Pathogenesis of Salmonella-associated arithritis in the rat.

The distribution of joint lesions in rats with Salmonella-associated arthritis (SSA), as determined in a detailed survey, resembles to a great extent the pattern of small joint involvement in human rheumatoid arthritis. Such lesions, though regularly induced in the rat by the intravenous injection of live S.enteritidis, could not be evoked by the heat-killed organisms injected by various routes with and without extrinsic adjuvants. Efforts to transfer SAA from sensitized donors to either normal or primed recipients, employing lymphoid ce-ls from several sources, also failed repeatedly. Two observations, however, virtually exclude the possibility that joint damage in SAA can be the direct result of sustained intra-articular sepsis. First, the inoculation of as many as 10-3 viable inflammation. Second, the incidence of SAA was significantly lower in weanling rats in the adult controls although the growth and distribution of intravenously injected S. enteritidis was virtually identical in the two groups. Together these observations indicate that the joint damage occurring in SAA is determined by the host and not by the infecting organism. From this, it seems fair to conclude that the destructive arthritis characteristic of this syndrome is immunologically mediated.