64. Non-infectious hoof diseases in cattle Flashcards
Non-infectious hoof diseases in cattle?
Laminitis
Sub-clinical laminitis
sinking of the pedal bone
sole ulcer
white line disease
toe necrosis
heel erosion
morpholoical deformities
hard/soft feet
Laminitis?
Laminitis:
- most common disease, biggest economic impact (intensive farming – dairy, bulls)
- multifactorial, numerous predisposing factors, not completely understood
three froms of laminitis?
Three forms:
• acute – grain overload (pathogenesis like in horses) – usually not characterized by lameness (quick
progression, high mortality)
• subclinical/subacute – most important
• chronic – can be originated from acute or subclinical
Subclinical laminitis ethiology and predisposing factors?
Subclinical laminitis:
Etiology, predisposing factors:
• Subacute rumen acidosis (SARA):
o Long-term concentrate feeding – easily fermentable (non-structural) carbohydrates ↑
Streptococcus bovis and Lactobacillus spp. ↑ – lactate↑ – ruminal pH↓ – Allisonella
histaminiformans (acidity tolerant, produces histamine from histidine) ↑ - histamine,
lactate and endotoxins in the bloodstream– disturbance of hoof-horn production
• Heat stress:
o Ruminal pH is regulated by bicarbonate excreted into the saliva (buffer)
o slow, deep breaths - respiratory alkalosis – bicarbonate excretion with urine – buffer ↓
o severe heat stress– salivation – buffer ↓
o decreased buffer capacity can exacerbate SARA
Calving:
• Relaxine production begins 4 weeks before calving (relaxation of the pelvic ligaments) – relaxine
can have an effect on the fixation of the pedal bone (not proven but likely) – can cause sinking of
the pedal bone
• Relaxine is only in effect around the time of calving
Flooring:
• Hard floor around calving – stresses destabilized pedal bone – deformity, sinking –problem
becomes permanent
Pathogenesis of subclinical laminitis?
Pathogenesis:
• Disturbance of hoof-horn production:
o Histamine, other vasoactive agents (endotoxins) – disturbance of function of pedal blood
vessels– local hyperaemia– blood vessels rupture – blood and plasma in the tissues –
pink/yellow discoloration of the horn, thrombi – further disruption of blood flow, hypoxia,
lack of nutrients in the corium – soft, sensitive horn
o (EGF – epidermal growth factor – produced during GI tract inflammations (SARA) in large
quantities – disturbance of keratinocyte function in the hoof)
• Sinking of the pedal bone (P3):
o Suspension of the pedal bone –connection between laminae and lamellae –collagen fibers
o Relaxine, MMP (matrix metalloproteinase) – collagen fibers stretch – pedal bone
sinks/rotates
o Hoof wall separates from pedal bone –flexion of the hoof wall
Clinical signs of subacute laminitis?
Clinical signs:
• Observation and examination of groups at risk (fresh cows, heifers - develops more easily but also
heals more easily)
• Not always lame in the early stages
Examination of movement and feet?
Examination of movement:
- Careful steps, tiptoeing, lameness
- Legs placed under the body when standing, arched back
Examination of the feet:
- Swelling of the coronary band
- Oedema around the dewclaws
- Haemorrhages on the tip of the toe and the sole – can also be caused by trauma
- Abnormalities of the white line
Local and general consequences of subacute laminitis?
Local consequences:
- Sole ulcers
- White line disease
- Toe necrosis
- Slipper foot: sign of chronic laminitis, hoof wall is ridged, striped, dorsal wall overgrows, abnormally
acute angle with the ground or it even curls up – can be fixed by trimming temporarily but. the
connection between the laminae and the lamellae cannot be restored – culling
General consequences:
- Loss in bodyweight
- Decreased milk production
- Suboptimal reproduction
- Immunosuppression
- Culling ↑
Therapy and prevention of subacute laminitis?
Therapy:
- Individual treatment is too late at the time of diagnosis – not economical
- Herd level: exploration of risk factors, prevention
Prevention:
- Prevention of SARA, ruminal pH monitoring
- Soft floors in calving barn, space to lie down
- Hygiene – avoid inflammation processes
- Special attention to heifers
Sole ulcer origins and pathogenesis?
Sole ulcer (pododermatitis circumscripta):
Common in intensive farming (dairy, bull fattening) especially in winter
Origins:
- Trauma (hard, rocky floors)
- Consequence of subclinical laminitis
Pathogenesis:
• Weakened (pressure of the pedal bone) or injured solar horn – environmental bacteria –ulceration,
even abscesses
• Characteristic place: hind leg, lateral claw, on the border between the sole and the heel bulb
Sole ulcer clinical signs and therapy?
Clinical signs:
- Lameness – hind leg
- Bloodstain on the floor/bedding – bleeding ulcer
Therapy:
• Hoof trimming:
o area around the ulcer should be trimmed without cutting into the ulcer itself and to avoid
the animal placing weight on the ulcer after trimming
o Block on the sound claw - pressure ↓
o Avoid chemical agents – healing time↑
• Usually full health cannot be restored - culling
White line disease ethiology and pathogenesis?
White Line Disease:
Etiology and predisposing factors are similar to those of the sole ulcer
Pathogenesis:
• White line is comprised of soft horn – connection between laminae and lamellae is weakest at the
palmar/plantar end of the abaxial wall + digital cushion presses the hoof wall outward – laminitis –
white line weakens – white line haemorrhage
• Weakened white line – bacteria or foreign bodies – ascending infection -abscessation – white line
separation
• Characteristic place: hindleg lateral claw, abaxial side, near the heel bulb one- or two-sided
Clinical signs of white line necrosis?
Clinical signs:
• Lameness – only visible early if one-sided, if two-sided, the gait remains symmetrical until one foot
worsens considerably compared to the other
- Special gait – hind legs are thrust outward when walking - weight on the medial claw
- Pus/blood on the floor/coronary band
- Foot:
o Discoloration of the white line (pink or even black)
o Widening of the white line
o Pus/blood around the white line
Consequences of white line necrosis?
Consequences:
- Ascending infection to the coronary band – abscess – pus on the coronary band
- Involvement of other structures:
o distal interphalangeal (DIP) joint
o bursa of the deep flexor tendon – rupture – retroarticular abscess
o proximal interphalangeal (PIP) joint
o swelling of the digital cushion – local swelling – diff. diag.: foot rot
Therapy of white line necrosis?
Therapy:
• Hoof trimming:
o cut away the white line until no black discoloration is visible
o abscess:
n elliptical cut on the abaxial wall – free draining
n white pus – can be sterile (reaction to laminitis)
n black pus – probably contaminated
o Consequences – see later
• Usually does not heal fully - culling
Toe necrosis ethiology?
Toe necrosis (Toe-tip necrosis):
Etiology and pathogenesis:
• Subclinical laminitis – sinking of the pedal bone – damage to the surrounding tissues – bleedingincreased pressure – necrosis (if the pedal bone rotates, it can pierce through the sole -
osteomyelitis)
- Pain in the heel area – walking on toe-tip – thinning of sole horn – trauma- infection – necrosis
- Transportation (mainly young beef cattle – USA) – long periods of standing- Local hyperaemia in the
feet – damaged blood vessels – bleeding –Necrosis
Toe necrosis anatomical background and clinical signs?
Anatomical background:
• Arteria digitalis palmaris/plantaris propria III/IV axialis – main blood supply – branches – after going
through the pedal bone branches emerge between the bone and the hoof wall – can be damaged
by pressure
Clinical signs:
- Lameness
- Bleeding/visible necrosis on the toe
Therapy of toe necrosis?
Therapy:
- Only in uncomplicated cases
- Hoof trimming:
o opening the necrotic area, cleaning, local AB
o if the necrosis is extensive, amputation of the toe tip under local
- if the pedal bone is affected, more aggressive amputation
- block on the sound claw
- if it does not worsen, after applying local AB, the area can be sealed with methyl-methacrylate
- Systemic AB is advised
Heel erosion cause?
Heel Erosion
- dairy herds, wet, on bedding contaminated with urine/faces, especially in winter
- origins not known, often found together with subclinical laminitis and DD
- on its own it usually does not cause lameness – no accurate data on incidence
Heel erosion clinical signs?
Pathogenesis, clinical signs:
• Initially approx. 0.5 cm wide erosions on the heel, these later merge and create black grooves
parallel to the coronary band on the axial wall – no lameness yet
Two possible ways:
• Horn thickens on the heel, especially on the lateral claw of the hind limb + axial thinning of the hoof
horn – sole slopes inward – tarsus bends medially – different weight distribution – usually with sole
ulcer
• heel horn almost completely denudes – different weight distribution – sometimes with sole ulcer
Therapy of heel erosion?
Therapy:
- Hoof trimming
- Weekly foot baths from October (with formalin is possible)
- Hygiene
Morphological deformities?
Morphological Deformities:
Forms:
- Overgrown hoof: dorsal wall grows longer than 7.5 cm
- Slipper foot: see before
- Scissor claw: one or both claws grow over the midline and cross each other
- Corkscrew claw: overgrown dorsal wall twists and gets between the abaxial and heel wall- double
sole
Treatment:
• Hoof trimming
Hard/soft feet?
Hard/Soft feet:
• Hard horn:
o Tie-stalls, wood shavings/sawdust for bedding
o Horn breaks easily - infections
o Treatment: softer bedding, standing on grass, grazing
• Soft feet:
o Wet bedding contaminated with urine/faeces
o Treatment: hard, dry flooring, hydrated lime, copper-sulphate foot bath
