Transcript Measles is an acute highly contagious viral disease caused by

MMR
Measles, Mumps &Rubella
Measles
DEFINITION
•
Measles is an acute highly contagious viral
disease caused by measles
• Agent- RNA virus ( Paramyxo virus family,
genus Morbillivirus )
Host factors
• Age- All age person is susceptible;
90% of contact people acquire the
disease 6 months to 3 years even up to
10 years
• Incidence equal in both sexes
• Immunity – life long immunity
• Malnourished children are susceptible
Measles Epidemiology
• Reservoir
Human
• Transmission
Respiratory
Airborne
• Temporal pattern
Peak in late winter–spring
• Communicability
4 days before to 4 days after
rash onset
Measles Pathogenesis
• Respiratory transmission of virus
• Replication in nasopharynx and regional
lymph nodes
• Primary viremia 2-3 days after exposure
• Secondary viremia 5-7 days after exposure
with spread to tissues
Measles Clinical Features
• Incubation period 10-12 days
Prodrome
• Stepwise increase in fever to
40°C or higher for 4 days.
• Cough, coryza, conjunctivitis ( 3 Cs )
• Koplik spots
Measles Clinical Features
Rash
• 2-4 days after prodrome, 14 days after
exposure
• Maculopapular, becomes confluent
• Begins on face and head
• Persists 5-6 days
• Fades in order of appearance
DIAGNOSIS
• 1 .Epidemiologic data;
• 2 .Clinical manifestations;
• 3. Laboratory findings:
. 3 .1 .Multinucleated giant cells are
detected in nasopharyax mucosa
secretions;
• 3 .2 .Measles virus can be isolated in
tissues culture;
. 3 .3 . Antibody titer;
• 3 .4 . WBC is relative low .
treatment
•
1 .General therapy: rest, nursing and
diet
• 2. Symptomatic therapy: fever and
cough,
• 3.Support threapy:r-globulin
traditional chinese herbs may be
used ;
• 4.complications of treatment
PREVENTION
• 1 .Control source of infection;
• 2 .Interruption of transmissions ;
• 3 .Protection of the susceptible person:
3.1 . Active immunization
Lived attenuated measles vaccine.
plan immune:8m,7j
epidemic stage:before 2 m
contactor:with in 2 days
Contraindications:pregnancy
3.2 . Passive immunization
placenta globulin or gamma globulin.
<5 days
prevent onset
>5 days
relieve symptoms
Introduction
Mumps is an acute respiratory tract
infectious disease caused by mumps
virus, it occurs primarily in school-aged
children and adolescents.
The most prominent manifestation is
nonsuppurative swelling and tenderness
of the salivary glands with one or both
parotid glands involved in most cases.
Epidemiology
 Sources of infection:
Patients in early course of the disease,
hosts under covert infection.
The period of peak contagion before or
at the onset of parotitis.
Route of transmission :
Via droplet nuclei or direct
contact,fomites
Etiology
 Mumps virus (Paramyxovirus
parotitis) belongs to Paramyxoviridae
family. RNA virus.
 Epidemic features:
Endemic throughout the world.
The peak incidence in winter and spring.
Mode of transmission: droplet
Age and gender : 5-15 years
School-aged children at high risk and
girls common.
Post-infection immunity is stable and
long-lasting.
Clinical Manifestations
 Incubation period:
averages 16 to 18 days
with a range of 2 to 4 weeks.
 Prodromal symptoms include low- grade fever,
anorexia, malaise and headache.
 Parotid tenderness and ipsilateral earache
within 1 or 2 days after the illness onset,then
parotid is visibly enlarged and go to maximum
size over next 2 to 3 days accompanied severe
pain and normal or high temperature. One
parotid enlarges after the other. The orifice of
Stensen’s duct is edematous and erythematous.
Parotid returns to normal size within a week.
Patients with parotitis have difficulty with
pronunciation and mastication. Citrus fruits and
juices exacerbates the pain.
Other salivary glands involved include
submandibular adenitis and sublingual adenitis.
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Clinical meningitis occurs in 15% of
patients with mumps. Its onset averages 4-5
days after parotitis but may before, after or in
the absence of parotitis. Clinical features are
headache, vomiting, fever and nuchal rigidity.
CSF pleocytosis. Prognosis is benign.
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The onset of orchitis is abrupt with high
temperature, chills , testicular pain and
swelling. Impaired fertility is rare.
Diagnosis
 In most instances, the diagnosis of mumps is
made on the basis of a exposure history and
of parotid swelling and tenderness
accompanied
other symptoms.
 Laboratory confirmation is unnecessary in
typical cases, exception the absence or
recurrence of parotitis and extrasalivary
glands
involved. Serologic tests,viral isolation.
Amylase and lipase.
Prognosis
Benign and self-limited
Major death causes are severe mumps
encephalitis
treatment
 There is no specific anti-viral drug therapy.
 Treatment is supportive by treating symptoms, using
antipyretics and analgesics.
Child care
 The child must rest in bed until the fever goes away.
 Isolate the child, to prevent spreading the disease to
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other.
Use analgesics and anti-pyretic to ease symptoms.
Avoid food that require chewing.
Avoid sour foods that stimulate saliva production.
Drink plenty of water.
Use cold compress to ease the pain of swelling
glands.
Prevention
 A live attenuated vaccine is available (MMR).
 It contains mumps, measles and rubella attenuated
virus strains.
 Administered in one dose, intramuscularly or
subcutaneously.
 The vaccine is protective.
 Rubella is an acute, contagious viral infection. While
the illness is generally mild in children, it has serious
consequences in pregnant women causing fetal death
or congenital defects known as congenital rubella
syndrome (CRS).
 The name rubella is derived from a Latin term meaning
"little red."
 Rubella is sometime called German Measles or 3-day
Measles.
 The synonym "3-day measles" derives from the typical
course of rubella exanthema that starts initially on the
face and neck and spreads centrifugally to the trunk and
extremities within 24 hours.
 It then begins to fade on the face on the second day and
disappears throughout the body by the end of the third
day.
 It is a generally mild disease caused by the rubella virus.
 Agent – RNA virus (Togo virus family), Genus
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Rubivirus.
Source of infection – Respiratory secretion
Host -3-10 yrs
Immunity –life long
Environmental factors –winter and spring season
Transmission – droplet, vertical transmission
I.P – 2-3 weeks average 18 days
Symptoms
 In children, the disease is usually mild, with
symptoms including a rash, low fever (<39°C),
nausea and mild conjunctivitis. The rash, which
occurs in 50–80% of cases, usually starts on the face
and neck before progressing down the body, and
lasts 1–3 days. Swollen lymph glands behind the ears
and in the neck are the most characteristic clinical
feature. Infected adults, more commonly women,
may develop arthritis and painful joints that usually
last from 3–10 days.
 When a woman is infected with the rubella virus
early in pregnancy, she has a 90% chance of passing
the virus on to her fetus.
Congenital rubella syndrome
 Children with CRS can suffer hearing impairments,
eye and heart defects and other lifelong disabilities,
including autism, diabetes mellitus and thyroid
dysfunction – many of which require costly therapy,
surgeries and other expensive care.
 The highest risk of CRS is in countries where women
of childbearing age do not have immunity to the
disease (either through vaccination or from having
had rubella). Before the introduction of the vaccine,
up to 4 babies in every 1000 live births were born
with CRS.
 0–28 days before conception - 43%
chance
 0–12 weeks after conception - 51%
chance
 13–26 weeks after conception - 23%
chance
 Infants are not generally affected if
rubella is contracted during the third
trimester
Vaccination
 he rubella vaccine is a live attenuated strain that has
been in use for more than 40 years. A single dose
gives more than 95% long-lasting immunity, which is
similar to that induced by natural infection.
 Rubella vaccines are available either in monovalent
formulation (vaccine directed at only one pathogen)
or more commonly in combinations with other
vaccines such as with vaccines against measles (MR),
measles and mumps (MMR), or measles, mumps
and varicella (MMRV).