Bovine neurology Flashcards
1
Q
Give examples of genetic neurological conditions in cattle
A
- Hydrocephalus (Holstein, Hereford, Ayrshire, Charolais)
- Cerebellar hypomyelinogenesis (Shorthorn, Hereford, Angus)
- Progressive ataxia (Charolais)
2
Q
What are congenital neurological conditions in cattle commonly associated with?
A
Infectious or toxic insults during pregnancy
3
Q
Outline the aetiology of cerebellar hypoplasia in cattle
A
- Genetic condition (rare)
- congenital condition
- In utero infection of calves with BVD virus
4
Q
Describe the epidemiology of cerebellar hypoplasia in cattle
A
- Infection of naiive cows during pregnancy with BVD
- Limited effects on dam, virus crosses placental barrier and infects calf
- Infection between 90-130 days gestation can lead to cerebellar hypoplasia (and other problems e.g. microphthalmia)
- Single cases, occasionally small storms e.g. batch calving groups
5
Q
Outline the pathogenesis of cerebellar hypoplasia in cattle
A
- Cerebellum concerned with fine motor coordination of voluntary movement
- Hypoplasia leads to dysfunction leading to clumsy, jerky movements
6
Q
Describe the clinical signs of cerebellar hypoplasia in cattle
A
- Ataxia and incoordination
- Wide based stance
- Hypermetria and intention tremors
- Lateral recumbency and inability to stand in severe cases
7
Q
How is cerebellar hypoplasia of cattle diagnosed?
A
Based on clinical signs
8
Q
Outline the treatment of cerebellar hypoplasia in cattle
A
None, mildly affected often cope if maintained in low stress environments
9
Q
Outline the prevention of cerebellar hypoplasia in cattle
A
- Affected calves indicate active circulation of virus in herd so herd level investigation required
- Control programme for BVD is in place
- Remove persistently infected individuals
10
Q
Describe the aetiology of meningitis/meningoencephalitis in cattle
A
- Inflammation of meninges and/or encephalon
- Usually bacterial or viral, infection in farm species
- Streptococcus spp, E coli in young
- Histophilus somnus in cattle
- Pasteurella multocida and Mannhemia haemolytica in lambs
11
Q
Describe the epidemiology of meningitis/meningoencephalitis in cattle
A
- Most commonly sporadic disease of young (3-10 days) calves/lambs
- Failure of passive transfer and high environmental bacterial contamination
- Bacteraemia leads to navel ill/joint ill and less commonly meningitis
12
Q
Describe the pathogenesis of meningitis/meningoencephalitis in cattle
A
- Localisation of septic foci in meningeal vessels, occasionally progressing to encephalon
- Hyperaemia, opacity and accumulation of pus
- Swelling
13
Q
Describe the clinical signs of meningitis/meningoencephalitis in cattle
A
- Initially depression, weakness, lack of suck reflex, low head carriage, neck extension
- Leads to ataxia, recumbency, lack of menace, episcleral congestion
- Leads to stupor, hyperaesthesia, opisthotonus and death
- Other signs: polyarthritis, hypopyon, omphlophlebitis, diarrhoea
14
Q
Outline the diagnosis of meningitis/meningoencephalitis in cattle
A
- Clinical signs
- CSF tap (not required for treatment, may show increased protein and WBC count, turbidity and can culture)
15
Q
Describe the treatment of meningitis/meningoencephalitis in cattle
A
- Prognosis poor unless early treatment
- High doses of braod spec, bacteriocidal, BBB crossing antibiotics: 3rd gen cephalosporins, florfenicol, TMPS combinations
- NSAIDs
- Supportive treatment e.g. fluids and nursing
16
Q
Describe the prevention of meningitis/meningoencephalitis in cattle
A
- Neonatal managment
- Passive transfer of immunity via colostrum must be ensured
- Clean environment, disinfect regularly
- Navel dressing
17
Q
Describe the aetiology of otitis media in cattle
A
- Infection usually bacterial
- Often mixed infection
- Ascending infection up eustachian tube following pneumonia
- Haematogenous spread (navel/joint ill in calves)
- Rarely an extension of otitis externa
18
Q
What are the common pathogens in otitis media in cattle?
A
E coli, Pseudomonas spp., Acinetobacter spp., Mycoplasma bovis
19
Q
Describe the epidemiology of otitis media in cattle
A
- Usually younger calves and lambs
- Sporadic single cases, some group outbreaks reported
20
Q
Describe the clinical signs of otitis media in cattle
A
- Head tilt, possible ataxia, circling/falling towards affected side
- Occasionally ear drooping (inflammation of facial nerve)
- Purulent discharge if tympanic membrane ruptured
- Pyrexia/anorexia/dull in advanced disease
21
Q
Outline the diagnosis of otitis media in cattle
A
- Clincial signs
- Further investigation possible similar to small animals, but rarely necessary
- NB trauma may be a differential, higher risk than in small animals
22
Q
Outline the treatment of otitis media in cattle
A
- Antibiotics: brad spec, long course 3-4 weeks
- NSAIDs
- Irrigation following rupture of tympanic membrane possible
23
Q
Outline the prevention of otitis media in cattle
A
Difficult, prevent pneumonia and navel/joint ill
24
Q
Describe the aetiology of hypovitaminosis A in cattle
A
- Primary deficiency of vit A or carotene in diet
- Secondary deficiency caused by problems with digestion, absorption or metabolism (Less common)
25
Describe the epidemiology of hypovitaminosis A in cattle
- Usually young housed cattle on diets lacking green plant material i.e. straw and cereals without mineral and vit supplementation
- May be maternal deficiency leading to congenital deficiencyand disease in young calves
- Neonates should have high levels of vit A in colostrum
26
Describe the pathogenesis of hypovitaminosis A in cattle
Required for:
- Rhodopsin photo-receptor
- Maintenance of epithelial tissue and mucus membranes
- Normal bone growth
- Also leads to damage to peripheral nerve roots and increased intracranial pressure
27
Describe the clinical signs of hypovitaminosis A in growing cattle (not congenital)
- Night blindness leading to complete blindness
- Rough, dry coat, poor quality hoof horn
- Paralysis, initially show weakness and incoordination
- Encephalopathy seen as convulsions and other nervous signs
28
Describe the clinical signs of hypovitaminosis A as a congenital disease of young calves
- Born blind (optic nerve constriction)
- Other ocular problems e.g. microphthalmos
- Tonic-clonic convulsions
29
Outline the diagnosis of hypovitaminosis A in cattle
- History and clinical signs
- Vitamin A levels in plasma <10ug/100ml
- High CSF pressure (theoretical)
30
Outline the treatment of hypovitaminosis a in cattle
- Parenteral administration of vit A at 400iu/kg BW (rapid response unless chronically affected)
- Ensure ongoing daily requirements met by diet
31
Outline the prevention of hypovitaminosis A in cattle
- Daily requirement 40IU/kg BW
| - Ensure cattle and sheep of all ages receive green forage or are supplemented with minerals and vitamins
32
What is cerebrocortical necrosis also known as?
Polioencephalomalacia
33
Describe the aetiology of polioencephalomalacia in cattle
- Deficiency of vit B (thiamin)
- Normal requirements absorbed from rumen produced by microflora
- Primary deficiency: inadeuate production/absorption, unclear aetiology
- Secondary deficiency: presence of thiaminases in rumen of bacterial production of plants
- High levels of sulphate in diet
- Brain dependent on carbohydrate in diet, absorbed thiamine converted to thiamine pyrophosphate (TPP), which is coenzyme in TCA and other carb metabolism processes
34
Give examples of bacterial thiaminases
- Bacillus thiaminolyticus
- Clostridium sporogenes (Thiaminase type 1)
- Bacillus anaerinolyticus (thiaminase type II)
35
Give examples of plant thiaminases
- Bracken fern
| - Horsetail
36
Describe the epidemiology of polioencephalomalacia
- Sporadic, often small clusters of cases
- Most common vitamin deficiency
- Usually young, often fast growing/well fed calves (4-18mo) and lambs (4-8mo) on low fibre diets
- Often associated with chagne in diet
- Occasionally single cases in adults
37
Describe the post mortem findings in polioencephalomalacia
- Brain pale, swollen, flattened gyri, sometimes yellow discolouration
- Necrotic cortical tissues in cerebrum with laminar configuration
- Affected regions have bright white autofluorescence when viewed with UV light (pathognomic)
- Histopath shows necrosis esp. in cortex
38
Describe the clinical signs of polioencephalomalacia in cattle
- Initially dull, diarrhoeic
- then neuro signs: staggering, high head carriage/star gazing, wandering
- Blind, no menace response
- Hyperaesthesia to tactile and auditory stimuli
- recumbency, muscle tremors, intermitent opisthotonus, convulsion, periods of flaccid and spastic paresis
- Death in 1-4 days if untreated
39
What are the pathognomic signs of polioencephalomalacia in cattle?
Wide based stance and stargazing
40
Outline the diagnosis of polioencephalomalacia in cattle
- History and clinical signs
| - Response to treatment
41
Describe the treatment of polioencephalomalacia in cattle
- Thiamine hydrochloride IV, 10-15mg/kg repeat for 2-3 days
- Nursing to reverse pathology, reduce other symptoms
- Maintain hydration and management of whole animal
42
Describe the prevention of polioencephalomalacia in cattle
- If case identified, watch others in group carefully and treat early if any clinical signs
- Increase fibre/reduce concentrate in diet
- Ensure no thiaminase plants on pasture
43
What is silage eye?
Ocular lesions caused by listeriosis
44
Describe the aetiology of malignant catarrhal fever
- Ovine herpesvirus-2 in UK
- Do not cause disease in sheep
- Usually acute or peracute disease, chronic disease seen occasionally
- Less common vs listeriosis but more severe
45
Describe the epidemiology of malignant catarrhal fever
- Sporadic single cases in yearling/adult cattle, occasionally mini outbreaks
- Direct or indirect contact with pregnant or lambing sheep
- Deer can also be affected
- Cattle to cattle transmission does not occur
- Incubation period 3-8 weeks
46
Describe the pathogenesis of malignant catarrhal fever
- Lymphoid hyperplasia and infiltration
| - Vasculitis
47
Describe the clinical signs of malignant catarrhal fever
- ANorexia and agalactia
- High pyrexia (41-41.5) and tachycardia
- Profuse mucopurulent nasal discharge
- Corneal opactity, eyelid oedema, congestion and discharge, blepharospasm
- Extensive necrosis of buccal mucosa
- Occasionally neurological signs weakness, nystagmus, head pressing)
- Occasionally mild and chronic disease seen
48
How can MCF be differentiated from FMDV?
- MCF will have no coronary band lesions
| - FMDV has no ocular signs
49
Describe the clinical pathology results of MCF
- Leukopaenia
- Virus isolation difficult and problematic
- Serology may be of value in clinical cases although some do not/have not seroconverted
50
Describe the post mortem findings of MCF
- Lesions (haemorrhagic and erosive) often extensive in GIT, UT and RT
- Enlarged, oedematous, harmorrhagic lymph nodes
- Histopath shows necrotising vasculitis, perivascular and mononuclear cell cuffing in most organs
51
Describe the diagnosis of MCF
- History and clinical signs highly suggestive
- Viral antigen PCR can be attempted
- Seroconversion (care)
- PM findings
52
Outline the treatment and prevention of MCF
- Invariably fatal, euthanasia on welfare grounds
- No vaccine
- Prevent by preventing sheep to cattle contact
53
Outline the aetiology of Thromboembolic Menincoencephalitis (TEME) in cattle
Fulminating bacteraemia caused by Histophilus somnus
54
Describe the epidemiology of TEME in cattle
- Young growing cattle
- Usually induced by significant stress
- Uncommon cause of disease in UK, more common in feedlots in US
- Resp. form most common presentation in Uk
- Lots of concentrate feeding leading to liver abscesses, which can then seed out and spread around body e.g. to brain
55
Describe the clinical signs of TEME in cattle
- Pyrexia, anorexia, depression
- Somnolence (aka sleepy calf disease)
- Ataxia and proprioceptive deficits
- Occasionally blindness and nystagmus
- Opisthotonus, convulsions and coma if untreated
- Pneumonia, pleuritis, myocarditis
- Joint effusions/swelling leading to lameness
- Focused lesion e.g. in spinal cord may caused hindlimb ataxia (common in sheep, cattle)
56
Describe the diagnosis of TEME
- Clinical signs
- Culture from CSF, blood, synovial fluid
- Acute and convalescent serology
57
Describe the treatment of TEME
- Antibiotics (oxytet - crosses BBB, penicillins, florfenicol)
- NSAIDs
- Nursing
- Need to start treatment quickly, affects prognosis
58
Describe the prevention of TEME
- Prevent/limit stress
| - No vaccine in UK
59
Describe the aetiology of lead poisoning in cattle
Licking/chewing of lead objects e.g. paint, vehicle batteries, soil from lead mines, engine sump oil, putty, grease
60
Explain the epidemiology of lead poisoning in cattle
- Young more at risk due to lining of intestines having higher number of calcium channels than older
- These channels can absorb lead due to having the same latency
61
Describe the clinical signs of peracute lead poisoning in cattle
Sudden death depending on dose
62
Describe the clinical signs of acute lead poisoning in cattle
- Muscle fasciculations (esp. head and neck)
- Jaw champing, frothing, bruxism
- Staggering gait and head pressing
- Blindness
- Opisthotonus
- Tonic-clonic convulsions
- Bellowing
- Diarrhoea
63
Describe the clinical signs of lead poisoning in cattle
- Less severe vs acute
| - Diarrhoea, depression and poor doing predominate
64
Describe the pathogenesis of lead poisoning in cattle
- Not fully understood
- Damage to BBB allowing passage of toxins
- Disturbance of cellular memrbanes
65
Describe the post mortem findings of lead poisoning in cattle
- No gross lesions of acute
| - If less acute, abomastitis and enteritis, congestion of the lungs, degeneration of liver and kidney
66
Describe the diagnosis of lead poisoning in cattle
- History and clinical signs
- LEad in heparinised blood sample >0.4ppm diagnostic
- Lead in kidney >20ppm diagnostic
67
Describe the treatment of lead poisoning in cattle
- IV chelating agent which is an easily excretable non-ionisable, soluble complex e.g. sodium calcium edetate (Ca-EDTA)
- Euthanasia as is often unsuccessful
- Report heavy metal contamination to APHA
- Oral agents: precipiate soluble Pb into insoluble forms, reduce uptake, e.g. magnesium sulphate
- Supportive treatments e.g. sedatives, IV fluids, careful nursing
68
Outline the prevention of lead poisoning in cattle
- Search environment for source
| - Move all animals from pasture if in doubt
69
Explain the importance of lead poisoning in cattle to human health
- Contaminated milk and meat prevent risk
- FSA 1990 makes it offence to sell products which could compromise human health
- All cases of Pb poisoning investigated by VLA on behalf of FSA
- Need to ensure potentially contaminated produce does not enter food chain
- Blood sample affected/potentially affected animals before sale
70
Briefly outline other heavy metals that may cause neurological signs
- Arsenic, mercury
- Much less common vs Pb
- Arsenic compounds found in herbicides, insecticides, wood preservatives
71
Describe the pathogenesis of organophosphate poisoning in cattle
- Block cholinesterases at cholinergic nerve ends and myoneural junctions
- Lead to persistence of acetylcholine and continued stimulation
- stimulation of PSNS, skeletal muscles and CNS
72
How may organophosphates be absorbed?
Orally, dermally or by inhalation
73
Describe the clinical signs of organophosphate poisoning
- Profuse salivation, nasal discharge, dyspnoea, cough, excess lacrimation, miosis, diarrhoea, sweating
- Muscle fasciculation, stiffness leading to paralysis
- Profound CNS depression
74
Outline the diagnosis of organophosphate poisoning in cattle
- Clinical signs and history
| - (reduction in cholinesterase activity in blood or brain tissue)
75
Outline the treatment of organophosphate poisoning in cattle
- Atropine sulphate (blocks acetylcholine): 0.1mg/kg BW slow IV, or 0.4mg/kg BW SC
- Repeat after 48 hours if necessary
76
How does ionophore poisoning occur?
- Monensin used as growth promotor and coccidiosat
| - Excessive feeding or over-supplementation by error
77
Describe the clinical signs of ionophore poisoning
- Diarrhoea
- Dullness
- Weakness
- Tachycardia
- Neurological signs
- Heart failure due to myocardial effects
78
Outline the treatment of ionophore poisoning
No treatment other than supportive measures
79
What is mycotoxicosis?
Umbrella term for toxicosis due to consumption of toxins produced by moulds and fungi
80
How does mycotoxicosis occur?
Ingestion of plants or badly stored feed stuffs in wet and warm conditions (where moulds and fungi have grown)
81
Outline the importance of mycotoxicosis to humans
Risk to humans via direct consumption or indirectly by consumption of contaminated animal products e.g. milk
82
Describe the clinical signs of mycotoxicosis in cattle
More commonly abortion than neurological signs
83
Describe the aetiology of aflatoxicosis in cattle
- Aflatoxins are metabolites produced by range of fungi growing on spoiled/spoiling animal feeds
- Cattle and sheep affected if ingest affected feed stuffs
- Toxins include: B1, B2, G1, G2 and second generation metabolites M1 and M2
84
What is the main source of aflatoxins?
Aspergillus flavus
85
Describe the epidemiology of aflatoxicosis
- Wet/warm storage conditions of feed
- Sheep and cattle relatively resistant to effects
- Can affect any age group
- Usually all individuals in a group affected
- Can affect human health via milk
86
Describe the pathogenesis of aflatoxicosis
- Hepatosis and hepatic insufficiency
| - Mutagenesis and teratogenesis
87
Describe the clinical signs of aflatoxicosis in cattle
- Dependent on dose consumed
- Vague signs of ill health/poor performance
- Blindness, circling, bruxism, frothing, tenesmus and diarrhoea, photosensitivity, abortion
- Recumbency, convulsions and death
88
Describe the diagnosis of aflatoxicosis in cattle
- CLinical signs (often vague)
- Sensitive assays for levels in feeds, urine, blood, milk and other tissues (chromatography, ELISA)
- Elevation go live enzymes in acute case
89
Outline the treatment of aflatoxicosis in cattle
None, supportive only
90
Outline the prevention of aflatoxicosis in cattle
- Proper feed storage
- Do not feed mouldy food
- Measure levels in feed
- Commercial products can be mixed with feed which bind toxins and prevent absorption in the gut
91
How does plant poisoning commonly occur in cattle?
- Hunger if kept on sparse pasture
- Keeping animals on unimproved pasture
- Curiosity esp. in youngstock
- Drainage or clearance work
- Garden clippings thrown over hedges
92
List common plants that may cause neurological signs
- Ragwort
- Bracken
- Horsetail
- Hemlock
- Hemlock Water dropwort (aka dead man's fingers)
- Black nightshade
- Rhododendron
- Laburnum
93
List important infectious neurological disease of cattle
- BSE and Scrapie
- Aujeskys
- Rabies
- Gid
94
What are the key aspects for the treatment of ruminant neurological idsease?
Antibacterial and anti-inflammatory treatment
95
What are the key criteria for antibacterials to treat neurological conditions in cattle?
- Must cross BBB and achieve high enough concentration
- Must be bacteriocidal
- Must be active against causal pathogen
96
List and justify some logical choices of antibacterials for the treatment of neurological conditions in ruminants
- Penicillins: use small animal preparations as can be used IV, large animal preps have limited routes of admin
- 3rd generation cephalosporins: purely for individual cases, no metaphylaxis, are critically important but may be justified in neuro cases
- TMPS combinations
- Florfenicol
97
List and evaluate components of anti-inflammatory teatment for ruminant neurological conditions
- Cerebral oedema and inflammation common, leads to problems
- Steroids: treat cerebral oedema + inflammation, may interfere with immune response and decrease BBB, dex 1-2mg/kg
- NSAIDs: broad anti-inflamm and analgesia, no data on efficacy in farm animal neurodisease
- Frusemide: diuretic, 1-2mg/kg IV but rare due to limited access in pure farm animal practice
- Dimethyl sulphoxide (DMSO): not licensed for food producing animals
98
Describe the implications of diagnosing a neurological condition for the individual and rest of herd/flock
- Diagnosis of meningitis/meningoencephalitis suggests poor management of herd e.g. poor maternal antibody transfer, dirty environment, need to consider herd welfare and health
- Listeriosis indicates herd problem as is commonly transmitted via poor silage: consider future protection of bales/batches of food
- Be aware that initial neuro case of Listeria may mean abortion cases in the future
