- Etiology
- Pathogenesis
- Pathology
- Epidemiology
- Prevention
- Management & Treatment
- Complications
- Prognosis
- Clinical Case Studies
- Study Questions
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
Measles is a highly contagious viral disease.
The rash of rubeola (measles) starts at the hairline 2–3 days into the illness and moves down the body, typically sparing the palms and soles. It begins as discrete erythematous lesions, which become confluent as the rash spreads. Koplik’s spots (1- to 2-mm white or bluish lesions with an erythematous halo on the buccal mucosa) are pathognomonic for measles and are generally seen during the first 2 days of symptoms. They should not be confused with Fordyce’s spots (ectopic sebaceous glands), which have no erythematous halos and are found in the mouth of healthy individuals. Koplik’s spots may briefly overlap with the measles exanthem.Rubella is a contagious disease.
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
In 1997 it was the sixth leading cause of death worldwide; it is still the leading cause of blindness in African children. The causative agent of measles is paramyxovirus, which has an incubation period of 7 to 12 days, and infection occurs most commonly in winter and spring.
Measles is contagious 3 days before and 5 days following onset of the rash. It begins with a prodrome of gradually increasing fevers (>40° C), headache, coryza, dry hacking cough, and an impressive bilateral conjunctivitis (the three C's). The prodrome occurs 2 to 4 days before the rash. Koplik spots are clustered, white lesions (“grains of salt on a wet background”) that may appear on the buccal mucosa opposite the second molars during the prodromal period ( Fig. 18.1 ). They are pathognomonic if present. The erythematous, nonpruritic, maculopapular rash first appears at the hairline and behind the ears and then spreads inferiorly. As the rash involves the trunk and extremities, the discrete macules coalesce. After 1 week the rash fades. Diagnosis of measles is typically made clinically; however, laboratory diagnosis via serologic assay is available. Treatment of measles is supportive. Administration of vitamin A is associated with a reduction in risk for mortality in children younger than 2 years, as well as a reduction in postmeasles pneumonia complications. Complications of measles include blindness, pneumonia, laryngotracheobronchitis, otitis media, myocarditis, and encephalitis.
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
In 1997 it was the sixth leading cause of death worldwide; it is still the leading cause of blindness in African children. The causative agent of measles is paramyxovirus, which has an incubation period of 7 to 12 days, and infection occurs most commonly in winter and spring. Measles is contagious 3 days before and 5 days following onset of the rash. It begins with a prodrome of gradually increasing fevers (>40° C), headache, coryza, dry hacking cough, and an impressive bilateral conjunctivitis (the three C's). The prodrome occurs 2 to 4 days before the rash. Koplik spots are clustered, white lesions (“grains of salt on a wet background”) that may appear on the buccal mucosa opposite the second molars during the prodromal period ( Fig. 18.1 ). They are pathognomonic if present. The erythematous, nonpruritic, maculopapular rash first appears at the hairline and behind the ears and then spreads inferiorly. As the rash involves the trunk and extremities, the discrete macules coalesce. After 1 week the rash fades. Diagnosis of measles is typically made clinically; however, laboratory diagnosis via serologic assay is available. Treatment of measles is supportive. Administration of vitamin A is associated with a reduction in risk for mortality in children younger than 2 years, as well as a reduction in postmeasles pneumonia complications. Complications of measles include blindness, pneumonia, laryngotracheobronchitis, otitis media, myocarditis, and encephalitis.
The best protection against rubella is MMR (measles-mumps-rubella) vaccine.
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
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A recent 18-year-old immigrant from Kenya presents to a university clinic with fever, nasal congestion, severe fatigue, and a rash. The rash started with discrete lesions at the hairline that coalesced as the rash spread caudally. There is sparing of the palms and soles. Small white spots with a surrounding red halo are noted on examination of the palate. The patient is at risk for developing which of the following in the future?
The correct answer is A. You answered A.
The answer is A.(Chap. 24) Based on the characteristic rash and Koplik spots, this patient has measles. A rare but feared complication of measles is subacute sclerosing panencephalitis. His examination does not support epiglottitis as he has no drooling or dysphagia. His rash is not characteristic of acute HIV infection, and he lacks the pharyngitis and arthralgias commonly seen with this diagnosis. The rash is not consistent with herpes zoster, and he is quite young to invoke this diagnosis. Splenic rupture occasionally occurs with infectious mononucleosis, but this patient has no pharyngitis, lymphadenopathy, or splenomegaly to suggest this diagnosis. Due to widespread (and in some cases mandatory) vaccination, measles is very uncommon in the United States (as well as Central and South America); almost all cases are imported. However, countries with lower rates of vaccination still have endemic measles. Recent cases in the United States in unvaccinated children make this an important diagnosis for clinicians to consider in appropriate situations.