Measles
Measles (probably from Middle Dutch or Middle High German masel(e), meaning "blemish, blood blister")[11][12] is a highly contagious, vaccine-preventable infectious disease caused by measles virus.[3][5] Other names include morbilli, rubeola, 9-day measles, red measles, and English measles.[1][3] Symptoms usually develop 10–12 days after exposure to an infected person and last 7–10 days.[7] Initial symptoms typically include fever, often greater than 40 °C (104 °F), cough, runny nose, and inflamed eyes.[3][4] Small white spots known as Koplik spots may form inside the mouth two or three days after the start of symptoms.[4] A red, flat rash which usually starts on the face and then spreads to the rest of the body typically begins three to five days after the start of symptoms.[4] Common complications include diarrhea (in 8% of cases), middle ear infection (7%), and pneumonia (6%).[5] These occur in part due to measles-induced immunosuppression.[6] Less commonly, seizures, blindness, or inflammation of the brain may occur.[5][7] Measles is an airborne disease which spreads easily from one person to the next through the coughs and sneezes of infected people.[7] It may also be spread through direct contact with mouth or nasal secretions.[7] It is extremely contagious: nine out of ten people who are not immune and share living space with an infected person will be infected. Furthermore, measles's reproductive number estimates vary beyond the frequently cited range of 12 to 18,[13] with a 2017 review giving a range of 3.7 to 203.3.[14] People are infectious to others from four days before to four days after the start of the rash.[5] While often regarded as a childhood illness, it can affect people of any age.[15] Most people do not get the disease more than once.[7] Testing for the measles virus in suspected cases is important for public health efforts.[5] Measles is not known to occur in other animals.[16] Once a person has become infected, no specific treatment is available, although supportive care may improve outcomes.[7] Such care may include oral rehydration solution (slightly sweet and salty fluids), healthy food, and medications to control the fever.[7][8] Antibiotics should be prescribed if secondary bacterial infections such as ear infections or pneumonia occur.[7][16] Vitamin A supplementation is also recommended for children under the age of 5.[7] Among cases reported in the U.S. between 1985 and 1992, death occurred in 0.2% of cases,[5] but may be up to 10% in people with malnutrition.[7] Most of those who die from the infection are less than five years old.[7] The measles vaccine is effective at preventing the disease, is exceptionally safe, and is often delivered in combination with other vaccines.[7][17] Due to the ease with which measles is transmitted from person to person in a community, more than 95% of the community must be vaccinated in order to achieve herd immunity.[18][better source needed] Vaccination resulted in an 80% decrease in deaths from measles between 2000 and 2017, with about 85% of children worldwide having received their first dose as of 2017.[7] Measles affects about 20 million people a year,[3] primarily in the developing areas of Africa and Asia.[7] It is one of the leading vaccine-preventable disease causes of death.[19][20] In 1980, 2.6 million people died from measles,[7] and in 1990, 545,000 died due to the disease; by 2014, global vaccination programs had reduced the number of deaths from measles to 73,000.[21][22] Despite these trends, rates of disease and deaths increased from 2017 to 2019 due to a decrease in immunization.[23][24][25] Signs and symptoms Symptoms typically begin 7–14 days (typically 11-12 days) after exposure with a prodrome of fever, malaise, and cough.[5][3][6] The fever with measles increases in a stepwise fashion and peaks at 103 °F (39 °C) - 105 °F (41 °C).[5] After one to two days of prodromal illness, Koplik spots appear inside the cheeks opposite the molars as clusters of white lesions ("grains of salt") on reddened areas. They are pathognomonic for measles, but are present for only a short time and therefore are not always seen.[3] The classic symptoms include a fever, cough, coryza (head cold, fever, sneezing), and conjunctivitis, referred to as "the three C's", and a maculopapular rash.[26] The characteristic measles rash is classically described as a generalized red maculopapular rash that begins three to five days after the prodrome; on average, 14 days after exposure, but as few as 7 or as many as 21 days post-exposure.[5][6] The rash starts on the back of the ears or on the face and thereafter spreads to the rest of the body. It is caused by the cellular and humoral immune system's clearing of infected skin cells, as is the conjunctivitis. Measles conjunctivitis often also causes photophobia.[6] The rash is said to "stain", changing color from red to dark brown, before disappearing. Uncomplicated cases of measles typically improve within days of rash onset and resolve within 7–10 days.[6] People who have been vaccinated against measles but have incomplete protective immunity may experience a form of modified measles. Modified measles is characterized by a prolonged incubation period, milder, and less characteristic symptoms (sparse and discrete rash of short duration).[5] Because development of the rash and conjunctivitis requires a functional immune system, immunocompromised people may not be diagnosed as readily.[6]
ComplicationsComplications of measles are relatively common. Some are caused directly by the virus, while others are caused by viral suppression of the immune system. This phenomenon, known as "immune amnesia", increases the risk of secondary bacterial infections;[6][27][28][29] two months after recovery there is an 11–73% decrease in the number of antibodies against other bacteria and viruses.[30] Population studies from prior to the introduction of the measles vaccine suggest that immune amnesia typically lasts 2–3 years. Primate studies suggest that immune amnesia in measles is effected by replacement of memory lymphocytes with ones that are specific to measles virus, since they are destroyed after being infected by the virus. This creates lasting immunity to measles re-infection, but decreases immunity to other pathogens.[28] Complications may be directly related to the virus - e.g. viral pneumonia or viral laryngotracheobronchitis (croup) - or related to the damage measles virus causes to tissues and the immune system. The most serious direct complications include acute encephalitis,[31] corneal ulceration (leading to corneal scarring);[32] and subacute sclerosing panencephalitis, a progressive and fatal inflammation of the brain that occurs in about 1 in 600 unvaccinated infants under 15 months. Common secondary infections include infectious diarrhea, bacterial pneumonia, and otitis media.[6] The death rate in the 1920s was around 30% for measles pneumonia.[33] People who are at high risk for complications are infants and children aged less than 5 years;[15] adults aged over 20 years;[15] pregnant women;[15] people with compromised immune systems, such as from leukemia, HIV infection or innate immunodeficiency;[15][34] and those who are malnourished[15] or have vitamin A deficiency.[15][35] Complications are usually more severe in adults.[36] Between 1987 and 2000, the case fatality rate across the United States was three deaths per 1,000 cases attributable to measles, or 0.3%.[37] In underdeveloped nations with high rates of malnutrition and poor healthcare, fatality rates have been as high as 28%.[37] In immunocompromised persons (e.g., people with AIDS) the fatality rate is approximately 30%.[38] Even in previously healthy children, measles can cause serious illness requiring hospitalization.[34] One out of every 1,000 measles cases progresses to acute encephalitis, which often results in permanent brain damage.[34] One to three out of every 1,000 children who become infected with measles will die from respiratory and neurological complications.[34] Cause Measles is caused by the measles virus, a single-stranded, non-segmented, negative-sense, enveloped RNA virus of the genus Morbillivirus within the family Paramyxoviridae.[39][40] It is related most closely to rinderpest, a cattle virus eradicated in 2001, and canine distemper, a mammalian disease that causes neurologic deterioration.[5] There are 24 strains of measles virus divided into eight clades designated A-H.[39] The virus is one of the most contagious human pathogens and is spread by coughing and sneezing via close personal contact or direct contact with secretions.[34][40][39] It remains infectious for up to two hours via suspended respiratory droplets.[5] It is not easily spread by fomites, because the virus is inactivated within a few hours by ultraviolet light and heat.[6] It is also inactivated by trypsin, acidic environments, and ether.[5] Measles is so contagious that if one person has it, 90% of non-immune people who have close contact with them (e.g., household members) will also become infected.[5][41] Humans are the only natural hosts of the virus, and no other animal reservoirs are known to exist, although mountain gorillas are believed to be susceptible to the disease.[5][42] Risk factors for measles virus infection include immunodeficiency caused by HIV/AIDS,[43] immunosuppression following receipt of an organ or a stem cell transplant,[44] alkylating agents, or corticosteroid therapy, regardless of immunization status;[15] travel to areas where measles commonly occurs or contact with travelers from such an area;[15] and the loss of passive, inherited antibodies before the age of routine immunization.[45] Pathophysiology  Once the measles virus contacts the mucosa lining the respiratory tract, it binds to SLAM (signaling lymphocyte activation molecule, also known as CD150) on the surface of macrophages and dendritic cells. These cells then take up the virus. This process is mediated by the hemagglutinin protein (H) on the surface of the measles virus binding to SLAM and causing the fusion protein in the viral capsule (F) to change shape, allowing the envelope to fuse with the viral RNA and viral proteins entry. The L protein, an RNA-dependent RNA polymerase, then transcribes the viral negative-sense genome into a positive-sense mRNA, which is translated by the cell's native ribosomes into viral proteins. These immune cells pass the virus on to other groups of immune cells, including B cells, T cells, thymocytes, and hematopoietic stem cells, which disseminate the virus to other organs during the incubation period.[5][39] The initial period of infection in the lung lasts for two to three days, and ends with the first period of viremia. Five to seven days after infection begins, the second viremia occurs, and the virus infects epithelial cells.[5] The virus spreads along epithelial cells, initially in the respiratory tree via intercellular pores, and later in the linings of other organs and the respiratory tree via nectin-4 receptors. This causes the cough seen clinically, which aerosolizes the virus and enables it to spread.[5][6] DiagnosisTypically, clinical diagnosis begins with the onset of fever and malaise about 10 days after exposure to the measles virus, followed by the emergence of cough, coryza, and conjunctivitis that worsen in severity over 4 days of appearing.[47] Observation of Koplik's spots is also diagnostic.[48] Other diseases that may appear similar to measles include dengue fever, rubella, erythema infectiosum (also called fifth disease, caused by parvovirus B19), and roseola (also called exanthem subitum or sixth disease, caused by HHV6).[6] Laboratory confirmation is therefore strongly recommended, especially in non-endemic areas.[5] Laboratory testingLaboratory diagnosis of measles can be done with confirmation of positive measles IgM antibodies or detection of measles virus RNA from throat, nasal or urine specimen by using the reverse transcription polymerase chain reaction assay.[49][50] This method is particularly useful to confirm cases when the IgM antibodies results are inconclusive.[49] For people unable to have their blood drawn, saliva can be collected for salivary measles-specific IgA testing.[50] Salivary tests used to diagnose measles involve collecting a saliva sample and testing for the presence of measles antibodies.[51][52] This method is not ideal, as saliva contains many other fluids and proteins which may make it difficult to collect samples and detect measles antibodies.[51][52] Saliva also contains 800 times fewer antibodies than blood samples do, which makes salivary testing additionally difficult. Positive contact with other people known to have measles adds evidence to the diagnosis.[51] Biopsies and histopathologic examinations are not typically used to diagnose measles, but Warthin–Finkeldey cells, giant cells with multiple nuclei and eosinophilic inclusions, are frequently seen in affected lymphoid tissue but are not unique to measles.[1][53] Affected epithelium may have giant cells with viral inclusion bodies or Cowdry bodies.[53] Prevention Mothers who are immune to measles pass antibodies to their children while they are still in the womb, especially if the mother acquired immunity through infection rather than vaccination.[5][45] Such antibodies will usually give newborn infants some immunity against measles, but these antibodies are gradually lost over the course of the first nine months of life.[3][45] However, immunization with live vaccines is not recommended in pregnancy; pregnant people found to be non-immune to measles should be immunized after delivery.[54] Infants under one year of age whose maternal anti-measles antibodies have disappeared become susceptible to infection with the measles virus.[45] It is generally recommended that children be immunized against measles at 12 months, as part of a three-part MMR vaccine (measles, mumps, and rubella). The vaccine is generally not given before this age because younger infants respond inadequately to the vaccine due to an immature immune system. A second dose of the vaccine is recommended between the ages of four and five, to increase rates of immunity.[55][56] Adverse reactions to vaccination are rare, with fever and pain at the injection site being the most common. Life-threatening adverse reactions occur in less than one per million vaccinations (<0.0001%).[57] In areas with a high risk of measles infection, the World Health Organization (WHO) recommends the first two doses of vaccine be given earlier, at nine and eighteen months of age.[56] The vaccine should be given whether the child is HIV-infected or not.[58] The vaccine is less effective in HIV-infected infants than in the general population, but early treatment with antiretroviral drugs can increase its effectiveness.[59] Measles vaccination programs are often used to deliver other child health interventions as well, such as bed nets to protect against malaria, antiparasitic medicine, and vitamin A supplements, and so contribute to the reduction of child deaths from other causes.[60] The Advisory Committee on Immunization Practices (ACIP) of the US Centers for Disease Control and Prevention (CDC) recommends that all adult international travelers who do not have positive evidence of previous measles immunity receive two doses of MMR vaccine before traveling.[55][61] Birth before 1957 is presumptive evidence of immunity.[55] People born before 1957 are likely to have been naturally infected with the measles virus and generally need not be considered susceptible.[55][5][62] There have been false claims of an association between the measles vaccine and autism; this incorrect concern has reduced the rate of vaccination and increased the number of cases of measles where immunization rates became too low to maintain herd immunity.[15] Additionally, there have been false claims that measles infection protects against cancer.[17] Administration of the MMR vaccine may prevent measles after exposure to the virus (post-exposure prophylaxis).[63] Post-exposure prophylaxis guidelines are specific to jurisdiction and population.[63] Passive immunization against measles by an intramuscular injection of antibodies could be effective up to the seventh day after exposure.[64] Compared to no treatment, the risk of measles infection is reduced by 83%, and the risk of death by measles is reduced by 76%. However, the effectiveness of passive immunization in comparison to active measles vaccine is not clear.[64] The MMR vaccine is 95% effective for preventing measles after one dose if the vaccine is given to a child who is twelve months of age or older; if a second dose of the MMR vaccine is given, it will provide immunity in 97-99% of children.[34][40] Vitamin A and measles prevention"Vitamin A deficiency (VAD) is a major public health problem in low- and middle-income countries, affecting 190 million children under five years of age and leading to many adverse health consequences, including death."[65] Vitamin A deficiency is rare in the United States.[66] A meta-analysis of clinical trials conducted in countries where VAD is prevalent concluded that when children were supplemented with vitamin A, there was a 50% reduction in incidence of contracting measles.[65] By way of comparison, vaccination with two doses of the measles vaccine in childhood provides 97-99% protection at preventing measles.[34][55][40] Vitamin A supplementation is not thought to reduce the risk of death from measles.[66] Children given high doses of vitamin A from supplements or cod liver oil can accumulate to toxic levels and this can lead to hypervitaminosis A and liver damage.[66] A 2016 Cochrane review of two randomised controlled trials (RCTs) involving 260 children with measles compared vitamin A to placebo. Crucially, neither study reported blindness or other ocular morbidities as primary outcomes. One trial showed a temporary increase in serum retinol levels, but no sustained effect or impact on weight gain. The second trial found no significant difference in serum retinol levels or rates of undernutrition. Therefore, the authors concluded that no trials were found that assessed whether vitamin A supplementation in children with measles prevents blindness.[67] In the 2025 Southwest United States measles outbreak, centered in West Texas, some families continued to refuse vaccines and instead opted for giving vitamin A supplements or vitamins A- and D-containing cod liver oil to their children after Robert F. Kennedy Jr., promoted vitamin A as prevention and treatment.[68] Multiple children hospitalized for measles at Covenant Children's Hospital in Lubbock also showed signs of liver damage, a symptom of vitamin A toxicity.[66][68][69] As of May 2025, regardless of such serious side effects—and possibly resulting in increased disease spread—Kennedy, in his role as Secretary of Health and Human Services, has nevertheless continued to endorse vitamin A during the measles epidemic, along with other unscientific, non-vaccine measures, a response for which he has been widely criticized.[70] TreatmentThere is no specific antiviral treatment if measles develops.[34] Instead the medications are generally aimed at treating superinfections, maintaining good hydration with adequate fluids, and pain relief.[34] Supportive treatment can include ibuprofen or paracetamol (acetaminophen) to reduce fever and pain and, if required, a fast-acting medication to dilate the airways for cough.[71] Some groups, such as young children and the severely malnourished, are also physician-administered vitamin A, which acts as an immunomodulator that boosts the antibody responses to measles and decreases the risk of serious complications.[34][40][72] While vitamin A treatment does not cure the disease or reduce mortality in every age group,[73] two doses (200,000 IU) of vitamin A was shown to reduce mortality in children younger than two years of age.[40][74] In the 2025 U.S. outbreak, children are presenting at hospitals with measles and hypervitaminosis A because their parents were administering vitamin A sources (supplements or cod liver oil) as attempts of protection before the children became ill with measles.[68][69] Zinc supplementation for children with measles has not been sufficiently studied.[75] Similarly, there is no randomized clinical trial evidence for or against whether Chinese medicinal herbs are an effective treatment.[76] PrognosisMost people survive measles, though in some cases, complications may occur. About 1 in 4 individuals will be hospitalized and 1–2 in 1,000 will die. Complications are more likely in children under age 5, adults over age 20, and pregnant people.[54][77] Pneumonia is the most common fatal complication of measles infection and accounts for 56–86% of measles-related deaths.[78] Possible consequences of measles virus infection include laryngotracheobronchitis, sensorineural hearing loss,[79] and—in about 1 in 10,000 to 1 in 300,000 cases[80]—panencephalitis, which is usually fatal.[81] Acute measles encephalitis is another serious risk of measles virus infection. It typically occurs two days to one week after the measles rash breaks out and begins with very high fever, severe headache, convulsions and altered mentation. A person with measles encephalitis may become comatose, and death or brain injury may occur.[3] For people having had measles, it is rare to ever have a symptomatic reinfection.[82] The measles virus can deplete previously acquired immune memory by killing cells that make antibodies, and thus weakens the immune system, which can cause deaths from other diseases.[28][29][30] Suppression of the immune system by measles lasts about two years and has been epidemiologically implicated in up to 90% of childhood deaths in third world countries, and historically may have caused rather more deaths in the United States, the UK and Denmark than were directly caused by measles.[83][84] Although the measles vaccine contains an attenuated strain, it does not deplete immune memory.[29] Epidemiology no data 0 1–8 9–26 27–38 39–73 74–850  no data ≤ 10 10–25 25–50 50–75 75–100 100–250 250–500 500–750 750–1000 1000–1500 1500–2000 ≥ 2000 Measles is extremely infectious and its continued circulation in a community depends on the generation of susceptible hosts by birth of children. In communities that generate insufficient new hosts the disease will die out. This concept was first recognized in measles by M.S. Bartlett in 1957, who referred to the minimum number supporting measles as the critical community size (CCS).[85] Analysis of outbreaks in island communities suggested that the CCS for measles is around 250,000.[86] Due to the ease with which measles is transmitted from person to person in a community, more than 95% of the community must be vaccinated in order to achieve herd immunity.[18] In 2011, the WHO estimated that 158,000 deaths were caused by measles. This is down from 630,000 deaths in 1990.[87] As of 2018, measles remains a leading cause of vaccine-preventable deaths in the world.[19][88] In developed countries the mortality rate is lower, for example in England and Wales from 2007 to 2017 death occurred between two and three cases out of 10,000.[89] In children one to three cases out of every 1,000 die in the United States (0.1–0.2%).[90] In populations with high levels of malnutrition and a lack of adequate healthcare, mortality can be as high as 10%.[7][5] In cases with complications, the rate may rise to 20–30%.[medical citation needed] In 2012, the number of deaths due to measles was 78% lower than in 2000 due to increased rates of immunization among UN member states.[18] Between 2000 and 2016, global cases decreased by 84%; by 2019 cases had increased to a total of 870,000, the highest since 1996.[39]
Even in countries where vaccination has been introduced, rates may remain high. Measles is a leading cause of vaccine-preventable childhood mortality. Worldwide, the fatality rate has been significantly reduced by a vaccination campaign led by partners in the Measles Initiative: the American Red Cross, the United States CDC, the | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
