Skeletal muscle pathology in 2 siblings infected with Toxoplasma gondii

Calore, E.E.; Minkovski, R.; Khoury, Z.; Seguro, A.C.; Perez Calore, N.M.; Cavaliere, M.J.

Journal of Rheumatology 27(6): 1556-1559

2000


ISSN/ISBN: 0315-162X
PMID: 10852291
Document Number: 513023
Skeletal muscle can be the site of inflammatory diseases that lead to muscle weakness, pain and increased myogenic serum enzymes. Most of these myopathies are idiopathic but some cases are due to infectious agents. The pathological aspects of muscle biopsies of 2 Brazilian siblings who acquired toxoplasmosis at the same time and in similar conditions are described. One developed a tetraplegia that was confirmed to be due to inflammatory myositis due to Toxoplasma gondii (case 1). The other developed myocarditis, with heart failure, without skeletal muscle weakness (case 2). In both cases many T. gondii organisms were observed in the muscle biopsies, but only in case 1 was there an inflammatory myopathy with myofibre necrosis; the inflammatory cells were predominantly macrophages with some CD4+ cells and rare CD20+ cells. Expression of CD54 was observed in many inflammatory cells as well in endothelial cells in case 1, but only in endothelial cells in case 2. Treatment with clindamycin and corticosteroids resulted in only partial improvement in both cases: case 1 had residual muscle weakness and case 2 had residual cardiac insufficiency (requiring digoxin). These cases show that the presence of T. gondii in myofibres is not enough to induce inflammatory myositis with muscle cell necrosis, suggesting that immunological disturbances may contribute to the development of inflammatory myositis due to T. gondii.

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