ISSN 2398-2969      

Arthritis: septic

icanis

Synonym(s): Bacterial arthritis


Introduction

  • Joint inflammation caused by infection.
  • Usually single joint (especially larger appendicular), may be polyarthritic (less commonly).
  • Cause: usually direct introduction of infection via wound, foreign body, injection, surgery, etc; may be hematogenous spread from remote focus of infection.
  • Signs: acute onset lameness, swollen, painful joint(s).
  • 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, traumatically exposed joint surfaces, foreign bodies, infected surgery, contaminated injections.
  • Hematogenous spread secondary to systemic spread, eg skin infections, cystitis Cystitis , pyelonephritis Kidney: pyelonephritis , prostatitis Acute prostatitis , peritonitis Peritonitis , pneumonia Lung: bacterial pneumonia - primary focus of infection often not identified.
  • Extension of adjacent soft tissue or bone infection (osteomyelitis Osteomyelitis ).
  • Concommitant bacterial endocarditis Endocarditis: bacterial.
  • 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.
  • 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.
  • Montgomery R D, Long I R Jr, Milton J L, DiPinto M N & Hunt J (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 8 (3), 501-510 PubMed.

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