Equis ISSN 2398-2977

Joint: immune-mediated polysynovitis

Contributor(s): Steve Adair, Helen Herinckx, Clare Knottenbelt, Graham Munroe

Introduction

  • Cause: deposition of immune complexes, derived from foci of infection elsewhere, in capillary beds of synovial membrane   →   inflammation and synovitis.
  • History: other systemic diseases, eg pneumonia or diarrhea especiallyRhodococcus equi  Rhodococcus equi  ; stiffness and swellings of several limbs. Idiopathic cases are recorded in adults.
  • Signs: multiple shifting limb stiffness; multiple synovial distentions; evidence of other systemic diseases.
  • Diagnosis: synovial culture; synovial fluid cytology; identification of immune complexes in synovium.
  • Treatment: symptomatic. Systemic corticosteroids in adults with idiopathic form.
  • Prognosis: guarded to poor.

Pathogenesis

Etiology

  • Inflammatory foci elsewhere in body:
  • Auto-immune complexes may be involved in occasional causes and there may be a genetic predisposition in these individuals. Some of these cases may be triggered by vaccination or exposure to viruses.
  • Borrelia burgdorferi  Borrelia burgdorferi   has been suggested as a possible agent that could lead to this presentation but the evidence within the scientific literature is weak.
  • Idiopathic cases have been recorded in a number of adult horses that did not have any evidence of an underlying systemic disease.

Predisposing factors

General
  • Systemic infections.

Specific

  • Rhodococcus equiinfections.
  • Streptococcal infections.

Pathophysiology

  • Approximately one-third of foals withRhodococcus equipneumonia   Rhodococcus equi infection  exhibit immune-mediated non-septic polysynovitis. Indeed some clinicians believe it is an early manifestation of the disease process.
  • There are two proposed theories for this manifestation. The most commonly accepted is that immune complexes (antibody-antibody) formed elsewhere in the body are deposited in the capillary beds of synovial membranes of joints, sheaths and bursae    →   complement fixation, inflammatory reaction and synovitis.
  • The source of the immune complexes is usually foci of infection elsewhere in the body, most commonly the thorax. A less well accepted theory suggests that a bacteremia leads to a short-lived, septic polysynovitis which, following clearance of the organism from the body, leads to a longer-standing, non-septic inflammation in multiple synovial structures.
  • More unusually derivation of complexes may be of an auto-immune nature. Rheumatoid factor activity, where antibodies are raised against the Fc portion of the immunoglobulin, has been noted in the synovial fluid of foals withRhodococcus equipneumonia.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed papers

  • Recent references fromPubMedandVetMedResource.
  • Reuss S Met al(2009)Extrapulmonary disorders associated with Rhodococcus equi infection in foals: 150 cases (1987-2007).JAVMA235(7), 855PubMed.
  • Pusterla N, Pratt S M, Magdesian K G & Carlson G P (2006)Idiopathic immune-mediated polysynovitis in three horses.Vet Rec159(1), 13-15PubMed.
  • Lumsden J M (1990)Suspected immune-mediated polysynovitis and serositis in a horse.Aust Vet J67(12), 470-471PubMed.
  • Madison J Bet al(1988)Immune-mediated polysynovitis in four foals.JAVMA192(11), 1581-1584PubMed.
  • Sweeney C Ret al(1987)Rhodococcus equi pneumonia in 48 foals: response to antimicrobial therapy.Vet Microbiol14(3), 329PubMed.
  • Byars T Det al(1984)Non-erosive polysynovitis in a horse.Equine Vet J16(2), 141-143PubMed.


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