Large Animal Neurology Flashcards
(232 cards)
1
Q
are brain diseases more common in livestock or horses
A
livestock
horses more common to have spinal cord disease
2
Q
What might be a cause of Horner’s disease in horse
A
neck trauma- iatrogenic caused by injections
3
Q
the extent of joint movement
A
dysmetria
4
Q
What are challenging maneuvers used in an equine neurological examine
A
1) Head up and walk
2) Circling
3) Tail pull
4) backing
5) over a curb
6) Hill
7) blindfold
5
Q
How might you describe ataxia in a horse
A
1) Truncal sway
2) Proprioceptive deficits
3) Inconsistent foot placement
4) Irregular irregularities
5) Interference
6) Excessive lifting of feet and uncontrolled placement
7) Does not seem to know where feet are placed
6
Q
too little joint movement
-stiff / tin soldier
A
hypometria
7
Q
too much joint movement
-floating: lifting thoracic limbs too high
A
hypermetria
8
Q
What are signs of paresis in a horse
A
1) Toe dragging
2) Knuckling (on hills)
3) Stumbling
4) Inability to resist tail pull
9
Q
The ataxia score in horses is on a scale of
A
1 to 5
0: No neurological deficits
1: Neurologic deficits just detected at normal gait but worsened by backing, turning, loin pressure, or neck extension
2) Neurologic deficits easily detected at the walk and exaggerated by backing, turning, loin pressure, or neck extension
3) Neurological deficits prominent at the walk with a tendency to buckle or fall with backing, turning, loin pressure, or neck extension, postural deficits noted at rest
4) Stumbling, tripping, and falling spontaneously at a normal gait
5) Horse recumbent
10
Q
Grade this horse on ataxia scale:
No neurological deficits
A
Grade 0
11
Q
Grade this horse on ataxia scale:
Neurologic deficits just detected at normal gait but worsened by backing, turning, loin pressure, or neck extension
A
Grade 1
12
Q
Grade this horse on ataxia scale:
Neurologic deficits easily detected at the walk and exaggerated by backing, turning, loin pressure, or neck extension
A
Grade 2
13
Q
Grade this horse on ataxia scale:
Neurological deficits prominent at the walk with a tendency to buckle or fall with backing, turning, loin pressure, or neck extension, postural deficits noted at rest
A
14
Q
Grade this horse on ataxia scale:
Stumbling, tripping, and falling spontaneously at a normal gait
A
Grade 4
15
Q
Grade this horse on ataxia scale:
Horse recumbent
A
Grade 5
16
Q
What will you see in a horse with peripheral nerve damage / LMN
A
weakness predominates
postural deficits and ataxia (mild)
17
Q
What will you see in a horse with spinal cord damage
A
1) Paresis
2) Ataxia
3) dysmetria
4) spasticity
18
Q
What will you see in a horse with cerebellum damage
A
Ataxia
Intention tremors
19
Q
What will you see in a horse with damage to the vestibular system
A
Ataxia
Head tilt
Postural deficits pronounced
20
Q
What will you see in a horse with damage to brainstem
A
Ataxia
Weakness
Dysmetria
Dysphagia
anisocoria
dilated pupils possible
21
Q
What will you see in a horse with damage to the cerebral cortex
A
Postural deficits
Seizures
altered mentation
blindness
22
Q
You might see horner’s syndrome in horses with damage to the
A
C1-C5
C6-T2
23
Q
Damage to what spinal cord segment might you see a horse with urinary incontience, fecal retention, hypalgesia tail and perianal
normal thoracic and pelvic
A
S3-S5
24
Q
What might see you with damage to the coccygeal spinal segement in a horse
A
decreased tail tone
hypalgesia caudal tolesion
normal thoracic and pelvic
25
What might you see with damage to S3-S5 in a horse
1) Urinary incontinence
2) Fecal retention
3) Hypalgesia tail and perianal
*Normal thoracic and pelvic
26
What might you see with damage to T3-L3 in a horse
1) Proprioceptive deficits (rear)
2) Normal gait in front
3) Rear limb weakness
4) Spasticity, pelvic limbs
27
What might you see with damage to C6-T2 in the horse
1) Proprioceptive deficits, worse in front than in rear
2) Weakness
3) Thoracic limb muscle atrophy
4) +/- Horner's syndrome
28
What might you see in damage to C1-C5 in the horse
1) Spastic gait, worse in rear limbs
2) Proprioceptive deficits
3) Weakness
4) +/- Horner's syndrome
29
What is the main reason for cranial nerve disease in a horse
Guttural pouch disease (often affects CN 7 and/or 8)
30
What are the main causes of spinal cord disease in the horse **
1) Cervical Vertebral Compressive Myelopathy
2) Equine Protozoal Myeloencephalitis
3) Eqine Degenerative Myelopathy/ Equine Neuronal Dystrophy
4) Trauma
5) Neoplasia
** Wobbler, EDM, and EPM is the most common **
31
What will you see with radial nerve paralysis in the horse
non-weightbearing
dropped elbow
inability to advance the limb
Causes: humeral fracture, trauma, post anesthesia
32
What will you see with femoral nerve paralysis in the horse
1) Nonweight bearing
2) Flexion of stifle, hock, fetlock
3) Loss of sensation medially
Causes: trauma, post anesthesia, dystocia
33
T/F: there is no vaccine for equine protozoal myeloencephalitis
True
34
What are the 5 core vaccines for horses
1) Rabies
2) Tetanus
3) EEEV
4) WEEV
5) West Nile Virus
Risk based: Equine Herpes Virus 1/4 (1- doesnt do a lot against neurologic or abortion)
35
What are common cortical diseases in livestock
1) Polioencephalomalacia (PEM)
2) Salt toxicity / water deprivation
3) Lead poisoning
4) Vitamin A deficiency
5) Rabies
6) Transmissible Spongiform Encephalopathies
36
necrosis of the grey matter
polioencephalomalacia (PEM)
37
What is a main cause of polioencephalomalacia in livestock
thiamine (vitamin B1) metabolism dysregulation
decrease ATP-dependent Na/K and H20 transport across cell membranes leading to neuronal dysfunction and ultimately swelling and laminar cotrical necrosis
38
What is the pathogenesis of polioencephalomalacia in cattle
main cause
thiamine (vitamin B1) metabolism dysregulation
decrease ATP-dependent Na/K and H20 transport across cell membranes leading to neuronal dysfunction and ultimately swelling and laminar cortical necrosis
39
What are the clinical signs of polioencephalomalacia in livestock
1) Ataxia
2) Proprioceptive deficits
3) Altered mentation (aggression; lethargy)
4) cranial nerve deficits
5) Seizures, coma, death
6) Anorexia
7) Diarrhea
8) muscle tremors
9) head pressing, star gazing
10) Opisthotonus
11) Eye signs
40
What livestock is polioencephalomalacia most common in
small ruminants > cattle > camelids
41
cortical blindness *
an animal that is blind has an absent menance but a functional pupilary light reflex
*if they have this then cortex damage is likely
42
How do you diagnose polioencephalomalacia
history and clinical signs and response to treatment
Necropsy: edema, laminar necrosis, may fluoresce under UV light, findings also with Pb and Na toxicity
43
44
What is the prognosis of polioencephalomalacia
good prognosis- patient will likely respond well to thiamine treatment
44
How might livestock animals get salt toxicity or water deprivation
- High salt intake
-H20 deprivation followed by rapid H20 intake
44
Salt toxicity/ water deprivation pathophysiology
1) Na+ accumulates in neurons and CSF
2) Hyperosmolarity leads to reduced energy dependent Na+ transport and inefficient cell Na+ removal
3) Thirst receptors trigger H20 consumption
4) Water in the extracellular fluid then shifts intracellularly
5) CNS edema; increased intracranial pressure
6) Acute encephalopathy
45
What is the pathophysiology of lead toxicity
1) Entry through GI or respiratory systems
2) Sequestered in bone matrix
3) Pb is toxic to cells, especially in neurons and RBS
4) Pb inhibits enzymes at Cu, Zn, Fe binding sites
5) inhibits heme synthesis and decreases RBC life
6) Capillary dusfunction
7) CNS hemorrhage and edema
46
What is a major differential for cattle with rabies
Aujeszky's
47
a prion disease- protease resistance
induced conformational changes
disrupts normal cellular functions
found in all cell memebranes, especially neurons
Scrapie- Bovine Spongiform Encephalopathy
48
What is the only way to diagnose bovine spongiform encephalopathy in cattle
post mortem
49
How is bovine spongiform encephalopathy transmitted
1) feeding rendered animal proteins from infected animals
2) spontaneous mutation
50
How is scrapie transmitted
1) Horizontal and vertal - not inutero but in the placenta
not heritable
requires susceptible genotype and exposure
2) atypical: spontaneous mutation
51
How do the clinical signs of BSE differ from scrapie
Both: behavior changes, abnormal gait
BSE: Ptyalism, reluctance to be milk, fasciculations, proprioceptive deficits, licking
Scrapie: Pruritus, biting, licking, grinding teeth, more aware, weight loss, cannibslism
52
What symptom is signficant in sheeps with scrapie
Pruritus
53
How do you diagnose bovine spongiform encephalopathy
*No antemortem test
1) Histopathology for lesions
2) Western Blot
54
How do you diagnose scrapie
1) 3rd eyelid or rectal mucosal biopsy
2) Histopathology specific brain region
3) Genetic risk factor (all breeds are susceptible
55
gram + bacteria that grows in forages with pH >5.4 (improperly fermented silage)
also found in soil and GI
Listeria monocytogenes
56
What are the clinical signs of Listeria monocytogenes
Neurologic form:
-Fever (early), anorexia, lethargy, ataxia, head pressing
-CN V-XII deficits
Septicemic form
Abortion form
57
What cranial nerve deficits can be seen with Listerioisis
CN V-XII deficits
58
gram negative bacteria that causes thromboembolic meningoencephalitis
Histophilus somni
59
Histophilus somni causes
thromboembolic meningoencephalitis
-fever
-asymmetric signs frequent
-oculuar: retinal hemorrhages, hyphema, hypopyon
-respiratory, polyarthritis reproduction
60
What is the meningeal worm that affects sheeps, goats, and camelid
Paraelaphostrongylus tenuis
61
What is the pathogenesis of Paraelaphostrongylus tenuis
1) Adults in subarachnoid space and cerebrospinal venous sinuses of deer
2) Ova: released into blood and escapes via lungs
3) Slugs and snails (intermediate host)
4) Aberrant hot ingest organisms and within 2 weeks larvae migrate from GI to spinal cord and brainstem
62
How do you diagnose Paraelaphostrongylus tenuis
1) Endemic area or white tailed deer exposure
2) Posterior paresis
3) Ataxia
4) Proprioceptive deficits
5) CSF eosinophilia and increased protein
6) Necropsy
63
How do you treat Paraelaphostrongylus tenuis
1) Fenbendazole- treat larvae in CNS (ivermectin only affect circulating larvae)
2) Supportive care
Prognosis is fair to poor
Prevention is to prevent exposure to deer and use guinea fowl to eat intermediae hosts
Monthly ivermectin injections
64
Why shouldnt you use ivermectins to treat current Paraelaphostrongylus tenuis infestations?
Ivermectins only affect the circulating larvae
*Use fenbendazole to treat larvae in the CNS
65
What are the clinical signs of cerebellar disease in livestock?
1) Proprioceptive deficits
2) Intention tremor
3) Opisthotonus
4) Strabismus
5) Mystagmus
6) Hypermetria
66
What are some examples of cerebellar disease in large animals
1) Cerebellar hypoplasia
2) Staggers- grasses
3) Storage diseases
67
What CNS lesions can occur due to bovine viral diarrhea virus
1) Cerebellar hypoplasia - clinical signs at birth
2) Hydrancephaly
3) Hydrocephalus
4) Hypomyelinogenesis
*Days 90-170 of gestation
68
When are CNS lesions present in BVDV infections?
Days 90-170 of gestation
69
How might a cow get cerebellar hypoplasia from BVDV
natural infeciton during days 90-170 of gestation or vaccination with a modified live vaccine
70
How might spinal injuries occur in livestock
1) Trauma *
2) Abscess *
3) Abnormal bone mineralization
4) Lymphosarcoma
Common sites:
C2-C4; T10-T13; L3-L6
71
What are common peripheral neuropathies in livestock
Suprascapular n
Radial n
Femoral n
Sciatic n (Calving)
Peroneal n
Tibial n
Obturator n (calving)
72
What nerves are common peripheral neuropathies associated with calving paralysis? *
1) Sciatic Nerve
AND
2) Obturator Nerve
73
How do you treat calving paralysis in cows
1) Corticosteroids; NSAIDs
2) Support, floating, slinging
3) Hobbles (obturator nerve)
74
How do you determine if a horse has neurologic disease
1) Abnormal Behavior: Altered mentation, seizures, coma, circling, head pressing
2) Loss of function: Unable to swallow, muscle atrophy, inability to void urine
3) Abnormal gait:
75
How do you evaluate the hypoglossal nerve in the horse?
tongue tone
76
How do evaluate accessory nerve in the horse
cranial neck muscle symmetry
77
How do you evaluate the vagus nerve in the horse
"Slap" test for laryngeal abduction
78
How do you evaluate the glossopharyngeal nerve in the horse
test the ability to swallow
79
How do you evaluate the vestibulocochlear nerve in the horse
1) Head tilt/turn
2) circling/leaning
3) response to environmental sounds
80
How do you evaluate the facial nerve in the horse
1) facial symmetry
2) rostral tongue sensation
81
How do you evaluate the abducens nerve in the horse
1) eye position- retraction
2) lateral movement
82
How do you evaluate the trigeminal nerve in the horse
1) Cutaneous sensation
2) Tone of mastication muscles
3) Ability to Chew
83
How do you evaluate the trochlear nerve in the horse
Eye position
ventrolateral
84
How do you evaluate the oculomotor nerve in the horse
1) Pupillary light reflex
2) Eye position
3) medial movement
85
How do you evaluate the optic nerve in the horse
1) Menace response
2) Pupillary light reflex
3) Dazzle reflex
86
How do you test the olfactory nerve in the horse
detection of hidden treat
87
What cranial nerves are affected by the guttural pouch disease
5, 7, 8, 9, 10
88
What is a common way for a horse to get facial nerve dysfunction
trauama from tight halter
89
What should you do if you see deficits of cranial nerves 5, 7, 8, 9, or 10
inspect the guttural pouch on that side
90
What are the most common guttoral pouch diseases that can lead to cranial nerve deficits
1) Strep equi equi- retropharayngeal abscess leading to emphyema
2) Guttoral pouch mycosis
3) Temporohyoid Osteoarthropathy -styohyoid junction is enlarged
91
What do you see with cervical vertebral compressive myelopathy or Wobblers
all 4 limbs
1) Symmetrical ataxia
2) Dysmetria
3) Paresis
*normal mentation, intact peripheral nerve function
caused by focal spinal cord compression
92
CVCM affects primarily
young, large breed, fast growing, male horses
93
What is the most common cause of non-infectious spinal cord disease in the horse
CVCM (Wobblers)
94
What else do you see with CVCM
developmental orthopedic disease- multifactorial etiology, sometimes horses have OCD lesions elsewhere
95
How might older horses have CVCM
secondary to degenerative joint disease affecting articular process joints and possibly intervertebral disk space
96
How do you diagnose CVCM in horses
Survey Radiographs to see if there is good spacing for the spinal cord but do not give spinal cord information
final diagnosis is by CT myelography
97
How do you treat CVCM in horses
1) Dietary caloric restriction in growing horses only (<1-2 years of age)
2) Cervical vertebral interbody fusion surgery: 65-70% of horses improve and return to atheletic use
98
What kind of horses is dietary caloric restriction only helpful in for the treatment of CVCM
growing horses only that are <1-2 years of age
99
What causes EPM?
1) Sarcocystis neurona
2) Neospora hughesi
*Range of disease defined by range of opossum
100
Sarcocystis neurona has been found to cause
EPM
101
Neospora hughesi has been found to cause
EPM
102
Is EPM focal or multifocal
Multifocal progressive disease
103
What is the lifecycle of Sarcocystis neurona
1) Definitive host, opossum, where replicates
2) Horse ingests sporocyst (aberrant host)
104
What are the clinical signs of EPM
Variable- can involve the brain or the spinal cord
Spinal cord: asymmetry, muscle atrophy, ataxia, dysmetria, paresis
Brainstem:
CN VII, VIII
Seizures
Lethargy
105
can EPM cause symmetrical disease? ****
yes, occasionally therefore it is a main differential for CVCM
but it is primarily asymmetrical disease
106
How do you diagnose EPM
It can be very challenging because there are variable clinical signs and there is a high seroprevalence
1) Surface antigen on serum and CSF of SAG2, 4/3 ELISA
2) Confirm intrathecal antibody production via serum:csf titer ratio
107
Serum:CSF titer ratio to confirm intrathecal antibody production is important in EPM diagnosis but how might there be antibodies in the CSF *
1) Antibody production in the CNS
2) Leakage over an intact BBB
3) Leakage over a diseased BBB
4) Iatrogenic contamination during CSF collection
108
How do you treat EPM
1) Ponazuril- Marquis: disrupts the apicoplast organelle which is a chloroplast related organelle important in energy metabolism and cell division
28 day treatment with 63% efficacy
2) Sulfadiazine/pyrimethamine (ReBalance)
3) Diclazuril
109
Ponazuril is used to treat
EPM
110
What is the mechanism of action of Ponazuril
disrupts the apicoplast organelle which is a chloroplast related organelle important in energy metabolism and cell division
28 day treatment with 63% efficacy
111
EDM/eNAD is a
diffuse neurodegenerative disease caused by genetic and environmental factors with a predisposition to vitamin E deficiency
leads to symmetric ataxia and proprioceptive deficits
onset of 1-12 months of age then stabilizing within days to months
occasionally occurs in late-onset in older horses
112
What causes equine degenerative myelopathy *
diffuse neurodegenerative disease caused by genetic and environmental factors with a
predisposition to *vitamin E deficiency*
113
What are the clinical signs of EDM/eNAD
symmetric ataxia
proprioceptive deficits
decreased menace, lethargy, behavior change
114
How do diagnose EDM/ eNAD
1) Suggestive by excluding CVCM, EPM, or EHM
2) EDM confirmation in the bloodline
3) Low serum vitamin E <2ug/mL
4) Deficient dietary vitamin E
5) Post-mortem confirmation
115
How do you treat EDM/eNAD
1) Vitamin E supplementation
*Prognosis is poor, unlikely improvement of clinically affected animals is seen after supplementation
supplementation of breeding stock and young horses can reduce incidence and severity of the signs
116
What are the common peripheral neuropathies in horses
1) Radial nerve/ Brachial plexus
2) Suprascapular n
3) Fmeoral n
4) Obturator n
5) Sciatic n
Affected motor nerve leads to hypotonic/atonic effector muscle and muscle atrophy
117
What is Sweeney
Suprascapular nerve paralysis due to trauma to nerve at point of the shoulder
muscle atrophy of the supraspinatus, infraspinatus, and triceps leading to a very prominent scapular spine
abnormal gait with shoulder exo-rotation
used to see in old time with horses pulling carts and tack fixed in incorrect area
118
What 2 things will you see with a horse with Sweeney
1) muscle atrophy of the supraspinatus, infraspinatus, and triceps leading to a very prominent scapular spine
2) Abnormal gait with shoulder exo-rotation
119
What causes Sweeney
Trauma to the suprascapular nerve at the point of the shoulder
120
What muscles become atrophied with Sweeney
1) Supraspinatus
2) Infraspinatus
3) Triceps
121
What diseases are CORE for horses *
1) Rabies
2) Tetanus
3) Eastern Equine Encephalomyelitis
4) Western Equine Encephalomyelitis
5) West Nile Virus Encephalomyelitis
122
Rabies virus remains infectious in a carcass for
<24 hours
123
What animals serve as a reservoir for rabies
Bat
Skunk
Racoon
Fox
124
What occurs in the Centripetal stage of rabies
virus travels in the peripheral nerves to the CNS at ~1cm/day
125
What occurs during the central stage of rabies
the CSF contains virus
126
What occurs during the centrifugal stage of rabies
the saliva contains the virus
127
How do you diagnose rabies
post-mortem diagnosis: IFAT on brain tissue or presence of Negri bodies
128
What are the clinical signs of rabies in horses
1) Ataxia and paresis (43%)
2) Lameness (29%)
3) Recumbency (14%)
4) Pharyngeal paralysis (10%)
5) Colic (10%)
129
Horses with rabies develop a fatal encephalopathy within
5-7 days
130
Tetanolysin causes _______ while tetanospasmin is a ______
tissue destruction
neurotoxin- travels through lymphatics to NMJ and then to CNS. Blocks GABA and glycine of the Renshaw cells
131
tetanospasmin blocks ______ and _____ of the _________
blocks GABA and glycine of the renshaw cells of the spinal cord
132
What are the clinical signs of tetanus in horse
Develop within 5-10 days of infection
1) Increased sensitivity/anxiety
2) Altered facial expression: Risus sardonicus, protrusion of 3rd eyelid, spasms of the masseter (Lockjaw)
3) Colic
4) Drooling- swallowing is impaired
133
What altered facial expression in the horse do you see with tetanis
1) Risus sardonicus
2) Protrusion of the rd eyelid
3) Spasms of the masseter: Lockjaw
134
How do you diagnose tetanus in horse
1) Clinical signs
2) Vaccination status
135
How do you treat tetanus in horses
1) Protection from loud noises and light
2) Antibiotics
3) Tranquilizers
4) Tetanus toxoid
5) Tetanus antitoxin
prevent with tetanus toxoid
136
What is the reservoir host for west nile virus
birds
137
What is the reservoir host for eastern equine encephalitis virus
birds
138
What is the reservoir host for venezuelian equine encephalitis virus
rodents
139
What is significant about VEEV
there is a rodent reservoir host and horses serve as a secondary amplifying host
140
T/F: both humans and horses are dead-end hosts and cannot spread West Nile Virus to others in their area because they do not develop significant viremia
True
141
Why is west nile virus a reportable disease in horses
Because horses are more susceptible to west nile virus so when there are more cases of horses then cases in humans increase
142
What are the clinical signs of encephalomyelitis in horses
Inapparent infections with fever about 2 days after infection
10% of cases develop signs
Incubation 9-11 days
Clinical 5 days after infection
Signs: Changes in mentation, cranial nerve deficits (blindness, head tilt, dysphagia), muscle twitching, recumbency, death 2-3 days later
143
How do you treat equine encephalitides
1) supportive care
2) anti-inflammatories
3) Interferon
4) IgG
144
How do you diagnose Encephalitides in horses
IgM capture ELISA:
IgM elevated for 4-6 weeks
and it allows for differentiation of vaccine from the disease
145
How do you control for Encephalitides in horses
mosquito control (EEEV, WNV)
vaccination (WNV)
surveillance
146
What is the prognosis for West Nile Virus in horses
30% can recrudesce within 2 weeks
10# of recovered animals retain long-term complications
80% mortality when recumbent
147
What is the pathogenesis of EHV-1
1) Primary infection at the respiratory epithelium
2) Viremia
3) Infection of endothelial cells- thrombosis, vascular cuffing, and hemorrhage
4) Spinal cord grey and white matter - infrequently brainstem
148
What are the clinical signs of EHV-1
severity varies
1) asymmetric ataxia, dysmetria, paresis
2) Dog sitting- discrepancy between thoracic and pelvic limb signs
3) loss of tail tone
4) bladder incontinence
Recovery depends on extent of damage
149
Does EHV-1 cause symmetrical or asymmetrical ataxia
asymmetric ataxia,
dysmetria,
paresis
150
What are the risk factors of EHV-1
1) outbreak of fever and respiratory disease
2) following return from event
3) fall-winter-spring
4) tall breeds
151
What results in a horse to dog sit *
EHV-1 : ascending myelopathy -results in a significant discrepancy between thoracic and pelvic limb signs
results in dog-sitting, loss of tail tone and urinary incontinence (UMN bladder)
152
What posture do you see with EHM
ascending myelopathy -results in a significant discrepancy between thoracic and pelvic limb signs
results in dog-sitting, loss of tail tone and urinary incontinence (UMN bladder)
153
What is the mechanism of polioencephalomalacia
1) Decreased thiamine production- diet
2) Increased thiaminase activty
3) increased thiamine analogs
4) Dietary deficiency of thiamine
5) Increased sulfur diet or water (not thiamine responsive)
154
Thiamine is an important cofactor of
Transketolase
Pyruvate DH
155
What do you see with cortical diseases in livestock
Absent menace (CN II- blindness) - utilizes cortex
Functional pupillary light reflex ( CN II and III): utilizes the brainstem through the colliculi
156
Livestock with polioencephalomalacia have dorsomedia strabismus. What is happening *
Trochlear Nerve is impacted
not a true paralysis but due to cerebral edema
157
How do you prevent polioencephalomalacia
1) Supplement with thiamine
2) Adapt to high grain diets
3) Prevent free choice grain
4) Limit dietary sulfur
158
How do you treat polioencephalomalacia
1) Thiamine: Vitamin B1 (NOT Vit B complex)
2) Dexamethasone
3) NSAIDs if pregnant
4) Supportive care
159
How do you diagnose salt toxicity / water deprivation in livestock
1) History and clinical signs
2) Clinical Pathology:
-Serum/CSF Na+ >160mmol/L
-CSF/serum Na+ >1
-CSF osmolality >300 mOsm/L
-Feed analysis
-Necropsy /Histopathology
160
How do you treat salt toxicity / water deprivation
1) Slow decrease of serum sodium: 0.3-1.0 mEq/K Na+ /hr
2) Corticosteroids
3) Thiamin
4) Supportive care
*Prognosis is poor
161
How do you diagnose lead toxicity in livestock
History and clinical signs, looking around pasture
1) Radiographs: reticulum and cranioventral rumen
2) Blood or urine Pb (Pre and post EDTA if chronic)
3) Basophilic stippling on red blood cells
162
what changes to RBCs will you see with lead toxicity
basophilic stippling
163
How do you treat lead toxicity
1) Remove source
2) Ca EDTA chelation
3) Thiamine *
4) Corticosteroids
5) Cathartics
6) Supportive care
7) Rumectomy to remove lead, only if you know there are large pieces, likely unhelpful
Prognosis is variable
164
What are the ethical concerns regarding lead in livestock*
Lead can be found in milk, meat bones
No acceptable levels states
Not tested for or reportable in the USA
owners need to be made aware
Half life in blood is 48-2507 (average=90 days)
recommendation: not use for food or milk
165
What is the incubation period of rabies in cattle
3-6 months
166
What are the clinical signs of rabies in cattle
1) Dumb form- lethargy
2) Paralytic form: flaccid paralysis (most common in cattle)
3) Furious form: hyperexcitable, fear, rage
Others: vocalization, pruritus, ataxia, lameness, dysphagia
recumbency 3-5 days and death within 10 days
167
What is the most common form of rabies in cattle
Paralytic form: flaccid paralysis
168
What is the post exposure management to rabies in livestock
Based on State Health department
vaccinated livestock: revaccinate and observe for 45 days
unvaccinated livestock: slaughter immediately or quarantine for 6 months
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what are the two prion diseases of livestock
1) Scrapie
2) Bovine Spongiform Encephalopathy
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Is scrapies a heritable disease
NO but the susceptibility to it is
it requires susceptible genotype and exposure to the prion
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What are the clinical signs of BSE?
Cows over 5-6 years of age
-Behavior changes
-Ptyalism
-Reluctance to be milked
-Fasciculations
-Proprioceptive deficits
-Abnormal gait
-Licking
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What are the clinical signs of scrapie
Goats 2-4 years old
-Behavioral changes
-pruritus
-biting, licking, grinding teeth
-more aware goats
-weight loss
-abnormal gait /ataxia
-cannibalism
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Unlike BSE, is the diagnosis of scrapie possible antemortem
Yes- take a biopsy of the 3rd eyelid or rectal mucosal biopsy
variable between sheep and goats
you can also do histopath of specific brain region
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What sites can you biopsy for scrapies diagnosis
Lymphoid follicles in
1) rectal mucosa *
2) third eyelid *
3) tonsillectomy
4) Lymphoid biopsy
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How do you treat BSE and scrapie
There is no treatment
*It is progressive to death
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How do you control for BSE and scrapie
1) No feeding of ruminant derived protein
2) Prevention through genetic testing for resistance- only for classical scrapie in sheep
3) REPORTABLE DISEASE
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Genetic testing for prion diseases is only capable in *
classical scrapie in sheep
(atypical and goat scrapie are under investigation)
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The neurologic form of listeria likely occurs from ________ while the septicemic and abortion form likely occur from ______
Neuro: aersol exposure of conjunctiva or respiratory tract
Abortion/Septicemic: ingestion of infected soil or feed
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What cranial nerve deficits do you see with listeriosis
CN V- XII
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How do you diagnose listeriosis
1) History: access to silage
2) Clinical signs- fever, anorexia, lethargy, ataxia, head pressing
3) CSF: increased mononuclear cells, cloudy, increased protein
4) CSF culture
5) Necropsy, histopathology- microabscesses
6) IHC of brain
7) Brain tissue culture (difficult)
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How do you treat listeriosis
1) Long-term antibiotics (IV tetracycline after 5 days change to long acting), Penicillin, or chloramphenicol
2) Supportive care
3) Consider flock/herd treatment
4) Prognosis is good if caught early
5) Remove from source and prevent contamination
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What does the CSF of listeriosis show
monocytosis or lymphocytosis
cloudy
increased protein
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What is the risk of listeria *
ZOONOTIC
Listeria can be transmitted in the milk and milk products
therefore pasteurize milk for human or animal consumption
carriers can shed bacteria for extended periods of time
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What causes thromboembolic meningoencephalitis in livestock
histophilus somni
(gram - bacteria)
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What is the septicemic manifestation of histophilus somni
thromboembolic meningoencephalitis
-fever
-asymmetric signs frequent- brainstem and any CNs
-ocular: retinal hemorrhages, hyphema, hypopyon
-respiratory, polyarthritis, reproduction, ears, udder
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What are the clinical signs of thromboembolic meningoencephalitis
-fever
-asymmetric signs frequent- brainstem and any CNs
-ocular: retinal hemorrhages, hyphema, hypopyon
-respiratory, polyarthritis, reproduction, ears, udder
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What is the pathophysiology of thromboembolic meningoencephalitis
1) Respiratory disease
2) Septicemia
3) Formation of microthrombi and micronecrosis
4) Endothelial cells undergo cell death and expose subendothelial collagen initiating the clotting cascade and leading to thromboses
5) Activation of immune system and inflammatory processes
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How do you diagnose thromboembolic meningoencephalitis
1) History and clinical signs (respiratory disease)
2) CSF: increased protein and neutrophils, hemorrhage, and xanthochromia (yellow staining)
3) CBC- septicemia
4) Necropsy with histopathology and culture
-Suppurative meningitis
-Necrotic meningoencephalitis
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How do you treat thromboembolic meningoencephalitis
1) Antibiotics (oxytetracycline)
2) Prognosis is fair is caugt early
3) Prevention through vaccination although effiacy is questionable (might make signs worse)
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What is the meningeal worm that infects sheeps, goats, and camelids
Parelaphostrongylus tenuis
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What is the lifecycle of Parelaphostrongylus tenuis
1) adults live in the subarachnoid space and cerebrospinal venous sinuses of white tailed deer
2) Ova is released into the blood, escape via the lungs
3) Slugs and snails act as intermediate hosts
4) Aberrant hosts ingests organisms
5) within 2 weeks larvae migrate from GI to spinal cord and brainstem
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How do you diagnose Parelaphostrongylus tenuis
1) Endemic area- deer exposure
2) Posterior paresis
3) Ataxia
4) Proprioceptive deficits
5) CSF eosinophilia and increased protein
6) Necropsy
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Can you use ivermectins to treat Parelaphostrongylus tenuis
only kills circulating larvae (injections only)
use fenbendazole to treat larvae in the CNS and the treatment of this disease
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How do you diagnose bovine viral diarrhea virus
1) Clinical signs and testing for antibodies
2) Virus neutralization: antibodies present in precolostral blood if they have cerebellar hypoplasia
3) Usually not persistently infected - infected critical time (30-125 days)
*not compatible with life
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In damage to the cervical spine, hyperreflexia is present in the limbs. Which limbs is it greater in?
Pelvic > Thoracic
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damage to what spinal cord segment results in cattle dog sitting
thoracic spine
-if sternal: pelvic limbs extended and not tucked under
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In livestock, what ticks commonly cause tick paralysis
Dermacentor ticks- neurotoxin present in saliva of some
only takes 1
blocks acetylcholine release at NMJ
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What are the clinical signs of tick paralysis in cattle
-Ascending flaccid paralysis
-Increasing stumbling and weakness
-Increasing recumbency
-Respiratory failure and death
-anorexia
-Can have >1 aniaml affected
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What are differentials for tick paralysis in livestock
1) Parelaphostrongylus tenuis
2) Heat stress
3) Botulism
4) Rabies
5) Trauma, tumor, etc
*Ascending flaccid paralysis
-Increasing stumbling and weakness
-Increasing recumbency
-Respiratory failure and death
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How do you diagnose tick paralysis in livestock
1) tick search (shear)
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What is used to treat tick paralysis in livestock
1) tick search (shear)
2) Injectable ivermectin *
3) Supportive care
*Can take 2-3 days to recover even when caught early
*Prognosis worsens with increased duration and recumbency
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What will you see in cattle with radial nerve injury
-Dropped elbow
-Leg held in flexion with flexed carpus, pastern, and fetlock
-Dorsum of foot the ground
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What do you see in cattle with femoral nerve injury
-Hyperextension of the hip
-Babies: forced traction if born in posterior presentation
-Inability to fix stifle or flexion
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In cattle, the sciatic nerve is most commonly damaged due to
1) Forced extraction over oversized fetus
2) Improperly placed IM injections
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What are clinical signs of sciatic nerve damage in cattle
-Dropped and extended stifle
-Knuckling of fetlock
-Atrophy of hamstrings and muscles distal to stifle
If peroneal branch is injured:
-Hyperextension of hock
-Knuckling of fetlock and hock
-Cutaneous analgesia of cranial lateral limb distal to stifle
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What will you see if the peroneal branch of the sciatic is injured
-Hyperextension of hock
-Knuckling of fetlock and pastern
-Cutaneous analgesia of cranial lateral limb distal to stifle
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The peroneal nerve often gets damaged when animals _________________
recumbent or paretic animals because it very superficial
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The peroneal nerve is responsible for
Flexes muscles of hock
and extends the muscles of the digits
Therefore: damage to the peroneal nerve (commonly when animals are recumbent for long times) would result in:
-Hyperextension of hock
-Knuckling of fetlock and pastern
-Cutaneous analgesia of cranial lateral limb distal to stifle
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What would occur if the tibial nerve of the sciatic is injured
-Flexion of hock
-No dragging of toe
-Pelvic asymmetry
-Atrophy of gastronemius
-Cutaneous analgesia of caudal medial leg
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What are common ways for the tibial nerve to be damage in livestock
1) Improver IM injections
2) Dog bite wounds in sheeps and goats
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What supplies motor innervation to the adductor muscles
Obturator nerve
damage to this caused abduction of the limb (splayed leg)
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What is a common reason for cattle to damage the obturator nerve
pelvic trauma associated with dystocia
(well protected in small ruminants)
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How do you treat obturator nerve paralysis
hobbling of the legs (tie to two legs together) so that the animal cant splay their leg and they can walk
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What nerves are associated with calving paralysis
both the sciatic and obturator nerve
-inability to bear weight (sciatic and tibial n)
-knuckling of fetlock (peroneal)
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One of your clients calls you to evaluate a cow that has gradually been developing abnormal behavior. Over the past 2 weeks, the cow has appeared more anxious and restless. More concerning is that the owner saw the cow having difficulty walking and she fell down in the hind end. She was able to get up, but the owner is concerned there is progressive neurologic disease. You evaluate the cow and find her to be very sensitive to touch and sound. You also notice the cow is in poor body condition (weight loss) and indeed has trouble walking and especially seems uncoordinated and weak in the hind limbs. What is your next step?
Contact the state veterinarian
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Can tetanus be effectively vaccinated against in horses
Yes
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Can Equine Herpes Myeloencephalopathy be effectively vaccinated against in horses
NO
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Can CVCM be effectively vaccinated against in horses
NO
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Can rabies be effectively vaccinated against in horses
YES
220
Can West Nile Encephalitis be effectively vaccinated against in horses
Yes
221
Can Eastern and Western Encephalitis be effectively vaccinated against in horses
Yes
222
Can Equine Protozoal Myeloencephalitis be effectively vaccinated against in horses
NO
223
What is the best first line diagnostic test for West Nile Virus Encephalitis
Serum IgM capture ELISA
224
What is the best first line diagnostic test for Equine Herpes Myeloencephalopathy
PCR on nasal swabs
225
What is the best first line diagnostic test for CVCM
Neck radiographs
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What is the best first line diagnostic test for EPM
CSF and serum antibody testing
227
What is the best first line diagnostic test for CN VII and VIII deficits in horses
upper airway endoscopy
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You are concerned a valuable 1-year-old steer has developed polioencephalomalacia. The calf is not able to eat or drink effectively. You collect samples for diagnostic testing and start treatment. You are not concerned for lead toxicity based on environmental and nutritional evaluation. What treatments do you include?
-Transfaunation
-Oxytetracycline IV
-Dexamethasone
-Procain Penicillin IM
-Vitamin B1
-Fluid admin IV or oral
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You are presented with a 9 year old pet goat that suddenly developed neurological signs this morning. You examine him in the afternoon and the main findings are that the goat is circling to the right and has a head tilt to the right. There is no significant weakness. Which differential diagnoses do you consider?
-lead toxicity
-thiamine deficiency
-sulfur toxicity
-listeriosis
-salt toxicity
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