Young C3H mice infected with Toxoplasma gondii are a novel experimental model of communicating hydrocephalus.

The effects of leptomeningeal inflammation on the development of hydrocephalus are less understood than those of obstructing the flow of cerebrospinal fluid (CSF) in animal models. We succeeded in introducing a novel experimental model of hydrocephalus and analysed changes in histopathology and CSF flow in mice infected with an avirulent Fukaya strain of Toxoplasma gondii (T. gondii). Six to 7 week-old male mice were orally inoculated with a brain homogenate containing ten T. gondii cysts. The cerebral ventricles became enlarged in all C3H/HeN and C57BL/6 mice 4 weeks after T. gondii infection, but mildly in BALB/c mice. In addition to the lateral ventricle, the third and fourth ventricles and Sylvian aqueducts were dilated in all mice. Lymphocytes and monocytes infiltrated the subarachnoid space. Indian ink particles required more time to pass from the lateral ventricle to the cervical lymph nodes, although they reached the subarachnoid space. Computed tomography ventriculography demonstrated that the CSF was not obstructed during passage through the ventricular systems, but contrast remained static in the lateral ventricle only in infected mice. These results indicated that the infected mice developed communicating type hydrocephalus without obstructive or mass lesions in the ventricles. The hydrocephalus that arises in mice infected with T. gondii is considered a consequence of leptomeningeal inflammation that blocks CSF circulation at the subarachnoid space, implying that leptomeningeal inflammation is important in other types of hydrocephalus.