DR ANWAR AHMAD

COMMUNITY MEDICINE & PUBLIC HEALTH

KGMU, UP LUCKNOW

GERMAN MEASLES
 HISTORY - RUBELLA

 The Teratogenic property of

the infection was
documented by an
Australian ophthalmologist
Norman McAlister Gregg,
in 1941
 The virus was isolated in
1962
 An attenuated vaccine was
developed in 1967
 The name is derived from the Latin, meaning little red.
 Also called as three-day measles/German measles
 The synonym "3-day measles" derives from the typical course of rubella
exanthema that starts initially on the face and neck and spreads centrifugally to
the trunk and extremities within 24 hours. Then begins to fade on the face on the
second day and disappears throughout the body by the end of the third day.
 Rubella is also known as German measles because the disease was first
described by German physicians, Friedrich Hoffmann, in the mid-eighteenth
century.
 It is a generally mild disease caused by the rubella virus.
 Congenital rubella syndrome (CRS) described by Gregg in 1941
 Because of routine vaccination against rubella since 1970 , rubella is now rarely
reported.
Rubella Epidemic United States, 1964-1965
12.5 million rubella
cases
2,000 encephalitis
cases
11,250 abortions
(surgical/spontaneous)
2,100 neonatal deaths
30,000 CRS cases
Deaf - 11,600
Blind - 3,580
Mentally retarded - 1,800
The largest rubella epidemic in the
United States occurred in 1964-
1965, and resulted in the birth of an
estimated 30,000 infants with
congenital rubella syndrome. As
many as 85% of pregnant women
with clinical rubella delivered babies
with congenital rubella. The highest
percentage of congenital rubella
occurred when the pregnant
mothers had rubella during the first
trimester
EPIDEMIOLOGICAL
DETERMINANTS
 Agent factors
 Host factors
 Environmental factors
 Causative agent: Rubella virus
 ssRNA Virus of the Togaviridae
Family
 genus Rubivirus
 One antigenic type
 Diameter 50 – 70 nm
 Enveloped Spherical
 Virus carry hemagglutinin
 Virus multiply in the cytoplasm
of infected cell.
 Highly sensitive to heat,
extremes of pH & uv light.
 At 4°C, virus is relatively stable
for 24 hours.
Prevailing Genotypes

7
AGENT FACTORS cont.

B- Source of C- Period of
infection communicability
 CASES  It probably extends from a
 Subclinical week before symptoms to
 Clinical
about a week after rash
appears.
 Congenital from infected
 Infectivity is greatest
pregnant women to
when the rash is erupting.
fetus.
 There is no known
carrier state.
HOST FACTORS
A- Age
 Disease of childhood 3-10 yrs
age group.
 Following widespread
immunization campaigns
persons older than 15 yrs
account for 70% cases in
developed countries.
B- Immunity
 One attack results in life long
immunity.
 Infants of immune mothers
are protected for 4-6 months.
 In India, about 40% of child
bearing age group women
are susceptible to rubella.
Immunity - Rubella
 Antibodies appear in serum
as rash fades and antibody
titers raise
 Rapid raise in 1 – 3 weeks
 Rash in association with
detection of IgM indicates
recent infection.
 IgG antibodies persist for life
ENVIRONMENTAL FACTORS

 Disease usually occurs in seasonal pattern,

during the late winter & spring.
 Epidemics every 4-9 years.
 Person to person- via respiratory route:-
 Droplet from nose & throat
 Droplet nuclei (aerosols)

 Maintain in human population by chain

transmission.
 Acquired during pregnancy- vertical
transmission:-
 Virus can enter via the Placenta & infect the
foetus in utero (Congenital Rubella Syndrome).
 Between 14-21 days
Rubella Pathogenesis

 Respiratory transmission of virus

 Replication in nasopharynx and regional lymph nodes

 Viremia 5-7 days after exposure with spread to tissues

 Placenta and fetus infected via hematogenous spread

during viremia
Rubella Virus Developed in the nasopharynx

Respiratory Lymph Placenta

Tract Skin Nodes Joints or Fetus

• Cough • Mild
• Minor • Rashes arthralgia
sore • Lesions • arthritis • Placentitis
throat • Fetal
Damage
• Lymphadenopathy
 Transmitted Infects cells in
via respiratory the upper
Rubella virus droplets respiratory
tract

Virus
Virus replicates in Extends in the multiplies
the nasopharynx regional
lymph nodes

Infection is Virus can

established in be found in
the skin and Forchheimer’s Rashes the skin,
other tissues Spot may develops, blood and
including the develop cough etc. respiratory
respiratory tract tract
 Recent Diagnosis:
Vaccination infection doctor
Virus culture/
and proper suspects
blood test
interventions whether
With german patient has
measles measles
vaccine

German Measles left

untreated, it may cause
complications: Rubella
Arthritis, Encephalitis,
Purpura bronchitis,
abscesses in the ears
and pneumonia
 Occurs worldwide
 The virus tends to peak in countries with temperate climates
 Common in children ages 5-10 years old
 Human are only known reservoir.
 Host -3-10 yrs
 Source of infection – Respiratory secretion
 Infants with CRS may shed virus for a year or more
 Immunity –life long
 Occurs round the year, peak in late winter and spring season
 Transmission – droplet, vertical transmission
 I.P – 2-3 weeks average 18 days
 Rubella is world wide in distribution
 Epidemics occur every 4-9 years.
Rubella Clinical Features

 Incubation period 18 days (range 14-21 days)

 Prodrome of low grade fever

 Lymphadenopathy in second week

 Maculopapular rash 14-17 days after exposure

SIGNS AND SYMPTOMS

 RASH- After an incubation period of 14-21 days, the

primary symptom of rubella virus infection is the
appearance of a rash (exanthema) on the face which
spreads to the trunk and limbs and usually fades after three
days with no staining or peeling of the skin.The skin
manifestations are called "blueberry muffin lesions."
 LYMPH NODE- Tender lymphadenopathy (particularly
posterior auricular and suboccipital lymph nodes) persist
for up to a week.
 TEMPERATURE-Fever rarely rises above 38 oC(100.4 oF)

20
 Eye pain on lateral and upward eye movement (a
particularly troublesome complaint)
 Conjunctivitis
 Sore throat
 Headache
 General body aches
 Low-grade fever
 Chills
 Anorexia
 Nausea
 Forchheimer sign
Other manifestations & complications

 May produce transient

Arthritis, particular in
women.
 Serious complications
are-
 Thrombocytopenia
Purpura
 Encephalitis
Rubella Rashes
Rubella Rashes
Image in a 4-year-old girl with a 4-day history of low-grade fever,
symptoms of an upper respiratory tract infection, and rash.
Courtesy of Pamela L. Dyne, MD.
Posterior auricular tender lymphadenopathy
Forchheimer’s Spot

 Fleeting enanthema
 Pinpoint or larger
petechiae that usually
occur on the soft palate
in 20% of patients
 Similar spots can be
seen in measles and
scarlet fever.
Systemic events of Rubella Infection

28
Main Clinical Events During Pregnancy

The clinical events occurring in the neonatal

age is more important and divided into two
major groups-
 1 Congenital Rubella
 2 Post Natal Rubella
 Occurs during the first trimester of
pregnancy.
 Affects the development of the fetus.
 may lead to several birth defects.
 Infection may affect all organs.
 May lead to fetal death or
premature delivery.
 Severity of damage to fetus
depends gestational age.
 Infants: virus is isolated from urine
and feces.
Rubella infection – At various trimesters

 Ist trimester infections lead to abnormalities in 85 % of

cases. and greater damage to organs
 2nd trimester infections lead to defects in 16 %
 > 20 weeks of pregnancy fetal defects are uncommon
 However Rubella infection can also lead to fetal deaths,
and spontaneous abortion.
 The intrauterine infections lead to viral excretion in
various secretion in newborn up to 12-18 months.
Rubella infection & Chance of CRS

 0–28 days before conception - 43% chance

 0–12 weeks after conception - 51% chance

 13–26 weeks after conception - 23% chance

 Infants are not generally affected if rubella is

contracted during the third trimester

 Sensorineural hearing loss – 58%  Liver and spleen damage
 Ocular abnormalities including
cataract, infantile glaucoma, micro-
ophthalmia and pigmentary
retinopathy occur in approximately
43%.
 Congenital heart disease
including patent ductus arteriosus
(pda) and pulmonary artery stenosis
- 50%.
 Bone lesions
 Psychiatric disorder
 Diabetes mellitus type 1
 Hypogammaglobulinemia
 Generalized lymphadenopathy
 Intrauterine growth restriction
 Hepatosplenomegaly,, hepatitis,
jaundice, thrombocytopenic purpura,
with petechiae and "blueberry
muffin" lesions
 Central nervous system
 Retardation, microcephaly
 Motor delay, behavioural disorders,
autism
 Intellectual disability (13%)
 A rare complication of pan
encephalitis can occur in second
decade with congenital rubella
syndrome may progress to death
 Problems in balance
Classical Triad of congenital Rubella

 Cataract
 Cardiac abnormalities
 Deafness
Salt and pepper retinopathy
 Post natal Rubella
 Occurs in Neonates and
Childhood
 Adult infection occurs through
mucosa of the upper
respiratory tract spread to
cervical lymph nodes
 Viremia develops after 7 – 9
day
 Lasts for 13 – 15 days
 Leads to development of
antibodies
 The appearance of antibodies
coincides the appearance of
suggestive immulogic basis for
the rash
 In 20 – 50 % cases of primary
infections are subclinical.
Diagnosis of Rubella in Adults

 ClinicalDiagnosis is unreliable
 Many viral infections mimic Rubella

 Specific diagnosis of infection with-

1 Isolation of virus
2 Evidence of seroconversion
Isolation and Identification of virus
 Nasopharyngeal or
throat swabs taken 6
days prior or after
appearance of rash is
a good source of
Rubella virus
 Using cell cultured in
shell vial antigens can
be detected by
Immunofluresecente
methods
 Culturing the Virus

 The virus can be

cultured and adopted
to continuous cell
lines
Rabbit kidney cells
(RK 13 )
and
Vero cells
Serology In Rubella
 Haemagglutination inhibition
test for Rubella is of Diagnostic
significance
 ELISA tests are greater
importance
 A raise in Antibody titers must
be demonstrated between two
serum samples taken at least
10 days apart.
 Or Detection of Rubella
specific IgM must be detected
in a single specimen.
Diagnosis of acute rubella in mother

 Fourfold rise in IgG titer between acute and

convalescent serum specimens
 Obtainedwithin 7 to 10 days after onset of rash
 Repeated 2 to 3 weeks later

 Presence of rubella specific IgM

 Positive rubella culture
 Can be isolated from nasal, blood, throat, urine,
or cerebrospinal fluid
 Generally isolated from pharynx one week before
to two weeks after rash.
 Diagnosis in infant
 Isolation of rubella virus
 Most frequently isolated from nasopharyngeal secretions
 Can be cultured from blood, urine, CSF, lens tissue, etc.
 Serial rubella-specific IgG levels at 3, 6, and 12 months
 Rubella-specific IgG antibodies that persist at higher concentration or longer duration than
expected from passive transfer of maternal antibody
 Maternal rubella antibody- half-life= 1 month, should decrease by 4 to 8 fold by 3 months of
age and should disappear by 6 to 12 months
 Can delay diagnosis
 Presence of rubella-specific haemagglutination inhibition (HAI) after nine
months of age
 Demonstration of rubella-specific IgM antibodies
 Demonstration of Rubella antibodies of IgM in a new born is diagnostic value. As IgM group do
not cross the placenta and they are produce in the infected fetus.
 Most useful in infants younger than 2 months, but may persist for up to 12 months
 False- negative-20% of infected infants tested for rubella IgM may not detectable titers before 1
month.
 If clinically consistent and test negative after birth, should be retested at 1 month
 False- positive- rheumatoid factor, viral infections (EBV, IM, parvovirus), and heterophile
antibodies
 Rubella is a mild self limited illness.
 No specific treatment or Antiviral treatment is
indicated.
 Isolation and quarantine
 Increase fluid intake
 Encourage the patient to rest
 Good ventilation
 Encourage the patient to drink either lemon or
orange juice
 Provide health teaching about Rubella (cause,
immunizations)
Treatment for acute maternal rubella
infection

 Acetaminophen for symptomatic relief

 IgG- controversial, CDC recommends limiting use of immune
globulin to women with known rubella exposure who decline
pregnancy termination.
 Glucocorticoids, platelet transfusion, and other supportive
measures for complications.
 Should be counselled about maternal-fetal transmission and
offered pregnancy termination, especially prior to 16 wks.
Gestation.
 After 20 wks. gestation- individualized management.
Recommendations

 Screening at first post-conceptual

appointment, first-trimester screening
 Routine screening of child-bearing age women
not recommended
 Routine vaccination of all women of
childbearing age not recommended
 Rubella vaccine is given to
children at 15 months of age
as a part of the MMR
(measles-mumps-rubella)
immunization.
 The vaccine is live and
attenuated and confers lifelong
immunity.
 Given to children 12 and 15
months and again between 3-6
years of age
 Treatment, Prevention, Control
in childbearing age women
 No specific treatment
is available
 CRS can be prevented by
effective immunization of
the young children and
teenage girls, remain the
best option to prevent
Congenital Rubella
Syndrome.
 The component of Rubella
in MMR vaccine protects
the vaccinated
 MMR Vaccine
48

 The MMR vaccine is a mixture of three live attenuated

viruses, administered via injection for immunization against
measles, mumps and rubella virus strain RA 27/3 . It is
generally administered to children around the age of one year,
with a second dose before starting school (i.e. age 4/5). The
second dose is not a booster; it is a dose to produce
immunity in the small number of persons (2-5%) who fail to
develop measles immunity after the first dose, the vaccine
was licensed in 1963 and the second dose was introduced in
the mid 1990s. It is widely used.
 Contraindications= immunodeficiency disorder, history of
anaphylaxis to neomycin, and pregnancy
 Side effects- arthritis, arthralgia, rash, adinopathy, or fever.
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