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
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 8 (3), 501-510 PubMed.