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Lecture 13
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List clinical signs associated with polioencephalomalacia (polio).
acute onset of ataxia, tremor, blindness, opisthotonos, convulsions, recumbency
ruminations unaffected
usually no fever
cranial nerve function is normal except for blindness
neuroexam revealed central blindness and dorsomedial strabismus
Why should you do a rumen fluid evaluation in cases of polioencephalomalacia?
polio can be a sequela to grain overload
How can we diagnose polioencephalomalacia?
clinical signs, history, and response to thiamine
lab tests (few readily available)
What can be used as evidence for a polio diagnosis but is not confirmatory?
RBC transketolase activity (should be low)
tissue thiamine concentrations (may be normal)
postmortem thiamine concentrations of heart, brain, and 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
What can be found on necropsy of polio cases?
swollen, slightly yellow cerebrum
cerebellar and/or cerebral herniations may occur in the acute disease
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
List risk factors associated with polio.
plants containing thiaminase —> Bracken fern, Nardoo fern
some drugs such as Amprolium (thiamine analog)
alteration of the rumen microflorae
sulfur —> increased intake or cruciferous plants
What other differentials must be ruled out for polio diagnosis?
acute lead poisoning
water deprivation/sodium toxicosis
Histophilus meningoencephalitis
Rabies
coccidiosis with nervous involvement
vitaminA deficiency
pregnancy toxemia
type D clostridial entertoxemia
Listeriosis
Describe the pathogenesis of polio.
gray matter necrosis from lack of glycolysis (ATP production) with resulting brain edema
dysfunction of the ATP dependent Na/K pump leads to cellular swelling which leads to pressure necrosis of gray matter
ATP generation come from glycolysis —> transketolase is the rate limiting enzyme, thiamine is a co-factor for transketolase
ruminants depend on ruminal microbial thiamine production
How can we treat polio?
parenteral supplementation of thiamine (vitamin B1)
supportive care with correction of the rumen environment (transfaunation, forage feeding), fluid support, ± anti-inflammatories, soft bedding, eye lube
What species is known as the meningeal worm?
Parelaphostrongylus tenuis
List clinical signs of a meningeal worm infection.
head tilt
incoordination
difficuty rising
downers (usually still alert)
progressive weakness in the rear
List risk factors associated with meningeal worm.
proximity to water —> presence of snails/slugs
proximity to white tail deer
season —> late summer/early fall
Describe the pathophysiology of meningeal worms.
meningeal worm in white tail deer lay eggs —> eggs move from CNS to lungs where larvae hatch —> larvae are coughed up and consumed then passed in feces —> larvae are taken up from the environment by small and slugs —> snails and slugs are eaten by ruminants —> larvae hatch in the GI tract then migrate to nervous tissue —> larvae die in nervous tissue of aberrant host —> resulting inflammation leads to clinical signs
How can we diagnose a meningeal worm?
signalment and physical exam are suggestive and often show pelvic limb ataxia
currently the standard is an eosinophilic pleocytosis on CSF tap
definitive diagnosis is technically larvae in spinal cord
How can we treat cases of meningeal worm?
anti-inflammatories —> flunixin, meloxicam, sometimes steroids
anthelmentics —> fenbendazole ± ivermectin
supportive care —> separate from herd, passive range of motion, deep bedding
may need extensive management or bounce back quickly —> can get worse before they get better
How can we prevent infection with meningeal worm?
restricting access to ponds
gravel track around fencing
deer fencing
guinea fowl to eat snails/slugs
camelids can be managed with monthly ivermectin injections for prevention
List clinical signs of nervous coccidiosis.
seizures: opisthotonos, tonic clonic movement, medial strabismus, and snapping of the eyelids
muscle tremors
periods of normalcy
no characteristic lesions on necropsy
How can we treat nervous coccidiosis.
sulfonamides, amprolium, and supportive care, ± anticonvulsants
What are common sites to find lymphosarcoma in cattle?
heart (right atrium)
abomasum
spinal cord (extradural lesions)
retrobulbar area
Spinal cord tumors are generally caused by what neoplasia?
lymphosarcoma
What abnormality results from thinning brain due to fluid accumulation such as in vitamin A deficiency or as a hereditary condition in Hereford, charolais, dexter, holdtein, and jersey cattle?
hydrocephalus
What abnormality is defined as a congenital absence of brain due to failure to grow or cellular necrosis due to viral disease such as BVD or bluetongue?
hydrancephaly
What can cause peripheral neuropathy of the brachial plexus?
injury to the shoulder —> trauma, fracture, penetrating wound
What are signs indicating peripheral neuropathy of the brachial plexus?
complete flaccidity of the affected limbs due to absence of sensation ± ipsilateral horner’s syndrome
What can cause peripheral neuropathy of the radial nerve?
trauma or excessive recumbency during anesthesia or hoof trimming restraint
What are signs indicating peripheral neuropathy of the radial nerve?
limb position varies based on where 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 tricep muscle atrophy
What can cause peripheral neuropathy of the femoral nerve?
traumatic overextension of hip and stifle, or excessive traction during dystocia
What are signs indicating peripheral neuropathy of the femoral nerve?
inability to fix and extend the stifle —> hoof usually stays flat on the ground, absent patellar reflex
What can cause peripheral neuropathy of the femoral nerve?
often damaged with traction from dystocia
What are signs indicating peripheral neuropathy of the femoral nerve?
limb hangs behind the animal
stifle is dropped and extended
hoof rests on dorsal surface
chronic injury will lead to profound muscle atrophy
What can cause peripheral neuropathy of the peroneal nerve?
recumbent postpartum dairy cattle
What are signs indicating peripheral neuropathy of the peroneal nerve?
hyperextension of the hock
flexion of fetlock and pastern
dorsal hoof drags on ground
may bear weight if placed in position manually
What can cause peripheral neuropathy of the tibial nerve?
dog bite injuries or injections to the caudal leg at the level of the stifle
What are signs indicating peripheral neuropathy of the tibial nerve?
“stringhalt” like movement —> exaggerated flexion of stifle and tarsus
asymmetric pelvis —> lower side is the affected side
atrophy of gastrocnemius
What can cause peripheral neuropathy of the obturator nerve?
cattle have a shallow acetabulum and small round ligament which predisposes obturator nerve to injury during dystocia
What are signs indicating peripheral neuropathy of the obturator nerve?
hoppy pelvic limb gait
severe pelvic abduction “splay leg”
What can cause peripheral neuropathy of the facial nerve?
trauma, infection, inflammation, masses
What are signs indicating peripheral neuropathy of the facial nerve?
facial muscle atrophy, prolapsed lips, exposure keratitis
How can we treat peripheral neuropathy of the facial nerve?
supportive care
assisted feedings and cleaning out of cheek pouches
electroacupuncture
What are the three key principles for therapy and management of peripheral neuropathy cases?
reduce swelling and inflammation at the site of injury
support and stabilize the denervated area
maintain the general health of the animal