NAVLE Musculoskeletal

Equine Arthritis: Septic and Non-Septic – NAVLE Study Guide

Arthritis in horses encompasses a spectrum of inflammatory joint diseases that significantly impact equine health, performance, and welfare.

Overview and Clinical Importance

Arthritis in horses encompasses a spectrum of inflammatory joint diseases that significantly impact equine health, performance, and welfare. Understanding the distinction between septic (infectious) arthritis and non-septic arthritis (including osteoarthritis/degenerative joint disease) is critical for NAVLE success. Septic arthritis represents a true veterinary emergency requiring immediate intervention, while osteoarthritis (OA) accounts for approximately 60% of all equine lameness cases and is the leading cause of poor performance in athletic horses.

Route Description Common Bacteria
Hematogenous Most common in FOALS; spread from umbilicus, lungs, or GI tract Enterobacteriaceae (E. coli most common), Salmonella, Actinobacillus
Traumatic/Wounds Penetrating injuries, lacerations near joints; most common in ADULTS Mixed flora: Gram-positive, Gram-negative, and anaerobes
Iatrogenic Post intra-articular injection or surgery; increased risk with corticosteroids Staphylococcus aureus, Streptococcus spp., coagulase-negative Staphylococci
Adult Horses Foals
Lameness: Acute onset, moderate to severe (AAEP 3-5/5), rapidly progressive Joint effusion: Marked swelling, heat, pain on palpation Systemic signs: Variable; fever, tachycardia in severe cases Wound/drainage: May be present; draining joints may be LESS lame Fever: Often PRECEDES lameness Lameness: May develop 8-24 hours after infection; sometimes subtle Multiple joints: Common with hematogenous spread Recumbency: Increased lying time; decubital ulcers Septicemia signs: Depression, poor suckle, diarrhea

Part 1: Septic Arthritis

Definition and Pathophysiology

Septic arthritis (SA) is a joint infection caused by bacterial invasion of the synovial space. It represents a potentially life-threatening or career-ending emergency requiring immediate veterinary attention. The synovial membrane is highly susceptible to infection because it lacks a basement membrane, allowing rapid bacterial colonization.

Pathophysiologic Cascade: Bacterial invasion triggers an inflammatory response with release of cytokines (IL-1, TNF-alpha) and degradative enzymes (matrix metalloproteinases). This leads to synovial membrane inflammation, fibrin accumulation, cartilage degradation, and potentially subchondral bone destruction. Without treatment, irreversible cartilage damage can occur within 24-48 hours.

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