Exam 2 Flashcards
Testing Cranial Nerves
Olfactory (CN I)
• Do they find the treats?
Optic (CN II)
• Menace response (slowly so no air; not present in young foals)
• Pupillary light reflex (usually slow)
III, IV, VI
• Ability to move and position eye (fixed strabismus)
V, VII
• Sensory & motor of muscles of face
• Can they sense things you touch and move appropriately
• Ears, eyes, nose, mouth
VIII
• Head tilt
• Nystagmus (slow phase to side of lesion)
• Deafness – common in blue eyed paint horses (blindfold)
IX, X
• Dysphagia
XII
• Pull out tongue and see if replaces
• Unilateral muscle atrophy of tongue
Non cranial nerve portions of neuro exam
Opthalmic Exam
• Evaluate nerve ending for CN II
• Cataracts?
Gait Eval
o regular walking
o circle walking
o curb walking
o hill walking
o standing tail pull
o walking tail pull
Neck Mobility
o Head should be able to touch flank
o Head should go high & between front legs
o Palpate transverse processes manually
Identifying Sacral Nerve Damage
o Urination
o Defecation
o Tail tone
o Anal tone
o Perineal sensation
Neurologic Lesion Localization
Brain:
• mentation, behavior
Brain stem:
• cranial nerves
Cervical spinal cord:
• all four limbs
Thoracolumbar spinal cord:
• rear limbs
Sacral nerves:
• urination, defecation
Head trauma; Types of Damage, Treatment, Prognosis
Types of Damage
• Direct impact – occipital, sphenoidal, temporal bones
• Direct & contracoup impact – inner, middle ear, basilar bones, optic nerves
Treatment
• Osmotic diuretics for edema (mannitol, hypertonic saline)
• NSAIDs
• Anti-convulsants if needed
• Corticosteroids (controversial)
• Supportive care
Prognosis
• Variable
• Response to treatment best indication
• Keep them on their feet!
Head trauma; First Aid
• Is airway patent?
• What is level of consciousness?
• Pupils – size, symmetry, response
_ Bilateral nonresponsive mydriasis = grave prognosis
_ Watch for central blindness due to optic nerve trauma
• Assess motor function if standing
• Monitor respiratory patterns
Juvenile Idiopathic Epilepsy
o Autosomal dominant in (Egyptian) Arabians
o Seizure activity begins days to 6
months of age
o Seizures stop between 1 and 2 years
o Partial or full seizures, post-ictal phase
o May require medication
o Long-term prognosis excellent
Causes of Seizures
Most common
• Hepatoencephalopathy
• Trauma
• Infectious disease
• Toxins
• Intracarotid injection
Neonates
• Hypoxic-ischemic damage
• Metabolic issues
• Congenital abnormalities
• Epilepsy (only in Arabians)
Seizures; Diagnosis, Therapy
Diagnosis of Seizures
o History, signalment
o CBC, chem,
o Test for specific diseases
o CSF
o EEG, CT, MRI
(mass?)
Therapy
o Treat underlying disease
o Anti-convulsants: diazepam(acute),
phenobarbital (maintenance)
o Other anti-convulsants: potassium bromide, phenytoin, primidone
Intracarotid Injection; What? Symptoms
Accidental injection of drug into carotid artery
Symptoms
• Cortical blindness (can improve)
• Self-trauma & seizure
• Brain trauma
Equine Leukoencephalomalacia; How, symptoms, diagnosis, treatment
o Corn contaminated with Fusarium moniliforme -> toxin fumonisin B1
o Summer drought, followed by a wet period
o 3 – 4 weeks after ingestion, acute onset signs
Symptoms
• Anorexia, depression,
• ataxia, circling, blindness, head pressing
• Recumbency, seizures, death in 2-3 days
Diagnosis
• Fumonisin in feed
• CSF – xanthochromia, increased protein, pleocytosis
• Necropsy – focal liquefactive necrosis, sometimes hepatic involvement
Treatment
• Supportive
• Check other horses & remove feed
Nigropallidal Encephalomalacia; How? Symptoms
o Yellow-star thistle (Centaurea soltitialis) or Russian knapweed (Acroptilon repens)
o Some horses develop a craving; toxic in hay also
o Ingestion of large amounts over weeks to months
o Lesions in substantia nigra, globus pallidus
o Young horses most common
o No treatment/recovery
Symptoms
• Sudden onset clinical signs
• Retracted lips, continuous chewing movements
• Aimless walking, circling, ataxic, tetraparetic
• Impaired eating and drinking
• Unable to chew and propel food to pharynx
• Usually can swallow
Narcolepsy; True Vs Sleep Deprivation
True
• Hereditary, rare
• Spontaneous collapse, daytime sleepiness
• May be triggered by specific events
Sleep Deprivation
• Limited recumbent sleep – likely very common
• Pain associated with recumbency
• Environmental factors
• Social-behavioral factors
Peripheral Vs Central Traumatic Lesions
Peripheral
• Head tilt toward lesion
• Nystagmus fast phase away from lesion
Central
• Head tilt away from lesion
• Nystagmus any direction
Temporohyoid Osteoarthropathy Pathogenesis, Diagnosis, Treatment, Prognosis
Pathogenesis
• May begin w/ middle ear infection
• May be primary noninfectious arthritic condition
• Hyoid bone fuses ->
• Any movement can cause breakage ->
• Fracture affects CN VII & VIII deficits
OR
• Acute seizures & death
ALSO
• May have CN IX & X signs (dysphagia)
Diagnosis
• Endoscopy of guttural pouch
• Rads
• CT or MRI
Treatment
• standing basihyoid- ceratohyoid disarticulation
• NSAIDs, +/- antibiotics may help
• Treat corneal ulcer if present
Prognosis
• Most stabilize & improve over 6-12 mo
• Risk of bilateral dz
• Risk of new Fx
Cerebellar Abiotrophy; who?, Symptoms, Diagnosis, Prognosis
o Arabian foals
o Autosomal recessive
o Premature death of purkinje cells
Symptoms
• 6-4wks old
• Intention tremor of the head
• Symmetric ataxia
• Hyperextension of the limbs
• Base-wide stance
• Lack of menace reflex?
• Visual with normal
Diagnosis
• Presumptive based on signs
• Genetic testing
• Histology
Prognosis
• No treatment available
Occipitoatlantoaxial Malformations; Basics, Diagnosis, Treatment
o Congenital malformation
o Arabian horses; autosomal recessive;
o DNA test available for one form
o Neurologic signs result from spinal cord compression
o Onset of signs birth - 6months
Diagnosis
• Confirm with imaging (radiographs, CT, MRI)
Treatment
• No available treatment
Cervical Vertebral Stenotic Myelopathy; Type I Vs Type II
Type I
• Developmental disease in young, fast-growing horses (<2 years of age)
• Most common at C3, C4, C5
• Often young, fast-growing, male horses
• Nutritional imbalances in Cu, Ca, P may play a role
• Concurrent OCD?
Type II
• Older horses with
degenerative
joint disease
• Most common at
C5, C6, T1
• Especially
common in Warmblood breeds
Cervical Vertebral Stenotic Myelopathy; Common name, Pathophysiology, Clinical Signs, Treatment, Prognosis w/ Sx
o “wobblers”
Pathophysiology
• Multiple sites of compression may be present
• Can occur as far caudally as C7 – T1
• May present with acute onset after relatively minor trauma
• Compression may be “static” or “dynamic”
Clinical Signs
• Primarily Upper motor neuron – ataxia, general proprioceptive deficits
• Usually symmetric signs
• Pelvic limbs usually more severely affected if lesion is C1 – C5
• Thoracic limbs may be same or worse if C6 – T1
• May be worse with flexion or extension of the neck (dynamic)
Treatment
• Surgery – “basket” stabilization
• Restricted energy and protein diet
• Time – turn out and wait
Prognosis w/ Sx
• 80% improve one neurologic grade
• 40% improve two grades or more
• Up to 1 year for full recovery
Cervical Vertebral Stenotic Myelopathy; Diagnosis
Rads
Minimal Sagittal Ratio
• minimum sagittal diameter of the spinal canal divided by the maximum sagittal diameter of the vertebral body
• Narrow = <52% at C3/4, C4/5, C5/6
and/or <56% at C6/7
Myelogram
• Best method for definitive diagnosis
• Neutral, flexed, & extended views
• 50% or greater reduction in width of dorsal and ventral dye columns directly opposite each other
Equine Degenerative Myeloencephalopathy; Basics, Predisposing Factors, Diagnosis, Prognosis, Treatment
o Diffuse degenerative neurologic disease
o Classically described as symmetrical ataxia, proprioceptive deficits all four limbs in young horses (6 months to 2 years of age)
o Pigment retinopathy in some affected Warmblood horses
Predisposing Factors
• Genetic predisposition + environmental factors
• Insufficient Vit E in diet especially early in life (lack of fresh green grass)
Diagnosis
• Difficult antemortem
• Measure serum Vit E (may be normal)
• Plasma and CSF phosphorylated neurofilament heavy chain (new / accuracy?)
• Definitive diagnosis requires necropsy
Prognosis
• Poor
Treat
• Supplement Vit E Non racimic (better for prevention)
Equine Motor Neuron Dz; Basics & Clinical Signs
o Risk peaks at about 16 years of age
o Typically seen in horses that have been vitamin E deficient for > 18 months
o Horses usually have not had access to fresh green grass pasture
o Affects lower motor neurons
o Associated muscles atrophy
o Lesion similar to amyotrophic lateral sclerosis (Lou Gehrig’s disease)
Clinical Signs
• Excellent appetite
• Muscle wasting, weightloss
• Abnormal stance
• Weakness, trembling, recumbency
• Paraphimosis
• Ocular lesions
Equine Motor Neuron Dz; Diagnosis, Treatment, Prognosis
Diagnosis
• History, clinical signs
• Mild to moderate increases in CK
• Low plasma vitamin E
• Biopsy of sacrocaudalis dorsalis medialis muscle
Treatment
• Move to new environment
• Vitamin E as described for EDM
Prognosis
• W/ treatment
• 40% improve
• 40% stabilize
• 20% progress
Suprascapular Nerve Injury; aka, acute vs chronic
o AKA Sweeney
Acute traumatic injury
• Outward rotation of the shoulder
Chronic Traumatic Injury
• Visible atrophy
Radial Nerve Paralysis; How? Clinical SIgns
o Trauma around elbow due to lateral recumbency or humeral fx
Clinical Signs
• Can’t flex shoulder or extend limb
• Dorsum of hoof on ground
• Not weight bearing
EPM Life Cycle, Predisposing factors, Diagnosis
Life Cycle
o Definitive host eats meat (OPO) ->
o Sporocyst in feces ->
o Horse eats feces on accident ->
o Sarcocyst encysts in muscle
Predisposing Factors
o 1-5 years old
o Racing or showing
o Spring, summer, fall
o Wildlife, especially opossums
o Wooded terrain surrounding the farm
o Previous EPM on the farm
o Recent adverse health event
Diagnosis
o Serum:CSF titer ratio <100 STRONGLY correlates w/ EPM
o PE
o Neuro exam
o Rule out other diseases
o Detection of IgG in serum & CSF (only shows exposure)
o Necropsy
EPM Clinical Signs
o May be >1 year after infection
o Encited by stress, preganancy, decreased immunity, steroid use
Spinal Cord
• Ataxia, asymmetry, atrophy
Brain
• Depression, Blindness, Circling, Recumbency
EPM Treatment
Sulfadiazine + pyrimethamine
• >3mo
• 70% improve
Ponazuril
• 28 days
• 60% improve
Diclazuril
• Top dress for feed
• 28 days
• 67% improve
o Supportive care
o NSAIDs
o Vit E
o Levamisole
No response in 30 days is poor prognosis
EHV-1 Vs EHV-4
EHV-4
• Respiratory dz
EHV-1
• Neuro dz
• abortion
Equine Herpes Transmission, Pathogenesis
Transmission
• Shed via nasal secretion & aerosol
• Sniffing aborted fetuses
• Horses as young as 11 days can be infected despite maternal Abs
Pathogenesis
• Replication n respiratory tract ->
• Local lymph nodes w/ in hours ->
• Cell associated viremia ->
• Latency ->
• Travel / stress ->
• CNS endothelial cells ->
• Vasculitis & reactive thrombosis
Equine Herpesvirus Myeloencephalopathy; Basics, Clinical Signs, Diagnosis
• All ages accept young
• Pregnant/nursing mares highly susceptible
• Incubation 2-10days
• May be associated w/ abortion or resp dz
• Biphasic fever may come prior to neuro signs
Clinical Signs
o Rapid onset
o Ataxia worse in hindlimbs
o Bladder paralysis (dribbling urine)
o May have central or CN signs
Diagnosis
o PCR or isolation of nasal secretions or buffy coat
Equine Herpesvirus Myeloencephalopathy; Treatment, Prognosis, Prevention
Treatment
o NSAIDs
o Heparin
o Support rectal/bladder function
o Soft bedding
o Support sling
Prognosis
o Fair-good if standing
o Poor if recumbent
o Months to recover
o Some have residual effects
Prevention
o Separate horses into small groups
o Minimize stress
o Isolate new arrivals
o Vx does not prevent neuro dz (may decrease nasal shedding)
Rabies Pathophysiology
• Virus enters via animal bite ->
• Replicates in muscle at site of bite ->
• Infects nerve in PNS & moves by retrograde transport ->
• Replicates in dorsal root ganglion and travels up spinal cord to brain ->
• Brain infected ->
• Travels from brain to eyes, kidneys, salivary glands
Rabies; Clinical Signs, Diagnosis
Clinical Signs
• Fever, lethargy, anorexia
• Lameness, ataxia, paresis
• Hyperesthesia, hyperactivity, aggression
• Depression, blindness, pharyngeal paralysis
• Loss of tail, anal tone
• Recumbency, seizures, death
Diagnosis
• Post-mortem FA of brain
Equine Core Vaccines
o Tetanus
o West Nile virus
o Rabies
o Eastern equine encephalomyelitis
o Western equine encephalomyelitis
Eastern Equine Encephalitis; Vector, Clinical Signs, Diagnosis, Treatment, Prognosis, Control
Vector
o Mosquito
Clinical Signs
• High fever
• Anorexia
• Stiffness
• Forebrain signs
• Recumbency, coma, death
• Sometimes inapparent infection (mild fever)
Diagnosis
• IgM capture ELISA
Treatment
• Support
• Flunixin Meglumine
• Anti-convulsants
Prognosis
• 90% mortality
Control
• Vx (twice yearly in endemic areas)
• Mosquito control
West Nile Virus; CLinical Signs, Diagnosis, Treatment, Control
Clinical Signs
• Inapparent infection (80%)
• Weakness & ataxia (90%)
• Lethargy, depression
• Muscle fasciculations
• Fever
• Changes in mentation/behavior
• Recumbency
• CN abnormalities
Diagnosis
• IgM antigen capture ELISA
Treatment
• Supportive care
• Flunixin meglumine
• Hyperimmune plasma
Control
• Control mosquitos
• Vaccinate (core)
Tetanus; Agent, Clinical Signs, Treatment
Agent
• Clostridium tetani
• G(+), anaerobic rod
• Soil & feces worldwide
• Exotoxins produced in anaerobic environment
• Incubation days – months
• Tetanospasm toxin affects inhibitory neurons -> blocks glycine, GABA -> muscle spasms
Clinical Signs
• Contaminated wounds, injury, surgery sites
• Extensor rigidity / muscle spasms
• Sardonic grin
• Prolapsed 3rd eyelid
• Sweating/hyperthermia
• Recumbency, death
Treatment
• Debride, irrigatewound
• Metronidazole
• Tetanus antitoxin IM, IV, SC, intrathecal
• Tranquilizers or muscle relaxants
• Supportive care
Tetanus Vaccination
• Annual booster
• Booster mares 4-6wks prior to parturition
Foals from Vx Dams
• 3 dose series of tetanus toxoid @ 4-6 MO
Foals from Non-Vx Dams
• Tetanus antitoxin at birth
• 3 dose series of tetanus toxoid @ 1-4 MO
Botulism; Transmission, Clinical Signs, Diagnosis
Transmission
• Toxins A (PNW), B, C, or D from Clostridium botulinum
• Ingestion of feed w/ preformed toxin
• Ingestion of C. botulinum & toxin production in GI
• Infection of wound w/ C. botulinum
Clinical Signs
• 1-10 day incubation
• Sudden death
• Progressive weakness
• weak eyelid, tongue, tail tone (first signs)
• Mydriasis, sluggish pupils
• Intestinal hypomotility, ileus, colic
• Recumbency, respiratory paralysis
Diagnosis
• Isolate spores in GI or feed
• Toxin in GI contents, feed, tissue, serum
Botulism; Treatment, Prognosis, Prevention
Treatment
• Support
• Antitoxin (not available once toxin binds)
• GI cathartics
• Metronidazole
Prognosis
• Most adults die
• Foals have good chance w/ treatment
Prevention
• Vx pregnant mares w/ type B toxoid
• Vx foals w/ type B toxoid
• Vx in endemic areas
Cardiac Dz; Presenting Signs
o Exercise intolerance/poor performance
o Syncope, collapse or “seizure”
o Weakness
o Failure to grow and thrive
o Cough, dyspnea, exercise induced pulmonary hemorrhage
Cardiac Dz; PE Findings
o Arrhythmia
o Murmur
o Jugular pulsation
o Pericardial friction rub
o Generalized venous distension
o Poor perfusion
o Ventral pitting edema
o Cough, dyspnea, tachypnea
o Tachycardia
Cardiac Auscultation
Left side
• Cranial to bicep – Pulmonic valve
• Bicep and dorsal to P – Aortic valve
• Caudal to tricep – Mitral valve
Right Side
• Tricep – Tricuspid valve
Heart Sounds
S1
• Closure of AV valves
S2
• Closure of aortic & pulmonic valves
S3
• Rapid ventricular filling
S4
• Atrial contraction
Systolic Vs Diastolic Murmur
Systolic
• Synchronous w/ pulse
• Short part of cycle (if HR slow)
Diastolic
• NOT Synchronous w/ pulse
• long part of cycle (if HR slow)
Ancillary Diagnosis for Arrhythmia
Electrocardiography
• Evaluation of arrhythmia
• Base-Apex lead system
• White at base of neck
• Red on chest behind elbow
• Black almost at withers
2nd Degree AV Block
o Normal in fit, healthy horses
o High resting parasympathetic tone
o Arrhythmia disappears with exercise, excitement
o You may auscultate an isolated S4 sound at the time of the “missing” beat!
Ventricular Tachycardia; Treatment
Treat if
• Rate > 80 BPM
• Multifocal
• R on T
Treat w/
• Lidocaine
• Mg sulfate
• Quinidine
• Procainamide
A Fib; Prognosis, Treatment
o Common pathologic arrhythmia
Prognosis depends on
• Duration of arrhythmia
• Presence of underlying heart dz
Treatment
• Cardioversion w/ Quinidine
• Transverse electrical cardioversion (TVEC)
Physiologic Murmurs
o Common in fit horses, neonates, systemic dz
o Usually systolic
o Usually < grade III/VI
o Soft “blowing” murmur
o Localized
o May be intermittent
Pathologic Murmurs
Systolic
• Regurgitation of mitral or tricuspid (most common)
• Aortic or pulmonic stenosis
• Congenital VSD (common)
Diastolic
• Aortic regurgitation (most common)
Heart Failure; Signs, diagnosis
o Tachycardia
o Edema & jugular pulse
o May have tricuspid or mitral regurgitation
o May have arrhythmia
Diagnosis
• Measure cTNI
• Check selenium
Sign of Patent Ductus Arteriosus
o Continuous murmur in foal
Thrombophlebitis; Cause, Clinical Signs, Diagnosis, Treatment
Cause
• Complication of jugular injection or catheter
Clinical Signs
• Heat, swelling, pain
• May have systemic signs
• Complete thrombosis -> venous distension, edema of head
Diagnosis
• Clinical exam
• Ultrasound
Treatment
• Antimicrobials
• Anti-inflammatories
Aortoiliac Thrombosis; Clinical Signs, Diagnosis, Prognosis
Clinical Signs
• Lameness (often exercise associated)
• Collapse
• Cool extremities, poorly palpable pulses
• Acute, severe pain
Diagnosis
• Feel clot on rectal exam
• Ultrasound of affected vessels
Prognosis
• poor
Parts of Respiratory Tract Visible through Radiograph Vs Ultrasound
Rads
• Upper airway
• Dentition
• Thorax (parenchymal dz)
US
• Fluid, fibrin, or mass/abcess in pleural surface
• better diagnostic
• can’t see parenchyma
Transtracheal Wash Vs Broncheoalveolar Lavage
Transtracheal Wash
o Sterile
o Lower respiratory tract
o Endoscope or percutaneous
o Culture & cytology
o Macrophages normal
o Should have < 20% neutrophils
Bronchoalveolar Lavage
o Non sterile
o Lower respiratory tract
o Endoscope or special tube
o Cytology for inflammation/hemorrhage
Structures in the guttural pouch
Medial
• CN VII – XII (Not VIII)
• Sympathetic trunk
• Internal carotid
Lateral
• External carotid artery & vein
• CN VII
Guttural Pouch Tympany; congenital Vs acquired, Treatment, Prognosis
Congenital
• Arabians
• Fillies
Acquired
• Inflammation
Treatment
• decompress
Prognosis
• Good
Guttural Pouch Empyema; Bacteria, Clinical Signs, Diagnosis, Treatment, Prevention
o Strep equi
Clinical Signs
• Fever
• Enlarged Guttural pouch
• Lymph node enlarged
• Purulent nasal discharge
• NO SIGNS: Shed!!
Diagnosis
• Endoscopy
• 3 washes 2 weeks apart (NO nasal swab)
• Culture
• PCR for M protein
• SeM ELISA (for complicated)
Treatment
• Lavage & removal
• +/- surgery
• topical antibiotics through lavage
• NSAIDs
Prevention
• Immunity after infection
• Vx (poor efficacy)
Guttural Pouch Empyema; Complications & Tretment for Purpura hemorrhagica
Complications
• Dyspnea
• Dysphagia
• Bastard strangles (abscess)
• Myositis
• Purpura hemorrhagica
Treatment for Purpura hemmorhagica
• Corticosteroids
• Supportive care
• Discuss prognosis with owner
• No antibiotics (unless ongoing infection)
Cells found on Normal BAL
o 5% NT
o 50-55% macro
o 35-40% LT
o +/- 1% mast cells
Severe Asthma; Basics, Pathogenesis, Clinical Signs
o AKA recurrent airway obstruction
o Genetic predisposition + allergen
o > 7yo
Pathogenesis
• Neutrophils ->
• Bronchospasm ->
• mucus plugs ->
• smooth muscle hyperplasia ->
• airway wall thickening ->
• fibrosis ->
• difficulty breathing
Clinical Signs
• Heave line
• Cough
• Anorexia
• Weight loss
• Nare flaring
Severe Asthma; Diagnosis, Control, Prognosis
Diagnosis
• Respond to steroids?
• Sedation & butorphanol ->
• Bronchoalveolar lavage & cytology
• > 25% non-degenerative neutrophils & churchmann’s spirals
Control
• No cure
• Minimize exposure to Ag
• Corticosteroids (fluticasone IN)
• Bronchodilators (albuterol/clebuterol)
• Ciclesonide (horse inhaler)
• Manage environment
Prognosis
• Progressive
• Euthanize once advanced
Mild Asthma; Basics, Diagnosis, Treatment
o AKA inflammatory airway dz
o Multifactorial
o Allergens important
o All ages (often young)
o Reversible
Diagnosis
• Mucus on endoscopy
• 10-15% non-degenerative NT OR >1-5% EO OR >2-5% mast cells on BAL & cytology
Treatment
• Control environment
• Corticosteroids
• IFN-alpha
• Mast cell inhibitors (Neocromil or cromolyn)
Exercise Induced Pulmonary Hemorrhage (EIPH); Pathogenesis, Clinical Signs, Diagnosis, Treatment
Pathogenesis
• High transmural Pressure +
• High capillary Pressure +
• Negative intrathoracic Pressure ->
• Capillary stress failure
Clinical Signs
• Epistaxis (7% of horses)
• Excessive swallowing
• Cough
• Sudden death
Diagnosis
• Blood on endoscopy
• RBCs or hemosideropahges on BAL
Treatment
• No treatment
• Furosemide (probably doesn’t help)
• Nasal strips (probably doesn’t help)
Treatment for Respiratory Dz & Abortions due to EHV
Respiratory Dz
• Rest
• NSAIDs
• Support
EHV Abortion
• Uterine lavage
• NSAIDs
• Antibiotics if retained placenta
Equine Viral Arteritis; Pathophysiology, Clinical Signs, Diagnosis
Pathophysiology
• Inapparent carrier stallions ->
• Virus in urine, semen, respiratory secretions ->
• aerosolized -> upper airway resp -> macrophages -> endothelium ->
• abortion
Clinical Signs
• Ventral edema
• Fever
• Conjunctivitis & rhinitis
• Cough
• Dyspnea
• Abortions
• Fatal pneumonia in foals
Diagnosis
• PCR of nasopharyngeal swab, conjunctival swab, blood (use EDTA)
• Virus isolation
Equine Viral Arteritis; Positive PCR, Treatment, Prevention
If Positive
• Notifiy state
• Quarantine
• Suspend breeding
Treatment
• Rest
• Support
• Fluids
• NSAIDs
• Furosemide for edema
Prevention
• Biosecurity
• Vx (false positive on PCR)
Equine Influenza; Who, Clinical SIgns, Diagnosis, Positive PCR, Prevention
o H3N8
o Young animals
o Donkeys/mules
Clinical Signs
• Biphasic fever
• Nasal discharge
• Submandibular LN swelling
• Dry cough
• Limb edema
Diagnosis
• PCR of nasopharyngeal swab or transtracheal wash
If Positive Result
• Notigy state
• Quarantine 21d post clinical case
• Biosecurity
Prevention
• Vx every 6 mo
• Vx 4-6wks pre foaling
• Vx foals 3-6mo
Pleurodynia
Pleural pain that results in
• Shallow breathing
• Reluctance to move
• Abducted elbows
• Intolerant to rebreathing exam
• Painful on percussion / pressure on thorax
• Painful cough
Pleuropneumonia; Causes, Clinical Signs, Diagnosis
Causes
• Travel >4hr
• Anesthesia
• Previous respiratory dz or choke
Clinical Signs
• Crackles/wheezes/silence
• Tachypnea
• Fever
• Pleurodynia
• Dyspnea
• Ventral edema
• Chronic low BCS
Diagnosis
• Thoracic ultrasound
• Drain + thoracic radiographs
• Trans tracheal wash culture/cytology
• Pleural fluid may be sterile
Pleuropneumonia; Common Bacteria
G+
• Strep Zooepidemicus (99%)
• Staph aureus
G-
• Pasturella
• Acinobacillus
• Klebsiella
• E coli
• Bordetella
Anaerobes
• Bacteroides fragilis (most common anaerobe)
• Clostridium
• Fusobacterium
Or mixed
Pleuropneumonia; Treatment, Complications, Prognosis
Treatment
• Inhaled Penicillin (G+), gentamicin (G-), metronidazole (anaerobes)
• Po antibiotics once under control
• O2 if needed
• Flunixin meglumine
• Support
Complications
• Laminitis
• Thrombosis
• Sepsis / endotoxemia
• Diarrhea
Prognosis
• Good if caught early
• Worse if anaerobic bacteria
Where to catheterize a horse
• lateral thoracic
• cephalic
Neonatal Pneumonia; Causes, Common Bacteria, DIagnosis, Treatment
Causes
o Systemic infection in utero or post-partum
o Failure of passive transfer
o Aspiration due to weakness or dysphagia
Common Bacteria
o E. coli,
o Klebsiella
o Strep Zoo
Diagnosis
o Blood culture
o TTW w/ culture & cytology (if not in resp distress)
o Arterial blood gas
o Rads
o Ultrasound
Treatment
o Broad spectrum antibiotics
o Anti-inflammatories
o Intranasal O2
o Bronchodilators
Acute Respiratory Distress Syndrome (ARDS) Basics, Diagnosis, Treatment
o Atypical interstitial pneumonia
o <8MO
o respiratory distress
Diagnose
• Thoracic rads
Treatment
• Intranasal O2
• Corticosteroids
• Bronchodilators
• Antimicrobials
EHV-1 in foals; Pathophysiology
• Mare infected w/ EHV-1 ->
• Weak foal ->
• Progressive pneumonia ->
• Secondary bacteria ->
• Unresponsive to treatment
Pneumonia Causes in Immunosuppressed Foals
Pneumocystis carinii
• Diagnose w/ cytology
• Treat w/ TMS
Adenovirus (SCID)
• Fatal bronchopneumonia
Other common pathogens
Rhodococcus equi; who, extrapulmonary lesions, diagnosis, treatment, prognosis, prevention
o G+ aerobic
o Young foals
o Immunosuppressed adults
o Immunosuppressed humans
o Infected early in life
Extrapulmonary Lesions
• Ulcerative colitis & diarrhea
• Ulcerative lymphangitis
• Arthritis & osteomyelitis
• Abscesses
• Immune mediated, polysynovitis, thrombocytopenia, anemia
Diagnosis
• Thoracic ultrasound
• Thoracic rads
• Blood work
• TTW cytology culture for definitive diagnosis
Treatment
• rifampin + azithromycin (orange urine)
• NSAIDs
Prognosis
• No treatment for abscess
• Worse prognosis extrapulmonary
• No VX
Prevention
• Hyperimmune plasma
• Give 1-2L at birth
• Decreases severity of dz
Parasitic Pneumonia; parasite, who, diagnosis, treatment
o Parascaris equorum
o 4mo – 1yo
o migration in lungs causes inflammation & eosinophils
o adults are immune
Diagnosis
• TTW or BAL for eosinophils & larvae
• Blood work
Treatment
• Multiple doses fenbendazole
• Tube w/ water-oil
