Exam 2 - neuro 2 Flashcards
infectious equine neuro dzz?
EEE, WEE, WNV, Rabies
EHV
EPM
neuroborrelliosis
developmental neuro dz?
CSM
nutritional or metabolic neurologic dz?
EDM
EMND
idiopathic neuro dz?
polyneuritis
toxins that cause neuro dz?
tetanus
botulism
neoplasia that causes neuro signs?
melanoma
diffuse CNS dzz?
viral encephalitides
EHV
neuroborrelliosis
upper motor neuron dzz?
CSM
EDM, NAD, EPM
lower motor neuron dzz?
EMND, botulism, tetenus, equine polyneuritis syndrome
multifocal neuro dz?
EMP
infectious, diffuse CNS and spinal cord dzz:
viral encephalitides
equine herpes myeloencephalitis
neuroborrelliosis
EMP
what family of virus are EEE, WEE and VEE part of?
genus?
arboviruses
togaviridae
what type of genetic material do EEE, WEE and VEE have?
single stranded RNA viruses
what are the reservoir hosts of EEE, WEE and VEE?
birds, rodents, reptiles
t/f
the reservoir hosts do not show signs of virus
true
they are asymptomatic sylvatic hosts
what is the vector for EEE, WEE and VEE?
mosquito
what are the dead end hosts for EEE, WEE and VEE?
horse and human
what is the geographical distribution of EEE?
east of the Mississippi
what is the geographical distribution of WEE?
west of the Mississippi
what is the geographical distribution of VEE?
Mexico and South America
sometimes SW US border states
the US has been free of which encephalitis (E, W, V) virus since 1971?
VEE
rank the virulence of EEE, WEE and VEE from greatest to least
EEE > VEE > WEE
mortality rates highest for EEE in horses and humans
t/f
EEE, WEE and VEE are all reportable dzz
true
what is the common name for EEE?
sleeping sickness
does EEE have enzootic or epizootic cycles?
both enzootic and epizootic cycles
how is EEE transmited?
during what season does this occur?
mosquito
summer months
t/f
EEE has a slow progression and onset
false
fast progression of 2-14 days
typically die w/in 2-3 days
what is the human mortality rate for EEE?
75-100%
what is the common clinical presentation for EEE?
what are the early symptoms?
- uncommon in foals less than 3 mos old
- early symptoms: fever, malaise, anorexia, “colic”
what is the pathogenesis of EEE?
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
what acute clin signs occur with EEE?
ataxia head pressing hyper excitability somnolent, depressed, stupor - flaccid lips, tongue protrusion recumbent, unable to rise seizures coma death
what pathology is associated with EEE?
- 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
how to dx EEE ante mortem?
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
t/f
full recovery occurs readily after EEE
false
recovery is rare
if it does occur, animals have permanent or long term neuro deficits
EEE px:
vaccination - works well
mosquito control
how often should EEE vacc be boostered?
4-6 mos in endemic areas
12 mos in non endemic areas (MO)
what family and genus is west nile virus in?
arbovirus
genus flavirius
t/f
west nile virus is considered endemic in US
true
what species does west nile virus affect?
humans
horses
what animal is the reservoir for west nile virus?
birds [sparrows, robins, crows]
what is the vector for west niles virus?
mosquito
what is the peak outbreak for west nile virus?
spring to fall
september to october
what is the mortailtiy rate for west nile virus?
28-38%
what % of horses develop c/s of west nile virus?
5%
t/f
most infections of west nile virus are likely asymptomatic
true
what c/s are seen with west nile virus?
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
what % of west nile virus patients will see full recovery?
how long will it take?
90% within 1-6 months
how long after initial onset of west nile virus will patients appear to recover?
w/in 3-5 days of onset
may see recrudescense of c/s 7-10 d after apparent recovery
t/f
the prognosis of west nile virus is better if the horse remains standing
true
dx of WNV?
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
WNV tx?
supportive care - nutrition, IV fluids, sling support, paddled stall
antiinflammatory therapy: banamine, DMSO
vit E
hyperimmune plasma (maybe)
INF cl, high dose glutamate therapy
WNV px?
vacc and mosquito control
how often to vaccinate for WNV?
q6-12 mos and before mosquito season peaks
t/f
rabies is not a concern for horses
false
t/f
rabies has distinct c/s that look different from neurological dzz
false
rabies can look like any other neurological dz - should be on ddx list for any patient with acute onset neuro symptom
how long after exposure can symptoms appear?
up to 6 mos
how fast is the progression of rabies?
rapid after first symptoms appear - patients die w/in 1 week
what are the 2 forms of rabies?
furious - hyper excitable, fearful, aggressive
dumb - depressed
dx rabies?
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
c/s rabies?
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
what is the pathognomonic sign for rabies? it may not always be present
negri bodies w/in neuronal and glial cells
what happens if an animal unvaccinated for rabies gets bitten by wildlife?
quarantined for 6 mos
what happens to an unvaccinated animal that bites a human?
euthanized and tested
what happens to a vaccinated animal if it bites a human?
quarantined for 6 mos
how frequently is a rabies vaccine necessary?
annually
what happens if a vaccinated animal gets bitten by wildlife?
booster horse immediately for rabies and all other animals on property
quarantine animals for 6 mos
what is the etiology for equine herpes myeloencephalitis?
EHV 1
t/f
the MC clinical manifestation of EHV 1 is neuro dz
false - other clin manifestations are more common than neurologic dz [upper resp virus]
how contagious is EHV1?
highly contagious
when does infection with EHV 1 occur MC in horse life?
early life
what is the MC strain of EHV1 seen in EHM cases?
neuropathic strain
what type of mutation enhances viral replication of EHV1?
mutation I DNA polymerase gene
ORF 30 of DNA polymerase gene - single nucleo tide switch - sub asparagine to aspartic acid
what aspect of EHM and EHV1 infection causes a greater potential for neurologic dz and larger outbreaks?
significant viremia in those infected
what does the wild type / non neuropathic strain of EHV1 cause?
it is not apathogenic
it causes neurologic dz but to a lesser extent - a lower degree of viremia
EHM pathology?
- vasculitis win CNS -> microthrombosis and ischemia
- deficits depend on area of spinal cord affected but there is an affinity for the caudal cord
c/s of EMH?
- biphasic fever: over 103* for over 3 days
- maybe respiratory signs: influenza like, malaise, inappetance, lethargy
- neuro: manifest for days after fever resolves
what neuro signs occur with EMH?
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
what is prognosis of EMH?
- good IF NOT recumbent w/in 3 days of onset of neuro signs
- complete recovery possible but many have permanent deficits
- POOR if recumbent
what complications occur with EMH?
pneumonia
2* infections
bladder rupture
Mm necrosis
dx EMH / EHV1?
which test detects shedding and which test detects viremia?
nasopharyngeal swab or lavage: RT-PCR, detects shedding
whole blood EDTA sample: RT-PCR detects viremia
EMH tx?
supportive care - sling, IV fluids, nutrition, bladder, catheterization
abx to px 2* infection
anti inflammatory - banamine, DMSO, steroids
anti viral therapy - acyclovir, valcyclovir
t/f
after EMH case, facility must be quarantined for 6 months
false
quarantine for 21-28 days
EMH px?
biosecurity at horse events and hospitals
vaccination
what is the purpose of EMH vaccine?
to maintain herd immunity and to dec shedding
how often should a horse get EMH vacc?
q 6 mos
prior to entering a high risk area if not vaccinated in last 90 days
what is etiology of EMP? [equine protozoal myeloencephalitis]
protozoan parasite of equine CNS
sarcocystis neurona
neospora hughesi
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
true and true
what is the MC age of cases for EPM?
1-5 yo
over 13 y
how are horses infected with S. neurona?
ingesting food/water contaminated by opossum feces and infective sporocysts
what species is the definitive hose of s neurona?
how is it infected with the protozoa?
opossum
eats muscle tissue of the IM hosts, which contain the latent sarcocysts
what are the intermediate hosts of S neurona?
how do the acquire the protozoa?
skunks racoons, cats, etc
they ingest sporozoites / sporocytes that are passed in the feces of the DH
how does the s neurona affect the IH?
forms latent sarcocysts in muscle tissue
what species is the dead end host of s neurona?
horse
t/f
for EPM, the protozoa gains access to most horses
false - few horses
how/why does the protozoa gain access into the CNS of some horses?
- individual immune susceptibility
- stress induced immune suppression
- numbers of parasites during exposure
- special strains parasite
what are some risk factors of EPM?
- presence of opossum near premise
- wooded area
- warmer season
- stress - exercise, transport, injury, parturition, show horses
- high stocking density
- diminished immunity
EPM onset acute or insidious?
either
t/f
EPM can cause damage to any part of the CNS
true
c/s of EPM?
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
if damage to grey matter occurs in EPM, what signs occur?
focal Mm atrophy
if damage to white matter occurs in EPM, what signs occur?
ataxia
describe horner’s syndrome and the signs?
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)
EPM pathology?
multifocal, non suppurative myelencephalomeningitis
spinal cord path MC occurs than brain or brain stem path b/c protozoa migrate to spinal cord
EPM dx?
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
t/f
serology offers good dz tests for EPM?
false - serology is unreliable unless you get negative
EPM tx?
anti protozoal drugs
anti inflammatory therapy
vit E
immune stim
t/f
compounded meds offer specialized treatment for EPM
false - avoid compounded drugs - adverse events and death occur
EPM Px?
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
what is the etiology of neuroborrelliosis?
Borrelia burgdorferi
how is borrelia burgdorferi transmitted?
Ixodes scapularis tick - black legged deer tick
neuroborrelliosis dx?
difficult ante mortem
serologic testing - specific aby titers in blood and in CSF
c/s of neuroborrelliosis?
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
Tx neuroborrelliosis?
tetracycline abx
what do each constituent of the outer surface proteins indicate?
OSP a, c and f
a = inc in vaccinated animals c = early infection (3 wks after infection) f = chronic infection (5-8 wks after infection)
UMN dzz?
cervical vertebral stenotic myelopathy (CSM)
equine degenerative myopathy (EDM) and neuroaxonal dystrophy (NAD)
EMP
what is the common name for cervical vertebral stenotic myelopathy?
wobbles syndrome
what is nature of CSM?
developmental
orthopedic dz
vertebral canal fails to develop adequate diameter
cord is damaged as result of vertebral impingement and movement
common presentation of CSM?
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
CSM dx?
survey cervical radio graphy
saggittal diameter ratio
less than 50% suggests compression
myelography - neutral, flexed and extended views
50% attenuation of dorsal dye column
CSM management?
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
what is the nature of degenerative myeloencephalopathy and neuroaxonal dystrophy?
dzz of axonal degeneration in the CNS
c/s of EDM/NAD?
age of development
symmetrical ataxia, abnormal base wide stance, proprioceptive deficits in all 4 limbs
12 mos - 2 years
where are lesion in NAD?
in brain stem only, less severe form
where are EDM lesions?
white matter of spinal cord, brain stem
EDM and NAD neuro exam findings?
- 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
risk factors of EDM/NAD?
- dry lot, insecticides, exposure to wood preservatives, lack of dietary vit E possibly
dx EDM/NAD?
low plasma vit E, low CSF vit E
EDM/NAD tx?
vit E
what is localization of equine motor neuron dz (EMND)?
LMN
is EMND hereditary? what is classic presentation?
young adults - avg 9 yo
NOT Inherited
cause of EMND?
insufficient dietary vit E - imbalance btwn oxidants and anti-oxidants
what region of CNS affected in EMND?
alpha motor neurons in ventral horn of the spinal cord and brainstem
anti gravity Mm
what human dz is EMND commparable to?
ALS - lou gehrig dz
EMND c/s?
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
pathology in eye of EMND?
retinal - lipopigment accumulation in pigment epithelium - brown pigment deposition in fundus
EMND dx?
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
EMND tx?
vit E natural a tocopherol (RRR isomer)
polyneuritis equi pathogensis?
progressive immune degradation of peripheral nerves of the horse
“cauda equine neuritis”
any peripheral nn affected
p2 myelin protein aby
what type of inflammation of nerve roots during polyneuritis equi?
granulomatous inflammation
what dz is polyneuritis equi comparable to in the dog?
coonhound paralysis in the dog
what is primary presentation in the acute form of polyneuritis equi?
hyperesthesia of perineal or head region
what is primary presentation of chronic form of polyneuritis equi?
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
what is common name of tetanus?
‘lock jaw’
what is etiology of tetanus?
toxins produced by clostridium tetani - soil organism - cause rigid muscle paralysis
often inoculated during castration, puncture wounds, tail docking
what does tetanolysin toxin cause?
tissue damage
what does tetanospasmin cause?
neurotoxin
how susceptible are horses to tetanus toxins?
very susceptible
tetanus dx?
c/s
what effects do tetanus neurotoxins have on neurotransmitter?
inhibition of release of inhibitory NTs - resulting in tetanic muscle contraction
tetanus c/s:
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
tetanus tx?
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
botulism etiology?
common name?
clostridium botulinum neurotoxin
forage poisoning
what syndrome in foals occurs with tetanus?
shaker foal syndrome
1-3 mos of age
how might a horse acquire botulism?
wound botulism
ingestion of pre formed toxin [dead animals]
what is onset of botulism?
acute onset weakness
slow to eat grain - dysphagia
can present as outbreak
botulism c/s?
weak muscle fasciculations camped under stance Cr N deficits - mydriasis, sluggish, PLRs, ptosis, dysphagie constipation and urine retention ileus recumbency respiratory distress death
where does botulism toxin bind on NT?
to terminal of alpha motor neuron at neuromuscular jxn
inhibition of vesicle tethering and release of NT Ach -> flaccid muscle paralysis
dx botulism?
c/s
mouse bio assay
PCR
botulism Tx?
antiserum - will not target toxin once in nerve terminals
supportive care
botulism prognosis?
fair or milder cases - poor for rapidly progressive cases
botulism px?
toxoid vacc
t/f
neurologic neoplasia is common in horses
false
rare
what types of neoplasia are seen in neurologic horese?
which are “NOT true neoplasms”?
- cholesterinic granulomas in ventricles [not true neoplasm]
- pituitary adenoma [not true neoplasm]
- melanoma [in grey horses]
- lymphosarcoma [schwann cell tumors]
