Equine Neuro Flashcards
(292 cards)
1
Q
Evidence of cerebral disease
A
abnormal mentation
seizures
head pressing
compulsive walking
ataxia
blindness (lack of menace, pos PLR)
2
Q
Evidence of brainstem disease
A
CN deficits
altered consciousness
Gait deficits
3
Q
Evidence of cerebellar disease
A
ataxia with wide-based stance
intention tremor
maybe absent menace
strength is preserved
4
Q
Spinal cord segment involved: C1-C5 Clinical signs
A
all 4 limbs (pelvic > thoracic)
-UMN deficits to thoracic and pelvic limbs
5
Q
Spinal cord segment involved: C6 to T2 Clinical signs
A
all 4 limbs affected (thoracic >pelvic)
-LMN to thoracic limbs
-UMN to pelvic limbs
6
Q
Spinal cord segment involved: T3-L3 Clinical signs
A
pelvic limbs only affected
-UMN to pelvic limbs
7
Q
Spinal cord segment involved: L4-S1 Clinical signs
A
pelvic limbs only affected
-LMN to pelvic llimbs
8
Q
Spinal cord segment involved: S3-S5 Clinical signs
A
urinary incontinance, fecal retention, hypalgesia to tail and perineal areas
9
Q
Spinal cord segment involved: Coccygeal Clinical signs
A
decreased tail tone, hypoaglesia caudal to lesion
10
Q
UMN signs
A
exaggerated (hypermetric gait, exaggerated reflex, increased muscle tone
11
Q
LMN signs
A
weakness, dragging feet, reduced to absent reflexes, decreased muscle tones
12
Q
Cranial nerves:
A
1: olfactory
2: optic
3: oculomotor
4: trochlear
5: trigeminal
6: abducens
7: facial
8: vestibulocochlear
9: glossopharyngeal
10: vagus
11: accessory
12: hypoglossal
13
Q
Nerves involved in menace response
A
afferent: optic nerve
through occipital cortex
efferent: facial nerve
14
Q
nerves involved in pupillary light reflex
A
afferent: optic nerve
efferent: oculomotor nerve
15
Q
Where is the lesion located if pLRS are intact but menace is absent?
A
through occipital cortex
–cortical–cortical blindness
16
Q
What nerves are involved in eye position?
A
trochlear: innervates superior/dorsal oblique
abducens: innervates retractor bulbi and lateral rectus
oculomotor: innervates all rest
17
Q
Ventrolateral strabismus– what cranial nerve is damaged?
A
CN3
18
Q
dorsal deviation of medial angle (strabismus)– what cranial nerve is damaged?
A
CN 4
19
Q
Medial strabismus– what cranial nerve is damaged?
A
CN 6
20
Q
What nerves are involved in palpebral refelx?
A
afferent trigeminal nerve
efferent: facial nerve
21
Q
What supplies motor innervation ot the tongue?
A
hypoglossal nerve
22
Q
Signs of cranial VIII: vestibulocochlear nerve involvement
A
nystagmus (fast phase away)
head tilt (poll towards)
widebased stance
ataxia
circling (toward)
hearing
23
Q
What cranial nerves are invovled in dysphagia
A
IX: glossopharyngeal
X: Vagus
XII: hypoglossal (tongue tone)
24
Q
Which cranial nerve innervates the trapezius muscle?
A
XI: accessory nerve
25
What is the grading scale for ataxia?
0: no neuro deficits
1: subtle nero deficits
2: mild neuro deficits (apparent at all times)
3: moderate deficits at all times (obvious to all observors at all times)
4: severe neuro deficits & danger of folling
5: recumbent, unable to stand
26
Describe C/S of horners syndrome
vagosympathetic trunk; miosis, ptosis, prolapse of nictitating membrane, enotphthalmus
horse: ipsilateral sweating, poor airflow through affected nostril
27
What are differentials for horses with cerebral C/S?
alpha viruses: WEE, EEE/VEE
WNV
Rabies
Trauma
Leukoencephalomalacia
Mass: PPID, abscess, cholesterole granuloma, neoplasia
meningitis
juvenile epilepsy of arabians
28
What are differentials for horses with cerebellar C/S?
cerebellar abiotrophy
trauma
29
what are differentials for horses with brain stem C/S?
vestibular disease
THO
Trauma
Horners syndrome
Nigropallidal encephalomalacia
30
What are differentials for horses with spinal cord C/S?
EHM
EPM
NAD/EDM
Trauma
cervical vertebral compressive myelopathy
Mass: abscess, neoplasia, hematoma
occipitoatlantoaxial malformation
verminous meningecephalopmyelitis
31
What are differentials for horses with neuromusclar C/S?
EMND
botulism
tetanus
polyneuritis equi
lead poisoning in horses (chronic polyneuritis)
32
What are reservoir for EEE/WEE
birds
EEE: snakes potentially
VEE: small rodents
33
What is the vector for EEE/WEE/VEE?
mosquito
34
What is the amplifying host for VEE?
horses
35
What are clinical signs seen with EEE/WEE/VEE?
fever
cerebral signs (head pressing, compulsive walking, abnormal mentation)
36
What is the reservoir for WNV?
birds
37
What is the vector for WNV?
mosquito
38
What clinical signs are seen with WNC?
mentation change, muscle fasciculations
weakness/ataxia assymetric
CN abnormalities
fever
depression
39
WNV diagnosis
serum IgM capture ELISA (elevated with disease, not vaccination)
40
What are wildlife reservoirs of rabies?
skunks
bats
raccoons
41
Rabies diagnosis
hippocampus and brainstem
--negri bodies (aggregates of viral proteins and nucleic acids
-direct flourescent antibody
-intercerebral inoculation of mice with CNS tissue
42
Cerebellar abiotrophy is heritable in what breed?
ariabians
-- 2 to 6 months of age
43
Cerebellar abiotrphy clinical signs
ataxia
wide-based stance
intention tremor, absent menace
normal strength
44
Vestibular disease clinical signs
head tilt
circling
pathologic nystagmus
assymetric ataxia: ipsilateral extensor hypotonus & contralateral extensor hypertonus
45
What is the most common C/S of temperohyoid osteoarthropathy (THO)?
CN VII and CN VIII signs
46
Cervical vertebral malformation spinal cord compression has C/S of
ataxia worse in hind limbs than forelimbs
47
Signalment of horses with cervical vertebral malformation?
young, fast-growing horses
48
Cervical vertebral malformation diagnosis
cervical vertibral radiographs: minimum ratios: <52% are abnormal for C2-C6 ,<56% abnormal for C6-C7
Myelogram: neutral, felxed, extended
49
What are radiographic abnormalities of cervical vertebrae?
flare of caudal epiphysis (ski slope)
subluxation/malalignment
abnormal ossification
dorsal laminar extensions
50
Diagnosis of cervical spine compression on myelogram
20% or greater reduction in dural diametercompared to adjacent mid-body diameter
--50% or greater reduction on dorsal dye column
51
Equine degenerative (EDM) is seen in what horses?
genetically susceptible individuals deficient in vitamin E in first year of life (young horses)
52
Equine degenerative (EDM) breeds predisposed
mrogan
appaloosa
lusitano
53
Equine degenerative (EDM) C/S
symmetric ataxia & paresis (hind limbs >forelimbs)
spasticity
54
Equine degenerative (EDM) neuronal degenreation seen on histo
EDM: spinocerebellar tracts of cervicothoracic spinal cord
--axonal necrosis, spheroids (Swollen axons)
55
Prognosis Equine degenerative (EDM)
Poor- even with tx of vit E
56
What is the definitive host of sarcocystis neurona?
opposum
57
EPM C/S
assymmetric ataxia
weakness
muscle atrophy
+/- CN abnorma
+/- cerebral signs (mentation change, seizures)
58
What are the 3 FDA approved tratments for EPM?
ponazuril (marquis)
diclazuril (protazil)
sulfadizine/pyrimethamine (Rebalance)
59
EHV-1 clinical signs
symmetric posterior weakness and ataxia
ascending
urine dribbling
poor tail and anal tone
+/- fever
60
EHM CSF
xanthochromic
61
EHM diagnosis
nasal swab PCR: shedding
whole blood PCR: lymphocyte assoc viremia
62
What is the analagous disease in humans to equine motor neuron disease?
Lou Gerigs Disase (ALS)-- assoc with Vit E def
63
Equine motor neuron disease C/S
muscle wasting and weakness
fasciculations
64
Equine motor neuron disease Diagnosis
serum vit E levels
tail head mm biopsy (sarcocaudalis dorsalis m)
65
Equine motor neuron disease treatmnet
+/- response to natural Vit E supplementation
66
Clostridium tetani toxin?
tetanospasmic (classic toxin) and tetanolysin
--> irreversibly binds presynaptic inhibitory interneurons (Renshaw cell)-- blocks inhibitory synapses by inhibtiing NT release (glycine and GABA)--> disinhibition of motor neurons
**SPASTIC PARALYSIS
67
Tetanus disease is caused by
inoculation of organism in anaerobic wound (ie subsolar abscess)
68
tetanus c/S
spastic paralysis
- "Sawhorse" stance, rigit tail, stiff gait
-hyperesthesia
-prolapse of nictating membrane
69
Tetanus treatment
-antibiotics: stop toxin production from vegetative form
-tetanus antitoxin: neutralize unbound toxin
-diazepam, sedatives: control muscular spasm
-supportive care
-tetanus toxoid: generate active immunity
70
What are the 3 routes of transmission of clostridium botulinum?
1. forage poisoning: ingestion of preformed toxin
2. wound botulism: anaerobic
3. toxicoifnectious botulism (ingestion of spores)
71
What is the cause of shaker foal syndrome?
clostridium botulinum-- toxicoinfectious botulism ingestion of spores
72
What are clinical signs of shaker foal syndrome
muscle fasciculations
bunny hopping
dysphagia
73
describe the pathogenesis of botulism
botulinum neurotxin at presynpatic cholinergic NM junction
--> binds to SNARE proteins in nerve terminal
--> prevents fusion of prsynaptic vesicle at NM junction
--> prevents release of acetylcholine
**FLACCID PARALYSIS
74
What are clinical signs of BOtulism?
Flaccid paralysis
-weakness, poor muscle tone
-dysphagia
-hypoventilation
75
Botulism treatment
-eliminate source of toxin: antibiotics
-bind circulating toxin: antitoxin
-supportive
76
What anitbiotics are contraindicated in the treatment of botulism?
gentamicin
procaine (PPG)
**because potentiate NM blockade
77
What are C/S of cauda equina/polyneuritis equi
tail and anal spincter paralysis, peirneal anesthesia, CN deficits
78
What are palliative treatments for cauda equina?
corticosteroids
rectal and bladder evacuation
79
What are the most competent reservoir for WNV in US?
1. passerine (true perching birds)
2. Charadrii form (shore bird) spp
80
Who are the dead end hosts of WNV?
horses
humans
81
How is WNV transmitted to horses?
unknown mosquito species
82
WNV clinical signs are predominantly due to?
lesions in gray matter-- hindbrain, spinal cord **majority of lesions
83
Describe the progression of C/S seen with WNV?
initial presentation-- mild obtundation
--> progress to stupor
--> narcoleptic episodes-- midbrain/hindbrain, facial tongue involvement, vestibular signs, ataxia, limb weakness
84
What are differentials for WNV?
alphaviral encephalomyelitis (EEE, WEE)
rabies
verminous or bact encephalitis
EPM
brain or SC trauma
cervical stenotic vertebral myelopathy
hepatic encephalopathy
compressive mass in calvaria/vertebral canal
85
What are common reported residual effects with horses that recover from WNV?
gait abnormalities
behavioral changes
mm atrophy
lethargy
86
When horses flip over backwards, why is there facial nerve deficits?
courses through facial canal within petrosal bone
87
The basioccipital and basisphenoid bones are susceptible to fracture due to the dsitracting force of what mm?
rectus capitus ventralis mm
88
Optic nerve injuries occur with flipping over backwards ifor what reason?
stretched/damaged with violent gyrations d/t head impact fx through optic canals
89
When a horse pitches its head first into ground when running, it can fracture the atlas cranially causing trauma to what CN?
hypoglossal nerve
**trauma as it exits hypoglossal foramen
90
Cattle injure what cranial nerve when they are clampedi n the head catch?
CN VII: Facial N.
**"stanchion head
91
What kind of breathing pattern is seen with cerebral injury?
Cheyne-stokes breathing (hyperventilation)
92
What is the main differentiating factor between central vs peripheral C/S?
peripheral: horizontal/rotary nystagmus-- fast phase away from lesion
central: spontaneous vertical nystagmus
93
What retinal changes are seen with traumatic optic nerve blindness (in 2 to 4 weeks)?
pallor of optic disk
Dec number and caliber of retinal vessels
linear peripappillary pigment
94
Equine thiamine deficiency can be seen with ingestion of what?
diets that contain thiaminases:
-bracken fern (pteridium aquilinum)
horse tails (Equistium avense)
-amprolium
95
What C/S are seen with equine thiamine deficiency?
ataxia
CP deficits
heart block bradycardia
blindness
wt loss
dysuria
hypothermia of extremities
periodic muscular fasciculations
convulsions (terminal development)
96
Why are intracarotid injections uncommon in cattle?
d/t omohyoid mm lies between carotid a and jugular
97
What are drugs that cause cortical necrosis when injected into carotid a:
pheonthiazine tranquilizers
chloramphenicol
chloral hydrate
barbiturate anesthetics
phenylbtuazone
calcium gluconate
Naiodide
98
What is the pathogenesis of an intracarotid injection leading to neuro signs?
intense vasospasm
--> ischemia
--> progress to Ca ion influx, anaerobic metabolism, loss of function and accumulation of excitatotoxi aa, free radicals and eicosanoids
99
Cholinesteric granulomas in horses are seen in what part of the brain?
choroid plexus-- 4th and lateral ventricles
100
A cholinesteric granuloma should be suspected in horses with what C/S
forebrain dysfunction and brain stem
**suspect in horses with waxing/waning forebrain dysfunction
101
What is the etiology of cholinesteric granulomas?
chronic inflammatory reaction to cholesterol-- extravasated from breakdown RBCs w//in choroid plexus
102
What is the method of choice for Dx of cholinesteric granuloma?
CT
103
What is seen on necropsy with a cholinesteric granuloma?
brownish mass ~3cm in diamater and attached to choroid plexus
104
What is the cause of equine luekoencephalomalacia?
ingestion of fumonsin toxins produced by fusarium certicilloids or fusarium proliferatum (fungi) infecting corn/corn by products
105
What C/S are seen with equine luekoencephalomalacia?
Neuro signs (cerebral): obtundation, dementia, head pressing, blindness, lack of menace, limb ataxia/weakness
hepatic: high liver enzymes, icterus, mm petechiation
CV: dec cardiac contractility, inc systemic vascular resistance
106
Which species is most susceptible to fumonsin toxins?
horses
107
How is an antemortem diagnosis of equine luekoencephalomalacia?
>10 ppm in feed: B1, B2, B3
108
What are differentials for equine luekoencephalomalacia?
traumatic brain injury
arboviral encephalitidies
hepatic encephalopathy
EPM
botulism
109
What is seen on necropsy of horses with equine luekoencephalomalacia?
vascular damage: liquefactive necrosis, degen or malacia of white matter, flattening of cortical gyri, yellowing of white matter, feltainous fludi in CNS lesions, CNS hemorrahge
visceral organs: hepatic conestion, centrilobular necrosis, hemorrahgic enteritis& cystitis
110
What are idiopathic causes of epilepsy?
genetic predisposition (known or suspected): juvenile idiopathic epilepsy of arabian foals of egyptian lineage, arabian lavender foal syn, familial epilepsy of various cattle breeds
unknown cause (no structural cause
111
What are structural causes of epilepsy?
cerebral disorders:
-vascular
-inflamm/infectious
traumatic
anomalous/developmental
-neoplastic
-degenerative dzes
112
What is the most common cause of epilepsy in ruminants?
polioencephalomalacia
113
What is the most common cause of structural abnormalities leading to epilepsy?
skull fractures
--> cerebral hemorrhage, cerebral edema, neoplasia, cholinesteric granuloma, vasculitis, meningoencephalitis, abscess, IC bascular events, leukocencephalomalacia, congenital abnorm, EPM
114
Define generalized seizures
involving neural networks of both cerebral hemispheres
**generalized bilateral motor activity
115
Define focal seizures
involving one side of forebrain
**lateralized motor signs or sensations
116
What are autonomic signs of generalized the seizures?
salivation
urination
defecation
117
When are clinical signs seen with juvenile idiopathic epilepsy?
2 months old (2d-6months)
118
juvenile idiopathic epilepsy: what are post ictal clinical signs?
profound & persistent obtundation
-obtundation
-cortical blindness (last sign to resolve, several days, hrs to 2 weeks)
-loss of maternal bond & interest in suckling
119
Define cataplexy
path intrusion of REM sleep into wakefullness or at onset of sleep
120
define narcolepsy
tendency for abrupt transitions from wakfullness into non-REM sleep
121
What are equine breeds known to have narcolepsy/cataplexy?
american mini horse
lipizzaner
suffolk
shetland
fell pony
122
What are ruminant breeds known to have narcolepsy/cataplexy?
suffolk lamb
spanish fighting bulls
Guernsey bull
brahman bull
123
Rabies is shed in what secretions?
saliva
124
Rabies is inactivated by
dried/exposed to UV light
125
Describe the pathogenesis of rabies
binds to acetylcholine receptors of peripheral n migrates to CNS through peripheral N, spinal rootlets and SC traveling to brain along nerve tracts into CSF
**spreads centrifugally to salivary galnds and nasal epithelium
126
How does Rabies causing neuron destruction lead to death?
multifocal loss of lower motor n and autonomic dysfunction
--> leads to cardiorespiratory paralysis as virus infects medullary centers of brainstem
127
What are the forms of rabies disease?
dumb: mentally depressed
furious: hyperexcitable, fearful or enraged
paralytic: dumb with flaccid paraperesis, tetraparesis, teraplegia
128
What bacteria are most commonly isolated from foals and calves with meningitis?
Gram neg enteric bacteria:
escherichia coli
salmonella spp
klebsiella spp
129
What bacteria are commonly isolated from goat kids?
mycoplasma spp
130
What bacteria is commonly isolated from juvenile cattle in feedlots with meningitis?
Histophilus somni
listeria monocytogenes
131
CSF analysis indicative of meningitis
color: turbit, white amber in color, may foam when shaken, may clot
+/- xanthochromia
WBC: calves >100 neuts/uL, 20 - 270 mg/dL protein
gluc: <50% of corrresponding serum
132
What is the recommended antibiotic treatment with calves with gram negative enteric bacterial meningitis?
florfenicol
133
What is the recommended antibiotic treatment for horses with meningitis?
3rd generation cephalosporins:
-ceftazidime
-ceftizoxime
-ceftriaxone
-cefoprazone
-ceftazxime
134
If cannot use 3rd generation cephalosprins and suspect enteric organisms, what antibiotic is recommended
Na ampicillin (better spectrum than PPG)
135
EHV-1 can manifest in what forms?
respiratory disease
reproductive disease
neurologic disease
136
How is EHV-1 transmitted?
inhalation or ingestion
respiratory secretions, most commonly:
-- direct or indirect contact
--aerosol, short distance, less important
137
What is the incubation period of EHV-1
2 to 10 days
138
How long does EHV-1 remain infective in the environment?
for 14 days and on horse hair for 35 to 42 days
139
How does EHV-1 evade the immune response?
EHV-1 downregulated MHC-1 expression to evade immune response
**trigeminal ganglion and lymphoreticular system
140
Describe the pathogenesis of EHV-1 respiratory disease:
after inhalation/ingestion
--virus infects cells of nasopharyngeal epitheliuma nd assoc lymphoid tissue
--> infection & erosion of resp epithelium--> respiratory disease
141
Describe pathogenesis of EHV-1 neurologic disease
virus infected phagocytic cells migrate into circulation--> viremia assoc with mononuclear cells, T lymphs
-- intracellular location is protection from immune sys & antibodies
-->endotheliotropism-- vasculitis, thrombosis of arterioles
--spinal cord, brain --> neuro disease
--placental endothelial cells-- reproductive disease
142
EHV-1 non-neuroapthic genotype
A2254= N752
143
Neuropathic genotype
G2254=D752
144
Can either strain of EHV-1 cause neurologic disease?
yes: N752 and D752
145
What are risk factors for the development of EHV-1?
-risk based on viral, host and environ factors
-presence of EHV-1 and/or shedding horse with susceptible horses
-season: late autumn, winter, spring
-Age >3 years; mares >20 years of age
-past exposure
-biphasic fever
-stress assoc with weaning, transport, intro of new horses, secondary infection, immune suppression
-mares more commonly affected: ponies and smaller breed less common
-magnitude and duraiton of viremia
-infection with D752 genotype
-geographic region (NZ, AUS less common)
-vaccination within 5 weeks of event
146
What are potential differentials for EHV-1/EHM?
EPm
cervical vertebral malformation
vertebral fx/trauma
viral encephalitis (WNV, EEE, WEE)
equine degnerative myelopathy
rabies
botulism
intoxication
anaplasma phagocytophilum
borrelia burgdorferi
147
PCR testing for EHM/EHV-1 recommendation from AAEP guidelines
PCR for glycoprotein B (gB) gene, then PCR for N752D mutation
148
In acute suspected cases of EHV-1/EHM that are initially negative, when should you retest?
in 24 to 72 hours
149
EHV-1 serology, what is indicative of recent infection?
four-fold rise indicates recent infection
150
What is the mechanism of action of acyclovir against EHV-1?
synthetic purine nucleoside analog
-- inhibits viral DNA polymerase and viral replication
-- inhibitory action against several human herpresviruses
--inhibitory effect on EHV-1 in invitro
--> prevents viremia, reduces nasal shedding severity and abortion
151
The prodrug of acyclovir gets higher bioavailability, what drug is this?
valacyclovir: 27 mg/kg q8h for 2 days, then 18 mg/kg a12h for 1 to 2 weeks
152
The greatest effect of valacylovir was seen when?
greatest effect when administered prophylactically
153
What are differentials to rule out with headshaking in horses?
skull lesions
alelrgic rhinitis
vasomotor rhinitis
otitis externa/media/interna
trombicula autumnalis (harvest mite)
sinus sx
cervical arthritis
ocular lesions
alelrgic oconjucntivitis
blocked lacrimal ducts
fungal sinusitis
THO
mites/ticks-- external ear canal
guttural pouch mycosis
onchocerca dermatitis
dental problems
154
What diagnostic is used to determine integrity of auditory pathway of inner ear adn medulla oblongata
auditory evoked potentials
155
What should you suspect when a horse with vestibular disease, shows clinical signs of systemic sepsis (fever, tachycardia, tachypnea), limb ataxia/weakness, other CN deficits, obtundation?
extension of infection along fracture line to meninges
156
Antibiotic Treatment of otitis media/interna
**should directed with culture
-- gramp ps: PPG, Kpenn, ceftiofur sodium
Staph: enrofloxacin
oral tx: TMS, chloramphenicol
157
Temperohyoid osteoarthropathy is a progressive disease, with enlargement and sclerosis of:
stylehyoid bone
tympanic bulla
petrous portion of the temporal bone
158
Fusion of the Temporohyoid joint causes interference in the coordinated movement of what structures?
tongue
hyoid apparatus
larynx
159
WIth THO, what causes stress on fused joints?
chewing
swallowing
vocalizing
veterinarian-- passing NG tube, dental work
160
What is a normal schirmer tear test?
normal >20 mm
**injury to parasymp. lacrimal brach of facial nerve causes decreased tear production
161
Fusion of THJ causes a sudden onset of C/S
CN VII and VIII deficits
**toward the affected side: head tilt, neck turn, body lean, tight circling
162
What are the percentages of hroses that died as a consequence of THO with what treatment options?
medical therapy: 13/20- 65%
certahyoid ostectomy 1/25 4%
partial stylohyoid ostectomy 1/8 12.5%
163
What are management changes to help prevent the progression of THO?
cribbing collars-- prevent cribbing
bitless bridle
minimize dental/other prof procedures
164
What is the cause of equine nigropallidal encephalomalacia?
yellow star thistle: centaura solstitalis
Russian knapweed: rhapoticem repens
165
What are characteristic C/S of equine nigropallidal encephalomalacia?
faciala nd lingual dystonia
variable: obtundation (mild-mod)
behavioral signs
ataxia
166
What do horses that have nigropallidal encephalomalacia do when drinking?
immerse the muzzle deep into bucket to force water to back of pharnyx
167
What are the toxic principles of yellow star thistle/russian knapweed?
repin- sequeseterpen lactone
-- high affinity for neural tissue- inhibit dopamine release
168
Nigropallidal encephalomalacia lesions are similar to human toxic envorment parkinsomism, seen where?
lesions globus pallidus and susbtantia nigra pars reticulata
169
What are the most common fungal organisms cultured in guttural pouch mycosis?
Aspergillus fumigatus
Emericella nidulans
170
In guttural pouch mycosis, what causes the epistaxis, local pain and. neurologic signs
erosion of major vessels and major nerves involved
medial pouch: CN 9-12, cranial cervical ganlgion, postganglionic sympathetic n, internal carotid a
lateral pouch: external carotid a, facial n VII paralysis
171
Definitive diagnosis of guttural pouch mycosis is performed with what diagnostic?
endoscopy
-- can see other C/S: dorsal displacement of soft palate, inability to swallow, larygneal hemiplegia
172
What treatment has the best prognosis for cure in guttural pouch mycosis?
15 days to 5 weeks after arterial catheterization for fungal plaques
173
What are differentials for epistaxis (guttural pouch mycosis)
EIPH
ehtmoid hematoma
guttural pouch or pharyngeal neoplasia
tracheobronchial foreign bodies
174
What are differentials for dysphagia (guttural pouch mycosis)?
hyoid apparatus fracture
pharyngeal & guttural pouch fistula
cleft pallate
esophagitis
pharyngeal paralysis
bacteria, viral & mycotic CNS infections
FB entrapment in mouth/esophagus
pharyngeal neoplasia
PB poisoning
175
Horners syndrome: damage to sympathetic nerve supply along pre/post ganglionic nerves orders?
First order: brain stem-- ipsilat brain stem (rare), spinal cord (T1-T3)-- horses met neoplasia & EPM
Second order: cranial thoraic nerve roots, spinal nerves, cervical sympthatic trunk
Third order: CCG (cranial cervical ganglion) in the skull and behind the eye
176
Preganglionic sympathetic motor fibers that innervate structures of the head originate from where?
the first 3 thoracic segments
177
Cattle with horners syndrome have what C/S?
dryness of ipsilateral planum nasale
-- mediation of norm sweat gland secretion by postganglionic symp. fibers & alpha adrenergic receptors in cattle
178
Using hydroxyamphetamine (1% solution) as a diagnostic causes release of norepinephrine form postganglionic sympathetic neurons, no response (no pupillary dilation) indicates:
postganglionic nerve damaged
179
Horners syndrome:
Using hydroxyamphetamine (1% solution) as a diagnostic causes release of norepinephrine form postganglionic sympathetic neurons, response (pupillary dilation) indicates:
preganglionic n damage
180
Horners syndrome:
After administration of hydroxyamphetamine and no response is elicited, then what can be administered?
topical adinistration of epinephrine
--> activates iris musculature produces mydraisis within 20 m, within 40 m if preganglionic disorder
181
Horners syndrome:
Topical administration of phenylephrine solution (2.5 to 10 %) causes pupillary dilation is indicative of what lesion location?
postganglionic lesion
-- INC d/t denervation hypersensitivity
182
Horners syndrome: if administer epinephrine parenterally, what C/S are seen in effected horses?
affected horses sweat profusely over affected side of face
**does not differentiate post to pre-ganglionic lesions
183
What is the treatment in xylazine associated horners syndrome?
condition disappears spontaneously
184
With horners syndrome caused by necrotizing perivascular drug injection, what treatment can be performed?
immediate dilution or irrigation or both (lg vol of saline infiltrated into perivascular tissues)
185
With abnormalities seen in CN IX, X and XI, what C/S are seen
dysphagia
dysphonia (stridor, roaring)
inspiratory dyspnea
186
CN X deficits (visceral efferent component) can be caused by what other diseases in ruminants?
vagal indigestion
ruminal distension with fluid
ruminal tympany
abomasal stasis
+/- hypochloremic, hypokalemic met alkalosis
187
define abiotrophy
spontaneous premature degeneration resulting from an inborn error of development
188
cerebellar abiotrophy is described in what breeds?
arabian
gotland pony
eriskay pony
189
What is the genetic basis for cerebellar abiotrophy in arabians?
mutY homolog gene (MUTYH)
**single nucleotide polymorphism upstream of MUTYH gene
190
cerebellar abiotrophy inheritance in arabians is
autosomal recessive
191
C/S of cerebellar abiotrophy in arabians is seen at what age?
6 weeks to 4 months
192
What are C/S of cerebellar abiotrophy?
basewide posturing in thoracic limbs
head tremors
+/- menace response
gait: wobble side to site, swaying, learching, stiff thoracic limbs/paddling
193
Does blindfolding exacerbate signs of cerebellar abiotrphy?
No
194
What is the diagnostic for cerebellar abiotrophy?
homozygosity for cerebellar abiotrophy allele--> 20 to 30 hair roots of vet genetics
195
Cerebellar hypoplasia is seen with what infection?
BVDV at 90 to 170 days pregnancy
196
conditions promoting poisoning with locoism (swainsonine tox)
hot dry weather
scarcity of alternative forage
horses prone to grazing v cattle
cattle-- chornicly exposed addicted to locoweed
197
swainsonine toxic principle
indolizidine alkaloid
198
what is the pathogenesis of locoism (swainsonine tox)?
potent inhibition of mammalian alpha-D-mannosidase and golgi-mannosidase II
199
What are clinical signs of locoism (swainsonine tox)?
cerebellar signs: high stepping gait, intention tremor of head,
ataxia
obtundation
dysphagia
200
Why are weak calves seen from cattle diagnosed with locoism (swainsonine tox)?
abnormal suckling behavior
-- indolizidine alkaloids secreted in milk
201
in utero calves exposed to locoism (swainsonine tox) have what C/S
weak/fail to thrive
flexural limb contractions
lateral carpus rotation
202
locoism (swainsonine tox) can potentiate the C/S of what disease?
core pulmonale
203
In sheep, the immunosuppressive effects of locoism (swainsonine tox) can predispose to:
-pyogenic infections
-- pneumonia
--keratoconjunctivitis
-- foot rot
204
locoism (swainsonine tox) defintive diagnosis
alpha- D-mannosidase, swainsonine-- blood concentrates measured with assays
***swainsonine measurements on blood samples collected within 2 days of eating locoweed
205
what liver abnormalities are seen with locoism (swainsonine tox)?
INC liver enzymes (INC AST, ALP)
-- liver prominent vacuolation of hepatocytes
206
What the is the pathogenesis behind the secondary fungal metablolites indole diterpenoid tremorgens?
act by blocking K outflow from cells via inhibition of cell membrane large conductance Ca-activated K channels
207
What is the associated fungus with Perennial Rygrass staggers?
Neotyphodium lolii
208
What are conditions that increase the toxicity of perennial ryegrass pastures?
-high proportions of endophyte infected plants
-late seasons growth
-hot,dry, summer and fall after wet spring
-ryegrass domination of pastures
ambient temperature higher than 23C
-ryegrass that is allowed to flower before consumption and close grazing
209
what is the toxic principle of rye grass staggers produced by the fungus neotyphodium lolii?
lolitrem B
210
When are clinical signs of rye grass staggers seen after introduction to pasture?
5 to 10 days onto endophyte rich pastures (as early as 48h, as late as 2 weeks)
211
Horses show what C/S with grass staggers?
-fine muscle fasciulcations & tremors-- esp shoulders, chest & thoracic limbs
-apparent after exercise
-fine tremors of eyes during ophtho exam
-wide based gait
-trunkal sway
-rapid stumbling
**blindfolding makes these signs worse (consistent with bilateral vestibular disease)
-hyperresponsiveness-- C/S worsen with handling
212
Ruminants show what C/S with grass staggers
-limb stiffness
-unpredictable inconsistent leg movement
-hypermetria
-head tremor
-falling
-generalized tetanic convulsions
-variable progression of ataxia
-vestibular, veneral proprioceptive then cerebller
213
Treatment of rye grass staggers?
recover days to weeks, handle infrequently.
214
What is the toxic principle of PasPalum staggers?
indole diterpene metabolite: paspalitrem B (mostly), also A & C
215
What are preventative measures for Paspalum staggers?
mowing toxic pastures and removing
burning infected seed heads
216
What is the definitive host of Sarcosystis neurona?
opposum: didelphis virgiania- N. America
217
What are intermediate hosts of sarcocystis neurona?
nine-banded armadillo
striped skunk
raccoon
domestic cat
218
What is the aberrant host of sarcocystis neurona?
Horses
219
What stage of Sarcocystis neurona is ingested by the hrose?
sporocyst
220
What is the mechanism of entry into the CNS of sacocystis neurona and Neospora hughesi ?
leukocyte associated parasitemia
221
On histology which life stage is observed of sarcocystis neurona/Neospora hughesi in cytoplasma of nerons, mononuclear phagocytes, or capillary enodthelial cells?
free merezoites
222
what are risk factors for infection of sarcocystis neurona and neospora hughesi?
-prevoius dx EPM
-INC exposure to opposums in environment, feces consistently identified
-- physiologic stress important role in onset of disease:
-primary use of the horse-- show and race horses
-recent transport
-recent adverse health problems, parturition, management changes
223
What is serum S. neurona antibody PPV?
A negative test strong evidence that the horse doesn't have EPM
224
What ist he only way tot distinguish horses with EPM from exposed horses?
detect specific ab made within the CNS
-- western blot
-serum to CSF ab ratios
--C values
225
IS PCR of CSF for S. neurona DNA useful?
**useful for PM diagnosis
false negatives are common-- enzymes destroy DNA in CSF, merezoites rarely enter CSF
226
What percentage of horses with moderate to severe neurologic signs due to EPM improve?
60% improve 1 grade
227
What percentage of horses have a complete recovery from neurologic signs due to EPM?
10-20% have a complete recovery
228
What percentage of horses with neurologic signs due to EPM suffer at least one relapse?
10-20%
229
Equine degenerative myeloencephalopathy/neuroaxonal dystrophy clinical signs?
acute insidious onset
-symmetric ataxia
-trunk/limb paresis
-age 1-12 m
-posture/gait wide based (hypometric (aspsicity)
-usu mroe severe in hind limbs
**neurogenic mm atrophy note seen in EDM/NAD
230
Equine degenerative myeloencephalopathy/neuroaxonal dystrophy diagnostic?
consistently associated with low serum/plasma vitamin E
normal >2 microg/ml
marginal 1.5-2 microg/ml
deficient <1.5 microg/ml
231
What role does vitamin E have in the body?
-neuroprotective effects
-inhibition of oxidation of CNS membrane lipids
-falcification axonal transport macromolecules
-preventing accumulation of oxidized cholesterol (oxysterol) in lipid peroxidation and demyelination
232
How to diagnose Equine degenerative myeloencephalopathy/neuroaxonal dystrophy?
low serum/plasma vit E:
marginal-low (<2 microg/ml)
collect 3 blood samples over 24 hours
*store blood without contact to rubber stopper
**diagnosis of exclusion
233
absorption of vitamin E requires what?
fat-- give with feed or oil
234
DDX for Equine degenerative myeloencephalopathy/neuroaxonal dystrophy
EPM
trauma
wobblers (CVCM)
EHV-1 (EHM)
235
Which horse breeds have a familial predisposition for the development of Equine degenerative myeloencephalopathy/neuroaxonal dystrophy?
-standardbreds
-paso finos
-Norwegian fjords
-arabians
-welsh ponies
-haflingers
236
What are the histological hallmarks of Equine degenerative myeloencephalopathy/neuroaxonal dystrophy?
spheroids, axonal loss and secondary demyelination w/in caudal brain stem adn spinal cord
237
eNAD and EDM are clinically indistinguishable, with EDM being a more advanced form of the disease. What are the differences between these diseases?
eNAD: histological lesions are confined to the cuneate and gracile nuclei of the caudal medulla oblongata
EDM: lesions are more widespread and include demyelination within the ascending tracts of the spinal cord
238
what are risk factors for the development of Equine degenerative myeloencephalopathy/neuroaxonal dystrophy?
-application of insecticde
-exposure to wood preservatives
-frequent time spent on dirt lots
239
Once clinical signs of ataxia are present in horses with Equine degenerative myeloencephalopathy/neuroaxonal dystrophy, is supplementatin with alpha tocopherol beneficial?
-- supplementation will not improve neurologic deficits
-progression of disease can be halted through supplementation
--C/S typically stabilize at 2 years of age
240
What is the best management practice in the prevention of Equine degenerative myeloencephalopathy/neuroaxonal dystrophy?
maintain pregnant mares, foals, weanlings, yearlings and 2 year old horses on lush green pastures
241
Is treatment of postanesthetic myelopathy and encephalopathy rewarding?
no-- majority of cases euthanized d/t progressing C/S
242
What are clinical signs observe diwth postanesthetic myelopathy & encephalopathy?
apparent in recovery
-paraperesis
-ataxia
-recumbency
-paraplegia
-cutaneous hypoagesia
-areflexia of hind quarteres
-dementia
-pacing
-cortical "central" blindness
243
What are the 5 groups of occipitalatlantoaxial malformation?
1. Heritable conditin Arabian horses
2. Congenital assymetric OAAMs
3. Assym atlantoccipital fusion
4. duplication of axis or atlas
5. symmetric OAAms iin nonArabian horses
244
What are clinical signs of occipitalatlantoaxial malformation?
-+/- abnormal head position
-sudden unexpected death
-stillbirth
-sudden death
-reluctance to move head/neck
-symmetric C/S: hyperreflexia, hypertonia, weakness, ataxia in all 4 limbs, hold head in extension "weathervane posture"
245
What are reasons for congenital vertebral malformations?
- disruption in early gestation spinal cord development
--> genetic defects, mechanical injury, teratogens, nutrient deficiency microbial infections, maternal abnormalities
246
What are viruses that cause congenital vertebral malformations?
schmalenberg virus
akabane virus
aino virus
cache valley virus
247
What are teratogenic viruses that do not cause congental vertebral maloformations?
blue tongue
BVD
border disease
248
Spina bifida is seen in what livestock breeds?
charolais calves
hereford calves
249
define acquired torticollis
neck mm contract, cause head to twist to one side
250
What horse breed is predisposed to torticollis?
draft horses
251
What species are most susceptible to tetanus?
horses
small ruminants
cattle
252
Which neurotoxin is produced by Clostridium tetani?
tetanospasmin
253
Tetanospasmin bind irreversibly where in the nervous system?
to presynpatic inhibitory interneurons, preventing hte release of GABA/glycine inhibitory NTs
**growth of new nerve terminals required
254
What is seen on gram stain of wound exudate with horses with tetanus?
drumstick shaped, gram pos bacilli
255
What are classic C/S of tetanus?
-trismus: INC masticatory mm tone
-risus sardonicus-- rigidity of facial expression
-prolapse of membrane nictitans (horses prominant, cattle incosistent, sheep no observed)
-"sawhorse stance"- limbs and neck head in extended posture
-"pump handle" tail- tail evelated
256
What is an effective fluid additive in patients with tetanus?
magnesium-- b/c blocks neruomuscular transmission, interferes wtih vatecholamine release from nerves and adrenal medulla, antagonizes action so ca, (spares resp mm)
257
What are the goals in treatment of tetanus?
1. provide mm relaxation
2. enxure good footing
3. eliminate infection
4. neutralize unbound toxin
5. maintain hydration & nutrition
6. establish active anti-toxic immunity
258
the virulence factor tetanolysin does what in tetanus?
damages healthy tissue -- anaerobic conditions
259
What is polyneuritis equi?
a progressive granulomatous polyganglioradiculneuritis of cauda equina
260
Cauda equine C/S:
dysuria
tail rubbing
cutaneous & muscular hyperestehsia around hind quarters
paresis: tail, bladder, rectum (fecal retention), anal sphincter, penis, neurogenic tail atrophy
lumbosacral nerve roots involved: pelvic limb weakness, mm atrophy
spinal n roots: discrete areas of mm atrophy
+/- CN involvement-- variable
261
What are differentials for polyneuritis equi?
ca spine fx/luxations
EHM
sorghum-sudan gass tox
rabies
other infectious dzes involving ca spine and/or lower urinary tract
262
What is seen on muscle biopsy with polyneuritis equi?
mononuclear neuritis: sacrocaudalis dorsalis mm
263
Treatment of polyneuritis equi?
corticosteroids-- early on in dz course
general supportive care: fluid therapy, manual rectal & bladder evaucation
**with careful management can live for months
264
What gait is seen with sorghum toxicity?
hopping gait in hind limb
** pelvic limb ataxia, worsens with backing
265
What are C/S seen with sorghum toxicity?
flaccid distended bladder-- cystitis secondary to urinary retention
--> progress to pyelonephritis- fatal
pelvic limb ataxia
266
What is the toxic principle of sorghum toxicity?
unknown
267
What are the two stringhalt syndrome?
1. classical stringhalt: persistent condition of individual horses involving one limb
2. pasture assoc/Australian stringhalt: inovles both pelvic limbs; outbreaks in horses in pasture
268
Describe the stringhalt gait?
abrupt hyperflexion of hock and stifle
269
The stringhalt gait is exacerbated by?
excitement, cold weather, hard exercise
backing, sharp turning, when horse goes down slope, sudden stops, transition from standing to walking
270
What is the cause of classical stringhalt?
unknown cause
271
Pasture associated stringhalt primarily effects what nerves?
primarily large myelinated axons of peripheral nervous system
--> long nerves: recurrent laryngeal nerve, peroneal and tibial branch of sciatic nerve
272
What histologic changes show evidence of nerve regeneration?
regenerative nerve clusters
"onion bulb" formations
Schwann cell proliferation
273
Differ between the two types of cervical stenotic myelopathy
type 1: focal or multifocal stenosis of vertebral canal, C1-C6
Type 2: boney and ST imingement-remodeling of articular process joints of ca cervical vertebrae, C5-T1
274
What are risk factors for the development of cervical stenotic myelopathy in foals?
genetic
physical
dietary factors
COD articular process & metaphyseal growth plates
275
What are normal intervertebral sagittal ratios to be known for diagnosis for cervical stenotic myelopathy?
ratio <0.52 C4: C6
ratio <0.54 C7
**89% sensitivity and specificity for spinal cord compression
276
What is Equine motor neuron disease?
acquired neurodegenerative disorder in ventral horns, gray matter, spinal cord and brainstem nuclei
277
What are clinical signs of equine motor neuron disease?
**do not. have ataxia
-skeletal mm denervation-- mm weakness, carry head below shoulders
-"horse on a ball" stance
-fundic exam: horizontal band of pigment above optic disk at tapetal-non-tapetal junction
278
What abnormalities are seen on bloodwork with equine motor neuron disease?
vit E levels: low-normal
CK/AST: mild-mod INC
CSF: no cytology abnormalities, +/- INC TP, INC CK
279
What is diagnostic on muscle biopsy for equine motor neuron disease?
sacrocaudalis dorsalis mm (biopsy of tailhead mm)
-- rich in T 1 myofibriers- sensitive to denervation
**neurogenic atrophy-- variable numbers of angular atrophied fibers
280
What are the three forms of botulism?
1. forage poisoning- ingestion of preformed toxin (most common form)
2. toxicoinfectious- germination of ingested spores in GIT-- shaker foal syndrome (T. B)
3. wound- cotaminated of wounds with spores and vegetative growth
281
Botulism toxin (BoNT) inactivates what protein?
inactivates SNARE (soluble N-ethylmalide sensitive factor attachment protein receptor
282
What is the significance of botulism toxin inactivating SNARE?
prevents docking and fusion of synaptic vesicles containing acetylcholine
--> prevents exocytosis and relase of neurotransmitter at neuromuscular junction
-->flaccid paralysis of striated mm
283
Shaker foal syndrome is caused by
C. botulinum T B
284
When is shaker foal syndrome caused by C. botulinum T B age typically seen?
peak age 4 weeks (70% 2-6 weeks)
285
How is botulism diagnosed?
1. botulinum toxin in serum, GI contents, tissues or wounds
2. antibody against botulinum toxin in serum
3. C. botulinum spores in GIT contents or suspect feed materials
286
Clinical signs of botulism are dose dependent, and what are they
low dose: dysphagia, progression 5 to 7 days, recover with minimal tx
high dose: recumbency 8-12 h, death within 48h
dysphagia- green nasal discharge
generalized mm weakness
increased effort to swallow
287
What are differentials for muscular weakness and dysphagia in horses?
-infectious encephalomyelitis: EPM, EEE, WEE, VEE, EHM, WNV
-generalized myopathy: nutritional, seasonal, PSSM
-equine motor neuron dz
-grass sickness
-HYPP
-heavy metal toxicosis
288
What are differentials in cattle for muscular weakness and dysphagia?
hypocalcemia
hypokalemia
sulfur toxicity
listeriosis
epidural lymphosacroma
organophosphate tox
289
BoNT T B toxoid vaccine is effective at preventing disease, however what are reasons for failure of vaccine protection in foals?
-insufficient ab production in dam
-failure of passive transfer
-overwhelming toxin production
-loss of passive immunity
290
Tick paralysis is caused by what tick spp in the US?
Dermacenter andersoni
291
Equine grass sickness is what kind of dz
debilitating, often fatal dysautonomia (polyneuropathy)
292
What is the cause of equine grass sickness?
unknown
(toxic principle- hypoglycin A in ACer spp seeds)
