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MSK2 > Farm animal MSK disease 3 > Flashcards

Farm animal MSK disease 3 Flashcards

1
Q

Discuss the prognosis for vertical fissures in cattle

A
  • Generally good
  • Some can be difficult to treat, require multiple trims before wall normal
  • If periople permanently damaged, leading to continued production of defective wall, long term prognosis is poor
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2
Q

Outline the aetiology of horizontal fissures in cattle

A
  • Interruption of wall horn production at coronary band
  • Any severe toxic condition e.g. mastitis, metritis, acute acidosis
  • Will be complete circumferential fissure around all 8 claws
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3
Q

Outline the clinical signs and presentation of horizontal fissures in cattle

A
  • Often asymptomatic unless fissure and underlying laminae infected or granuloma produced
  • if get production of thimbles of wall and sole on all claws, movement of this relative to rest of wall results in lameness, infection and granulomas
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4
Q

Outline the treatment of horizontal fissures in cattle

A
  • If infection present, open crack and drain abscess
  • Resect granulation tissue
  • Often all claws affected so no blocks
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5
Q

Discuss the prognosis for horizontal fissures in cattle

A
  • prognosis varies depending on severity of disease

- Sometimes thimbles grow out and are shed asymptomatically, other times may have to cull affected animal

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6
Q

Explain the difference between horizontal fissures and hardship lines in cattle

A
  • Hardship lines = incomplete disruption of horn production, producing thin wall
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7
Q

Discuss the aetiology of fracture of the distal phalanx in cattle

A
  • Uncommon
  • Trauma during bulling (slipping off cows) or slipping off steps
  • Flouride poisoning (herd “outbreaks”)
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8
Q

Describe the clinical signs of fracture of the distal phalanx in cattle

A
  • Acute onset severe lameness, no other obvious clinical signs
  • If medial claw of front feet affected, animals stand with forelimbs crossed
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9
Q

What is required for definitive diagnosis of distal phalanx fracture in cattle?

A

Radiography

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10
Q

Discuss the treatment and prognosis for fracture of the distal phalanx in cattle

A
  • Distal phalanx well splinted by hoof capsule
  • Only need to apply block to unaffected claw
  • Prognosis good unless complicating factors e.g. fluoride poisoning
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11
Q

Outline the aetiology of interdigital skin hyperplasia in cattle

A
  • Chronic irritation of interdigital area e.g. chronic infection or impaction
  • Foul in the foot may predispose to condition later in llife
  • Hereditary component suggested
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12
Q

Outline the clinical signs of interdigital hyperplasia in cattle

A
  • Skin hyperplasia often asymptomatic, noted during routine foot trimming or inspection
  • Lame if overgrowth becomes infected or pinched during movement
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13
Q

Outline the treatment and prognosis for interdigital skin hyperplasia in cattle

A
  • If infected, treating infection treats lameness
  • If pinching, dish out horn from interdigital area
  • In severe cases or where corrective trimming ineffective, surgically remove hyperplastic skin under local or IVRA
  • Good prognosis
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14
Q

How may interdigital skin hyperplasia be prevented

A

Ensure underfoot conditions are optimal during the winter housing period

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15
Q

Outline the aetiology of suprascapular paralysis in cattle

A
  • C6 and C7 outflow innervates supraspinatus and infraspinatus
  • Usually damaged by trauma to prescapular or scapular area
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16
Q

What would the following clinical signs be most suggestive of in a cow?
Thoracic limb advanced normally but abducts when weight bearing, shortened stride, atrophy of infra and supraspinatus

A

Suprascapular paralysis (NB atrophy can be complete)

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17
Q

Outline the aetiology of radial paralysis in the cow

A
  • Excessive traction on limb e.g. calving, trauma to scapulohumeral area, prolonged recumbency
  • C7, 8 and T1 give motor innervation to carpus and digit extensors, and sensation to lateral aspect of limb
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18
Q

What would the following signs be most suggestive of in a cow?
Forelimb held in flexion with elbow dropped, evidence of scuffing on the dorsal hoof wall

A

Radial paralysis

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19
Q

What may be seen if only the distal portion of the radial nerve is damaged in a cow?

A

Innervation to elbow normal, but carpus and fetlock are held in flexion

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20
Q

Describe the aetiology of brachial plexus paralysis in cattle

A
  • Excessive traction of limb e.g. calving, traumatic abduction, prolonged lateral recumbency
  • C5 to T2 outflow = radial, median and ulnar nerves
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21
Q

List your differentials for the following clinical signs in a cow:

  • Flaccid left forelimb
  • Non-weight bearing
  • Hoof dragging on the foor
A
  • Brachial plexus paralysis (most likely if no other signs)
  • Scapulohumeral luxation
  • Fracture (e.g. humeral)
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22
Q

Describe the aetiology of obturator paralysis in a cow

A
  • Damaged during dystocia usually, often due to foetal oversize
  • L4, 5 and 6 outflow make up obturator nerve, innervates adductor muscles of HL
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23
Q

Describe the aetiology of femoral paralysis in a cow

A
  • Usually damaged in calves during dystocia caused by hiplock
  • Calf’s limbhyperextended during traction
  • Femoral nerve composed of outflow from L4, 5 and 6, innervates iliopsoas and quads
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24
Q

What are the following signs indicative of in a calf?

  • HL virtually non-weight bearing
  • Stifle cannot be extended
  • Limb hangs in flexed position with digits resting on floor
A

Femoral nerve paralysis

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25
Q

Describe the aetiology of sciatic paralysis in cattle

A
  • Commonly injured during dystocia caused by foetal oversize
  • occasionally by prolonged periods of lateral recumbency and iatrogenically through IM injections into HL
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26
Q

What are the following signs indicative of in a cow?

  • HL non-weight bearing
  • Stifle and hock held in extension and distal joints of foot are flexed
  • Foot is knuckled over
  • Limb is dragged along by extension of the hip
A

Sciatic paralysis

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27
Q

Describe the aetiology of tibial paralysis in the cow

A
  • Damage is rare, usually caused by extensive trauma to gastrocnemius area
  • Supplies motor innervation to extensors of hock and flexors of digit
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28
Q

Describe the clinical signs of tibial paralysis in the cow

A
  • Weight bearing shifted onto heels

- Animal walks with jerky motion

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29
Q

Describe the aetiology of peroneal paralysis in the cow

A

Damaged during periods of prolonged recumbency or sudden falls that damage the lateral aspect of the stifle joint

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30
Q

Describe the clinical signs of peroneal paralysis in the cow

A

Fetlock flexed (knuckled over) and hock extended, weight bearing but tends to stumble

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31
Q

Outline the general treatment for peripheral nerve paralysis in cattle

A
  • Relies on keeping animal comfortable e.g. deep soft bedding, non-slip surfaces
  • Anti-inflammatory drugs to reduce swelling
  • Supportive dressings in some cases
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32
Q

Discuss the prognosis for peripheral nerve damage in cattle

A
  • Bruising or swelling of the nerve usually respond well to conservative management
  • Prognosis for complete rupture very poor
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33
Q

Discuss the aetiology of white muscle disease in cattle

A

Selenium and vitamine E deficiency, and high levels of poly unsaturated fatty acids in the diet

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34
Q

Discuss the clinical signs of white muscle disease in cattle

A
  • Muscular dystrophy in growing animals
  • Peracute: sudden death
  • Acute: lateral recumbency, dull, respiratory disease, tachycardia, dead within 24h
  • Subacute: stand and walk stiffly, reluctant to move, weakness, eat normally
  • Chronic: ill thrift, poor weight gain, lower survival rate
  • Retained cleansing, metritis, cystic ovarian disease
  • Heinz body anaemia in growing calves
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35
Q

Discuss the clinical signs of white muscle disease in sheep

A
  • Muscular dystrophy in lambs
  • lambs born weak/die within a few days
  • Acute: 0-4 months, stand and walk stiffly, weak, ddx joint ill
  • Chronic: ill thrift, poor weight gains, lower survival rate
  • High embryonic mortality, infertility in ewes
  • Heinz body anaemia in growing lambs
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36
Q

How can white muscle disease be diagnosed in cattle?

A
  • PM: white plaques in myocardium, white striations in skeletal muscle
  • Erythrocyte GSHPx
  • Serum/plasma CK (elevated)
  • Response to supplementation
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37
Q

Discuss the treatment and prevention of white muscle disease in cattle

A
  • Parenteral (SC, IM) injection of SE, usually combined with vit E (e.g. Vitenium), usually re-dose q1-2 weeks, or depot (Deposel)
  • Addition to feedstuffs
  • Selenium boluses (+Co, Cu often)
  • Free access minerals
  • Medicated water
  • Drenching
  • Application of Se salts to soils
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38
Q

Which cattle breeds are predisposed to spastic paresis?

A

German and dutch Friesians, Aberdeen Angus

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39
Q

Discuss the clinical signs and presentation of spastic paresis in cattle

A
  • Chronic and progressive contraction of gastrocnemius muscle
  • 6weeks-6months of age
  • Hock nearly straight
  • Stiff stilted gait
  • Limbs may jerk intermittently at rest
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40
Q

Discuss the treatment of hock cellulitis/bursitis/trauma

A
  • Usually no treatment needed unless infected

- Most lesions resolve over summer months when outside

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41
Q

What is the following presentation typical of in a cow?

Bilateral dropped hocks to floor level

A

Gastrocnemius rupture (usually occurs at musculotendinous junction and usually bilateral)

42
Q

Discuss the treatment and prognosis of gastrocnemius rupture in a cow

A
  • NSAIDs e.g. meloxicam
  • Close confinement with limbs splinted in extension for number of weeks to allow healing and fibrosis
  • Prognosis guarded, unlikely to fully recover, re-rupture may occur
43
Q

List the NSAIDs licensed for use in cattle in the UK

A 
Carprofen
Meloxicam
Flunixen
Ketoprofen 
Tolfenamic
44
Q

What are the key risk factors for the development of foot lameness in cattle?

A
  • Standing on hard ground
  • Hoof overgrowth
  • Periparturient increase in movement of pedal bone
  • Loss of fat from digital cushion (weight loss)
  • Poor underfoot conditions
  • Poor hygiene of foot trimming equipment
45
Q

How can the risk of foot disease resulting from long periods of standing be mitigated in cattle?

A
  • Promote lying by improving cubicle comfort
  • Cubicle training for heifers for post-calving period
  • Limit standing time waiting for milking
46
Q

How can the risk of foot disease resulting from the periparturient increase in pedal bone movement be mitigated in cattle?

A

Provide periparturient animals with best accommodation to minimise risk

47
Q

How can the risk of foot disease resulting from weight loss be mitigated in cattle?

A
  • Minimise BCS loss to peak yield

- Identify and treat animals early to limit impacts of disease

48
Q

How long should cows ideal spend lying down?

A

12 hours

49
Q

How many cubicles should be provided to cows?

A

5-10% more cubicles than cows

50
Q

Discuss the bedding for cow cubicles

A
  • If uncomfortable leads to hock and hip abrasions, ulcerations
  • Should be absorbent, dry and comfortable
  • Deep straw: very comfortable but increased risk of mastitis
  • Sand: soft when lying, hardens when standing (easier), but abrasive
  • Mattress and mats lots of variation, can be good but expensive, make sure cubicles good first
51
Q

Describe the ideal cow cubicle design

A
  • Must have sufficient lunge zone (~90cm)

- 2.2m long, 1.2m wide

52
Q

Outline how heifers may be managed pre-calving in order to reduce the incidence of post-calving lameness

A
  • Cubicle training during rearing (at least one month in cubicles before calving)
  • Expose to concrete before calving to allow foot to adapt
53
Q

Outline how a fresh cow group may be managed in order to reduce post-calving lameness

A
  • Separate fresh cow group

- Provide best cubicles at low stocking rate, or v clean straw yard 4-6 weeks after calving

54
Q

Discuss the importance of diet in the prevention of foot lameness

A
  • Low fibre diet = more sole haemorrhage and sole ulceration
  • Minimise BCS loss to peak yield
  • Avoid SARA (although not related to claw horn lesions)
55
Q

What should the ideal cow track allow?

A
  • Rapid flow of cows without chasing
  • Comfortable and easy travel
  • Minimise damage and risk of lameness
  • Keep cows clean
  • Reduce loss of pasture due to poaching
  • Support some vehicle use if absolutely necessary
56
Q

What possible substrates should be used for cow tracks?

A
  • Oolitic limestone
  • Pine peelings, wood chip, rape straw
  • Chalk or sand
  • Shellet/soft stone
  • Concrete/tarmac kept free of stones ok, ideally with softer covering e.g. quarry belting/cow carpet
57
Q

What does the addition of biotin (B7) to the diet protect against and which cows are at particular risk?

A
  • White line disease

- Esp. high yielding cows on high concentrate (SARA may reduce B vitamin production)

58
Q

Discuss the use of footbaths for the prevention of foot lameness in cattle

A
  • 2-7 days/week
  • Must keep clean
  • 1 litre of foot bath per cow passage
59
Q

Compare the footbathing solutions that may be used in cattle

A
  • Formalin 2-5% (carcinogenic, hardens feet)
  • Copper/zinc sulphate 5%, safer vs formalin, toxic to cows, build up in environment
  • 1%peracetic acid
  • 1% hypochlorite
60
Q

Discuss the importance of biosecurity in the prevention of foot lameness in cattle

A
  • Digital dermatitis infectious
  • Maintain closed herd where possible
  • Care re. fomites e.g. boots, PPE, foot trimming equipment, machinery
61
Q

Discuss the slurry management in the prevention of foot lameness in cattle-

A
  • Scrape slowly, methodically, as often as possible
  • Hand scrape areas not reached mechanically
  • repair/improve concrete to prevent pooling of stale slurry
  • Automatic scrapes are risk factor for digital dermatitis (waves cover feet)
62
Q

Describe the clinical signs of scald/strip/interdigital dermatitis in sheep

A
  • Inflammation of skin between claws
  • Reddening, hair loss
  • White/grey scum
63
Q

Describe the clinical signs of footrot in sheep

A
  • Smell
  • Grey ooze
  • Underrunning of horn hoof near to skin between claws
  • Underrunning horn anywhere
64
Q

What pathogens are associated with the development of footrot in sheep?

A

Dichelobacter nodosus and Fusobacterium necrophorum

65
Q

Explain the pathogenesis of footrot in sheep

A
  • D nodosus and F necrophorum found in all sheep
  • D nododus is the main cause, causes the under-running
  • F necrophorum is a commensal that then invades and worsens the condition
66
Q

Compare interdigital dermatitis and virulent foot rot in sheep

A
  • Same thing, different degrees of disease
  • D nodosus higher load in ID than VFR
  • F necrophorum is an opportunist that then causes progression to VFR
67
Q

Discuss the treatment of foot rot in sheep

A
  • Need to treat ID and VFR = lower lameness prevalence
  • ID may be more infectious
  • Need to treat and separate affected sheep from flock to prevent environmental accumulation
68
Q

Describe the appearance of contagious ovine digital dermatitis

A
  • Highly invasive, painful lesion starting at coronary band
  • Rapid invasion and underrunning of hoof wall
  • Horn missing
69
Q

What pathogens are involves in contagious ovine digital dermatitis?

A

Spirochaetes/treponemes, also D nodosus

70
Q

Outline the treatment and management of contagious ovine digital dermatitis

A
  • Long acting injectable antibiotic e.g. Tilmicosin
  • Topical oxytet
  • Quarantine new sheep
71
Q

Outline the aetiology of toe granulomas in sheep

A
  • Non-infectious
  • Either from chronic unresolved footrot
  • Or overtrimming into sensitive part of foot
72
Q

Outline the treatment of toe granulomas in sheep

A
  • Very difficult, need to cut away granuloma
  • Ring block using 2% lidocaine or IVRA into superficial leg vein of 2% lidocaine 10ml max
  • Pare away loose and underrun horn , expose base of granuloma
  • Must have tourniquet on leg before cutting away granuloma at base
  • Cauterise site of granuloma with hot iron
  • Ensure no bleeding
73
Q

Outline the aftercare following treatment of a toe granuloma in sheep

A
  • Do not bandage
  • Dress with antibiotic aerosol spray e.g. oxytet
  • If necessary use parenteral antibiotic (e.g. footrot) - pen+strep 2x normal dose, oyxtet normal dose
74
Q

Outline the aetiology of white line disease in sheep

A

Unknown, may be similar to other species

75
Q

What is shelly hoof in sheep?

A
  • Presentation of white line disease where soil/debris accumulates laterally at white line
  • Half moon appearance of separation of white line
  • Often no lameness until abscess then acutely lame
  • No underrunning of hoof
76
Q

How is shelly hoof treated?

A

Trim back and expose pocket

77
Q

Describe the typical presentation of toe abscesses in sheep

A
  • Sudden onset extreme lameness with pain and heat, no obvious swelling
  • Small localised black spot at white line
  • Pus may track up and break out at coronary band
78
Q

Outline the treatment of toe abscesses in sheep

A
  • Do not trim acute cases

- Avoid parenteral antibiotics until pus has burst out - poultice foot to encourage this

79
Q

Describe the variety of white line separation lesions that may occur in sheep

A
  • Minor: usually no infection, not lame, short distance of separation, not detected unless pare foot along WL
  • Moderate: no infection, not usually lame, half moon appearance once pared
  • Major: shelly hoof, when detached wall is trimmed see half moon appearance, impaction of mud/debris, pus
80
Q

Outline the treatment for white line disease with extensive separation

A
  • Pare away detached horn, care not to go too deep
  • Antibiotic spray if infected
  • If pus burst out, no paring
  • Leave to recover for at least a week, after which loosened horn pared away carefully
81
Q

Outline the treatment of early acute cases of white line separation

A
  • Careful paring along course of white line, may release pus
  • Not too deep
  • If pus found, poultice foot for 1/2 days to soften horn and encourage bursting
82
Q

Discuss the use of parenteral antibiotics in the treatment of white line disease in sheep

A
  • May delay resolution of separation

- Antibiotics used in expensive pedigree animals

83
Q

How do foot abscesses develop in sheep?

A
  • Often sequel to trauma or infection

- May follow excessively strong foot bathing

84
Q

Give your differentials for the following clinical signs in a sheep:

  • Extreme pain, swelling and heat in the foot
  • Discharging sinus at the coronary band releasing pus
A
  • Foot abscess
  • Toe abscess
  • White line disease
  • Contagious ovine digital dermatitis (Coronary band involvement)
85
Q

Discuss the use of foot trimming in sheep

A
  • Routine foot trimming has no benefits, but can cause lameness
  • Trimming horn may delay healing in foot rot
  • Overgrown feet does not cause lameness, but may become overgrown if infected
86
Q

Outline the five point plan for footrot in sheep

A
  • Avoid spread of infection
  • treat individuals quickly and effectively
  • Quarantine brought in sheep
  • Cull out persistent offenders
  • Vaccinate to protect against foot rot
87
Q

After how many incidences of lameness should a sheep be culled?

A

2-3 incidences of lameness

88
Q

When would the vaccine against foot rot be most effective?

A

Best used if have a high level of lameness, in order to reduce to a level where other methods can then be used instead, but always use in conjunction with other methods

89
Q

Discuss the use of footbathing for the prevention of footrot

A
  • Footbath must be clean, clean feet before use, stand on hard surface after footbathing
  • 10% zinc sulphate for at leas 2 mins, or 3% formalin as walk through
  • Will not TREAT footrot
90
Q

List the management factors that influence lameness in pigs

A
  • Flooring
  • Housing system
  • Stocking density and group size
  • Growth rate
  • Nutrition
91
Q

Outline the lesions may develop in pigs as a result of slatted floors

A
  • Sole bruising in piglets, heel flaps in older pigs
  • Bursitis and capped hock in older pigs
  • If sharp edges, coronary band injuries in piglets
92
Q

Outline the lesions that may develop in pigs as a result of solid concrete floors without bedding

A
  • Hard: sole bruising in piglets, bursitis and capped hock in older pigs
  • Rough: sole erosion in piglets, skin abrasion in piglets, calluses in older pigs
93
Q

Outline the lesions that may develop in pigs as a result of solid floors with bedding

A
  • Soft: hoof overgrowth in older pigs

- Damp: toe erosion in older pigs

94
Q

Discuss how housing system influences lameness in pigs

A
  • EU requirement to group house sows from 4 weeks after service until one week before farrowing
  • Group is more natural, social interaction, increased exercise, less superficial joint damage
  • But also increased aggression leading to lameness, claw lesions, body lesions
  • Stable groups reduce this risk
95
Q

Discuss how group size and stocking density influence lameness in pigs

A
  • Pigs in larger groups tend to have higher limb lesions and lameness scores
  • Increased lameness later in finisher stage especially due to increased body size
96
Q

Discuss how growth rate influences lameness in pigs

A
  • Leg weakness more evident in pigs with higher lean tissue growth rates
  • Every 100g increase in daily gain results in an increase of 20% in the risk of exhibiting signs of OCD
97
Q

Discuss how nutrition influences lameness in pigs

A
  • Directly related to claw, bone and cartilage physiology, direct affects limb healthy via weight gain
  • Vitamins and minerals important
  • Feed specific diets to replacement gilts to support bone development and fat deposition
98
Q

List the 5 most common infectious/congenital causes of lameness in pigs

A
  • Bacterial arthritis
  • Erysipelas
  • Splayleg
  • Mycoplasma
  • OCD (leg weakness)
99
Q

What is bacterial arthritis in pigs also known as?

A

Joint ill

100
Q

List the pathogens commonly involved in bacterial arthritis in pigs, indicating which is the most important

A
  • Strep suis (most important)
  • Actinobacillus suis
  • Haemophilus parasuis (Glassers disease)
  • Trueperella pyogenes

MSK2 (29 decks)

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