Measles, also known as rubeola, is one of the most contagious infectious diseases, with at least a 90%

secondary infection rate in susceptible domestic contacts. Despite being considered primarily a childhood
illness, measles can affect people of all ages.
Essential update: Measles in US increases threefold
Although the elimination of endemic measles transmission in the US in 2000 was sustained through at
least 2011, according to a CDC study, cases continue to be caused by virus brought into the country by
travelers from abroad, with spread occurring largely among unvaccinated individuals. In 88% of the cases
reported between 2000 and 2011, the virus originated from a country outside the US, and 2 out of every 3
individuals who developed measles were unvaccinated. Moreover, the director of the CDC noted that, in
2013, US measles cases increased threefold from the previous median, to 175 cases.
[1, 2]
Most of these
cases were outbreaks in children whose parents had refused immunization.
This trend of increased incidence has continued into 2014. From January 1 to May 23, 2014, 288
confirmed cases were reported to the CDC, a figure that exceeds the highest reported annual total
number of cases (220 cases in 2011) since measles was declared eliminated in the United States in
2000. Of the 288 cases, 200 (69%) occurred in unvaccinated individuals and 58 (20%) in persons with
unknown vaccination status. Nearly all of the 2014 cases reported thus far (280 [97%]) were associated
with importations from at least 18 countries. Eighteen states and New York City reported measles
infections during this period, and 15 outbreaks accounted for 79% of reported cases, including a large
ongoing outbreak in Ohio primarily among unvaccinated Amish persons, with 138 cases reported thus
far.
[3]

Signs and symptoms
Onset of measles ranges from 7-14 days (average, 10-12 days) after exposure to the virus. The first sign
of measles is usually a high fever (often >104
o
F [40
o
C]) that typically lasts 4-7 days. The prodromal
phase is also marked by malaise; anorexia; and the classic triad of conjunctivitis, cough, and coryza (the
3 Cs). Other possible prodromal manifestations include photophobia, periorbital edema, and myalgias.
Enanthem
Koplik spotsbluish-gray specks or grains of sand on a red basedevelop on the buccal mucosa
opposite the second molars
Generally appear 1-2 days before the rash and last 3-5 days
Pathognomonic for measles, but not always present
Rash
On average, the rash develops about 14 days after exposure
Mild pruritus may also occur
Blanching, erythematous macules and papules begin on the face at the hairline, on the sides of the
neck, and behind the ears
Within 48 hours, the lesions coalesce into patches and plaques that spread cephalocaudally to the trunk
and extremities, including the palms and soles, while beginning to regress cephalocaudally, starting
from the head and neck
Lesion density is greatest above the shoulders, where macular lesions may coalesce
The eruption may also be petechial or ecchymotic in nature
Patients appear most ill during the first or second day of the rash
The exanthem lasts for 5-7 days before fading into coppery-brown hyperpigmented patches, which then
desquamate
Immunocompromised patients may not develop a rash
Clinical course
Uncomplicated measles, from late prodrome to resolution of fever and rash, lasts 7-10 days
Cough may be the final symptom to appear
Modified measles
Occurs in individuals who have received serum immunoglobulin after exposure to the measles virus
The incubation period may be as long as 21 days
Similar but milder symptoms and signs may occur
Atypical measles
Occurs in individuals who were vaccinated with the original killed-virus measles vaccine between 1963
and 1967 and who have incomplete immunity
A mild or subclinical prodrome of fever, headache, abdominal pain, and myalgias precedes a rash that
begins on the hands and feet and spreads centripetally
The eruption is accentuated in the skin folds and may be macular, vesicular, petechial, or urticarial
See Clinical Presentation for more detail.
Diagnosis
Although the diagnosis of measles is usually determined from the classic clinical picture, laboratory
identification and confirmation of the diagnosis are necessary for public health and outbreak control.
Laboratory confirmation is achieved by means of the following:
Serologic testing for measles-specific IgM or IgG titers
Isolation of the virus
Reverse-transcriptase polymerase chain reaction (RT-PCR) evaluation
Measles-specific IgM titers
Obtain blood on the third day of the rash or on any subsequent day up to 1 month after onset
The measles serum IgM titer remains positive 30-60 days after the illness in most individuals but may
become undetectable in some subjects at 4 weeks after rash onset
False-positive results can occur in patients with rheumatologic diseases, parvovirus B19 infection, or
infectious mononucleosis
Measles-specific IgG titers
More than a 4-fold rise in IgG antibodies between acute and convalescent sera confirms measles
Acute specimens should be drawn on the seventh day after rash onset
Convalescent specimens should be drawn 10-14 days after that drawn for acute serum
The acute and convalescent sera should be tested simultaneously as paired sera
Viral culture
Throat swabs and nasal swabs can be sent on viral transport medium or a viral culturette swab
Urine specimens can be sent in a sterile container
Viral genotyping in a reference laboratory may determine whether an isolate is endemic or imported
In immunocompromised patients, isolation of the virus or identification of measles antigen by
immunofluorescence may be the only feasible method of confirming the diagnosis
Polymerase chain reaction
RT-PCR, if available, can rapidly confirm the diagnosis of measles
[4]

Blood, throat, nasopharyngeal, or urine specimens can be used
Samples should be collected at the first contact with a suspected case of measles
Case reporting
Immediately reporting any suspected case of measles to a local or state health department is imperative.
The US CDC clinical case definition for reporting purposes requires only the following:
Generalized rash lasting 3 days or longer
Temperature of 101.0F (38.3C) or higher
Cough, coryza, or conjunctivitis
For reporting purposes for the CDC, cases are classified as follows:
Suspected: Any febrile illness accompanied by rash
Probable: A case that meets the clinical case definition, has noncontributory or no serologic or virologic
testing, and is not epidemiologically linked to a confirmed case
Confirmed: A case that is laboratory confirmed or that meets the clinical case definition and is
epidemiologically linked to a confirmed case; a laboratory-confirmed case need not meet the clinical
case definition
See Workup for more detail.
Management
Treatment of measles is essentially supportive care, as follows:
Maintenance of good hydration and replacement of fluids lost through diarrhea or emesis
IV rehydration may be necessary if dehydration is severe
Vitamin A supplementation should be considered
Postexposure prophylaxis should be considered in unvaccinated contacts; timely tracing of contacts
should be a priority. Patients should receive regular follow-up care with a primary care physician for
surveillance of complications arising from the infection.
Vitamin A supplementation
The World Health Organization recommends vitamin A supplementation for all children diagnosed with
measles, regardless of their country of residence, based on their age,
[5]
as follows:
Infants younger than 6 months: 50,000 IU/day PO for 2 doses
Age 6-11 months: 100,000 IU/day PO for 2 doses
Older than 1 year: 200,000 IU/day PO for 2 doses
Children with clinical signs of vitamin A deficiency : The first 2 doses as appropriate for age, then a third
age-specific dose given 2-4 weeks later
Background
Measles, also known as rubeola, is one of the most contagious infectious diseases, with at least a 90%
secondary infection rate in susceptible domestic contacts. It can affect people of all ages, despite being
considered primarily a childhood illness. Measles 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.
After an effective measles vaccine was introduced in 1963, the incidence of measles decreased
significantly. Nevertheless, 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. The incidence of measles in the United States and worldwide is increasing, with outbreaks
being reported particularly in populations with low vaccination rates.
[6]

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,
[7]
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 contributed to a recent resurgence of measles in countries where
immunization rates have fallen to below the level needed to maintain herd immunity.
[8, 9]

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.
Supportive care is normally all that is required for patients with measles. 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. Infection is
transmitted via respiratory droplets, which can remain active and contagious, either airborne or on
surfaces, for up to 2 hours. 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.
Measles virus infection causes a generalized immunosuppression marked by decreases in delayed-type
hypersensitivity, interleukin (IL)-12 production, and antigen-specific lymphoproliferative responses that
persist for weeks to months after the acute infection. Immunosuppression may predispose individuals to
secondary opportunistic infections,
[10]
particularly bronchopneumonia, a major cause of measles-related
mortality among younger children.
In individuals with deficiencies in cellular immunity, measles virus causes a progressive and often fatal
giant cell pneumonia.
In immunocompetent individuals, wild-type measles virus infection induces an effective immune
response, which clears the virus and results in lifelong immunity.
[11]

Etiology
The cause of measles is the measles virus, a single-stranded, negative-sense enveloped RNA virus of
the genus Morbillivirus within the family Paramyxoviridae. Humans are the natural hosts of the virus; no
animal reservoirs are known to exist. This highly contagious virus is spread by coughing and sneezing via
close personal contact or direct contact with secretions.
Risk factors for measles virus infection include the following:
Children with immunodeficiency due to HIV or 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 before the age of routine immunization
Risk factors for severe measles and its complications include the following:
Malnutrition
Underlying immunodeficiency
Pregnancy
Vitamin A deficiency