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FARM ANIMAL > 22.5.4: Neurological conditions of ruminants > Flashcards

22.5.4: Neurological conditions of ruminants Flashcards

1
Q

Metabolic diseases of ruminants producing neurological signs

A
  • Pregnancy toxaemia
  • Nervous ketosis
  • Cerebrocortical necrosis (CCN)
  • Swayback
  • Hypovitaminosis A
  • Hypomagnesaemia
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2
Q

Clinical signs of pregnancy toxaemia (early stages)

A
  • Separation from group
  • Apparent blindness - seems alert but does not want to move even if dog present
  • Bump into obstacles
  • Head-pressing
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3
Q

Clinical signs of pregnancy toxaemia (later stages)

A
  • Marked drowsiness
  • Facial twitching, jaw champing, salivation
  • Deviations of head position
  • Star-gazing and ataxia
  • Seizures -> marked drowsiness seen between seizures
  • Ketone breath
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4
Q

Clinical signs of pregnancy toxaemia (final stages)

A
  • Recumbency (this occurs after 3-4 days)
  • Comatose state lasting 3-4 days
  • If foetal death occurs, ewe appears to recover but secodary toxaemia results in deterioration and death
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5
Q

If a ewe with pregnancy toxaemia appears to start to recover (without any treatment being administered) what might you be suspicious of?

A
  • Suspicious that foetus(es) have died
  • Need to take care that toxaemia does not end up killing the ewe
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6
Q

Treatment of pregnancy toxaemia

A
  • Parenteral glucose - start with this to stop the animal dying😀 e.g. 5-7g glucose IV, may need to repeat 6-8x daily
  • IV fluids: Hartmann’s saline
  • Oral propylene glycol - 100ml daily. In milder cases, this alone may be effective.
  • Consider inducing if in early stages of disease; if you do not think ewe will survive between induction and parturition, consider C-section🔪
  • Consider eye lube - can’t blink so may get exposure keratitis
  • Consider implications and management for rest of the flock
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7
Q

Prevention and control of pregnancy toxaemia

A
  • When clinical cases occur, monitor rest of flock and treat affected animal immediately - prognosis is poor especially once recumbent
  • Ensure there is a rising plane of nutrition in the second half of pregnancy; if need be restrict feed in early pregnancy to allow this
  • Recommend scanning and feeding singles/twins/triplets separately if possible
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8
Q

Describe the aetiology of nervous ketosis

A
  • Uncommon presentation of ketosis
  • Likely due to isopropanolol (the breakdown product of acetone)
  • Hypoglycaemia likely to contribute
  • Ketone bodies further exacerbate signs
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9
Q

True/false: nervous ketosis cows, although displaying abnormal mentation, are usually placid.

A

False
They are dangerous and will only stop when they walk into something that doesn’t move.
Take care around these cows.

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10
Q

Clinical signs of nervous ketosis AND what differential should also be on your list when you see these

A

Sudden onset neurological signs in short recurring bouts
* Circling and aimless wandering
* Crossing limbs and ataxia
* Apparent blindness, walking into objects, head-pressing
* Hyperaesthesia
* Mild tremors

Key differential: ⚠️BSE⚠️

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11
Q

Diagnosis of nervous ketosis

A
  • Clinical signs
    +
  • BHB concentration >3.0 mmol/L
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12
Q

Treatment of nervous ketosis

A
  • 💉IV glucose (500ml of 50% solution) -> will produce a rapid improvement but this is transient and will only last 3-4hrs
  • Oral propylene glycol - 300ml once daily for 5 days
  • Glucocorticoids - limited evidence base, may be justifiable in v sick cases. Thought to help due to glucose repartitioning.
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13
Q

What is another name for cerebrocortical necrosis (CCN)?

A

Polioencephalomalacia

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14
Q

Aetiology of CCN

A

There is a deficiency in thiamine (Vitamin B)
* High concentration of thiaminases are formed in the rumen (we don’t know why this happens) -> these destroy the thiamine produced by microbes
* Thiamine is an important component of metabolic enzymes. Without it, there is increased pyruvate.
* This has a negative effect on glucose pathways -> damage to cerebral neurones.

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15
Q

What is sulphur-induced CCN and which animals is it most commonly seen in?

A
  • Seen in animals fed diets high in sulphates
  • Young cattle on feedlots (6-18 months old)
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16
Q

Describe the typical presentation and clinical signs of CCN

A
  • Usually seen in young, growing animals -> weaned lambs and calves most commonly
  • There is typically a history of recent dietary change (about 2 weeks prior) -> this causes disruption of the rumen microflora

Clinical signs - this is a condition of the cerebrum so we see abnormalities of mentation:
* Sudden onset blindness
* Aimless wandering and circling
* Head pressing
* Star gazing
* Progress over 12-24hrs to lateral recumbency and opisthotonos
* Death in a few days if untreated

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17
Q

This lamb was weaned approx 2 weeks ago. Over the past 12hrs it has progressed from aimless wandering and circling to its current posture. What is your diagnosis and how will you treat the lamb?

A

This lamb has CCN
* Treat with Vitamin B1 given IV slowly (initial treatment)
* Then follow up with up to 5 doses every 3hrs (can be IV or IM)

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18
Q

You obtain the brain of a lamb that died after showing neurological signs. The brain fluoresces under UV light. What is your diagnosis?

A

CCN

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19
Q

You suspect CCN in a lamb. What else might be on your differential list?

A
  • Meningitis
  • Lead poisoning
  • Vitamin A deficiency
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20
Q

How do you definitively diagnose CCN ante-mortem?

A

You can’t however history + clinical signs + response to treatment are highly suggestive.
* To definitively diagnose, need PM -> brain fluoresces under UV light

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21
Q

True/false: sulphur-induced CCN will response to thiamine given as treatment.

A

False
It will not respond

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22
Q

Treatment and control of CCN

A
  • Thiamine (Vitamin B1) 10mg/kg given slowly IV
  • Then repeat every 3hrs up to 5 doses - can give IV or IM
  • Use B1 products - often multivitamins will not have high enough B1 needed; if you only have multivitamins available, use a high volume of them
  • Supportive care: may need dexamethasone 1mg/kg if cerebral oedema

Ongoing management
* Supplementation of diet with thiamine for ongoing control (3 mg/kg dry matter - may need higher on some farms) - cases tend to be sporadic on farm so may not need to do this
* Ensure adequate roughage in diet
* Ensure sulphur in diet is appropriate

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23
Q

A ruminant is presenting with neurological signs. You are concerned about CCN and meningitis. Do you:
a) PM the ruminant and send for post-mortem so that you can ascertain the cause and implement herd-wide measures
b) Take a CSF sample to rule out meningitis
c) Take a blood sample to assess Vitamin B1 levels and diagnose CCN if present
d) Treat for both meningitis and CCN

A

a) PM the ruminant and send for post-mortem so that you can ascertain the cause and implement herd-wide measures
b) Take a CSF sample to rule out meningitis
c) Take a blood sample to assess Vitamin B1 levels and diagnose CCN if present - no, you cannot diagnose CCN this way!
d) Treat for both meningitis and CCN - this is cheap and effective - consider stewardship implications and choose an appropriate antibiotic if you are going to do this

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24
Q

Which species can be affected by swayback and what causes it?

A

Swayback = copper deficiency of dams during mid-pregnancy.

Sheep and goats can be affected.

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25
Q

What are the 3 presentations of swayback?

A
  1. Congenital cerebrospinal swayback - rarer but requires immediate euthanasia
  2. Progressive spinal swayback - more common
  3. Cerebral oedema - reported in Wales only, progresses to death in 1-2 days
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26
Q

Clinical signs of congenital cerebrospinal swayback

A
  • Lambs born dead or weak, unable to stand
  • Liveborn lambs that are recumbent with spatic paralysis of all lmbs
  • Movement that is uncoordinated and erratic
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27
Q

Clinical signs of progressive spinal swayback

A
  • Stiff, staggering gait, hindlimb ataxia (swaying gait)
  • Signs develop at 3-6 weeks old
  • Most common form of swayback
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28
Q

Clinical signs of cerebral oedema swayback

A
  • (Reported in Wales only🏴󠁧󠁢󠁷󠁬󠁳󠁿)
  • Similar to progressive spinal swayback: stiff, staggering gait but develops more quickly
  • Progresses to death in 1-2 days
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29
Q

True/false: in cases of swayback, the lambs are most severely affected, but the ewes will also show neurological signs, albeit milder ones.

A

False
Ewes do not show neurological signs with swayback; the lambs present with this. Eventually, copper deficiency in ewes/does will show itself as poor skin and ill thrift.

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30
Q

What post-mortem finding is seen particularly in goat kids with swayback?

A

Cerebellar hypoplasia
This can happen in lambs too but this is rare

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31
Q

Diagnosis of swayback

A
  • Usually based on history and clinical signs
  • Blood copper NOT reflective of copper status
  • Consider liver biopsies of 6-10 animals to assess flock level -> do this pre-tupping so you know if you will need to supplement during pregnancy
  • Treatment trial can be useful
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32
Q

Treatment of swayback

A
  • Oral supplementation of copper
  • Severely affected lambs have a poor prognosis
  • Prevention is better! Ensure ewes have adequate copper supplementation in diet in mid-pregnancy.
  • Remember that sheep are more likely to die of overdose than underdose so take care with not overdoing the oral dosing/boluses/injections
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33
Q

General treatment of the ruminant with neurological signs (that will cover a lot of bases)

A

Glucose + Vitamin B1 + NSAIDs (±antibiotics if suspicious of meningitis)

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34
Q

Antibiotic choice for bacterial meningitis

A
  • TMPS IV
  • Oxytetracycline IV
  • (Could give high dose penicillin/amoxicillin but we can only give these IM; prefer to give something that can go IV)

Theoretically, oxytetracycline doesn’t cross the BBB but in practice this doesn’t seem to matter and it achieves good results.

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35
Q

Clinical signs of hypovitaminosis A

A
  • Night blindness (earliest clinical sign)
  • Corneal keratinisation, mucoid ocular discharge, photophobia
  • Skeletal muscle paralysis; weakness and ataxia starts in hindlimbs (young animals)
  • Encephalopathy -> shows as convulsions (young animals)
  • Dry, brittle hooves and reduced repro performance (adults)
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36
Q

Primary vitamin A deficiency

A

Diet is deficient in vitamin A

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37
Q

Secondary vitamin A deficiency

A
  • Associated with chronic liver or enteric disease (e.g. fluke)
  • Failure of carotene to vitamin A
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38
Q

Treatment of hypovitaminosis A
What response to treatment would you expect?

A
  • Vitamin A supplementation at 400IU/kg (10-20x maintenance requirement)
  • Ensure adequate dietary vitamin A: 40IU = minimum daily requirement for all species, may need to increase if pregnant/lactating
  • Response to treatment is rapid: encephalopathy typically resolves in 48hrs; blindness does not improve
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39
Q

Which statement is correct?
a) Ruminants have poor storage capacity for magnesium, so will become deficient within weeks if they do not ingest any for a while
b) Ruminants have good storage capacity for magnesium so can easily become overwhelmed and suffer liver disease if levels in feed become too high
c) Ruminants cannot store magnesium so must ingest enough to meet their requirements every day.

A

c) Ruminants cannot store magnesium so must ingest enough to meet their requirements every day.

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40
Q

Clinical signs of acute hypomagnesaemia

A
  • Hyperaesthesia
  • Ataxia
  • Collapse
  • Seizures (tonic clonic)
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41
Q

Clinical signs of subacute hypomagnesaemia

A
  • Wild facial expression
  • Hypermetria
  • Muscle tremors
  • Spasmodic urination and defecation
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42
Q

What effect does low serum magnesium have on the body?

A

Low serum magnesium = alterations in nerve impulses to muscles

43
Q

These cows died suddenly. You are not suspicious of anthrax. Why not?

A
  • Markings in the grass suggest thrashing/muscle contraction before death
  • Suspicious of hypomagnesaemia (grass staggers)
44
Q

What is another name for hypomagnesaemia?

A

Hypomagnesaemia tetany; grass staggers

45
Q

What history and season might make you suspicious of hypomagnesaemia?

A
  • Grass staggers is typically seen in cows at pasture in spring/autumn with (older) suckling calves at foot
  • Lots of milk demand -> increased magnesium losses into milk
  • Recent history of release to lush pasture: young, fast-growing grass has lower magnesium content so the cows are able to obtain less magnesium in their diet
  • Recent history of fertiliser usage especially fertiliser high in potassium; farms with high potassium levels on pasture will have high magnesium requirements
46
Q

You suspect a live cow to have grass staggers. What sample will you take and how will you run this?

A
  • Take blood sample in lithium heparin (green) blood tube
  • Can send to external lab or run in house
  • Check Mg levels; might as well also check Ca and P at the same time
47
Q

A cow died suddenly and the farmer wants to know why. She had a calf at foot and was recently put out to pasture. The farmer used potassium fertiliser on this pasture not too long ago. What sample will you take fromthe cadaver to confirm your diagnosis?

A
  • Take sample of vitreous humour (fluid at back of eye)
  • Use 14G/16G needle and aspirate with syringe
  • Aqueous humour is easily contaminated by iris tissue so try to avoid this
  • This is done because magnesium levels in the vitreous humour are stable after death for longer than magnesium levels in blood
  • Your diagnosis is hypomagnesaemia.
48
Q

Treatment of hypomagnesaemia

A
  • This is an emergency 🚑 ‼️
  • Sedate if seizuring
  • Remain calm and quiet; any excess stimulation could kill the cow
  • Provide IV calcium with a small amount of magnesium included in this
  • Then provide SC magnesium
  • DO NOT GIVE A WHOLE BOTTLE OF MAGNESIUM IV (BLACK TOP IV = DEATH ⚫️☠️)
49
Q

Prevention of hypomagnesaemia

A
  • Supplement diet with magnesium (typically included in TMR, concentrates for dairy cows); could give magnesium salts
  • Graze suckler cows on lower risk pastures
  • Could consider calving earlier in winter so cows are housed until calves are weaned BUT this is unlikely to be a practical solution for a farm
50
Q

How can you supplement magnesium and what are the pros and cons of each method?

A
  • Daily oral drenching
  • ✅ Ensures each cow is dosed
  • ❌ Time consuming and would need to catch cows daily
  • Top dressing pasture
  • ✅ Easy and only need to do every 1-3 yrs depending on pasture type
  • ❌ Variability in individual cow consumption, need equipment
  • Magnesium in drinking water
  • ✅ Easy, cost effective
  • ❌ Need to make sure alternative water available, individual cow variability, need to check daily
  • Salt licks
  • ✅ Easy to use
  • ❌ Variability in cow consumption
51
Q

What is meant by top dressing pasture?

A

Sprinkling salt all over the pasture (done for prevention of hypomagnesaemia)

52
Q

Which breeds of cattle and sheep is hydrocephalus sometimes hereditary in?

A
  • Cattle - Holstein, Hereford
  • Sheep - Suffolk
53
Q

What are the possible mechanisms by which hydrocephalus may arise?

A
  • Increased CSF production
  • Obstruction of outflow
  • Decreased CSF absorption
54
Q

Describe the prognosis for hydrocephalus

A
  • Poor
  • Neonates often stillborn
  • If born alive have to consider welfare implications; hydrocephalus is reported to cause severe headaches in humans
  • Often seen alongside other congenital abnormalities; some may survive to slaughter weight
55
Q

Which breeds is cerebellar hypoplasia sometimes hereditary in?

A
  • Hereford
  • Shorthorn
  • Ayrshire
  • Aberdeen Angus
56
Q

Clinical signs of cerebellar hypoplasia

A
  • Recumbency, opisthotonus
  • Generalised ataxia
  • Hypermetric gait
  • May get no menace response even when expected for age (the menace response goes through the cerebellum)
57
Q

BVDv infection at how many days gestation could lead to cerebellar hypoplasia?

A

100-200 days gestation

58
Q

Treatment and prognosis of cerebellar hypoplasia

A
  • No treatment
  • Prognosis - dependent on clinical signs
  • Consider size of animal in future - tolerable ataxia now may make it hard to handle in future
  • Do not breed from this animal
59
Q
A

Hydrocephalus

60
Q
A

Cerebellar hypoplasia

61
Q

What is the most common neurological abnormality seen in calves affected by BVDv in utero?

A

Cerebellar hypoplasia

62
Q

True/false: when affected by Border Disease virus, lambs are known as hair little shakers due to the clinical signs. The most consistent clinical signs across all breeds is the presence of an unusual, curly coat.

A

False
Lambs are called “hairy little shakers” and often get coat abnormalities but not all breeds do e.g. Scottish Blackface lambs will not get a curly coat, but may show other signs.

63
Q

This lamb has had clinical signs from birth. What are you suspicious of and why?

A

Border Disease virus
* Small with conformational abnormalities: short legs, short spine, domed head
* Curly coat
* If videod, would see muscle tremors, jerking/shaking movement, head bobbing

64
Q

Treatment and control of Border Disease virus

A
  • No treatment available
  • Lambs may survive initially but do not thrive and are at increased risk of concurrent disease e.g. pneumonia
  • Identify and remove PI lambs
  • Avoid buying in infected animals
  • Vaccination not available
65
Q

Causative agent of Listeriosis

A

Listeria monocytogenes

66
Q

Syndromes reported with listeriosis

A
  • Encephalitis/meningitis
  • Abortion
  • Keratoconjunctivitis/uveitis
  • Septicaemia (rare)
  • Gastroenteritis (weaned lambs; rare)
  • Spinal myelitis (rare)
  • Mastitis (rare but public health risk)
67
Q

Risk factors for listeriosis

A
  • Poor nutritional status
  • Suppressed immunity e.g. pregnancy, parturition
  • Sudden weather changes (typically dry to very wet)
68
Q

Aetiopathogenesis of listeriosis

A
  • Associated with silage feeding/poorly made or poorly stored silage
  • Bacteria is ingested and accesses trigeminal nerves through abrasions of buccal mucosa or gum lesions
  • There is an ascending infection from the trigeminl nerves to the brainstem
69
Q

In which species, sheep or cattle, would you expect to see sporadic occurence of listeriosis vs outbreaks?

A

Cattle - typically sporadic occurrence
Sheep and goats - often flock outbreaks especially abortive syndrome

70
Q

Diagnosis of listeriosis

A
  • Presumptive from clinical signs and history
  • Definitive diagnosis only possible post-mortem: may see signs of inflammation/infection in CSF e.g. raised neutrophils, brain histopathology
71
Q

Diagnosis of listeriosis

A
  • Presumptive from clinical signs and history
  • Definitive diagnosis only possible post-mortem: may see signs of inflammation/infection in CSF e.g. raised neutrophils, brain histopathology
72
Q

Why are antibody tests not of value for diagnosis of listeriosis?

A

Listeria monocytogenes is ubiquitous in the environment and most ruminants test positive on antibody tests.

73
Q

Clinical signs of listeria encephalitis/meningitis

A

Initial stages
* Depressed, separation from flock
* Try to run away when approached but are ataxic and fall easily
* Pyrexia >40C

Later stages
* Recumbency and severe depression (happens more rapidly in small ruminants)
* Facial paralysis
* Hyperalgesia
* Drolling and flaccid tongue common
* Absent palpebral reflex may lead to exposure keratitis

Final stages
* Death due to respiratory failure in 2-4 days (sheep/goats) or 1-2 weeks (adult cattle)

74
Q
A

Listeria encephalitis/meningitis

75
Q

Treatment and prognosis of listeriosis

A
  • Early treatment needed for success; guarded to poor prognosis
  • Drug of choice: penicillin double dose every 12-24hrs for 10-14 days
  • Oxytetracycline reportedly effective in cattle but not sheed (10-14 day course)
  • Supportive care
  • NSAIDs or glucocorticoids
76
Q

sPrevention and public health implications of listeriosis

A
  • Avoid feeding poor quality silage
  • Zoonotic⚠️
  • Foodborne: unpasteurised milk, cheese (usually through faecal contamination of these products); bacteria can replicate at fridge temperature
77
Q

Causative agent and epidemiology of louping ill

A
  • Tick borne (Ixodes ricinus) flavivirus that causes encephalitis
  • Common in Scotland
  • Primarily affects sheep especially in a rough hill grazing system
78
Q

Clinical signs and treatment of louping ill

A
  • Muscle tremors
  • Nibbling
  • Ataxia
  • Drooling
  • Death after 1-3 days
  • Animals that survive retain immunity for life

Treatment is limited to supportive care

79
Q

Definitive diagnosis and mortality of louping ill

A
  • Diagnosis: brain histology
  • High mortality (60%) in naïve animals; 5-10% in previously exposed animals
80
Q

True/false: there is no zoonotic risk with louping ill.

A

False
There is a zoonotic risk through tick bites or injury with contaminated equipment but this is rare

81
Q

Clinical signs of TSEs

A
  • Circling
  • Generalised ataxia
  • Dullmentation
  • Weight loss in spite of a good appetite
  • Scrapie -> compulsive itching

⚠️ Notifiable if suspected ⚠️

82
Q

Clinical signs of nervous coccidiosis

A
  • Enteric signs (haemorrhagic diarrhoea) precede neuro signs
  • Clinical signs typical of cerebral disorders:

Depression, ataxia -> recumbency, opisthotonus -> seizures -> death 1-5 days after signs

  • Poor prognosis
  • Uncommon
83
Q

Causative agent of Gid

A
  • Gid = Coenurus cerebralis
  • This is the intermediate stage of Taenia multiceps which is a dog and wild canid tapeworm
  • The parasite ends up the brain/spinal cord
  • All domestic ruminants can be affected but sheep most common
84
Q

Clinical signs of Gid

A
  • Signs depend on area affected
  • Cerebrum: blidness, ataxia, collapse, dull mentation, head pressing, circling
  • Spinal cord: gradual development of paralysis
  • Most common: slowly developing unilateral blindness
  • Compulsive circling also seen
  • Acute stages: sheep can exhibit irritation signs e.g. salivation, frenzied running
85
Q

Causative agent of tetanus

A

Clostridium tetani
* Soil-dwelling spore-forming bacteria
* Spores are highly resistant and can remain in the environment for years
* Following anaerobic incubation, spores replicate and produce exotoxins
* Toxins enter through puncture wounds/navels, tail docking and dehorning sites

86
Q

Clinical signs of tetanus

A
  • Initially muscle stiffness
  • Inability to open mouth (lockjaw) and drooling
  • Anxious, alert expression -> pricked ears, dilation of nares
  • Constipation and difficulty urinating
  • Tail held away from body (elevated tail head)
  • Death due to resp arrest in 3-4 days sheep, 5-10 days cattle
87
Q

Treatment and prognosis of tetanus

A
  • Prognosis is poor; consider euthanasia
  • If early/mild:
  • Tetanus antixoin
  • Penicillin (double dose every 12-24hrs)
  • Sedation if convulsions
  • Supportive care and nursing
88
Q

Causative agent of botulism

A

Clostridium botulinum
* Soil dwelling spore forming bacteria; spores highly resistant
* During vegetative growth spores produce neurotoxins
* Toxins ingested in poorly made.stored forage or forage contaminated with bird faeces
* Poultry manure is implicated esp when ued to fertilse pastures that animals later graze on

89
Q

Clinical signs of botulism

A
  • Sheep initially present with muscle sitffness and ataxia then progress to flaccid paralysis in the later stages of the disease
  • Cattle show flaccid paralysis
  • Signs develop 3-17 days after exposure but this can happen quicker
  • Loose tongue as can’t hold it in mouth
  • Generalised weakness that progress fromthe hindlimbs forwards to the forelimbs, neck, head and throat
  • Obvious muscle tremors
90
Q

Treatment of botulism

A
  • Prognosis is grave so euthansia recommended
  • If early (before recumbency) then treat with antitoxin and supportive care. This is expensive so reserved for high value animals
91
Q

Prevention of tetanus and botulism

A
  • Vaccinate - clostridial vaccine
  • Don’t feed poor quality/contaminated silage
92
Q

What is the most common mechanism by which bacteria reach the brain and spinal cord and form abscesses?

A
  • Haematogenous spread (brain) or direct spread e.g. from injury, IM injection
93
Q

Clinical signs and treatment of brain abscesses

A
  • Clinical signs variable to the part of the brain that is affected (these are space-occupying lesions)
  • Treatment with antibiotics can be attempted but often poor because there is poor penetration of the lesion by the antibiotic
94
Q

Clinical signs, diagnosis and treatment of Visna

A
  • Visna = neurological form of Maedi Visna
  • Very rare in UK
  • Slow onset signs relating to demyelinating encephalitis:
  • Progressive loss of condition and hindlimb ataxia -> eventually complete paralysis
  • Circling, blindness, aimless wandering
  • Mays have perids of normalcy

Diagnosis is by serum ELISA and can be confirmed with brain histopathology🧠

Disease is always fatal. There is no treatment so must euthanise.

95
Q

Which animals are most likely to be affected by lead toxicity?

A

Young curious cattle at pasture who will eat things

96
Q

Clinical signs of acute lead toxicity

A
  • Tremors
  • Staggering
  • Blindness
  • Twitching of face, neck and ears
  • Progression to seizures and death in 12-24hrs
97
Q

Clinical signs of subacute lead toxicity

A
  • GIT dysfunction (rumen atony, constipation followed by foul-smelling diarrhoea)
  • Dull demeanour
  • Blindness
  • Muscle twtiching
  • Death in 3-4 days

Sheep show neuro signs less often than cattle

98
Q

Treatment of lead toxicity

A

Supportive care
* Sedate animals with severe neuro signs
* Provide IV fluid therapy
* Remove the animal from the source of lead

Chelation therapy
* Calcaium EDTRA given slowly IV for 3-5 days
* Side effects include renal and GI toxicity
* Can add thiamine at dose of 2mg/kg IV

99
Q

Cause of hypernatraemia in calves

A
  • Excessive sodium ingestion in the absence of adequate water
  • e.g. high sodium milk with no access to water
  • Electrolyte solutions with too much Na
100
Q

Clinical signs of hypernatraemia in calves

A
  • Cerebral oedema -> muscle tremors, seizures, ataxia, opisthotonos
  • May just have high mortality with no obvious neuro signs
101
Q

Diagnosis of hypernatraemia in calves

A
  • Blood sample if live
  • Aqueous or vitreous humour if dead; can also send brain either fresh or fixed
102
Q

Treatment of hypernatraemia in calves

A
  • Difficult -> consider euthanasia
  • IV fluids -> match Na concentration of the calf and then slowly sodium concentration over several days
103
Q

Prevention of hypernatraemia in calves

A
  • Ensure free access to water at all times
  • Be careful with electrolytes espcially home made ones

FARM ANIMAL (56 decks)

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