Serious central nervous system (CNS) disturbances, and death in some instances, occurred in 23 (18%) of 125 Meriones unguiculatus (Mongolian jirds) infected with Dipetalonema viteae. D. viteae was found in the CNS of 17 (74%) of these animals. The principal signs observed were hemiplegia, paraplegia, and ataxia. The majority of cases developed between 30 and 90 days following infection (range: 19 days to 191/2 months). Infection with as few as 19 larvae and as many as 200 resulted in invasion of the CNS. One worm at most was found in the CNS of any animal. All worms in the CNS were 5th stage, the majority being gravid females. Most worms were found in subcutaneous sites, and in and on the surface of muscles; they also penetrated the spleen, liver, stomach wall, and epicardium. Inflammatory lesions developed early in the infection, and many organisms were encapsulated and eventually killed. Various types of lesions encountered in the CNS and in other organs are described and discussed. The evidence indicates that invasion of the CNS is a fortuitous event, the worm entering through a foramen in the base of the skull or between vertebrae. Attention is directed to the possible invasion of the CNS of man by filariae. D. viteae developed to maturity in M. hurrianae, but not in Pachyuromys duprasi natronensis; in neither of these 2 species did invasion of the CNS occur. Various nematodes have been reported to invade the central nervous system (CNS) of man and animals. Among the filarial worms one species, Setaria digitata, has been principally incriminated as a cause of disease. The natural hosts of S. digitata are cattle and water buffalo (Shoho, 1956), and in these animals the parasite resides in the peritoneal cavity. In certain strains of abnormal hosts (sheep, goats, horses), the immature organism may invade the CNS to give rise to lumbar paralysis, or as it has subsequently been termed, cerebrospinal nematodiasis (Innes, Shoho, and Pillai, 1952). Such invasion may also occur in the normal host, but with a considerably lower frequency (Shoho, 1956). The experimental production of cerebrospinal nematodiasis in goats in Japan was reported by Ishii et al. (1953). Comprehensive reviews of the disease have been published by Innes, Shoho, and Received for publication 14 June 1973. * Laboratory of Parasitic Diseases, NIAID, NIH, Bethesda, Maryland 20014. Present address: Department of Biology, University of Notre Dame, Notre Dame, Indiana 46556. t Laboratory of Experimental Pathology, National Institute of Arthritis and Metabolic Diseases, NIH, Bethesda, Maryland 20014, and Armed Forces Institute of Pathology, Washington, D. C. 20305. Present address: Department of Pathology, University of Arkansas Medical Center, Little Rock, Arkansas. Pillai (1952), Innes and Shoho (1953), Shoho (1955), Innes and Saunders (1962), and Ander on (1968). One other filarial species has been found to invade the CNS of mammals. A case was r ported in Japan of the presence of adult worms of Dirofilaria immitis in the lateral ventricles of a dog suspected to be rabid (Taguchi, Takehara, and Uriu, 1959), and cerebral infarction caused by several adult D. immitis was observed in a dog in the United States (Patton and Garner, 1970). Presumptive evidence exists of the invasion of the CNS of man by Acanthocheilonema perstans based on the findings of microfilariae resembling those of A. perstans in the spinal fluid in association with neurological disorders (Dukes et al., 1968). The present study concerns the invasion of the CNS of the jird, Meriones unguiculatus, by the filarial worm Dipetalonema viteae under experimental laboratory conditions, with the production of severe disease, and death in some instances. The study was initiated when it was observed in the first group of infected jirds intended for stock infections that a number of animals exhibited CNS disorders associated with the presence of D. viteae in the nervous system. A preliminary report of some of the findings has been published previously (Weinstein and Highman, 1965).