Measles is highly contagious and is spread from person to person by aerosols. It enters the susceptible host by the respiratory route.
The virus initiates infection and replicates locally in the trachea and bronchial epithelial cells of the respiratory tract. After 2–4 days, the virus spreads systemically in lymphocytes, perhaps carried by pulmonary macrophages, and causes viremia. Wide dissemination of the virus causes infection of the conjunctiva, respiratory tract, urinary tract, lymphatic system, blood ves-sels, and the central nervous system (CNS). The characteristic rash seen in measles is caused primarily by cytotoxic T cells attacking the measles virus-infected epithelial cells in the skin.
Measles causes immunosuppression, characterized by decrease in eosinophils and lymphocytes (both B and T cells) and depres-sion of their response to activation by mitogens. Also, the con-dition is associated with marked decrease in interleukin-12 production and leads to antigen-specific lymphoproliferative responses that are present for weeks to months after the acute infection.
Cell-mediated immunity (CMI) plays an important role to control measles infection. Therefore, measles virus in individu-als with deficiency in cellular immunity causes progressive and often fatal giant cell pneumonia without a rash. The antibodies do not have any role in conferring protection against measles virus, because the viruses spread from cell to cell. However, maternal antibodies in infants protect against measles during first 6 months of life.
Immunosuppression caused by measles in the infected indi-viduals may predispose individuals to bronchopneumonia, a severe bacterial infection and a major cause of measles-related mortality among young children. Nevertheless, one attack of measles confers lifelong immunity.