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IP 11 Equine Medicine > Exam 2 - neuro 2 > Flashcards

Exam 2 - neuro 2 Flashcards

1
Q

infectious equine neuro dzz?

A

EEE, WEE, WNV, Rabies

EHV

EPM

neuroborrelliosis

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2
Q

developmental neuro dz?

A

CSM

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3
Q

nutritional or metabolic neurologic dz?

A

EDM

EMND

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4
Q

idiopathic neuro dz?

A

polyneuritis

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5
Q

toxins that cause neuro dz?

A

tetanus

botulism

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6
Q

neoplasia that causes neuro signs?

A

melanoma

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7
Q

diffuse CNS dzz?

A

viral encephalitides
EHV
neuroborrelliosis

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8
Q

upper motor neuron dzz?

A

CSM

EDM, NAD, EPM

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9
Q

lower motor neuron dzz?

A

EMND, botulism, tetenus, equine polyneuritis syndrome

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10
Q

multifocal neuro dz?

A

EMP

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11
Q

infectious, diffuse CNS and spinal cord dzz:

A

viral encephalitides
equine herpes myeloencephalitis
neuroborrelliosis
EMP

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12
Q

what family of virus are EEE, WEE and VEE part of?

genus?

A

arboviruses

togaviridae

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13
Q

what type of genetic material do EEE, WEE and VEE have?

A

single stranded RNA viruses

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14
Q

what are the reservoir hosts of EEE, WEE and VEE?

A

birds, rodents, reptiles

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15
Q

t/f

the reservoir hosts do not show signs of virus

A

true

they are asymptomatic sylvatic hosts

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16
Q

what is the vector for EEE, WEE and VEE?

A

mosquito

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17
Q

what are the dead end hosts for EEE, WEE and VEE?

A

horse and human

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18
Q

what is the geographical distribution of EEE?

A

east of the Mississippi

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19
Q

what is the geographical distribution of WEE?

A

west of the Mississippi

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20
Q

what is the geographical distribution of VEE?

A

Mexico and South America

sometimes SW US border states

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21
Q

the US has been free of which encephalitis (E, W, V) virus since 1971?

A

VEE

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22
Q

rank the virulence of EEE, WEE and VEE from greatest to least

A

EEE > VEE > WEE

mortality rates highest for EEE in horses and humans

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23
Q

t/f

EEE, WEE and VEE are all reportable dzz

A

true

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24
Q

what is the common name for EEE?

A

sleeping sickness

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25
Q

does EEE have enzootic or epizootic cycles?

A

both enzootic and epizootic cycles

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26
Q

how is EEE transmited?

during what season does this occur?

A

mosquito

summer months

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27
Q

t/f

EEE has a slow progression and onset

A

false

fast progression of 2-14 days
typically die w/in 2-3 days

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28
Q

what is the human mortality rate for EEE?

A

75-100%

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29
Q

what is the common clinical presentation for EEE?

what are the early symptoms?

A
  • uncommon in foals less than 3 mos old

- early symptoms: fever, malaise, anorexia, “colic”

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30
Q

what is the pathogenesis of EEE?

A

infection spreads to WBC - can be cleared with good humeral immunity if it does not spread to the spleen/liver endothelium

2nd stage of viremia: spreads to CNS

see cerebral and CNS signs in 3-5 days

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31
Q

what acute clin signs occur with EEE?

A 
ataxia
head pressing
hyper excitability
somnolent, depressed, stupor - flaccid lips, tongue protrusion
recumbent, unable to rise
seizures
coma
death
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32
Q

what pathology is associated with EEE?

A
  • severe inflammation, necrosis [malacia], hemorrhage, swelling
  • severe lesions in cerebral cortex, thalamus and hypothalamus
  • perivascular cuffing - PMNs and mononuclear cells
  • brain stem: herniation of occipital lobes under tentorial process and cerebellum into foramen magnum AND mydriasis, irregular breathing arrhythmias and death
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33
Q

how to dx EEE ante mortem?

A

c/s
season
geography
questionable vacc hx

high or rising aby titer - Hemagglutination inhibitor test

IgM specific ELISA
RT-PCR to demonstrate viral genome

CSF: elevated protein and nucleated cell count - inc NTs

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34
Q

t/f

full recovery occurs readily after EEE

A

false

recovery is rare

if it does occur, animals have permanent or long term neuro deficits

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35
Q

EEE px:

A

vaccination - works well

mosquito control

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36
Q

how often should EEE vacc be boostered?

A

4-6 mos in endemic areas

12 mos in non endemic areas (MO)

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37
Q

what family and genus is west nile virus in?

A

arbovirus

genus flavirius

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38
Q

t/f

west nile virus is considered endemic in US

A

true

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39
Q

what species does west nile virus affect?

A

humans

horses

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40
Q

what animal is the reservoir for west nile virus?

A

birds [sparrows, robins, crows]

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41
Q

what is the vector for west niles virus?

A

mosquito

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42
Q

what is the peak outbreak for west nile virus?

A

spring to fall

september to october

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43
Q

what is the mortailtiy rate for west nile virus?

A

28-38%

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44
Q

what % of horses develop c/s of west nile virus?

A

5%

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45
Q

t/f

most infections of west nile virus are likely asymptomatic

A

true

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46
Q

what c/s are seen with west nile virus?

A

fever

change in personality, behavior - hyperexictability followed by sleep like behavior, hyperesthesia

muscle fasciculations - muzzle, face chewing, rapid blinking

ataxia to inability to rise - paraparesis to tetraplegia, often asymmetrical; looks similar to laminitis initially

Cranial nerve deficits

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47
Q

what % of west nile virus patients will see full recovery?

how long will it take?

A

90% within 1-6 months

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48
Q

how long after initial onset of west nile virus will patients appear to recover?

A

w/in 3-5 days of onset

may see recrudescense of c/s 7-10 d after apparent recovery

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49
Q

t/f

the prognosis of west nile virus is better if the horse remains standing

A

true

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50
Q

dx of WNV?

A

c/s
geographical loc
season

blood samples from early in dz:
IgM capture ELISA
RT-PCR for WN genome

CSF: elevated prot and monomuclelar pleocytosis

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51
Q

WNV tx?

A

supportive care - nutrition, IV fluids, sling support, paddled stall

antiinflammatory therapy: banamine, DMSO

vit E

hyperimmune plasma (maybe)

INF cl, high dose glutamate therapy

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52
Q

WNV px?

A

vacc and mosquito control

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53
Q

how often to vaccinate for WNV?

A

q6-12 mos and before mosquito season peaks

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54
Q

t/f

rabies is not a concern for horses

A

false

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55
Q

t/f

rabies has distinct c/s that look different from neurological dzz

A

false

rabies can look like any other neurological dz - should be on ddx list for any patient with acute onset neuro symptom

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56
Q

how long after exposure can symptoms appear?

A

up to 6 mos

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57
Q

how fast is the progression of rabies?

A

rapid after first symptoms appear - patients die w/in 1 week

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58
Q

what are the 2 forms of rabies?

A

furious - hyper excitable, fearful, aggressive

dumb - depressed

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59
Q

dx rabies?

A

post mortem - submit entire brain on ice but not frozen

FAB is MC and fastest test used - 98% sensitive - mouse innoculation - takes 5-6 days

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60
Q

c/s rabies?

A

prodromal signs: colic, lame, listelss, anorexia, hydrophobia

aggression, behavior changes, paralasys/paresis, fever, hyperesthesia, puritis, self mutilation, ataxia, propulsive circling, head pressing, yawning

less common: dysphagia, pytalism, vocalization, tenesmus

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61
Q

what is the pathognomonic sign for rabies? it may not always be present

A

negri bodies w/in neuronal and glial cells

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62
Q

what happens if an animal unvaccinated for rabies gets bitten by wildlife?

A

quarantined for 6 mos

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63
Q

what happens to an unvaccinated animal that bites a human?

A

euthanized and tested

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64
Q

what happens to a vaccinated animal if it bites a human?

A

quarantined for 6 mos

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65
Q

how frequently is a rabies vaccine necessary?

A

annually

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66
Q

what happens if a vaccinated animal gets bitten by wildlife?

A

booster horse immediately for rabies and all other animals on property

quarantine animals for 6 mos

67
Q

what is the etiology for equine herpes myeloencephalitis?

A

EHV 1

68
Q

t/f

the MC clinical manifestation of EHV 1 is neuro dz

A

false - other clin manifestations are more common than neurologic dz [upper resp virus]

69
Q

how contagious is EHV1?

A

highly contagious

70
Q

when does infection with EHV 1 occur MC in horse life?

A

early life

71
Q

what is the MC strain of EHV1 seen in EHM cases?

A

neuropathic strain

72
Q

what type of mutation enhances viral replication of EHV1?

A

mutation I DNA polymerase gene

ORF 30 of DNA polymerase gene - single nucleo tide switch - sub asparagine to aspartic acid

73
Q

what aspect of EHM and EHV1 infection causes a greater potential for neurologic dz and larger outbreaks?

A

significant viremia in those infected

74
Q

what does the wild type / non neuropathic strain of EHV1 cause?

A

it is not apathogenic

it causes neurologic dz but to a lesser extent - a lower degree of viremia

75
Q

EHM pathology?

A
  • vasculitis win CNS -> microthrombosis and ischemia

- deficits depend on area of spinal cord affected but there is an affinity for the caudal cord

76
Q

c/s of EMH?

A
  • biphasic fever: over 103* for over 3 days
  • maybe respiratory signs: influenza like, malaise, inappetance, lethargy
  • neuro: manifest for days after fever resolves
77
Q

what neuro signs occur with EMH?

A

atacia
paresis
symmetrical, pelvic limbs
dec tail tone and anal sphincter tone - constipation
bladder paralysis/dysuria - dribbling urine / incontinence, urine scalding
recumbency

intracranial signs rare

78
Q

what is prognosis of EMH?

A
  • good IF NOT recumbent w/in 3 days of onset of neuro signs
  • complete recovery possible but many have permanent deficits
  • POOR if recumbent
79
Q

what complications occur with EMH?

A

pneumonia
2* infections
bladder rupture
Mm necrosis

80
Q

dx EMH / EHV1?

which test detects shedding and which test detects viremia?

A

nasopharyngeal swab or lavage: RT-PCR, detects shedding

whole blood EDTA sample: RT-PCR detects viremia

81
Q

EMH tx?

A

supportive care - sling, IV fluids, nutrition, bladder, catheterization
abx to px 2* infection

anti inflammatory - banamine, DMSO, steroids

anti viral therapy - acyclovir, valcyclovir

82
Q

t/f

after EMH case, facility must be quarantined for 6 months

A

false

quarantine for 21-28 days

83
Q

EMH px?

A

biosecurity at horse events and hospitals

vaccination

84
Q

what is the purpose of EMH vaccine?

A

to maintain herd immunity and to dec shedding

85
Q

how often should a horse get EMH vacc?

A

q 6 mos

prior to entering a high risk area if not vaccinated in last 90 days

86
Q

what is etiology of EMP? [equine protozoal myeloencephalitis]

A

protozoan parasite of equine CNS

sarcocystis neurona
neospora hughesi

87
Q

t/f

depending on the area, the seroprevalence of EPM can be quite high - around 90%

despite this, the incidence of new cases is very low

A

true and true

88
Q

what is the MC age of cases for EPM?

A

1-5 yo

over 13 y

89
Q

how are horses infected with S. neurona?

A

ingesting food/water contaminated by opossum feces and infective sporocysts

90
Q

what species is the definitive hose of s neurona?

how is it infected with the protozoa?

A

opossum

eats muscle tissue of the IM hosts, which contain the latent sarcocysts

91
Q

what are the intermediate hosts of S neurona?

how do the acquire the protozoa?

A

skunks racoons, cats, etc

they ingest sporozoites / sporocytes that are passed in the feces of the DH

92
Q

how does the s neurona affect the IH?

A

forms latent sarcocysts in muscle tissue

93
Q

what species is the dead end host of s neurona?

A

horse

94
Q

t/f

for EPM, the protozoa gains access to most horses

A

false - few horses

95
Q

how/why does the protozoa gain access into the CNS of some horses?

A
  • individual immune susceptibility
  • stress induced immune suppression
  • numbers of parasites during exposure
  • special strains parasite
96
Q

what are some risk factors of EPM?

A
  • presence of opossum near premise
  • wooded area
  • warmer season
  • stress - exercise, transport, injury, parturition, show horses
  • high stocking density
  • diminished immunity
97
Q

EPM onset acute or insidious?

A

either

98
Q

t/f

EPM can cause damage to any part of the CNS

A

true

99
Q

c/s of EPM?

A

asymmetrical abnormalities
multifocal neuroanatomical localization

UMN and LMN deficits
ataxia (UMN) with focal skeletal muscle atrophy (LMN)

manifestations: focal skeletal M atrophy - masseter, gluteal, quadriceps, triceps

acute onset ataxia/weakness
head tilt, facial N paralysis, dysphagia
seizures and behavorial changes 
recumbency
horner's syndrome
mild lameness, not block out
radial N paralysis
100
Q

if damage to grey matter occurs in EPM, what signs occur?

A

focal Mm atrophy

101
Q

if damage to white matter occurs in EPM, what signs occur?

A

ataxia

102
Q

describe horner’s syndrome and the signs?

A

unilateral signs of loss of sympathetic innervation

damage to vagosympathetic trunk or Cranial cervical - trauma to c6-T2, extravascular jugular IV injections, guttural pouch dz

ptosis, miosis, enopthalmus, protrusion of 3rd eyelid, patchy sweating (face, neck)

103
Q

EPM pathology?

A

multifocal, non suppurative myelencephalomeningitis

spinal cord path MC occurs than brain or brain stem path b/c protozoa migrate to spinal cord

104
Q

EPM dx?

A

c/s of neuro deficits

r/o other differentials:
x ray spine to r/o wobbles
CSF analysis to r/o other dzz

demonstrate prod of aby against S neurona in the CSF
western blot or IFAT are good too

response to anti protozoal tx

105
Q

t/f

serology offers good dz tests for EPM?

A

false - serology is unreliable unless you get negative

106
Q

EPM tx?

A

anti protozoal drugs
anti inflammatory therapy
vit E
immune stim

107
Q

t/f

compounded meds offer specialized treatment for EPM

A

false - avoid compounded drugs - adverse events and death occur

108
Q

EPM Px?

A

feed off ground, fresh water, px wildlife access to pasture/stall

metaphylaxis to Px infection
ponazuril to at risk horses every 7 days
or daily low dose diclazuril

109
Q

what is the etiology of neuroborrelliosis?

A

Borrelia burgdorferi

110
Q

how is borrelia burgdorferi transmitted?

A

Ixodes scapularis tick - black legged deer tick

111
Q

neuroborrelliosis dx?

A

difficult ante mortem

serologic testing - specific aby titers in blood and in CSF

112
Q

c/s of neuroborrelliosis?

A

lethargy, anorexia, wt loss
fever, neck and back pain, ataxia, weakness
muzzle fasciculations, tremors
polysynovitis, uveitis
dysphagia, vestibular dz, facial paralysis
recumbency
beh changes, seizure

113
Q

Tx neuroborrelliosis?

A

tetracycline abx

114
Q

what do each constituent of the outer surface proteins indicate?
OSP a, c and f

A 
a = inc in vaccinated animals
c = early infection (3 wks after infection)
f = chronic infection (5-8 wks after infection)
115
Q

UMN dzz?

A

cervical vertebral stenotic myelopathy (CSM)
equine degenerative myopathy (EDM) and neuroaxonal dystrophy (NAD)
EMP

116
Q

what is the common name for cervical vertebral stenotic myelopathy?

A

wobbles syndrome

117
Q

what is nature of CSM?

A

developmental
orthopedic dz

vertebral canal fails to develop adequate diameter
cord is damaged as result of vertebral impingement and movement

118
Q

common presentation of CSM?

A

any age and breed but common in
young male thoroghbreds btwn 4 m and 4 y

progressive symmetrical ataxia in pelvic limbs - sometimes evident in all 4 limbs - hindlimbs more abnormal than forelimbs

circling, raising head, walking over obstacles or inclines worsen signs

119
Q

CSM dx?

A

survey cervical radio graphy
saggittal diameter ratio
less than 50% suggests compression

myelography - neutral, flexed and extended views
50% attenuation of dorsal dye column

120
Q

CSM management?

A

conservative if less than 1 yo - pacedration
rest, anti inflammatories, vit E/se supplemenetation

sx: modified cloward technique “basket surgery”, arthrodesis of adjacent vertebrae, expensive

euthanasia - sx is expensive and horse will not return to full athletecism after

121
Q

what is the nature of degenerative myeloencephalopathy and neuroaxonal dystrophy?

A

dzz of axonal degeneration in the CNS

122
Q

c/s of EDM/NAD?

age of development

A

symmetrical ataxia, abnormal base wide stance, proprioceptive deficits in all 4 limbs

12 mos - 2 years

123
Q

where are lesion in NAD?

A

in brain stem only, less severe form

124
Q

where are EDM lesions?

A

white matter of spinal cord, brain stem

125
Q

EDM and NAD neuro exam findings?

A
  • gain analysis consistent w UMN deficits - symmetrical ataxia - pelvic limbs and advance to forelimbs
  • dysmetria, pacing gate
  • diminished reflexes (LMN) in long standing cases
  • thoracolaryngeal slap test reflex
  • local cervical and cervoci facial refleces
  • cutaneous trunci reflexes
126
Q

risk factors of EDM/NAD?

A
  • dry lot, insecticides, exposure to wood preservatives, lack of dietary vit E possibly
127
Q

dx EDM/NAD?

A

low plasma vit E, low CSF vit E

128
Q

EDM/NAD tx?

A

vit E

129
Q

what is localization of equine motor neuron dz (EMND)?

A

LMN

130
Q

is EMND hereditary? what is classic presentation?

A

young adults - avg 9 yo

NOT Inherited

131
Q

cause of EMND?

A

insufficient dietary vit E - imbalance btwn oxidants and anti-oxidants

132
Q

what region of CNS affected in EMND?

A

alpha motor neurons in ventral horn of the spinal cord and brainstem

anti gravity Mm

133
Q

what human dz is EMND commparable to?

A

ALS - lou gehrig dz

134
Q

EMND c/s?

A

weakness, muscle fasciculations
M atrophy, quadriceps, triceps, gluteals
narrow based stance - tail and head posture
black pigmentation of teeth
constantly shifting weight, difficulty / ataxia when restrained
fundic lesions - retinal pigment accumulation

  • hooves tucked under and muscle atrophy in limb girdle muscle groups
135
Q

pathology in eye of EMND?

A

retinal - lipopigment accumulation in pigment epithelium - brown pigment deposition in fundus

136
Q

EMND dx?

A

elevated serum AST activity
low serum vit E
EMG - neurogenic atrophy
muscle biopsy - neurogenic atrophy - sacrocaudalis dorsalis medialis Mm - type 1 fibers are good samples for EMND dx

137
Q

EMND tx?

A

vit E natural a tocopherol (RRR isomer)

138
Q

polyneuritis equi pathogensis?

A

progressive immune degradation of peripheral nerves of the horse

“cauda equine neuritis”
any peripheral nn affected

p2 myelin protein aby

139
Q

what type of inflammation of nerve roots during polyneuritis equi?

A

granulomatous inflammation

140
Q

what dz is polyneuritis equi comparable to in the dog?

A

coonhound paralysis in the dog

141
Q

what is primary presentation in the acute form of polyneuritis equi?

A

hyperesthesia of perineal or head region

142
Q

what is primary presentation of chronic form of polyneuritis equi?

A

paralysis of tail, anal sphincter, bladder and rectum

dysuria, urine scald, penile paralysis
impaction colic
pelvic limb involvement - less common
other nerves: CrN 5, 7, 8

143
Q

what is common name of tetanus?

A

‘lock jaw’

144
Q

what is etiology of tetanus?

A

toxins produced by clostridium tetani - soil organism - cause rigid muscle paralysis

often inoculated during castration, puncture wounds, tail docking

145
Q

what does tetanolysin toxin cause?

A

tissue damage

146
Q

what does tetanospasmin cause?

A

neurotoxin

147
Q

how susceptible are horses to tetanus toxins?

A

very susceptible

148
Q

tetanus dx?

A

c/s

149
Q

what effects do tetanus neurotoxins have on neurotransmitter?

A

inhibition of release of inhibitory NTs - resulting in tetanic muscle contraction

150
Q

tetanus c/s:

A 
saw horse stance ***
elevation of tail head
grimmace / sardonic grin - retracted lips, erect ears
protrusion of 3rd eyelid
colic
dysphagia
generalized stiffness, immobilization
recumbency
respiratory failure
death
151
Q

tetanus tx?

A

tetanus immunoprophylaxis - antiserum and boost tetanus toxoid

tx wounds appropriately
penicillin
ace, robaxin

intrathecal tetanus anti serum
supportive care - dec external stimuli - fluids, nutrition

recovery can take weeks

152
Q

botulism etiology?

common name?

A

clostridium botulinum neurotoxin

forage poisoning

153
Q

what syndrome in foals occurs with tetanus?

A

shaker foal syndrome

1-3 mos of age

154
Q

how might a horse acquire botulism?

A

wound botulism

ingestion of pre formed toxin [dead animals]

155
Q

what is onset of botulism?

A

acute onset weakness
slow to eat grain - dysphagia

can present as outbreak

156
Q

botulism c/s?

A 
weak muscle fasciculations 
camped under stance
Cr N deficits - mydriasis, sluggish, PLRs, ptosis, dysphagie
constipation and urine retention
ileus
recumbency
respiratory distress
 death
157
Q

where does botulism toxin bind on NT?

A

to terminal of alpha motor neuron at neuromuscular jxn

inhibition of vesicle tethering and release of NT Ach -> flaccid muscle paralysis

158
Q

dx botulism?

A

c/s
mouse bio assay
PCR

159
Q

botulism Tx?

A

antiserum - will not target toxin once in nerve terminals

supportive care

160
Q

botulism prognosis?

A

fair or milder cases - poor for rapidly progressive cases

161
Q

botulism px?

A

toxoid vacc

162
Q

t/f

neurologic neoplasia is common in horses

A

false

rare

163
Q

what types of neoplasia are seen in neurologic horese?

which are “NOT true neoplasms”?

A
  • cholesterinic granulomas in ventricles [not true neoplasm]
  • pituitary adenoma [not true neoplasm]
  • melanoma [in grey horses]
  • lymphosarcoma [schwann cell tumors]

IP 11 Equine Medicine (10 decks)

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