Camelidae and Cervidae Lameness – NAVLE Study Guide

Overview and Clinical Importance

Lameness in camelids (llamas and alpacas) and cervids (deer and elk) represents an important diagnostic challenge on the NAVLE. These species have unique anatomical features, distinct disease predispositions, and specific management considerations that differentiate them from other large animal species. Understanding the causes, clinical presentation, and treatment of lameness in these animals is essential for veterinary practice in mixed practices and zoological settings.

Camelids are considered excellent orthopedic patients due to their relatively low body weight, tolerance of external coaptation devices, ability to ambulate on three legs postoperatively, and acceptance of prolonged recumbency. Cervids present unique challenges due to their stress susceptibility, flight responses, and the emerging threat of chronic wasting disease (CWD) which can present with neurological signs mimicking musculoskeletal disorders.

Part I: Camelidae Lameness

Unique Anatomical Features

Camelids have several anatomical peculiarities that distinguish them from other large animal species and affect their musculoskeletal conditions:

Foot Structure: Camelids bear weight on both P2 (second phalanx) and P3 (third phalanx) rather than just on P3 as with most large animal species. There is no navicular bone. They walk on double pads with a claw (nail) in front. The claw is non-weight-bearing but provides traction and propulsion. A digital cushion supports both P2 and P3.

Joint Anatomy: In most camelids, the medial and lateral compartments of the fetlock joint are separate (unlike in cattle). The superficial digital flexor tendon has a direct fascial connection to the proximal suspensory ligament, so issues with one tend to impact both.

Limb Conformation: Mild bilateral carpal valgus is prevalent in both llamas and alpacas and is considered normal within certain limits.

Common Causes of Lameness in Camelids

Vitamin D Deficiency and Hypophosphatemic Rickets

South American camelids are highly susceptible to vitamin D deficiency, particularly during winter months at locations away from the equator and at low altitudes. This manifests clinically as hypophosphatemic rickets in growing animals.

Pathophysiology

Vitamin D is synthesized in the skin through UV light exposure. During winter, reduced UV light leads to vitamin D deficiency, resulting in secondary hypophosphatemia. Llamas and alpacas appear to poorly absorb dietary vitamin D and have a higher requirement compared to other ruminant species.

Clinical Signs

• Stunted growth compared to age-matched herdmates
• Angular limb deformities (especially carpal valgus)
• Shifting leg lameness with joint enlargement (especially carpus)
• Hunched back posture (kyphosis) due to pain
• Lethargy and decreased appetite
• Reluctance to move
• Swollen, painful joints

Risk Factors

• Fall-born crias (September-February) at highest risk
• Dark-coated animals (reduced UV absorption)
• Nursing crias 3-6 months of age
• Geographic location away from equator
• Low altitude regions with cloudy winters

Diagnosis

• Serum biochemistry: Low phosphorus, variable calcium, low 25-hydroxycholecalciferol (vitamin D3)
• Radiography: Metaphyseal and epiphyseal flaring, physeal ectasia (widening), irregular growth plates
• Note: Blood samples must be processed promptly (spin off plasma) for accurate vitamin D measurement

Treatment and Prevention

Angular Limb Deformities (ALD)

Angular limb deformity is defined as valgus (lateral/outward) or varus (medial/inward) deviation of a limb. The deformity is named for the joint at which the deviation begins and the direction of the deviated portion.

Etiology

• Vitamin D deficiency/hypophosphatemic rickets (most common)
• Dystocia with limb manipulation
• Prematurity
• Congenital/genetic factors
• Trauma to growth plate

Treatment Options

Fracture Management in Camelids

Camelids are considered excellent orthopedic patients due to: relatively low body weight, tolerance of external coaptation devices, ability to ambulate on three legs postoperatively, acceptance of prolonged recumbency, stoic nature, and high commercial value motivating owner compliance with treatment.

Common Fracture Sites

The most common fractures in camelids (in order of frequency) are: Metacarpus/Metatarsus (approximately 50%), Tibia (approximately 12%), Radius/Ulna (approximately 7%), Humerus (less than 5%), and Femur (variable).

Treatment Options

Prognosis and Complications

Complication rates vary widely (23-87% in studies) depending on definition of complications. Common complications include: lameness (most common), osteomyelitis, malunion/delayed union/nonunion, sequestrum formation, implant failure, and soft tissue complications. Open fractures are more likely to have complications associated with healing, repair, and infection than closed fractures.

Shoulder Luxation in Alpacas

Shoulder luxation is an important cause of sudden-onset, non-weight-bearing forelimb lameness in camelids, particularly in male alpacas following fighting. The injury occurs when the animal lands and twists simultaneously during combat.

Clinical Presentation

• Sudden onset, severe non-weight-bearing lameness
• History of fighting (males) or trauma

Diagnosis and Treatment

• Radiographs to confirm and rule out concurrent fractures
• Closed reduction under heavy sedation (ideally same day as injury)
• Sling application to maintain inward pressure on humerus for approximately 2 weeks
• Stall rest with anti-inflammatory medications
• Surgical reduction may be required if delayed or recurrent

Exam Focus: If delayed more than 24 hours, muscle contraction makes closed reduction extremely difficult. Males with shoulder luxation are prone to recurrence if permitted to fight again; separate from other breeding males.

Septic Arthritis in Camelids

Septic arthritis in camelids occurs mainly secondary to lacerations, traumatic injuries, or penetrating wounds. Bacteremia in neonates (failure of passive transfer) may result in joint sepsis, although this is less common in camelids than in foals.

Important Anatomical Consideration

Communication between all joint compartments may vary within the carpus and tarsus of individual llamas. Therefore, each compartment should be sampled separately for joint fluid cytology and contrast radiography to determine joint communications before treatment.

Diagnosis

• Severe lameness with joint distention, heat, and pain
• Synovial fluid: cloudy/turbid, greater than 30,000 WBC/mL, protein greater than 4 g/dL
• Cytology: greater than 80% neutrophils, degenerative changes
• Culture may be negative even with true sepsis

Treatment

• Joint lavage and drainage
• Systemic antimicrobials (2-3 weeks minimum)
• NSAIDs for pain and inflammation
• Facilitated ankylosis may be considered for distal interphalangeal joint

Part II: Cervidae Lameness

Overview of Cervid Musculoskeletal Disease

Cervids (deer, elk, moose, caribou, reindeer) present unique challenges for lameness evaluation due to their stress susceptibility, flight responses, and limited opportunities for physical examination. Important causes of lameness include infectious diseases (treponeme-associated hoof disease), trauma, degenerative conditions, and systemic diseases that can mimic musculoskeletal disorders.

Treponeme-Associated Hoof Disease (TAHD) in Elk

Treponeme-associated hoof disease (TAHD), also called elk hoof disease, is a serious emerging condition primarily affecting Roosevelt and Rocky Mountain elk in the Pacific Northwest United States. It was first identified in southwestern Washington elk herds between the late 1990s and early 2000s.

Etiology

The disease is caused by treponeme bacteria, related to those causing digital dermatitis (hairy heel wart) in cattle and contagious ovine digital dermatitis (CODD) in sheep. Whether the disease can be shared between livestock and elk is currently unknown.

Clinical Signs

• Lameness ranging from mild to severe non-weight-bearing
• Deformed, overgrown, broken, or sloughed hooves
• Painful lesions causing abnormal gait
• May affect any elk, young or old, male or female
• Some bulls develop contralateral antler deformities

Diagnosis

• Clinical examination by trained veterinarians
• Laboratory testing to identify treponeme bacteria
• Post-mortem examination of hooves
• Differentiate from trauma, other hoof diseases, or chronic wasting disease

Treatment and Management

Treatment of free-living wildlife is extremely difficult. In livestock, similar hoof diseases are treated with repeated antibiotics and foot baths, but these interventions are not practical for wild elk populations. Management focuses on monitoring, surveillance, and population-level approaches.

Chronic Wasting Disease (CWD) - Differential for Cervid Lameness

Chronic wasting disease (CWD) is a fatal, neurological transmissible spongiform encephalopathy (TSE) affecting deer, elk, moose, and reindeer. While primarily a neurological disease, CWD can present with clinical signs that may initially appear as musculoskeletal issues, making it an important differential for lameness in cervids.

Etiology

CWD is caused by misfolded prion proteins (PrP) that accumulate in the brain and nervous system. It is transmitted through direct animal contact and environmental contamination (saliva, urine, feces, carcasses). Prions persist in the environment for years.

Clinical Signs

Important Points

• Incubation period: 18-24 months average before clinical signs appear
• CWD is ALWAYS FATAL - no vaccine or treatment exists
• Diagnosis requires post-mortem testing of lymph nodes or brain tissue
• Currently detected in 36+ US states, 4 Canadian provinces, and Scandinavia

Traumatic Injuries in Cervids

Trauma is a significant cause of lameness in both wild and farmed cervids. Vehicle collisions are particularly common, with over 1.5 million deer-vehicle collisions occurring annually in the United States.

Fracture Management Considerations

• Wild cervids: Extremely difficult to treat; stress of capture and restraint often contraindicated
• Conservative management (rest, minimal disturbance) may allow some fractures to heal
• Fractures above the tarsus/carpus in wild deer may be left to natural healing or euthanasia considered
• Farmed cervids: Treatment similar to other ungulates when feasible
• Long-acting neuroleptics can reduce anxiety during treatment

Foot Rot and Infectious Pododermatitis

While true contagious foot rot (Dichelobacter nodosus) is primarily a disease of sheep, deer and other cervids can be affected by similar hoof infections. Fusobacterium necrophorum by itself can lead to severe foot disease in deer.

Clinical Signs

• Lameness affecting one or more feet
• Interdigital swelling and inflammation
• Foul-smelling necrotic discharge
• Separation of hoof horn in severe cases

Memory Aids

Camelid Lameness: "VITAMIN D-FAN"

Vitamin D deficiency - most common metabolic cause Infection (septic arthritis, osteomyelitis) Trauma (fractures, shoulder luxation) Angular limb deformities Management issues (overgrown nails, wet conditions) Interdigital dermatitis Neonatal septicemia (crias)

D-FAN = Dark-coated, Fall-born, At low Altitude, during wiNter - Risk factors for rickets!

CWD Clinical Signs: "WASTED"

Weight loss (progressive) Ataxia/stumbling Salivation excessive Thirst/urination increased Ears drooping Death always (100% fatal)