Mumps and Measles virus

Retno Budiarti, dr,M.Kes

Microbiology deparment
Medical Faculty
Hang Tuah University
Paramyxoviridae
The viral genome is linear, negative-
sense, single-stranded, nonsegmented
RNA, about 15 kb in size
Virion: Spherical, pleomorphic, 150 nm or
more in diameter (helical nucleocapsid )
Envelope: Contains viral glycoprotein (G,
H, or HN) (hemagglutinin or
neuraminidase) and fusion (F)
glycoprotein
replication
Virus Attachment, Penetration, and Uncoating
viruses attach to host cells via the hemagglutinin
glycoprotein (HN, H, or G protein). Next, the
virion envelope fuses with the cell membrane by
the action of the fusion glycoprotein F1 cleavage
product. Fusion by F1 occurs at the neutral pH
of the extracellular environment, allowing
release of the viral nucleocapsid directly into the
cell.
Transcription, Translation, and RNA
Replication

mRNA transcripts are made in the cell

cytoplasm by the viral RNA polymerase
Viral proteins are synthesized in the
cytoplasm
synthesis of a positive-strand antigenome
intermediate template, Full-length progeny
genomes are then copied from the
antigenome template.
Maturation

The virus matures by budding from the cell

surface. Progeny nucleocapsids form in the
cytoplasm and migrate to the cell surface.
During budding, most host proteins are excluded
from the membrane.
The neuraminidase activity of the HN protein of
parainfluenza viruses and mumps virus
presumably functions to prevent self-aggregation
of virus particles.
Mumps Virus Infections

Mumps is an acute contagious disease

characterized by nonsuppurative enlargement of
one or both salivary glands.
Mumps virus mostly causes a mild childhood
disease, but in adults complications including
meningitis and orchitis are fairly common. More
than one-third of all mumps infections are
asymptomatic.
Pathogenesis & Pathology

Humans are the only natural hosts.

Primary replication occurs in nasal or
upper respiratory tract epithelial cells.
Viremia then disseminates the virus to the
salivary glands and other major organ
systems. Involvement of the parotid gland
is not an obligatory step in the infectious
process.
 The incubation period about 1418 days.
Virus is shed in the saliva from about 3 days
before to 9 days after the onset of salivary
gland swelling.
About one-third of infected individuals with
inapparent infections but are equally capable
of transmitting infection.
virus replicate in epithelial cells in various
visceral organs. Virus frequently infects the
kidneys and can be detected in the urine of
most patients. Viruria may persist for up to 14
days after the onset of clinical symptoms. The
CNS is also commonly infected and may be
involved in the absence of parotitis.
Clinical Findings

one-third are subclinical, including the majority of infections

in children under 2 years of age. The most characteristic
feature is swelling of the salivary glands, which occurs in
about 50% of patients.
A prodromal period of malaise and anorexia is followed by
rapid enlargement of parotid glands as well as other salivary
glands. Gland enlargement is associated with pain.
CNS involvement is common (1030% of cases).
The testes and ovaries may be affected, especially after
puberty.20- 50% of men who are infected with mumps virus
develop orchitis (often unilateral). Atrophy of the testis may
occur as a result of pressure necrosis, Mumps oophoritis
occurs in about 5% of women.
Immunity
Immunity is permanent after a single infection. There is
only one antigenic type of mumps virus
Ab to the HN glycoprotein, the F glycoprotein, and the
internal nucleocapsid protein develop in serum following
natural infection.
Ab against the HN correlate well with immunity,
subclinical infections are thought to generate lifelong
immunity. In immune individuals, IgA antibodies secreted
in the nasopharynx exhibit neutralizing activity.
Passive immunity is transferred from mother thus, it is
rare to see mumps in infants under 6 months of age.
Isolation and Identification of Virus

The most appropriate clinical samples for

viral isolation are saliva, CSF, and urine
Monkey kidney cells are preferred for viral
isolation.
CPE of mumps virus consist of cell
rounding and giant cell formation. An
isolate can be confirmed as mumps virus
by hemadsorption inhibition using mumps-
specific antiserum.
Serology

Ab rise can be detected using paired sera:

a fourfold or greater rise in ab titer is
evidence of mumps infection.
ELISA is useful because it can be
designed to detect either mumps-specific
IgM antibody or IgG antibody.
Mumps IgM is uniformly present early in
the illness and seldom persists longer than
60 days.
Epidemiology

Mumps occurs endemically worldwide. Mumps is primarily

an infection of children. highest incidence in aged 59
years,. In children under 5 years of age, mumps may
commonly cause upper respiratory tract infection without
parotitis.
Mumps is quite contagious; most susceptible individuals
in a household will acquire infection from an infected
member. The virus is transmitted by direct contact,
airborne droplets, or fomites contaminated with saliva or
urine.
About one-third of infections with mumps virus are
inapparent, but the patient can transmit the virus to
others. Individuals with subclinical mumps acquire
immunity.
Treatment, Prevention, & Control

There is no specific therapy.

Immunization with attenuated live mumps virus
vaccine is the best approach to reducing
mumps-associated morbidity and mortality rates.
An effective attenuated live-virus vaccine made
in chick embryo cell culture is available. It
produces a subclinical, noncommunicable
infection. Mumps vaccine is available in
combination with measles and rubella (MMR)
live-virus vaccines.
Measles (Rubeola) Virus Infections

Measles is an acute, highly infectious

disease characterized by fever, respiratory
symptoms, and a maculopapular rash.
Pathogenesis & Pathology
virus gains access to the human body via the
respiratory tract, where it multiplies locally; the
infection then spreads to the regional lymphoid
tissue, multiplication occurs.
Primary viremia disseminates the virus, which then
replicates in the res.
Finally, a secondary viremia seeds the epithelial
surfaces of the body, including the skin, respiratory
tract, and conjunctiva, where focal replication
occurs.
Measles can replicate in certain lymphocytes,
which aids in dissemination throughout the body.
Pathogenesis & Pathology
During the prodromal phase (24 days) and the
first 25 days of rash, virus is present in tears,
nasal and throat secretions, urine, and blood. The
characteristic maculopapular rash appears about
day 14 just as circulating ab can detectable, the
viremia disappears, and the fever falls.
The rash develops as a result of interaction of
immune T cells with virus-infected cells in the
small blood vessels and lasts about 1 week. (In
patients with defective cell-mediated immunity, no
rash develops.)
Involvement of the cns is common
Clinical Findings

incubation period of 812 days, measles is typically a 7- to

11-day illness (with a prodromal phase of 24 days followed
by an eruptive phase of 58 days).
The prodromal phase : fever, sneezing, coughing, running
nose, redness of the eyes, Koplik's spots, and lymphopenia.
The cough and coryza reflect an intense inflammatory
reaction involving the mucosa of the respiratory tract.
The conjunctivitis is commonly associated with photophobia.
Koplik's spotspathognomonic for measlesare small,
bluish-white ulcerations on the buccal mucosa opposite the
lower molars. These spots contain giant cells and viral
antigens and appear about 2 days before the rash.
Clinical finding
The fever and cough persist until the rash
appears and then subside within 12 days.
The rash, which starts on the head and
then spreads progressively to the chest,
the trunk, and down the limbs, appears as
light pink, discrete maculopapules that
coalesce to form blotches, becoming
brownish in 510 days. The fading rash
resolves with desquamation..
complication
The most common complication of measles is otitis
media (59% of cases).
Pneumonia, caused by secondary bacterial infections
(<10% of cases in developed countries,>2080% in
developing countries.
Complications involving the cns are the most serious.
Subacute sclerosing panencephalitis, the rare late
complication of measles infection (1:300,000), begins
insidiously 515 years after a case of measles; it is
characterized by progressive mental deterioration,
involuntary movements, muscular rigidity, and coma. It is
usually fatal within 13 years after onset. exhibit high
titers of measles ab in csf and serum
Isolation and Identification of Virus

Nasopharyngeal and conjunctival swabs, blood

samples, respiratory secretions, and urine.
Monkey or human kidney cells or a
lymphoblastoid cell line are optimal for isolation
Measles virus grows slowly; typical cpe
(multinucleated giant cells containing both
intranuclear and intracytoplasmic inclusion
bodies) take 710 days to develop
Serology

Serologic confirmation of measles

infection depends on a fourfold rise in
antibody titer between acute-phase and
convalescent-phase sera or on
demonstration of measles-specific IgM
antibody in a single serum specimen
drawn between 1 and 2 weeks after the
onset of rash.
ELISA, HI, and Nt tests
Epidemiology

The virus is highly contagious, there is a single

serotype, there is no animal reservoir,
inapparent infections are rare, and infection
confers lifelong immunity.
Transmission occurs predominantly via the
respiratory route (by inhalation of large droplets
of infected secretions). Hematogenous
transplacental transmission can occur when
measles occurs during pregnancy.
Measles is endemic throughout the world.
Treatment, Prevention, & Control

Vitamin A treatment in developing countries has

decreased mortality and morbidity. Measles virus is
susceptible in vitro to inhibition by ribavirin, but clinical
benefits have not been proved.
A highly effective and safe attenuated live measles virus
vaccine has been available since 1963. monovalent
form, and in combination with live attenuated rubella
vaccine (MR) and live attenuated rubella and mumps
vaccines (MMR).
Mild clinical reactions (fever or mild rash) will occur in 2
5% of vaccinees, but there is little or no virus excretion
and no transmission.