Chronic erysipelas polyarthritis in pigs is considered to be an animal model closely resembling human rheumatoid arthritis. In an experimental study using SPF pigs infected with Erysipelothrix rhusiopathiae several immunopathological aspects were studied for up to 14 months after infection. After an initial febrile phase a progressive polyarthritis and discospondylitis developed at 2 weeks after infection. Quantitative determination of IgG and IgM revealed a significant increase in these immunoglobulins both in the serum and the synovia from arthritic joints. Arthritic joints containing viable Erysipelothrix bacteria at termination of the experiment have a higher content of IgG and IgM than bacteriologically negative joints. During the entire experiment the rheumatoid factor titer, determined by the Waaler Rose test, remained relatively low with increases and decreases. The Erysipelothrix antibody titers are highly significant. The total complement activity in the serum increases discontinuously and shows fluctuations similar to those of the rheumatoid factor titer. The highest enzyme activities of acid phosphatase and lactate dehydrogenase are demonstrable in the synovial fluid of arthritic joints with positive bacteriological or immunohistological findings. These joints also have the greatest numbers of IgG-producing plasma cells. By means of immunohistological methods Erysipelothrix antigen can be demonstrated in macrophages of the proliferating synovial membrane. Finally, there is a discussion of the pathogenic significance for the perpetuation of chronic polyarthritis of Erysipelothrix persisting in arthritic joints in spite of focal immune reactions.

Severe polyarthritis was induced in 42 SPF piglets by subcutaneous and intraarticular infection in one joint of the bacterium Erysipelothrix rhusiopathiae (Serotype B, strain T 28), which in its chronic stage morphologically resembles human c.P. The light and electron microscopic examination of the articular cartilage and synovial membrane reveals a parallel evolution of hyaline cartilage degeneration, and activation and proliferation of synovial lining cells. The initial cartilage alteration with demasking of collagen fibrils and focal degeneration of chondrocytes in the erysipelas model is caused by direct action of the microbial agent, fibrin and few granulocytes Erysipelothrix bacteria and neutrophilic granulocytes are able to invade the superficial and intermediate cartilage layers. This model is not considered a suppurative infectious arthritis. In chronic villous erysipelas polyarthritis, which develops without the presence of neutrophils in the cartilage, the invasively growing synovial pannus dominates, which deeply destroys the pre-damaged cartilage, resulting in macroscopic focal or wide-spread cartilage erosion. We consider the poorly vascularized cartilage and the particular fibrosis suitable sites for the extremely long (up to three years) persistence of this microbial agent. The persistence of the agent is considered necessary for the persisting immunological reactions and the perpetuation of erysipelas polyarthritis. With longer duration (1-3 years) of experimental erysipelas polyarthritis the number of bacteriologically positive arthritic joint decreases. Microscopically, the causative bacteria may only sporadically identified.

Comparative studies in man indicate a possible primary infectious aetiology of chronic polyarthritis, in spite of the pathogenetically important immunological processes and proven genetical predisposition [17]. This presumption is supported by the wide range of spontaneous, chronic polyarthritides in animal species. One of these primary infectious, secondarily mediated by immunological mechanisms and genetically predisposed, spontaneous diseases is the erysipelas infection.

The chronic Erysipelas-polyarthritis in pigs has been considered an animal model resembling human rheumatoid arthritis. Fifteen specifically pathogenfree (SPF) pigs 45 days old were experimentally infectec with strain T 28 of Erysipelothrix rhusiopathiae-bacteria. During the subsequent 32 weeks several enzymatic, immunohistological and microbiological parameters were monitored. Compared to 5 age and sex matched healthy controls the infected pigs showed increased activity of plasma acid phosphatase starting 4 weeks after the infection. Acid phosphatase activity was usually enhanced in synovial fluid of chronically ill animals. Histochemically increased activity of acid phosphatase, beta-glucuronidase and beta-acetylglucosaminidase was found in lining cells and fibroblasts of the synovial membrane of chronically diseased joints. Immunohistochemically Erysipelas-antigen was demonstrated in the synovial membrane even of those inflamed joints from which no living bacteria had been isolated. The microbiological and immunohistochemical results correlated positively with the enzymehistochemical data. The release of lysosomal enzymes from cells of the synovial membrane in chronically diseased joints due to the influence of Erysipelas-bacteria and the possible implications of persistent bacteria on the perpetuation of chronic Erysipelas-polyarthritis are discussed.