A potentially dangerous viral illness that causes fever and a rash. Measles mainly affects children, but can occur at any age. It is spread primarily by airborne droplets of nasal secretions. It can be transmitted during the incubation period (eight to 14 days after infection) and up to seven days after symptoms appear.

Symptoms and signs 

The illness starts with a fever, runny nose, sore eyes, cough, and a general feeling of being unwell. After three to four days, a red rash appears, usually starting on the head and neck and spreading to cover the body. The spots sometimes join to produce large red blotches, and the lymph nodes may be enlarged. After three days, the rash starts to fade and the symptoms subside.


The most common complications are ear and chest infections, which usually develop two to three days after the rash has appeared. Diarrhoea, vomiting, and abdominal pain may occur. Febrile convulsions are also common, but are not usually serious. In a tiny minority of cases, encephalitis (inflammation of the brain) occurs, causing headache, drowsiness, and vomiting. Seizures and coma may follow, sometimes leading to brain damage or even death. In very rare cases, a progressive brain disorder called subacute sclerosing panencephalitis develops several years after infection. If a woman has measles during pregnancy, the infection may be fatal to the fetus; however, there is no evidence that measles causes birth defects.


There is no specific treatment. Plenty of fluids and paracetamol are given for fever. In addition, antibiotic drugs may be given to treat bacterial infections that occur as complications.


To help prevent measles, immunization with the MMR (measles, mumps and rubella) vaccination is recommended at between 12 and 15 months of age. This measure produces immunity in about 90 per cent of cases, with a booster shot given before a child enters school or nursery school.

Below: link to pictures of measles

Measles pictures

Measles in more detail - non-technical

Measles in great detail - technical


Measles is a single-stranded RNA virus that is spread by aerosolized droplets and is highly transmissible. It causes a spectrum of disease ranging from mild in the well nourished to severe in the malnourished or immunosuppressed: mortality is 3 to 10% in Africa.

Clinical features—10 to 14 days after infection the viral prodrome typically consists of runny nose and fever, sometimes also diarrhoea or convulsions; signs include mild conjunctivitis, red mucosae, and (on the buccal mucosa) Koplik’s spots. After 14 to 18 days a morbilliform rash first appears on the forehead and neck, then spreads to involve the trunk and finally the limbs. Other manifestations include severe conjunctivitis (especially in those who are vitamin-A deficient), pneumonitis and enteritis (which may cause profuse diarrhoea). Early complications include (1) pneumonia—caused by secondary bacterial infection and responsible for most deaths; (2) stomatitis—caused by herpes simplex virus and/or candidal infection; (3) enteritis—due to candidal or bacterial superinfection; (4) eye infection—corneal ulceration may be caused by some combination of measles itself, herpes simplex infection, vitamin A deficiency, and use of traditional eye medicines; more than half of childhood blindness in Africa is related to measles; (5) skin and other infections, e.g. pyoderma; (6) encephalitis—occurs in 0.1 to 0.2% of cases; probably attributable to a neuroallergic process; mortality is 10 to 15%, and 25% of children are left with permanent neurological disability. Late complications include malnutrition, giant cell pneumonia and subacute sclerosing panencephalitis.

Diagnosis and treatment—diagnosis is primarily clinical, but signs may be less clear cut in vaccinated subjects. Detection of measles-specific IgM antibody or detection of measles antigen in saliva or urine may clinch the diagnosis if the rash is mild or atypical. Management is supportive, including administration of vitamin A, and with prompt treatment of secondary infections.

Prevention—(1) Passive immunization—human immunoglobulin is highly effective if given within 2 or 3 days of exposure and should be administered to those in whom vaccination is contraindicated. (2) Active immunization—live vaccine is often given in the developed world as one component of a trivalent mumps/measles/rubella (MMR) vaccine at 14 to 16 months of age. However, this is not appropriate for children in developing countries, who are infected by measles at a much earlier age, where substantial successes in controlling the disease has been obtained with a strategy combining (a) catch-up—a one-time mass campaign covering everybody aged 9 months to 14 years, regardless of previous measles or immunization; (2) keep-up—achieving a high coverage for each birth cohort; (3) follow-up—subsequent mass campaigns covering all children every 3 to 5 years; and (4) mop-up—campaigns that target children who are difficult to reach or during outbreaks.


Measles is an acute, highly transmissible RNA viral infection of humans that is spread by aerosolized droplets. It causes much death and suffering, especially among poor children in developing countries. Its severity varies according to host and socioeconomic factors, not to antigenic variation or alteration in virulence of the virus. There is no reservoir of infection other than in humans and no evidence of a carrier state and as there is an effective vaccine, global eradication is possible but a dauntingly high vaccine coverage of more than 95% will be needed. The virus causes a generalized infection coupled with severe damage to the immune system due to destruction of T lymphocytes, disturbance of the Th1/Th2 cytokine balance, and impaired antigenic presentation. The chief clinical features result from infection of the skin, mucous membranes, and respiratory tract. Death, which occurs in up to 15% of hospitalized children in Africa, results from secondary infections and immunosuppression. Attack rates in home contacts are very high (of the order of 90%) and long-life immunity follows the disease but not vaccination. Supplemental immunization activities allowing repeated vaccination every 3 to 5 years in endemic countries have lowered measles deaths dramatically. However, although global coverage by measles immunization in 2005 was 77%, at least 20 million children are infected annually and 345 000 die, mainly in sub-Saharan Africa where immunization coverage is low.


Measles has been the archetypical childhood infection, known and feared by all parents. Nearly everybody contracted this most infectious of childhood diseases. Measles was the single biggest cause of childhood deaths. In the prevaccination era, 6 million children may have died annually of measles. With advances in coverage during the last 25 years, the current estimate (2007) is 197,000 deaths, still the most important of the vaccine-preventable infections. The severity and age of infection varies markedly between poor and rich countries. In the West, most children were infected between 3 and 6 years of age, when they attended nursery and primary schools. Mortality was low (<0.05%) and morbidity, although considerable when compared to many other common viral infections, was limited. Most cases occurred in the winter and spring, with a biannual epidemic pattern. Widespread immunization has dramatically reduced both the number of cases and complications in high income countries.

In low income countries, measles is still severe and behaves differently. It kills between 3 and 10% of children in the community and some 10 to 20% of those admitted to hospital. Mortality from measles is considerably higher in Africa (3–10%) than in Asia or South America (1%). West Africa has the highest case fatality rates.

There are many reasons for this increase in severity: children are infected at 1 to 2 years of age; severe malnutrition leads to prolonged, severe measles. Overcrowding is another strong determinant, for secondary and tertiary cases in large families are at great risk of death. Exposure to a large dose of the virus when in close contact with the index case may be the critical factor. The severity of measles depends on the severity of disease in the index case. The high mortality found in West Africa is due to this region having the largest polygamous and extended families, which increase the risk of intense exposure. When females stay at home and are constrained in their social contacts, mortality is higher in girls than boys. There is also a high case fatality in children with chronic disease, including kwashiorkor, tuberculosis, and HIV infection. Hospital wards and clinics in developing countries have been important centres of disease transmission.

Though measles may have permanent sequelae, recent research has provided limited support for the previous belief in long-term excess morbidity and mortality after the first 6 weeks of measles infection. Long-term consequences may also depend on intensity of exposure. Index cases apparently have better long-term survival than secondary cases, suggesting a beneficial effect of mild measles infection. Long-term morbidity is most likely to be experienced by young children who have severe measles following intensive exposure.

Measles immunization has dramatically decreased the number of cases, but measles deaths through vaccine failures are not infrequent. Immunized cases are characterized by a prolonged incubation period, a short prodrome, mild symptoms, and a favourable outcome. The mild measles of immunized cases leads to less risk of transmission or transmission of less severe disease. Immunization reduces the number of children being susceptible in the same household and hence reduces the risk of intensive exposure (Table 1).

However, immunization may have negative consequences on herd immunity for an increasing number of unvaccinated children, or children who have responded poorly to the vaccine will reach adulthood without having been exposed to measles. Thus, vaccinated people will have lower antibody levels than naturally infected people, which is particularly important because young immunized mothers will transfer lower antibody levels to their offspring. In West Africa, children of immunized mothers have only half the antibody levels of children of naturally infected mothers and they become susceptible as early as 3 to 5 months of age.

It has been argued that measles vaccines only saved ‘weak’ children who were likely to die anyway. However, many epidemiological studies, including small randomized trials, have shown remarkable reductions in all cause mortality after standard measles vaccine. In Bangladesh, measles vaccination was associated with a 49% reduction in all-cause mortality from the age of 9 months, even though acute measles accounted for only 10 to 12% of deaths. This unexpected benefit was not related to prevention of measles. In most studies, this nonspecific benefit is particularly marked for girls. More recent studies have shown that the combination of measles vaccine with other vaccines or vitamin A supplements may influence the nonspecific effects on child survival.

Popular beliefs

In most cultures, measles has a specific local name and is a much feared disease. Popular understanding is centred around the rash, which if it stays within the body will lead to severe disease. This belief has some basis in truth for the prodrome is prolonged in severe cases, and a proportion of deaths reportedly occur before the appearance of the rash during very severe epidemics. Therapeutic practices, such as rubbing the skin with palm oil or kerosene, are aimed at eliciting the rash quickly. In West Africa it is believed that cooling keeps the rash within the body, so the child may be bedded in warm sand or covered with blankets, and is not washed or given cold water to drink.

The virus and its antigens

Measles mainly infects humans, but like the other closely related morbilliviruses (such as rinderpest or canine distemper virus) it is able to cross species to infect other primates and, on occasions, dogs. It contains a single strand of RNA, is highly pleomorphic, and ranges from 100 to 300 nm in diameter. The virus propagates by budding from the cell membrane, from which it acquires an envelope. The membrane of infected cells and the virion envelope contain two surface glycoproteins, the haemagglutinin (H) and fusion (F) proteins, and a nonglycosylated matrix (M) protein, which forms the inner layer. The H protein, which allows attachment of the virus to cells, via the CD46 or CDw150 receptors, is the main target for neutralizing antibodies. The F protein is responsible for fusion and syncytium formation of infected cells. CD46 is a ubiquitous membrane cofactor protein, which together with five other proteins, protects cells from complement activation and lysis. Some wild-type viruses, but not all, bind to the receptor but do not down-regulate it, thus preventing lysis and allowing efficient viral replication. The CDw150 receptor (also known as signalling lymphocyte activation molecule, SLAM) is expressed on immature lymphocytes and on effector memory T cells, and is rapidly induced on T and B cells after activation. The internal components or nucleocapsid consist of RNA, the nucleoprotein (N), which is the major protein, the phosphoprotein (P), and the large protein (L). The F protein is remarkably stable, the H protein shows minor antigenic variation, but the N protein, which contains a variable region in the C-terminal, is highly divergent among different strains of virus. Genetic analysis of Haemagglutinin and Nucleoprotein genes allowed molecular surveillance of the measles virus to track the international spread of the virus. There is also variation in the M protein, which some claim is related to persistent infection. 

Pathogenesis and the immune response

The measles virus, which is thermolabile and survives best at low humidities, is spread to susceptible contacts in droplets during sneezing and coughing. First, it infects and multiplies in the epithelium of the upper respiratory tract or the conjunctivae. Some 4 to 6 days later, the virus is found in the reticuloendothelial tissue of the liver and the spleen after passage through lymph nodes and spread via the blood. Here it multiplies, causing fusion of cells to form giant cells with many nuclei. Viral antigens, which can be found by immunofluorescent techniques in and on the surface of both these cells and lymphocytes, now induce the immune response. First, natural killer cells and cytotoxic T cells mount a cell-mediated reaction that contains the virus and limits its spread within cells. Later, B cells are primed to produce antibody. Defects in the cellular immune system, as in severe malnutrition, cancer, or primary and secondary immunodeficiencies, allow widespread multiplication of the virus to cause fatal giant cell pneumonia.


Table 1  Impact of measles immunization on the transmission and severity of measles


Outcome measurements
  • Bissau
  • 1980–1982
  • Senegal
  • 1983–1990
  • Bissau
  • 1991
Case fatality ratio: vaccinated / unvaccinated (95% CI) Acute mortality within 1 month 0.39 (0.13–1.14) 0.0 (0–0.92) 0.30 (0.13–0.72)
Delayed mortality from 1 month to 3 years     0.44 (0.22–0.90)
Secondary attack rate ratio according to vaccinated/unvaccinated index cases   0.28 (0.10–0.79) 0.36 (0.15–0.87)  

Based on data from Aaby P, et al. (1986). Vaccinated children get milder measles infection: a community study from Guinea-Bissau. J Infect Dis, 154, 858–63, and Samb B, et al. (1997). Decline in measles case fatality ratio after the introduction of measles immunization in rural Senegal. Am J Epidemiol, 145, 51–7.

Around day 8, the measles virus is carried by the blood, either free or in mononuclear cells, to the target tissues, which are epithelia of the skin, eye, lung, and gut. Again, the agent multiplies to cause a bright erythema of the mucosae and Koplik’s spots (see below), which are foci of viral multiplication. At this stage, measles virus may be cultured from nasopharyngeal secretions, and antigen can be detected by immunofluorescent techniques in the characteristic giant cells of the buccal mucosa, in epithelial cells, and in both B and T lymphocytes in the blood.

The rash, appearing around days 14 to 16, is the sign of a strong and complicated allergic reaction to the virus in epithelia. The extent and severity of the rash, which reflects the clinical severity of the disease, is determined by the number of target cells infected. Histological examination shows virus in the disrupted epidermis, in the corium, and in capillary endothelium. These tissues are infiltrated by mononuclear cells together with antibody, immune complexes, and complement. An intact cell-mediated immune response is essential to generate the rash and clear the virus, for if impaired, as in the case of children with leukaemia, or occasionally in severe kwashiorkor, the virus multiplies unchecked and no rash appears. Some 2 or 3 days after the start of the rash, around day 17 or 18, the virus can no longer be cultured from epithelia, for infected cells have been disrupted and the free virus neutralized by antibody. The first antibody to appear is to the nucleoprotein antigens. The second to appear, which is largely responsible for neutralization of the virus, is to the haemagglutinin. Finally, the antibody to the fusion glycoprotein appears in a low titre. This antibody stops cell-to-cell spread of the virus. At this stage the child is markedly immunosuppressed and thus susceptible to secondary infections of the eyes, mouth, gut, and lungs. Latent viruses, such as herpes simplex or cytomegalovirus, may be reactivated and in turn cause further damage to the immune system. The delayed hypersensitivity reaction, as measured by skin tests to old tuberculin or candida antigen, is absent or severely impaired.

By the third week, day 21, as the patient recovers, antibody is in full production. Levels remain elevated for the rest of the patient’s life, either because of repeated subclinical infections or because the virus persists in latent form in the spleen and other organs, so stimulating antibody. Occasionally, the virus persists in the brain in a damaging form to cause subacute sclerosing panencephalitis (see below).

The mechanisms of immunosuppression are complex. The CD4+ and CD8+ cytotoxic T-cell response, which is exuberant, may result in the destruction of infected T cells and dendritic cells thus leading to their depletion, deficient antigen processing, and generalized immunosuppression. Cross-binding of the CD46 cellular receptor down-regulates interleukin 12 (IL-12), a crucial cytokine in the development of Th1 and delayed hypersensitivity responses. Infection of CDw150+ lymphocytes, which are predominantly of the Th0/Th1 type, results in suppression of lymphoproliferation and cell death. Thus, measles ultimately dampens the Th1 response, resulting in a skewing towards a Th2 cytokine response and susceptibility to intracellular and other pathogens. However, this immunosuppression may be in the interest of the host by limiting further autoallergic damage of infected tissues.

Pathogenesis in the underprivileged, in the malnourished, and in the HIV-infected

Measles is severe, prolonged, and carries a high case fatality rate due to secondary infections in children of the developing world, as it was formerly in the underprivileged in Europe. Two explanations are offered. Crowding leads to a high dose of measles virus and also increases the chances of secondary infection. The period of incubation has been found to be short, around 10 to 12 days, in severe and fatal cases, consistent with the concept of infecting dose as a mechanism of severe disease. Alternatively, or in tandem, malnutrition diminishes the immune response to the virus, allowing great proliferation of virus and subsequent damage to the host. The immune response follows, which generates a severe and widespread rash followed by prolonged immunosuppression. Secondary bacterial infections with, e.g. Streptococcus pneumoniae, or latent infections such as herpes simplex or Mycobacterium tuberculosis occur in the wake of this intense damage to the immune system, often killing or maiming the child. Virus persists in lymphocytes and epithelial cells for up to 30 days after the start of the rash. Anorexia, increased catabolism, protein loss from the gut, and further malnutrition exaggerate the problem, which is worst in the weanling child.

The death rate after measles in hospitalized infants is higher in HIV-infected children, and prolonged viral shedding occurs in these children. Thus, in regions of high prevalence, HIV-infected children may be important unrecognized transmitters of the virus. Asymptomatic HIV-infected children respond normally to vaccination, but those with AIDS are less likely to respond and may be threatened by persistent infection.

Clinical features

There is a spectrum of severity ranging from mild in the privileged and well nourished to severe in the blatantly malnourished or immunosuppressed. However, the rule is not inviolate and other factors such as the age and dose of infection are probably as important in determining the severity of disease. Measles, often severe, occasionally infects unvaccinated young adults or those who have lived in isolated communities. The clinical features of measles and some complications are discussed below.

Prodrome (days 10–14)

A diagnosis of measles is often missed at this stage, when fever coupled with a runny nose, and sometimes complicated by convulsions, is the main feature. Other signs are mild conjunctivitis, red mucosa, Koplik’s spots, and diarrhoea. Koplik’s spots are found in the buccal mucosa. They are small, irregular, bright-red spots with a minute bluish-white speck in the centre of each of them. The prodrome is prolonged in severe cases, and reduced in individuals with modified measles due to maternal antibodies or the prophylactic use of immunoglobulin.

Rash (days 14–18)

The morbilliform rash first appears on the forehead and neck and then spreads, over a period of 3 to 4 days, to involve the trunk and finally the limbs.

In children in Africa and other parts of the developing world the rash is often red, confluent, raised, very extensive, and sometimes accompanied by bleeding into the skin and gut. Later, the rash blackens (postmeasles ‘staining’), then the skin peels causing extensive desquamation. Other epithelial surfaces are inflamed, the severity matching that of the rash. Cough may be hoarse and coupled with inspiration difficulty if the larynx and trachea are inflamed. Signs of pneumonitis are apparent, which in severe cases may cause cyanosis or be complicated by mediastinal and subcutaneous emphysema. Conjunctivitis, especially in those who are vitamin A deficient, can be severe. Enteritis may cause profuse diarrhoea with a resulting loss of protein, and malabsorption of food and water. The mouth is painful and red, which adds to the misery of the child, who becomes anorexic and may even refuse to suck the breast. In the uncomplicated case, as is usual in the West, the convalescent period is short, usually lasting less than a week. Complications should be suspected if fever persists while the rash is fading or desquamating.


Early complications (days 18–30)

As a result of the widespread, severe allergic reaction to the measles virus signified by the rash, the patient is left severely immunosuppressed and is susceptible to infection.


This causes the most deaths (Table 2) and is heralded by a rise in fever, leucocytosis, and respiratory difficulties. Lobar pneumonia is usually caused by S. pneumoniae, but bronchopneumonia, which is more common, results from other bacteria, such as Staphylococcus aureus, or secondary viral infections with, e.g. herpes simplex or adenovirus. A variety of other organisms such as Gram-negative bacteria, cytomegalovirus, fungi, M. tuberculosis, and Pneumocystis jirovecii should be considered as potential lung pathogens in the malnourished or immunocompromised child.

Stomatitis and enteritis

Chronic diarrhoea and a sore mouth caused by candidal infection are common complications of measles in children in the developing world. The gut is often superinfected with bacteroides spp., Escherichia coli, pseudomonas spp., and S. aureus, which results in malabsorption and protein loss. Deep ulcers caused by herpes simplex virus erode the corners of the mouth, gums, and inner surface of the lips causing much misery, illness, and pain.

Eye infections

Corneal ulceration leading to impaired vision or blindness is common after measles, especially in malnourished and vitamin A-deficient children (Fig. Several studies from Africa have shown that more than half of childhood blindness is related to measles. The mechanisms are still under discussion. In northern Nigeria, herpes simplex was found in 47% of active corneal ulcers after measles, and measles virus in 12%: the children often had evidence of oral herpes. In a study in Tanzania, blindness precipitated by measles was associated with vitamin A deficiency (50%), herpes simplex infection (21%), and the use of traditional eye medicine (17%).

Skin and other infections

Pyoderma is common after measles. In the malnourished patient, deep eroding ulcers may bore through the skin even into bone. When originating in the mouth they are known as cancrum oris or noma. Otitis media is also common.


This is a rare, but much feared, complication found in approximately 1 to 2 per 1000 cases. The onset is usually between 4 and 7 days after the start of the rash, but, rarely, it may occur within 48 h or up to 2 weeks from the onset. In addition to seizures, there is often fever, irritability, headache, and a disturbance in consciousness that may progress to profound coma. The disorder is probably attributable to a neuroallergic process. Lymphocytes from the cerebrospinal fluid have been shown to respond to myelin basic protein, as in experimental allergic encephalomyelitis. The virus cannot be isolated from cerebrospinal fluid, which contains lymphocytes and raised levels of IgG but normal levels of measles antibody. Mortality and morbidity are high: 10 to 15% of patients die and 25% of children are left with permanent brain damage. Treatment is supportive; dexamethasone has no convincing beneficial effect.

Late complications

This is the most frequent complication, for children of the developing world often lose a lot of weight during measles and may take many weeks to regain it. Those originally underweight, who have had severe measles, are at greatest risk, for anorexia in these children is prolonged, much protein is lost from the gut, and secondary infections, which lead to marasmus or marasmic kwashiorkor, are frequent. Measles has been shown to persist in the epithelia and lymphocytes of the severely malnourished for 30 or more days after the rash.

Persistent infection


Giant cell pneumonia is found in patients with defects in cell-mediated immunity. Children with leukaemia or kwashiorkor are particularly vulnerable, as are those with symptomatic HIV infection. The lung disease may develop weeks after measles, and in most cases the rash of measles has been absent and thus the diagnosis may not be suspected. The diagnosis is made by virological and/or histological examination of lung tissue. Most of these children die.

Subacute sclerosing panencephalitis (SSPE)

Persistent measles virus infection in the brain is responsible for this rare, progressive disease of the brain, which is found in 0.1 to 1.4 per million children after measles. The child with SSPE has usually experienced normal measles, albeit at a young age, 5 to 10 years earlier. The first indication is a disturbance in intellect and personality. Behavioural disorders and deterioration in school work are frequently mentioned. There then follows, over a period of weeks and months, myoclonus-like seizures, signs of extrapyramidal and pyramidal disease, and finally a state of decerebrate rigidity followed by death. The electroencephalogram shows a characteristic regular series of high-amplitude, spike-like waves. Very high titres of measles complement-fixing and haemagglutinin-inhibiting antibody are present both in serum and cerebrospinal fluid. Treatments for SSPE have included the use of transfer factor, plasmapheresis, and antiviral drugs, but to no avail.

Table 2  Complications and mortality in inpatients with measles, northern Nigeria, July–December 1978


  No. Died Percentage dead
Pneumonia 169 32 18.9
Gastroenteritis 65 9 13.8
Marasmic kwashiorkor 25 6 24.0
Laryngotracheobronchitis 21 4 19.0
Encephalitis 10 4 40.0

Reproduced from Parry EHOP (ed) (1984). Principles of medicine in Africa, 2nd edition. Oxford University Press, Oxford.

Multiple sclerosis, autism, Crohn’s disease

There is no convincing evidence that measles virus or immune responses to it have a causative role in these diseases. The alleged association between the measles, mumps, and rubella (MMR) vaccine, autism, and Crohn’s disease was based on weak science and has now been convincingly refuted by larger and stronger epidemiological studies. Subsequent molecular studies have failed to confirm the original finding of measles virus and genomic RNA in diseased bowel. The false alarm raised by this report caused a substantial reduction in the number of children vaccinated against measles in the United Kingdom.


This is primarily clinical, although signs may be less clear-cut in vaccinated subjects. Thus, in areas of high vaccine coverage the detection of measles-specific IgM antibody by enzyme-linked immunoassay or, better still, the detection of measles antigen in saliva or urine may clinch the diagnosis if the rash is mild or atypical. Subclinical measles is common in vaccinated children after exposure to measles: the diagnosis is made by detecting a fourfold or greater rise in measles antibody within 2 to 6 weeks of exposure. It is not clear if such cases are infectious.

Treatment of measles and its complications

No effective antimeasles drug exists, yet some children do benefit from treatment in hospital. The following criteria indicate severe measles and a need for hospital admission: a widespread, confluent rash darkening to deep red or purple; signs of laryngeal obstruction; subcutaneous emphysema; marked dehydration; blood in the stool or more than five stools a day; convulsion or loss of consciousness; severe secondary pneumonia; corneal ulceration; severe ulceration of the mouth and skin. These signs should be taken particularly seriously when the child is underweight or frankly malnourished.

Hydrate the child orally or intravenously. Treat lobar pneumonia with benzylpenicillin, and bronchopneumonia with amoxicillin or, if severe, with combined antibiotics such as gentamicin and cloxacillin. Antibiotic eye ointments relieve discomfort and possibly prevent secondary infections of measles conjunctivitis. Antibiotics (topical and systemic) and vitamin A should be given routinely for the treatment of eye ulcers. If herpes simplex virus is the cause, use aciclovir topically or, when severe, systemically. Candida infections of the mouth or gut often respond dramatically to nystatin. Feeding, by tube if necessary, needs careful planning and presentation, for the anorexic infected child will be in severe negative energy balance due to a greatly increased catabolic rate. Case fatality rates are 30 to 50% lower in those children in hospital treated with vitamin A. This should be given orally at the time of diagnosis in a dose of 100 000 IU for children below 12 months of age and in a dose of 200 000 IU for older children. If eye signs of vitamin A deficiency are present, the initial dose should be repeated the next day and again 1 to 4 weeks later.

The prophylactic use of antibiotics such as amoxicillin or co-trimoxazole to prevent secondary infections after measles is a widespread practice based on slender evidence. The only community randomized placebo controlled trial was small: those children who received co-trimoxazole had less pneumonia and conjunctivitis and had a significantly higher weight gain (see Table 3.


Passive immunization with human immunoglobulin is highly effective if given within 2 or 3 days of exposure, in a dose for children of 0.2 ml/kg. Immunoglobulin should be given to those in whom vaccination is contraindicated such as immunocompromised children with kwashiorkor, cancer, or AIDS or, if severe, combined antibiotics such as gentamycin and amoxicillin. If S. aureus is suspected, use gentamycin and cloxacillin.

The currently used vaccines are live strains, attenuated by culture in chick fibroblasts. The Edmonston–Zagreb strain, which has been cultured in human diploid cells, is also widely used. It is more effective than other vaccines in the presence of antibody, and should be used in a standard dose if vaccinating infants below 9 months of age, or if a booster dose is required. The complications of vaccination are few and generally mild. Fever of moderate severity is infrequent, and a mild rash with some signs of upper respiratory tract infection occurs rarely. Underweight children respond normally to the vaccine, as do ill children attending the outpatient department and those on the ward. As clinics and hospitals are major sites of transmission of the virus in the developing world, all susceptible children in these places should be vaccinated unless immunocompromised.

The measles vaccination policy for low income countries has seen major changes in the last 25 years. The optimal age for vaccination in the developed world is between 14 and 16 months, when maternal antibody has disappeared. However, this recommendation could not be applied to children in developing countries, because there measles infects at a much earlier age. In 1982, the World Health Organization recommended vaccination at 9 months of age but, by then, 5 to 15% of children may have had measles. This policy was not based on good evidence; it is not known if vaccination at 9 months is better in saving children than vaccination at 7, 8, or 10 months of age, or a two dose regime in infancy.

Table 3  Prophylactic antibiotic to prevent complications after measles in Guinea-Bissau


  • Co-trimoxazole
  • (n = 46)
  • Placebo
  • (n = 38)
  • Adjusted odds ratio
  • (95% CI)
Pneumonia 1 (2%) 6 (16%) 0.14 (0.01–1.50)
Hospitalization 0 3
Diarrhoea 3 (7%) 5 (13%) 0.17 (0.01–1.55)
Severe fever 6 (13%) 11 (29%) 0.36 (0.09–1.43)
Stomatitis 4 (9%) 7 (18%) 0.43 (0.08–2.26)
Conjunctivitis 12 (26%) 17 (45%) 0.31 (0.10–1.03)
Weight gain (g/day) 32 15

(Adapted and reproduced from Garly M-L, et al. (2006). Prophylactic antibiotics to prevent pneumonia and other complications after measles: community based randomised double blind placebo controlled trial in Guinea-Bissau. BMJ, 333, 1245–50.)

Through the 1990s it became clear that several doses of measles vaccines were needed to improve measles control. The developed countries have used two-dose strategies with a second dose being given at school entry or to young teenagers. Latin America has obtained major successes with a combination of improved vaccination coverage and regular immunization campaigns providing a second opportunity for measles vaccination. The strategy has the following elements: (1) catch-up—a one-time mass campaign covering everybody between 9 months and 14 years of age regardless of previous measles or immunization; (2) keep-up—achieving a high coverage for each birth cohort; (3) follow-up—subsequent mass campaigns covering all children every 3 to 5 years; and (4) mop-up—campaigns that target children who are difficult to reach or during outbreaks. As a result of this strategy, Latin America has been declared free of internal measles transmission since 2002. Since there is no immediate risk of measles infection, the age of routine vaccination has been raised to 12 months as this is believed to be associated with better antibody responses.

The Latin American model has been transferred to other regions. Rebranded as SIA (supplementary immunization activities), it has assured a spectacular success in reducing measles mortality in Africa. The goal of reducing global measles deaths by 50% by 2005 compared to 1999 has been met. However, these campaigns which are donor driven are expensive and should not be seen as a substitute for an inadequate immunization service.

Elimination or eradication

Global measles eradication has yet to be made official policy. However, the Americas have attained elimination (i.e. no internal transmission of the virus), and three other regions are pursuing such a policy. Measles satisfies the criteria for eradication for there is no animal reservoir, it is only transmitted between humans, it is easy to diagnose, and vaccines are available. Measles elimination can be accomplished for prolonged periods in defined geographical regions provided there is sufficient funding and political will. This was obtained for the first time in the Gambia in the mid 1960s as part of the smallpox eradication and measles vaccination campaigns.

However, eradicating measles will be a daunting task. First, it is the most infectious of diseases and will require vaccine coverage of greater than 95%. When there is no risk of infection, it will be increasingly difficult for parents to appreciate the necessity for vaccination especially as risk, although small, is perceived. Secondly, herd immunity will become a problem as with less exposure to the virus vaccine induced immunity will wane more rapidly. Thirdly, Africa will be a stern test for due to political instability, wars, and natural disasters it will be difficult to maintain sufficiently high coverage. Fourthly, with the growing HIV epidemic, there is a risk that the vaccine may be less effective and that infected individuals will be difficult to diagnose and excrete virus for long periods. Fifthly, with the growing fear of bioterrorism, it is unlikely that all immunization can be stopped in the posteradication era. Lastly, but most difficult, will be to assure long-term funding as donors have a tradition of changing priorities.

The international health community is split over whether eradication can be attained with the Latin American strategy using existing vaccines or whether new vaccines and delivery systems such as aerosolization are needed. New vaccines, which can be given in early infancy, or two-dose strategies using the standard vaccine at 4 and 9 months of age, might be necessary to contain measles in the developing world. Coverage of at least 95% of all susceptible children, including those between 3 and 9 months of age, with a vaccine that is at least 95% effective is assumed to be necessary if the virus is to be eradicated. Current vaccines do not meet these standards except when two doses have been given in national campaigns. New vaccines such as the modified vaccinia Ankara (MVA) recombinant virus, a nonreplicating mutant of horsepox made to express the F and H proteins, or a DNA vaccine expressing these proteins may possibly fulfill such exacting requirements, for they have been shown to protect macaques from measles. High titre vaccines were used to vaccinate young infants, but were discontinued when an unexplained increase in mortality in girls was found 1 to 3 years after vaccination. Thus, new vaccines need long-term monitoring in order to fully understand the potential nonspecific immunological interactions that may occur between the many vaccines in use and with infections that are common in infants.

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Further reading 

Aaby P, et al. (1983). Measles mortality, state of nutrition, and family structure. A community study from Guinea-Bissau. J Infect Dis, 147, 693–701. [Groundbreaking paper showing measles mortality depends on family structure and intensity of exposure but not nutrition.]
Aaby P, et al. (1986). Vaccinated children get milder measles infection: a community study from Guinea Bissau. J Infect Dis, 154, 858–63.
Aaby P, et al. (1995). Non-specific beneficial effects of measles immunization: analysis of mortality studies from developing countries. BMJ, 311, 481–5.[Abstract/Full Text]
Aaby P, et al. (2003). Differences in female-male mortality after high-titre measles vaccine and association with subsequent vaccination with diphtheria—tetanus-pertussis and inactivated poliovirus: re-analysis of West African studies. Lancet, 361, 2183–88. [An interesting theory invoking nonspecific effects of vaccines.][CrossRef] [Web of Science] [Medline] 
Aaby P, et al. (2003). The survival benefit of measles immunisation may not be explained entirely by the prevention of measles disease. Int J Epidemiol, 32, 106–115.[Abstract/Full Text]
de Quadros CA, et al. (1996). Measles elimination in the Americas. Evolving strategies. JAMA, 275, 224–229.
Duke T, et al. (2003). Measles: not just another viral exanthema. Lancet, 361, 763–73. [An excellent review.][CrossRef] [Web of Science] [Medline] 
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Garly ML, et al. (2006). Prophylactic antibiotics to prevent pneumonia and other complications after measles: community based randomized double blind placebo controlled trial in Guinea Bissau. BMJ, 333, 1245–1250. [The only randomized controlled trial of prophylactic antibiotics for measles in Africa.][Abstract/Full Text]
Jaye A, et al. (1998). Ex vivo analysis of cytotoxic T lymphocytes to measles antigens during infection and after vaccination in Gambian children. J Clin Invest, 102, 1969–77. [The largest and most complete study of cytotoxic T-cell responses in natural measles.] [Web of Science] [Medline] 
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Moss WJ, Ota MO, Griffen DE (2004). Measles: immune suppression and immune responses. Int J Biochem Cell Biol, 36, 1380–84. [A succinct review of an important aspect of measles.][CrossRef] [Web of Science] [Medline] 
Moss WJ, et al. (2006). Global measles elimination. Nat Rev Microbiol, 4, 900–908.[CrossRef] [Web of Science] [Medline] 
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Whittle HC, et al. (1979). Severe ulcerative herpes of mouth and eye following measles. Trans R Soc Trop Med Hyg, 73, 66–9.[CrossRef] [Web of Science] [Medline] 
Whittle HC, et al. (1999). Effect of sub-clinical infection on maintaining immunity against measles in vaccinated children in West Africa. Lancet, 353, 98–101.[CrossRef] [Web of Science] [Medline] 
Wolfson LJ, et al. (2007). Has the 2005 measles mortality reduction goal been achieved? A natural history modelling study. Lancet, 369, 191–200.[CrossRef] [Web of Science] [Medline]