USMLE – Measles
Measles (rubeola) virus is the cause of 1.5 million deaths per year among third world children, who by reasons of poor nutrition are 10 to 1000 times more likely to die of measles pneumonia than are Western children. In the United States, the incidence of measles has decreased dramatically since 1963, when a measles vaccine was licensed. However, epidemics of measles affecting as many as 10,000 children still occur among unvaccinated individuals and among vaccinated individuals who did not develop protective immunity (primary vaccine failure).
Measles virus is an RNA virus of the paramyxovirus family that includes mumps, respiratory syncytial virus (the major cause of lower respiratory infections in infants), and parainfluenza virus (the cause of croup). There is only one strain of measles virus. It has an envelope that contains a hemagglutinin that binds to many host cells by CD46, a complement regulatory protein that inactivates C3 convertases. Measles virus is spread by respiratory droplets and multiplies within upper respiratory epithelial cells and mononuclear cells, including Band T lymphocytes and macrophages. A transient viremia spreads the measles virus throughout the body and may cause croup, pneumonia, diarrhea with protein-losing enteropathy, keratitis with scarring and blindness, encephalitis, and hemorrhages (“black measles”). Most children, however, develop T cell-mediated immunity to measles virus that controls the viral infection and produces the measles rash, a hypersensitivity reaction to viral antigens in the skin. The rash does not occur in patients with deficiencies in cell mediated immunity but does occur in agammaglobulinemic patients. Antibody-mediated immunity to measles virus protects against reinfection. Subacute sclerosing panencephalitis and measles inclusion body encephalitis (in immunocompromised individuals) are rare late complications of measles caused by hypermutated, “defective” viruses that cannot produce matrix or envelope proteins.
The blotchy, reddish brown rash of measles virus infection on the face, trunk, and proximal extremities is produced by dilated skin vessels, edema, and a moderate, nonspecific, mononuclear perivascular infiltrate. Ulcerated mucosal lesions in the oral cavity near the opening of Stensen ducts (the pathognomonic Koplik spots) are marked by necrosis, neutrophil exudate, and neovascularization. The lymphoid organs typically have marked follicular hyperplasia, large germinal centers, and randomly distributed multinucleate giant cells, called Warthin-Finkeldey cells, which have eosinophilic nuclear and cytoplasmic inclusion bodies. These are pathognomonic of measles and are also found in the lung and sputum. The milder forms of measles pneumonia show the same peribronchial and interstitial mononuclear infiltration seen in other nonlethal viral infections. In severe or neglected cases, bacterial superinfection may be a cause of death.