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685 Cards in this Set

  • Front
  • Back
5 Viral Respiratory Diseases of Horses
1. Equine Influenza
2. EHV (Rhinopneumonitis)
3. EVA
4. Equine Adenovirus
5. Equine Rhinovirus
Transmission of EI
Envelope in EI contains...
Contains Neuroanimnase and Hemmagglutin
Rare sequele to EI
Why do you always have to update vaccines with EI?
Antigenic Shift
EI: more severe in young or old?
Diagnosis of EI
1. Virus Isolation
2. FA or ELISA
3. Serology (4 fold incr.)
common sequele to EI
Post Viral Allergic Pneumonitis: chronic pneumonitis, COPD, bact. and guttural pouch infections, bronchitis and pneumonia
How often do you vaccinate against EI?
Every 3-4 months
Booster 2-4 wks before show because if only 10 days or less then could have transiet dz.
Transmission of EHV
Inhalation or Ingestion
MC age for EHV
Stain of EHV that can cause abortion and CNS signs
Dx of EHV
Virus Isolation
FA Stain
(note: ELISA can't disting. between EHV 1 & 4
When to vaccinate pregnant mares against EHV?
5,7, 9 months gestation
How often to vaccinate foals against EHV?
Every 3 months
EVA is most prevelent in this breed?
Transmission of EVA
Respiratory Secretions and Venereally
Carriers of EVA
CS are febrile, serous nasal discharge that may become purulent, leukopenia, pharyngeal lymphoid hyperplasia, abortions and CNS signs
CS are acute onset of fever, coughing and nasal discharge
CS are fever, limb edema and stiffness, palpebral edema, rhinitis, conjunctivitis, urticaria, papular eruptions on muc mem., abortions
What 3 things do you worry about in an overweight horse?
1. Lipidosis
2. Laminitis
3. Arthritis
What 3 things do you worry about in an underweight horse?
1. Not enough feed
2. Parasites
3. Teeth
where do teeth get sharp on the maxilla?
on the mandible?
buccal surface on the maxilla and lingual surface on the mandible
(on the top the teeth are sharp on the cheek side and on the bottom the teeth are sharp on the tongue side)
EHV-1 Causes
EHV-2 causes
EHV-3 causes
Coital Exanthema
EHV-4 causes
Respiratory probs
Exuberant Granulation Tissue aka
proud flesh
cause of proud flesh?
poor wound management
An inflammatory response involving the DORSAL lamina of the hoof
4 Causes of Laminitis
Carb overload
Retained Placenta
Excessive Work or Stress
Stance with Laminitis
Sawhorse Stance: rear limbs are placed under body
With Laminitis, where is the positive hoof test at?
The Toe
MC place for laminitis to occur?
Forelimbs (toe pain)
Chronic CS of Laminitis?
Feet Cool to the Touch
No digital pulse
Dropped Sole
Diverging Hoof Growth Lines
Rotation on P3
Dx of Laminitis?
Rads showing rotation of P3
Nerve Block that shows improvement
Nerve Block to Dx Laminitis?
Palmar Digital Nerve Block
Tx/pain relief for acute laminitis?
Bute, Banamin
Frog Support used with Acute Laminitis?
Lily pads
Heart Bar Shoe
Way to reduce stress on lamina with laminitis
Wedge pad heel that reduces the pull of the DDF
Vasodialators used with Laminitis?
Nitroglycerin Patches
Why is heparin used to treat laminitis?
Activates reticuloendothelial system
Decreases clotting in foot microvasculure
Used to reduce inflammation in laminitis?
General Treatment for Acute Laminitis?
Pain Meds, Frog Support, Heels that reduce strain on DDF, Vasodialators, Heparin, Anti-inflammatories
Surgical Treatment for Chronic Laminitis?
1. Dorsal Hoof Wall Resection
2. Full thickness hoof wall resection
3. DDF Tenotomy
4. Inferior Check Ligament Desmotomy
Dorsal Hoof Wall Resection
remove toe and reshape hoof parallel to P3
Full thickness hoof wall resection
drain necrotic debris, allows for new hoof growth
DDF Tenotomy
For pasture soundness only
Inferior Check Ligament Desmotomy
Reduces the pull of the DDF

Allows for an athletic career
MC cause of lameness
Subsolar Abcess
cause of subsolar abcess
1. Puncture wounds at the frog
2. Puncture wounds at the white line from gravel
where do puncture wounds at the frog drain?
At the heel between the sensitive and insensitive frog
where do puncture wounds at the white line drain?
At the coronary band
Tx of Subsolar Abcesses?
Estab. Ventral Drainage
Maintain Drainage with Epson Salt and Ichthammol
Antibiotics in foals
Mares repro barriers
1. Vulva lips
2. Vestibular Sphincter: vulvovestibular junction
3. Cervix
Normal Vulvar Conformation
The dorsal commisure of the vulva should be even or tightly below the bony floor of the pelvis
pustules or ulcerations on the labia of mares or the penis of stallions
Equine Coital Exanthema
safe to breed horse with Coital Exanthema when?
3 weeks after lesions go away
Treat Melanoma (small nodules that can metastisize) of the vulva with?
Treat ACC (granulomatous or plaquelike lesions, rarely metastisizes)
MC psuedohermaphrodite?
Male Psuedohemaphrodite: Hypoplastic testicles, elongated rudimentary vulva with penile homologue instead of clitorus, XX, male behav
Location of Persistant Hymen?
Vulvovestibular Junction
Tx of Persistant Hymen?
should be broken down to allow fluid to exit, can breed 2-3 wks later
First Degree Perineal Laceration
Laceration thru the dorsal vulvular commisure and mucosa of the vestibule
Tx for Primary Perineal Laceration
Second Degree Perineal Laceration
Laceration thru the dorsal vulvular commisure, vestibular mucosa, submucosa, muscular layer
Third Degree Perineal Laceration
Laceration thru the rectal floor, vestibular ceiling, and anal sphincter
Vericose Veins in the Mare?
Chronic slow loss of blood from the vulva late in gestation
Tx for vericose veins in the mare?
Can be surgically ligated
Cause of urine pooling?
During estrus, the cervix relaxes and uterine tone decreases so urine pooling can occur
Urine Pooling can cause these 3 things?
1. Endometritis
2. Vaginitis
3. Cervicitis
Treatment for urine pooling?
Flush large volumes of saline or antibiotics before cover, Caslicks, or surg correction with a urethral extension
Asending infection can result in endometritis
Uterine Infection
Desending infection
Benign Portions of mesonephric tubules may be a rare cause of secondary infections
Gartner's ducts
Dx degnerative uterine disease
Endometrial biopsy
Seen on endometrial biopsy with degen uterine dz
1. Glandular degen
2. lymphatic abnorm
3. endometrial atrophy
4. endometrial cysts
Uterine Neoplasm (rare)
Caused by contamination after breakdown in uterine defense mechanisms due to breeding, examination, and poor perineal conformation
Uterine Defense Mechanisms
1. Uterine Contraction
2. Phagocytosis by neutrophils
3. Repro anatomy barriers (vulva, vestib sphincter, cervix)
MC cause of endometritis
Streptococcus zooepidemicus
Absolute prognostic indicator of active inflammation
Presence of neutrophils in the lumen when doing endometrial cytological eval.
Seen on ultrasound with Endometritis
Demonstration of uterine fluid by ultrasound (7-12 days after ovulation)
Tx of Endometritis?
Lavage enhanced by Oxytocin
Antibiotic therapy
Reportable venereally transmitted bacterial endometritis
Contagious Equine Metritis
Etiology of CEM
Taylorella equigenitalis
Asymptomatic carrier of CEM
Discharge with CEM
Copious Grey Exudate for short duration
CEM is localized in the mare where?
the Clitorus
Media to grow CEM
Chocolate Agar
Tx for CEM
Scrub clitorus with chlorhex then pack with nitrofurazone or chlor hex ointment
Cervix location during Diestrus
Closed and lies in the middle of the cranial face of the vagina with a round rosette appearance
Cervix location during Estrus
Softens and opens, dropping toward the vaginal floor as it relaxes
when are pregnancy losses the greatest in the mare?
before day 35 (before the embryo enters the uterus)
Pediculosis aka
Sucking Louse found on the mane, tail, and distal legs
Haematopinus asini
Biting louse found on the dorsolateral trunk
Damalinia equi
Season that lice is most common?
Dx lice
acetate tape
Psoroptic aka
Body Mange
Psorpties equi
Otitis Externa
Psoptes caniculi or hippotis
Quarantine how long with psoroptic mange?
7-12 wks
Tx for psoroptic mange and sarcoptic mange
Don't use this in the horse for mange because it causes depression, ataxia, and progressive large intestinal impaction
Rare, reportable mange in horses that has been eradicated?
Sarcoptic mange
Chorioptic mange aka
Leg Mange
Quarantine for how long with chorioptic mange
10 wks
Causes pruritis, erythema, alopecia and crust formation along legs
Chorioptic mange
MC breed affected with Chorioptic mange: feathers in fetlock region
Draft horses
Chorioptic: surface mange or deeper?
Etiology of demodex in horses?
Demodex caballi and equi
Rare mange associated with immunosuppressive conditions or therapies?
Trobiculosis aka
Free living larva that normally feed on small rodents: associated with pruitic papules and wheals on horses
Dx Chiggers?
Colorful larvae id in the center of a wheal or papule
More common in cows, but seen in horses that live close to cows
Hypodermiasis aka?
stage of warbles that penetrate the skin and produce a breathing hole?
CS: SQ nodules and cysts over the dorsal back
aka for summer sores
Etiology for Habronemiasis
Habronema musca
Drashia megastoma
Summer sores life cycle
Adults live in the stomach
Eggs and larva are passed in the feces
Ingested by maggots of flies
Flies deposit larva on horse mouth
CS occur when the larva are deposited in other places (prepuce)
Summer sores may cause this reaction
Common findings with habronemia
Nonhealing wounds
Proud flesh (exuberant granulation tissue)
Discharge and granules with habronemia?
Serosanginous or hemorrhagic

Yellow granules
DX habronemia?
id larva on granule exam or tissue biosy
Onchocerca of nuchal ligament
O. gutturosa
Onchocerca of CT of flexor tendons and suspensory ligaments of the fetlock
O. reticulata
Onchocerca of the funicular portion of the nuchal ligament
O. cervicalis
Intermediate host for Onchocerca
Cullucoides gnats
Onchocerca: hypersensitivity to the microfilaria along the ...
the *ventral midline*, face and neck
ocular lesions with Onchocerca
keratitis, uveitis, peripaular choroidal sclerosis
depigmentation of the bulbar conjunctiva
Dx of Onchocerca
Micro exam of skin biopsy with an eosinophilic granulomatous reaction to the parasite around the microfilaria
Oxyuriasis aka
where does pinworm adult female lay her eggs
out of the horses anus
CS of pinworms
Rubbing tail on fence posts, trees, etc
Dfdx of pinworms (4)
1. Food allergy
2. culicoides hypersensitivity
3. lice
4. stable vice
Premature/dysmature foal
any sick foal
barker foal, hypoxiod ischemic
Neonatal maladjustment syndrome
lymphopenia, decreased IgM, lymphoid hypoplasia
Combined immunodeficiency
COPD aka
Allergic Airway Disease
COPD signs can appear after this vaccine
Flu vax
COPD: allergy to...
spores of hay molds=indoor
pollens in pasture=outdoor
type of dyspnea due to bronchitis from COPD
Expiratory dyspnea
heave line is hypertrophy of these muscles
External abdominal oblique
Seen on TTW with COPD
Healthy neutrophils (segs)
lg amnt of mucous
(curschmann's spirals)
response to this with suspected COPD means postive dx
atropine or glycopyrolate
Corticosteroids (dex, triamcilinolone, beclamethasone)
Bronchodialtors (brethine, clenbuteral, albuterol)
Hyposens test
Infectious degen disease of the frog that results in black necrotic material in this region
Thrush associated with these 3 things..
1. filthy stalls
2. failure to clean frog reg.
3. lack of frog pressure
Tx of Thrush?
Debride diseased frog
Pick feet daily
Mild Antiseptics
Shock aborber between cartilage and cortical bone
Subchondral bone
_________(incr. or decr) PG's and HA's with Arthritis
_________(incr. or decr) vol., protein count with Arthritis
Configuration of collagen fibrils with arthritis
Arthritis: inflamm. induces
Cytokines, kkinins, PG E, thromboxanes, leukotrienes, and prostacycline
Synovial fluid analysis with aseptic arthritis
total leukocytes: norm or slightly elevated
increased lymphocytes
increased protein
Synovial fluid analysis with septic arthritis
Predominance of segmented neutrophils
Pathogneum of septic arthritis
Segs greater than 30,000 in synovial fluid
Seen with septic arthritis on rads
subchondral bone reabsorption
periosteal bone formation
uses 90m-methylene diphosphonate isotope and reflects relative blood flow in tissue
Neuclear scintigraphy
Tx of Arthritis
Antiarthritics like PSGAG's (adequan)
joint lavage
Ocular trauma can result in
How much of their body wt shuld foals consume in a day?
Uses to assess malnutrition
If foal can't suckle, how do you feed
Nasogastric tube
Why shouldn't you force feed with foals?
Aspiration pneumonia
Onchocerca of the funicular portion of the nuchal ligament
O. cervicalis
Intermediate host for Onchocerca
Cullucoides gnats
Onchocerca: hypersensitivity to the microfilaria along the ...
the *ventral midline*, face and neck
ocular lesions with Onchocerca
keratitis, uveitis, peripaular choroidal sclerosis
depigmentation of the bulbar conjunctiva
Dx of Onchocerca
Micro exam of skin biopsy with an eosinophilic granulomatous reaction to the parasite around the microfilaria
Oxyuriasis aka
where does pinworm adult female lay her eggs
out of the horses anus
CS of pinworms
Rubbing tail on fence posts, trees, etc
Dfdx of pinworms (4)
1. Food allergy
2. culicoides hypersensitivity
3. lice
4. stable vice
Premature/dysmature foal
any sick foal
barker foal, hypoxiod ischemic
Neonatal maladjustment syndrome
lymphopenia, decreased IgM, lymphoid hypoplasia
Combined immunodeficiency
COPD aka
Allergic Airway Disease
COPD signs can appear after this vaccine
Flu vax
Common condition associated w/ severe straining or tearing of flexor tendons
Bowed Tendons
Causes of Bowed Tendons
1.Hyperextension of the fetlock
2.Trauma w/ exercise
3.Muscle fatique w/ exhaustion
4.External trauma
5.Improper bandaging
MC Cause of Bowed Tendons
Hyperextension of the fetlock
3 types of Bowed Tendons
1.High bow – w/in carpal sheath
2.Mid bow – between carpal and digital sheaths
3.Low bow – caudal to P1
MC limbs for bowed tendons
rule outs for bowed tendons
Cellulitis and suspensory desmitis
Immed tx for bowed tendons
1.For three days
2.Ice 20 minutes every 6 hours
5.Stall rest
7.Poultice bandages
Follow up therapy for bowed tendons
1.U/S 4 days post injury and then every 30 days
2.Stop DMSO and possibly bute
3.Stall rest until heat is gone
4.Support bandages and controlled hacks for 4-8 weeks
Surgical treatments for bowed tendons
1.Proximal check ligament desmotomy
2.Tendon splitting
3.Volar ligament transection
Tendon splitting
Allows for collagen reconstruction of core tendon- In association w/ proximal check desmotomy
Volar ligament transection
-SDF tendinitis-Restricted movment of SDF through fetlock canal- Notching of sheath over volar annular ligament
prognosis with bowed tendons
20% return to previous level of training
aka lumpy wool and Strawberry fot rot, cutaneous streptotrichosis, rain rot, rain scald, dew poisoning
Dermatophilosis etiology
Dermatophilus congolensis
Infection of the epidermis characterized by exudative dermatitis w/ scab formation
·Seen in cattle, sheep and goats most commonly (occasionally horses)
causes of Dermatophilosis
Prolonged wetting by rain, high humidity, high temp and flies and ticks can increase it
Dermatophilosis: how do scabs look?
Scabs look raised and circular
Dermatophilosis: Lumpy wool
pyramid-shaped masses of scabs on wool
Dermatophilosis:· Strawberry foot rot
skin from coronet to carpus or hock
Tx of Dermatophilosis
PPG or streptomycin injections
where is dermatophysis seen?
·In horses it is seen on the rump, limbs and face
Bacterial pneumonia in foals: common primary
Primary – Streptococcus zooepidemicus and Rhodococcus equi
Bacterial pneumonia in foals
Secondary to sepsis
E coli, Actinobacillus equuli & suis, Klebsiella pneumonia, and Salmonella
Bacterial pneumonia in foals
Secondary to virus
Influenza, EAV, EHV-1,2,4, or Rhino
Bacterial pneumonia in foals
Others often seen in combination with above organisms are
Pasteurella multocida and Bordetella bronchiseptica
bacterial pneumonia of the foal caused by
overcrowding, poor housing, transportation, rough handling, inadequate nutrition, dehydration, poor ventilation, FPT, poor vaccination of mare
Clinical signs of bacterial pneumonia of the foal
a.Fever – early
b.Resp rate > 30 bpm
c.Flared nostrils, exaggerated rib movement and abdominal effort
d.Exercise intolerance, cyanosis, weakness and reluctnce to move – esp R. equi infection
e.Mucopurulent nasal discharge
f.Coughing – exacerbated by exercise or restraint
g.Auscultation shows increased bronchial and tracheal sounds, esp in cranioventral lungs
h.R. equi foals may show nonseptic synovitis, D+ and uveitis
Rhodococcus equi
8-10 weeks old, when passive immunity declines
Two clinical forms of Rhodococcus equi
a.Subacute – diffuse miliary pyogranulomatous pneumonia, usually die w/in days
b.Chronic – pneumonia, compromised resp fxn and untrhiftiness
Inflammation of the pleural surface w/ exudation into the pleural space
Horses are ...more prone or less prone... to pleural fluid accumulation b/c arterial supply to pleura is from sytemic circulation (not pulmonary circulation)
more prone
In the horse (not other spp), it is...
secondary to pneumonia or pulmonary abscesses
Pleuritis/pleuropneumonia MC secondary to...
most common Pleuritis/pleuropneumonia in horses recently transported
Clinical signs with Pleuritis/pleuropneumonia
·Clinical signs
a.Fever, ADR
b.Nasal discharge – mucopurulent to serohemorrhagic
c.May see halitosis, wt loss and edema and pleural pain
d.Dyspnea, Tachypnea
e.O may complain of low grade colic or laminitis signs
f.Auscultation – can hear all but bronchial sounds
best prognostic indicator for Pleuritis/pleuropneumonia
ODOR – , can detect putrid smell (anaerobic bactreial infection)
Dx of Pleuritis/pleuropneumonia
Thoracocentresis for cell cont, cytology, protein, Gram stain, bacterial culture and senstivity, aneaerobic bacterial culture and mycoplasmal isolation
Tx of Pleuritis/pleuropneumonia
antimicrobial therapy and drains
Etiology of Tuberculosis in horses
Mycobacterium avium, bovis or tuberculosis
how is tb in horses spread?
Ingestion and inhalation, hematogenous spread causing acute miliary tuberculosis in lung or specific organ involvement w/ nodular lesions
Nutritional D+ in foals caused by
Caused by overfeeding milk or sudden intro of grain or roughage, or ingestion of sand, dirt or wood
Gastroduodenal ulcers in foals caused by
a. High grain diet or severe malnutrition
b. May be other causes including stress, NSAIDs, infectious agents
Clinical signs of Gastroduodenal ulcers
Clinical signs are bruxism (grinding teeth), ptyalism, low volume D+, colic and anorexia, lie in dorsal recumbancy
tx of Gastroduodenal ulcers
- H2 blockers (Cimetidine & Ranitidine)
- antacids (Aluminum hydroxide)
- Sucralfate
- proton pump inhibitor Omeprazole
- Prostaglandin E analog Misoprostel
- Metoclopromide – stimulate GI motility and enhance gastric empyting
- Bethanechol – cholinergic agonist
cause of septicemia in foals
Caused by bacteria through the blood stream from resp, GI, umbilicus, placenta or locatlized infection (jt ill, navel ill, pneumonia, encephalitis)
MC cause of septicemia in foals
E. coli
Clincial signs with septicemia in foals
a.ADR – depression, lethargy
b.Petechial and echymotic hemorrhaging in MM and ears
c.Shock or coma
d.Pneumonia, D+, ecepthalitis, uveitis, septic arthritis
e.Owner will think mare stepped on her foal
f.Neutropenia most often with toxic changes
Dx of septicemia in foals
IgG of < 800
Tx of septicemia in foals
colostrum IV if less than 12 hours old, Ab therapy
Parturition problems in the mare Number one cause is
presentation problem
Causes of prolonged gestation are:
a. Draft breeds
b. Mule crosses
c. Fescue
sequela of dystocia in a mare
a. Laminitis
b. Retained placenta
c. Metritis
fatal problem in older mares
ruptured middle uterine artery
low calcium
indications for induction on partuition in the mare
a.Owner conventince
b.Prolonged gestation
c.Urterine atony
d.Periparturent colic
e.Impending prepubic tendon rupture
f.Problem mare (steps on foal)
g.Preparturent leakage of colostrum
h.Nurse mare – used for colostrum only
guidelines for induction of partuition in the mare
a.Foal is in correct PPP
b.Gestation over 320 days
c.Full mammary development
d.Cevix is dilated at least 3-4 findgers
e.DO NOT induce if the mare has a systemic dz, there is a foul smelling discharge, or will have an abortion
DOC for induction of partuition in the mare
watch for this during partuition in the mare
‘red bag’ or premature placental separation
Moldy sweet clover – contains
dicurmarol which inhibits blood clotting
botulism occurs with
large round bales and ensilted forage w/ inadequate storage
tall fescue toxicity
N. coenophialum causes prolonged gestation, thickened placenta, abortion and agalacia
red clover toxin and CS
slaframine, slobbering (black spots on leaves and stems)
blister beetle toxin and CS
cantharidine, contaminate of alfalfa hay; causes D+, colic and synchronous diaphragmatic flutter
problem with Corn grain mold: Fusarium moniliforma
Corn and CSM
aflotoxins w/ Aspergillus
Monensin and Lasaocid, mixing errors w/ cattle feed; D+, colitis and death
can produce bilateral panophthalmitis in foals w/ pneumonia
Rhodococcus equi
exophthalmos and blindness from frontal sinus and retrobulbar inflammation
Cryptococcus neoformans
retrobulbar abscess and orbital cellulits and exophthalmos
Steptococcus equi
caused by infecton of adjacent paranasal and nasal sinus cavities or guttoral pouch inflammation
Orbital cellulitis
Habronemiasis or onchocerciasis cause this ocular prob
Marginal blepharitis
Moraxellaacute conjunctivits w/ ocular disharge and superficial keratitis
pink eye
EHV-2 causes
transmitted to conjunctival sac by Musca fly
Thelazia lacrymalis
Loss of corneal epithelium accompanied by stromal cellular infilatrates and stromal edema
Infectious keratitis
·Most frequent eye problem of the horse
·Group of diseases involving the inner coats of the eye
classic cause of uveitis
Classic cause is Coliform or mycoplasma-associated omphalophlebitis, septicemia and infectious arthritis
hyperreactivity to any exciting stimulus via prostaglandins
recurrent uveitis
Signs of recurrent uveitis:
b.Aqueous flare, keratic ppts, and synechia
c.Changes in the pupil
Clostridial myositis
Clostridial chauvoei, septicum and perfringens
TX: Clostridial myositis
aggressive, high doses of PPG & wound drainage to induce an aerobic environment
transmission of Clostridial myositis
Direct inoculation or sporulation in muscle necrosis and anaerobic environment (severe wounds)
CS of Clostridial myositis
a.Life threatening situation
b.Fever, ADR, injected membranes
c.Signs of septic shock
d.Painful and edematous at site of infection
Moderate to severe muscle contusion w/ susequent calcification
Fibrotic myopathy (ossifying myositis)
MC area for Fibrotic myopathy
semitendiosus (and semimembranosus or biceps femoris)
Show characteristic gait deficit at a walk with fibrotic myopathy
protraction of the hindlimb followed by a brief period of retraction before the stance phase
will palpate this with fibrotic myopathy
Will palpate a firm, nonpainful mass at the musculotendinous junction
fibrotic myopathy Does not improve w/
local anesthesia or NSAIDs
tx of acute fibrotic myopathy
systemic and topical antiinflammatories
tx of chronic fibrotic myopathy
sx tx w/ semitendinosus tenotomy
Most common muscle disorder of horses
Exertional phabdomylolysis
AKA tying up, Monday morning sickness
Exertional phabdomylolysis
causes of Exertional phabdomylolysis
·Possible etiologies include electrolyte imbalances, hypothyroidism, Vit E/sel def
·Fillies and horses on high nutritional planes are most commonly affected
·Occur w/ exercise
clin path with Exertional phabdomylolysis
increased CK and AST
Increased tissue pressure w/in an osteofascial compartment – compromising local circulation and function
Compartment syndrome
compartments syndrome most commonly caused by
hypotension and poor positioning during anesthesia
always check this part of placenta after birth
· Always check placenta (chorioallantois) after a birth to ensure it is intact (can fill with water to check)
Clinical signs of Retained Placenta:
a.Toxic metritis
MC tx of retained placenta
other tx of retained placenta
a.Oxytocin – most common and best tx
b.Fill chorioallantois w/ warm saline to stretch receptors and allow endogenous release of oxytocin
c.Sytemic and local Abs
d.Uterine lavage
f.Prophylactic measures of laminitis (Banamine, pack feet)
Chronic end stage renal disease causes anemia how?
decrease in erythropoietin production
causes Aplastic anemia and bone marrow depression, defect in blood forming organs or is idiopathic
Estrogens (Estradiol, estrone, estriol, Zeranol, Diethylstilbestrol DES)
how does Congenital methemoglobinemia cause anemia
lack of methmoglobne reductase causing cyanosis b/c iron is not kept in reduced state
how does Nitrate toxicity cause anemia
– acquired methemoglobinemia causing cyanosis b/c iron is not kept in reduced state
how does Benzocaine toxicity cause anemia
acquired methemoglobinemia causing cyanosis b/c iron is not kept in reduced state
how does Acetemenophen toxicity cause anemia
overwelms hexose monophosphate pathway where glutathione reductase is needed to protect the RBC from oxidants (Heinz body formation – denatured Hb)
other causes of anemia in horses
·Thyroid hormones
·Pituitary hormones
·adrenocrotical hormones
·Hypoadrenocortisism – Addisons
Variable flexion of fetlock at birth
May walk on dorsal surface
Congenital fetlock flexural deformities
MC area for Congenital fetlock flexural deformities
conservative tx for Congenital fetlock flexural deformities
-Splints to force weight bearing on toe
– may correct in a few days
– binds Ca in the muscle
-Casts or splints may be dangerous
surgical tx for Congenital fetlock flexural deformities
-Inferior check ligament desmotomy
-Deep digital flexor tenotomy
-Superficial flexor tenotomy
occurs with Acquired fetlock flexural deformities
Normal at birth, then develops...
Club foot
Upright pastern
Knuckling fetlock
causes of Acquired fetlock flexural deformities
1. 2° to lamenessa. Foot abscess
b. OCD
c. Trauma
2. Improper nutrition Excess energy intake
b. Imbalance tendon to bone growth (grows too fast)
Club foot at 5 months old due to:
Growth at distal metacarpal physis
Deep flexor tendon – MCIII to P3 or Inferior check ligament
Fetlock knuckling at 6-18 months old due to:
Growth at distal radial physis
Superficial flexor tendon (P1 & P2)
-Radius to P1 & P2
-Superior check ligament
Degrees of severity of Acquired fetlock flexural deformities
Stage I – hoof < 90°
Stage II – hoof > 90°
shoeing treatment for Club foot
a.Shorten heel and extend toe
b.Reverse wedge shoe pad
c.Increase tension on deep flexor tendon
shoeing treatment for Fetlock knuckling
Elevate the heel
b.Wedge pad
c.Reduces tension on deep flexor tendon
d.Increases tension on SDF
sx tx for Club foot
inferior check ligament desmotomy
origin and insertion for inferior check ligament
Origin in palmar carpal fascia
Insertion is mide deep flexor tendon
tx for Fetlock knuckling is
Superior check ligament desmotomy
origin and insertion of Superior check ligament
Origin is caudal radius
Insertion is superificial flexor tendon
salvage procedure: Acquired fetlock flexural deformities
Superficial flexor tenotomy
prognosis with club foot
prognosis with knuckling
fair to guarded
with this condition Newborns rock back on bulbs of heels so that sole of foot does not bear weight
Flexor tendon weakness in foals
Flexor tendon weakness in foals MC in which limbs
tx for flexor tendon weakness
1.Rasp heels to remove fulcrum
2.Extended heel glue shoe
3.Cast and other support is NOT INDICATED b/c foal hoof wall is very thin
MC area for Angular limb deformities
Most common in distal radial physis (metaphysis & epiphysis, not diaphysis)
area for valgus? varus?
Carpal valgus
Fetlock varus
causes of angular limb deformities
1.Premature birth – weak supporting structures or hypoplasia of carpal tarsal bones
2.Fetal malposition
b.Metaphysis – most common
Weak collateral support
-PE shows switching between varus and valgus deformity
-Easy to manipulate joints into correct position
-Rads show normal osseous structures
Hypoplasia of carpal bones
-Angular deformity
-First 2 weeks of life of limbs
-Cannot be straightened out w/ manipulation
-Rads show lack of carpal bone development
-Axis lines cross the joint
Epiphyseal dysplasia
-Angular deformity
-Defect cannot be corrected w/ manipulation
-2° to metaphyseal dysplasia or cupboidal bone hypoplasia
-Rads show abonormal shaped epiphysis and axis lines across the epiphysis
Metaphyseal dysplasia
-Most common cause of angular deformites
-Can not correct w/ manipulation
-Rads show axis lines cross the physis & widening and roughening of physis on convex side
Weak collateral support tx
Stall or small paddock turnout No external coaptaiton needed
Hypoplasia of carpal bones tx
-External stabilization w/:
a.Tube casts or splints
b.Wt bearing w/ foot exposed
c.Prevents flexor tendon laxity
d.Limbs are kept straight until cuboidal bones ossify
e.Fair prognosis if caught before bones start to collapse
Epiphyseal tx
-Tube cases if seen early enough
-Periosteal stripping
-Guarded prognosis
Metaphyseal dysplasia tx
-Medical tx
a.Confinement and time of 30 days in a small paddock
b.Usually considerable improvement
c.Splints and tube casts (not used anymore) to correct minor problems, labor intensive
staples or screw and wire to slow growth on convex side, needs general anesthesia; is the most aggressive tx, can accomplish more changes in less time; hardware must come out when leg is straight
Transphyseal bridging
hemicircumferential transection and periosteal elevation on concave side of leg, easy to do in the field; no implant to remove
Periosteal stripping –
remove wedge of bone to correct angle after growth plate closure, rare
Wedge osteotomy
Glandular, lymphatic or endometrial atrophy
Degenerative Uterine dz
neoplastic ovarian diseases
granulosa theca cell tumors, teratoma, adenocarcinomas
Most common ovarian neoplasm
granulosa theca cell tumors
granulosa cell tumors produce
testosterone causing masculine behavior
appearance of granulosa cell tumors on ultrasound
honey comb
·Germ cell origin
·See bone, skin, teeth, cartilage and hair
·Contralateral ovary may be normal and so she may be ovulating normally
·Orginate from epithelial tissue and are located on surface of ovulatory fossa
·Wt loss, colic, recurring abdominal fluid
·Rarely pathological
·Common – may be confused w/ ovarian tumors
·Occurs w/ excessive amount of hemorrhage after ovulation
·Can have normal ovarian cyclic activity
·Will shrink over time
Ovarian hematomas
Sequela of FNA of ovarian cysts
Ovarian abscesses
Follicular and luteal cysts that are normally found in the bovine ...
DO NOT exist in the horse
Mares can have multiple preovulatory follicles, ovarian hematomas or prolonged estrus cystles during the breeding season, but are not
true ‘cystic’ conditions
normally a mare ovulate ____ follicle during each estrous cycle
If there is multiple ovulations, the mare should be bred....
12-24 hours before the ovulation of the most promising follicle
Most common cause of abortion in mares
prevention of twins
pinching via U/S before day 35 (before establishment of endometrial cups)
causes prolonged gestation, dystocia , thickened placentas, and agalactia
Needed from ovaries to maintain pregnancy for first 50 days of gestation
excessive accumulation of fluid in allantoic cavity
excessive accumulation of fluid in amniotic cavity is rare (one case reported)
most common causing brain damage in foal
viral causes of abortion in mares
a.Equine herpes virus
b.EVA – equine arteritis virus
diseases causing decreased progesterone cause abortion such as..
Glucocorticoid administration
babesiosis, colic, navicular dz, weaning a baby
bacterial causes of abortion
a.Leptospirosis – serovar pomona most commonly involved
b.Bacterial placentitis – transcervical, hematogenous, intrauterine
mycotic causes of abortion in mares
Aspergillus, Absidia, Mucor
Inflammation disruption of suspensory ligament esp in TB & SB
Suspensory desmitis
MC sites for Suspensory desmitis
Most common sites:
1.Proximal to sesamoids
2.Attachment to MCIII
Suspensory desmitis caused by
Caused by:
1.Trauma associated w/ exercise
2.Callous from enlarged splints
CS of Suspensory desmitis
Mild pain on palpation
Marked enlargment of ligament
Usually a lameness prior to injury
tx for suspensory desmitis
Conservative Tx same as above w/ Bowed tendons except longer healing timeSx tx is ligament splitting
which flexor tendon is lacerated?
-toe up
-fetlock slightly dropped
-when toe is held down, fetlock is lose to normal
DDF tendon
which flexor tendon is lacerated?
-fetlock dropped in weight bearing
-toe is normal on ground
SDF tendon
which flexor tendon is lacerated?
-toe is raised
-fetlock on or close to ground
-when toe is held down, fetlock is close to the ground
DDF & SDF tendon
which flexor tendon is lacerated?
-toe is raised
-fetlock in on the ground
-when toe is held down, fetlock is on the ground
Suspensory, DDF, SDF tendon
mc area for Laceration of extensor tendons
proximal dorsal cannon bone
mc area in forelimb Laceration of extensor tendons
common digital extensor tendon
mc area in hindlimb Laceration of extensor tendons
Long digital extensor tendon
tx of forelimb Laceration of extensor tendons
-Check for joint involvment by performing arthrocentesis away from the wound
-BS Abs
-Appropriate bandaging and support
-External coaptation for 3-4 weeks
tx of hindlimb Laceration of extensor tendons
-Check for joint involvment by performing arthrocentesis away from the wound
-BS Abs
-Appropriate bandaging and support
no external copitation
can occur in young foals at pasture than have been ran until fatiqued
Common digital extensor tendon rupture
tx of Common digital extensor tendon rupture
Stall rest for 2-3 weeks
Splinting of carpus
Sx NOT indicated
Lateral digital extensor tendon will take over fxn of common
Caused by:
1.Too much work too young
2.Common injury in training horses (TB, QH)
Bucked shins
gait with Bucked shins
Shortened anterior phase of stride
leg affected with Bucked shins
Inside leg more severely affected – left leg in TB
Bucked shins rads show
Show doral thickening of MCIII
Deep palpation of anterior MCIII will exhibit pain
Medical tx
Bucked shins
1.Rest for 60 days
4.Pin firing & blistering
sx tx
Bucked shins
1.For dorsal cortical fx
2.Bucked shin the 2nd time
3.Osteostixis- Drill holes into cortex of cannon bone-Multiple fxs- Cast recovery
4.Intracortical internal fixation – compression lag screw across fx
5.Stall confinement for 60 days/30 days of handwalking
6.Follow up rads in 60 days
Epistaxis during intense exercise in racehorses and polo ponies (not endurance horses)
EIPH – exercise induced pulmonary hemorrhage
what happens to cause EIPH
Pulmonary capillary rupture when capillary blood pressure increases during strenuous exercise
heart abnorm noted with EIPH
Atrial fibrillation
tx for EIPH
Vit C?
Rest for 3-6 mos?
Change environ?Bronchodilators don’t work
etiology of epm
Sarcocystic neurona
host for epm
Usually occurs in young (1-6 years) in eastern US
cs of epm
Multfocal, asymmetric, UMN & LMN dz
Can mimic any neurologic syndrome
dx of epm
1.Definitive dx only at necropsy
2.Serum Western blot – limited value
3.CSF Western blot or PCR – interpreted as meaning the horse has EPM, but horse may be normal
tx of epm
1.Folic acid inhibitors – sulfa + pyrimethamine – synergistic drugs for 1-3 months
2.Diclazuril – anticoccidial drug kills the organism
3.Nitrazonxanide (NTE)
6.Folic acid – b/c using folic acid inhibitors causes anemia and doesn’t affect efficacy of drugs
7.Strongid C – daily wormer
8.NSAIDs w/ DMSO and bute may be helpful
Anatomy of horse esophagus is
cranial 2/3 skeletal muscle
4 layer of esophagus –
cs of choke
Stretching of head & neck
Repeated swallowing
Food and water at nostrils
tx choke
Heavy sedation to drop head (xylazine, ace)
Water lavage w/ stomach tube and pump
If lavage doesn’t work, use general anesthesia w/ cuffed tube & oxytocin and sx remove
Ab for aspiration pneumonia
Esophagotomy for difficult obstructions or perforations – ID carotid and LRLN, incise next to obstruction, open healing, feed via stomach tube
cs of gi ulcers
a.Most are not apparent
e.Colic signs – dorsal recumbency
most common layer for ulcers in adult horses
Nonglandular mucosal ulcers:
Squamous mucosa adjacent to the margo plicatus
Ulcers are caused by:
a.Secondary to D+
b.Seconarday to Pneumonia
c.NSAIDs use
tx for ulcers
H2 antagonist therapy
layer of LPS is responsible for the pathophysiologic effects of endotoxin in mammals
Lipid A,
Endotoxemia - Septic shock
a.C/V collapse
b.Inadequate perfusion to vital tissues
d.Multisytem organ failure
the component for the pathogenicity of Gram negative enterbacteria
One of the cell walls of Gram-negative bacteria consists of LPS (lipopolysaccharid)
Abnormal arytenoid cartilage function due to atropy of intrinsic muscles (dorsal cricoarytenoid muscle) of larynx b/c of the tortuous and unusual course of the left recurrent laryngeal nerve
Laryngeal hemiplegia - Roarer
cs w/ Laryngeal hemiplegia
exercise intolerance or audible respiratory noise
dx of
endoscopic exam – evaluate larynx at rest and during strenuous exercise
see on endoscope w/ LH
a.There will be no artytenoid cartilage abduction
b.Slap test can assist in dx
Normal Cardiac arrhythmias
·P wave is normally split
·Wandering atrial pacemaker – P wave will look morphologically different each time; due to large SA node causing a shift in conduction
·QRS is predominantly negative
·T wave is extremely variable – most T wave changes have little significance
·Normal arrythmias:
a. 1° AV block
b. 2° AV block
c. Sinus arrhtyhmia
·Tall spiked T wave
·Dimishished P wave and atrial standstill
·AV block
·Surpraventricular tachcardia
·Speeding and slowing of heart w/ respiration
·High vagal tone and increased HR should abolish this arrhythmia
Sinus Arrhythmia
1° AV block
·Conductio delay causing a prolonged P-R interval
·High vagal tone in the resting horses and not w/ cardiac pathology
2° AV Block
·Electrical activity is inermittently completely blocked at the AV node
·Common in horses
·NORMAL – homeostatic mechanism to control blood pressure
·Atropine or glycopyrollate can be used to R/O pathology in these horses b/c it will go away w/ parasympatholytic agents
·Mobitz type I – most common, w/ progressvely lengthening P-R interval in the beats preceding the block
·Mobitz type II w/ a fixed P-R interval is less common but also normal
Most common clinically significant arrhythmia in the horse
Atrial fibrillation
Atrial fibrillation Characterized by
wavy baseline known as ‘F’ waves
tx Atrial fibrillation
Side effects of quinidine
vasodilation and hypotension
Advanced 2° or 3° AV block
a.Atropine and glycopyrrolate – parasympathlytic (anticholinergics)
b.Dopamine – sypthomimetic
c.Na bicarb – hyperkalemia, insulin, and dextrose
d.Ca may have a cardioprotective effect in yperkalemia – Ca gluconate
·No conduction through AV node; atrium and ventricles are completely dissociated
·Will see promenent jugular pulses
3° AV block
AV block is occurring for prolonged P-R periods or present at high heart rates
Advanced 2° AV block
P waves occur earlier than normal
Atrial premature depolarizations (APDs)
most rectal tears occur
Most tear occur dorsally, apporx. 12 inches cranial to anus in pertoneal cavity
4 grades of rectal tears
Grade 1: mucosa and submucosa
Grade 2: muscular layer, intact mucosa
Grade 3: All tissue except serosa (3a) or mesorectum (3b)
Grade 4: all layers
Immediate tx of rectal tears
Broad Abs,
Refer immediately
Tx of Grade 3 rectal tears
Rectal liner
Suturing tear intrarectum
Empyting of colon via enterotomy and daily lavage of tear
Empyema & Mycosis
Accumulation of pus within the pouch cavity
Empyema & Mycosis:Chronic sequella
URT infections, esp Strangles (Strep.)
cs w/ Empyema
Mucopurulent discharge most evident when head is lowered
Dyspnea and dysphagia from collapse of the nasopharynx
Chondroid – inspissated exudate, may cause outward distension
dx of Empyema
Endoscope or catheter placement will show stream of discharge from gp opening
X-ray will see fluid line
tx of Empyema
Daily irrigation w/ Isotonic saline through catheter
Feed & water on ground to establish drainage
Guttural pouch Mycosis
Fungal dz of gutteral pouch roof, can affect internal carotid
cs gutteral pouch mycosis
Epistasix not associated w/ exercise is most common sign by erosion of int carotid in medial compartment
Neuro signs:Dysphagia
Pain on deglutition
Parotid pain
Head tilt
Abnormal resp noise
Laryngeal hemiplegia
(R sided – rare)
Facial paralysis
Horner’s syndrome
gutteral pouch mycosis
unilat or bilat
tx of gutteral pouch mycosis
Amphotericin B
Sx ligation of internal carotid artery
Reported in young horses (Standardbred and TWH)
Cause unknown – Mycobacteria paratuberculosis?
Often compared to Crohn’s dz in people
Chronic D+/granulomatous enteritis
Lesions involving the small intestine with Chronic D+/granulomatous enteritis
Affected bowel is thickened w/ mononuclear cells
Villus atrophy common (malabsorption)PLE
Loss of dopamine negative feedback causes Pars intermedia pituitary adenoma, causing excess cortisol production by adrenal cortex via Ý POMC, a precursor to ACTH and b-endorphin.
Equine Cushings Dz
increased Temp
what kind of colic?
anterior enteritis, Colitis
increased pulse
what kind of colic?
Ischemia, obstruction, displacement
increased gastric reflux
what kind of colic?
anterior enteritis
MC NSAIDS used in equine vet med
a. Banamine
b. Phenylbutazone
c. Dipyrone
d. Ketoprofen
· Inhibit cyclooxygenase enzyme-mediated production of eicosanoids form arachidonic acid in the cell membrane
Side effects from NSAIDS
a.GI ulceration
b.Protein loss
c.Abdominal pain
e.Ulceration of the right dorsal colon – phenylbutazone
f.Paplillary necrosis – renal toxicity from phenylbutazone
Anti-ulcer meds
· H2 antagonists
Cimetindine – Tagamet
Anti-ulcer meds
· Proton pump inhibitors
Omeprazole – Prolosec
Anti-ulcer meds
· PGE2
Anti-ulcer meds
Cytoprotective agents
H 2 Blocker MOA
Blocks histamine stimulated gastric acid secretion
ulcer tx
Tagamet + antibiotic
if only use tagament:
Ulcers will come back after medication is stopped b/c H. pyloric bacteria
Uses of H 2 Blocker
gastric ulcer tx, chronic gastritis, reflux exophogitis, prophylactically prior to mast cell removal
Examples of H2 Blockers
Ranitidine (Zantac)
Fomotidine (Pepcid)
Nizatidine (Axid)
Cimetidine (Tagamet)
MOA of proton pump inhib
· Blocks ALL acid producers b/c blocks protone pump, blocks 100%, gastric acid is completely inhibited
what is PGE1 used for?
·Prevents NSAID-induced gastric ulcers
·Scavenge hydroxyl radicals generated by neutrophils during inflammation and reperfusion
use DMSO to treat?
·Tx endotoxemia and cerebral edema
why no greater than a 10 percent solution should be administered at a relatively slow rate with DMSO
Wear on teeth from cribbing is where?
·Excessive wear on rostral margin of upper central incisors
Dental bud is split during development, usually with incisors
Supernumerary teeth
brachygnathia, the upper jaw is longer than the lower jaw
Parrot mouth
prognathia, the lower jaw is longer than the upper jaw
Sow mouth/monkey mouth
·Maxilla is wider than the mandible
·Sharp edges on buccal of upper and lingual of lower
Shear mouth
aka for First premolar
wolf tooth
Removal of dental caps
deciduous teeth of premolars that can impede the eruption of underlying permanent tooth
Preanesthesia in a horse
a.withold food for 12 hours (not water)
b.Mineral oil 6 hours before sx
c.Atropine or Isoproterenol only when anesthesia used will induce bradycardia (atropine will cause ileus)
d.Sedate with Xylazine or Detomidine
Anesthesia in a horse
a.Induction agents – GG, Thiopental, Ketamine, Telazol, Profofol
b.Inhalation – Halothane (more potent and more lipid soluble, but more myocardial depression), Isoflurane (peripheral vasodilation), Sevoflurane
Blood pressure during anesthesia
ideal MAP is 60-90
Apnea: anesthesia complication
·Early induction period of anesthetic b/c high plasma protein concentration
·Too deep anesthesia
·Doxapram can be used as a respiratory stimulant that also initiates relase of endogenous epinephrine and causes an inr HR and BP
When does hypoxemia occur?
Is when PaO2 is less than 60 (should be > 90)
what do you treat hypoxemia with?
a.Dobutamie infusion – increases oxygen delivery to tissue
b.Clenbuterol - b2 agonist
c.minimizing time in dorsal recumbency
Neuropathies during surgeries caused by
a.improper positioning during anesthesia
b.malignant hyperthermia
c.prolonged sx
d.excessive anesthetic depth
e.low PaO2, ß BP or acidosis
Neuropathies during surgeries prevented by
a.maintaining light anesthesia and c/v fxns
b.avoid excessed preanesthetic especially phenothiazines
c.Adequate padding
d.Support of upper front and hind legs
e.Balanced electrolytes and Ca gluconate (maintain muscle contraction)
f.Dobutamine, dopamine or ephedrine to maintain adequate BP
g.Don’t put horse under until surgeon is ready
h.Dantrolene – muscle relaxation
i.Diazepam – muscle relaxation
j.Na bicarb – correct metabolic acidosis
what can be used for standing sedation in horses?
·ace + (Xylazine &/or Butorphanol, Meperidine, Pentazocine &/or xylazine)
·Xylazine + (Butorphanol, Pentazocine)
·Detomidine + Butorphanol
Intercoccygeal Epidural
·Lidocaine (5-10 mL) –fast & short
·Xylazine in saline – slow & long
·Lidocaine + Xylazine w/ saline – fast and long
Lumbosacral or suarachnoid epidural
·Detomidine in saline &/or morphine
·Butorphanol + lidocaine
Injectable anesthetics
·Thiopental – long, rough recovery
·GG/Thiopental – better muscle relaxation, poor analgesia
·Xylazine/Ketamine – (xylazine 5 min before ketamine), smooth induction and recovery, inadequate muscle relaxation
·xylazine/Ketamine/Butorphanol – give w/ xylazine, improved analgesia
·Xylazine/Ketamine/Diazepam – improved muscle relaxation
·GG/Xylazine/Ketamine – narcosis, analgesia & muscle relaxation, smooth recovery, reverse w/ yohimbine, tolazoline, atipamezole
·Detomidine/Ketamine – recovery depends on duration of anesthesia
·GG/Detomidine/Ketamine – same as triple drip above, but recovery slightly longer
·Xylazine/Telazol – relatively smooth recovery & may require more than one attempt
·Detomidine/Telazol – same as above
·Propofol – short term, rapid redistribution and hepatic metabolism
·Profofol/GG – lasts longer
why vasoconstriction with laminitis
increased cortisol, incr. catecholamine vasoactivity and insulin antagonism, coritsol ties up insulin receptors needed for vasodilation, causing chronic vasoconstriction
ADH antagonism from excess cortisol or decr ADH secretion from posterior pituitary due to expansion of intermediate lube into posterior pituitary
Diabetes Insipidus
initiating insulin insensitivity
Diabetes Mellitus
behavior change in older horses can be caused by...
beta endorphin in CSF
cause of hirutism
thermo dysfxn by tumor pressure on hypothalamus, or incr androgens by adrenal cortex
TOC for Equine Cushings
TRH stim –
CD have incr cortisol w/ TRH
DOC for Equine Cushings
Dopamine agonist (Pergolide medylate)
autosomal recessive microdeletion of 5 basepairs of DNA-PKcs in Arabian foals
Cell receptors on T cells and Ig on B cells don’t mature
Signs are pneumonia and profound lymphopenia
ß IgG even with colostrum intake at 100 days old
Hypoplasia of all lymphoid tissue
Equine CIDs (SCIDs)
Fairly severe colic signs followed by depression and mild pain
Anterior Enteritis
seen with Anterior Enteritis
NG reflux (orange brown)
Tap has high protein and low WBC
Tap is yellow serosanguinousDepression, fever
Rectal multiple loops of SI, thickness of wall on U/S
Potomac horse fever aka
Equine monocytic ehrlishiosis
Potomac horse fever etiology
Ehrlichia risticii
CS with Potomac horse fever
Fever, leukopenia, explosive D+
Vax protocol for Potomac horse fever
Two vaccinations 3-4 weeks apart in spring followed by a booster in the fall in high risk areas
Most common form of thoracic tumor
CS with lymphosarcoma
Clinical signs are inappetance, wt loss, vetral edema, dyspnea, pleural effusion and distension of jugular veins
Coughing when mediastinal mass was compressing the major bronchi and trachea
What signs will the horse show w/ peritonitis?
Brick red MM
What is the bloodwork like of a horse w/ peritonitis?
Acidotic – accumulation of lactic acid
Increased Fibrinogen
Leukopenia w/ L shift
What does the tap fluid look like with peritonitis?
Huge buffy coat
Bright, cloudy yellow
Acute – segs
Chronic MÆ
Sepsis – degenerative segs
What is the tx of peritonitis?
Banamine for analgesia
Correct fluid, protein, C/V, electrolytes to tx endotoxic shock
Usually can’t wait for blood culture, so give broad spectrum Ab (Penicillin, Gentamycin, Metranidazole)
Only do lavage if not responding to Ab
Warn owners this is a long term therapy
Who are most likely to get uroperitoneum
What is the tap look like in uroperitoneum
CREA will be twice that of blood
What are PE findings and bloodwork of uroperitoneum
Distension of ventral abdomen
Electrolytes change, decr Na, incr K
Could have cardiac arrythmia
What is the tx of uroperitoneum
Give NaCl & glucose
If ECG is abnormal, give bolus of glucose
Drain abdomen before surgery
prevents erection in stallion
Stallion ring scar
Abscesses could indicate what in a stallion
bastard strangles (strep)
eval penis on stallion BSE for....
scars, adhesions, lacerations, Squamous Cell Carcinoma, Sarcoids, Cutaneous habronema, & melanoma
history of little ejaculate or loose heads
have impaction of ampulla
tx of impaction of ampulla
Tx is to milk ampulla toward urethra, strip and repeat ejaculate
location of the epididymus in the stallion
dorsomedial side of testicle
how do testicles lay in a horse?
in a bull?
horizontal in a horse

vertical in a bull
to evaluate sperm in a stallion...
Collect twice, one hour apart. Evaluate 2nd ejaculate.
daily sperm output
collect for 5-7 days, 3 days that are the same in a row
to get a mare pregnant...
begin on 2nd day of estrus and breed every other day
to get a mare pregnant should have ____ progressively motile sperm
Need 500 x 106 progressively motile sperm
morphologically normal sperm?
Should have 75% morphologically normal sperm
3 cultures taken from stallion
1.Sinus of urethra
2.Urethral opening both pre and post ejaculate (especially in aged stallions)- Pseudomonas aeroginosus- CEM – cutaneous equine metritris in chocolate agar
Inflammation of blood vessels
Peripheral vascular dz – vasculitis
causes of vasculitis
b.Equine granulocytic ehrlichiosis
c.Equine viral arteritis
d.Purpura hemorrhagica – immune mediated cutaneous vasculaitis; involved w/ Steptococcus, influenza, or EHV; febrile, ventral edema
Toxin secreted by Clostridium tetani in soil heavily contaminated w/ feces
incubation for tetanus
2-4 weeks
3 Toxins secreted by Clostridium tetani
1.Tetanolysin – increases tissue necrosis
2.Tetanospasmin – binds to nerves & inhibits the inhibitory interneurons in ventral horn of spinal cord
3.Nonspasmogenic toxin overstimulation of sympathetic nervous system
CS of tetanus
Prolapse of 3rd eyelid (DDx HYPP)
Stiff gait initially
Sawhorse stance
Flared nostrils, lips retraced, erect ears (Sardonic expression)
Tx of tetanus
Non sitmulating environment – dark stall, ears plugged w/ mineral oil soaked cotton
Sedate w/ Ace at 4-6 hour intervals
Sedate w/ Chloral hydrate, valuim, sodium pentobarbital
Muscle relaxantes in combo w/ sedatives – GG IV drip, Methocarbamol
Slings or deep bedding
Penicillin to tx originating wound infection
Antitoxin at high doses
Parenteral nutrition and IV electrolytes
prognosis for tetanus
Good if:
1. Horse can drink
2. Remain standing
3. Survive more than one week
is the vax for tetanus against the organism or the toxin?
the toxin
tetnus antitoxin can cause this liver dz
highly fatal liver dz called Theiler’s dz
avoid using tetnus antitoxin if
vaccinated or older than 2
Cervical Vertebral stenosis/malformation/malarticulation
aka wobblers
cervical vertebral instability (dynamic) at C3-4 in weanlings
1. CVI
cervical static stenosis at C5-6 in older horses
Vertebral instability with wobblers leads to...
soft tissue (muscle and ligament) hypertrophy causing spinal cord compression
causes of wobblers
a.overfeeding imbalances esp of Ca Ph, Co & Zn
c.osteochondrosis involving the epiphyseal plate or articular process
d.heredity – but osteochondrosisi is an inherited condition, and wobblers is a form of osteochondrosis)
common signalment for wobblers
Young TB or TWH males when training begins
most obvious gait abnorm with wobblers
in hindlimbs
tx for wobblers is usually
most common equine arbovirus and most mild
reportable EE

100% mortality
% mortality with VEE
transmission of EE
Reservoir – birds and small mammals (VEE)
Vector – very specific spp. Of mosquitos
highest incidence of EE in what months?
Highest incidence in August and September – important for vaccination schedule
pathology seen with EE
CSF pleocytosis of small mononuclear cells w/ a slight increase in protein (esp in WNV)
Gross lesions of edema &hemorrhage w/ EEE
CS with EE
altered consciousness
CN dysfxn
Dx of EE
Viral isolation from cold brain
High titer
Ddx with EE
Moldy corn
Good nursing care – NSAIDs, IV DMSO; seizure meds; forced feeding
Dex is controversial in viral dzs but ma decrease viral inflammation
Zoonosis of EE
Horse is dead end host for EEE and WEE
Horses act as sentinels for humans
VEE horse is NOT dead end host
etiology of lyme's disease
Borrelia burgdorfere (a spirochette)
vector for lymes disease
Ixodes scapularis (deer tick)
CS for lymes disease
Intermittent (shifting leg) lameness
seen with stage I lymes dz
Erythema chronicum migrans (ECM) rash
Flu-like symptoms Fatique
seen with stage II lymes dz
Neurological signs
Cardiac signs (AV block)Arthritis
seen with stage III lymes dz
CNS signs
Chronic arthritis
tx for lymes dz
MC tick born dz in US
Lymes dz
most common pemphigus in the horse
Pemphigous folliaceous
Where does pemphigous folliaceous occur?
In below the stratum corneum (subcorneal) or in the stratum granulosum (intragranular) of epidermis
first CS with Pemphigous folliaceous
Depigmentation, Pustules, crusts or erosions On face and ears (periocularly and around the mouth) Fever/anorexia in cat & horse
second CS seen with Pemphigous folliaceous
Generalized seborrhea
Coalescing papules
third CS seen with Pemphigous folliaceous
Footpad Hyperkeratosis
what do you see on cytology/impression smear with pemphigus folliacus
Neutrophils & acantholytic cells with possible eosinophils – but not dx
ANA test with pemphigus folliacus
pos or neg
seen on skin biopsy with pemphigus folliacus
Most Dx
Subcorneal or intragranular pustular dermatitis with acantholytic cells
seen on direct EF with pemphigus folliacus
Intercellular staining within the epidermis(looks like a fishnet)
Seizures: abnorm motor or sensory impairment
seizures due to...
Episodes of impariment or loss of consciousness or abnormal motor impariment due to paroxysmal cerebral dysrhythmia
extracranial causes of seizures...
1. hypoglycemia
2. hyperglycemia
3. renal disease
4. hyperlipidemia
5. hyperkalemia
6. hypocalcemia
7. hyperthermia
8. infectious agents
9. toxicosis
10. neoplasia
11. hydrocephalus
12. cardiac arrhythmias
see with lactation tetany (hypocalcemai)
see violent respirations w/ thumps, muscle fibrillation, tetanic convulsions
see hyperkalemia with...
HYPP, ruptured bladder in foal
see hyperlipidemia in...
stressed ponies & minis
hyperthermia causes...
swelling of the brain
infectious agents causing seizures
tetanus; botulism
toxicosis causing seizures
Strychnine, lead, arsenic, organophosphates
neoplasia causing seizures
a.Pituitary adenoma – uncommon cause of seizures
c.Cholesteatoma – cholesterol granuloma plugs up ventricle causing blindness b/c pressure on optic chiasm
Intracranial causes of seizures...
1. viruses
2. bacterial meningitis
3. cerebral abcesses
4. verminous encephalitis
5. EPM
6. Fungal encephalitis
7. head trauma
8. vascular accidents
9. idiopathic epilepsy
viruses that cause intracranial causes of seizures
Togaviruses (EEE, WEE, VEE), rabies
seen with bacterial meningitis
foals, uveitis, incr fibrinogen, incr WBC, discolored iris, pus in anterior chamber
cause of Cerebral abscesses
strangles or trauma
tx Verminous encephalitis with?
larvacidal anthelmintis
common cause of seizures
head trauma
vascular accident causing intracranial cause of seizure
Neonatal Maladjusment Syndrome – hypoxic ischemic encephalopathy due to dystocia; ‘dummy foal’
tx Idiopathic epilepsy with
tx w/ Phenobarbital or Diphenylhydantoin
idiopathic epilepsy in arab foals...
Egyptian lineage, self limiting; tx for acute seizures w/ Valium
most common botulism
Clostridium botulinum Type B
route of infection with botulism
1.Ingestion – preformed toxin in forage/silage, usually type C & D
2.Wound – rare
3.Toxicoinfectious – ‘Shaker Foal Syndrome’; spores ingested, cause gastric ulcers
pathogenesis of botulism
Toxin binds to neuromuscular jxns causing pralysisi of cholinergic nerve fibers by blocking release of Ach
CS with botulism
Afebrile progressive muscular paralysis
Weakness, restlessness, incoordination
Inability to rise, shaking as rising (‘shaker foal’)
Sternal recumbancy w/ head at flanks
Dysphagia often first sign
Decreased tongue and tail tone
DX of botulism
Toxin in feces, serum or tissue
Tentative dx by finding toxin in feed
Tx of botulism
1.Antiserum – from Upenn, very expensive
2.Restrict movement
3.Ventilation and O2 tx
4.Abs – avoid ones that potentiate neuromuscular weakness – Ags, Tetracycline, & procaine penicillin
5.IV penicillin is recommended
6.DON’T use metranidazole
7.Avoid edpson salt
8.DON’T use parasympathomimetic drugs (Neostimine) b/c may increase mortality
prevention of botulism
Vaccinate pregnant mares during last part of pregnancy to prevent shaker foals
tx with spinal cord trauma
1.Corticosteroids or NSAIDs – Solu-delta cortef is very helpful in tx of human spinal trauma victims
2.Very high DMSO
3.Mannitol – expensive – may cause brain edema via hypertonicity
5.Sx tx – initial decompression or later decompression after callus formation
6.Euthanasia – if paralysis
MC spinal cord trauma area
C1-C2 broken dens most common
common history with spinal cord trauma
Peracute onset & nonprogressive
Signs depend on level of injury (T2-S2 involve hind limbs only)
General Overall Vaccination Schedule
Give all vaccines initally at 2 injections 4 weeks apart and then booster annually
Encephalities & PHF
how often do you booster?
booster twice a year
how often do you booster?
booster every 3 months
how often do you booster?
needs only one initial shot
how often do you booster?
initially give 3 injections at 3 week intervals, foals at 1 year old, and then no annual booster is necessary
General Overall Vaccination Schedule
Give all vaccines initally at 2 injections 4 weeks apart and then booster annually
Encephalities & PHF
how often do you booster?
booster twice a year
how often do you booster?
booster every 3 months
how often do you booster?
needs only one initial shot
how often do you booster?
initially give 3 injections at 3 week intervals, foals at 1 year old, and then no annual booster is necessary
Gram positive spore forming anaerobic bacteria
Pathogen of Tetanus
Extensive tissue damage or deep penetrating wound causes exotoxins to travel w/in the motor neurons to the CNS where it inhibits postsynaptic inhibitory impulses in the spinal cord
CS with tetanus
‘lockjaw’ – tonic spasms and hyperesthesia; sawhorse stance
Vax protocol: tetanus
Foal in high risk area
give antitoxin after birth and then give toxoid every 2-3 months until 3 months old
Vax protocol:tetanus
vaccinate w/ antitoxin at 5-8 weeks old and then booster at 3 months old
Vax protocol:tetanus
during last 4-6 weeks before birth
Vax protocol: tetanus
give toxoid annually
Vax protocol: tetanus
Adults w/ extensive wound or deep penetrating wound that is up to date on tetanus shot
another injection of toxoid to increase Ab
Vax protocol: tetanus
Adults w/ wounds that is NOT up to date on tetanus
1500 IU of antitoxin and toxoid simultaneously in different IM arease and repeated in 30 days
associated w/ administering antitoxin in horses over 2 years old; hepatic failure (heptoencephalopathy)
· Theilers disease
Sleeping sicknesses
Viral Equine Encepthalopathies
EEE, WEE, VEE transmitted by
transmitted by hematophgous insects (mosquitos)
dead end host for EEE, WEE, VEE
highest mortality rate of Viral Equine Encepthalopathies
Vaccination protocol for EEE, WEE, VEE:
give between 2-6 months old at 4-6 week intervals
Vaccination protocol for EEE, WEE, VEE:
booster twice a year in endemic areas
Common in racetracks, show grounds, sale barns and breeding farms
Vaccination protocol:
a. Foals and adults should be boostered every 3-4 months with IN (intranasal)
b. Booster 2-4 weeks before anticipated exposure (show, sale)
c. Avoid vaccinating w/in 10 days of competitiion b/c vaccine may cause transient disease
3 syndromes with EHV-1
a.Abortion – vasculitis causes placental detachment and hypoxia to the fetus
c.Neurological – rectal incontinence, urinary incontinence, loss of tail tone, dog sitting, posterior paralysis
most common cause of respiratory dz outbreaks in horses in KY
· EHV-4
· Causes a vasculitis via the leukocytes – can remain latent
EHV-1 is spread how
· Spread via nasal secretions and aborted fetuses and remains active in environment for 14 days in on horse hairs for 42 days
EHV-1 Vax: labeled for use in pregnant mares at 5,7, and 9 months gestation
Killed - Pneumobort
Recovering EHV horses quarantine for how long?
4 wks
is it neccessary to vaccinate non-pregnant horses for EHV-1?
only if they are close to broodmares
vax every 3-6 mon
when to vax horse against rabies?
only in endemic areas
Causes behavior change from aggressiveness to depression; colic, lameness may be complaint
vax protocol: rabies:
for foal
3 months of age, one shot
vax protocol: rabies:
for adult
annually w/ 2 mL IM w/ killed
type of paralysis with rabies
Causes progressive ascending paralysis
etiology of strangles
Streptococcus equi spp equi
type of strep with strangles
beta hemolytic
Clinical findings with strangles
· Fever, thick mucopurulent nasal discharge, swelling and absessation of head LNs
how long can recovered horses spread strangles
· Recovered horses can spread for up to 4 months
Vaccination protocol for strangles for foals only on endemic farms with IN (intranasal)
a. M protein or bacterin – 3 doses 3 weeks apart then at 1 years old
b. Enzyme extract – 2 injections 3 weeks apart then at 1 years old
can develop after vaccination of horses previously sensitized to streptococcual antigens
Purpura hemorrhagica (edema)
why don't vax adult horse for strangles?
risk of Purpura hemorrhagica (edema)
vax protocol for PHF
Two vaccinations 3-4 weeks apart in spring followed by a booster in the fall in high risk areas
etiology of EVA
transmission of EVA
Aerosol transmission of nasal secretions and venereally through infected semen
CS with EVA
Edema – scrotal, preputial, hindlimb, nasal and ocular discharge, and abortion
vax protocol with EVA
a.Vaccinate Seronegative mares 3 weeks before being bred to a positive stallion w/ attenuated live virus
b.Vaccinated horses are then seropositive and subject to export restrictions
Shaker foal syndrome etiology
Clostridium botulinum
pathophys of Botulism
Germinate in ulcerated areas of GI tract and produce exotoxins that block Ach release at neuromuscular jxns
CS of Botulism
· Signs are foals that tremble and become paretic, may cause respiratory paralysis
vax protocol for botulism
a. Mares – 3 times every month w/ last dose 4 weeks before parturition
b. Foals are protected by ingesting colostrum
etiology of anthrax
· Bacillus anthracis
edema with anthrax
· Ventral edema – die w/in 2-4 days
vax protocol with anthrax
a.Avirulent noncapsulated spore vaccine on annual basis in endemic arease and face of outbreak to reduce losses
b.Vacicnate 4 weeks before warm, dry summer months and the booster 3 weeks later
c.Given SQ
d.Do not give Ab after vaccination
etiology of ascarids in horses
Parascaris equorum
where do they hatch and develop
Hatch in small intestins and migrate through liver then to the lungs (coughed and swallowed) and then develop in smallintestines
CS with ascarids
Pot belly, respiratory signs
can ascarids cause colic?
yes it is an Ascarid-induced colic when they cause an impaction
deworming foals for ascarids
· Start foals at 2 months old, then worm every 2 months
· If heavy burden is expected, use slow-acting compounds to prevent intestinal obstruction or rupture
Most pathogenic of all endoparasites
Large and small strongyles
which is most damaging Strongyle?
Large (Strongylus vulgaris)
b/c L migrate extensively through intestine vasculature – their prevelence has almost been eliminated b/c of anthelmintics
what CS do small strongyles cause?
cause Wt loss, D+ and colic
life cycle of small strongyle
a. ingestion of L3 on grass, develop into adult in the cecum and colon.
b. Molt from EL3 à LL3 à L4 in mucose and submucosa of cecum and colon forming a fibrous cyst for 30-60 days
c. L4 emerge (can take up to 2.5 years) causes an intense inflammatory reaction
d. This is called Larvae Cyathostomiasis – chronic D+, severe wt loss, protein losing enteropathy
have developed a resistance to benzimidazole wormers
tx for strongyles
Moxidectin (Quest)
what stage of strongyles does moxidectin kill?
LL3 and L4 w/ a single dose
another tx for strongyles that will get 90% of EL3
Double dose of Fendbendazole (Panacur) for 5
etiology of bots
Gastrophilus fly larva
where do bots live in the horse?
· Inhabit stomach and large intestine
how horse infected with bots
· Adult flies lay eggs (nits) on horse hair
· Horse licks the eggs and they hatch and burrow in horse’s tongue, then migrate to the stomach and attach to the epithelium for several months
tx of bots
· Ivermectin effectively removes bots
· Give 1 month after nits are seen on horses legs and repeat after the last frost kills the adult flies
D+ and unthriftiness in suckling foals
Strongyloids westeri
transmission of Strongyloids westeri
via mare’s milk
when to treat for Strongyloids westeri
· Tx mares 12 ours after birth
· Foals at 3 weeks old
· Adult females create perineal irritation while laying eggs around anus
· Affected horses lose hair form the tail and rump during scratching attempts
tapeworms of horse
Anoplocephala maga and perfoliata
intermediate host for horse tapeworm
how horse infected with tapeworms?
· Horse ingests mite and tapeworm emerge and attached to mucosa in distal small intestine and proximal large intestine
· Grow to egg-laying adults in intestine
type of floatation to dx tapeworms?
· Sedimentation techniques are more reliable than floatation b/c ova do not easily rise in solution
tx for tapeworms in horses?
Strongid (Pyrantel pamoate) at high doses is very effective
how to "clean pastures" for parasite control?
physical removal of feces one to two times a week
rotation: parasite control
a. Slow rotation – use only one class of drugs over one year; reduces chance of resistance in small strongyles
b. Fast rotation – alternating different classes of wormers w/in one year
when to worm?
a. Worm when egg producing adult strogyles peak
b. North – spring and early summer and a botacide in the fall after a frost
c. Cannot seasonally worm in the south b/c the climate favor prolonged periods of strongyle transmission
d. Young horses (< 1 ½ years old) should be wormed in fixed intervals for ascarid control
acessment of deworming program?
a. Assess 2 weeks after deworming via fecal floatation
b. < 10 % of herd should have ova – if more could have a resistance problem, or did not deworm properly
c. If failure is detected, then use a modified McMaster or Wisconsin technique to assess
d. Strongyle should be < 100 eggs/gram
how long should you test after deworming?
2 wks
strongyles should be under ___eggs per gram
Excessive Flexion on Hindlimbs
dropped elbow: which nerve is damaged?
Radial N Paralysis
where is the pain seen on hoof testers with laminitis?
Gait of horse with laminitis
short strides
place feet down quickly
Etiology of Thrush
Fusobacterium necrophorum
Obel Grade 1
Foot Discomfort without pain
A short, stilted gait at a trot
No lameness
Obel Grade 2
Some discomfort and lameness as seen by a stilted gait at the walk
Forefeet are lifted without difficulty
Obel Grade 3
Reluctance to move
Resists lifting of forefeet
Obel Grade 4
Horse does not move his feet without being forced
Lamintis can be a sequele to these diseases
Colitis X
P3 rotates in how many days after onset of acute laminitis
3-4 days
Used for pain relief with laminitis
Flunixin Meglumine
Tx used to restore digital blood flow with laminitis
Isoxsuprine Hydrochloride
Sodium Heparin
Tx for chronic laminitis
D-I Methionine
Hoof Wall Resection