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 cruzi RA strain disclosed electromyographic signs (EMG) of neuropathic damage, while those infected with the myotropic CA-I strain showed EMG suggestive of primary muscle involvement. Although both strains induced inflammatory infiltrates in hamstring muscles (HM), damage was more severe in mice infected with CA-I. In sciatic nerves (SN) of mice infected with the RA strain, increased inflammatory changes, amastigote nests, 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. The RA strain induced chronic leptomeningitis in spinal cord (SC), while infiltrates were limited to spinal roots and dorsal ganglia in animals infected with CA-I. In mice infected with RA, phenotypic analysis of inflammatory lesions showed a consistent predominance of CD8+ T cells in nervous tissue throughout the course of infection and in HM during 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+ cells in SN was only detected during the acute phase and in HM during the late chronic phase; B lymphocytes bearing surface IgM were present in all studied tissues at 270 days pi. In addition, positive fluorescence for mouse IgG was observed at 120 days pi in muscle interstitium. These results strongly suggest that T. cruzi strain-dependent mechanisms are involved in the development of neuromyopathic damage.