VIROLOGY - LECTURE FIFTEEN
RUBELLA (GERMAN MEASLES) VIRUS
Dr. Margaret Hunt
MBIM 650/720 LECTURE: 70 (part)
READING: Murray et al., Microbiology, 3rd Ed., Chapter 59 pp. 499-502
review of structure and properties of rubella virus. Discussion
of viral pathogenesis and disease, epidemiology, prevention and
measles, mumps and rubella viruses are confined to man and occur
worldwide. They are all spread primarily via the aerosol route. Each of
these viruses exists as a single serotype. MMR vaccine contains live,
attenuated forms of all three of these viruses.
Rubella virus is a
member of the Togavirus family. Mumps and measles viruses are members of
the Paramyxovirus family.
"little red" also known as German measles) is a mild disease in
children and adults, but can cause devastating problems if it infects
the fetus, especially if infection is in the first few weeks of
Electron micrograph of rubella virus CDC/Dr. Erskine Palmer
Structure of rubella virus
Rubella virus is the
only member of the Rubrivirus genus of the Togavirus family.
Unlike most Togaviruses it is NOT arthropod borne, but is acquired
via the respiratory route.
It is an enveloped (toga=cloak), non-segmented, positive sense, RNA virus
and replicates in the cytoplasm.
Its nucleocapsid has icosahedral symmetry.
There is only one major antigenic type.
ASPECTS OF RUBELLA
replication of virus
although virus is shed (Mild sore throat, coryza,
infectious 5 days before to 3 days after symptoms
Rash of rubella on skin of child's back. Distribution is similar
to that of measles but the lesions are less intensely red. CDC
Infant with congenital rubella and "blueberry muffin"
Lesions are sites of extramedullary hematopoiesis
and can be associated with several different congenital viral
infections and hematologic diseases. CDC
Face of adult with rubella. CDC/Barbara Rice
short-lived, atypical; immunopathology (Ag-Ab complexes)
posterior triangle of neck or behind ear
(circulating immune complexes)
Baby born with rubella: Thickening of the lens of the eye that
causes blindness (cataracts) CDC
Mims et al. Medical Microbiology, 1993, Mosby.
CHILDREN AND ADULTS
Man is the only host.
Virus is spread via an aerosol route and occurs throughout the world.
Initial site of
infection is the upper respiratory tract. The virus replicates
locally (epithelium, lymph nodes) leading to viremia and spread to
other tissues. As a result the disease symptoms develop.
Rash (if it occurs)
starts approximately 2 weeks after initial infection. There is probably an
immunological basis for rash (since it occurs as antibody titers rise).
The patient is infectious from about 1 week before onset of rash to
about 1 week after. Disease results in low grade fever, rash, sore throat,
rash begins on the face and lasts from 12hr to 5days. Some individuals
(especially adults and especially women) get arthralgia
and sometimes arthritis which usually clears up in a few weeks.
T-cell immunity plays
an important role in recovery. IgM may persist for up to a year. There are
also IgG, IgA responses.
extremely rarely (1 in 6000 cases) - rubella encephalopathy (headache,
vomiting, stiff neck, lethargy, convulsions) may occur about 6 days after
rash. It usually lasts only a few days and most patients recover (no
sequelae),. If death occurs, it is within few days of onset of symptoms.
The risk to a fetus is
highest in the first few weeks of pregnancy and then declines in terms of
both frequency and severity, although there is still some risk in second
trimester. Virus infects the placenta and then spreads to the fetus.
If non-immune mothers are infected in the first trimester, up to 80% of
neonates may have sequelae:
(psychomotor retardation, mental retardation)
(cataract, glaucoma, retinopathy)
There may also be
variety of other problems including bone lesions, pneumonitis etc..
In most cases, there
is neural involvement - lethargy, irritability, motor tone problems,
mental retardation, motor disabilities, abnormal posture, neurosensory
Virus from congenital
infections persists after birth.
Those with congenital infections can infect others after birth for a year
or more. Virus occurs in naso-pharyngeal secretions, urine and feces.
Later on, patients
with congenital rubella syndrome may develop additional complications
including diabetes mellitus (up to 20%), thyroid dysfunction, growth
hormone deficiency, ocular complications.
This is an extremely
virus disease. It usually develops in the teens with death within 8
years. Most often it is associated with congenital rubella and may be
associated with childhood rubella.
DIAGNOSIS OF RUBELLA
Many (possibly 50%)
infections are apparently subclinical and many infections go unrecognized,
even if symptoms develop (rash is not always present).
Infections with many
other agents give similar symptoms to rubella (e.g. infection with human
parvovirus, certain arboviruses, many of the enterovirus group of
picornaviruses, some adenoviruses, EBV, scarlet fever, toxic drug
Serological tests or
isolation of virus (immunofluorescence) are needed to confirm infection of
Man is the only host.
Rubella occurs world wide.
Periodic epidemics occur in an unvaccinated population.
Natural infection protects for life (there is a single serotype).
A live vaccine
(attenuated strain) is available. Since only one serotype, a univalent
attenuated vaccine can provide lifelong immunity. The vaccine strain does
not spread to family members.
It is important that
women are vaccinated prior to their first pregnancy. United States
recommendations are for childhood vaccination to prevent epidemics,
combined with vaccination of susceptible, non-pregnant adolescent and
adult females. The vaccine is contraindicated for pregnant women, but when
unwittingly used, no problems have been seen. If the patient is pregnant
and seronegative, the pregnancy should be monitored carefully and the
patient vaccinated postpartum.
There is no specific
treatment. Supportive care should be used