not develop clinical measles. Three classes of immune globulin (IgA, IgG, and IgM) are produced and are detectable in the serum and nasal mucus of vaccinated subjects (Bellanti et al., 1969).

The standard test of immunity to measles is based on the detection of serum antibodies by the enzyme-linked immunosorbent assay method. Although the titers of these antibodies induced by the vaccine tend to be somewhat lower than those resulting from natural infection (Schwarz and Anderson, 1965), immunity acquired by vaccination is long-lasting (Krugman, 1983).


Following the administration of mumps vaccine, seroconversion is slower and the antibody titers achieved are lower than those following natural infection. A neutralizing antibody response can be detected in some recipients 2 weeks after vaccine administration; in others, it can be delayed for up to 6 weeks (Hilleman et al., 1968a,b). It is assumed that this immunity is long-lasting, but this has not yet been established.


Clinical Description

Encephalopathy refers to any acute or chronic acquired abnormality of, injury to, or impairment of the function of the brain. Symptoms can include alterations in state of consciousness or behavior, convulsions, headache, and focal neurologic deficits. Encephalitis refers to an encephalopathy caused by an inflammatory response in the brain. This is usually manifested with systemic constitutional symptoms, particularly pleocytosis of the cerebrospinal fluid (CSF). However, the terms encephalopathy and encephalitis have been used imprecisely and even interchangeably in the literature. The discussion that follows uses the terminologies of the authors of the reports. However, if the authors used the term encephalitis, but there was no documentation of pleocytosis in the CSF, "encephalitis" is used in quotation marks. The annual incidence of encephalitis for the years 1950 to 1981 in Olmsted County, Minnesota, was 7.4 per 100,000 people (Beghi et al., 1984; Nicolosi et al., 1986). The incidence in children less than age 1 year was 22.5, in children between ages 1 and 4 years it was 15.2, and in children between ages 5 and 9 years it was 30.2 per 100,000. Other estimates of encephalopathy for children less than age 2 years were somewhat lower than those reported by Beghi et al. and Nicolosi et al. cited above. Other estimates for annual incidence range from 5 per 100,000 people (Walker et al., 1988) to 10 per 100,000 people (Gale et al., 1990). Chapter 3 contains a discussion of encephalopathy.

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