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.