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Measles



Measles

Measles (also known as Rubeola) is an infection of the respiratory system and is a highly contagious, serious disease caused by a virus; specifically a paramyxovirus of the genus Morbillivirus. Morbilliviruses, like other paramyxoviruses, are enveloped, single-stranded, negative-sense RNA viruses. The measles virus normally grows in the cells that line the back of the throat and lungs. Measles is a human disease and is not known to occur in animals.

Globally, it remains one of the leading causes of death among young children, despite the availability of a safe and effective vaccine. An estimated 164,000 people died from measles in 2008 – mostly children under the age of five.

Targeted vaccination campaigns have had a major impact on reducing measles deaths. From 2000 to 2008, nearly 700 million children aged 9 months to 14 years who live in high risk countries were vaccinated against the disease. Global measles deaths decreased by 78% during this period.

Contents

Signs and Symptoms
Causative Agent
Mode of Transmission
Diagnosis
Incubation Period
Pathogenesis/Pathophysiology
Prevention
Treatment
Prognosis
Complications
References

Signs and Symptoms

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Symptoms may include:

  • Bloodshot eyes
  • Cough
  • Fever
  • Light sensitivity (photophobia)
  • Muscle pain
  • Rash
    • Usually appears 3 – 5 days after the first signs of being sick
    • May last 4 – 7 days
    • Usually starts on the head and spreads to other areas, moving down the body
    • Rash may appear as flat, discolored areas (macules) and solid, red, raised areas (papules) that later join together
    • Itchy
  • Redness and irritation of the eyes (conjunctivitis)
  • Runny nose
  • Sore throat
  • Tiny white spots inside the mouth (Koplik’s spots)

Causative Agent

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Paramyxovirus, genus Morbillivirus

Mode of Transmission

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The highly contagious virus is spread by coughing and sneezing, close personal contact or direct contact with infected nasal or throat secretions.

The virus remains active and contagious in the air or on infected surfaces for up to two hours. It can be transmitted by an infected person from four days prior to the onset of the rash to four days after the rash erupts.

Measles outbreaks can result in epidemics that cause many deaths, especially among young, malnourished children.

In countries where measles has been largely eliminated, cases imported from other countries remain an important source of infection.

Diagnosis

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Clinical diagnosis of measles requires a history of fever of at least three days together with at least one of the three C’s (cough, coryza, conjunctivitis). Observation of Koplik’s spots is also diagnostic of measles.

Alternatively, laboratory diagnosis of measles can be done with confirmation of positive measles IgM antibodies or isolation of measles virus RNA from respiratory specimens. In children, where phlebotomy is inappropriate, saliva can be collected for salivary measles specific IgA test. Positive contact with other patients known to have measles adds strong epidemiological evidence to the diagnosis. The contact with any infected person in any way, including semen through sex, saliva, or mucus can cause infection.

Incubation Period

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Symptoms usually begin 8 – 12 days after you are exposed to the virus. This is called the incubation period.

Pathogenesis/Pathophysiology

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Measles virus

The measles virus initially infects the respiratory epithelium and is transmitted via respiratory droplets. It is highly transmissible with an infectivity rate of 76%, even greater than that of varicella. Prior to the measles vaccine, infection with the measles virus was simply considered a part of life.

Instead of replicating in the respiratory epithelium, as was once thought, replication appears to occur in the regional lymph nodes. Replication in regional lymph nodes eventually leads to viremia. Infection of the endothelial cells ensues, causing an enanthem (Koplik’s spots). Epithelial cells are also infected, leading to the well-known cutaneous eruption of measles.

The measles virus is a single stranded RNA virus of the genus Morbillivirus and family Paramyxoviridae. Measles virus has 2 membrane glycoproteins called hemagglutinin and fusion. Both of these glycoproteins appear to be important for infection with the measles virus.

Hemagglutinin appears to be involved with receptor binding and fusion, with fusion of the virus with host cells. Expression of hemagglutinin activates the alternative complement pathway.

The Edmonston strain of the measles virus and vaccines derived from this strain bind to the cell surface protein CD46, also known as membrane cofactor protein. CD46 is a regulator of the complement activation gene and inhibits activation of the alternative complement pathway. Four isoforms of CD46 exist in humans, and all are capable of binding measles virus.

An additional cellular receptor for the measles virus has recently been identified called SLAM (signaling lymphocyte-activation molecule) or CDw150 expressed on some T and B cells. SLAM is capable of binding strains of the measles virus that also bind CD46 (the Edmonston strain) as well as strains that do not bind CD46 such as the KA strain.

Infection with the measles virus leads to a prolonged immunosuppression, which accounts for much of the morbidity and mortality associated with this disease. Cell-mediated immunity decreases, clinically evidenced by the conversion of positive tuberculin skin test results to negative following infection or vaccination. The mechanism of this immunosuppression is being elucidated.

Following infection with the measles virus, a shift from cell-mediated immunity (a TH-1 response) to humoral immunity (a TH-2 response) occurs. Expression of the TH-2 cytokine interleukin (IL)–2 is increased, supporting antibody formation, and TH-1 cytokines IL-2, IL-12, interferon (IFN)–gamma decrease.

IL-12 is a crucial cytokine for the development of cell-mediated immunity. It is necessary for delayed-type hypersensitivity, induces production of IFN-gamma, and plays a role in activation of T cells and natural killer cells. It was found that infection of monocytes, the primary producer of IL-12, with the measles virus via CD46 led to decreased production of this cytokine. It was also found that activated dendritic cells also had a significant decrease in production of IL-12, leading to proliferation of the measles virus and apoptosis of infected dendritic cells and T cells. These findings support the hypothesis that measles virus infection of antigen-presenting cells plays a critical role in the immunosuppression observed following infection with the measles virus.

Primates are the only hosts for measles virus, and no animal model exists that replicates the clinical findings of measles infection typical in children.

Prevention

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  • The most effective way to prevent measles is through immunization.
    • Children in the United States routinely receive the measles-mumps-rubella (MMR) vaccine according to a published immunization schedule. This vaccine protects against both red measles and German measles. Vaccination (or written refusal) is required for entry into school.
    • Doctors usually give the first dose of the measles immunization at 12-15 months of age.
    • Doctors give a second dose of the immunization when the child is 4 to 6 years old.
    • Although most children tolerate the vaccine well, a few may develop fever and even a rash from five to 12 days after the immunization. Adult women who get the vaccine may notice short-term aching in their joints.
    • The vaccine is about 95% effective in preventing measles of either type. That means that a small number of people who get the vaccine may still be able to get measles.
    • The vaccine should not be used in people with egg allergies.
    • Rarely, the measles vaccine can cause a measles-like illness. This is most common in people with weak immune systems, such as those with advanced HIV or those on chemotherapy. In such patients, the risk of vaccination should be balanced carefully against the risk of getting measles.
    • Women who may become pregnant should have a blood test to be sure they are immune to rubella (“German measles”).
  • Both types of measles are still common in areas that do not offer immunization and in people who have not been immunized.
  • As with all other contagious illnesses, covering the mouth when coughing or sneezing and good hand-washing practices will help prevent the spread of the diseases.
  • A special immunization — immune globulin — may be necessary for certain high-risk people after they are exposed to measles. These include children younger than 1 year, children with weakened immune systems, and pregnant women. If exposure to measles had occurred, contact the physician to determine if there is a need for immune globulin.

Treatment

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There is no specific treatment for the measles.

The following may relieve symptoms:

  • Acetaminophen (Tylenol)
  • Bed rest
  • Humidified air

Severe complications from measles can be avoided though supportive care that ensures good nutrition, adequate fluid intake and treatment of dehydration with WHO-recommended oral rehydration solution. This solution replaces fluids and other essential elements that are lost through diarrhea or vomiting. Antibiotics should be prescribed to treat eye and ear infections, and pneumonia.

Some children may need vitamin A supplements. Vitamin A reduces the risk of death and complications in children in less developed countries, where children may not be getting enough vitamin A. People who don’t get enough vitamin A are more likely to get infections, including measles. It is not clear whether children in more developed countries would benefit from supplements.

Prognosis

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Those who do not have complications such as pneumonia do very well.

Complications

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Complications with measles are relatively common, ranging from relatively mild and less serious diarrhea, to pneumonia and encephalitis (subacute sclerosing panencephalitis), corneal ulceration leading to corneal scarring. Complications are usually more severe amongst adults who catch the virus.

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References

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1. “WHO, Measles”

2. “Wikipedia, Measles”

3. “MedlinePlus, Measles”

4. Dörig RE, Marcil A, Chopra A, Richardson CD. The human CD46 molecule is a receptor for measles virus (Edmonston strain). Cell. Oct 22 1993;75(2):295-305.

5. Manchester M, Liszewski MK, Atkinson JP, Oldstone MB. Multiple isoforms of CD46 (membrane cofactor protein) serve as receptors for measles virus. Proc Natl Acad Sci U S A. Mar 15 1994;91(6):2161-5.

6. Naniche D, Varior-Krishnan G, Cervoni F, et al. Human membrane cofactor protein (CD46) acts as a cellular receptor for measles virus. J Virol. Oct 1993;67(10):6025-32.

7. Tatsuo H, Ono N, Tanaka K, Yanagi Y. SLAM (CDw150) is a cellular receptor for measles virus. Nature. Aug 24 2000;406(6798):893-7.

8. Karp CL, Wysocka M, Wahl LM, et al. Mechanism of suppression of cell-mediated immunity by measles virus. Science. Jul 12 1996;273(5272):228-31.

9. Fugier-Vivier I, Servet-Delprat C, Rivailler P, Rissoan MC, Liu YJ, Rabourdin-Combe C. Measles virus suppresses cell-mediated immunity by interfering with the survival and functions of dendritic and T cells. J Exp Med. Sep 15 1997;186(6):813-23.

10. “eMedicine, Measles”

11. “eMedicineHealth, Measles”

12. “Internet Archive, Prevention of Eye Blindness – Document”

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