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CVSOH 4 > Bovine Musculoskeletal > Flashcards

Bovine Musculoskeletal Flashcards

1
Q

What are the top 3 issues affecting dairy herds in the UK?

A

Lameness, mastitis and fertility

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2
Q

What is the impact of lameness on cow welfare?

A

Pain and discomfort
Susceptibility to other disease
Yields
Reproductive performance
Behavioural changes

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3
Q

What are the behavioural changes caused by lameness?

A
  • Increased lying times – longer bouts
  • Which can cause a reduced feed intake
  • Suppression of oestrus expression
  • Can cause reduced visits to robot in automatic milking systems
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4
Q

What are the direct costs of lameness in cows?

A

Treatment cost
Vet time
Farmer time
Milk discard
Decreased milk yield

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5
Q

What are the indirect costs of lameness in cows?

A

Increased risk of culling
Effects on fertility
Risk of further lameness cases
Risk of secondary disease

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6
Q

What is the best way to identify the prevalence of lameness in UK dairy herds?

A

Mobility scoring

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7
Q

What is the cost of lameness to the average UK dairy herd?

A
  • If the average case costs £330 and the average case of lameness “lasts” 5 months
  • So a lame cow costs £2.20 per day
  • Average 200 cow herd with 25% lameness = £110 a day = £40,150 a year
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8
Q

Define the coronary band, wall and periople.

A

Coronary band – junction between skin and shorn, produced the wall horn

Wall – formed at a rate of 5mm/month, migrates down hoof

Periople – junction between skin and horn at coronary band , arms waxy coat to hoof

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9
Q

Define the sole, white line and heel.

A

Sole – formed for papillae on sole, wall and sole meet at white line

White line – join between wall and sole, point of weakness

Heel – soft sponge horn

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10
Q

Describe the position of the pedal bone/P3.

A
  • Centrally within hoof, mainly attached to dorsal wall
  • Flexor tendon attached to palmar/planter edge
  • Navicular bone between tendon and P2
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11
Q

What is the function and position of the corium/stratum germinativum?

A

Produces horn

  • Fills space between sole and P3, vulnerable to pinching
  • Blood vessels, nerves and other support structures - very sensitive
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12
Q

If the digital cushion is made from fat and connective tissue in which animals may the digital cushion be less effective?

A

Old and thin cows and heifers

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13
Q

Describe the structure of the laminae in the bovine foot.

A
  • Junction between the wall and P3
  • Sensitive dermal laminae from P3
  • Insensitive epidermal laminae from hoof wall
  • Interdigitate like interlacing fingers
  • Suspends P3 within the hoof capsule
  • Affected by hormonal changes around calving
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14
Q

What is the normal size of the hoof?

A

Anterior wall – 80mm (60-90mm)

Anterior wall to ground – 45-50˚

Heel height – 25-35mm in young, 30-45mm in old

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15
Q

Why does it take time for the horn of the bovine foot to repair?

A

Slow growth rates – approximately 5mm per month

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16
Q

What is hoof growth rate affected by?

A
  • Loading - increased loading = increased growth)
  • Claw - outside > inside on the hind feet
  • Nutrition
  • Age
  • Breed
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17
Q

Where do wall and sole growth originate?

A

Wall growth – starts from the coronary band, downwards to the toe

Sole growth – starts from the sole corium (quick), downwards and forwards

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18
Q

What are the cow factors of horn wear?

A

Horn quality
Hoof conformation
Limb conformation
Udder size and structure

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19
Q

What are the external factors of horn wear?

A

Underfoot conditions – surface abrasiveness, slurry dept

Management factors – walking distances, foot trimming, housing programme

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20
Q

What are the factors affecting horn quality?

A
  • Lameness
  • Damage to the corium or coronary band
  • Underfoot conditions
  • Foot bathing
  • Systemic illness (hardship lines)
  • Nutrition – low biotin or high concentrates
  • Breed and age
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21
Q

Describe normal weight bearing on the hoof.

A

Should have weight bearing around the outside of the foot, around the outside of the foot and onto the heel, shouldn’t be any on the sole so shouldn’t have any pinching.

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22
Q

Describe normal weight bearing of the limbs and claws.

A

Forelimbs – 60% bodyweight, more on inside claw, larger inside claw

Hindlimbs – 40% bodyweight, more carried on outside claw, large outside claw

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23
Q

Where is somewhere you don’t really get overgrowth on the bovine foot?

A

Heels

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24
Q

What is the result of toe overgrowth?

A
  • The wall is worn more rapidly at the heel, heel undermined by slurry heel in winter
  • Further overgrowth at toe = NWB
  • Shifts weight further back (45˚)
  • Sole corium pinched, pain whilst walking
  • Sole bruising/haemorrhage causes inflammation and sole ulceration
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25
Q

What is the result of sole overgrowth?

A

Overgrowth at the toe leads to thickening of the sole

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26
Q

What may cause the disparity in claw size when weight bearing on the lateral hind claw?

A
  • Irritation and sole overgrowth
  • Increased pressure and pain in lateral claw
  • Abduction of the limb
  • Increased weight on medial claw, decreased wear on lateral claw
  • Overgrowth at toe forces hocks together
  • Decreased weight bearing on lateral claw
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27
Q

If a cow is walking on an overgrown claw, what structure is at risk of being damaged?

A

Corium

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28
Q

What is the aetiology of septic arthritis in calves?

A

Tertiary spread of infection, umbilicus or generalised bacteraemia - T. pyogenes, E. coli, Strep. spp., Staph. spp. and Salmonella

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29
Q

What are the clinical signs of septic arthritis in calves?

A

Lameness followed by joint heat, pain and swelling

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30
Q

How is septic arthritis in calves usually diagnosed?

A

Presenting signs

Differentiated from other joint pathologies, such as intra-articular fractures

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31
Q

How is septic arthritis uncommonly diagnosed in calves?

A

For unresponsive cases or where worried about AMR:

  • Arthrocentesis – large volumes of turbid, clotted fluid containing large amounts of protein and many PMN’s
  • Aseptic samples for culture
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32
Q

How is septic arthritis in calves treated?

A
  • 2 weeks of broad spectrum parenteral antibiotics – amoxicillin, oxytetracycline
  • NSAIDs
  • Less commonly - open joint lavage, best prognosis if performed in acute stage
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33
Q

What is the prognosis of untreated septic arthritis in calves?

A

Severe joint damage

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34
Q

How is septic arthritis in calves prevented?

A

Good calving hygiene and application of topical naval dressing

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35
Q

What is the occurrence and cause of septic arthritis in older animals?

A

Uncommon. Similar to joint ill, often penetrating injury

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36
Q

What is the aetiology of hip dislocation?

A
  • Usually seen in adult cows after traumatic abduction (“partial splits”) of hind legs
  • Soon after calving, when relaxation of ligaments maximal
  • Femoral head displaced craniodorsally in most cases
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37
Q

What are the clinical signs and presentation of hip dislocation?

A
  • Down cows – with history of recent calving/seeing slipping
  • Acute onset lameness, usually non weight bearing
  • Craniodorsal dislocation – the pelvis and hips will often appear asymmetrical if viewed from behind
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38
Q

How are hip dislocations diagnosed?

A

Manipulation of leg, which can be difficult with large muscle mass = restriction movement and crepitus

Usual triangle of the pelvis can become much reduced and hip pops out, moving cranially and dorsally

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39
Q

How is hip dislocation treated?

A

Depends on size/weight of animal and how soon after dislocation we see them:
- Euthanasia if non-reducible (majority of cases)
- Replaced by manipulation (if small/light weight)

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40
Q

How are hip dislocations replaced by manipulation?

A
  • Soon after dislocation
  • Heavily sedated (xylazine)
  • Forcible replaced by combination of rotation to loosen the soft tissue contraction, leverage and pressure on the femoral head
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41
Q

What is the prognosis of hip dislocations?

A

Good provided cases are uncomplicated (no fractures) and replacement attempted early

Poor if dislocated for a while

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42
Q

Name 2 aetiological agents of mycoplasma arthritis. What do each cause?

A

Mycoplasma bovis – arthritis

Mycoplasma wenyonii – hind limb oedema

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43
Q

What is the pathogenesis of mycoplasma bovis arthritis?

A
  • Cow to cow spread – close and repeated contact over short distances
  • Asymptomatic carriers?
  • Mastitis, calf respiratory disease
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44
Q

What is the pathogenesis of mycoplasma wenyonii arthritis?

A
  • Blood borne
  • Spread in herd vaccination?
  • Udder oedema, lymphadenopathy, pyrexia
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45
Q

What are the clinical signs and presentation of mycoplasma arthritis?

A
  • Severe arthritis in calves and adult cattle
  • Severe lameness
  • With/without one or more swollen lower limb joints in which damage rapidly occurs
  • In conjunction with mastitis?
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46
Q

How is mycoplasma arthritis diagnosed?

A
  • Antibody tests
  • Culture?
  • PCR
  • Based on signs if known to be present in a herd
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47
Q

How is mycoplasma arthritis treated?

A

Oxytetracycline or tylosin

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48
Q

Name 4 rare bone and joint diseases that can affect cows.

A

Hip dysplasia
Osteomyelitis
Patellar luxation
Generative joint disease

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49
Q

Describe hip dysplasia in cows.

A

Gradual onset hindlimb lameness in growing animal 4-12 months

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50
Q

Describe osteomyelitis in cows.

A

Uni or multifocal, possible salmonella related in calves, penetrating trauma in adults

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51
Q

Distinguish dorsal and medial/lateral patellar luxation in cows.

A

Dorsal – sporadic, mature cattle. Leg held out stiff/behind, suddenly snaps forward in jerky action, may be intermittent

Medial or lateral – rare, congenital. Stifle collapses when weight borne, unilateral or bilateral may be secondary to femoral nerve paralysis

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52
Q

What are the most common causes of bovine lameness in the foot?

A

Sole ulcers
White line disease
Local sole bruising
Digital dermatitis
Foul in the foot

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53
Q

What structure protects the corium from pinching by P3?

A

The digital cushion

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54
Q

What is the aetiology of sole ulcers?

A
  • Happening inside the foot that has worked its way out – insult takes a while to be seen as it grows from the corium
  • Disruption of claw horn formation
  • Weight of cow borne through suspension of P3 in hoof capsule. Relaxation of supporting structures around calving, which allows this caudal movement of P3
  • Compounded by standing on concrete, thin cows (= thin digital cushion), poor conformation/insufficient routine foot trimming
  • Pinching
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55
Q

What causes pinching of the corium between P3 and sole?

A
  • Hoof overgrowth
  • Underdeveloped digital cushion in heifers
  • Standing on hard surfaces
  • Relaxation of support for P3 around calving
  • Shape of P3
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56
Q

What is the result of pinching between P3 and the sole?

A

Degeneration of corium in coriosis > poor quality horn production and cessation of horn production

Sole haemorrhage

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57
Q

Distinguish mild and sever sole ulcers.

A

Mild sole ulcers = incorporation of blood into horn = sole haemorrhage

Severe (standard) sole ulcers = horn production completely arrested = sole ulcer

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58
Q

What are the clinical signs of sole ulcers?

A
  • Lameness
  • Haemorrhagic discolouration means complete cessation of horn production at sole ulcer site
  • Lateral claw of hind feet, medial claw of fore feet
  • Possible secondary infection
  • Deep digital sepsis in extreme cases
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59
Q

How are sole ulcers treated?

A
  • Decrease pressure on pinched corium
  • Corrective trimming and decrease height of affected claw and dish
  • Remove underrun
  • Foot blocks
  • NSAIDs
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60
Q

What is the prognosis of sole ulcers that are not simple horn overgrowth?

A

Chronic coriosis may require regular corrective trimming. Deep digital sepsis, chronic bony changes

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61
Q

How are sole ulcers and coriosis prevented?

A
  • Regular foot trimming to prevent overgrowth
  • Good underfoot conditions
  • Avoid standing times – rubber mats, turn them out
  • Nutrition and BCS (thin cows go lame)
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62
Q

What is the aetiology of white line disease?

A
  • Junction of sole and wall = area of weakness
  • Dirt and stones impact causing infection carried through to corium
  • White line seals over meaning infection is trapped
  • Pus is produced and expands within potential space causing pain
  • Abscess may progress – usually under running the sole, occasionally up the wall. Eventually pus breaks out, usually at heel or coronary band
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63
Q

What are the clinical signs of white line disease?

A
  • Lameness
  • Lateral claw more commonly affected
  • Swelling – advanced with/without large abscess
  • Leg abducted to bear weight on medial claw
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64
Q

How is white line disease diagnosed?

A
  • Impaction and abscess if trimmed and explored
  • Black holes
  • Pain if “tweak” claw with hoof testers
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65
Q

How is white line disease treated?

A
  • Trim and balance both claws
  • Explore impacted white line, drain abscess, remove under run sole (at least enough to prevent re impaction)
  • Foot blocks
  • Parenteral antibiotics if necrotic corium
  • NSAID
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66
Q

How long are blocks left on and why?

A

Wouldn’t leave block on for longer than a month so that not too much weight and pinching is put through the claw with the block on it

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67
Q

When are white line disease lesions harder to treat?

A

Tracks up wall
Deep digital sepsis

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68
Q

How is white line disease prevented?

A
  • Underfoot condition – sharp stones, rough concrete, not being bathed in slurry that would cause feet to not be hard enough
  • Avoid walking long distances on hard surfaces or rough tracks
  • Biotin in the diet – hardens the white line
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69
Q

What is the aetiology of digital dermatitis?

A
  • Spirochete bacteria
  • Likely deep tissue invasion
  • Spreads in contaminated slurry/water
  • Fomite spread e.g. knives
  • Subclinical carrier status
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70
Q

What are the clinical signs of digital dermatitis?

A
  • Interdigital area behind heel bulbs
  • Small circular (1-4 cm), moist browny grey exudative areas of epidermal liquefaction and matting of the surrounding hair
  • Raw dermal granulation tissue if diphtheritic debris cleaned – intensely painful
  • “Papilliform” form – long thick strands of keratin protrude from the underlying granulation bed
  • Variable lameness
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71
Q

How is digital dermatitis treated on an individual level?

A
  • Clean – anaerobic bacteria so cleaning and exposing to air will often cure
  • Topic antibiotic – oxytetracycline sprays, soluble powders such as lincospectin, tylan?
  • Topical non-antibiotic – copper/zinc containing gels
  • Systemic antibiotics
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72
Q

How is digital dermatitis treated at herd level?

A
  • Ensure feet are clean first
  • Treatment bath
  • Antibiotics not representative of good AM use
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73
Q

What is the prognosis of digital dermatitis?

A
  • Good
  • Front of foot causes damage to periople, which impairs production of wall, causing under running and vertical wall cracks
  • Herd immunity seems to develop over time
  • Herd eradication unlikely
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74
Q

How is digital dermatitis prevented?

A
  • Improve housing hygiene with increased scraping
  • Hygiene of foot trimming equipment
  • Foot bathing
  • Disinfectant
  • Quarantine of new stock
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75
Q

What is the effect of involvement of non-healing sole ulcers and white line lesions?

A
  • Acute onset, severe claw lesions
  • Stippled appearance
  • Seen in herds with DD presence
  • Difficult and unrewarding to treat
  • Can result in digit amputation
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76
Q

What is the aetiology of foul in the foot/foul interdigital necrobacillosis?

A
  • Acute necrotising inflammation of interdigital skin
  • Fusobacterium necrophorum +/- Secondaries (T. pyogenes, Streptococcus spp.)
  • Damage to skin – FB’s, rough underfoot condition
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77
Q

What are the clinical signs of foul interdigital necrobacillosis?

A
  • Sudden onset moderate to severe lameness
  • Swelling of soft tissues above and around the coronary band and between the digits - forced apart
  • Swollen, hot, inflamed and painful to the touch
  • “Split” which discharges pus and lumps of necrotic tissue
  • Swelling may track higher up the leg as infection invades
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78
Q

How is foul interdigital necrobacillosis treated?

A
  • Check interdigital space for FB’s
  • NSAID
  • Parenteral antibiotics – milking/beef, cost/withdrawal
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79
Q

What antibiotic would be appropriate to choose to treat Fusobacterium necrophorum (and others)?

A

Amoxicillin and oxytetracycline – gram negative

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80
Q

How is foul interdigital necrobacillosis prevented?

A
  • Improve underfoot conditions – increased mucking out
  • Formalin foot baths
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81
Q

Poor quality/stone filled farm tracks may lead to which foot lesion?

A

White line disease

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82
Q

What are the characteristics of foul in the foot?

A

In interdigital space, requires FB penetration

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83
Q

Where would you expect to see a sole ulcer?

A

Axial aspect inside of the foot

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83
Q
A
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84
Q

What is the treatment indicated for a sole ulcer?

A

Foot trimming, block and NSAIDs

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85
Q

What is the aetiology of acute laminitis in cows?

A
  • Severe toxic incident – ruminal acidosis/toxic metritis/mastitis
  • Vasoactive mediators
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86
Q

What are the clinical signs of acute laminitis in cows?

A

Unwillingness to move
Weight on heels

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87
Q

What else can be seen at the site of sole ulcers and caused by coriosis?

A

Sole haemorrhage

Sole haemorrhage > sole ulcer

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88
Q

What causes sole haemorrhage?

A
  • Laxity of ligaments around calving
  • Movement of P3
  • Compression of corium
  • Due to increased standing times and standing on concrete, overgrowth of hoof
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89
Q

Why might cows get sole bruising?

A
  • Turn sharply on hard surfaces (bullying)
  • Rough concrete
  • Soft feet - standing in water or slurry
  • Bulling/dismounting
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90
Q

What is slurry heel?

A
  • Erosion of soft heel horn
  • Usually incidental finding when trimming
  • Asymptomatic, but can alter conformation predisposing to other issues
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91
Q

What other condition might occur when there is pooling of slurry on yards?

A

Digital dermatitis

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92
Q

What are vesicle fissures/sand cracks?

A
  • Hot, dry conditions
  • Often asymptomatic unless pinching of laminae
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93
Q

What is the rate of horn growth?

A

5mm/month

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94
Q

What are horizontal fissures/hardship lines?

A
  • Complete circumferential horizontal
  • Following severe toxic condition
  • Often round all 8 claws
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95
Q

What causes interdigital skin hyperplasia/corns/fibromas/granulomas?

A
  • Chronic irritation of the interdigital area
  • Infection or impaction of dirt/small stones
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96
Q

What are the clinical signs of interdigital skin hyperplasia/corns/fibromas/granulomas?

A
  • Chronic lesions/abnormal gait and poor foot conformation from walking differently from a sole ulcer for example
  • Often asymptomatic
97
Q

If surgery of the digital is undertaken – which licensed local anaesthetic is to be used?

98
Q

Describe fracture of the distal phalanx?

A
  • Acute onset lameness
  • Cross legged stance – often medial claw so try to take weight off and stand more on lateral claw
  • No other lesions detected in foot
99
Q

When might deep digital sepsis occur?

A
  • Complication of other disease – sole ulcers, WLD, Foul, Horizontal and Vertical fissures
  • Infection gains entry to deeper structures of foot
100
Q

nfection tracks in through the foot – what structures could it affect?

A

Digital cushion, P3 and DIP joint

101
Q

What is the principle of therapeutic foot trimming?

A
  • Early detection and early treatment
  • Don’t wait until toxic
  • Use Dutch 5 step technique
  • Isolate lesion
  • Remove under run and diseased horn
  • Decrease weight bearing on disease claw
  • Foot blocks?
  • Bandages?
102
Q

What is the local analgesia used for therapeutic foot trimming?

A
  • Local infiltration
  • Nerve blocks
  • Intra-venous regional anaesthesia
  • Procaine used
103
Q

How is IVRA done?

A
  • Apply tourniquet
  • Identify vein
  • Just cranial to accessory digit
  • Care not to leave on too long
  • Care on removal of tourniquet
104
Q

How long are foot blocks left on?

105
Q

What NSAIDs are available in cattle?

A

Meloxicam, ketoprofen, flunixin, carprofen

106
Q

Describe NSAID use for lameness in cattle.

A
  • Evidence to support benefit over trimming alone
  • Ketoprofen – 0 day milk withdrawal
  • Meloxicam – longer analgesic effect, so use in beef cows
107
Q

How are dressings used in foot problem patients?

A
  • Protect diseased area
  • Apply topical treatment – Astringent, Antibiotics
  • Now less popular – creating anaerobic environment, may trap muck in
  • Increase weight bearing on diseased claw?
  • 48 hours maximum
108
Q

What type of procedure are digit amputations?

A

Viewed as a treatment failure/salvage procedure

109
Q

What are the indications for digit amputations?

A
  • Deep digital sepsis
  • Toe necrosis
  • Non-healing white line lesions and sole ulcers
  • Trauma – degloving or disarticulation
110
Q

What are the pre-operative considerations?

A
  • Is culling more appropriate?
  • How good is the post-operative care? If management bad then will get infected so little point
  • Analgesia and palliative care – is the cow likely to be less painful in the longer term?
111
Q

What are the contraindications for digit amputations?

A
  • Imperfect contralateral claw
  • Severe, ascending tenosynovitis
  • Lameness affecting another limb
112
Q

What is the surgical approach for digit amputations?

A
  1. Apply tourniquet
  2. Give IVRA
  3. Hemi-circumferential incision approximately 1cm proximal to the coronary band
  4. Longitudinal incision in the interdigital space
  5. Place clean embryotomy wire into the incision at the level of P2 and make a transverse cut
  6. Apply a pressure bandage over stump of the digit
113
Q

Distinguish the 3 methods for digit amputations.

A

1 - disarticulation of the DIP joint
2 - amputation through P2
3 - amputation through P1

114
Q

What is the post operative care used for digit amputation?

A
  • Change the pressure bandage every 48 hours (7 days) until a complete, healthy layer of granulation tissue has formed
  • Systemic antibiotics – min 5 days
  • Repeat NSAIDs
115
Q

What are the complications of digit amputations?

A
  • Haemorrhage
  • Ischaemia and sloughing
  • Premature culling
  • Infection, dehiscence, osteomyelitis, ascending tenosynovitis
116
Q

What is the prognosis of digit amputation?

A
  • Should be viewed as a salvage procedure
  • Should not be expected to calve in again
117
Q

What is the aetiology of hock cellulitis/bursitis/trauma?

A
  • Result of trauma suffered during winter housing period
  • Rub hock on cubicle beds, cubicle frames and other objects
118
Q

What are the clinical signs of hock cellulitis/bursitis/trauma?

A
  • Initial hair loss over bone protuberances causes swelling because of soft tissue damage and development of tarsal bursitis
  • Early cases = not lame
  • Severe cases skin can ulcerate causes development of a secondary infectious bursitis and even infectious arthritis
  • Moderate lameness if swelling is severe or infected
119
Q

How is hock cellulitis/bursitis/trauma diagnosed?

A

Swollen and damaged hock in winter housed animals

120
Q

How is hock cellulitis/bursitis/trauma treated?

A
  • Not usually necessary unless secondary infection exists
  • Most lesions almost completely resolve during the summer months when animals are out of winter housing
  • Antibiotics will usually relieve the lameness
  • Do not incise and drain
121
Q

How is hock cellulitis/bursitis/trauma prevented?

A

Identify and correct the underlying cause – coarse sawdust, hard/abrasive mattresses, sparse bedding

122
Q

What is carpal bursitis?

A
  • Common in winter housed cattle
  • Resolves in the summer months
  • Large swollen carpi
  • If severe, lesions can be aseptically drained
123
Q

What is the aetiology of white muscle disease?

A
  • Diet deficient in Vitamin E/Selenium (antioxidants)
  • Congenital and delayed forms
124
Q

What are the clinical signs and presentation of white muscle disease?

A
  • Weak or still born calves
  • Ill thrift
  • Stiffness, inability to stand/increased recumbency
  • Respiratory distress and sudden death if respiratory or cardiac muscle affected
125
Q

How is white muscle disease treated?

A

Injectable forms available of vitamin E/selenium

126
Q

How is white muscle disease prevented?

A
  • Silage analysis/soil testing
  • Oral boluses/drenches
  • Supplementing feed in areas of known deficiency
127
Q

What is the aetiology of spastic paresis?

A

Unknown, German and Dutch Friesians and Aberdeen angus breeds so may be genetic

128
Q

What are the clinical signs and presentation of spastic paresis?

A
  • Chronic and progressive contraction gastrocnemius
  • 6 weeks and 6 months
  • Hock nearly straight
  • Animals walk with a stiff and stilted gait
  • Limbs may jerk intermittently at rest
129
Q

How is spastic paresis treated?

A

Surgical resection of gastrocnemius and superficial flexor tendons

Neurectomy of tibial nerve

130
Q

How is spastic paresis prevented?

A

Hereditary predisposition

Affected animals should not be used for breeding

131
Q

What is the aetiology of gastrocnemius rupture?

A

Unclear, associated with prolonged recumbency excessive weight and possible mineral imbalance

132
Q

What are the clinical signs and presentation of gastrocnemius rupture?

A
  • Muscles ruptures usually at the musculotendon junction
  • Usually bilaterally
  • Weight bearing is impossible, hock drops almost to floor
133
Q

How is gastrocnemius rupture treated?

A

Close confinement, limbs splinted in extension

134
Q

What is the prognosis for gastrocnemius rupture?

A

Guarded, animals are unlikely to recover fully, re-rupture may occur

135
Q

Name a bovine congenital malformation.

A

Flexural limb deformities

136
Q

What is the aetiology of flexural limb deformities?

A
  • Relatively common congenital abnormality
  • Some breeds – Belgian Blues
  • Associated with limb position in a cramped uterus?
137
Q

What are the clinical signs of flexural limb deformities?

A
  • Varying degrees of rigid flexion usually fore limbs
  • Less commonly extensor rigidity in the hocks
  • Usually bilateral
138
Q

How are flexural limb deformities diagnosed?

A
  • Signalment – neonate
  • History – often in herds with previous cases but not necessarily
  • Clinical presentation
139
Q

How are flexural limb deformities treated in milder cases?

A

Mild cases usually self limiting

Physiotherapy and walking on hard surfaces may help – want them in larger groups instead of smaller pens by themselves in order to encourage that movement

140
Q

How are flexural limb deformities treated in more severe cases?

A
  • More serious may be necessary to splint
  • Severe cases surgery can be helpful – rare, referral
141
Q

What is the prognosis of flexural limb deformities?

A
  • Good in mild cases
  • Treatment of severe cases can be difficult and disheartening
  • May be worth if after a few days of no improvement having that talk with the farmer about how worth it treatment is and if they want to continue – case specific
142
Q

Does oxytet work for flexural limb deformities?

A

No evidence, physio is key

143
Q

Where do you stand when foot trimming?

A

Lateral side
When trimming medial claw, will have to reach other

144
Q

How do you hold the knife when foot trimming?

A

Always keep 2 hands on the handle of the knife

145
Q

How are the aims of creating a normal banaced foot with the Dutch 5 stage method ensured?

A
  • Correction of overgrowth
  • Even weight bearing
  • Allowing a diagnosis and treatment of lameness
  • Preventing new lameness
146
Q

Which forelimb and hindlimb claws bear the most weight?

A

Forelimb = medial
Hindlimb = lateral

147
Q

Which claw do you begin foot trimming on?

A

Always begin your foot trimming with the claw that bears less of the body weight, so start with lateral forelimb and medial hindlimb

148
Q

What are the first 3 steps of the Dutch 5 step method (routine)?

A
  1. Correct the length of the claw – start with the claw that bears less of the weight and used hoof nippers to trim the toe.
  2. Level the claw using hoof knives to remove the sole horn. We want to do this until the sole horn is at a depth of 5-8mm
  3. Match the toe length and level of the weight bearing claw to the correct claw now. We want claws that are balanced and level with each other. You can use the handle of your hoof knife to check that the soles are both flat.
149
Q

What is step 4 of the Dutch 5 stage method to foot trimming?

A

To shift weight away from the lesion

150
Q

How is weight shifted away from the lesion in step 4 of the Dutch 5 stage method?

A

Trimming the sole horn in the caudal 2 3rd of the sore toe, providing the sole horn is thick enough to do so

Placing a hoof block on the healthy claw, providing the healthy claw has no lesions or bruising

151
Q

What is step 5 in the Dutch 5 stage method?

A

Remove all underrun horn and sharp edges. Underrun horn is visible as cracks, where dirt has become trapped

152
Q

How is underrun horn removed in step 5 of the Dutch 5 stage method?

A

Trimming the horn over the heals – be conservative

Underrun horn and sharp edges will usually be present around ulcers and cases of white line disease – try and avoid cutting into exposed soft tissue (corium/quick) in these cases

153
Q

What is the aetiology of limb fractures?

A
  • Severe trauma
  • Limb fractures often comminuted, open and grossly contaminated
154
Q

How are limb fractures diagnosed?

A

Manipulation often reveals atypical movement and crepitus unless fracture is high up the limb – hard to do with these huge animals and muscle mass, so get farmer to help. Really important to get good manipulation to get diagnosis. Stethoscope on area to listen for crepitus or get someone to manipulate limb while you listen to the heart and assess for change in heart rate for indication of pain.

Radiographs of the lower limb only

155
Q

What are the differential diagnoses for limb fractures?

A

Differentiate from other non-weight bearing lameness - dislocations, severe nerve damage

156
Q

Why do the prognoses of limb fractures depend on the signalment of the animal?

A

Heavier animals and fractures higher up the limb – much more difficult to treat and effectively immobilise

Young animals with uncomplicated breaks – fixation of distal limb fractures possible

157
Q

What are the treatment options for limb fractures in bovine?

A
  • Reduction can be difficult especially if delayed
  • Internal and external fixations – often casts
  • Usually casting (cost)
158
Q

What is the aetiology of tuber coxae fractures?

A

Lateral falls
Pushing/racing through narrow entrances

159
Q

What are the clinical signs of tubercoxae fractures?

A

Often an incidental finding but usually obvious, displaced bone fragment ventrally. Animal moving normally, no pain usually associated, not part of weight bearing apparatus

161
Q

How are tuber coxae fractures treated?

A
  • No treatment indicated
  • Respond well to box rest
  • Although sequestra > open draining tract develops
162
Q

What is the aetiology of pelvic symphysis fractures?

A

Occasionally pelvic symphysis separation during calving, particularly in assisted, pelvis pulled away from spine

163
Q

What are the clinical signs of pelvic symphysis fractures?

A
  • Sunken spine at sacrum
  • May be incidental finding
164
Q

How are pelvic symphysis fractures treated?

A
  • No treatment possible – can move around okay but not a great idea to have her calve again
  • May prevent future vaginal deliveries, go as a cull after lactation finished
165
Q

How are pelvic fractures diagnosed?

A
  • Crepitus during walking or palpation
  • Rectal and vaginal examination can be helpful
166
Q

What are the possible differential diagnoses for pelvic fractures?

A

Dislocations, and pelvic haematomas and abscesses

167
Q

How are pelvic fractures treated?

A
  • Slaughter? If NWB and painful
  • Initial period of closely confined box rest? Painful but WB
  • Poor prognosis
168
Q

How are cows treated for femur fractures and why?

A

We can’t do immobilisation of upper limb fracture, adult animal of significant weight so can’t immobilise. Meloxicam won’t do much and not appropriate to rest of straw bed. Best action is euthanasia

169
Q

Describe the innervation of the radial nerve.

A
  • C7, C8 and T1
  • Motor innervation of carpus and digit extensors
  • Sensation to lateral side of limb
170
Q

How can radial nerve damage occur?

A
  • During calving and excessive traction on limb
  • Trauma to the scapulohumeral area
  • Recumbency
171
Q

What is the result of proximal radial nerve damage?

A

Limb held in flexion with the elbow dropped cranial wall of the hoof “scuffs” the floor during locomotion

172
Q

What is the result of distal radial nerve damage?

A

Carpus and fetlock held in flexion

173
Q

Where is the suprascapular nerve?

A

Cv6, Cv7
Scapular/prescapular

174
Q

What is the result of suprascapular nerve paralysis?

A
  • Limb abducts when weight bearing
  • Supra/infraspinatus atrophy
175
Q

Where is the radial nerve?

A

Cv7-8, T1
Scapular/humeral

176
Q

What is the result of radial nerve paralysis?

A
  • Calving traction
  • Flexed limb
  • Dropped elbow
  • Cranial hoof scuffs floor
177
Q

Where is the brachial nerve?

178
Q

What is the result of brachial nerve paralysis?

A
  • XS traction or abduction
  • No muscle control/tone in forelimb
  • Flaccid, non-weight bearing limb
179
Q

Describe the innervation of the obturator nerve.

A
  • L4, L5 and L6
  • Innervates the adductor muscles of the hind limb
180
Q

What is the aetiology of obturator nerve damage?

A

Dystocia due to foetal oversize = crushed nerve running through pelvic canal

181
Q

What is the result of obturator nerve damage?

A
  • Inability to adduct the limb leading to abduction
  • Animals may slip causing severe abduction and trauma to the leg, hip and pelvis, and dislocations and fractures
182
Q

Why must care be taken when doing intramuscular injections around the sciatic nerve?

A
  • Sciatic nerve damage iatrogenically
  • Especially in low BCS cows
183
Q

Where is the femoral nerve?

184
Q

What is the result of femoral nerve paralysis?

A
  • Hyperextension of calf leg during calving
  • Limb hangs flaccid
  • Stifle cannot be extended
185
Q

Where is the sciatic nerve?

186
Q

What is the result of sciatic nerve paralysis?

A

Knuckling
Stifle and hock extended

187
Q

Where is the tibial nerve?

A

Branch of sciatic

188
Q

What causes tibial nerve paralysis?

A

Major gastric region trauma

189
Q

What is the result of tibial nerve paralysis?

A
  • Hock flexed
  • Digits extended
190
Q

Where is the peroneal nerve?

A

Branch of sciatic

191
Q

What causes peroneal nerve paralysis?

A

Calving or lateral stifle trauma

192
Q

What is the result of peroneal nerve paralysis?

A
  • Hock extended
  • Fetlock flexed
193
Q

Can we treat nerve damage?

A

Unlike fractures, this is something we are often able to treat but it is a lot of work for the farm so this must be considered

194
Q

How is nerve damage treated?

A

Anti-inflammatory drugs
Nursing care
Supportive dressings

195
Q

How do anti-inflammatory drugs treat nerve damage?

A

To reduce swelling around damaged nerves. Can be NSAIDs or steroids or a combination (this is okay for a one off injection and gives maximum effect to reduce swelling)

196
Q

What nursing care is done to treat nerve damage?

A
  • Easy access to food and water
  • Regular turning/lifting – get blood flow
  • Keeping animal comfortable
  • “Non slip” surfaces
197
Q

How so supportive dressings treat nerve damage?

A

Hold the limb in correct position (shackles)

198
Q

Post calving this cow can stand but has a flexed fetlock – what nerve has been damaged?

A

Peroneal – still weight bearing but knuckling forward on fetlock

199
Q

What treatment would be appropriate for peroneal nerve damaged?

A

Meloxicam (lasts a few days), ketoprofen (no milk withdrawal so useful if animal recently calved and producing a lot of drugs) and dexadresson (steroid). Not used in combination but perhaps meloxicam and dexdresson

200
Q

What sources of lameness data are used/recorded on farm?

A

Foot trimmer records - might not reflect causes of lameness

Treatment - may represent only more severe lameness cases

201
Q

Name 4 categories of housing and husbandry when analysiing a farm for lameness risk factors.

A

Underfoot surfaces and cow flow
Cow comfort, standing and lying times
Underfoot hygiene and foot bathing
Stockmanship

202
Q

What aspects contribute to underfoot surfaces and cow flow on farms?

A
  • Building design for cow flow
  • Underfoot surfaces
  • Farm tracks
203
Q

How should building design be designed for cow flow to avoid lameness?

A

Avoid narrow walkways with sharp corners, sharp protrusions, blind alleys (bullying) and overstocking

Water troughs = 0.2m per cow
Feed troughs = 0.7m per cow

204
Q

How should underfoot surfaces be designed to avoid lameness?

A
  • Avoid slipper, overly rough, sharp aggregate surfaces
  • Sand on concrete - leads to excess wear and thin soles
  • Rubber mats
205
Q

How can farm tracks be designed to avoid lameness on farms?

A
  • Single file, place feet, “pick” track
  • Increased lameness when forced to move quickly
  • Ideal “Cow Tracks” = permeable membrane, stone base, pine peelings on surface
206
Q

How are cubicles designed for cow comfort when getting up and down?

A

To get up, cows push themselves forwards a bit amount on hindlegs before pushing upon forelegs so need to design cubicles that will allow these movements

207
Q

What are the 3 aspects of cubical comfort?

A
  • Cubicle lying surface (most important)
  • Cubicle hardware/design
  • Stocking rates
208
Q

How can cubicle comfort tested?

A

Test using knee drop/knuckle test

209
Q

How can cows tell us about poor cubicle comfort?

A
  • Stall standing index: comfort quotient = standing / touching beds
  • Hock lesions
  • Positioning in cubicles (lying or standing)
210
Q

What are the hardware and design components of cubicles?

A

Lunge space
Step
Bed length
Groupings
Numbers of cubicles - 5% extra
Accessibility
Prioritisation in hierarchy

211
Q

Compare Cantilever vs Newton rigg cubicles.

A

Cantilever has less metal work for legs to become trapped in so better than newton rigg to allow get up/down movement

212
Q

What are the advantages and disadvantages of loose yards?

A

More comfortable/higher lying times

Poorer hygiene/increased mastitis risk

213
Q

How can underfoot hygiene be maintained on farms to avoid lameness?

A
  • Regular scraping - 2x daily
  • Wide passageways spread slurry over a larger area
214
Q

What are aims of foot bathing?

A

Clean feet, harden feet, control pathogens

215
Q

What substances are used for foot baths on farms to avoid lameness?

A
  • 2-5% formalin – carcinogenic and toxic, handle with care
  • 2-5% copper sulphate – can be toxic on pasture (when spread in slurry)
  • 2.5-5% zinc sulphate – use of parlour washings/hypochlorite circulation wash
216
Q

What is the efficacy of a prewash before foot baths?

A

Has been shown to reduce contamination in treatment footbath, just ensure feet are clean. In parlour, have to be careful about spraying onto the udder. If 2 footbaths, they defecate after the first and footbath becomes full of slurry

217
Q

What should the dimensions of footbaths be?

A

Footbaths should be long enough so that each foot enters the solution twice and deep enough so the solution reaches the top of the coronary band

218
Q

How can we get early detection of lameness with stockmanship?

A
  • Foot trimming including lesion identification and treatment via therapeutic trimming
  • Mobility scoring
219
Q

How does nutrition affect lameness development?

A
  • Good quality horn relies on adequate levels of zinc, sulphur and biotin in the diet
  • Additional dietary supplementation with biotin
220
Q

What is the link between thin cows and lameness?

A

Thin cows go lame – post calving condition loss, <2 associated with increased lameness, thin digital cushion

Lame cows go thin – effect on milk production, effect on other disease and recurrence of lameness

221
Q

How are heifers managed to prevent lameness?

A
  • Lameness can be very high 3-4 months of first lactation as they go through a lot of changes in the first lactation
  • Bullying/social changes
  • Increased time standing as they are learning about cubicles and how to use them
  • Incomplete digital cushion development
  • Udder development which will change the way they walk
  • Concrete, especially when reared on straw or grass
222
Q

What are the prevention strategies of lameness on farms?

A
  • Cubicle training
  • Introduce adult diet
  • Separate group for early lactation/first lactation
  • Focus on first 60 days in milk
  • Pre-calving trim
223
Q

How is mobility scoring used to determine prevalence of lameness?

A

0 to 3 scoring scale
2 and 3 = lameness prevalence

224
Q

Describe score 0 mobility scoring.

A
  • Walks with even weight bearing and rhythm on all 4 feet
  • Flat back
  • Long fluid strides

No action needed

225
Q

Describe score 1 mobility scores.

A
  • Steps uneven (rhythm or weight bearing) or strides shortened
  • Affected limbs or not able to pick out a specific limb (just not quite right)

Preventative foot trimming and further observation

226
Q

Describe score 2 mobility scores.

A
  • Uneven weight bearing on a limb that is immediately identifiable
  • Shortened strides
  • Back arch

Treatment, lift foot to investigate, see to asap

227
Q

Describe score 3 mobility scores.

A

Can’t keep up with brisk human walking pace

Treatment, urgent attention, do not make cow walk far, culling in most severe cases

228
Q

What are the issues with mobility scoring?

A
  • Repeatability
  • Reliability – only detecting severe lesions?
229
Q

How are records analysed?

A

Date, cow id, claw affected, diagnosis, severity, treatment and response to treatment, ideally cow age and days calved

Can calculate:
- Annual incidence
- Annual incidence by diagnosis
- Number of cases per lactation
- Monthly incidence
- Consider what is a new case (lag period)

230
Q

What are the potential problems with the data collected?

A
  • Understanding/classification of lesions
  • Cases identified and treated in the parlour may not get recorded
  • Are these lame cows or does the data include foot trimmers reports
  • Missing data
231
Q

What are the risk factors associated with sole haemorrhage and sole ulcers?

A

Stockmanship – poor trimming protocol, technique. Acclimatisation of heifers to cubicles. Thin walls

Cow comfort, lying and standing times – too much time standing, poor cubicle comfort, extra attention around calving period

232
Q

What are the risk factors associated with white line disease?

A

Underfoot surfaces and cow flow – sharp turns, blind ending passageways, poor tracks

Stockmanship – biotin, poor trimming protocol/technique, acclimatisation of heifers to cubicles

233
Q

What are the risk factors associated with digital dermatitis?

A

Underfoot hygiene and foot bathing – foot bathing protocols, poor slurry management

Stockmanship – biosecurity infected cows in the herd

234
Q

What is a score 0 hair loss and lesion?

A

Lesions or hairless patches smaller than 2cm in diameter or no hair loss or lesions

235
Q

What is a score 1 hair loss and lesion?

A
  • 1 or more hairless patches larger than 2cm in diameter
  • Scars should only be included if they are at least 3mm wide
236
Q

What is a score 2 hair loss and lesion?

A
  • 1 or more lesions (damage, wound, scab) larger than 2cm in diameter
  • Scratches or cuts should only be included if they are at least 3mm wide
237
Q

How do areas of hair loss and lesions occur on the head and neck?

A
  • Incorrect neck barrier height
  • Protruding items
238
Q

How do areas of hair loss and lesions occur on the front legs?

A
  • Cubicle comfort
  • Amount and type of bedding
  • Protruding items
239
Q

How do areas of hair loss and lesions occur on the hock and hindleg?

A
  • Cubicle comfort
  • Amount and type of bedding
240
Q

How do areas of hair loss and lesions occur on the rest of the body?

A
  • Broken cubicle fittings
  • Protruding/low hanging items in housing or cow flow area
241
Q

Which NSAID has a zero day milk withdrawal?

A

Ketoprofen

CVSOH 4 (35 decks)

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