FELINE CHRONIC PROGRESSIVE POLYARTHRITIS

  • 1 January 1980
    • journal article
    • research article
    • Vol. 41  (4) , 522-535
Abstract
Cats (20) with a chronic progressive polyarthritis were studied. The disorder occurred exclusively in male cats, and all but 6 of the cats were between 1.5 and 5.0 yr of age. There were 2 forms of the disease as determined by radiographic changes: joint instability and deformity and clinical course. The most prevalent form of the disease was characterized by osteopenia and periosteal new bone formation surrounding affected joints. Marginal periarticular erosions and collapse of the joint spaces with fibrous ankylosis occurred with time, but joint instability and deformities were not seen. The 2nd form of the disease was characterized by severe subchondral marginal erosions, joint instability and deformities. The periosteal proliferative form resembled Reiter''s arthritis of man and the deforming type resembled human rheumatoid arthritis. The disease began as tenosynovitis and synovitis, with subsequent changes in the articular cartilage and periosteal bone. Histopathologic changes in these cats were similar to those occurring in chronic Reiter''s and rheumatoid arthritis of man. Chronic progressive polyarthritis of cats was not caused by identifiable bacteria or mycoplasma, but was etiologically linked to feline leukemia virus (FeLV) and feline syncytia-forming virus (FeSFV) infections. The FeSFV was isolated from the blood or was detected by a serologic test in all cats with the disease, whereas FeLV was isolated or identified by immunofluorescence technique in 60% of the cats. Arthritis could not be reproduced by inoculation of cell-free synovial tissue from diseased cats or with tissue culture fluid containing FeSFV and FeLV isolates. Arthritis apparently was an uncommon manifestation of FeSFV infection that occurred in predisposed male cats. Feline leukemia virus may not have been directly involved in the disease, but may have acted in some way to potentiate the pathogenic effects of FeSFV.