1. P R E S E N T E D B Y : D R . A A M I R
M O D E R A T E D B Y : D R . S H U G U F T A
RUBELLA
2. HISTORY
Discovered in 18th century –
thought to be variant of measles
Congenital rubella syndrome
(CRS) described by Gregg in 1941
Rubella virus first isolated in 1962
by Parkman and Weller
An attenuated vaccine was
developed in 1967
3. INTRODUCTION
Generally mild disease caused by the rubella virus.
Acute exanthematous viral infection of children and adults.
From Latin meaning “little red”
First described as distinct clinical entity in German literature- German
measles
Also called as three-day measles & “THIRD DISEASE”
Because of routine vaccination against rubella since 1970 , rubella is
now rarely reported.
8. Epidemiology
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
9. RUBELLA IN INDIA
40-45% of women in the
childbearing age are susceptible
to Rubella.
Over 40000 babies are born with
birth defects every year because
of Rubella infection during
pregnancy in India.
11. Genotypes 1A, 1E, 1F, 2A and 2B have been isolated in China.
Genotype 1J has only been isolated from Japan and the Philippines.
Genotype 1E is found in Africa, the Americas, Asia and Europe.
Genotype 1G has been isolated in Belarus, Cote d'Ivoire and Uganda.
Genotype 1C is endemic only in Central and South America.
Genotype 2B has been isolated in South Africa.
Genotype 2C has been isolated in Russia
12. Modes of Transmission
1. Person to person- via
respiratory route:-
Droplet from nose & throat
Droplet nuclei (aerosols)
Maintain in human population by
chain transmission.
13. 2. Acquired during pregnancy-
vertical transmission:-
Virus can enter via the Placenta
& infect the fetus in utero
(Congenital Rubella Syndrome).
14. Communicability
Moderately contagious
Patients are most contagious
when the rash is erupting
Shed virus from 7 days before
until 5-7 days after the onset of
the rash
Infants with congenital rubella-
transmit the infection to those
who care for them
17. 2- Source of infection 3- Period of
communicability
CASES
Subclinical
Clinical
Congenital from infected
pregnant women to fetus.
There is no known carrier state.
It probably extends from a
week before symptoms to about
a week after rash appears.
Infectivity is greatest
when the rash is erupting.
AGENT FACTORS(Contd.)
18. 1.AGE 2.IMMUNITY
Disease of childhood 3-10 yrs
age group.
Following widespread
immunization campaigns
persons older than 15 yrs
account for 70% cases in
developed countries
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.
HOST FACTORS
19. 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
20. ENVIRONMENTAL FACTORS
Disease usually occurs in
seasonal pattern -
late winter & early spring.
Epidemics every 4-9 years.
24. ACQUIRED RUBELLA
Prodrome -Low grade fever,
malaise , anorexia
Lymphadenopathy in second
week
Maculopapular rash 14-17 days
after exposure
Children have milder disease
than adults
Many, if not most, cases of
postnatal rubella are subclinical.
25. Sign & Symptoms
RASH
Primary symptom- appearance of a
rash (exanthema)on the face
Spreads to the trunk and limbs
Usually fades after three days with no
staining or peeling of the skin.
The skin manifestations are called
"blueberry muffin lesions."
26. LYMPH NODE-
Tender Lymphadenopathy
Posterior auricular lymph nodes
Posterior cervical nodes
Sub occipital lymph nodes
Persist for up to a week.
28. Pathognomonic Sign
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.
Not diagnostic
29. Complications
May produce transient
Arthritis or Arthalgia, particular
in women.
Serious complications are-
Thrombocytopenia
Purpura
Encephalitis
30. Main Clinical Events During Pregnancy
The clinical events occurring in the
neonatal age is more important and
divided into two major groups-
31. Congenital Rubella Syndrome(CRS)
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.
36. Rubella infection – At various trimesters
First 2 months of gestation-65% to 85% chance of being affected,
multiple congenital defects or
spontaneous abortion, or
Both
Rubella during the third month-30% to 35% chance of developing a
single defect
Fourth month -10% risk for a single congenital defect
Fetal damage (deafness alone) -rubella occurs up to the 20th week of
gestation
37.
38. DIAGNOSIS OF ACQUIRED RUBELLA
Clinical Diagnosis is unreliable
Many viral infections mimic Rubella
Specific diagnosis of infection with-
1. Isolation of virus from clinical specimen( nasopharynx, urine etc)
2. Evidence of seroconversion
#.Significant rise in IgG by any standard serologic assay
(enzyme immunoassay)
#.Positive serologic test for IgM Rubella antibody
39. 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
40. Using cell cultured in shell vial -antigens can be detected by Immuno-
fluorescence methods
41. Culturing the Virus
The virus can be cultured and
adopted to continuous cell
lines
Rabbit kidney cells (RK
13 )
Vero cells
Identified by characteristic
Cytopathic effect on cell
cultures.
42. Serology In Rubella
Hemagglutination inhibition
test for Rubella is of Diagnostic
significance
ELISA tests are greater Importance,
Passive latex agglutination test,
and Radial hemolysis test
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.
43. Diagnosis of Acute Rubella in Mother
Fourfold rise in IgG titer between acute and
convalescent serum specimens
Obtained within 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 1 week before to 2 weeks after rash.
45. Diagnosis in Infant
Isolation of rubella virus
Most frequently isolated from nasopharyngeal secretions
Can be cultured from blood, urine, CSF, lens tissue, amniotic fluid.
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
46. Presence of rubella-specific hemagglutination 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.
Most useful in infants younger than 2 months, but may persist for up to 12
months
RT-PCR results may be positive before the appearance of rubella IgM
antibodies
47. 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),
Heterophile antibodies
48. TREATMENT
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)
49. Treatment For Acute Maternal Rubella Infection
Acetaminophen for symptomatic relief
IgG- controversial, CDC recommends limiting use of immunoglobulin
to women with known rubella exposure who decline pregnancy
termination.
Glucocorticoids, platelet transfusion, and other supportive measures
for complications.
Should be counseled about maternal-fetal transmission and offered
pregnancy termination, especially prior to 16 wks Gestation.
After 20 wks. gestation- individualized management
50. Recommendations
Do:-
Screening at first post-
conceptual appointment, first-
trimester screening
Don’t:-
Routine screening of child-
bearing age women not
recommended
Routine vaccination of all
women of childbearing age not
recommended
51. PREVENTION
Rubella vaccine is given to
children at 15 months of age
as a part of the MMR.
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
52. Prevention of Child Bearing Age Women
Immunization of:
Young children
Teenage girls
Best to prevent Congenital Rubella
Syndrome(CRS)
Component of Rubella in MMR
protects the vaccinated
53. Vaccination of Women of Childbearing Age
Ask if pregnant or likely to become so in next 4 weeks
Exclude those who say “yes”
For others
explain theoretical risks
vaccinate
54. VACCINES
Vaccine Trade Name Licensure Discontinued
HPV-77:DE5 Meruvax 1969 1979
HPV-77:DK12 Rubelogen 1969 1979
GMK-3:RK53 Cendevax 1969 1979
RA 27/3* Meruvax II 1979 Still in use
55. RUBELLA VACCINE
Composition Live virus (RA 27/3
strain)
Efficacy 95% or more
Duration of Immunity lifelong
Schedule at least 1 dose
Should be administered with measles
and mumps as MMR or with measles,
mumps and varicella as
MMRV(ProQuad)
56. CHARACTERISTICS:
Lyophilized (freeze-dried) powder
Reconstituted with sterile, preservative-free water
Vaccines contains
Small amount of human albumin
Neomycin
Sorbitol
Gelatin
57. IMMUNIGENICITY &VACCINE EFFICACY
RA 27/3 rubella vaccine
is safe
more immunogenic than rubella vaccines used previously
95% or more of vaccinees aged 12 months and older develop serologic evidence
of rubella immunity after a single dose.
58. RUBELLA IMMUNITY
Documentation of one dose of rubella-containing vaccine on or after
the first birthday
Serologic evidence of immunity
Birth before 1957 (except women of childbearing age)
Birth before 1957 is not acceptable evidence of rubella immunity for
women who might become pregnant
Only serology or documented vaccination should be accepted
59. MMR ADVERSE EFFECTS
Rubella vaccine is very safe.
Most adverse events reported following MMR vaccination (such as
fever and rash) are attributable to the measles component.
Some adverse events being:
Fever
Rash
Chronic arthralgias
Chronic arthritis
Transient peripheral neuritic complaints
Recurrent joint symptoms
Collagen disease
60. MMR CONTRAINDICATIONS
History of anaphylactic reactions
to neomycin
History of severe allergic reaction
to any component of the vaccine
Pregnancy
Immunosuppression
• Moderate or severe acute illness
• Recent blood product
• Personal or family
(i.e., sibling or parent) history of
seizures of any etiology (MMRV
only)
61. Rubella Vaccination in INDIA
MR vaccine was introduced in
National Immunization Schedule
in 2017
Phased introduction, at present in
five states namely
Karnataka,
Tamil Nadu,
Goa,
Lakshadweep and
Pondicherry. (As of Feb’ 2017)
First dose at 9-12months(until
5yrs)
Booster -16-24months
62. Strategies to Decrease Rubella and CRS
Vaccination of Susceptible Post pubertal Females
Vaccinate susceptible adolescents and young adults of childbearing age
Emphasizing immunization for college students
Vaccinating women postpartum and post abortion
Vaccination can be carried out at:
Family planning clinics,
Sexually transmitted disease (STD) clinics,
As part of routine gynecologic care
63. Hospital Rubella Programs
Vaccinating susceptible hospital personnel
Both male and female
e.g., volunteers, trainees, nurses, physicians
Ideally, all hospital employees should be immune.
Editor's Notes
Schematic representation of the translation and processing strategy of the RV ns and structural proteins. The RV genome comprises two long nonoverlapping ORFs, with the 5′ ORF coding for the ns proteins and the 3′ ORF coding for the structural proteins. A polyprotein precursor, p200, is translated from the 5′ ORF of the RV genomic RNA and undergoes cis cleavage to produce two ns proteins, p150 and p90. The locations of the putative amino acid motifs for methyltransferase (M), X motif, papain-like cysteine protease (P), helicase (H), and replicase (R) are indicated on the 5′ ORF. The RV structural proteins are synthesized from a 24S subgenomic RNA transcribed from the 3′ ORF. A polyprotein precursor, p100, is translated from the subgenomic RNA and undergoes several posttranslational modifications to ultimately produce the mature capsid (C), E2, and E1.
E1 and E2 are transmembrane
glycoproteins, and C is the capsid protein that surrounds the
RNA of the virion.
Hemagglutinin and complement-fixing antigens
are composed of varying proportions and mixtures of E1, E2, and
C. E1 is important in attachment, fusion, hemagglutination, and
neutralization