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Lent term fourth year > Lameness in cattle > Flashcards

Lameness in cattle Flashcards

1
Q

Distribution of lameness causes

A

> 90% from hoof and hoof skin
Of this 85% is hind feet and 15% front feet
Within hind feet, 85% related to LATERAL claw vs in front feet, lateral and medial = distribution

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2
Q

What is the suspensory apparatus of the hoof

A

Dense collagenous fibres that extend from P3 to lamellae of hoof wall to supend P3 within hoof capsule

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3
Q

What is the white line

A

= junction between the wall and the sole

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4
Q

Rate of hoof production by the corium and how does this change after parturition

A

5mm/month
- Slows down after parturition

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5
Q

How does the cow mobility score work

A

From 0-3
0 = good mobility
1 = slight impairment but affected limb not obvious; use preventative measures
2 = impaired mobility where affected limb identifiable - get seen within 48 hours
3 = severely impaired mobility; should be seen within 24 hours

Should ideally be done on whole herd every 2 weeks

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6
Q

4 most common conditions causing foot lameness

A

Sole ulcer
White line disease
Digital dermatitis
Foul of the foot

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7
Q

Basics of how sole ulcers form

A

Failure of suspensory apparatus + inadequacy of digital cushion changes pedal bone support
-> Allows movement of bone within hoof capsule
Get excessive force on horn producing tissues; causes sole ulcers

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8
Q

What can cause inadequacy of digitial cushion

A

In severe negative energy balance, fat may be mobilised from here

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9
Q

What causes white line disease

A

Shearing forces; when moving in unnatural directions e.g backwards or sharp exits
+ poor surfaces can tear wall from sole and weaken the white line

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10
Q

Factors causing failure of the suspensory apparatus

A

1) Laminitis: inflammation in hoof capsule due to endotoxins (e.g from metritis/toxic mastitis) + lactate, histamine (can enter circulation following ruminal acidosis); causes disruption of microcirculation in chorium; get inflammmation, ischaemic damage, oedema, haemorrhage
-> THEN: MMPs are activated which degrade collagen in apparatus

2) Hoofase = substance in hooves of periparturient animals which activates MMPs

3) Oestrogens and relaxin; released around parturition to loosen pelvic ligaments but also at on foot ones

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11
Q

What does position of ulcers on foot relate to

A

MOvement of P3
- Downward displacement/rotation –> sole haemorrhage and ulcer
- Rotation of apex causes toe ulcer
- Sinking of rear portion gives heel ulcers

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12
Q

Why do we get more lameness from back feet

A

Due to attachment of the limbs
- IN front limb the muscle-tendon sinew at shoulder acts as a shock absorbant
- IN back limbs it is skeletal attachment so shock stays in leg

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13
Q

Why do we get more lameness from lateral claw on back legs

A

Because longer than medial so more weight bearing

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14
Q

How can subacute ruminal acidosis affect hoof horn keratin

A

Production requires biotin (vit B7, vit H) which is made by ruminal microbes
- BUT don’t make as much with acidosis

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15
Q

What is the key predisposing cause to claw horn lesions in cattle

A

confinement on hard usrfaces

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16
Q

Why do cows go lame 2 months after parturition

A

Because all the risk factors are around parturition BUT takes time for deficity in hoof horn growth to show

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17
Q

Risk factors around parturition

A

> Relaxins and oestrogens cause loosening of suspensory apparatus
Risk of toxic mastitis/metritis + ruminal acidosis can contribute to laminitic changes
Standing for long periods on concrete yards for milking
Body condition loss in early lactation can cause loss of digital cushion function

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18
Q

What are the causative agents in digital dermatitis

A

Spirochetes treponema species
- Then get secondary invasion from others e.g Fusobacterium, campylobacter

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19
Q

M0-M4.1 scoring of digital dermatitis

A

0 = normal
1 = early lesions <2cm
2 = acute, active ulcerative lesions >2cm
3 = healing stage; covered in scab
4 = late chronic lesions; may be dyskeratotic or proliferative
M4.1 = CHORNIC M4 stage AND acute M1 stage

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20
Q

WHen to change foot bath

A

After 1 cow passage/L

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21
Q

Treatment for digitial dermatitis

A

Individuals: give local antibiotics and antisepsis
- If not working can give pencillin/cephalosporin systemically

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22
Q

Types of foot baths and size they should be

A

Formalin, copper, Zn, paracetic acid
should be >10cm deep to cover coronary band + 3m long to allow several steps to be taken

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23
Q

What two bacteria together cause foul of the foot

A

= Fusobacterium necrophorum
+ Prevotella melaninogenia

These are opportunistic environmental pathogens

24
Q

Clinical signs of foul of the foot

A

Lameness, symetrical swelling of hoof, fissue in interdigital skin with necorsis underneath, smelly

25
Q

Treatment for foul of the foot

A

Parenteral antibiotics e.g oxytetracycline, amoxycillin (broad spectrum)
+ NSAIDs
+ Corrective claw trimming

26
Q

Cause of slurry heel

A

Dichelobacter nodosus causes chronic interdigital dermatitis which spreads across heels and causes errosion of heel via keratin digesting proteases
- Get other causes of lameness after
+ irritation causes skin hypertrophy and fibroma formaion

27
Q

How to do IVRA

A

Place tourniquet distal to carpus or tarsus
Inject 20-30ml LA into superficial vein
Effective block within 10 mins; don’t leave on for >1 hour

28
Q

What length of foot do to we want when foot trimming and what degree

A

8.5cm; around 50 degrees

29
Q

Which claw do we start with for routine trimming

A

MORE NORMAL one
i.e on hind will be medial one
On fore will be lateral one

30
Q

Dutch 5 step trimming method (basics)

A

1: Trim toe length to 8.5cm
2. Match untrimmed claw to this
3. DIsh soles to take weight away (avoid ulcers)
—– This is routine
THEN corrective
4. Relieve weight from pinful claw via trimming + adding block
5. Remove under-run horn

31
Q

If doing digit amputation which joint do we amputate at

A

Prox interphalangeal joint

32
Q

What are the 4 success factors in control of lameness

A

1) Low infection pressure
2) Good horn quality
3) Early lameness detection
4) Low forces on feet

33
Q

Can feet get back to normal after a solar ulcer

A

NO! This = end stage
- once corium damaged will never be same

34
Q

What is downer cow syndrome

A

= pathology that develops after prolonged period of recumbency
- These secondary changes can become main reason animals is unable to stand even after primary issues resolved

35
Q

3 main things causing secondary recumbency as part of downer cow syndrome

A

Ischaemic muscle damage
Nerve pressure/damage
Traumatic muscle damage

36
Q

Two most significant causes of recumbency in cows

A

1) Dystocia related injuries
2) Hypocalcaemia

37
Q

What blood biochemistry might we be interested in with a down cow

A

1) Minerals e.g Ca2+, Mg2+, phosphorus to look at metabolic deficiencies
2) CK, AST, LDH: to assess degree of muscle damage and help with prognosis

38
Q

Methods to assist a cow to its feet

A

Tail lift
Nets/slings
Bagshaw hoists; clamp tightened over ileem wings; welfare concerns
Floatation tanks

39
Q

Causes of swinging leg lameness

A

i.e not seen when stnading just when moving
= Degenerative conditions and dislocation

40
Q

Causes of weight bearing lameness

A

fractures, septic arthritis

41
Q

cause of white muscle disease

A

Vit E (poor forage) + selenium (poor soil) deficiencies
OFten triggered by increase in activity e.g at turn out

Bloods: show low Vit E and selenium + see markers of muscle damage (CK and AST)

42
Q

What deficiencies can cause osteomalacia/osteoporosis

A

Calcium, copper, phopshorys

43
Q

What deficiency causes rickets and what signs do we see

A

Phosphorus/vit D deficiency in young animals
> Enlarged epiphses, high change of fraction, limb bending, rosary formation (on ribs)

44
Q

Diseases of skin and subcut that can cause lameness

A

1) Non-septic effusinos due to pressure with poor housing; get effusions in joints/tendon sheaths
2) Cellulitis/tarsal bursitis: due to ascending infection from foot or penetrating wound

45
Q

Cause of miscellaneous spastic paresis causing trying to handstand

A

OVeractive stretch reflex in gastrocnemius
Need to section tibial nerve

46
Q

Which nerve paralysis causes atrophy of muscles around the shoulder blade (Sweeney)

A

Subscapular paralysis

47
Q

Damage to what nerves during birth causes a dropped forelimb in calves

A

Brachial plexus

48
Q

Which nerves are often seen temporarily paralysed following recumbency

A

Radial nerve: see dropped elbow
Peroneal nerve: fetlock knuckles over
Sciatic nerve: limb held further forward

49
Q

Difference in presentation between hip dislocation in cranio-dorsal vs cranio-ventral direction

A

Cranio-dorsal more common; lame but ambulatory
Cranio-ventral; down

50
Q

Fractures of tuber coxae/ileum wing in dairy cattle

A

Not unusual; only causes issues with open wounds of bone sequestration

51
Q

When would we expect to see sacroiliac luxation and subluxation

A

In perinatal period because of pelvic muscle and ligament relaxation (also in oestrus)

52
Q

Which stifle ligament is it common for breeding bulls to injure when dismounting

A

Cranial cruciate

53
Q

What is patellar fixation and how do we fix it

A

When patella is fixed upwards so we can’t flex the stifle
Treat via dissection of the medial patellar ligament

54
Q

What is patellar luxation and how do we fix it

A

Seen in fast growing cattle; often secondary to femoral nerve paralysis

Should treat via shortening of anterior-tibio-patellar ligament or tightening joint capsule

55
Q

What does ability to move hock freely suggest

A

Rupture of peroneus tertius (part of reciprocal apparatus)

56
Q

Which muscle has probably ruptured if we see scapula blade protruding dorsally and what predisposes to this

A

Serratus ventralis
Vit E/selenium deficiency

57
Q

What are contracted tendons and what are predisposing factors

A

Congenital defect of forelimb flexor tendons
- Suggested due to restricted movement in utero
– Large, bull calves and beef calves
Manganese deficiency may be involved

Lent term fourth year (38 decks)

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