RUBELLA

GERMAN MEASLES

DR ANWAR AHMADCOMMUNITY MEDICINE & PUBLIC HEALTH

KGMU, UP LUCKNOW

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

RUBELLA INTRODUCTION

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

AGENT FACTORSA- Agent

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

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AGENT FACTORS cont.

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.

B- Source of infection

C- Period of communicability

HOST FACTORS

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.

A- Age B- Immunity

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.

MODE OF TRANSMISSION

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).

INCUBATION PERIOD

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

PATHOGENESIS

Rubella Virus Developed in the nasopharynx

Respiratory Tract Skin

Lymph Nodes Joints

Placenta or Fetus

• Cough• Minor

sore throat

• Rashes• Lesions

• Lymphadenopathy

•Mild arthralgia• arthritis

• Placentitis• Fetal Damage

PATHOPHYSIOLOGY

Rubella virus

Transmitted via

respiratory droplets

Infects cells in the upper respiratory

tract

Virus multiplie

s

Extends in the regional lymph nodes

Virus replicates in the nasopharynx

Infection is established in the skin and other tissues including the respiratory tract

Forchheimer’s Spot may develop

Rashes develops, cough etc.

Virus can be found

in the skin,

blood and respirator

y tract

PATHOPHYSIOLOGY

Diagnosis: doctor suspects whether patient has measles

Virus culture/

blood test

Recent infection

With german measles vaccine

Vaccination and proper interventio

ns

German Measles left untreated, it may

cause complications: Rubella Arthritis,

Encephalitis, Purpura bronchitis, abscesses

in the ears and pneumonia

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 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)

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OTHER SIGNS AND SYMPTOMS

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

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.

Systemic events of Rubella Infection

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Main Clinical Events During Pregnancy

The clinical events occurring in the neonatal age is more important and divided into two major groups-

1 Congenital Rubella2 Post Natal Rubella

CONGENITAL RUBELLA SYNDROME

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

MANIFESTATION OF CONGENITAL RUBELLA

Sensorineural hearing loss – 58%

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 Liver and spleen damage

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

Clinical Diagnosis is unreliableMany viral infections mimic RubellaSpecific 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 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 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

MEDICAL 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)

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

PREVENTION

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, Controlin 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

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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