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Updated: Jun 26, 2026

Parasite Induced Genetically Driven Autoimmune Chagas Heart Disease in the Chicken Model
Published on: July 29, 2012
The neuromuscular pathology of experimental Chagas' disease
H A Molina1, R L Cardoni, M T Rimoldi
1Department of Neuropathology, Instituto de Investigaciones Neurológicas Dr. Raul Carrea, FLENI, Buenos Aires, Argentina.
Abstract:
In this work, we describe skeletal muscle, neuromuscular junction, nerve and spinal cord lesions in the mouse model system of Chagas' disease. Myositis was a common finding and Trypanosoma cruzi amastigote nests were frequently found in the muscle fibers. Angular atrophy, targetoid fibers, groups of atrophic fibers, fibrosis, myofiber necrosis and phagocytosis of cellular debris were also observed. The neuromuscular junction studies showed degeneration of intramuscular nerve fibers, swelling and distortion of nerve endings and multiple ramifications on the same muscle fiber. Collateral, terminal and ultraterminal axonal sprouts were also present. Inflammatory neuropathy was seen in all of the infected mice. Demyelination, axonal degeneration, remyelination and axonal regeneration were observed in the transverse sections. There was an average reduction of 29% in the total number of myelin fibers. The teasing of single myelin fibers showed segmental and paranodal demyelination and remyelination more frequently than axonal degeneration and regeneration. The lumbar spinal cords presented inflammatory cell infiltration associated with tissue destruction. Amastigote nests were found in 3 out of the 8 infected mice studied. There was a mean loss of 21% of the large cytoneurons of the anterior horn of the lumbar spinal cord.
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