Multiple sclerosis (MS) is an acquired inflammatory disease of the central nervous system (CNS) of uncertain etiology. On the basis of the available evidence, it seems probable that MS is a complex disease in which exposure to one or more environmental agents predisposes genetically susceptible individuals to develop immunologically mediated CNS demyelination and axonal injury. In terms of the environment, the degree or type of exposure to solar ultraviolet radiation, smoked meat, vitamin D, vaccines, organic solvents, cigarette smoking, cold damp weather, workplace environment, and stress have all been suggested as predisposing to MS; however, it is likely on epidemiologic considerations that any such contribution is probably secondary rather than primary (see Chapter 1). There is also considerable indirect support for the role of infection in initiating and perhaps perpetuating the inflammatory pathology that results in neurologic symptoms and disability (1,2). Over the past decade, several novel exogenous agents have been identified in MS brain or cerebrospinal fluid (CSF) (3-5), raising the possibility that antiviral or antibacterial drugs could alter disease prognosis. While the specificity of these findings is in doubt, interest in an infectious cause of MS remains strong.

This chapter comprises a critical review of evidence for and against an infectious etiology of MS.

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