Introduction

• Joint inflammation caused by infection.
• Usually single joint (especially larger appendicular) with direct inoculation, may be polyarthritic (less commonly) if hematogenous.
• Cause: usually direct introduction of infection via wound, cat bite, foreign body, injection, surgery, etc; may be hematogenous spread from remote focus of infection. The joint affected may have been traumatized recently.
• Signs: acute onset lameness, swollen, painful joint(s) or gradual onset with mild clinical signs.
• Diagnosis: bacteriological culture and sensitivity of synovial fluid sample.
• Treatment: specific antibiotic therapy +/- joint lavage.
• Prognosis: depends on early diagnosis and treatment before irreversible joint damage has occurred.

Pathogenesis

Etiology

Single joint - commonly carpus, hock, stifle, hip.

• Penetrating wounds, cat bites, traumatically exposed joint surfaces, foreign bodies, infected surgery, contaminated injections.
• Hematogenous spread secondary to systemic spread, eg skin infections, cystitis Cystitis: bacterial, pyelonephritis  Pyelonephritis, prostatitis, peritonitis Peritonitis, pneumonia  - primary focus of infection often not identified.
• Extension of adjacent soft tissue or bone infection (osteomyelitis  Osteomyelitis).
• Concommitant bacterial endocarditis Endocarditis.
• Smaller joints of foot - usually due to penetrating wounds or spread from contiguous infection.

Polyarthritis

• Usually secondary to omphalophlebitis, mammary or uterine infection, streptococcal pharyngitis, septicemia, eg bacterial endocarditis.
• The formation and subsequent deposition of antigen-antibody complexes lead to inflammation in multiple joints.
• Often young relatively immunoincompetent animals.

Specific

• Factors affecting defense mechanisms.
• Immunosuppressive drugs.
• Joint trauma.

Pathophysiology

• Initially affects synovial membrane, later joint cavity.
• Infection    →   inflammation of synovium    →   hypercellular synovial fluid (polymorphs).
• Lysosomal granules released by polymorphs and synovial cells engulf bacteria    →   enzyme release    →   destruction of cartilage matrix    →   mechanical damage by pressure and grinding of joint movement.
• Fibrin deposits form in synovial fluid    →   deposited on cartilage surface    →   limit normal exchange of cartilage metabolites and nutrients to and from synovial fluid    →   further cartilage degeneration.
• Degree of articular damage depends on number, type and virulence of organism; local and general resistance of patient.
• Ligaments may be weakened by infection    →   joint instability, eg cranial cruciate rupture    →   significant progression of lameness.
• Cartilage destruction and exposure of subchondral bone - bony bridges develop between adjacent bones and around abscesses which form within exudate    →   fibrous or bony ankylosis    →   decreases range of joint movement.

Timecourse

• Days.

Diagnosis

Treatment

Outcomes