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Mice injected intravenously with Mycoplasma arthritidis developed a chronic arthritis which persisted through at least 269 days. Rats similarly treated developed an acute short-term infection. The mouse disease was characterized by periods of remission and exacerbation and was proliferative in nature, gradually spreading to adjacent joints. M. arthritidis strain 158 P10 was found to be less arthritogenic for mice than for rats, but further passage of this strain in mice substantially increased its virulence. Unlike rats, mice appeared to be susceptible to a "toxin" of M. arthritidis and they developed a necrotic spreading abscess after subcutaneous administration of the organisms. Histopathological studies revealed that mice varied greatly in the degree of joint inflammation, destruction, and repair. The disease was characterized by (i) an initial acute phase with infiltration of the articular and periarticular tissues with polymorphonuclear leukocytes and a mild hyperplasia of the synovial membrane; (ii) a mixed acute-chronic phase in which new areas of acute inflammation developed alongside areas of chronic lesions; (iii) a chronic phase followed which was characterized by massive synovial proliferation with mononuclear cell infiltration, irregularity in the articulating cartilage, pannus formation, and "punched out" defects in cortical bone near cartilagenous osseous junctures. The clinical course and histopathological characteristics of the chronic phase of mouse arthritis induced by M. arthritidis closely resembled those of rheumatoid arthritis of man.
Cole et al. (Fri,) studied this question.