This page is for referring vets. If you are a pet owner please click here.

Review Article: Atypical Arthritis

Arthritis is a very broad term referring to any condition resulting in inflammation of the joints. It is generally subdivided into three major categories; osteoarthritis, immune-mediated arthritis and infectious arthritis.

Osteoarthritis is a common degenerative disease for which diagnosis and treatment options are likely to be familiar.  On the other hand, immune-mediated and infectious arthropathies are seen much less frequently.  Treatment options and prognosis may vary dramatically depending on underlying aetiology and it is therefore useful to be familiar with the various different clinical presentations and diagnostic tools available.

Infective arthopathies

Primary infective arthopathies usually affect a single joint, resulting in obvious lameness and swelling.  In fact, since culture from synovial fluid is notoriously difficult, an infectious process should generally be assumed if there is only one joint involved.  However, certain infectious agents can induce polyarthritis (table 1, below)) and multiple joints may be affected if sepsis or endocarditis is an underlying trigger. 

Infectious Arthopathies and their Clinical Features

fig.1 — mediolateral radiograph of carpus. There is periarticular soft tissue swelling and a focal loss of bone density spanning the radiocarpal joint.

fig. 2 — STIR-MR-scan of carpus (radiograph fig.1) revealing extent of bony pathology across entire joint.

Bacterial infections are most common and result from either direct penetration or haematogenous spread (the later is more common in patients with pre-existing joint disease).  Diagnosis requires synovial fluid analysis (neutrophilic pleocytosis) with cytologic identification or culture of the infectious organism.  The radiographic appearance changes with time.  In the early stages, changes are minimal with soft tissue swelling and/or widening of the joint space secondary to joint effusion.  In chronic cases, radiographic changes may  include subchondral bone destruction, narrowing of the joint space and periosteal proliferation.  Fibrotic or bony ankylosis may also occur in severely affected cases.  MRI may be helpful in defining the extent of the pathology (see figs. 1&2). 






Immune-mediated arthopathies

In contrast to infectious arthritis, immune-mediated arthopathies generally affect multiple joints and may also involve other body systems (table 2, below). Generalised stiffness and pyrexia, with or without other systemic signs are most common. Only one third of patients with immune-mediated disease have obvious lameness, swelling or local lymphadenopathy. In fact, polyarthritis is one of the most common causes of pyrexia of unknown origin (PUO) and multiple joint taps (at least three joints) are often indicated where there is no obvious cause for persistent pyrexia.

Immune-mediated Arthropathies and their Clinical Features

Patients may develop primary (idiopathic) disease and certain individuals are believed to be genetically predisposed to immune-mediated pathology (as a result of their DLA allele composition). Secondary immune-mediated disease is triggered by an underlying infection, neoplasia or drug/vaccination reaction; base-line blood work and imaging is therefore essential in order to exclude this possibility before idiopathic disease can be diagnosed.

fig. 3 — dorsoplantar radiograph of talocrural joint. There are multiple punctuate lesions within the bones of the tarsus typical of the erosive form of the disease

fig. 4 - dorsopalmar view of metacarpophalangeal joints of a dog with chronic, immune mediated polyarthritis—there is a combination of widened (digits II & V, indicating joint effusion) and collapsed (digit III, indicating loss of articular cartilage) joint spaces & periarticular new bone formation.

Immune-mediated pathology results from cytotoxicity (type II hypersensitivity), immune-complex disease (type III hypersensitivity), cell-mediated immunity (type IV hypersensitivity) or a combination of these. However, as with infectious arthropathies, synovial fluid analysis invariably yields a neutrophilic pleocytosis regardless of underlying pathology. A distinction can often be made with histology (+/- immunohistochemistry) but synovial biopsy is rarely performed. In the clinical situation arthritis is therefore classified on its radiographic appearance, as either erosive (rheumatoid and periosteal proliferative) or non-erosive. In erosive forms (fig. 3), chronic synovitis leads to the proliferation of granulation tissue which invades articular cartilage eventually eroding into subchondral bone and resulting in joint deformity and secondary peri-articular new bone formation (fig. 4). In contrast, peri-articular soft tissue swelling may be the only radiographic feature noted in non-erosive disease.  Again, MR-imaging can be used to highlight pathology in joints that appear radiographically normal (particularly within the subchondral bone and periarticular soft tissues).  It is increasingly being used at Downs Referrals to obtain a more detailed assessment of the extent of joint disease.  This helps when deciding between treatment modalities (particularly on deciding whether surgery is appropriate) as well as increased accuracy when offering a prognosis.


Treatment and prognosis

If an underlying aetiology is not immediately apparent then NSAIDs are the mainstay of therapy while awaiting a diagnosis.

Medical treatment of infectious arthritis depends on the identified agent and, where possible, should be based on culture and sensitivity results (see table 1). Surgical debridement and serial joint lavage may also be required but this is usually reserved for those cases that fail to respond to medical management.

The prognosis for an infected joint largely depends on the specific organism involved and the degree of damage at presentation. In the case of immune-mediated disease, initial treatment is with corticosteroids (usually immunosuppressive doses of prednisolone). Additional immunosuppressive therapies such as cyclophosphamide or azathioprine are added in refractory cases. Any underlying disease should be treated specifically and patients should be monitored closely for secondary infections following immunosuppression. Monitoring can be done using synovial fluid cytology but most often the steroid dose is tailored according to clinical response. Relapse is not infrequent and steroid doses should be tapered cautiously. Although the clinical signs will eventually resolve in most cases, some patients do require life long therapy and erosive forms in particular may carry a poor prognosis (table 2, above).