GENUS MORBILLIVIRUS
MEASLES (Rubeola)
MEASLES (RUBEOLA)
• Ancient disease, no clear extinction was made between measles or other
exanthematous diseases including smallpox.
• Thomas Syndenham (1960) accurately described measles.
• Viral origin was established by Goldberger and Anderson in 1911 through inoculation of
blood filtrates and nasopharyngeal secretions from Patients.
• Virus was isolated in monkey and human kidney cells by Enders and Peebles in 1954.
MEASLES VIRUS
• Roughly spherical, often pleomorphic particle, 120 to 250nm in diameter, tightly coiled helical
nucleocapsid surrounded by lipoprotein envelope on its surface hemagglutinin (H) spikes.
• Envelope has F protein which mediates cell fusion and haemolytic activities.
• Agglutinates monkey erythrocytes but there’s no elution as the virus doesn't posses
neuraminidase activity.
• Grows well on human or monkey kidney and human amnion cultures for primary isolation.
• Isolates can be adapted for growth on continuous cell lines (HeLa, Vero) and in amniotic sac of
hen’s eggs.
• Cytopathic effects consists of multinucleate syncytium formation, with numerous acidophilic
nuclear and cytoplasmic inclusions.
• Multinucleate giant cells (Warthin- Finkeldey cells) are seen in lymphoid tissues of patients.
• Labile, readily heat inactivated, ultraviolet light, ether and formaldehyde.
• Can get stabilised by molar magnesium sulphate, so that it resists heating
at 50֯C for 1hour.
• Measles virus is antigenically uniform.
• Shares antigen with viruses of canine distemper and bovine rinderpest.
CLINICAL FEATURES
• Takes 9 to 11 days from exposure time to infection for first signs of clinical disease to
appear.
• Consist of prodromal malaise, fever, conjunctival injection, cough and nasal discharge.
• Rashes appears after 3-4 days of prodromal illness.
• Before a day or two the rash begins, Koplik’s spots develop on the buccal mucosa,
occasionally on conjunctiva and intestinal mucosa.
• Illness subsides within a day or two of rash’s appearance.
• Red maculopapular rash of measles appears on forehead first, spreads downwards, to
disappear in the same sequence 3-6 days later, leaving behind a brownish
discolouration and finely granular desquamation.
• Patients recover uneventfully, but few develop complications due to virus (croup,
bronchitis) or to secondary bacterial infection (pneumonia, otitis media).
• Rarely, virus may cause fatal giant cell pneumonia, particularly in children with
immunodeficiencies or severe malnutrition.
• Complications are common and serious in developing countries.
• Most serious complication is meningoencephalitis.
• Survivors have neurological sequelae.
• A rare late complication is subacute sclerosing panencephalitis (SSPE).
• Protracted diarrhea is often seen as a complication in children in poor nations.
• Virus may be recovered from stools of patients with measles enteritis.
• Occurs as a suppression of delayed hypersensitivity after measles infection, which may
last for weeks or few months.
• Mantoux and other skin tests may be negative during this period.
• Underlying tuberculosis may become worse.
• Recovery of measles is associated with the improvement of allergic eczema or asthma,
Hodgkin’s disease or lipoid nephrosis
• Measles induces labour in pregnant women.
• Results in spontaneous abortion or premature delivery.
• Virus may cross the placenta and infect the fetus during maternal measles but there’s no
evidence of teratogeny.
• Thrombocytopenia may develop, leading to purpura and bleeding from mouth, intestines
and genitourinary tract.
PATHOGENESIS
• virus enters body through respiratory tract or conjunctiva and multiplies locally and in the
adjoining lymph nodes.
• Spreads to reticuloendothelial system through blood.
• After multiplication, a secondary viremia transports virus to epithelial surfaces including the skin,
mouth, respiratory tract and conjunctiva.
• Pathogonomic Koplik’s spots (small bluish white ulcerations) on buccal mucosa opposite to lower
molars contain giant cells, cytoplasmic and intranuclear inclusions and virion components,
indicating local viral replication.
• Viral replication evidence can be seen in vascular endothelial cells at the sites of the
skin rash.
• Rash is an immune reaction between T-lymphocytes and cells in which viral replication
takes place.
• Virus can be isolated from blood, washed leucocytes, tears and respiratory secretions
during the 2-4 days of prodromal period.
• Can be recovered from urine upto 4 days after the appearance of skin rash.
LABORATORY DIAGNOSIS
• Diagnosis is self-evident in case of typical case of measles.
• In atypical cases and differentiation from rubella, laboratory tests are useful.
• Measles virus antigen can be defected in these cells by immunofluorescence.
• Multinucleated giant cells can be diagnosed in Giemsa – stained smears of nasal secretions.
• Virus can be isolated from nose, throat, conjunctiva and blood during prodromal phase and upto
2 days after rash appearance.
• Virus can be obtained from urine.
• Primary human or monkey kidney and amnion cells are most useful.
• Cytopathic changes may take upto a week to develop.
• Earlier diagnosis of viral growth is possible by immunofluorescence.
SEROLOGICAL DIAGNOSIS
• Specific neutralisation, hemagglutination inhibition and complement fixing antibodies develop
early.
• A 4 fold rise in titre is looked for using sera collected during the acute phase and 10-21 days
later.
• Demonstration of measles-specific IgM in a single specimen of serum drawn between 1 and 2
weeks after the onset of the rash is confirmatory.
• False negatives may occur if the serum is taken earlier than 1 week before or later than the 2
weeks after the onset of the rash.
• Demonstration of high titre measles antibody in the CSF is diagnostic of SSPE.
EPIDEMIOLOGY
• Endemic and produces epidemics (seen in late winter or early winter) every 2-3 years.
• Disease has maximum incidence in children of 1-5 years.
• Uncommon in first 6 months of life due to the presence of maternal antibody.
• One attack confers solid immunity.
• People are natural hosts of measles.
• Monkeys are often infected but they seem to acquire the infection from humans.
• Patients are infectious from 3 days before to the onset of symptoms until the rash desquamates.
• Infectivity is maximum at the prodrome and diminishes rapidly on the onset of rash.
• Spread by direct contact with respiratory secretions and aerosols by coughing and sneezing.
• Virus enters through respiratory tract and conjunctiva.
• In nonimmune, infection results in clinical disease.
PROPHYLAXIS
• Normal human gammaglobulin given within 6 days of exposure can prevent or modify the
disease, depending on the dose.
• Valuable in children with immunodeficiency, pregnant women and others at special risk.
• Safe and effective live attenuated measles vaccine is available.
• Original live vaccines used the Edmonston strain developed by multiple passage through human
kidney, amnion and chick embryo cultures.
• Have high risk of febrile rash (vaccination measles), further attenuation became necessary.
• Schwartz and Moraten strains so developed were safe but effective only in children older then 15
months.
• Edmonston- Zagreb strain, attenuated by passage in human diploid cells, is preferred as vaccine
strain because it is able to produce seroconversion even in infants 4-6 months old.
• Recommended age for measles vaccination in developing countries is 9 months while
in advanced nations is 15 months.
• Vaccine is either given by itself, or in combination, as the MMR vaccine.
• A single subcutaneous injection provides protection beginning in about 12 days and
lasting for over 20 years.
• Contraindications are immunodeficiency, untreated tuberculosis and pregnancy.
• Live attenuated vaccine is developed which can e given intranasal aerosol in young
babies and gives good protection irrespective of the presence of maternal antibodies.

Genus morbillivirus

  • 1.
  • 2.
    MEASLES (RUBEOLA) • Ancientdisease, no clear extinction was made between measles or other exanthematous diseases including smallpox. • Thomas Syndenham (1960) accurately described measles. • Viral origin was established by Goldberger and Anderson in 1911 through inoculation of blood filtrates and nasopharyngeal secretions from Patients. • Virus was isolated in monkey and human kidney cells by Enders and Peebles in 1954.
  • 3.
    MEASLES VIRUS • Roughlyspherical, often pleomorphic particle, 120 to 250nm in diameter, tightly coiled helical nucleocapsid surrounded by lipoprotein envelope on its surface hemagglutinin (H) spikes. • Envelope has F protein which mediates cell fusion and haemolytic activities. • Agglutinates monkey erythrocytes but there’s no elution as the virus doesn't posses neuraminidase activity. • Grows well on human or monkey kidney and human amnion cultures for primary isolation. • Isolates can be adapted for growth on continuous cell lines (HeLa, Vero) and in amniotic sac of hen’s eggs. • Cytopathic effects consists of multinucleate syncytium formation, with numerous acidophilic nuclear and cytoplasmic inclusions. • Multinucleate giant cells (Warthin- Finkeldey cells) are seen in lymphoid tissues of patients.
  • 4.
    • Labile, readilyheat inactivated, ultraviolet light, ether and formaldehyde. • Can get stabilised by molar magnesium sulphate, so that it resists heating at 50֯C for 1hour. • Measles virus is antigenically uniform. • Shares antigen with viruses of canine distemper and bovine rinderpest.
  • 5.
    CLINICAL FEATURES • Takes9 to 11 days from exposure time to infection for first signs of clinical disease to appear. • Consist of prodromal malaise, fever, conjunctival injection, cough and nasal discharge. • Rashes appears after 3-4 days of prodromal illness. • Before a day or two the rash begins, Koplik’s spots develop on the buccal mucosa, occasionally on conjunctiva and intestinal mucosa. • Illness subsides within a day or two of rash’s appearance. • Red maculopapular rash of measles appears on forehead first, spreads downwards, to disappear in the same sequence 3-6 days later, leaving behind a brownish discolouration and finely granular desquamation. • Patients recover uneventfully, but few develop complications due to virus (croup, bronchitis) or to secondary bacterial infection (pneumonia, otitis media).
  • 6.
    • Rarely, virusmay cause fatal giant cell pneumonia, particularly in children with immunodeficiencies or severe malnutrition. • Complications are common and serious in developing countries. • Most serious complication is meningoencephalitis. • Survivors have neurological sequelae. • A rare late complication is subacute sclerosing panencephalitis (SSPE). • Protracted diarrhea is often seen as a complication in children in poor nations. • Virus may be recovered from stools of patients with measles enteritis. • Occurs as a suppression of delayed hypersensitivity after measles infection, which may last for weeks or few months. • Mantoux and other skin tests may be negative during this period.
  • 7.
    • Underlying tuberculosismay become worse. • Recovery of measles is associated with the improvement of allergic eczema or asthma, Hodgkin’s disease or lipoid nephrosis • Measles induces labour in pregnant women. • Results in spontaneous abortion or premature delivery. • Virus may cross the placenta and infect the fetus during maternal measles but there’s no evidence of teratogeny. • Thrombocytopenia may develop, leading to purpura and bleeding from mouth, intestines and genitourinary tract.
  • 8.
    PATHOGENESIS • virus entersbody through respiratory tract or conjunctiva and multiplies locally and in the adjoining lymph nodes. • Spreads to reticuloendothelial system through blood. • After multiplication, a secondary viremia transports virus to epithelial surfaces including the skin, mouth, respiratory tract and conjunctiva. • Pathogonomic Koplik’s spots (small bluish white ulcerations) on buccal mucosa opposite to lower molars contain giant cells, cytoplasmic and intranuclear inclusions and virion components, indicating local viral replication.
  • 9.
    • Viral replicationevidence can be seen in vascular endothelial cells at the sites of the skin rash. • Rash is an immune reaction between T-lymphocytes and cells in which viral replication takes place. • Virus can be isolated from blood, washed leucocytes, tears and respiratory secretions during the 2-4 days of prodromal period. • Can be recovered from urine upto 4 days after the appearance of skin rash.
  • 10.
    LABORATORY DIAGNOSIS • Diagnosisis self-evident in case of typical case of measles. • In atypical cases and differentiation from rubella, laboratory tests are useful. • Measles virus antigen can be defected in these cells by immunofluorescence. • Multinucleated giant cells can be diagnosed in Giemsa – stained smears of nasal secretions. • Virus can be isolated from nose, throat, conjunctiva and blood during prodromal phase and upto 2 days after rash appearance. • Virus can be obtained from urine. • Primary human or monkey kidney and amnion cells are most useful. • Cytopathic changes may take upto a week to develop. • Earlier diagnosis of viral growth is possible by immunofluorescence.
  • 11.
    SEROLOGICAL DIAGNOSIS • Specificneutralisation, hemagglutination inhibition and complement fixing antibodies develop early. • A 4 fold rise in titre is looked for using sera collected during the acute phase and 10-21 days later. • Demonstration of measles-specific IgM in a single specimen of serum drawn between 1 and 2 weeks after the onset of the rash is confirmatory. • False negatives may occur if the serum is taken earlier than 1 week before or later than the 2 weeks after the onset of the rash. • Demonstration of high titre measles antibody in the CSF is diagnostic of SSPE.
  • 12.
    EPIDEMIOLOGY • Endemic andproduces epidemics (seen in late winter or early winter) every 2-3 years. • Disease has maximum incidence in children of 1-5 years. • Uncommon in first 6 months of life due to the presence of maternal antibody. • One attack confers solid immunity. • People are natural hosts of measles. • Monkeys are often infected but they seem to acquire the infection from humans. • Patients are infectious from 3 days before to the onset of symptoms until the rash desquamates. • Infectivity is maximum at the prodrome and diminishes rapidly on the onset of rash. • Spread by direct contact with respiratory secretions and aerosols by coughing and sneezing. • Virus enters through respiratory tract and conjunctiva. • In nonimmune, infection results in clinical disease.
  • 13.
    PROPHYLAXIS • Normal humangammaglobulin given within 6 days of exposure can prevent or modify the disease, depending on the dose. • Valuable in children with immunodeficiency, pregnant women and others at special risk. • Safe and effective live attenuated measles vaccine is available. • Original live vaccines used the Edmonston strain developed by multiple passage through human kidney, amnion and chick embryo cultures. • Have high risk of febrile rash (vaccination measles), further attenuation became necessary. • Schwartz and Moraten strains so developed were safe but effective only in children older then 15 months. • Edmonston- Zagreb strain, attenuated by passage in human diploid cells, is preferred as vaccine strain because it is able to produce seroconversion even in infants 4-6 months old.
  • 14.
    • Recommended agefor measles vaccination in developing countries is 9 months while in advanced nations is 15 months. • Vaccine is either given by itself, or in combination, as the MMR vaccine. • A single subcutaneous injection provides protection beginning in about 12 days and lasting for over 20 years. • Contraindications are immunodeficiency, untreated tuberculosis and pregnancy. • Live attenuated vaccine is developed which can e given intranasal aerosol in young babies and gives good protection irrespective of the presence of maternal antibodies.