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Togaviridae: Rubella (German Measles)

The document discusses two virus families: Togaviridae and Rhabdoviridae. For Togaviridae, it notes that rubella virus causes a mild rash disease called German measles but can cause birth defects if a woman is infected during pregnancy. For Rhabdoviridae, it states that rabies virus is the most significant pathogen, causing a disease transmitted via animal bites that leads to hydrophobia, paralysis, and death if left untreated. Vaccines exist to prevent both rubella and rabies.

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Nikita SHARMA
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75 views3 pages

Togaviridae: Rubella (German Measles)

The document discusses two virus families: Togaviridae and Rhabdoviridae. For Togaviridae, it notes that rubella virus causes a mild rash disease called German measles but can cause birth defects if a woman is infected during pregnancy. For Rhabdoviridae, it states that rabies virus is the most significant pathogen, causing a disease transmitted via animal bites that leads to hydrophobia, paralysis, and death if left untreated. Vaccines exist to prevent both rubella and rabies.

Uploaded by

Nikita SHARMA
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as DOCX, PDF, TXT or read online on Scribd
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TOGAVIRIDAE

Introduction
The Togaviridae (togaviruses) can be classified into the following major genera: Alphavirus,
Rubivirus, and Arterivirus.No known arteriviruses cause disease in humans, so this genus is not
discussed further.Members of the Togaviridae are responsible for two very different kinds of
human disease.All alphaviruses are transmitted by arthropods, and cause encephalitis, arthritis,
and rashes.

Rubella virus is the only member of the Rubivirus group; it is discussed separately because its
disease manifestation (German measles) and its means of spread differ from those of the
alphaviruses.Rubella virus is the agent of a mild rash disease but can also cause congenital
abnormalities in the fetus when acquired by the mother early in pregnancy.

Rubella (German Measles)


Rubella is one of the five classic childhood exanthems, along with measles, roseola, fifth
disease, and chickenpox.Rubella, meaning “little red” in Latin, was first distinguished from
measles and other exanthems by German physicians; thus the common name for the disease,
German measles.In 1941, an astute Australian ophthalmologist, Norman McAlister Gregg,
recognized that maternal rubella infection was the cause of congenital cataracts.Maternal rubella
infection has since been correlated with several other severe congenital defects.This finding
prompted the development of a unique program to vaccinate children to prevent infection of
pregnant women and neonates.

 Characteristics Rubella virus is spherical and enveloped.

The diameter is from 40 to 90 nm.Icosahedral nucleocapsid.Genome is composed of a single


molecule of positive RNA.The envelope contains two E proteins that mediate fusion of viral and
cellular membranes.mRNA is translated into a single polyprotein.The virus buds from cell
membrane.The virus contains hemagglutinin.

Epidemiology Humans are the only host for rubella.

The virus is spread in respiratory secretions and is generally acquired during childhood.Spread of
virus, before or in the absence of symptoms, and crowded conditions, such as those in day-care
centers, promote contagion.Approximately 20% of women of childbearing age escape infection
during childhood and are susceptible to infection unless vaccinated.Programs in many states in
the United States test expectant mothers for antibodies to rubella.

Pathogenesis
Rubella virus is not cytolytic but does have limited cytopathologic effects in certain cell lines,
such as Vero and RK13.The prodromal period lasts approximately 2 weeks.Rubella infects the
upper respiratory tract and then spreads to local lymph nodes, which coincides with a period of
lymphadenopathy.This stage is followed by establishment of viremia, which spreads the virus
throughout the body.

 Immune Response

Antibody is generated after the viremia, and its appearance correlates with the appearance of the
rash.The antibody limits viremic spread, but cell-mediated immunity plays an important role in
resolving the infection.Only one serotype of rubella exists, and natural infection produces lifelong
protective immunity.Most important, serum antibody in a pregnant woman prevents spread of the
virus to the fetus.Immune complexes most likely cause the rash and arthralgia associated with
rubella infection.Arthritis is joint pain with inflammation, whereas arthralgia is joint pain without
inflammation

Congenital Infection
The virus may persist in tissues, such as the lens of the eye, for 3 to 4 years and may be shed up
to a year after birth.The presence of the virus during the development of the baby’s immune
response may even have a tolerogenic effect on the system, preventing effective clearance of
the virus after birth.Immune complexes that produce further clinical abnormalities may also form
in the neonate or infant.

Laboratory Diagnosis
Isolation of the rubella virus is difficult and rarely attempted.The presence of the virus can be
detected by RT-PCR detection of viral RNA.The diagnosis is usually confirmed by the presence
of antirubella-specific IgM.A fourfold increase in specific IgG antibody titer between acute and
convalescent sera is also used to indicate a recent infection.Antibodies to rubella are assayed
early in pregnancy to determine the immune status of the woman; this test is required in many
states.When isolation of the virus is necessary, the virus is usually obtained from urine and is
detected as interference with replication of echovirus 11 in primary African green monkey kidney
cell cultures (heterologous interference).

Treatment, Prevention, and Control


No treatment is available for rubella.The best means of preventing rubella is vaccination with the
live cold adapted RA27/3 vaccine strain of virus.The live rubella vaccine is usually administered
with the measles and mumps vaccines (MMR vaccine) at 15 months of age.The primary reason
for the rubella vaccination program is to prevent congenital infection by decreasing the number of
susceptible people in the population, especially children.As a result, there are fewer seronegative
mothers and smaller chance that they will be exposed to the virus from contact with the
children.Because only one serotype for rubella exists, and humans are the only reservoir,
vaccination of a large proportion of the population can significantly reduce the likelihood of
exposure to the virus.

RHABDOVIRIDAE
Introduction
The members of the family Rhabdoviridae (from the Greek word rhabdos, meaning “rod”) include
pathogens for a variety of mammals, fish, birds, and plants.Rabies virus is the most significant
pathogen of the rhabdoviruses.Until Louis Pasteur developed the killed-rabies vaccine, a bite
from a “mad” dog always led to the characteristic symptoms of hydrophobia and certain death.

Characteristics

Bullet-shaped, RNA virus. Helical nucleocapsid.


Glycoprotein (G protein) spikes are responsible for viral attachment to cellular receptors.The
genome is single-stranded (-) RNA.The virus contains virion-associated RNA transcriptase “the L
protein”, which produces five viral mRNAs.The M protein is the major structural protein, lies
beneath the lipid membrane.The nucleoprotein (N) protects RNA from degradation by RNase
enzymes, NS “nucleocapsid small”

Classification

Rhabdoviruses infecting mammals belong to two genera in Rhabdoviridae familyLyssavirusIt


contains rabies virus and related viruses (Lagos bat virus, Mokola, Duvenhage).Genus
vesiculovirus:It contains vesicular stomatitis virus (VSV) and related viruses like Chandipur
(arbelius)
 Pathogenesis Reproduces in muscle at bite site
Incubation period of weeks to months, depending on inoculum and distance of bite from central
nervous systemInfects peripheral nerves and travels to brainReproduction in brain causes
hydrophobia, seizures, hallucinations, paralysis, coma, and deathSpreads to salivary glands of
nonhuman animals, from which it is transmittedPost-exposure immunization can prevent disease
due to long incubation period

 Laboratory Diagnosis

The occurrence of neurologic symptoms in a person who has been bitten by an animal generally
establishes the diagnosis of rabies.Unfortunately, evidence of infection, including symptoms and
the detection of antibody, does not occur until it is too late for intervention.Laboratory tests are
usually performed to confirm the diagnosis and to determine whether a suspected individual or
animal is rabid (postmortem).The hallmark diagnostic finding has been the detection of
intracytoplasmic inclusions consisting of aggregates of viral nucleocapsids (Negri bodies) in
affected neurons.

Treatment and Prophylaxis


The first protective measure is local treatment of the wound.Subsequently, immunization with
vaccine in combination with administration of one dose of human rabies immunoglobulin (HRIG)
or horsy antirabies serum is recommended.Passive immunization with HRIG provides antibody
until the patient produces antibody in response to the vaccine.A series of five vaccinations is then
administered over the course of a month.The slow course of rabies disease allows active
immunity to be generated in time to afford protection.

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