EXPERIMENTALLY-INDUCED SEPTIC ARTHRITIS IN CHIMPANZEES INFECTED WITH MYCOPLASMA-HOMINIS, MYCOPLASMA-PNEUMONIAE, AND UREAPLASMA-UREALYTICUM

Mycoplasma hominis was isolated in pure culture from septic synovial a spirates from an individual (patient A) during 16 different bouts of e xacerbation over a 70-month period of observation. Two isolates, 10(7) and also 10(6) color-changing units (CCU) of the 1620 isolate and 5 X 10(4) CCU of the 1628 isolate, caused inflammation in chimpanzees ino culated intraarticularly. Inflammation was also induced with 10(7) CCU of the 2010B isolate, serovar VII of Ureaplasma urealyticum, recovere d from an agammaglobulinemic individual (patient B) with septic polyar thritis and with 3 X 10(6) CCU of the PI-1428 isolate of Mycoplasma pn eumoniae. Inflammation persisted for up to 36 days and was self-limiti ng. The aspirates contained up to 220,000 white blood cells/mm(3) and up to 10(7) CCU/mL. There was good correlation between the severity of inflammation and the numbers of organisms, but antibody was not detec ted in aspirates during the peak severity of disease. As the numbers o f organisms decreased, detectable levels of antibody increased, thus s uggesting that antibody may have been bound to antigen. Chimpanzees pr eviously infected with either the 1628 isolate of M. hominis or the 20 10B isolate of U. urealyticum were protected on challenge with > 100 t imes the minimal dose causing arthritis. Chimpanzees showed little or no inflammation when inoculated intraarticularly with 5 X 10(8) CCU of the type strain PG-21 of M. hominis or with the type strain CO of U. urealyticum or when inoculated intravenously with 3 X 10(8) CCU of the arthrogenic 1620 isolate of M. hominis.