This document summarizes information about Mumps and Rubella. Mumps is caused by the mumps virus, an RNA paramyxovirus. It causes swelling of the parotid glands. The virus is transmitted through respiratory droplets. Complications can include orchitis. Vaccination with the MMR vaccine provides protection. Rubella, also known as German measles, is caused by the rubella virus, an RNA togavirus. It causes a rash and lymphadenopathy. Congenital rubella syndrome can occur if a pregnant woman is infected, causing birth defects. The rubella vaccine is a live attenuated vaccine that provides lifelong immunity in 95% of cases. Global vaccination strategies

1. Mumps
&
Rubella
Dr. Rahul Netragaonkar
Professor
Dept. Of Community Medicine
ZMCH Dahod

2. • Mumbling Speech - Mumps :
• Name "mumps" comes from
"lump" or "mumble."

3. Mumps
• Acute viral illness
• Parotitis and orchitis described by Hippocrates
in 5th century BC
• Viral etiology described by Johnson and
Goodpasture in 1934
• Frequent cause of outbreaks among military
personnel in pre vaccine era

4. MUMPS
• Acute infectious disease due to “myxovirus
parotiditis” ; RNA paramyxovirus
(Genus Rubulavirus) affecting mainly
glands and nervous system
• Clinically the disease is recognized by
enlargement of one or both parotid glands
with tenderness.
• Worldwide distribution.
• Morbidity is high. Mortality is less.

5. Mumps Epidemiology
• Reservoir Human
Asymptomatic infections
may transmit
• Transmission Respiratory drop nuclei
• Temporal pattern Peak in late winter and spring
• Communicability Three days before to four
days after onset of active
disease

6. MUMPS
• AGENT FACTORS:
• A)Agent: Myxovirus parotiditis is a RNA
virus of the myxovirus family. The virus
can be grown in chick embryo or tissue
culture. There is only one serotype.

7. Mumps Virus
• Paramyxovirus
• RNA virus
• One antigenic type
• Rapidly inactivated by chemical agents, heat,
and ultraviolet light

8. MUMPS
• The virus can be
• A)Isolated from the saliva or from swabs taken
from the surface of STENSON’S DUCT.
• Virus has also been found in the blood, urine,
human milk, and in the CSF.
• A) PERIOD OF COMMUNICABILITY:
• Usually 4-6 days before the onset of symptoms
and a week thereafter.
  The period of maximum infectivity is just
before and at the onset of parotitis.

9. • SOURCE OF INFECTION: Both clinical and
sub clinical cases.
• Sub clinical cases accounts for 30-40% of all
cases.

10. MUMPS
• A) SECONDARY ATTACK RATE:
• Estimated to be about 86%

11. HOST FACTORS
• a)AGE AND SEX: Mumps is the most
frequent cause of parotitis in children in the
age group of 5-15 years.
 The average age of incidence of mumps is
higher than with measles, chicken pox or
whooping cough.

12. MUMPS
• MODE OF TRANSMISSION:The disease
is spread mainly by droplet infection and
after direct contact with an infected person.
• INCUBATION PERIOD; Varies from 2-3
weeks usually 18 days.
• CLINICAL FEATURES:30-40% of cases
are sub clinical characterized by pain and
swelling in either one or both parotid glands
and involves the sublingual submandibular
glands.

13. Mumps Pathogenesis
• Respiratory transmission of virus
• Replication in nasopharynx and regional
lymph nodes
• Viremia 12-25 days after exposure with spread
to tissues
• Multiple tissues infected during viremia

14. Mumps Clinical Features
• Incubation period 14-
18 days
• Nonspecific prodromal
phase of myalgia,
malaise, headache,
low-grade fever
• Parotitis in 30%-40%
• Up to 20% of
infections
asymptomatic

15. Mumps Clinical Case Definition
• Acute onset of unilateral or
bilateral tender, self-limiting
swelling of the parotid or other
salivary gland lasting more than
2 days without other apparent
cause

16. MUMPS
 The disease tends to be more severe in adults
than in children.
 IMMUNITY: One attack clinical or sub clinical
will induce life long immunity.
 ost infants < 6 months of age are immune
because of maternal antibodies.
• ENVIRONMENTAL FACTORS:
• Mumps is largely an endemic disease. Cases occur
throughout the year – but peak incidence in
wintertime of the year – but peak incidence in
winter and spring. Over crowding linked to
epidemics

17. 17
Complications of Mumps
Frequent but not serious:
• Orchitis (25-40%): 7-10 days after parotitis,with high fever
(Unilateral in 75% orchitis cases, Most common extra-salivary gland
manifestation in adults)
• Epididymitis
• Pancreatitis (4%)
• Mild form of meningitis
• Thyroiditis, Neuritis, Hepatitis,Ovaritis,
• Oophoritis (5% adult women)
• Spontaneous abortion(25% in pregnancy)
Rare:
Hearing loss, Polyarthritis, Encephalitis, Cerebellar ataxia

18. • Mumps infection in post-pubertal males
can result in swelling of the testicles in
22-30% of affected individuals.
• Such swelling may then lead to marked
atrophy (shrinkage) of the testicle with
poor sperm production as the result.

19. Mumps Laboratory Diagnosis
• Isolation of mumps virus
• Detection of mumps antigen by PCR
• Serologic testing
– positive IgM antibody
– significant increase in IgG antibody between
acute and convalescent specimens

20. MUMPS
• PREVENTION: VACCINE:
• Recommended for children over one year of
age.
• Its use may be considered in susceptible
adults, especially males.
• Mumps vaccine should not be administered
to pregnant women, who are severely ill or
who are on Immuno suppressive therapy

21. Mumps Vaccine
• Composition Live virus (Jeryl Lynn strain)
• Efficacy 80% (1 dose)
• Duration of
Immunity Lifelong
• Schedule At least 1 Dose should be administered
with measles and rubella as MMR or with measles,
rubella and Varicella as MMRV

22. Mumps (MMR) Vaccine
Indications
• One dose (as MMR) for preschool-age children
12 months of age and older and persons born
during or after 1957 not at high risk of mumps
exposure
• Second dose (as MMR) for school-age children
and adults at high risk of mumps exposure (i.e.,
healthcare personnel, international travelers and
students at post-high school educational
institutions

23. MMR Adverse Reactions
• Fever 5%-15%
• Rash 5%
• Joint symptoms 25%
• Thrombocytopenia <1/30,000 doses
• Parotitis* rare
• Deafness* rare
• Encephalopathy <1/1,000,000 doses
*reactions usually attributed to the mumps component

24. MMR Vaccine
Contraindications and Precautions
• Severe allergic reaction to vaccine
component or following a prior dose
• Pregnancy
• Immunosuppression
• Moderate or severe acute illness
• Recent blood product

25. Vaccine Storage and Handling
MMR Vaccine
• Store 35o
- 46o
F (2o
- 8o
C) (may be
stored in the freezer)
• Store diluent at room temperature or
refrigerate
• Protect vaccine from light
• Discard if not used within 8 hours
reconstitution

26. MIG
• a) IMMUNO GLOBULIN:
• A specific Immuno globulin (MIG) is available.
• CONTROL: The control of mumps is difficult
because the disease is infectious before a
diagnosis can be made. Due to long I.P, sub
clinical cases, - it is difficult to control mumps.
• Isolation of cases.
• Disinfection of the articles.
• Contacts kept under surveillance

27. RUBELLA (GERMAN
MEASELS
• RUBELLA or German Measles
is an acute child hood infection
usually mild of short duration (3
days) and accompanied by low-
grade fever, lymphadenopathy
and a maculopapular rash.
 Infection in early pregnancy
may result in serious congenital
defects like PDA, cataract and
deafness. Rubella in pregnancy
can also cause spontaneous
abortion and stillbirth.

28. RUBELLA HISTORY
• HISTORY:
• 1941 – Norman Gregg – reported rubella
infection in pregnancy WHICH IN TURN
linked to congenital anomalies including
congenital cataracts.
• 1962 – The virus was isolated.
• 1967 – Live attenuated vaccine was
developed.

29. Epidemiological Determinants
AGENT:
• It is a RNA virus of the Toga virus
family.
• Virus can be recovered from the cases
of Rubella, from naso- pharynx, throat,
blood, CSF and urine.
• It can be propagated in cell culture.

30. SOURCE OF INFECTION
• Clinical or sub clinical cases of
rubella. Most of the infections are
sub clinical. Infants born with
infection may shed the virus, for
many months. Vaccine virus is not
communicable.

31. AGENT&HOST FACTORS:
• Period of Communicability
• Less communicable than
measles.
• Probably one week prior to
symptoms to a week after
appears.

32. HOST FACTORS
• a) AGE: Mainly a disease of child hood in age
group of 3 – 10 yrs.
• - Persons aged > 15. Yrs now account for over
70% of cases in developed countries. This is
changing epidemiological pattern with wide
coverage of immunization.
• IMMUNITY: One attack results life long
immunity. 40% women of childbearing age may
remain susceptible to rubella

33. EPIDEMIOLOGY
• ENVIRONMENTALFACTORS: Seasonal
variation is present, temperate zones every
4-9 yrs.
• TRANSIMISSION: Droplets from nose and
throat and droplet nuclei transmit the virus
directly from person to person during
communicability period.
• -The portal of entry is via respiratory route.
• - Vertical transmission is also present.

34. CLINICALF EATURES
• CLINICAL FEATURES: 50-65% of infections
are asymptomatic.
• a)PRODROMAL: Symptoms like coryza, sore
throat, and low-grade fever – herald the onset of
viraemia.
• b)LYMPHADENOPATHY:Posterior auricular
lymph nodes, and posterior cervical group will be
enlarged 7 days before rash appearance and it
continues 10-14 days after the rash. Some times
no lymphadenopathy.

35. CLINICALFEATURES
• a) RASH: Appears first on face. Rash is
like minute, discrete, pinkish, macular rash
and not confluent. Rash spreads to trunk and
extremities. Rash disappears by 3 rd day.
• b) COMPLICATIONS:
• - Arthralgia
• - Encephalitis (rare)
• - Thrombocytopenia purpura
• Congenital anomalies of newborn baby

36. DIAGNOSIS OF RUBELLA
• By virus isolation and serology.
1. - Throat swabs should be cultured for virus
isolation. Most widely used test is
haemagglutination inhibition test (HAI).
• - 4-fold rise in HI antibody titer in paired sera
or presence of – IgM in a single serum sample
after 2 weeks of rash is diagnostic of rubella.
• - More sensitive serological tests include
Elisa test and radio immune assay.

37. Congenital Rubella Syndrome
• Refers to infants born with defects secondary to
intrauterine infection or with defects some time after birth.
Congenital infection is diagnosed by
- Rubella infection inhibits cell division. – reason for
congenital malformation and low birth weight.

38. CONGENITAL RUBELLA SYNDROME
• - Common congenital defects are
deafness, cardiac malformations,
cataracts, glaucoma, retinopathy,
microcephalus, cerebral palsy,
IUGR, hepato – splenomegaly and
mental and motor retardation.
• The first trimester of pregnancy
infection affects the fetus and
newborn baby with congenital
defects, > abortion, stillbirth,
PDA, cataract and deafness

39. PREVENTION
• Active immunization with live attenuated vaccine.
• RUBELLA VACCINE: 1979 – RA 27/3 vaccine (human
diploid fibroblast) – produces higher antibody titer with
good immune response.
• Administration in a single dose 0.5 ml S.C
• Sero conversion occurs in more than 95% vaccinees.
Immunity persists for 14-16 yrs.
• Infant should not be vaccinated.
• Pregnancy – is contra indication for immunization.
• Recipients of the vaccine should be advised not to
become pregnant for next 3 months

40. Vaccination strategy
• Combined vaccine MMR.
VACCINATION STRATEGY:
• - First to protect women of child bearing age
(15-34/39)
• Then interrupt transmission of rubella by
vaccinating all children 1-14 yrs.
• Subsequently all children at one-year age.

41. 41
Prevention of Rubella
Immunization
• Rubella vaccine: RA 27/3 strain,0.5 ml,
SC,Life long immunity in 95%
• C/I for immunization: Pregnancy
• Recipients of vaccine should be advised not to
become pregnant in 3 months after getting
vaccine
• MMR vaccine

42. 42
Vaccination strategy for Rubella
• First protect women in 15-39 yr age
• Second interrupt transmission by vaccinating
children aged 1-14 years
• Third, all children at age 1

45. 45
Global Measles and Rubella Strategic Plan 2012-2020
In 2012, the M&R Initiative launched a new Global Measles
and Rubella Strategic Plan which covers the period 2012-2020.
• By the end of 2015 the plan aims:
to reduce global measles deaths by at least 95%
compared with 2000 levels;
• To achieve regional measles and rubella/congenital
rubella syndrome (CRS) elimination goals.
• By the end of 2020 the plan aims:
to achieve measles and rubella elimination in at least 5
WHO regions.

46. 46
The strategy focuses on the implementation of 5 core components:
• Achieve and maintain high vaccination coverage with 2 doses of
measles- and rubella-containing vaccines;
• Monitor the disease using effective surveillance, and evaluate
programmatic efforts to ensure progress and the positive impact of
vaccination activities;
• Develop and maintain outbreak preparedness, rapid response to
outbreaks and the effective treatment of cases;
• Communicate and engage to build public confidence and demand
for immunization; and
• Perform the research and development needed to support cost-
effective action and improve vaccination and diagnostic tools.