RUBELLA

Guided by – Dr.Sanjay
Presented by –Tejaswini K.S
Sakshi S.P
 CONTENTS
1)INTRODUCTION
2)HISTORY
3)EPIDEMOLOGICAL
DETERMINANTS
4) INCUBATION PERIOD
5) DIAGNOSIS
6)CRS
7) CONTROL and
PREVENTION
8) VACCINE
 INTRODUCTION

• Rubella or german measles is an acute

childhood infection, usually mild, of short
duration (approximately 3 days)
• It is accompanied by low-grade fever,
lymphadenopathy and a maculopapular
rash.
• Infection in early pregnancy may result in
serious congenital defects, including death
The disease is worldwide in distribution and
tends to occur in epidemics, in non-immunized
populations, every 6 to 8 years
 HISTORY
• Rubella was considered a mild and benign
disease until 1941
• Later when Norman Gregg, an ophthalmologist
reported an epidemic of congenital cataracts
associated with other congenital defects in
children born to mothers who had rubella
during their pregnancies (2).
• This discovery changed the concept that
rubella is not merely a benign disease of
childhood but also one with teratogenic
potential.
• In 1962, the virus was isolated;
in 1967, an attenuated vaccine was
developed
 Epidemiological determinants
Agent factors-
(a) AGENT: Rubella is caused by an RNA virus of the
togavirus family. Only one antigenic type of the virus
seems to exist. The virus has been recovered from the
naso- pharynx, throat, blood, CSF and urine. It can be
propagated in cell culture.
(b) SOURCE OF INFECTION: Clinical or subclinical
cases of rubella. A large number of rubella infections
are, in fact, subclinical. This represents one of the major
differences between measles and rubella.
There is no known carrier state for postnatally acquired
rubella. Infants born with congenital rubella may shed the
virus for many months. The vaccine virus is
not communicable.
(c)PERIOD OF COMMUNICABILITY: Rubella is much less
communicable than measles, probably because of the
absence of coughing in rubella. It is difficult to state the
exact period of infectivity. It probably extends from a week
before symptoms to about a week after rash appears.
Infectivity is greatest when the rash is erupting .
 Host factors-
(a) AGE: Mainly a disease of childhood particularly in
the age group 3 to 10 years. Persons older than 15
years now account for over 70 per cent cases in
developed countries – this is similar to the changing
epidemiological pattern with measles, following
widespread immunization campaigns against the
disease.
(b) IMMUNITY: One attack results in life-long
immunity; second attacks are rare. Infants of Immune
mothers are protected for 4 to 6 months.
It is estimated that 10 to 40 per cent of the
population could reach adulthood without
experiencing rubella infection in the absence of
immunization.

• Thus many women of child-bearing age may

remain rubella-susceptible. Studies in India indicate
that approximately 40 per cent of women of child-
bearing age are susceptible to rubella.
Environmental factors-
Disease usually occurs in a seasonal pattern i.e. in
temperate zones during the late winter and spring, with
epidemics every 4-9 years.
Transmission-
1) The virus is transmitted directly from person to person
by droplets from nose and throat, and droplet nuclei
(aerosols), from one week before onset of rash to one week
after it has faded.
2) The portal of entry is via the respiratory route. The virus
is maintained in human population by chain transmission.
3) The virus can cross the placenta (vertical transmission)
and infect the foetus in uterus, leading to congenital rubella
in the newborn.
Incubation period

2 to 3 weeks; average 18 days.

Clinical features

A large percentage of infections (50 to 65 per cent) are

asymptomatic. In a typical case, the clinical features comprise the
following:
(a) PRODROMAL: The prodromal symptoms (coryza, sore throat,
low-grade fever) herald the onset of viraemia. They are generally
mild and insignificant, and less frequent in children.
(b) LYMPHADENOPATHY: In susceptible individuals, the
enlargement of the post-auricular and posterior cervical lymph nodes
appears as g. early as 7 days before the appearance of the rash.
(c)RASH: The rash is often the first indication of the
disease in children. It appears first on the face,
usually within 24 hours of the onset of prodromal
symptoms.
• It is a minute, discrete, pinkish, macular rash and
not confluent as the rash of measles. Conjunctivitis
may occur. The rash spreads rapidly to the trunk
and extremities
• The rash spreads much faster and clears more rapidly
than the rash of measles. It disappears altogether by the
third day. The rash is an inconstant feature of the disease
• The incidence of rubella infection without rash may
be upto 25%.

(d) COMPLICATIONS- In rare instances arthralgia

may occur in several joints in adults, especially young
women. Encephalitis, Thrombocytopenic purpura,
congenital malformations has also been observed as
a complication.
 DIAGNOSIS-
• Because of its mildness and variability of
symptoms, the disease can go unrecognized
unless it is an epidemic.
• A definitive diagnosis of rubella is possible
only through virus isolation and serology.
Throat swabs should be cultured for virus
isolation. The haemagglutination inhibition
(HI) test is a standard serological test for
rubella.
• ELISA tests are preferred
 CONGENITAL RUBELLA-
Congenital rubella syndrome (CRS) refers to infants
born with defects secondary to intrauterine
infection or who manifest symptoms or signs of
intrauterine infection sometime after birth .
• Congenital infection occurs if the infant has IgM
rubella antibodies shortly after birth or if IgG
antibodies persist for more than 6 months, by
which time maternally derived antibodies would
have disappeared.
• Viral excretion may last for 12-18 months after
birth, but the level of shedding gradually
decreases with age.
• Rubella infection inhibits cell division, and this is
probably the reason for congenital malformations
and low birth weight .
• The classic triad of congenital defects are
deafness, cardiac malformations and cataracts.
• Other resulting defects include glaucoma,
retinopathy, microcephalus, cerebral
palsy, intrauterine growth retardation, hepato-
splenomegaly, mental and motor
retardation. These defects occurring singly or in
combination have become known as “congenital
rubella syndrome
CONTROL
1.Isolation of case in good ventilation room

2. No specific treatment or Antiviral

treatment is indicated

3. Encourage the patient to take rest

4. Increase fluid intake

 Prevention
Active immunization against rubella is now possible with
live attenuated vaccines. The goal of rubella
immunization is the prevention of rubella infection
during a future pregnancy

RUBELLA VACCINES:
• In 1979 the RA 27/3 vaccine, produced in human
diploid fibro-blast has replaced all the other vaccines
because RA 27/3 vaccine induces immune response
more closely paralleling natural infection than the
other vaccines
• Rubella vaccine is also available as combined measles,
mumps and rubella (MMR) vaccine.
 VACCINE-
• Children should get two doses
of MMR vaccine, starting with
the first dose at 12 to 15
months of age, and the second
dose at 4 through 6 years of
age
• Children can receive the
second dose earlier as long as it
is at least 28 days after the first
dose.
Recent update
Reported rubella cases declined 97%, from
670 894 cases in 102 countries in 2000 to 17
865 cases in 78 countries in 2022.
Thank you