In uncomplicated infection recovery begins soon after the appearance of the rash. However, complications will occur in up to 40% of all patients, the risk of a complication being higher for the very young or for adults and in undernutrition. Mortality is highest in infants and younger children. Complications most commonly are respiratory, and pneumonia causes most measles-associated deaths. The pneumonia risk is higher with immune suppression, which can be induced systemically by the virus itself or local immune dysfunction can occur locally within the lungs. The pneumonia infecting agent can be the measles virus itself, another secondary virus, or by secondary bacterial infections. Measles virus in immunocompromised patients will cause
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Post-measles encephalomyelitis will affect approximately one in 1,000 patients, usually older children and adults. The encephalomyelitis usually occurs within 2 weeks following onset of the rash and is characterized by recurrence of fever plus seizures and various other neurological abnormalities. The absence of measles virus in the brain, periventricular demyelination, and demonstration of an immune response to a myelin basic protein all suggest post-measles encephalomyelitis occurs due to an autoimmune disorder that is triggered by the measles virus. Other CNS complications of measles can occur months to years after acute infection: measles inclusion body encephalitis and subacute sclerosing panencephalitis (SSPE), both caused by persistent measles virus infection. Measles inclusion body encephalitis is fatal and is due to progressive neurological deterioration that affects individuals with defects of cellular immunity. SSPE occurs in about one in 10,000–100,000 patients, most often children infected before 2 years old, and usually 5–15 years after measles infection. It is characterized by seizures plus progressive deterioration of cognitive and motor functions and eventual death. [Measles immunization has led to a dramatic decrease in the incidence of
Post-measles encephalomyelitis will affect approximately one in 1,000 patients, usually older children and adults. The encephalomyelitis usually occurs within 2 weeks following onset of the rash and is characterized by recurrence of fever plus seizures and various other neurological abnormalities. The absence of measles virus in the brain, periventricular demyelination, and demonstration of an immune response to a myelin basic protein all suggest post-measles encephalomyelitis occurs due to an autoimmune disorder that is triggered by the measles virus. Other CNS complications of measles can occur months to years after acute infection: measles inclusion body encephalitis and subacute sclerosing panencephalitis (SSPE), both caused by persistent measles virus infection. Measles inclusion body encephalitis is fatal and is due to progressive neurological deterioration that affects individuals with defects of cellular immunity. SSPE occurs in about one in 10,000–100,000 patients, most often children infected before 2 years old, and usually 5–15 years after measles infection. It is characterized by seizures plus progressive deterioration of cognitive and motor functions and eventual death. [Measles immunization has led to a dramatic decrease in the incidence of