Rubella;

Mumps; Influenza;
 Rubella
Rubella was considered a mild and benign disease until 1941 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

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 nasopharynx, 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 RUBEL LA major differences between measles and rubella.

(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 1- 5 days after the appearance of rash;

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
 Transmission
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.

The portal of entry is via the respiratory route.

The virus is maintained in human population by chain transmission. The virus can cross the placenta
(vertical transmission) and infect the foetus in utero, 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 feature s 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 early
as 7 days before the appearance of the rash. This, however, is not pathognomonic since cases of clinical rubella without enlargement of lymph nodes
have been documented. The glands may be found enlarged for
10 to 14 days after 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. by which time it is often no longer apparent on the face.

(d) COMPLICATIONS : In rare instances arthralgia may occur in several joints in adults, especially young women. Encephalitis is very rare.
Thrombocytopenic purpura has also been observed as a complication. Mention has beenmade already about the congenital malformations.

Complications — Complications of rubella are infrequent except in the developing fetus.

Hemorrhagic complications (eg, thrombocytopenic purpura, cerebral, gastrointestinal, and
intrarenal hemorrhage) are estimated to occur in approximately 1 per 3000 cases and are more
frequent among children than adults. Other complications are observed more frequently among
teenagers and adults. Postinfectious encephalitis occurs in about 1 per 6000 rubella cases,
usually within a week of the exanthem, but may occur without any rash. Although the prognosis
is generally good, fatal cases have been reported. Progressive rubella panencephalitis is a rare
and devastating complication
 Prevention
Active immunization against rubella is now possible with live attenuated vaccines. The goal of rubella
immunizationis the prevention of rubella infection during a future
pregnancy.

RUBELLA VACCINES: Since the isolation of the virus in 1962, several live attenuated vaccines have been
developed. In 1979 the RA 27/3 vaccine, produced in human diploid fibro-blast has replaced all the other
vaccines. This is because RA 27/3 vaccine induces higher antibody titres and produces an immune response
more closely paralleling natural infection than the other vaccines . There is evidence that it largely prevents
subclinical superinfection with wild virus.

Vaccination strategy

In the light of the experience gained during the past years, the immunization strategies to prevent
congenital rubella infection have been modified - the priorities being first to protect women of child-
bearing age (15- 34 or 39 years of age) and then to interrupt transmission of rubella by vaccinating all
children currently aged 1-14 years, and subsequently all children at one year of age. The programme
would then revert to one of routine universal immunization of all children at age 1 (preferably using
combined measles- rubella or measles-mumps rubella vaccines).
 Mumps
An acute infectious disease caused by an RNA virus classified as genus Rubulauirus of the family
paramyxoviridae which has a predilection for glandular and nervous tissues. Clinically, the disease is
recognized by nonsuppurative enlargement and tenderness of one or both the parotid glands. Other organs
may also be involved.

Constitutional symptoms vary, or may be in apparent. The disease occurs throughout the world. Although
morbidity rate tends to be high, mortality rate is negligible.

In most parts of the world, the annual incidence of mumps in the absence of immunization is in the range of
100-1000 cases/100,000 population with epidemic peak every 2-5 years. Natural infection with this virus is
thought to confer lifelong protection
Mumps
Agent factors

(a) AGENT : The causative agent, Myxouirus parotiditis is a RNA virus of the myxovirus family. The virus can
be grown readily in chick embryo or tissue culture. There is only one serotype.
(b) SOURCE OF INFECTION : Both clinical and subclinical cases. Subclinical cases which account for 30-
40 per cent of all cases (2) appear to be responsible for maintaining the cycle of infection. The virus can be
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 on occasion in the CSF.
(c) PERIOD OF COMMUNICABILITY : Usually 4-6 days before the onset of symptoms and a week or more
thereafter. The period of maximum infectivity is just before and at the onset of parotitis. Once the swelling
of the glands has subsided, the case may be regarded as no longer infectious.
(d) SECONDARY ATTACK RATE : Estimated to be about 86 per cent.

Host factors
(a) AGE AND SEX : Mumps is the most frequent cause of parotitis in children in the age group 5-9 years. The
average age of incidence of mumps is higher than with measles, chickenpox or whooping cough. However,
no age is exempt if there is no previous immunity. The disease tends to be more severe in adults than in
children.
(b) IMMUNITY : One attack, clinical or subclinical, is assumed to induce lifelong immunity. There is only one
antigenic type of mumps virus, and it does not exhibit significant antigenic variation (3). Most infants below
the age of 6 months are immune because of maternal antibodies.

Mode of transmission
The disease is spread mainly by droplet infection and after direct contact with an infected person.

Incubation period
Varies from 2 to 4 weeks, usually 14-18 days.
 Clinical Features
Mumps is a generalized virus infection. In 30-40 per cent of cases mumps infection is clinically non-apparent. In
clinically apparent cases. it is characterized by pain and swelling in either one or both the parotid glands but may also
involve the sublingual and submandibular glands.

Often the child complains of "ear ache'' on the affected side prior to the onset of swelling. There may be pain and
stiffness on opening the mouth before the swelling of the gland is evident.

Mumps may also affect the testes, pancreas, CNS, ovaries, prostate, etc. In severe cases, there may be fever, headache
and other constitutional symptoms which may last from 3-5 days. The swelling subsides slowly over 1-2 weeks.

COMPLICATIONS : Though frequent, are not serious. These include orchitis, ovaritis, pancreatitis, meningoencephalitis,
thyroiditis, neuritis, hepatitis and myocarditis.

Testicular swelling and tenderness denote orchitis, which is the most common extrasalivary gland manifestation of
mumps in adults.

It is unilateral in about 75 per cent of cases. High fever usually accompanies orchitis, which develops typically 7-10 days
after the onset of parotitis in about 25-40 per cent of post-pubertal men;

Mumps infection in the first trimester of pregnancy is associated with a 25% incidence of spontaneous abortion,
although congenital malformations following mumps infection in pregnancy have not been reported
 Prevention

VACCINATION : Highly effective live attenuated vaccine is now available for the prevention
of mumps.

A single· dose (0.5 ml) intramuscularly produces detectable antibodies in 95 per cent of
vaccinees. The duration of long-term immunity is not known. It is recommended for routine
immunization for children over 1 year of age, either alone or in combination with other virus
vaccines, eg. in MMR vaccine or as a quadrivalent vaccine with varicella. A second dose is
recommended for children at 4-6 years of age i.e., before starting the school.
Influenza (Flu)
Influenza Viruses
How Flu Spreads

• People with flu can spread it to others up to about 6 feet away;

• Flu viruses spread mainly by droplets made when people with flu cough,
sneeze or talk; these droplets can land in the mouths or noses of people who
are nearby or possibly be inhaled into the lungs.

• People with flu are most contagious in the first three to four days after their
illness begins. Most healthy adults may be able to infect others beginning 1
day before symptoms develop and up to 5 to 7 days after becoming sick.
People at High Risk For Flu
Complications
Prevention

Vaccination

Everyone 6 months and older should get a flu vaccine every season with rare exceptions.
Vaccination is particularly important for people who are at high risk of serious
complications from influenza. People at High Risk of Developing Flu-Related Complications
has a full list of age and health factors that confer increased risk.