Exam 1 Flashcards
Lecture 1
Bovine Hoof Lameness
-Interdigital Erosion
-Heel Erosion
-Interdigital hyperplasia/fibroma “corn”
-Papillomatous Digital Dermatitis “Hairy hell wart”
-Traumatic Pododermatitis “Subsolar Abscesses”
-Solar Ulcers (Rusterholz ulcer)
-Foreign body
Lameness Exam
Part -1 Hands free
Signalment: age, breed, sex.
History
-Chief complaint
-Number of limbs affected
-Onset and progression
-Prior treatments/Diet
-Purpose of the animal (pet or meat or dairy)
-Date to harvest or sale
Hands Free
-Examination starts from afar: don’t miss the forest for the “trees”
-Muscular asymmetry: Acute vs. chronic
-Inflammation: joints, tendons, coronary band.
-Lameness severity: Grade 1, 2, 3, 4, 5
Lameness Exam
Part -1 Hands free
Grade 1 - Normal
-Stands and walks normally
-Level back
-Makes long confident strides
Grade 2
-Stands with back flat
-Arches back during walk
-Gait is slightly abnormal
Grade 3
-Stands and walks with back arched
-Short strides with one of more legs
-Slight sinking of dew claw in limb opposite to the affected limb may be evident
Grade 4
-Arched back standing and walking
-Favoring one or more limbs but can
-Still bear some weight on limbs
-Sinking of the dew-claws is evident in the limb opposite to the affected limb
Grade V
-Pronounced arching of back
-Reluctant to move
-Almost complete weight transfer off the affected limb
The Lame Bovid Exam Hands Free
Locomotion
-“Down on sound”
-Short strides
-Toe in or out
Standing Posture/Conformation
-“cow-hocked”
-Post legged
-Overgrown toes
-Short heels
The lame bovid Exam - Part 2 (Hands on)
BE SAFE!!!
-Restrain all extremities: ropes/halters/ratchet straps
45 Min MAX tilt time
-Radial Nerve paralysis
-Bloat
-Aspiration pneumonia
Always start with the foot
Clean the hooves
-Hooves account for 80% of lameness
-Often hind limb and lateral claw
Weight bearing digits
-Front - medial claw
-Hind - lateral claw
Odor/Trauma/Heat
Flexion/Extension/Crepitus (gas under the skin)
Hoof Testers
-ALL parts, ALL digits, EVERY TIME
-Percussion
-Draining tracts/Pus: hoof knife, Swiss knife
-Dark areas/Bruising
-Foreign material
Exam Part 2 (hands on)
Upper limb
-Tendon/Ligament/Muscle rupture
-Cranial cruciate ligament trauma: Cranial drawer test standing. Joint instability (lateral recumbency)
-Coxofemoral luxation (takes more diagnostics)
-Greater trochanter location
-Bilateral symmetry
-Transrectal palpation (always good bc may find other things)
The Lame Bovid Exam Part 3 (Diagnostics)
Ultrasound
-Joint
-Tendon sheaths
-Bone
-Soft tissue
Radiographs
-Orthogonal views always
-Obliques - sometimes
Cytology
-Arthrocentesis
Regional blocks
-Intraarticular, venous, peripheral nerve
Anatomy of the hoof Review
-Lateral claw
-Medial claw
-Bulb of heel
-Wall
-Axial wall
-Abaxial wall
-White line
-Sole
Laminae
-Insensitive lamina
-Sensitive lamina: Laminar corium
Diseases of the Distal Limb/Hoof
Interdigital Necrobacillosis (Footrot)
Interdigital Necrobacillosis (Footrot)
Pathogenesis
-Breech in skin barrier (opportunistic bacteria)
-Anaerobic environment production. Symbiotic relationship between organisms, Lowered oxygen tension
-Host evasion: Leukotoxins and lipopolysaccharides
Clinical signs
-Soft tissue trauma
-Tissue necrosis
-Distal limb swelling
Diagnosis
-Combination of signs
-Distal limb swelling: coronary band area
-Fetid interdigital odor (wear gloves)
-Culture - not beneficial
-MAYBE leukotoxin A antitobody ELISA
Treatment
-Antimicrobial: TALUTHROMYCIN
-CEFTIOFUR, TETRACYCLINE, FLORFENICOL
-Clean and deride toes floss, twine.
Pain medication
-Flunixin meglumine: transdermal or injectable
-Meloxicam
-Gabapentin
Never bandage: worsens anaerobic environment
Prognosis
-Good in uncomplicated cases
-If no improvement within 24-48 hours, then look for another problem
Control and Prevention
-Reduce access to standing water/mud
-Hygiene
-Dry bedding
-Foot baths: Formalin, copper sulfate, antibiotic formulations
-Vaccination (+/-)
Heel Erosion
AKA
-Bovine Contagious Interdigital Dermatitis
-Slurry “heel/foot”
Etiology
-Chronic skin irritation
Dichelobacter nodosus
-Fusobacterium necrophorum and Treponemes can be concurrent
Pathogenesis
-Superficial inflammation, wet conditions
Clinical Signs
-Mild lameness
-Heel horn erosion
Diagnostics
-Clinical signs - erosion of heel
Treatment
-Hoof care and trimming (most of the time it is all that is needed)
-Antibiotics …. if deeper structures involved (SDF, DDF, etc)
Prognosis
-Good
Control and prevention
-Hygiene improvement (BEST)
-Topical antibiotics: oxytetracycline
-Footbaths +/-
-Vaccine?
Interdigital Hyperplasia/ Fibroma “CORN”
Etiology
-Heritable
-Hoof conformation
-Secondary problem
-“wear and tear”
-Chronic inflammation
Clinical signs
-Uncommon cause of lameness by itself
-Growth of tissue in interdigital space
-Forelimb: bulls
-Hindlimbs: cows
-Repeatable sensitivity to area
Inadequate footing causes spreading of the hooves
Treatment
-Conservative management
-Treat associated infections
-Provide adequate footing
-Debulk tissue: regional anesthesia (Bier Block)
-Wire claws together
-Bandage
-Antibiotic of choice
Debulking Procedure
-Bier Block
-Sharp wedge incision #20 Blade
-Bandage
-Wire claws together
-Post Op care
Prognosis
-Good
-May require subsequent debulking
-Predispose to other infections?
Control and prevention
-Genetic selection
-Flooring/ground management
-Hoof care
Papillomatous Digital Dermatitis
AKA
-Hairy Heel Wart
Etiology
-Tremponema spp. invasion
-Spirochete bacteria
Pathogenesis
-Beef or Dairy
-Muddy wet conditions
-Invasion of bacteria
-Loss of Stratum Granulosum
-Dermis inflammation
Clinical Signs
-Mild Lameness of any digit
-M1, M2, M3, M4 (chronic infection) M0 (M5)
Diagnosis
Characteristic papillomatous and ulcerated
-Usually interdigital space of limbs
-Skin biopsy?
Treatment
-OXYTETRACYCLINE (individual) topical
-2g of powder in the lesion
-Parenteral Ceftiofur/penicillin (more efficient for larger herds)
Footbaths copper sulfate, formalin, tetracycline
Prognosis
-Good but management is difficult
-High recurrence rate
-Reduced weight gains
Control and Prevention (Goal)
-Hygiene
-Footbaths
-Biosecurity: prevent from getting it in herd (closed herd)
Hairy heel wart
Hairy heel wart
Traumatic Pododermatitis
AKA
-Subsolar Abscess
-Sole Abscess
Etiology
-Trauma
-Puncture/bruising
-Inappropriate hoof trimming
-Secondary laminitis
Clinical Signs
-Can cause SEVERE lameness
-Soft or discolored sole appearance or visible tract
Diagnosis
-Hoof testers
-Radiographs +/-
-Rule out P3 osteomyelitis
Punctuate, black lesion
Treatment
-Pare our defect (sometimes the entire sole)
-Regional anesthesia (Bier Block)
-Wooden block on adjacent digit
-Often more effective for pain than NSAIDs
-Antibiotics only if deep structures involved
Prognosis
-Good
-Immediate lameness improvement
Control and prevention
-Reduce traumatic flooring: rocks, slippery surfaces, etc.
-Proper hoof care
Sole Ulcers
AKA
-“Rusterholz ulcer”
Etiology
-Combination of risk factors
-Hoof conformation: long toe length or short heels. Corkscrew claw
-Thin soles: excessive hoof trimming or wear
-Laminitis
-Chronic exposure to manure/urine slurry
Pathogenesis
- Depends on underlying causes
-Multi-factorial
Leading theory: Contusions
-Corium and germinal epithelium
-Flexor tuberosity of distal phalanx
Clinical Signs
-Varying degrees of lameness (can be severe)
Diagnosis
-Ulcer at specific region of hoof
-Severe or chronic ulcers can affect deeper structures: P3, distal interphalangeal joint, tendons
Treatment
Pare out ALL undermined sole
-+/- wooden block on adjacent claw
-+/- pain medication
-Resolve underlying condition if identified
Prognosis
-Good if deeper structure not involved
Control and Prevention
-Prevent underlying condition
-Often considered metabolic problem (laminitis)
Foreign Body
Clinical Signs
-Sudden Lameness
-After milking parlor
-Pen change
-Depends on location. Hoof or interdigital space
Diagnostics
-Radiographs
+/- Ultrasound
Treatment
-Remove foreign body
-+/- antibiotics
-In/near deeper tissues
Prognosis
-Good if not structures involved
-Control and prevention: remove material from environment
Lecture 2
Bovine Lameness - Distal Limb
Sole Bruise
Sand crack “vertical hoof fissures”
Scissor Claw
Laminitis
White line disease
Corkscrew claw
Tenosynovitis
Phalangeal factures
Pedal Osteitis/Osteomyelitis
Sole Bruise
Etiology
-Trauma to the sole: rocks, gravel, uneven floor, long hours of standing, stress forces.
Clinical signs
-Mild lameness: underlaying structure problem?
Diagnosis
-No parable deep tract to a sole ulcer
-Discoloration of the sole epidermis
-Dislodge of rocks on examination
Treatment
-Remove from flooring
-Sole saver pads
-Abscess can develop: remove sole and clear it up, it will be fine
Prognosis
-Good
-Make sure not laminitis/sole ulcer
Prevention
-Fix flooring
-Reduce time standing
-Proper hoof trimming
Sole Bruise Sole Saver pad
Vertical hoof fissures
Sand Crack “Vertical Hoof Fissures”
AKA Vertical hoof fissures
Etiology
-Inferior hoof wall
-Dry environment most typically
-Laminitis
-Damage to coronary band
-Stress forces: heavier/Larger cattle
-Pastured animals more than confined
Pathogenesis
-As the hoof wall dries, it becomes brittle and cracks - starts to separate
-Dry sandy environments (similar issues in horses)
Clinical Signs
-Uncommon cause of lameness
-Result of impacted material in crack
-85% of cases are front lateral claws
Diagnosis
-Easy to visualize and determine extent
-Seldom affects sensitive lamina
Treatment
-Dremel crack, allows to drain
-Radiographs optional
-Prevent debris impaction
-Not usually fill crack , optional cover with hypoxy
Prognosis
-Good
Control and prevention
-Corrective trimming and hoof care
-Topical oil
-Practical?
Thimble Claw “Horizontal hoof fissures”
Etiology
-Any interference with hood growth
Metabolic condition
-Laminitis
-Interrupted growth at coronary band
-Hardship or stress line: something happen during the life of the animal, lack of adequate nutrition maybe.
Pathogenesis
-Intermittent disruption of hoof growth causes horizontal fissure that must grow out and be worn off
Clinical signs
-Uncommon cause of lameness by itself
-More useful as indicator of underlying condition and how long
Heel growth 1cm/month
Toe growth 0.5 cm/month
-Both vary with surface exposure: concrete vs. dirt
0.25 inches/month walk around knowledge
Diagnosis
-Visual inspection
Treatment
-Fix underlying condition
Prognosis
-Good given no other complications
Control and prevention
-Adequate footing
-Proper diet
-Routine hoof care
Scissor Claw - very common
Etiology
-Overgrown hooves
-Laminitis
Clinical signs
-Uncommon cause of lameness
+/- hardship grooves
-Too much pressure on toe
Treatment
-Frequent trimming (every 6 months)
Laminitis
AKA Founder - more equine name
Etiology
-Definition: weakening of suspensory apparatus of third phalanx
-Younger animals <3 yrs old
-Peripartum/transition period
-Rumen acidosis: high concentrate/low roughage diet
-Sequela to systemic inflammation/infection
Clinical signs
-Acute: painful, weight shifting, stiff gait, elevated heart and respiratory rate.
-Chronic: secondary hoof changes, sole ulcers, white line separation, bruising, stress rings.
Cow tries to put more weight on lateral hooves, crossing legs position
Diagnosis
-Clinical signs and history
-Check rumen motility: normal 2-3 times per minute.
Treatment
-Treat underlying cause
-Anti-endotoxemic drug administration
-Flunixin meglumine or polymexodine (expensive)
-Supportive care and corrective hoof trimming
Prognosis
-Fair to good
-Subsequent disease: white line disease, sole ulcers, bruising
Control and prevention
-diet management
-Reduce stressors - most important
White Line Disease
Etiology
-Inferior lamina development or separation
-Often sequela to laminitis
-Wet conditions
-Unbalanced weight bearing
-Inappropriate trimming
Pathogenesis
-Separation between sensitive and insensitive laminae at hoof wall and sole junction
-Organic debris becomes impacted
-Abscess development
-Retrograde infection towards coronary band
Clinical signs
-Varying degree of lameness
-Associated with movement between separated hoof portions
Diagnosis
-Visual inspection
-Most often abaxial wall of lateral claw hindlimb or medial claw in forelimb
Treatment
-Pare tracts and facilitate draining
-Partial removal of hoof wall may be warranted
Prognosis
-Good given no other complications
-Navicular bursitis and DIP joint infection complications
Control and prevention
-Adequate footing
-Proper diet
-Routine hoof care
Corkscrew Claw
Etiology
-Malalignment of middle P2 and distal P3 phalanges
-Low degree of heritability: mostly seen in black cattle
Pathogenesis
-Inappropriate curvature of P3 causes the claw rotation toward the axial plain
Clinical Signs
-Initial rotation starts in younger animals
-Any breed
-Higher prevalence in black hided animals
-Hind limb more than forelimb
Treatment
-Cull
-Corrective trimming every 6mts
Prognosis
-Good? fair?
Subsequent lateral collateral ligament strain, periostitis, subsolar abscesses/ulcers, bruising, chronic lameness - no normal part of the hoof left
Control and Prevention
-Not recommended as breeding prospects
Tenosynovitis
Etiology and Pathogenesis
-Aseptic: direct trauma
-Septic: progression of digital disease, penetrating wound
Distal tendon sheaths of common extensor of digits tendons
Clinical signs
-Severe lameness
-Draining wounds
-Visible viscous fluid draining
-Distended sheath: unilateral flexor tendons independent distal fetlock
-Proximal limb swelling
Tenosynovitis
Diagnosis
-Ultrasound
+/- radiographs: rule out foreign material, bone/joint involvement
Treatment
-Facilitate adequate draining HOSPITALIZED
-Sterile bandage changes daily 5-7 days
-Antibiotics: culture/sensitivity
-Pain medication
-Wooden block of adjacent claw +/-
-Amputation: depending on severity, purpose of animal, which limb, restraint availability
Prognosis
-Fair
-Adhesions, chronic lameness, expensive
-Unlikely to return to sound
Piece of wood superglued to hoof toe, allows better distribution of weight
Phalangeal Fractures
Diagnosis
-Swelling +/-
-Hoof makes visualization difficult
-Hood testers: hoof sensitivity
-Radiographs: ALWAYS ORTHOGONAL views
-Sequestrum common in P3 fractures sole approach
-Evaluate joint spaces carefully
-Gas present?
Treatment
-P2 and P3 fractures: wooden block on adjacent digit
-Pain medication
+/- antibiotics
-P1 fractures: wooden block or stabilize with cast “joint above and below”
-Half limb cast for comminuted fractures
-Bandage care is costly over 6-8 weeks
Prognosis
-P2 and P3 fractures good, may take a while and be expensive. Sequestrum is common
-P1 fracture largely depends on management capability. Good to guarded, high motion joint
Pedal Osteitis/Osteomyelitis
Etiology and Pathogenesis
-Chronic inflammation/infection
-Sequela to unmanaged disease
-Laminitis
-Trauma: breeding injuries, unstable flooring, older animals commonly present with P3, very painful, and completely bone gone
Clinical Signs
-Moderate to severe lameness
-Distal swelling
+/- abscessation
Diagnosis
-Radiographs
-Articular surface, number of bones affected, sequestrum present
Treatment
-Considerations: job, value, of animal, severity of the problem
-Cull
-Treat underlying condition
-Facilitated ankylosis abaxial, solar, bulbar
-Amputation
Toe tip necrosis
-Usually specific to young feedlot cattle
-First 21 days of placement
-Severe lameness due to trauma
-Multiple theories exist
-Treatment dependent on severity: amputation distal aspect of toe, claw amputation
Pedal osteitis/osteomyelitis
Toe tip necrosis
Lecture 3
Musculoskeletal
Non-infectious joint issues
Coxofemoral luxation
Cranial cruciate tear
Upward fixation of the patella
Lateral luxation of patella
Osteochondrosis
Degenerative joint disease and OA
Coxofemoral Luxation
One of the most common orthopedic issues of bovine hip
-1% in beef cattle
-8% in dairy cattle (more likely to slip on concrete)
-Traumatic: most of the time
-Hypocalcemia: weak when mounted and causes trauma
-Estrus behavior
-Inadequate flooring
-Dystocia - bilateral obturator nerve paralysis: retractive devices lead to trauma
-Iatrogenic from dystocia (calves)
Coxofemoral luxation Anatomy
Primary stabilization
-Ligament of the femoral head (red)
-Joint capsule (yellow)
Secondary stabilization
-Acetabular labrum (purple)
-Transverse acetabular ligament (blue)
-Gluteal muscles
-Bovids lack accessory ligament
Types of Coxofemoral Luxation and Frequency
- Craniodorsal
-Animal falls with joint ADDUCTED
-Greater trochanter struck
-Femoral head ligament and capsule tear
-Gluteal muscle pulls femoral head cranially - Caudoventral
-Animal falls with joint ABDUCTED
-Simultaneously rotation into obturator foramen.
-Can’t get up, hard to diagnose - Caudodorsal
- Cranioventral
Related to something striking the femur in a particular direction most of the time
Diagnosis
-Severe gluteal swelling
-Anatomy: Greater trochanter symmetry. Transrectal palpation can often feel the femoral head
-Radiographs
-Ultrasound: takes a lot of practice, but at least can tell not normal
-Find normal anatomy and see where the greater trochanter is, find hooks and pins.
Treatment
-Closed Reduction: external manipulation
-Open reduction: intra/extra articular correction
-Femoral head Ostectomy: not common
Closed Reduction
-Prognosis: 56-75% within 12 hrs. 8-43% within 24hr.
-Craniodorsal less trauma than caudoventral
-< 3 yr of age
-< 400 kg
-Often recurs, hobbles
Open Reduction
-Capsulorrhophy
-Prosthetic capsule
-Trochenteric transposition: not common, present destruction prevents it
-Toggle
-Combination
Prognosis: fair to good? Confounding problems, post operative care, biological factors, Age, weight, trauma extent.
Cranial Cruciate Tear CCL
-Cranial cruciate ligament (red)
-Caudomedial aspect of lateral condyle (proximally)
-Craniolateral to intercondylar imminence (distal)
Functions: limit excessive cranial displacement, prevents internal rotation
Cranial Cruciate Tear/Rapture
Etiology
-Acute trauma (younger animals). Breeding injury, falling
-Conformation: chronic hypertension of stifle, Degenerative joint disease, “post legged”
Clinical signs
-Moderate to severe lameness
Diagnosis
-Swollen stifle (acute) femoropatellar joint, medial femorotibial joint. Fluid tap where it is most swollen
-“Cranial drawer test”
-Joint instability while weight bearing
-Radiographs: cranial tibial displacement, Avulsion fractures/mineralization/DJD?
Treatment
-Financial considerations: value of animal, equipment.
-Medical management
-Surgical intervention: referral
-Cull/euthanize: most common
CCL tear/Rapture
Medical Management
-Lower value animals
-Partial tears
-<450 kg
-Strict confinement 2-3 months
-NSAIDs: Meloxicam, Gabapentin
Surgical Intervention
-High value animals
-Partial and complete tears
Methods
-Joint imbrication
-Gluteobiceps graft
-Bone tunnel method
-Post op care: 6-8 months
Prognosis
-No treatment: poor
-Surgical intervention: fair to good
-Complete lameness resolution reported
-Cows better than bull: 88% vs. 43%
-Weight and job related
Upward Patella Fixation
-Uncommon
-Cause: heritable? larger medial femoral condyle. Trochlear malformation
-Decreased muscle tone of quadriceps
-Femoral nerve damage association
-Nutritional
Diagnosis
-Intermittent “locked” hind limb at start of anterior stride
-No swelling
Treatment
-Depends on cause: genetic/nutrition/nerve trauma.
-Radiographs if possible
-Medial patella ligament desmotomy (not complicated): lidocaine locaoregional anesthesia. Sharp percutaneous incision.
Lateral Luxation of Patella
-Predominately reported in calves
-Causes: congenital
-Shallow trochlear ridges
-Dystocia: medial patella ligament
Treatment
-Femoropatellar imbrication
-Salvage
Osteochondrosis
OCD
-Disease of young, growing animals
-Abnormal endochondral ossification
-Failure or defect
Osteochondrosis Dissecans
-When cartilage flap is present
Osteochondritis
-Synovial inflammation
Pathogenesis
-Multifactorial?
History theory
-Disruption of endichondral ossification. Endochondral to metaphyseal blood flow
-Cartilage thickening
-Reduced blood supply to deeper structures
-Necrosis and “plug” development: spontaneous resolution, fissure/fragmentation
Pathogenesis continued
-Common predilection sites have thickened cartilage measurements in fetuses and neonates
-Nutrition: high grain diet - most often blamed as culprit
-Rapidly growing
-Genetics
Clinical Sigs
-Joint effusion
-Tarsocrural, femoropatellar
+/- lameness
-Higher incidence in purebred bulls
Diagnostics
-Arthrocentesis STERILE PREP!!
-Mild inflammation/protein increases
-TP<1g/dl and WBCs <5000/ul
-Radiographs: orthogonal views
-CT/MRI
-Ultrasound: depth and user skill limiting
Predilection sites
-Dependent on cited source
-Stifle»Tarsus»Fetlock
Stifle
-Lateral trochlear ridge»_space; Medial trochlear ridge»_space; trochlear groove»_space; Distal end of patella
Tarsus
-Distal intermediate ridge of the tibia»_space; lateral trochlear ridge of talus»_space; medial malleolus
Fetlock
-Dorsal aspect of sagittal ridge»_space; metacarpal/metatarsal condyles»_space; dorsal aspect of proximal phalanx
Treatment OCD
Medical management
-Stall rest
-Feed manipulation
-Slow growth
-NSAIDs
-Intraarticular treatment?
-Hyaluronic acid/GAGs
-Steroids
Stem cells?? PRP? IRAP? controversial
-Mesynchymal stem cell use has gained momentum globally.
-Staph mastitis treatment, show cattle lameness
Surgery
-Prognosis can be better
-Arthroscopy: debridement, reattach chondral flaps.
-Bone screws: bone cysts
Prognosis
-What is the goal? completely sound-show cattle: problematic
-Finish feeding period: fair to good
-Insurance dilemmas you may face: personal interpretation
-Prevention: Unknown at this time
Degenerative Joint Disease and Osteoarthritis
Clinical presentation
-Varies widely
-Minimal effusion: no palpable heat
-Any joint can become affected
-Distal/proximal interphalangeal joint
-Coxofemoral
-Stifle
**May be good to sue ultrasound to check for septic arthritis **
Diagnosis
-Challenging
-Radiographs: Osteophytes, joint space narrowing, subchondral bone sclerosis or cysts
-CT
-MRI
+/- ultrasound: effusion usually minimal
Treatment
-Medical management
-NSAIDs, Gabapentin, stall/pen rest, monitor diet
-Surgery
-Lesion amenable to treatment?
-Arthroscopy
-Worsens prognosis for other surgeries (CCL)
Prognosis
-Varies
-Reduced production
-Reduced milk, breeding difficulty.
-Poor if a result of previous infection
-Fair if from trauma
OA DJD
Lecture 4
Arthrogryposis
Contracted Tendons
Spastic Paresis “Elso Heel”
Spastic Syndrome
Gastrocnemius Tear/Avulsion
Peroneus tertius tear
Polymelia
Tibial Hemimelia
Downer Cow Syndrome
Arthrogryposis
Congenital contracture present at birth
-Genetics (can be tested)
Charlois cattle, Holstein, Angus
Charolais
-Spinal dysraphism
-Cleft palate
Holstein
-Vertebral malformation syndrome
-Agenesis
Angus
-Arthrogryposis multiplex/ “curly calf syndrome”
Other causes
-In-utero teratogen
-Lupines “CROOKED CALF”
-Viral infections: Akabane, Bluetongue, Schmallenberg.
Prognosis
-Poor
-Complicated by additional defects
-Unable to suckle
-Often born dead or die soon after
-Identify underlying cause, if there is one
-Dorsal tissue damage
Contracted Tendons
Cause
-Debatable
-Heritable: other congenital defects?
-In-utero malposition
-Must differentiated from arthrogryposis Taunt but not immovable
Treatment
-Caudal splints
-Slipper
-Tenotomy: SDF, DDF tendons, complications later
-Drug therapy? oxytetracycline?
Caudal Splint
-Location and function is key
-Adequate padding: especially accessory carpal
-Coronary band to elbow
-Hooves exposed: forces weight bearing. Exercise is important
-24 hours on and 24 hours off for about 3-4 days
Slipper application not a fan
-Forces weight on heel
-Types: PMMA (dental cement)
-Bovi-bond and block
-Slippers tend to pop off especially extreme cases, too much force exerted
forces stretch by putting more weight on the heel
Medical Management
-NSAIDs
-Need to be comfortable enough to exercise
Prognosis
- Either excellent or poor
-Worth trying
-Based on severity
-Sore development
-Supportive care
Spastic Paresis “ELSO HEEL”
-Young animals
-Onset at 2-9 months old
-Hind limb extension: unilateral or bilateral “SOLDIER WALK”
Cause
-Heritable
-Elso II - Friesian bull
-Adema 197 - British type bull
Treatment
-Cull
-Tibial neurectomy
-Grastocnemius tenotomy: DONT CUT SDF! transection
Prognosis
-Poor
-Corrective procedures: palliative at best, weight gain and production reduced
Spastic Syndrome
-Older animals
> 3 yrs old
-Progressive
Cause
-Heritable
Diagnosis
-Involuntary hindlimb extension
-Difficult standing
-Always look to be pushing forward
Prognosis
-Not recommended for breeding
-Culling recommended
-Can worsen to recumbency, Hobbles?
Gastrocnemius Tear/Avulsion
Causes
-Traumatic: hit by a car, 4-wheeler
-Secondary to metabolic disease causing the fall
-Additional nerve damage
-Locking loop repair doesn’t work well
Prognosis
-Poor to grave
-Unilateral vs. bilateral
-Support limb problems
Peroneus Tertius Tear
Traumatic
-Additional nerve damage
Medical management
-Pain medication
-Confinement
-Cull
Tibial Hemimelia (TH)
Congenital defect
-Simple autosomal recessive
-Shorthorns most notoriously
-Galloway
-Multiple breeds
Caudal abdominal hernias common
-Poor surgical candidates. Defect too large, not enough holding tissue, mesh does not hold.
Prognosis
-Poor
-Euthanasia recommended
Prevention
-Identify genetic carriers
Downer Cow Syndrome
AKA
-Compartment syndrome
-Crush Syndrome
-Downer
Cause
-Secondary problem
Top 5
Mastitis, Metritis, Musculoskeletal, Metabolic, Massive Infection
-Soft tissue muscle and nerve damage
Downer Cow Syndrome
Diagnostics
-CBC
-Chemistry
-Creatine Kinase (CK) muscle
-Aspartate Aminotranferase (AST) - liver, muscle, brain.
Values >171IU/L are 80% less likely to recover
-Lactase dehydrogenase (LDH) liver
CSF tap
-Can find lymphosarcoma/infection/inflammation
-Protein >0.39g/L or cell count >4.5
Look at ratio CK high AST low then Acute and vice versa
LONG HORN CATTLE can live long, so more likely to have lymphosarcoma in spinal cord
Treatment
-Prevent secondary complications
-Acute bloat
-Further muscle damage
-Recumbent care
-Rotate every 4-6 hours
-Passive range of motion (PROM)
-Hip lifter
-Float tank/aqua cow
Float tank/Aqua Cow
-Most ideal treatment
-Faster to treatment the better
-Down <24 hrs: 2.8 days avg floating
-Down >24 hrs: 5.3 days avg floating
-40-90% success rate, case selection
Pelvic Fractures
-Shaft of ileum
-Swaying gait
-Transrectal palpation
-Strict confinement
-Predispose to dystocia
Lecture 5
Infectious Nutritional Diseases
Hygromas
AKA
-Concrete Hocks
-Tarsal/Carpal Cellulitis
Chronic Cellulitis of epidermis, dermis and subcutis
-Periarticular to tarsus or carpus, DOES NOT involve the Joint
-Uncommon cause of lameness
Treatment
-LEAVE IT ALONE!
-Manipulation can introduce infection, much worse problem
-Aseptic prep and drain? risk
-Will come back
Prevention (CRUCIAL)
-Propper bedding
-Free stall design adjustment
-Neck rail placement
-Brisket tube placement
-Flex stalls
-Over/Under bedding
manure solids dry, recycled
Septic Arthritis/Osteomyelitis
Etiology and pathogenesis
-Primary: direct trauma seeding infection
-Secondary: extension of adjacent infection into joint
Hematogenous
-Predominantly calves: failure of passive transfer - E. coli
-Respiratory, alimentary, navel.
-Mycoplasma spp. challenging to confirm, mastitis milk, multiple joints (hallmark), Feedlot cattle
-Streptococcus spp. /Staphylococcus spp. Histophilus somni, Salmonella Dublin, E. coli especially calves Truepurella pyogenes
Clinical Signs
-Severe lameness (5/5)
-Draining wounds: viscous synovial fluid, pus
-Distented joints (carpus, tarsus, stifle, and fetlock), don’t forget the hip.
-Periarticular swelling, use ultrasound to determine joint involvement
-Systemic disease: pneumonia, endocarditis (necropsy or ultrasound), diarrhea, omphaphlebitis (inflammation navel)
Diagnosis
-Ultrasound
-Radiographs
-CBC: inflammatory leukogram, Left shift?
-Arthrocentesis
-Cytology
-Culture
-50% success rate at recovering pathogen, still try to culture, worth a shot.
-Blood culture? not very common, not terribly expensive
Septic arthritis/osteomyelitis
Septic Arthritis/Osteomyelitis
Treatment
-Joint lavage
-1st liter is most beneficial
-Antibiotics
-AMDUCA and withdrawal concerns
-Arthrotomy: if tissue is so thick they block needles. Tie over bandage
-Arthroscopy
-Large bore needle/Teat Cannulas: can break off
-Plaster of Paris Beads: antibiotic impregnated
-Ampicillin, Florfenicol, Gentemacin
-Withdrawals concern
-Pack wounds “slow release”
Arthrodesis
-Carpus, fetlock, proximal interphalangeal joint, distal interphalangeal joint.
-Amputation
-Prosthesis
Prognosis
-Good if Acute onset, no bony lesions
-Poor if Comorbidities, DJD, multiple joints, carpus/tarsus, Mycoplasma ssp. /T. pyogenes
Physitis
Etiology and pathogenesis
-Disburtance of endochondral ossification at the physis
-Most common developmental orthopedic disease
-Copper deficiency association
-Absorptive inhibition of zinc or molybdenum
-Divalent metal transporter 1 (DMT1)
-Rapid growth (genetic predisposition?)
-Diet (high CHOs, calcium imbalance)
-Slatted flooring
Clinical Signs
-Moderate to severe lameness
-Multiple areas can be affected
-Pain on palpation
+/- swelling, nodules heat
-Common locations: distal metacarpal/metatarsal, proximal physics P1
-Distal radius/tibia
-Similar locations in calves
Diagnosis
-Radiographs: sclerotic bone
-Ultrasound: concave appearance, irregular margins, fluid
-Culture and sensitivity
-Blood culture?
Treatment
-Diet manipulation if needed, take off CHOs
-Pain control NSAIDs, opioids (expensive for LA, morphine affordable, butephonol)
-Surgery
-Curette to healthy bone
-Septic material should be taken out
-Culture
-Post op care
Prognosis
-Good if early and aggressive treatment
-Concerns: infection, premature closure, angular limb deformities.
Clostridial Myositis “Blackleg”
AKA Blackleg
-Gram ( + )
-Produces endotoxins that are histotoxic
C. Cheauvoei
Pathogenesis
-Ubiquitous in environment
-Spore form
-Entry into the body: direct wound penetration of vegetative form
-Spore enter alimentary tract and settle in liver/muscle
-Becomes vegetative form when tissue devitalized
-Often associated with tetanus, microbe already in tissue, injury happens, or liver becomes compromised.
Classic, healthy young animal that suddenly dies, SQ emphysema, bubble wrap skin
Clostridial Myositis
C. Chauvoei gram +
Blackleg
Clinical Signs
- Healthy animals on high plane of nutrition
-Sudden death
-SQ emphysema (bubble wrap skin)
-Recent processing? usually more related to tetanus, dehorning, castration.
Diagnosis
-Necropsy: SQ emphysema, myonecrosis of affected areas
-Dark - colored
-Containing gas bubbles
-Serosanguinous fluid
-Rancid butter smell to tissue
-Can be confined to heart only
Treatment
-Usually fatal
-Penicillin IV
-Na, K, q4hrs or procaine form
-Historical drug of choice B-lactin drug
-Oxytetracycline: 6.6mg/kg q12-24hr
-Wound fenestration? permits oxygen into wound allowing less favorable environment for the bacteria
-Antitoxin probably the last effort
Prevention
-Vaccination
-“8-way vaccine” or “9-way” number of pathogens addressed by vaccine
-At least one dose of blackleg
-At least two doses for other clostridium spp.
-4-6mts of age ideally
-Often at processing, not always ideal timeframe
-Bury or burn diseased animals
White Muscle Disease
AKA
-Nutritional myodegeneration
-Nutritional rhabdomyolysis
Pathogenesis
-Oxidative damage to cell membranes and proteins
**Selinium is potent antioxidant (Vit E also) **
-Glutathione peroxidase: catalyzes reduction of H2O2 to water and oxygen
-Oxygen radicals scavengers
Clinical Signs
-Rapidly growing animals: deficient dams
-Selenium deficient areas or feed ration
Cardiac form: sudden death
Musculoskeletal form: stiff gait, rigid
Young animals on pasture are most susceptible
Diagnosis
-Chemistry: Marked elevations in CK, AST, LDH.
-Urinalysis: myoglobinuria, acute phase
-Selenium analysis: whole blood, muscle tissue
-Necropsy: coagulation necrosis, calcification, fibrosis
-Predilection sites in calves: left ventricle and septum. Type 1 muscle more commonly affected in yearling cattle.
-Sheep both ventricles can be affected
White Muscle Disease
Treatment
-Parenteral selenium
-0.055-0.067 mg/kg, can be toxic
-Vitamin E is preservative, not effective for treatment
-Oral vitamin E, water soluble, in feed, alpha-tocopherol
Prevention
-Adequate diet: legal limits exist
-Injectable forms: multimin, Bo-Se/Mu-Se
Prognosis
-Cardiac form: grave
-Musculoskeletal form: Fair-poor
Manganese Deficiency
AKA “Acorn calf”
-Enzyme cofactor
-Chondrodysplasia
-Teeth exposure: underdeveloped cartilaginous muzzle
-More prevalent in calves of 1st parity cows
-During winter: silage
-Divalent metal transporter 1 DMT-1: iron increase in diet decrease absorption of manganese
Rickets - very uncommon
-Disease of young, growing animals
-Largely nutritional: Phosphorus deficiency, Vitamin D deficiency, Calcium deficiency (rare)
-Predisposing factors: environmental (winter housing), ration/pasture deficiencies, genetics - not yet reported in cattle
Pathogenesis
-Growth plate mineralization failure
-Chondrocytes continue to elongate cartilage, possible reduction in type X collagen, prevents cell death.
-Blood vessel migration inhibition
-Results in rubbery, soft bones, wide growth plates, shorter bone length
Diagnosis
-Clinical signs and history
-Bowed limbs, physical swelling, lameness.
-Mineral evaluation: blood, rations/pasture mineral concerns if osteophasia
+/- radiographs
-Necropsy
Fescue Toxicity
AKA Fescue foot, Summer slump
Pathogenesis
-Tall fescue infected with Neotyphodium coenophialum
-Some texts use Epichloe coenophiala
Ergovaline: ergot alkaloid, vasoconstriction of arterioles
Clinical Sigs
-Within 21-42 days of exposure
-Lameness: particularly HIND LIMB. Swelling at coronary band, Gangrenous appearance develops. More common during winter
-Ears, tails, can also be affected
-Illthrift appearance with rough haricot and heat intolerant “summer slump”
-Unable to dissipate heat, severe clinical signs, fat necrosis
Fescue Toxicity
Diagnosis
-Cannot see Rhizome with the naked eye
->400-750 ppm in feed
-Testing fields: contact laboratory for sample: tillers, seed stems, seeds
-Histopathology: vascular thrombosis and necrosis
Prognosis
-Euthanasia recommended once lesions begin
Prevention
-Proper management of fescue pastures: 61% of fescue pastures infected in US
-Legume supplement
-Overseed with clover
-Sufficient strains
-Resistant strains
-Limit fertilization (nitrogen exacerbates toxicity)
Ergot Toxicity
AKA Ergotism
Etiology and pathogenesis
-Claviceps purpurea: fungus in Rye, other grains
-Ergot alkaloids: ergotamine and ergonovine (ergometrine)
-Vasoconstriction of arterioles, similar to ergot alkaloids
Diagnosis
-Visible plant infection
-Clinical signs and history
-Testing feed, hay, grain
Prognosis
-Poor if lesions develop.
-Immediate diet change
Prevention ideal
-Pasture control of known areas
Frosbite and Salmonellosis
Lecture 6
Musculoskeletal
Fracture overview and hoof trimming
Fractures
Most common: MTRH others rare
Cause
-Trauma
-High vs. low velocity trauma
-“Green-stick”
-Stepped on
-Caught in fences
-Iatrogenic
Nutritional
-Vitamin D
-Phosphorous
-Metacarpus/Metatarsus: ~50%
-Tibia: ~ 12%
-Radius/Ulna ~ 7%
-Humerus ~ <5%
-Rare: femur, pelvis, phalanges, vertebrae, ribs
Clinical signs
-Lameness 5/5
-Palpation: crepitus, distal limb pulses/temperature.
-Open/closed fracture common
Diagnosis
-Radiographs
-Ultrasound
-CT
Prognosis
Depends
Young <1 yr old
-Open and articular worst on distal limb
Adult > 2 yrs old
-Proximal limb, open, articular worst
Fractures - Repairs Basics
-Race to the finish: stabilization vs. fracture healing
-Stick to the basic principles
-Orthogonal views!!
-Mechanical, biological, situational factors
Basics to Hoof Trimming
Recommendation vary
-Beef, dairy, age, size, sex
-Toe length minimum - general 3.5-4 inches
-Heel length - 1.5 inches: usually not trimmed unless unbalanced
-Sole thickness: 0.25 inch (when soft to touch probably already too thin!)
Sedate bulls with Acepromazine
Clean the hoof
1. Shorten the toe: can use a grinder, Nippers (gotta be skilled with the angle) and sheers
2. Remove sole excess: knives or grinder
3. Level Heel
4. Balance claw and heel
5. Scallop out axial space “Slope the sole” be careful not to take out too much
If you miss up, Bovi-bond, bandaging - not aggressively tight just enough to stay on with antimicrobial
