11.20.2025 - LAM2 - food animal review
Locomotion & Lameness Evaluation
5-Point Dairy Cattle Locomotion Scoring System
Score 1 – Normal
Gait: Normal; stands and walks normally.
Back posture standing: Flat back.
Back posture walking: Flat back.
Score 2 – Mildly lame
Gait: Normal to slightly abnormal gait (subtle changes only).
Back posture standing: Flat back.
Back posture walking: Arches back during ambulation (arched topline only visible when walking).
Score 3 – Moderately lame
Gait: Shortened phase of the stride (short-striding).
Back posture standing: Stands with an arched back.
Back posture walking: Walks with an arched back (arched topline both at rest and in motion).
Score 4 – Lame
Gait: Obvious diminished weight bearing in one or more limbs; cow clearly favors one or more limb(s).
Back posture standing: Arched back topline when standing.
Back posture walking: Arched back topline when walking.
Score 5 – Severely lame
Gait: Inability or extreme reluctance to bear weight on one or more limbs; may be non-weight bearing or recumbent.
Back posture standing & walking: Constantly arched back (severe, persistent topline arch).
Radiographic / Clinical Findings & Severe Lameness
Common causes of severe lameness in cattle include:
Arthritis (septic or degenerative) of distal joints.
Fractured distal third metacarpal.
Deep digital sepsis.
Interdigital phlegmon (foot rot).
Euthanasia vs. Salvage in End-Stage Lameness
Score 5 locomotion is defined as “severely lame; inability or extreme reluctance to bear weight (non-weight bearing or recumbent)” with a constantly arched back.
Chronic grade 5 lameness implies prolonged, severe pain and non-weight-bearing / recumbency.
Sending such an animal to a sale barn or slaughter would not be consistent with humane care. Therefore, the appropriate decision for end-stage chronic grade 5 lameness is euthanasia rather than salvage.
Hoof Trimming & Non-Infectious Foot Lesions
Dutch 5-Step Hoof-Trimming Method
Step 1 – Trim the first claw
Hindlimbs: medial claw; Forelimbs: lateral claw.
Establish correct toe length: 8 cm.
Establish correct sole thickness: 7 mm.
Step 2 – Trim the second claw
Trim the second claw so that toe length matches the first claw and sole is level with the first claw (same sole thickness).
Step 3 – Model (dish) out sole ulcer site
Create a dish or model over zone 4 (typical Rusterholz sole-ulcer site) to reduce weight bearing over this area.
Step 4 – Therapeutic trimming
For painful claws: relieve weight off the painful claw, treat lesions appropriately, place a claw block on the sound partner claw to shift weight.
Step 5 – Therapeutic trimming: horn & heel work
Remove loose or under-run horn; remove hard ridges at the heels to prevent abnormal weight distribution.
These steps aim to restore proper length, balance, and weight distribution, unload diseased areas, and remove diseased horn.
Distinguishing Non-Infectious Lesions
Rusterholz sole ulcer
Zone: Zone 4 (typical sole-ulcer area under the flexor process of P3).
Clinical presentation: affects the lateral claw of the hindlimbs, especially in dairy cattle.
Lesion morphology: ulceration at the typical sole-ulcer site; exposed/protruding corium.
White line disease
Zone: Zone 3.
Clinical presentation: separation of the wall from the sole at the white line, can progress to the coronary band, causes subsolar separation (underrun sole).
Lesion morphology: cracks or separations in the white line with subsolar tracts.
Toe ulcer / abscess (toe-tip necrosis)
Zone: Zone 5 + white line lesions in zones 1 & 2.
Clinical presentation/etiology: often associated with cranial rotation of P3 in heavy bulls OR thin soles in all types of cattle.
Lesion morphology: ulcer or abscess at the toe tip; may have undermined wall and tracts toward P3.
Therapeutic Trimming Strategies
Rusterholz sole ulcer
Remove weight-bearing by applying a claw block to the healthy claw; sloping and thinning the horn around the protruding corium; remove all loose horn around the lesion.
White line disease
Remove all loose horn; debride tracts so infected or undermined horn is eliminated.
Toe ulcer/abscess (toe-tip necrosis)
Debride the lesion; remove undermined wall; specifically look for a sequestrum from P3.
General strategy from Steps 4–5
Unload the painful claw (blocks, trimming patterns); debride until all loose/underrun horn and infected material are removed; maintain appropriate toe length (8 cm) and sole thickness (7 mm) to prevent recurrence.
Infectious Foot Diseases
Identification, Agents, Lesions
Digital dermatitis (DD)
Also called hairy heel warts, strawberry foot.
Location: plantar aspect of hindlimbs.
Lameness: ± lameness; severity varies by disease stage.
Lesion character: “hairy” or strawberry-like erosive/proliferative lesions at the heel.
Agents: Treponema spp. (spirochetes) plus anaerobes.
Interdigital dermatitis
Also called stable footrot, slurry heel, scald.
Location: hindlimbs, both claws, interdigital skin.
Lameness: rare or mild; more of a superficial dermatitis.
Lesion character: mild infection in interdigital space; chronic cases lead to heel-horn erosion.
Agent: Dichelobacter nodosus.
Foot rot
Also called interdigital phlegmon, interdigital necrobacillosis.
Lameness: severe lameness, acute onset.
Lesion character: necrotizing inflammation of interdigital and digital tissues.
Agents: Fusobacterium necrophorum plus anaerobes.
Treatments & Footbath Management
Digital dermatitis
Individual treatment: bandage + tetracycline (topical).
Herd-level control: footbaths using: copper sulfate (CuSO₄), zinc sulfate (ZnSO₄), formalin, possibly antibiotics, thymol, or organic options.
Foot trimming where needed plus properly designed and managed footbaths as key tools in controlling lameness associated with DD.
Interdigital dermatitis
Treat only if lame; topical antibiotic + light bandage; improve hygiene: keep feet dry/clean.
Foot rot (interdigital phlegmon)
Systemic antibiotics; local debridement, topical antibiotics, light bandage; NSAIDs for pain/inflammation.
Preventive Protocols
Environmental hygiene is central:
Keeping feet dry and clean is explicitly mentioned for interdigital dermatitis and implied for DD/foot rot.
Footbath programs (with properly designed and managed baths containing CuSO₄, ZnSO₄, formalin, or other options) are the main herd-level biosecurity/hygiene strategy against digital dermatitis.
Prevention emphasizes:
Good housing and manure management (to reduce slurry exposure).
Routine footbaths.
Early treatment of clinical cases to reduce infectious load.
Musculoskeletal Disorders of the Hindlimb
Reciprocal Apparatus: Anatomy & Ruptures
Key Structures
Fibularis (peroneus) tertius
Gastrocnemius
Rupture of the Fibularis Tertius
Diagnosis: "Rupture of the fibularis (peroneus) tertius."
Effect on joint movement:
On stifle extension → tarsus (hock) does not extend normally; stifle and hock no longer move together.
Prognosis: Good with stall rest ± NSAIDs.
Rupture of the Gastrocnemius
Diagnosis: "Rupture of the gastrocnemius."
Effect on movement:
Extension of the stifle is impaired; flexion of the tarsus (hock) is affected, breaking the normal reciprocal movement.
Prognosis: Poor – euthanasia is recommended.
Prognosis Summary
Loss of the reciprocal apparatus disrupts linked flexion/extension of stifle and hock, and gastrocnemius rupture carries a grave prognosis compared to fibularis tertius rupture.
Patellar Abnormalities
Bilateral Lateral Patellar Luxation
Etiology: congenital (malformation of the stifle) or secondary to femoral-nerve paralysis (quadriceps muscle atrophy).
Clinical description: crouched position (dog-sitting posture); inability to extend the stifle, bear weight, or extend the affected limb.
Prognosis / treatment: guarded prognosis; few reported surgical options (lateral release, medial imbrication, trochlear wedge resection).
Upward Fixation of the Patella
Etiology: patella locked on the medial trochlear ridge of the femur; breed predisposition implied.
Clinical description: inability to flex the stifle; the stifle is locked in rigid extension; affected limb held in a caudal position; increased toe wear on that limb.
Prognosis / treatment: good prognosis with desmotomy of the medial patellar ligament; important differentials listed: spastic paresis (Elso heel), dorsal coxofemoral luxation.
Prognosis & Treatment Options
Fibularis Tertius Rupture
Prognosis: Good.
Treatment: Stall rest ± NSAIDs.
Gastrocnemius Rupture
Prognosis: Poor.
Treatment: Euthanasia.
Bilateral Lateral Patellar Luxation
Prognosis: Guarded.
Treatment: Limited options; a few reported surgical options (lateral release, medial imbrication, trochlear wedge resection).
Upward Fixation of the Patella
Prognosis: Good.
Treatment: Medial patellar ligament desmotomy.
Reticulorumen Anatomy & Physiology
Primary vs. Secondary Contractions, Pathways
Primary (Mixing) Contraction
Involves contractions of reticulum, then dorsal sac, then ventral sac, with involvement of cranial and caudal pillars.
Function is to mix ingesta and move it around the different sacs.
Secondary (Eructation) Contraction
Involves gas movement toward the cardia and esophagus for eructation.
Neural / Chemical Control of Rumen Motility
Key afferent signals:
Rumen distention (stretch receptors)
Moderate distention → increases rumen motility and rumination.
Severe distention (bloat) → cessation of rumen motility.
Abomasal distention
Decreases rumen motility, reducing flow of ingesta through the reticulum-omasal orifice into the abomasum.
Ingesta consistency (tension receptors)
Solid, fibrous mat → stimulates receptors → increases motility.
Highly fluid rumen ingesta → low muscle tension → decreases motility.
pH, VFA concentration, osmolality (chemoreceptors)
Decreasing pH (rumen acidosis) or increasing VFA concentration → suppresses rumen motility.
Buccal receptor stimulation during feeding → increases contraction rate.
Additional inhibitors of motility: systemic disease, increased sympathetic tone (stress, pain, fear).
Rumen Fluid Analysis (Physical, Chemical, Microscopic)
Physical Characteristics: Color, consistency, odor, and sedimentation activity test.
Microscopic Exam: Quantitative exam (counts of organisms) and qualitative exam (morphology, activity of protozoa and bacteria).
Chemical Characteristics / Tests:
pH
Methylene blue reduction test (MBRT) – assesses anaerobic fermentation / redox potential.
Glucose fermentation test – digestion of carbohydrates.
Cellulose digestion test – digestion of fibers.
Nitrate reduction test – digestion of protein.
Rumen fluid chloride – normal 15–30 mEq/L; elevated indicates abnormal gastric outflow or reflux.
Normal MBRT: methylene blue reduced within 2–6 minutes, indicating active anaerobic flora.
An abnormal MBRT (slowed reduction) would be associated with rumen acidosis or altered flora, especially with indigestible roughage or dietary problems.
Rumen Dysfunction & Bloat
Free-gas vs Frothy Bloat
Both are important conditions of the reticulorumen, but the document lacks detailed mechanisms.
Vagal indigestion Types I–IV and their pathophysiology are noted, with Type I being free gas bloat (failure to eructate).
Vagal Indigestion Types I–IV
Type I – Free gas bloat (failure to eructate)
Gas from rumen fermentation stays in dorsal cap instead of being expelled during secondary contractions.
Examples of diseases: pneumonia in calves, choke (esophageal obstruction).
Type II – Omasal transport failure
Feed bolus stops in the reticulum instead of moving into the omasum.
Disease examples: traumatic reticuloperitonitis (TRP), liver abscesses.
Type III – Abomasal stasis
Progression of feed is stopped in the antrum of the abomasum instead of moving toward the pylorus.
Examples: abomasal ulcers, abomasal impaction, foreign bodies or bezoars in the abomasum.
Type IV – Late pregnancy / pyloric outflow obstruction
Progression of feed stops at the pylorus instead of entering the cranial duodenum.
Examples: late gestation, pyloric lymphoma.
Abdominal Contour Patterns
Links body shape to intra-abdominal conditions:
Normal – normal contour.
Bloat – bilateral distension, more dorsal.
Ascites / intestinal obstruction – associated with these contours.
Hhydrops / severe ascites.
Cecocolic volvulus / abomasal volvulus.
OTF (omasal/abomasal impaction).
Various shapes: pear, apple, papple-type silhouettes with a specific case question linking papple shape to vagal indigestion.
Metabolic & Fluid Therapy Calculations
Fluid Deficit from % Dehydration
Formula:
ext{% dehydration} imes ext{body weight (kg)} = ext{fluid deficit (L)}
Bicarbonate Requirement & Isotonic Bicarb Volume
Amount of bicarbonate needed (mmol or mEq):
Adults:
Neonates:
This yields mmol (mEq) of bicarbonate required.
Volume of isotonic bicarbonate (1.3% NaHCO₃):
Isotonic bicarb contains 150 mmol/L.
Volume (L) needed:
In practice, correct half the calculated deficit, then reassess the patient.
Application to Clinical Cases
These formulas can be applied in cases of metabolic acidosis due to diarrhea, grain overload, or other causes.
Worked examples are not provided in this document.
Abomasal Physiology & Disease
Liptak Test and Abomasal pH
Liptak test: Needle aspiration of fluid at the location where you auscultate a ping; purpose is to differentiate LDA ping from a rumen void ping.
Abomasal content pH:
pH < 4.5 is stated as abomasal; an aspirated fluid from a left-sided ping site supports an abomasal origin (e.g., LDA) if pH < 4.5.
Abomasal Ulcer Types I–IV
Type I: Non-perforating ulcer with limited blood loss.
Type II: Non-perforating ulcer with severe blood loss (bleeding type).
Type III: Perforating ulcer with local peritonitis.
Type IV: Perforating ulcer with diffuse peritonitis.
Type II leads to clinical importance regarding blood transfusion calculations, though precise transfusion formulas are not provided.
Abomasal Displacements: Types
LDA (Left Displaced Abomasum)
RDA (Right Displaced Abomasum)
Abomasal Volvulus (counterclockwise rotation).
Digestive Triad (bloodwork) associated with abomasal displacement/volvulus:
Hypochloremic
Hypokalemic
Metabolic alkalosis (increased bicarbonate).
Urine pH in Ruminants:
Normal urine pH: 7.0–8.7 (alkaline).
In abomasal volvulus, urine becomes acidic, a notable clinical sign.
Neonatal Calf Diarrhea
Causative Agents and Age of Onset
Timeline for calf diarrhea agents with:
E. coli (ETEC, K99)
E. coli (EHEC)
Rotavirus
Coronavirus
Cryptosporidium
Clostridium perfringens
Salmonella
Giardia
BVDV
Nematodiasis
Coccidia (Eimeria)
Different pathogens have characteristic age-of-onset windows; age ranges are not specified in detail.
Diarrheal Mechanisms
Secretory Diarrhea
Defined as: fluid-filled intestines without mucosal damage or hemorrhage.
Associated agents: ETEC (enterotoxigenic E. coli), Rotavirus.
Mucohemorrhagic Enterocolitis
Characterized by: fresh blood and mucus in feces, mucosal damage, petechiation, and hemorrhage.
Associated agents: EHEC (enterohemorrhagic E. coli), Coronavirus, Salmonella, Coccidia, Type C Clostridium perfringens (hemorrhagic enterocolitis).
Malabsorption
Mechanism: decreased absorptive surface due to blunting/atrophy of villi.
Associated agents: Rotavirus, Coronavirus, Cryptosporidium (noted as “foul smelling”).
Treatment & Prevention (Colostrum, Hygiene)
Treatment should be targeted to the specific agent and mechanism (secretory vs hemorrhagic vs malabsorptive).
Prevention emphasizes good hygiene (implied) and colostrum management (volume, timing, IgG levels are not detailed).
Adult Ruminant GI Diseases
Johne’s, Salmonellosis, BVD, Winter Dysentery
Important adult GI diseases: Salmonella, Johne’s disease (paratuberculosis) = Mycobacterium avium subspecies paratuberculosis (MAP), BVD (bovine viral diarrhea), Bovine coronavirus (winter dysentery).
Malignant catarrhal fever (MCF): Ovine herpesvirus type 2 (North America), Alcelaphine herpesvirus type 1 (wildebeest-associated MCF).
Clinical features and diagnostic indicators for these diseases are not described in detail.
Clostridial Diseases
Clostridium perfringens (types A, C, D common in North America):
Type A: Causes abomasitis and enteritis in calves; linked to dietary factors and poor milk quality.
Type C: Causes hemorrhagic enterocolitis in calves less than 10 days old.
Type D: Causes enterotoxemia in lambs and goat kids (“pulpy kidney”).
Clostridium novyi
Type B: Infectious necrotic hepatitis (“black disease”) in adult sheep, secondary to liver damage caused by Fasciola hepatica.
Type D (hemolyticum): Causes bacillary hemoglobinuria (“red water”) in calves > 1 year old, also follows Fasciola infection.
Oral & Upper GI Diseases
Vesicular Diseases (VS, FMD, Bovine Papular Stomatitis)
Important vesicular diseases discussed, but details such as species affected, incubation time, zoonotic status, and reportable disease status are not provided.
Actinomycosis (“Lumpy Jaw”) vs Actinobacillosis (“Wooden Tongue”)
Actinomycosis is treated with sodium iodide.
Sodium iodide can cause iodinism; specific clinical signs of iodinism are not listed.
Distinct clinical presentations and etiologic agents for actinomycosis vs. actinobacillosis are mentioned but not detailed.
Summary
This extensive review PDF covers key areas including locomotion scoring, hoof trimming, foot lesions, musculoskeletal problems, reticulorumen function, and various gastrointestinal conditions. It includes questions for further understanding but lacks some specific answers, particularly for agent timelines and treatment protocols.