An 18-month-old boy, who is visiting family in San Antonio with his parents from Central America, presents with a 3-day history of fever, malaise, conjunctivitis, coryza, and cough. He had been exposed to a child with similar symptoms approximately 2 weeks prior. A day before, he developed a maculopapular rash that blanches under pressure (Figures 111-1 and 111-2). His shot records are unavailable but his mother states that his last vaccine was before age 1 year. He is diagnosed with measles and supportive care is provided.

Measles is a highly communicable, acute viral illness that is still one the most serious infectious diseases in human history. Until the introduction of the measles vaccination, it was responsible for millions of deaths worldwide annually. Although the epidemiology of this disease makes eradication a possibility, the ease of transmission and the low percentage of non immunized population that is required for disease survival have made eradication of measles extremely difficult.

• Last major outbreak in the US was during 1989 to 1990 and prompted a change in immunization policy in 1991, so that all children are to have two measles-mumps-rubella (MMR) vaccines before starting kindergarten.

• This practice interrupted the transmission of indigenous measles in the US by 1993 and reduced incidence of measles to an historic low (<0.5 cases per million persons) by 1997 to 1999.¹

• After an all-time low of 34 cases were reported in 2004 in the US, the annual incidence began to increase with most cases linked to international travel of inadequately vaccinated Americans to endemic areas. Incomplete vaccination rates facilitate the spread once the virus is imported to the US causing clusters of periodic outbreaks.¹

• The worldwide incidence of death from measles was effectively reduced from an estimated 733,000 deaths in 2000 to an estimated 164,000 deaths in 2008 with mass vaccination campaigns by the member countries of the World Health Assembly.² In 2008, about 83 percent of the world’s children received one dose of measles vaccine by their first birthday through routine health services—up from 72 percent in 2000.³

• Measles elimination is now considered a feasible target. The World Health Organization have renewed their commitment to eliminate measles transmission by 2015. This will require greater than 95 percent of the population receives two doses of the MMR vaccine.⁴

• Measles is caused by the measles virus, a member of the family paramyxoviridae, genus Morbillivirus (hence the name, morbilliform rash).

• It is highly contagious, transmitted by airborne droplets, and commonly causes outbreaks.

• Classic measles infection starts with the incubation phase that is usually asymptomatic and lasts for 10 to 14 days. It starts after entry of the virus into the respiratory mucosa with local viral replication. The infection then spreads to regional lymphatic tissues, and then throughout the body through the bloodstream.

• The prodrome phase starts with the appearance of systemic symptoms including fever, malaise, anorexia, conjunctivitis, coryza, and cough (Figure 111-3). The respiratory symptoms are caused by mucosal inflammation from viral infection of epithelial cells. Patients may develop Koplik’s spots, which are small whitish, grayish, or bluish papules with erythematous bases that develop on the buccal mucosa usually near the molar teeth (Figure 111-4). The prodrome usually lasts for 2 to 3 days.

• The classic measles rash (Figures 111-1, 111-2, and 111-5) is maculopapular and blanches under pressure. Clinical improvement in symptoms typically ensues within 2 days. Three to 4 days after the rash first appears, it begins to fade to a brownish color which is followed by fine flaking. The cough may persist for up to 2 weeks.

• Fever persisting beyond the third day of rash suggests a measles-associated complication.

• Immunity after measles infection is thought to be lifelong in most cases. Measles reinfection occasionally occurs, but it is extremely rare.

• Atypical measles is a measles variant that occurs in previously-vaccinated persons. Patients develop high fever and headache 7 to 14 days after exposure, and often present with a dry cough and pleuritic chest pain. Two to three days later, a rash develops that spreads from the extremities to the trunk. The rash may be vesicular, petechial, purpuric, or urticarial. Patients may develop respiratory distress, peripheral edema, hepatosplenomegaly, paresthesias, or hyperesthesia.

• The measles virus can cause a variety of clinical syndromes including the classic childhood illness and a less intense form in persons with suboptimal levels of anti measles antibodies.

• Measles virus infection can also result in more severe illness, including lymphadenopathy, splenomegaly, laryngotracheobronchitis (croup), giant cell pneumonia, and measles inclusion body encephalitis in immunocompromised patients.⁵ This form occurs in the very young, those with vitamin A deficiency, and in pregnant women.

• Postinfection neurologic syndromes can occur. Postinfectious encephalomyelitis is a demyelinating disease that presents during the recovery phase, and is thought to be caused by a postinfectious autoimmune response.⁶ The major manifestations include fever, headache, neck stiffness, ataxia, mental status changes, and seizures. CSF analysis demonstrates lymphocytosis and elevated proteins. Postinfectious encephalomyelitis has a 10 to 20 percent mortality rate, and residual neurologic abnormalities are common.⁶

• Subacute sclerosing panencephalitis (SSPE) is a progressive, fatal, neurological degenerative disease that may represent a persistent infection of the central nervous system with a variant of the virus. It usually occurs in patients younger than 20 years of age and 7 to 10 years after natural measles.⁷ Patients develop neurologic symptoms, myoclonus, dementia, and eventually flaccidity or decorticate rigidity.

• Measles in pregnancy is a rare entity in areas that practice vaccination. Premature births may be more common in gravid women with measles, but there is no clear evidence of teratogenicity.^8,9

• When measles occurs during pregnancy, maternal and fetal morbidity is increased. The virus is not responsible for congenital defects but can induce placental damage which may lead to fetal death. Major perinatal risks are also miscarriage and prematurity. When measles occurs in late pregnancy, congenital infection is possible.⁸