Morphological modifications of the choroid plexus in a rodent model of acute ventriculitis induced by gram-negative liquoral sepsis. Possible implications in the pathophysiology of hypersecretory hydrocephalus.

Gram-negative bacterial infections of the central nervous system are generally associated with high morbidity and mortality rates. In patients with ventriculitis induced by gram-negative liquoral sepsis, a reduction in cerebrospinal fluid formation has been reported, suggesting that gram-negative ventriculitis is able per se to alter the normal functioning of the choroid plexus. The aim of the present study was to analyse, for the first time in the rat, the effects of acute ventriculitis on the ultrastructure of the choroid plexus. A simple and inexpensive experimental model of acute ventriculitis was developed: we injected into the cisterna magna of rats 10(3) CFU of live Escherichia coli, inducing septic ventriculitis without major neurological deficits. Histological examinations of rodent choroid plexus 24 h after the injection revealed patches of altered epithelium, with swollen and vacuolated ependymal cells associated with leukocyte infiltration. Electron microscopy demonstrated a reduced number of microvilli and flattening of the epithelial surface. These results (a) indicate that gram-negative septic ventriculitis is able to induce visible ultrastructural alterations of the choroid plexus which (b) are consistent with a picture of marked reduction of the functioning epithelial choroid plexus surface, and (c) highlight the potential usefulness of our rodent acute ventriculitis model for developing treatment modalities.