Bovine Neurological disease Flashcards
(77 cards)
1
Q
What is the typical presentations of bovine neurological disease?
A
recumbency (downers) gait abnormalities abnormal head posture sick aint doing right difficulty eating blindness
2
Q
What should you try to assess with a distance exam?
A
- behavior
- vision
- gait
- ability to eat
3
Q
How do you examine the 12 cranial nerves? (restrained)
A
- vision
- sensation and response
- hearing
- vestibular system
- mastication and swallowing
4
Q
How do you do a spinal evaluation?
A
- examine the animal as moves freely and driven
- attempt to assess limb placement and motion
(requires experience)
5
Q
What is a key comonent of neurological disease (time)
A
the timeline–what is onset, progression?
acute, subacute, chronic
6
Q
What is the timeline of progression, treatment of polio?
A
Fairly rapid progression, rapid improvement with thiamine
7
Q
What is the timeline of progression of rabies?
A
rapid
8
Q
What is an issue with doing a neuro exam in calvess?
A
they are very stoical and hard to get a response to most stimuli
9
Q
What is an issue with downer cows?
A
It is difficult to assess limb function. May need to use panniculus, shock prod.
10
Q
What are additional diagnostic tests that can be used for neuro cows?
A
- chemistry–Mg, Ca, urea, glucose (hypocalcemia, hypomagnesiuma, urea poisoning, glucose–neuro ketosis) CK/AST—down cows
- CBC–meningitis, cerebral abscess
- CSF–menigitis, neoplasia, trauma
- lead
- vit A
11
Q
Are CBCs very useful?
A
no, the inflammation in the brain is rarely reflected in the CBC
12
Q
Are CSF taps useful?
A
could do in a calf but in a cow very very difficult
13
Q
What is the best diagnostic test for neurologic dz in cattle?
A
you
14
Q
How do you assess blindness in cattle?
A
- distant exam
- pupillary light reflex
- menace response
(check palpebral reflex first)
15
Q
what are three conditions typified by blindness?
A
- lead poisoning
- polioencephalomalacia. a) vit B1 deficiency, b) sulfate induced
- vitamin A deficiency
16
Q
What is the signalment for lead poisoning in cattle?
A
- any age, any animal, calves may be slightly more common
2. any bizarre behavior patterns (e.g. uncontrollable walking)
17
Q
What are characteristics on distance exam of lead poisoning?
A
- ataxia (drunkeness)
- weakness (recumbency)
- convulsions
- aimless wandering
- headpressing
6 opsithotonus - teeth grinding
- bellowing
9 . hyperasthesia
18
Q
What is the source of lead in lead poisoning?
A
car batteries
19
Q
What will you see when looking for a “car battery”
A
The individual lead sheets and old paper that separated them because the casing has been frozen and broken apart
Grey, white because the acid has dried–residue crystals
20
Q
What does lead taste like?
A
sweet, covered in salt crystals. cows like to pick it up and chew it
21
Q
What is a source of lead besides car batteries
A
1) paint
(white and green
usually an issue for bottle fed calves in an old barn)
2) crank case oil–not really major
22
Q
What are features on the physical exam of lead poisoning?
A
- Disruption of normal GI function (decreased rumination, mild bloat, tenesmus, constipation or diarrhea)
- blindness!
23
Q
What is more common, acute or chronic lead poisoning?
A
acute (1/2lb in cows, 2oz calve)
24
Q
How is lead poisoning diagnosed?
A
1) blood lead levels
25
What blood tubes must be used to analyze lead poisoning?
HEPARINIZED BLOOD SAMPLE (can't use EDTA because it binds lead)
26
What are ways can check for lead poisoning besides blood sample?
1. Ca-EDTA adminsitration and measure urinary excretion
2. measure urinary delta ALA excretion
3. fecal lead
4. radiograph
27
What can you do post mortem to diagnose lead?
1. lead in reticulum and rumen
| 2. check levels in KIDNEY (or liver)--kidney better
28
Do you teat lead poisoning in cows?
no
29
What are the theoretical treatments for lead?
1. remove access to lead
2. chelation therapy--Ca-EDTA to promote excretion
3. thiamine
4. rumenotomy
30
What are the problems with teatment of lead poisoned cows?
Not safe to eat even with treatment
31
What are the two types of polioecephalomalacia?
1. thiamine deficiency
| 2. sullfate toxicity
32
What are the signs on a distance exam of polio?
1. blindness
2. ataxia
3. tremors
4. recumbency
5. convulsions
6. opisthotonus
33
What is the pathophysiology of thiamine deficiency/polio?
1. thiamine normally made in rumen
2. thiamine needed for pentose phoshate pathway of glycolysis
3. main energy producing pathway in brain
4. without thiamine brain cells die
34
What are the causes for thiamine deficiency in cattle (that normally have thiamine made in rumen)
1. thiamine antagonists-amprolium--used for cocidiosis
2. rumen thaminases--produced by bacterial fermentation--IN RUMENAL acidosis--predisposition to colonization by thiaminase producing bacteria--
3. ingested preformed thaminases (braken fern), fish meal
35
Which animals usually get thiamine deficiency due to the colonization of bacteria that produce thiaminases?
1. feedlot--number
| 2. dairy
36
How is polio diagnosed and differentiated from lead?
They are blind BUT the eye responds to light (pupillary light reflex maintained)
GI motility is normally ok
otherwise signs very similar to lead poisoning
37
How do you finalize polio diagnosis?
```
1. PM examination of the brian
cerebral edema
mild yellow discoloration
FLouresces under UV light
2. no simple lab tests--eryhtrocyte transketolase
```
38
What is the treatment for polio?
1. Thiamine!
| 10mg/kg IV then 10mg/kg IM every 3 hours for 5 teatments
39
What is the prognosis for polio?
good if caught early!
40
What should you remember if one animal has gotten polio (thiamine deficiency)?
Leave a bottle because it is likely a feed issue and may have to treat others
41
Can sulfate toxicity be distinguished from thiamine deficiency?
NO not clinically or PM
42
What is the typical source of sulfate?
water (slough wter may be particularly bad in drought years)
43
What is the level of sulfate that is toxic?
2000-7000ppm range
44
What are sources of sulfate besides water?
1. hay and grain grown in highh sulfate areas
| 2. plans that accumulate sulfate--kochia, canadian thistle
45
What minerals can be protective against sulfate toxicity?
1. copper and molybdenum (high levels can protect from sulfate toxicity)
46
How is sulfate toxic
Not clear
May be that sulfate is converted to H2S in rumen, erucated, injaled and absorbed in lung and transported to the brain in blood where it exerts toxic effect
47
What happens if you treat an animal with thiamine that has sulfate toxicity?
they still die. thiamine treatment does not work
48
What do you do if cows are dying of sulfate poisoning?
fix the water problem--hard to get producer during august during harvest
49
What are the three syndromes of vitamin A deficiency?
1. adult cattle on scurb patsures
2. feedlot steers
3. neonatal calves
50
Why do adult cows with vit A deficiency have infertility?
vit A is required for corpus luteum (yellow)
51
What are the presenting signs for vit A?
```
night blindness-rare
blindness-esp feedlot steers
weak animals dying shortly after birth
repro problems
poor hair coat
paralysis
convulsions
```
52
What colour plants is vit A in?
green things--easily produced from beta carotene--carotenes freely available in green coloured feed
53
Where do neonates get their vitA?
in colostrum. VitA crosses the placent poorly (why colostrum is yellow)
54
Why does it take pastured animals a long time of poor feed to get vit A deficiency?
It takes months because they have good liver stores
55
How do feed lot animals get vit A deficiency?
toxicity of chlorinated napthalenes
56
What is vit A required for?
maintenance of epithelial surfaces
57
Why do animals get blindness with vit A
the low vit A means that epithelial surfaces are not maintained, replaced with keratinized epithelium, thickened arachnoid results in decreased CSF absorption and there is increased pressure on optic nerve and they go blind
(also failure to remodel bone as animal regrows)
58
How is vit A deficiency typically diagnosed?
1. response to therapy,
2. signs,
3. liver biopsy (other methods not practical)
4. plasma vit A
5. diet calculations
6. CSF pressure
7. optho exam
59
What is the treatment for vit A deficiency?
injectible vit A
60
What is the prognosis for calves with vit A deficiency if treated?
good, with improvement within 48hrs
61
What are the two ways mentation can be altered?
1. depression
| 2. excitability
62
What are the two causes of disease that affect forebrain?
1. infectious
| 2. metabolic
63
What are the signs of acetonemia/ketosis?
1. hyperexcitability
| 2. deranged licking
64
How is acetonemia/ketosis diagnosed?
urine dip stick
65
How is ketosis treated?
glucose IV, good quality feed
66
What animals get hypocalcemia?
1. post-partum dairy cows
| 2. late pregnancy beef cows
67
What is calcium needed for?
1. heart function
2. muscle function
3. brain function--hypocalcemic animals become hyperexcitable then depressed
68
What animals get hypomagnesemia?
1. often cattle on lush pasture
69
What is the progression of hypomagnesemia?
rapid
found dead with signs of struggling
(dead convulsing)
70
What is the treatment of hypomagnesemia
magnesium but must be careful not to give them too much
71
What are the signs of urea toxicity?
1. bizarre behavioral signs in animal fed a urea supplement
2. severe abdominal pain
3. frothing at the nose and mouth
4. hypersensitivity
5. aggression
6. muscle tremor weakenss
7. dypnea
8. bellowing
72
What is the pathogenesis of urea poisoning?
urea turned into ammonia in the rumen and causes the neuro effects
73
What is the history of urea poisoning>
1. animals fed urea suplements as cheap non-protein nitrogen source
2. urea as fertilizer
3. conversion of urea to ammonia is facilitated by soybean meal (urease)
74
How does death occur with urea poisoning?
resp depression
75
How is urea poisoning diagnosed?
blood ammonia--difficult to do, must be on ice, here they have to do at human hospital
76
What is the treatment for urea poisoning?
4L vinegar orally to acidify rumen
| rumen lavage
77
Is treatment for urea poisoning likel to be successful?
no
