The Possible Relationship of the Pleuropneumonialike Organisms to Reiter's Disease, Rheumatoid Arthritis and Ulcerative Colitis

Abstract

The pleuropneumonia-like group of organisms has long been identified with the problem of chronic arthritis in many animal species. In 1898, Nocard and Roux isolated the first member of this group from cattle suffering from pleurisy, pneumonitis, and in a considerable percentage of the cases, from joint involvement. In 1923, Bridre and Donatien found a similar organism in sheep and goats suffering from agalactia, a syndrome which includes mastitis with glandular atrophy and suppression of lactation, chronic arthritis, keratitis, vesiculo-pustular skin eruptions, and in males, scrotal inflammation. The organism was isolated from the milk, conjunctivae, joint fluid, and blood stream.1 Further members of this group of organisms were first isolated by Klieneberger in 1935 in cultures from rats infected with Streptobacillus moniliformis. In the following few years, many strains were isolated from rats both alone and in association with the streptobacillus. Of these, the L4 strain of Woglom and Warren caused a pyogenic polyarthritis in rats and the L7 of Findlay et al.2 caused a spontaneous as well as transmissible and experimental polyarthritis in rats. This strain could also produce an arthritis when injected into mice. In the course of studies on mouse toxoplasmosis, Sabin3 isolated a new filtrable agent, later shown4,5 to be a pleuropneumonia-like organism (called strain A). This organism caused a neurological disorder in mice, called rolling disease by Findlay et al.,5 but if inoculated into older, more resistant mice, it induced a polyarthritis rather than the cerebellar disease.6 Other strains (B, C, D, E) were subsequently isolated' from the conjunctiva, nasal mucosa, and sometimes the brain, lung, and trachea of normal carrier mice. Of these, strain B,5 on intravenous inoculation, produced a chronic, proliferative, progressive arthritis in mice which clinically and pathologically bears a striking resemblance to human arthritis. Clinically there were typical rheumatoid fusiform swellings of the involved joints which often went on to chronicity and ankylosis. The organisms could be isolated from infected joints as late as 70 days after intravenous injection, though the blood stream was rendered sterile in 2 to 3 days. These various mouse strains all induced antibody responses in the host, but did not cross agglutinate and were not serologically identical. Pleuropneumonia-like microorganisms have likewise been found in dogs and guinea pigs' though not in relation to arthritis and also as saprophytes in sewage and decaying matter.' The close similarity of this experimental infection in mice to human arthritis led several workers8-I to study under controlled