Mycoplasma arthritidis Pathogenicity: Membranes, MAM, and MAV1

Abstract

In 1937, W. A. Collier, working in Java, came into possession of a wild rat with unusual swellings in its hind legs. When injected into laboratory rats, material from the lesions induced a migratory, inflammatory polyarthritis (29). In 1938, two researchers from Columbia University discovered a “pyogenic filterable agent,” possibly a virus, that induced a severe systemic infection with joint swelling, hind limb paralysis, and rapid weight loss on intravenous (iv) injection (91). At the same time, Emmy Klieneberger and her colleagues at the Lister Institute in London were systematically characterizing and classifying an unusual group of microorganisms called “pleuropneumonia-like organisms” (PPLO), which were turning up with remarkable regularity in a wide variety of animals. They had seen phenomena similar to those reported by the other two groups in both wild and laboratory rats, and, using Klieneberger’s “special medium,” succeeded in isolating the responsible agents and identifying them as PPLOs. These agents were designated L4 and L7 (37, 53). The Columbia University strain was shown to be identical to L4 (52, 90), although Collier’s strain was lost at the beginning of World War II before it could be thoroughly characterized (52). Over the next few years, similar isolates turned up in a variety of settings (37, 53, 65). Transplanted rat lymphosarcoma tissue proved to be an especially prolific source (43–45, 47, 91).