Bovine Neurology Flashcards
Name 4 properties which are needed for antibiotics in neurology (6)
–Cross the blood – brain barrier and achieve high enough concentration
- Lipid soluble
- Low molecular weight (not protein bound)
- NB BB barrier more permeable if inflamed
–Bacteriocidal
•Natural intrathecal defence mechanisms are poor
Name 3 options for an antibiotic (4)
- Penicillin
- 3rd generation cephalosporins e.g. Ceftiofur
- Trimethoprim – sulphonamide combinations
- Florfenicol
Name 3 treatment options for treatig cerebral oedema (4)
–Steroids
•Dexamethazone 1-2mg/Kg
–May interfere with immune response and decrease BB barrier permeability
–NSAIDs
•Broad anti-inflammatory and analgesic affects. No published data on their efficacy in FA neurological disease
–Frusemide
•Diuretic. 1-2mg/Kg i/v
–Dimethyl sulphoxide (DMSO)
•Not licensed in food producing animals
What is a common consequence of many bovine neuro problems?
Cerebral oedema
What predisposes an animal to congenital neuro conditions?
–Often exposure to infectious or toxic insults during pregnancy
What are Holstein, Hereford, Ayrshire, Charolais predisposed to?
Hydrocephalus
What are Shorthorn, Hereford, Angus predisposed to?
Cerebellar hypomyelinogenesis
abnormally reduced myelination in the cerebellum;
charcterized clinically by severe neonatal tremor.
What are Charolais predisposed to?
Progressive ataxia
Cerebellar hypolasia:
A) What is the aetiology?
B) What is the epidemiology?
A)
–Genetic condition (rare, see previous)
–Congenital condition. In utero infection of calves with Bovine Viral Diarrhoea (BVD) virus (a Pestivirus)
B)
–Infection of a naïve cows during pregnancy with BVD virus (respiratory / nose to nose contact)
–Limited affects on the dam, however the virus can cross the placental barrier and infect the calf
–Infection between 90-130 days of gestation can lead to cerebellar hypoplasia (and other problems e.g. microphthalmia)
–Single cases, occasionally small storms e.g. batch calving groups
Cerebellar Hypoplasia:
A) What is the pathogenesis?
B) Name cliniccal signs
A)
–Cerebellum primarily concerned with fine motor coordination of voluntary movement
–Hypoplasia causes dyfunction leading to “clumsy” and jerky movements
B)
–Ataxia and incoordination
–Wide based stance
–Hypermetria and intention tremours
–Lateral recumbency and inability to stand in severe cases
Cerebellar Hypoplasia:
A) How do you diagnose?
B) How do you treat?
C) How do you prevent?
A) –Clinical signs
–Affected calves will be “persistently infected” (PIs) (See BVD teaching)
B)
–None. Mildly affected calves will often cope if maintained in low stress environments
C)
–Affected calves implies the presence of active circulation of virus in the herd. This must prompt further herd level investigation
Meningitis / Meningoencephalitis:
A) What is the aetiology?
B) What is the epidemiology?
A)
–Inflammation of the meninges and / or encephalon
–Usually associated with bacterial (or viral) infection in farm species
•Streptococcus spp., E.coli (young farm animals)
- •Histophilus somnus (cattle)
- •Pasturella multocida & Mannhemia haemolytica (lambs)
B)
–Most commonly a sporadic disease of young (3-10 days) calves and lambs
–Failure of passive transfer & high environmental bacterial contamination e.g. dirty indoor housing
–Bacteraemia → Navel ill / Joint ill and less commonly meningitis
Meningitis / Meningoencephalitis:
A) What is the pathogensis?
B) What are the clinical signs?
A)
–Localisation of septic foci in meningeal vessels occasionally progressing to encephalon
- Hyperaemia, opacity, accumulation of pus
- Swelling
B) – clinical exam is pretty much the same as a SA including menace response etc.
–Initially depression, weakness, lack of suck reflex, low head carriage, neck extension
–→ ataxia and recumbency, lack of menace, epischeral congestion (engorgement of the blood vessels that run across the white part of the eye)
–→ stupor, hyperaesthesia, opisthotonus (abnormal posturing caused by strong muscle spasms) and death
–Other signs may include polyarthritis, hypopyon ( involving inflammatory cells in the anterior chamber of the eye. It is a leukocytic exudate, seen in the anterior chamber, usually accompanied by redness of the conjunctiva and the underlying episclera), omphalophlebitis (inflammation of the umbilical cord stump) , diarrhoea
Meningitis / Meningoencephalitis:
A) How do you diagnose?
B) How do you treat?
A) –Clinical signs
–CSF tap ( protein & WBC count), turbid. Culture?
B)– Onset is critical! Need to be a prompt as possible!!
–Prognosis poor unless treated early
–High doses of broad spec, bacteriocidal antibiosis to cross B-B barrier
- 3rd generation cephalosporins e.g. ceftiofur
- Florfenicol
- Trimethoprim – sulphonimide combinations
–NSAIDs
–Supportive treatment e.g. fluids and nursing
How do you prevent Meningitis / Meningoencephalitis?
–Neonatal management
- Passive transfer of immunity
- Clean environment (calving / lambing areas, neonatal areas)
–Clean out and disinfect regularly
•Naval dressing
Otitis Media:
A) What is the aetiology?
B) What is the epidemiology?
A) –Infection (usually bacterial) of the middle ear
•Often mixed infection
–E.coli, Pseudomonas spp, Acinetobacter spp, Mycoplasm bovis
- Ascending infection up the eustachian tube following pneumonia
- Haematogenous spread (navel / joint ill in calves)
- Rarely extension of otitis externa
B) –Usually young calves and lambs.
–Sporadic single cases, although group outbreaks have been reported
Otitis media:
A) Name clinical signs?
B) How would you diagnose?
A) –Head tilt, possibly ataxia and circling / falling towards the affected side
–Occasionally ear drooping (inflammation of the facial nerve)
–Purulent discharge if the tympanic membrane is ruptured
–Pyrexia / Anorexia / Dull in advanced disease
B)
–Clinical signs
–Further investigation is possible (c.f. small animals) but rarely necessary
Otitis media:
A) How do you treat?
B) How do you prevent?
A)
–Antibiotics
- Broad spectrum, long courses (3-4wks)
- Fluoroquinolones?
- Which Abs are going to be able to access this site??
–NSAIDs
–Irrigation following rupture of the tympanic membrane is possible
B) –Difficult. Prevent pneumonia and navel / joint ill
Hypovitaminosis A:
A) What is the aetiology?
B) What is the epidemiology?
A)
–Primary deficiency of Vit A or carotene (precursor) in the diet (much more common)
•Carotene present in green plant material
–Secondary deficiency caused by problems with digestion, absorption or metabolism can occur
B)
–In the UK, usually young housed cattle on diets lacking green plant material e.g. straw and cereals without mineral & vitamin supplementation
–Alternatively, maternal deficiency can lead to congenital deficiency and disease in young calves
–Neonates receive high levels of vitamin A in colostrum (levels are low in milk)
What is vitamin A needed for?
- Essential component of the photo-receptor rhodopsin
- Maintenance of epithelial tissue and mucus membranes
- Normal bone growth
