Epidemiology and Risk Factors. Measles is one of the three major infectious diseases worldwide and causes about 1.5 million childhood deaths per year. y In the 1960s, prior to routine childhood immunization, more than 400,000 cases of measles were reported annually; in comparison, less than 4000 cases were reported annually in the early 1980s. From 1988 to 1990, the incidence of measles increased eightfold. y Between 1987 and 1990, 52,846 cases of measles were reported to the CDC.y This marked increase in the number of cases of measles was attributed to outbreaks among unvaccinated preschool-age children and to outbreaks among vaccinated school-age children who had received only a single dose of measles vaccine. y

Encephalitis is a rare complication of measles infection. It occurs in one of three distinct types: (1) postinfectious or autoimmune encephalomyelitis, which presents as a sudden recurrence of fever with an altered level of consciousness, seizure activity, and multifocal neurological signs during convalescence from measles; (2) subacute sclerosing panencephalitis (SSPE), which presents after a latent period of 6 years or more from an acute measles infection and has an insidious onset of neurological dysfunction associated with myoclonus and seizure activity; it progresses to coma and death within 1 to 2 years; and (3) subacute measles encephalitis (subacute inclusion body encephalopathy, progressive infectious measles encephalitis), which most commonly occurs in immunosuppressed individuals after a latent period of 1 to 10 months between the measles-like illness and the encephalitis. y y y Encephalomyelitis occurs in 1 per 1000 individuals who develop measles (mostly in older persons), and between 5 and 10 children per million who contract measles develop subacute sclerosing panencephalitis. y

Pathogenesis and Pathophysiology. Measles virus is spread by respiratory droplets, and only a small amount of virus is required to produce the infection. Virus replicates in the respiratory tract and then spreads to the local lymphatic tissues. Amplification of virus in the lymph nodes produces a primary viremia that results in the spread of virus to multiple lymphoid tissues and the skin, kidney, gastrointestinal tract, and liver. In these organs, the virus replicates in endothelial cells, epithelial cells, and monocytes and macrophages. Measles virus can be detected in peripheral blood leukocytes at the time of onset of prodromal symptoms and for several days after the onset of the rash. The fusion of the measles virus-infected cells leads to the formation of multinucleated giant cells, a pathological hallmark of this infection.^

Postmeasles encephalomyelitis (postinfectious encephalomyelitis, autoimmune encephalomyelitis) is a perivenular demyelinating disease rather than an inclusion body encephalitis. Histologically, the lesions resemble those induced experimentally by injection of animals with myelin proteins with adjuvant, that is, experimental, autoimmune encephalomyelitis.^ There is little evidence of virus in the brain, as assessed either by virus isolation and antigen and RNA detection or by the appearance of measles virus- specific antibody in the cerebrospinal fluid. y

The pathogenesis of subacute sclerosing panencephalitis and of subacute measles encephalitis has, however, been attributed to measles virus persistence in the central nervous system.y , y The histological features of SSPE include inflammatory infiltrates, glial nodules, degeneration of neurons, hyperplasia of astrocytes and microglia, and intranuclear inclusion bodies of Cowdry type A with abundant measles virus antigen. y The histological diagnostic features of subacute measles encephalitis include intranuclear eosinophilic, and sometimes intracytoplasmic, inclusion bodies in neurons and oligodendrocytes with abundant paramyxovirus nucleocapsids and measles virus antigen. y , y

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