis
transmission: flies or fomites (mechanical only)
CS: external abscess, internal abscess, ulcerative lymphagitis
dx: culture abscess or synergistic hemolysis inhibition test (SHITest)
tx: allow external abscess to mature, internal abscess needs systemic abx
which liver enzymes are indications of hepatocellular disease
SDH and AST
which liver enzymes are indications of biliary disease?
GGT & ALP
which enzymes are a measure of liver function?
bilirubin and bile acids
dorso-medial strabismus is indication that which nerve is abnormal?
CN 4 (trochlear) bc it innervates the dorsal oblique m.
medial strabsimus is indication that which nerve is abnormal?
CN 6 (abducent) bc it innervates lateral rectus and retractor bulbi
equine protozoal myeloencephalitis (EPM) transmitted by which parasite? who is DH? IH? CS Dx lesions tx
sarcocystis neurona
DH = opossum
IH = horse, racoon
CS: onset is sudden, asymmetrical, CN deficits = head tilt, facial paralysis, gait deficits = incoordination, weakness, asymmetric
dx = western blot
lesions = perivascular cuffing w/ mononuclear cells
tx = ponazuril and folic acid inhibitors: sulfadiazine and pyrimethamine
EPM = asymmetrical!!! this is in contrast to equine herpes which is symmetrical
EEE virus type vector CS lesion dx px prevention
togavirus
vector: mosquito (culiseta melanura/culex tasalis)
CS: transient viremia, biphasic fever, dementia, head pressing, seizures, blindness, CN deficits, hypermetria, ataxia
lesion: meningoencephalitis with primary involvement of gray matter
dx: CSF = neutrophilia, xanthrochromia; serum = IgM capture, ELISA
px = poor, 90% mortality
prevention: vaccinate - good for 6 months
WEE location virus type vector CS lesion dx px prevention
togavirus
location: midwest to western US
vector: mosquito (culex tarsalis)
CS: No viremia, otherwise just like EEE - biphasic fever, dementia, head pressing, seizures, blindness, CN deficits, hypermetria, ataxia
lesion: meningoencephalitis with primary involvement of gray matter
dx: just like EEE - CSF = neutrophilia, xanthrochromia; serum = IgM capture, ELISA
px = fair to poor <50% mortality
VEE location virus type vector who is the amplifier? CS lesion dx px prevention
togavirus
location: central and S. America, Tx, Fl, CO
vector: mosquito (culiseta melanura/culex tasalis)
horse is the amplifer of VEE; unlike WEE and EEE in which birds are the amplifiers
CS: constant and HIGH viremia otherwise just like EEE - biphasic fever, dementia, head pressing, seizures, blindness, CN deficits, hypermetria, ataxia
lesion: meningoencephalitis with primary involvement of gray matter
dx: just like EE - CSF = neutrophilia and xanthochromia; serum = IgM capture, ELISA
px = poor (>50% mortality)
WNV virus type vector CS dx px prevention
flavivirus
transmission: culex mosquito
CS: acute onset ataxia, fever, muscle fasiculations (primarily facial)
dx: IgM capture ELISA
px: lower morbidity and lower mortality compared to EEE
prevention: vaccination
equine herpes virus: EHV-1 primary concerns CS pathology diagnosis prevention
primary concerns: myeloenephalitis, abortion, rhinopneumitis
CS: rear symmetric ataxia (unlike EPM)
pathology: type 3 hypersensitivity, anterior vasculitis
dx: CS, viral isolation, CSF = xanthochromia, high protein, low cells
prevention: mares more susceptible, vaccination is NOT protective against neurologic form
moldy corn poisoning toxin season what does it cause CS dx tx
fumonisin B1
season: late fall/early spring
affects brain and liver causing severe coagulation necrosis of white matter - leukoencephalomalacia
CS: dementia, blindness, convulsion, death, toxic hepatopathy
dx: ID toxin in feed
tx: supportive care; often fatal in 48 - 72 hrs
what are the 3 disease syndromes in horses caused by botulism?
- forage poisoning - pre-formed toxin ingested via bad hay or silage - type B!
- toxico-infectious = “shaker foals” type B - toxin produced in GI tracts. seen in 1 - 3m foals bc their gastric acidity is not low enough to inhibit organism growth yet
- wound botulism - toxin produced in contaminated wound; less common
Botulism what does it do? CS dx tx
causes neuromuscular BLOCKADE of ACh at NMJ leading to flaccid paralysis
CS: ptyalism, dysphagia, DILATED pupils
dx: exclusion; isolation of organism
tx: polyvalent antiserum/anti-toxin
treating tetanus: toxoid vs anti-toxin
toxoid = inactivated intact toxin from C. tetani
- stimulates active immunity
- given 3 doses from 12w - 12m of age
anti-toxin = antibody to tetanus toxin
- confers passive immunity
- use this in un-protected animals (neonates and adults)
- will bind circulating toxin
Wobblers
doctor name
what are the two different types and what age groups are they seen in?
cervical stenotic myelopathy Cervical vertebral INSTABILITY = foals - dynamic compression during flexion & extension - mal-articulating cervical vertebrae - seen at C3-C4 and C4-C5
Cervical vertebral MALFORMATION = adults (2 - 4y)
- static compression
- common sites: C5-C6; C6-C7
CS of wobblers
hypometric hindlimbs w/ HYPERmetric forelimbs
dx and tx of wobblers
dx: rads, myelography, myeloscopy
tx: stall confinement, NSAIDs, restricted diet, arthrocentesis, sx (“basket” sx)
temperhyoid osteo-arthropathy
what is it
CS
Tx
when stylohyoid bone fuses with petrous temporal bone in GP. when this impinges on CN 7 or 8 it can lead to vestibular disease and/or facial nerve paralysis
CS: acute onset of vestibular disease - head shaking, pain associated with palpation of ear
Tx: medical: SMZ-TMP, NSAIDs; sx = stylohyoid or ceratohyoid ostectomy and tarsorrhaphy.
they can’t blink so you need to prevent KCS!
when does Rectus capitus/longus capitus avulsions occur?
when a horse rears and throw’s its head back and hits its head
grass staggers
CS
activity on GABA causing release inhibition
CS: ataxia, trembling, hypermetria
stringhalt
cause
hyperflexion of hocks
ingestion of dandelion
what is the dx of a systolic LEFT sided murmur in a healthy foal and how should you treat it?
likely physiologic - ignore
what is a continuous grade III heart murmur that is left sided in a foal?
PDA
what is a systolic RIGHT sided heart murmur in a foal?
VSD
what is a pansystolic grade 4 heart murmur with a thrill in a foal?
tetralogy of fallot
what are the clinical signs associated with R-sided heart failure in a horse?
high HR, jugular pulses, generalized venous distension and rarely ascites
what are the two treatment options for converting a horse in atrial fibrillation?
medical: quinidine
procedural: electroconversion
what drugs would you prescribe for a horse with signs of heart disease to slow down the heart rate, increase contractility and cause vasodilation?
digoxin - positive iontrope
ACE inhibitor: enalapril or quinalapril (vasodilator)
hydralazine - arterial dilator
what two valves are most commonly affected by degeneration and endocarditis?
mitral and aortic
elevations in what enzyme indicate damage to cardiac muscle?
cardiac troponin
what are 5 specific causes of myocardial disease?
- bacterial (staph, strep, clostridium)
- viral (EIA, EVA, flu)
- DCM - vitamin E / Selenium deficiency
- gossypol or cassia ingestion
- monensin toxicity
Theiler’s disease: what is it?
CS
Tx
idiopathic acute hepatic disease and serum hepatitis
- most common cause of acute hepatitis in the horse
- associated with tetanus antitoxin and admin of equine immune serum
- CS: hepatic insufficiency, icterus, hepatic encephalopathy, dark urine
- Tx: supportive therapy
Tyzzer’s disease
- agent
- pathophys
- CS
- lesions
- seen most often in who?
- Clostridium piliforme
- oral exposures to spores or contaminated feces results in acute focal bacerial hepatitis
- CS: low glucose, elevated liver enzymes, death is rapid
- lesions: focal areas of necrosis in liver, myocardium and intestines, paintbrush hemorrhage, hepatomegaly
- seen most often in young foals
