eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Measles

Author: Selina SP Chen, MD, MPH, Assistant Professor of Pediatrics, Department of Internal Medicine, John A Burns School of Medicine, University of Hawaii; Internal Medicine and Pediatric Hospitalist, Kapiolani Medical Center for Women and Children; Internal Medicine Hospitalist, Straub Clinic and Hospital
Coauthor(s): Glenn J Fennelly, MD, MPH, Director, Division of Pediatric Infectious Diseases, Jacobi Medical Center; Associate Professor, Department of Pediatrics, Albert Einstein College of Medicine
Contributor Information and Disclosures

Updated: Jun 10, 2009

Introduction

Background

Measles virus (MV), a negative-sense enveloped RNA virus, is a member of the Morbillivirus genus in the Paramyxoviridae family. Measles is a highly communicable acute disease. It is also known as rubeola and is marked by prodromal fever, cough, coryza, conjunctivitis, and pathognomonic enanthem (ie, Koplik spots), followed by an erythematous maculopapular rash on the third to seventh day. Infection confers life-long immunity.

A generalized immunosuppression that follows acute measles frequently predisposes patients to bacterial otitis media and bronchopneumonia. In approximately 0.1% of cases, measles causes acute encephalitis. Subacute sclerosing panencephalitis (SSPE) is a rare chronic degenerative disease that occurs several years after measles infection. Because of a failure to deliver at least one dose of measles vaccine to all infants in certain industrialized and developing nations, measles remains a common disease in certain regions and continues to account for nearly 50% of the 1.6 million deaths caused each year by vaccine-preventable childhood diseases.

Maternal antibodies play a significant role in protection against infection in infants younger than 1 year and may interfere with live-attenuated measles vaccination. A single dose of measles vaccine administered to a child older than 12 months induces protective immunity in 95% of recipients. Because measles virus is highly contagious, a 5% susceptible population is sufficient to sustain periodic outbreaks in otherwise highly vaccinated populations. A second dose of vaccine, now recommended for all school-aged children in the United States,¹ induces immunity in about 95% of the 5% who do not respond to the first dose. Slight genotypic variation in recently circulating strains has not affected the protective efficacy of live-attenuated measles vaccines.

Unsubstantiated claims that suggest an association between the measles vaccine and autism have resulted in reduced vaccine use and a recent resurgence of measles in countries where immunization rates have fallen to below the level needed to maintain herd immunity.^2,3 Considering that for industrialized countries such as the United States, endemic transmission of measles may be reestablished if measles immunity falls to less than 93-95%, efforts to ensure high immunization rates among people in both developed and developing countries must be sustained.

Vitamin A supplementation during acute measles significantly reduces risks of morbidity and mortality.

Pathophysiology

In temperate areas, the peak incidence of infection occurs during late winter and spring. Measles virus is spread by direct contact via respiratory droplets or, less commonly, by airborne transmission. Initial infection and viral replication occur locally in tracheal and bronchial epithelial cells. After 2-4 days, measles virus infects local lymphatic tissues, perhaps carried by pulmonary macrophages. Following the amplification of measles virus in regional lymph nodes, a predominantly cell-associated viremia disseminates the virus to various organs prior to the appearance of rash.

In individuals with deficiencies in cellular immunity, measles virus causes a progressive and often fatal giant cell pneumonia. Measles virus infection causes an immunosuppression marked by decreases in delayed-type hypersensitivity, interleukin-12 production, and antigen-specific lymphoproliferative responses that persist for weeks to months after the acute infection. Immunosuppression may predispose individuals to severe bacterial infection, particularly bronchopneumonia, a major cause of measles-related mortality among younger children.

Frequency

United States

The practice of administering 2 doses of live-attenuated measles vaccine to children to prevent school outbreaks of measles was implemented when the vaccine was first licensed in 1963. The immunization program resulted in a decrease of more than 99% in reported incidence. The last major US outbreak (1989-1991) affected more than 55,000 Americans and resulted in 123 deaths. 

Vaccination programs interrupted the transmission of indigenous measles virus in the United States by 1993 and reduced the incidence of measles to an historic low (<0.5 cases per million persons) by 1997-1999. From 1997-2004, the reported incidence was as low as 37-116 cases per year. Since November 2002, measles has not been considered an endemic disease in the United States. 

Despite the highest recorded immunization rates in history, young children who are not appropriately vaccinated may experience more than a 60-fold increase in risk of disease due to exposure to imported measles cases from countries that have not yet eliminated the disease. In 2006, a total of 49 confirmed cases were reported in United States.

International

Approximately 30 million measles cases are reported annually. Most reported cases are from Africa. In 1998, the cases of measles per 100,000 total population reported to the World Health Organization was 1.6 in the Americas, 8.2 in Europe, 11.1 in the Eastern Mediterranean region, 4.2 in South East Asia, 5.0 in the Western Pacific region, and 61.7 in Africa. Only 187 confirmed cases were reported in the Western Hemisphere (mainly in Venezuela, Mexico, and the United States) in 2006.⁴

Mortality/Morbidity

Common infectious complications include otitis media, interstitial pneumonitis,⁵ bronchopneumonia, laryngotracheobronchitis (ie, croup), exacerbation of tuberculosis, transient loss of hypersensitivity reaction to tuberculin skin test, encephalomyelitis, and diarrhea. Rare complications include hemorrhagic measles, purpura fulminans, hepatitis, disseminated intravascular coagulation (DIC), and SSPE. Transient hepatitis may occur during an acute infection. Approximately 1 of every 1,000 patients develops acute encephalitis, which often results in permanent brain damage. SSPE, a degenerative CNS disease, can result from a persistent measles infection. SSPE is characterized by the onset of behavioral and intellectual deterioration and seizures years after an acute infection (the mean incubation period for SSPE is approximately 10.8 years).

Measles is still a leading cause of death among children, despite the availability of an effective vaccine. Measles-related mortality, most often due to respiratory and neurologic complications, occurs in 0.1-0.3% of reported US cases. Measles caused an estimated 197,000 deaths worldwide in 2007.⁴  An estimated 85% of these deaths occur in Africa and Southeast Asia. Case-fatality rates are higher among children younger than 5 years. Highest fatality rates are among infants aged 4-12 months and in children who are immunocompromised because of human immunodeficiency virus (HIV) infection or other causes. From 2000-2007, deaths worldwide fell by 74% (from an estimated 750,000 to 197,000), thanks to the partnership of several global organizations.

Race

Measles affects people of all races.

Sex

Excess mortality following acute measles has been observed among females at all ages, but it is most marked in adolescents and young adults. Excessive non–measles-related mortality has also been observed among female recipients of high-titer measles vaccines in Senegal, Guinea Bissau, and Haiti.⁶

Age

Unvaccinated young children are at the highest risk. Age-specific attack rates may be highest in susceptible infants younger than 12 months, school-aged children, or young adults, depending on local immunization practices and incidence of the disease. Complications such as otitis media, bronchopneumonia, laryngotracheobronchitis (ie, croup), and diarrhea are more common in young children.

Clinical

History

• The incubation period from exposure to onset of measles symptoms ranges from 8-12 days. The first sign of measles is usually a high fever that usually last 4-7 days. The prodromal phase is marked by malaise, fever, anorexia, and conjunctivitis, cough, and coryza (the "3 Cs"). 
• Small white spots inside the cheeks can be seen during the early stage, prior to eruption of rash.
  
  

  

  Koplik spots in measles. Photograph courtesy of the World Health Organization (WHO).

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  Koplik spots in measles. Photograph courtesy of the World Health Organization (WHO).

• Rash usually occurs, on average, 14 days after exposure and starts on the face and upper neck and spreads to extremities. 
  
  

  

  Child with measles. Photograph courtesy of the Centers for Disease Control and Prevention (CDC).

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  Child with measles. Photograph courtesy of the Centers for Disease Control and Prevention (CDC).

• The entire course of uncomplicated measles, from late prodrome to resolution of fever and rash, is 7-10 days. Cough may be the final symptom to appear.
• Patients are contagious from 1-2 days before onset of symptoms. Healthy children are also contagious during the period from 3-5 days before the appearance of the rash to 4 days after the onset of rash. On the other hand, immunocompromised individuals can be contagious during the duration of the illness.

Physical

• Fever: A temperature often exceeding 104°F (40°C) begins with the prodrome and persists 7-10 days.
• Enanthem: Koplik spots (ie, bluish-gray specks or "grains of sand" on a red base) appear on the buccal mucosa opposite the second molars near the end of the prodrome. It is generally seen 2 days prior to the appearance of the rash and lasts until 2 days after the rash appears (see Media file 1). This enanthem begins to slough as the rash appears. Although this is the pathognomonic enanthem of measles, its absence does not exclude diagnosis.
• Rash: An erythematous and maculopapular rash that becomes confluent begins on the face and then proceeds to the trunk, extremities, palms, and soles; it lasts for about 5 days. Patients appear most ill during the first or second day of the rash. Desquamation and brown staining, which spares the palms and soles, may occur after one week. The rash may be absent in patients with underlying deficiencies in cellular immunity.
• Lymphoid involvement: Generalized lymphadenopathy, mild hepatomegaly, and appendicitis may occur because of generalized involvement of lymphoid tissue.

Causes

The highly contagious measles virus is spread by coughing and sneezing via close personal contact or direct contact with secretions.

• Risk factors for infection
  • Children with immunodeficiency due to HIV or acquired immunodeficiency syndrome (AIDS), leukemia, alkylating agents, or corticosteroid therapy, regardless of immunization status
  • Travel to areas where measles is endemic or contact with travelers to endemic areas
  • Infants who lose passive antibody prior to the age of routine immunization
• Risk factors for severe measles and its complications
  • Malnutrition
  • Underlying immunodeficiency
  • Pregnancy
  • Vitamin A deficiency

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