Neurological Disorders in Younger Cattle Flashcards
Neurological conditions that are evident from birth.
Congenital:
- viral associated.
– BVD virus (common and important).
– Schallenberg virus.
– Bluetongue virus.
Acquired:
- cerebral anoxia.
BVDV.
Naive adult cattle:
- usually subclinical.
- systemic.
– mild pyrexia +/- diarrhoea.
– reduced milk yield.
- repro.
– poor fertility, EED and abortion.
– congenital deficits/abnormalites.
–> internal hydrocephalus, cerebellar hypoplasia.
– production of persistently infected (PI) calves.
Internal hydrocephalus (congenital as a result of BVDV)…
1. Aetiology.
2. Clinical signs.
3. Tx and Px.
- BVD most common cause.
Can be inherited (e.g. bulldog calves). - Neuro deficits (e.g. depression/ataxia).
+/- abnormal skull shape.
Born weak and die in a few days or stillborn. - No tx, poor px.
Cerebellar hypoplasia (congenital as a result of BVDV)…
1. Aetiology.
2. Clinical signs.
3. Tx and Px.
- BVD most common cause.
Can be inherited. - Neuro deficits (largely proprioceptive).
- ataxia +/- wide based stance.
- intention tremor +/- hypemetria.
- inability to stand. - No tx and poor px.
Schmallenberg virus.
Vector born (midges).
Timing of infection:
- before pregnancy leads to dam immunity.
- during pregnancy leads to:
– congenital malformations +/- abortion / still birth.
– neuro signs in foetus.
Affects all ruminants (esp. sheep and cattle).
Clinical signs of Schmallenberg virus in calves / lambs?
Neuro signs (apparently normal outer appearance - rare).
- “dummy presentation”.
- bilateral blindness.
- ataxia.
- recumbency.
- inability to suck.
- Cerebral anoxia aetiology?
- Cerebral anoxia clinical signs?
- Px of cerebral anoxia?
- Tx of cerebral anoxia.
- +/- prolonged birth/dystocia +/- assistance.
- Usually unable to stand and show CNS signs.
- Poor.
- IV fluids spiked w/ bicarbonate to correct metabolic acidosis.
Colostrum by stomach tube.
Nursing.
What is CCN?
Cerebrocortical necrosis.
- common and important!
CCN aetiology?
Thiamine normally formed by rumen flora in sufficient quantities.
Thiamine is essential for glucose metabolism.
Glucose is most important energy source for brain.
CCN is caused by thiamine deficiency due to:
- thiaminases produced by certain rumenal bacteria.
- thiaminases in some plants (bracken/fern) and in mouldy/spoilt feed.
- lack of uptake in SI following enteritis.
Thiamine deficiency leads to cerebral oedema, pressure necrosis due to oedema, necrosis of cerebral cortex.
Epidemiology of CCN.
Most common neuro disorder of calves.
Usually housed but can occur at pasture.
Intensive feeding systems.
- low forage to concentrate ratio
- low dietary neutral detergent fibre.
Age:
- 2-7m.
- young cattle most at risk due to rapid growth and lower natural thiamine levels.
- occasionally adults.
CCN clinical signs.
Initially:
- depressed.
- bilateral, central blindness.
- aimless wandering.
Progressing to:
- ataxia.
- muscle tremors.
Ending with:
- collapse.
- convulsions.
- opisthotonus (turned head).
- mortality 25-50%.
Normal temperature.
Normal rumen activity.
Dx of CCN.
Clinical signs.
Response to tx w/ thiamine (vit B1).
PME:
- generally good BCS.
- swelling and coning of brain into foramen magnum (due to cerebral oedema).
- gyri yellow and soft (due to necrosis).
- fluorescence under UV light.
DDx of CCN.
Toxic:
- lead poisoning.
– difficult to distinguish from CCN.
– absent rumen contractions.
Nutritional:
- hypovitaminosis A.
– bilateral central blindness.
– papilloedema.
Infectious:
- meningitis.
– usually pyrexic.
– nystagmus.
- listeriosis:
– asymmetrical cranial nerve deficits.
– unilateral, central blindness.
– may be pyrexic.
CCN tx.
CCN px.
CCN prevention.
Tx:
- high doses of thiamine (vit B1) IV (every 3hrs for 5 occasions).
– can give IM if farmer to give.
- frusemide to reduce cerebral oedema.
Px:
- improvement in 24hrs, recovery may take a week.
Prevention:
- thiamine IM in face of outbreak.
- correct nutrition >60% forage in diet.
Meningitis aetiology.
Most commonly E coli (gram negative, facultative anaerobe).
May be from high levels of bacterial challenge (calf environment? - housed).
Low level of protection - failure of passive transfer.
Sequel to neonatal septicaemia +/- navel/joint ill.
Mean age 6d.
Systemic signs of meningitis +/- septicaemia?
Lethargy.
Loss of suck reflex.
Collapse.
Signs of shock.
+/- pyrexia.
Neuro signs of meningitis +/- septicaemia?
Bilateral nystagmus.
Head pressing.
Star gazing.
Tremors.
Opisthotonus.
Convulsions.
Tx of meningitis +/- septicaemia?
Systemic abx.
- must be able to cross BBB.
- first line – amoxycillin, TMPS or florfenicol.
NSAIDs.
Supportive therapy:
- nursing care.
- IVFT +/- glucose.
- heat lamp.
Middle ear disease aetiology?
Ascending infection from respiratory tract often w/ a recent hx of pneumonia.
Occasionally progression from otitis externa.
Mycoplasma bovis.
Incidence is sporadic.
Typically calves 3-5w old.
- Middle ear disease clinical signs.
- Middle ear disease tx?
- Head tilt towards affected side.
No cranial nerve deficits.
Calf remains BAR and feeding.
Usually no vestibular disease. - Systemic ABX appropriate to mycoplasma.
Risk factors for hypoglycaemia.
Neonates.
Inadequate colostrum intake.
Inadequate feeding.
Hypothermia.
Other systemic disease (esp. scour and septicaemia).
- Hypoglycaemia clinical signs.
- Tx of hypoglycaemia?
- Depression.
Weakness.
Ataxia.
Seizures, coma, death. - IV glucose.
Address risk factors.
- warming, appropriate feeding.
- Sources of lead poisoning.
- What do clinical signs of lead poisoning depend on?
- Lead paint, pipes, car batteries.
Soil in certain geographical areas. - Rate of exposure.
Magnitude of exposure.
Animal’s body mass.
- Neuro signs seen in acute high exposure and small body mass in young animals.
- GI signs seen in chronic low exposure and large body mass in older animals.
Lead poisoning clinical signs.
Peracute, acute, subacute and chronic forms.
Neurological signs:
- bilateral central blindness.
- muscle fasciculations.
- head pressing.
- bruxism, jaw champing and bellowing.
- hyperaesthesia and excitability.
- seizures.
