| First Author | Cookston M | Year | 1990 |
| Journal | Am J Pathol | Volume | 136 |
| Issue | 5 | Pages | 1137-45 |
| PubMed ID | 2349964 | Mgi Jnum | J:38146 |
| Mgi Id | MGI:85537 | Citation | Cookston M, et al. (1990) Eosinophilic myocarditis in CBA/J mice infected with Toxocara canis. Am J Pathol 136(5):1137-45 |
| abstractText | In humans, chronic eosinophilia has been associated clinically with endomyocardial fibrosis and myocardial damage. Mice infected with Toxocara canis have a marked eosinophilia, and develop eosinophil-rich granulomatous lesions in the soft tissues of the body, especially the lungs, liver, brain, and skeletal muscle. Few reports have described myocardial lesions associated with T. canis infections in mice. We examined the hearts of CBA/J mice killed at weekly intervals over an 8-week period for evidence of myocardial damage that might be attributable to eosinophils. Total white blood cell counts and eosinophil counts were obtained during this period, and revealed a peak white blood cell count of approximately 28,000 cells/mm3 at day 7 after infection and a peak eosinophil count of approximately 4,000 cells/mm3 at day 14 after infection. Myocardial lesions in the ventricular wall began as focal infiltrates of eosinophils and histiocytes, then progressed into granulomata containing necrotic debris. Collagen deposition was noted by day 21 after infection. By day 42 after infection, the lesions had contracted greatly because of a loss of cellularity, and consisted mainly of fibroblasts and hemosiderin-laden macrophages. Myocyte damage, characterized by increased eosinophilia and necrosis, was observed. T. canis-infected CBA/J mice thus offer a useful model to study eosinophil-dependent myocardial damage. |
