Bovine neurology Flashcards
1
Q
Antibacterial treatment
A
A number of conditions causing neurological signs are bacterial in origin. Antibiotic choice is very important:
- Cross the blood-brain barrier and achieve a high enough concentration
- lipid soluble
- low molecular weight (not protien bound)
- Bacteriocidal - natural intrathecal defence mechanisms are poor
- Active against causal pathogen
E.g. Penicillins, 3rd generation cephalosporins (ceftiofur), TMPS, Florfenicol
2
Q
Anti-inflammatory Treatment:
Cerebral oedema is a common consequence and needs to be treated.
A
-
Steroids
- Dexamethasone 1-2mg/kg
- might dampen immune response and reduce BBB permeability
- NSAIDs
-
Frusemide
- Diuretic 1-2mg/kg IV
-
Dimethyl sulphoxide (DMSO)
- not licensed in food producing animals.
3
Q
Genetic and Congenital conditions:
A
- Hydrocephalus (Holstein, Hereford, Ayrshire, Charolais)
- Cerebellar hypomyelinogenesis (Shorthorn, Hereford, Angus, Progressive ataxia (charolais
4
Q
Cerebellar Hypoplasia
A
- Aetiology - genetic condition, congenital condition (BVD)
- BVD virus can cross the placental barrier and infect the calf.
- infection between 90-130 days can lead to cerebellar hypoplasia and other problems e.g. microphthalmia
-
Pathogenesis
- cerebella involved with fine motor coordination of VOLUNTARY movement - ‘clumsy’, jerky movements
- ataxia and incoordination, wide based stance
- hypermetria and intention tremors
- lacteral recumbency, cannot stand
-
Diagnosis:
- clinical signs, PI calves
-
Treatment
- None - mildly affected calves can cope in low stress environments
-
Prevention
- affected calves implies presence of PI in the herd. This must prompt further investigation!
5
Q
Meningitis/ Meningoencephalitis
A
- usually associated with bacterial (or viral) infection
- Streptococcus sp, E.coli (young animals)
- Histophius somnus (cattle)
- Pasturella multocida and Mannhemia haemolytica (lambs)
- usually disease of young (3-10 days) calves and lambs
- poor passive transfer and high environmental contamination
- bacteriaemia - navel ill/ joint ill
-
Clinical signs:
- depression, weakness, no suck reflex, neck extension, loss of menace, ataxia, epischeral congestion, stupor, hyperaesthesia, opisthotonus and death
- polyarthritis, hypopyon (inflammatory cells in anterior chamber of eye), omphalophlebitis, diarrhoea
-
Diagnosis:
- clinical signs, CSF tap (increased protein and WBC), turbid, culture?
-
Treatment:
-
high dose of broad spectrum bacteriocidal ABs
- 3rd generation cephalosporins e.g. ceftiofur
- Florfenicol
- TMPS
- NSAIDs
- supportive treatment e.g. fluids and nursing
-
high dose of broad spectrum bacteriocidal ABs
-
Prevention:
- Passive transfer of immunity
- clean environment (lambing/calving areas) - disinfect
- naval dressing
6
Q
Otitis Media:
A
Aetiology:
- Infection (bacterial) - E.coli, Pseudomonas sp, Acinetobacter sp, Mycoplasma bovis
- Ascending infection - following pneumonia up eustacian tube
- Haematogenous spread (naval/joint ill)
- Extention of otitis externa
Epidemiology:
- young calves and lambs, sporadic single cases.
Clinical signs:
- Head tilt, ataxia, circling/ falling towards affected side
- ear droop (inflammation of facial nerve)
- purulent discharge if tympanic membrane rupture
- pyrexia/anorexia/dull
Diagnosis:
- clinical signs
Treatment:
- BS antibiotics, long course 3-4 weeks
- NSAIDs
- Irrigation following rupture of tympanic membrane
Prevention:
- Difficult, prevent pneumonia and navel/joint ill
7
Q
Hypovitaminosis A
A
Aetiology:
- Primary deficiency of vit A or carotene (precursor) in the diet - in green plant materials
- Secondary deficiency - digestion, absorption, metabolism problems
Epidemiology:
- Cattl housed lacking green plant material e.g. straw and cereals without supplementation (minerals and vitamins)
- Maternal deficiency can lead to congenital deficiency in calves
- Neonates recieve high vitamin A in colostrum (levels low in milk)
Pathogenesis;
- Vit A needed for photoreceptor rhodopsin
- maintenance of epithelial tissue and MM
- normal bone growth
Clinical signs:
- Growing cattle:
- Night blindness (no menace)
- rough, dry coat and poor quality hoof horn
- Paralysis (damage to peripheral nerve roots)
- encephalopathy (increase ICP) - nervous signs
- Congenital disease
- born blind - optic nerve obstruction
- microphthalmos
- tonic-clonic convulsions
Diagnosis:
- Hx and clinical signs, vitamin A plasma levels (<10μg/100ml)
- in theory, high CSF pressure can be used
Treatment:
- parenteral administration of Vit A at 400iu/kg
- ensure ongoing daily requirements met in the diet
Prevention:
- Daily requirement 40 IU/kg BW
- ensure green forage and supplemented with minerals and vitamins
8
Q
Cerebrocortical Necrosis (CCN)
aka Polioencephalomalacia
A
Aetiology:
- Deficiency of vitamin B1 (thiamin)
- either produced by bacteria or plants - normal requirements absorbed in rumen produced by microflora
- Primary deficiency - inadequate production/absorption
-
Secondary deficiency - thiaminases in the rumen
- bacterial production = bacillus thiaminolyticus/ Clostridium sporogenes (thiaminase Type I)
- Bacillus aneurinolyticus (thiaminase Type II)
- Plants - Bracken fern and Horsetail
- High levels of sulphate in the diet
Pathogenesis:
Brain is critically dependent on carbohydrate for energy. Absorbed thiamine is actively phosphorylated to thiamine pyrophosphate (TPP) which is a coenzyme in krebs (TCA) cycle.
Epidemiology:
- Sporadic cases, young fast-growing animals
- well fed calves (4-18 months) and lambs (4-8 months) on LOW FIBRE diets
- often associated with change in diet
PME:
- brain pale and swollen, yellow discoloration
- necrotic cortical tissues in cerebrum with laminar configuration
- bright white autofluorescence when viewed with UV light
- areas of necrosis, particularly cortex
Clinical signs:
- dull, diarrhoea
- staggering, ‘star gazing’, wandering, blind (no menace)
- hyperaesthesia
- recumbency, muscle tremors, opisthotonus, convulsions, flaccid and spastic paresis
- death in 1-4 days if left untreated
Diagnosis:
- hx and clinical signs, response to tx
Treatment:
- Thiamine hydrochloride IV, repeat regularly for 2-3 days
- nursing
- steroids to reduce cerebral oedema
Prevention:
- watch others in group and treat promptly
- increase fibre/ reduce concentrate in diet
9
Q
Listeriosis:
Very common disease in cattle and sheep.
A
Very common in older animals often relating to silage.
Causes neurological disease - travels through the buccal membrane and facial nerve causing drooping of one side of face and ears.
Treat and identify route of disease e.g. silage. This is a common cause of abortion in sheep.
10
Q
Malignant Catarrhal Fever (MCF)
A
Aetiology:
- Ovine herpesvirus -2 (OHV 2) - does not cause disease in host species e.g. sheep and wilderbeest
Epidemiology:
- sporadic single cases in yearling/adult cattle
- usually direct (or indirect) contact with pregnant or lambing sheep
- cattle to cattle transmission does NOT occur
- incubation 3-8 weeks
Pathogenesis:
- lymphoid hyperplasia and infiltration
- vasculitis
Clinical signs:
- anorexia and agalactia
- Pyrexia (41-41.5 degrees) and tachycardia
- mucopurulent nasal discharge
- corneal opacity, eyelid oedema, congestion, blepharospasm
- necrosis of buccal mucosa
- neuro signs- weakness, nystagmus, head pressing
Clinical pathology:
- Leucopenia
- serology might be useful, but not all have seroconverted
- lesions through GIT, UT, respiratory tracts
- haemorrhagic lymph nodes
- Histo
- necrotising vasculitis
- perivascular and mononuclear cell cuffing of most organs
Diagnosis:
- Hx - contact with sheep
- viral antigen PCR
- seroconversiom?
- PME
Treatment and prevention:
- no treatment - EUTHANASIA
- no vaccine
- prevent cattle having contact with lambing sheep
11
Q
Thromboembolic Meningoencephalitis (TEME)
A
Aetiology:
- Sudden and severe bacteraemia caused by Histophilus somnus
Epidemiology:
- Young growing cattle, usually induced by stress e.g. weaning
- ‘feedlot’ cattle in N America, uncommon in UK
- Respiratory form most common presentation seen in UK
Clinical signs:
- pyrexia, anorexia, depression
- Somnolence (sleepy calf disease)
- ataxia, proprioceptive deficits
- blindness, nystagmus, opisthotonus, coma
- pneumonia, pleuritis and myocarditis
- joint effusions/ swellings
Diagnosis:
- clinical signs, culture CSF, blood, synovial fluid
- acute and convalescent serology
Treatment:
- Antibiotics - oxytetracycline, penicillins, florfenicol
- NSAIDs
- Nursing
Prevention:
- Limit stress
- No vaccine in UK
12
Q
Toxicity and Poisoning
A
- Not uncommon, lots of different cases
- associated with neurological signs
- Hx and investigation of the environment.
13
Q
Lead Poisoning
Arsenic and mercury poisoning also associated with CNS signs. Arsenic compounds include herbicides, insecticides and wood preservatives.
A
By far the most common toxicity. Young ruminants more at risk, but in poultry, older animals more at risk.
- young ruminants are ingesting milk meaning more calcium channels in intestine and calcium and lead have similar valency so they are at more risk of absorbing lots of lead.
Aetiology:
- consumption of lead, licking objects in the environment e.g. paint, batteries, lead mines, engine oil, putty, grease
Clinical signs:
Peracute - sudden death
Acute - muscle fasiculations, jaw champing, frothing, bruxism, staggering gait, head pressing, blindness, opisthotonus, tonic-clonic convulsions, bellowing, diarrhoea.
Subacute/chronic - less severe signs, diarrhoea, depression, poor doing
Pathogenesis:
- Damage to BBB allowing passage of toxins, disturbing cellular membranes
PME:
- No gross lesions if acute
- less acute - Abomasitis and enteritis, congestion of lungs, degeneration of liver and kidney
Diagnosis:
- Hx and clinical signs - search environment
- lead in heparinized blood >0.4ppm diagnostic
- lead in kidney >20ppm diagnostic
Treatment:
- IV chelating agent - ca-EDTA, repeat for 3-4 days
- oral agents e.g. magnesium sulphate (bind Pb reducing uptake)
- supportive treatments
- sedatives e.g. alpha 2 e.g. xylazine
- fluids
- careful nursing
Prevention:
- search environment for source
- if in doubt, move animals and change pasture
Protecting Human Health:
- contaminated products are a risk to health
- Food safety act 1990
- all Pb poisoning cases are investigated by VLA on behalf of FSA
- blood sample affeted/ potentially affected animals before sale
14
Q
A
15
Q
Organophosphate Poisoning
A
- principally in insecticides/acaricides. carbonates are similar and used as molluscicides and herbicides.
Aetiology:
- block cholinesterases at cholinergic nerve endings and myoneural junctions –> persistence of acetyl choline and continued stimulation –> stimulation of PNS, skeletal muscles and CNS
Clincal signs:
- salivation, nasal discharge, dysponea, cough, lacrimation, miosis, diarrhoea, sweating
- muscle fasciculations, paralysis
Diagnosis:
- clinical signs
- reduction in cholinesterase activity
Treatment:
- Atropine sulphate (blocks acetylcholine) IV, then SC
- repeat after 48 hours if necessary
19
Q
Plant poisoning
- Ragowrt (hepatic encephalopathy)
- Bracken
- Horsetail
- Laburnum
A
- Relatively uncommon however:
- animals kept on sparse pasture - bog, woodland
- curiosity - especially young cattle in a novel environment
- drainage of clearance work
- garden clippings thrown over hedge
