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polio
thiamine enters during the cycle and creates ATP
ATP required for molecular pumps in the brain and nervous tissue to move water out of the cell
no ATP = swelling of nervous tissue
polio clinical signs
acute onset
ataxia, tremor
blindness
opisthotonos
convulsions
recumbency
ruminations unaffected
usually no fever
cranial nerve function is normal
polio neuro exam reveals
central blindness and dorsomedial strabismus
rumen fluid evaluation for polio
can be sequela to grain overload
rumen fluid pH can be normal but rumen protozoa were few and the large protozoa were dead
polio diagnostics
clinical signs, history, and response to thiamine
several lab tests
evidence of polio but not confirmatory
RBC transketolase activity should be low
tissue thiamine concentrations may be normal
postmortem thiamine concentrations of heart, brain, liver
blood pyruvate and lactate may be elevated
CSF may reveal a slight mononuclear pleocytosis and a mild protein elevation with xanthochromia
evidence of thiaminase
polio necropsy
provides the most evidence → may reveal a swollen, slightly yellow cerebrum
autofluorescence of a freshly cut surface of cerebral cortex placed under ultraviolet light is good presumptive evidence
with acute death, autofluorescence may not always be present
polio risk factors
plants containing thiaminase
some drugs like amprolium
alteration of the rumen microflora
sulfur
other differentials for polio
acute lead poisoning
water deprivation/sodium toxicosis
histophilus meningoencephalitis
rabies
coccidiosis with nervous involvement
vitamin A deficiency
pregnancy toxemia
type D clostridial enterotoxemia
listeriosis
pathogenesis of polio
gray matter necrosis from lack of glycolysis with resulting brain edema
dysfunction of the ATP-dependent Na-K pump leads to cellular swelling
ATP generation comes from glycolysis
ruminants depend on ruminal microbial thiamine production
what is the rate limiting enzyme in glycolysis?
transketolase
what is a co-factor for transketolase?
thiamine
polio treatment
parenteral supplementation of thiamine (vitamin B1)
10-20mg/kg initially then maintained with 5-10 mg/kg
supportive care → correction of rumen environment, fluid support
meningeal worm
parelaphostrongylus tenius
aberrant parasite migration through CNS
meningeal worm clinical signs
head tilt
incoordination
difficulty rising
downers
progressive weakness in the rear
meningeal worm risk factors
proximity to water → snails/slugs
proximity to white tailed deer
season → late summer, early fall
multiple species reported → llamas, sheep, goats, cattle, horses, moose
meningeal worm pathophysiology
MW in WTD lay eggs
eggs move from CNS to lungs → larvae hatch
coughed up and consumed → pass in feces
taken up from the environment by snails and slugs
snails/slugs eaten by non WTD ruminants, then larvae hatch in GI tract
meningeal worm diagnostics
signalment and PE → suggestive, often pelvic limb ataxia
currently the standard is an eosinophilic pleocytosis on CSF tap
definitive diagnosis is technically larvae in spinal cord
meningeal worm therapy
antiinflammatories → flunixin, meloxicam
anthelmentics → fenbendazole
supportive care → separate, passive range of motion, deep bedding
may need extensive management or bounce back quickly
meningeal worm prevention
restricting access to ponds
a gravel track around fencing
deer fencing
guinea fowl → will eat snails and slugs
camelids can be managed with monthly ivermectin injections
nervous coccidiosis
may have concurrent enteric coccidiosis
seizures, snapping of the eyelids
muscular tremors
periods of normalcy
no lesions on necropsy
sulfonamides, amprolium, and supportive care
feedlot disease/cold weather
70-100% case fatality rate
spinal cord tumors
uncommon, but primarily lymphosarcoma in older cattle
common sites → heart, abomasum, spinal cord, retrobulbar area
sometimes can be diagnosed on CSF tap
hydrocephalus
thinning brain due to fluid accumulation → vitamin A deficiency
inherited → hereford, charolais, dexter, holstein, and jersey
hydrancephaly
congenital absence of brain due to failure to grow or cellular necrosis (more common)
viral associated (BVD, bluetongue)
peripheral neuropathy of brachial plexus
injury to the shoulder → trauma, fracture, penetrating wound
complete flaccidity of the affected limb → absence of sensation, ± ipsilateral horner’s syndrome
peripheral neuropathy of radial nerve
often damaged from trauma or excessive recumbency
limb position varies based on where the nerve is injured
close to elbow → dropped elbow, scuffed toe, distal limb flexion
distal to elbow → knuckling of carpus, fetlock and pastern, but animal may bear weight
chronic presentations can have muscle atrophy
peripheral neuropathy of femoral nerve
traumatic overextension of hip and stifle, or excessive traction during dystocia
inability to fix and extend the stifle → hoof stays flat on the ground, absent patellar reflex
peripheral neuropathy of sciatic nerve
largest peripheral nerve
often damaged with traction from dystocia
limb hangs behind animal → stifle is dropped and extended, hoof rests on dorsal surface
peripheral neuropathy of peroneal nerve
branch of the sciatic nerve
common in recumbent postpartum dairy cattle
presentation → hyperextension of hock, flexion of fetlock and pastern, dorsal hoof drags on ground, may bear weight if placed in position manually
peripheral neuropathy of tibial nerve
supports extension to hock and digital flexors common sequelae to dog-bite injuries or injections to caudal leg at level of stifle
presentation → stringhalt like movement - exaggerated flexion of stifle and carpus
asymmetric pelvis
atrophy of gastrocnemius
peripheral neuropathy of obturator nerve
cattle have shallow acetabulum and small round ligament → predisposes the obturator nerve to injury during dystocia
clinical signs → hoppy pelvic limb gait, severe pelvic abduction “splay leg”
peripheral neuropathy of facial nerve
more common in horses
can be due to trauma, infection, inflammation, masses
facial muscle atrophy, prolapsed lips, exposure keratitis
treatment → supportive care, assisted feedings, electroacupuncture
peripheral neuropathy therapy and management
reduce swelling and inflammation at site of injury
support and stabilize the denervated area
maintain the general health of the animal
NSAIDs
bandaging, splinting, or casting
fluid therapy
range of motion exercises
float therapy
peripheral neuropathy prevention
consider the amount of traction used for dystocias → change angle, add more lube, move to C-section
quick recognition and treatment is key