EXPERIMENTAL CHAGAS-DISEASE - ELECTROPHYSIOLOGY AND CELL COMPOSITION OF THE NEUROMYOPATHIC INFLAMMATORY LESIONS IN MICE INFECTED WITH A MYOTROPIC AND A PANTROPIC STRAIN OF TRYPANOSOMA-CRUZI

C3H/HeN mice infected with the pantropic/reticulotropic Trypanosoma cr uzi RA strain disclosed electromyographic signs (EMG) of neuropathic d amage, while those infected with the myotropic CA-I strain showed EMG suggestive of primary muscle involvement. Although both strains induce d inflammatory infiltrates in hamstring muscles (HM), damage was more severe in mice infected with CA-I. In sciatic nerves (SN) of mice infe cted with the RA strain, increased inflammatory changes, amastigote ne sts, and myelin digestion chambers were consistently found during the course of infection. On the other hand, the CA-I strain produced minor inflammatory changes without detectable amastigotes in such tissue. T he RA strain induced chronic leptomeningitis in spinal cord (SC), whil e infiltrates were limited to spinal roots and dorsal ganglia in anima ls infected with CA-I. In mice infected with RA, phenotypic analysis o f inflammatory lesions showed a consistent predominance of CD8+ T cell s in nervous tissue throughout the course of infection and in HM durin g the chronic phase whereas natural killer cells were detected at 120 and 270 days pi. In mice infected with CA-I, a predominance of CD8+ ce lls in SN was only detected during the acute phase and in HM during th e late chronic phase; B lymphocytes bearing surface IgM were present i n all studied tissues at 270 days pi. In addition, positive fluorescen ce for mouse IgG was observed at 120 days pi in muscle interstitium. T hese results strongly suggest that T. cruzi strain-dependent mechanism s are involved in the development of neuromyopathic damage. (C) 1994 A cademic Press, Inc.