Felis ISSN 2398-2950

Arthritis: septic

Contributor(s): John Innes, Prof Walter Renberg, Eithne Comerford

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

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Treatment

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Carr A P (1997) Infectious arthritis in dogs and cats. Vet Medicine 92 (9), 786-797 VetMedResource.
  • Montgomery R D, Long I R Jr., Milton J L et al (1989) Comparison of aerobic culturette, synovial membrane biopsy and blood culture medium in detection of canine bacterial arthritis. Vet Surg 18 (4), 300-303 PubMed.
  • Brown S G (1978) Infectious arthritis and wounds of joints. Vet Clin North Am (3), 501-510 PubMed.


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