Measles morbillivirus

March 12, 2019 Gaurab Karki Virology 0




Measles morbillivirus:

  • Measles is an acute highly infectious disease characterized by fever, respiratory symptoms and a maculopapular rash.

General properties

  • General morphology as Paramyxoviruses
  • Roughly spherical with size of 120-250 nm in diameter, often pleomorphic.
  • Spikes on envelope contains haemagglutinin but no neuraminidase
  • The virus causes agglutination of erythrocytes (RBCs) but it is not followed by elution as the virus does not produce any neuraminidase activity.
  • Grows well on human or monkey kidney and human ammonion cultures. Isolates can be adapted for growth on continuous cell lines (Hela, Vero) and in the amniotic sac of hen’s eggs.
  • CPE consists of multinucleate syncytinum formation with numerous acidophilic nuclear and cytoplasmic inclusion.
  • Multinucleate giant cells are also found in the lymphoid tissue of patients.
  • The virus is labile and readily inactivated by heat, UV, ether and formaldehyde.
  • It can be stabilized by molar mgso4, so that it resist heating at 50 degree Celsius for 1 hour.
  • The measles virus is antigenically stable. It shares antigens with the viruses of canine distemper and bovine rinderpest.

Mode of transmission of Measles virus

  • Transmission occurs by direct contact with respiratory secretion and aerosols created by coughing and sneezing.
  • The virus enters the body through the respiratory tract and conjunctiva.
  • Haematogenous and transplacental transmission can occur when measles occurs during pregnancy.

Pathogenesis of Measles virus

  • Humans are the only natural host for measles virus although numerous other species, including monkeys, dogs and mice can be experimentally infected.
  • The virus gains access to the human body via the respiratory tract, where it multiplies locally.
  • The infection than spreads to the regional lymphoid tissue, where further multiplication occurs.
  • Primary viraemia disseminates the virus, which then replicates in the reticuloendothelial system.
  • Finally a secondary viraemia seeds the epithelial surface of the body, including the skin respiratory tract and conjunctiva, where focal replication occurs. The described events occur during the IP which typically lasts 8-12 days but may last up to 3 weeks in adults.
  • During the prodromal phase (2-4 days) and the first 2-5 days of rash, virus is present in tears, nasal and throat secretions, urine and blood.
  • The characteristics maculopapular rash appears about day 14 just as circulating antibodies become detectible and the viraemia disappears and the fever falls.
  • The rash develops as a result of interactions of immune T cells with the virus infected cells in the small blood vessels and last for about 1 week.
  • Involvement of CNS is common in measles. Progressive measles inclusion body encephalitis may develop in patients with defective cell mediated immunity.
  • A rare late complications of measles is subacute sclerosing panencephalitis (SSPE); a fatal disease that develops years after the initial measles infections and is caused by virus that remains in the body after acute measles infections.

Clinical manifestation of measles

  • Infections in non-immune host are almost always symptomatic.
  • Measles is a highly contagious febrile illness.
  • After an incubation period of 8-12 days, measles is typically a 7-11 days illness with a prodromal phase of 2-4 days followed by an eruptive phase of 5-8 days.

i. Prodromal phase of measles:

  • The prodromal phase is characterized by fever and three (C’s – coryza of nose, conjunctivitis usually associated with photophobia and Cough), Kopliks spots and lymphopenia.
  • The cough and coryza reflects an intense inflammatory reaction involving the mucosa of the respiratory tract.
  • Kopliks spots are small, bluish white ulceration of the buccal mucosa.
  • The fever and cough persists until the rash appears and then subside within 1-2 days. The rash starts on the head and the spreads progressively to the chest, the trunk and down the limbs which appears as light pink, discrete maculopapular that coalesce to form blotches and becomes brownish in 5-10 days. The fading rash resolves with desquamation.

ii. Modified measles:

  • Modified measles occurs in partially immune persons such as infants with residual maternal antibody.
  • The IP is prolonged, prodromal symptoms are diminished.
  • Koplik’s spots are usually absent and rash is mild.

iii. Atypical measles:

  • Atypical measles occurs in individuals who received the older inactivated vaccine and later exposed to a wild strain.
  • It may also rarely occur in persons vaccinated with attenuated vaccine.
  • It is characterized by a prolonged high fever, pneumonitis and the rash.
  • The rash characteristically begins peripherally and may be urticarial, macularpapular, hemorrhagic or vesicular.

iv. Complications of measles:

  • The most common complications of measles is otitis media occurring in 5-9 % of cases.
  • Pneumonia is life threatening complications of measles, caused by secondary bacterial infections.
  • Giant cells pneumonia is serious complication in children and adults with deficiencies in CMI.
  • Complications involving CNS are the most serious.
  • Acute encephalitis occurs in about 1:1000 cases.
  • Post infections encephalomyelitis is an autoimmune disease associated with an immune response to myelin base protein.
  • The mortality in encephalitis associated with measles is about 10-20 %. The majority of survivors have neurologic sequela.
  • Subacute sclerosing panencephalitis (SSPE) is a rare late complications of measles, occurs with an incidence of about 1:300000 cases.
  • It is a degenerative disease of the CNS caused by persistent measles infection. The disease begins 5-15 years after a case of measles. It is characterized by progressive mental deterioration, involuntary movements muscle rigidity and coma the condition is associated with the presence of an extremely high measles antibody titers in the blood and CSF.
  • Other complications of measles include bronchopneumonia, laryngotracheobronchitis (croup), diarrhoea.
  • Measles includes labor in some pregnant women, resulting in spontaneous abortion or premature delivery. The virus may across the placenta and infect the fetus during maternal measles.

Laboratory diagnosis of measles:

  • Typical measles is reliably diagnosed on clinical grounds.
  • Laboratory diagnosis is necessary in case of modified or atypical measles.

1. Specimens:

  • Respiratory specimens, conjunctival specimen, urine, blood and brain tissue.
  • Specimens are collected during the prodromal stage and the period following until 2 days after the appearance of the rash.

2. Microscopy:

  • Demonstration of multinucleated giant cells measuring up to 100 nm in diameter in Giemsa stained smears is diagnostic of measles.
  • Immunofluorescent study of exfoliated respiratory cells in nasopharyngeal secretion virus particles.

3. Antigen detection:

  • Measles antigen can be detected directly in epithelial cells in respiratory secretions, urinary sediments, pharyngeal secretions by direct immunofluorescent antibody test

4. Isolation and identification of virus:

  • Nasophayngal and conjunctival swabs, blood samples, respiratory secretions and urine collected from a patient during febrile period are appropriate sources of viral isolation.
  • Growth can be obtained in primary human or monkey kidney cells.
  • Growth occurs slowly with CPE containing both intra-nuclear and intra-cytoplasmic inclusion bodies in 7-10 days.

5. Serology:

  • Serologic confirmation of measles depends on a 4 fold rise in antibody tilter between acute phase and convalescent phase sera or demonstration of measles specific antibody in a single specimen drawn between 1 and 2 weeks after the onset of rash.
  • ELISA
  • Haemagglutinin Inhibition assay
  • Neuraminidase test

Treatment and control of measles:

  • Ribavirirn either intravenous or in aerosol form is evaluated now a days to treat severely affected adults and immunocompromised individuals with acute measles or SSPE.
  • However the drug is yet to be used for regular treatment of cases of measles.
  • Vitamin A treatment in developing countries has reduced mortality and morbidity.
  • Active immunization
  • A highly effective and safe attenuated live measles virus vaccine is available. It now uses Schwartz and Moraten attenuated strain of the original Edmonstron B strain.
  • The vaccine is available in monovalent form in combination with live attenuated Rubella vaccine (MR) and live attenuated rubella and mumps vaccine (MMR)- currently used for universal immunization of children.
  • Efficacy – 95 % (90-98%)
  • Duration of immunity- life long
  • Schedule- 2 doses – first at the age of 9 month- second at the age of 2 years
  • Passive immunization
  • Pooled sera containing antibody against measles virus confess passive immunity to infants and susceptible contacts of measles cases.

Measles morbillivirus