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Cerebral anomalies in congenital murine toxoplasmosis: a preliminary report
1Department of Infectious Diseases, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Gravid Nya: NYLAR strain mice were infected with Toxoplasma gondii on embryonic day 7. During the remaining 12 days of gestation, considerable fetal wastage occurred. At birth, pups were sickly and growth-stunted, and postnatal mortality was high. After 1 month, surviving weanlings were killed and autopsied. Coronal sections of the cerebrum revealed: numerous cortical and periventricular cystic cavitations, some undergoing calcification; ventricular enlargement and marked periventricular edema; subependymal nodules bulging into the ventricles; loss of subependymal germinal cells; and meningeal and perivascular inflammation. We suggest, as a working hypothesis, that hematogenously transported parasites invaded the vascular endothelium of the fetal cerebrum, inducing endothelial cell activation, recruitment of inflammatory cells, and focal inflammatory lesions in the endothelium. These inflammatory lesions triggered an intravascular coagulopathy, leading to the formation and deposition of microthrombi in cerebral capillaries and the development of numerous infarcts. Hypoxic-ischemic necrosis of the infarcted tissues led to the creation of the cystic cavitations.
Gravid Nya: NYLAR strain mice were infected with Toxoplasma gondii on embryonic day 7. During the remaining 12 days of gestation, considerable fetal wastage occurred. At birth, pups were sickly and growth-stunted, and postnatal mortality was high. After 1 month, surviving weanlings were killed and autopsied. Coronal sections of the cerebrum revealed: numerous cortical and periventricular cystic cavitations, some undergoing calcification; ventricular enlargement and marked periventricular edema; subependymal nodules bulging into the ventricles; loss of subependymal germinal cells; and meningeal and perivascular inflammation. We suggest, as a working hypothesis, that hematogenously transported parasites invaded the vascular endothelium of the fetal cerebrum, inducing endothelial cell activation, recruitment of inflammatory cells, and focal inflammatory lesions in the endothelium. These inflammatory lesions triggered an intravascular coagulopathy, leading to the formation and deposition of microthrombi in cerebral capillaries and the development of numerous infarcts. Hypoxic-ischemic necrosis of the infarcted tissues led to the creation of the cystic cavitations.