Measles, or rubeola, is a highly contagious disease with worldwide distribution that remains a leading cause of vaccine-preventable deaths in children.1 The peak incidence of infection occurs during the winter and spring months in temperate areas.2 The risk of mortality is highest in developing countries, with most deaths due to complications of the disease.3 In the United States, measles-related deaths occur in 1–3 of every 1,000 reported cases.2
Before the development of a vaccine, measles epidemics in the United States usually occurred in preschool and young school aged children.2,4 A successful immunization program for children and adolescents, particularly in urban areas, has resulted in a greater than 99% decrease in the reported incidence of indigenous measles since the vaccine was first licensed in the early 1960s.2 Yet, cases of measles continue to occur as a result of viral transmission from importation into the United States.2
Improved immunization programs in developing countries have also prevented outbreaks and reduced measles-associated morbidity and mortality. From 2000–2008, global mortality attributed to measles decreased by 78%, from 733,000 to 164,000 deaths.5 However, the reduction in mortality has leveled off and concerns exist regarding the ability of many countries with a high burden of measles mortality to continue effective measles eradication strategies.
Etiology and Pathogenesis
Measles virus, a member of the Paramyxoviridae family, is a heat-labile virus with an RNA core and outer lipoprotein envelope.2,4 Humans are the only natural hosts of the measles virus.2 Measles is spread by direct or airborne droplet exposure. The incubation period is typically 8–12 days, with patients being contagious from 1 to 2 days before onset of symptoms to 4 days after appearance of the rash.2 Both humoral and cell-mediated immunity are needed to control measles virus infection. Immunoglobulin M (IgM) antibodies are detected initially with onset of the rash, followed by a rise in measles-specific IgG titers. The humoral response controls viral replication and confers antibody protection, whereas the cell-mediated response eliminates infected cells.4 A transient immunosuppression occurs during measles virus infection, causing depressed delayed-type hypersensitivity and T-cell counts as well as an increased risk of bacterial infections.4 This process, as well as long-term immunity against measles, is not well understood but may be due to a weak T helper 1 response to the virus.6 Measles virus may use dendritic cells to target lymphoid tissue (CD150 lymphocytes) and disseminate virus throughout the body.7
The prodrome is typically characterized by fever (up to 40.5°C), malaise, conjunctivitis (palpebral, extending to lid margin), coryza, and cough (brassy or barking), which may last up to 4 days.2,4 Koplik spots, the pathognomonic enanthem of measles, begin as small, bright red macules that have a 1–2-mm blue–white speck ...