3 Measles

Measles (Rubeola)
Prof. Dr. Saad S Al Ani

Senior Pediatric Consultant
Head of Pediatric Department
Khorfakkan Hospital
Sharjah ,UAE
saadsalani@yahoo.com
Measles (Rubeola)
It is an acute viral infection

characterized by a final stage with
a maculopapular rash erupting
successively over the neck and
face, trunk, arms, and legs, and
accompanied by a high fever.
09/18/10 Prof. saad s al ani measles khorfakkan hospital 2

Etiology
 Measles virus, the cause of measles,
is an RNA virus of the genus
Morbillivirus in the family
Paramyxoviridae.
 Only one serotype is known

Epidemiology
 Measles is endemic throughout the
world.
 In the past, epidemics tended to occur
irregularly, appearing in the spring in
large cities at 2-4-yr intervals as new
groups of susceptible children were
exposed.

Epidemiology (Cont.)
 It is rarely subclinical.
 Prior to the use of measles
vaccine, the peak incidence
was among children 5-10 yr of
age.

Epidemiology (Cont.)
 Individuals born before 1957 are

considered to have had natural
infection and to be immune

TRANSMISSION
 Measles is highly contagious;

approximately 90% of susceptible
household contacts acquire the disease.
 Maximal dissemination of virus occurs
by droplet spray during the prodromal
period (catarrhal stage).

TRANSMISSION (Cont.)
 Transmission to susceptible contacts

often occurs prior to diagnosis of the index
case
 Infants acquire immunity transplacentally
from mothers who have had measles or
measles immunization.

 This immunity is usually complete for

the first 4-6 mo of life and wanes at a
variable rate.
 Some protection persists that may
interfere with immunization
administered before 12 mo of age.

 Most women of childbearing age in

the United States now have measles
immunity by means of immunization
rather than disease

 infants of mothers with measles

vaccine-induced immunity lose
passive antibody at a younger age
than infants of mothers who had
measles infection.
infection

 Infants of mothers who are susceptible

to measles have no measles immunity
and may contract the disease
simultaneously with the mother before or
after delivery

Incidence and percentage of import-associated measles
cases, by year – United States, 1985 to 2003
Centers for Disease Control and Prevention. Epidemiology of Measles – United States, 2001–2003.
MMWR 2004;53:713–716.)

Number of measles cases, by import status and week of
rash onset – United States, 2004
Centers for Disease Control and Prevention. Measles – United States. MMWR 2005;54:1229–1231

Number of confirmed measles cases and percentage of
routine infant measles vaccination coverage – the
Americas, 1980–2000.
Centers for Disease Control and Prevention. Progress toward interrupting indigenous measles
transmission – region of the Americas, January 1999–September 2000. MMWR 2000;40:986–990

Pathogenesis
 The essential lesion of measles is found
in the skin, conjunctivae, and the
mucous membranes of the
nasopharynx, bronchi, and intestinal
tract.
 Serous exudate and proliferation of
mononuclear cells and a few
polymorphonuclear cells occur around
the capillaries.

Pathogenesis (cont.)
 Hyperplasia of lymphoid tissue usually

occurs, particularly in the appendix,
where multinucleated giant cells of up
to 100 μm in diameter (Warthin-
Finkeldey reticuloendothelial giant
cells) may be found.
 In the skin, the reaction is
particularly notable about the
sebaceous glands and hair follicles.
 Koplik spots consist of serous exudate

and proliferation of endothelial cells
similar to those in the skin lesions.
 A general inflammatory reaction of the
buccal and pharyngeal mucosa extends
into the lymphoid tissue and the
tracheobronchial mucous membrane.

 Interstitial pneumonitis resulting

from measles virus takes the form of
Hecht giant cell pneumonia.
 Bronchopneumonia may occur from
secondary bacterial infection.

 In fatal cases of encephalomyelitis,

perivascular demyelinization occurs in
areas of the brain and spinal cord.
 In subacute sclerosing panencephalitis
(SSPE), there may be degeneration of
the cortex and white matter with
intranuclear and intracytoplasmic
inclusion bodies
Clinical Manifestations
 Measles has three clinical stages:

1. an incubation stage
2. a prodromal stage with an enanthem
(Koplik spots) and mild symptoms
3. a final stage with a maculopapular
rash accompanied by high fever.

The incubation period
 lasts approximately 10-12 days to the first
prodromal symptoms and another 2-4 days to
the appearance of the rash; rarely, it may be
as short as 6-10 days.
 Body temperature may increase slightly 9-10
days from the date of infection and then
subside for 24 hr or so.
 The patient may transmit the virus by the
9th-10th day after exposure and occasionally
as early as the 7th day, before the illness can
be diagnosed
The prodromal phase
 usually lasts 3-5 days and is characterized by:
* low-grade to moderate fever
* dry cough
* coryza
* conjunctivitis.
 These symptoms nearly always precede the
appearance of Koplik spots, the
pathognomonic sign of measles, by 2-3 days.

The prodromal phase (cont.)
 The conjunctival inflammation and
photophobia may suggest measles before
Koplik spots appear.
 In particular, a transverse line of conjunctival
inflammation, sharply demarcated along the
eyelid margin, may be of diagnostic
assistance in the prodromal stage. As the
entire conjunctiva becomes involved, the line
disappears.
Koplik spots
 An enanthem or red mottling is
usually present on the hard and
soft palates
 the pathognomonic sign of
measles:

Koplik spots (cont.)
 are grayish white dots, usually as
small as grains of sand, that have
slight, reddish areolae; occasionally
they are hemorrhagic.
 tend to occur opposite the lower
molars but may spread irregularly over
the rest of the buccal mucosa.

Koplik spots (cont.)
 Rarely they are found within the
midportion of the lower lip, on the
palate, and on the lacrimal caruncle.
 They appear and disappear rapidly,
usually within 12-18 hr.
 As they fade, a red, spotty
discoloration of the mucosa may
remain.

 Occasionally, the prodromal phase may be
severe, being ushered in by a sudden high
fever, sometimes with convulsions and even
pneumonia.
 Usually the coryza, fever, and cough are
increasingly severe up to the time the rash
has covered the body.
 The temperature rises abruptly as the rash
appears and often reaches 40°C (104°F) or
higher.

 In uncomplicated cases, as the rash appears

on the legs and feet, the symptoms subside
rapidly within about 2 days, usually with an
abrupt drop in temperature to normal.
 Patients up to this point may appear
desperately ill, but within 24 hr after the
temperature drops, they appear well.

The rash
 usually starts as faint macules on the:
* upper lateral parts of the neck
* behind the ears
* along the hairline
* posterior parts of the cheek.

The rash (cont.)
 The individual lesions become increasingly

maculopapular as the rash spreads rapidly
over the:
* entire face
* neck
* upper arms
* upper part of the chest
within approximately the first 24 hr

Maculopapular rash of measles
Korting GW: Hautkrankheiten bei Kindern und Jugendlichen, 3rd ed. Stuttgart, FK
Schattauer Verlag, 1982

The rash (cont.)
 During the succeeding 24 hr the rash

spreads over the back, abdomen, entire
arm, and thighs.
 As it finally reaches the feet on the
2nd-3rd day, it begins to fade on the
face.

Typical rash on day 2–3 of measles
(Courtesy of J.H. Brien.)

Rash on day 5 of measles showing typical confluence and density
on head with scattered lesions on the trunk. (Courtesy of J.H. Brien.)

The rash (cont.)
 The rash fades downward in the same

sequence in which it appeared.
 The severity of the disease is directly related
to the extent and confluence of the rash.
 In mild measles the rash tends not to be
confluent, and in very mild cases there are
few, if any, lesions on the legs.

The rash (cont.)
 In severe cases the rash is confluent,

the skin is completely covered,
including the palms and soles, and the
face is swollen and disfigured.
 The rash is often slightly hemorrhagic;
in severe cases with a confluent rash,
petechiae may be present in large
numbers, and there may be extensive
ecchymoses
The rash (cont.)
 The appearance of the rash may vary

markedly.
 Infrequently a slight urticarial, faint
macular, or scarlatiniform rash may
appear during the early prodromal
stage, disappearing in advance of the
typical rash.

The rash (cont.)
 Complete absence of rash is rare except :

1. in patients who have received
immunoglobulin (Ig) during the incubation
period
2. in some patients with HIV infection
3. occasionally in infants younger than 9 mo of
age who have appreciable levels of maternal
antibody.

The rash (cont.)
 In the hemorrhagic type of measles

(black measles), bleeding may occur
from the mouth, nose, or bowel.
 In mild cases the rash may be less
macular and more nearly pinpoint,
somewhat resembling that of scarlet fever
or rubella

The rash (cont.)
 Itching is generally slight.

 As the rash fades, branny desquamation
and brownish discoloration occur and
then disappear within 7-10 days.

 Otitis media
 bronchopneumonia
 gastrointestinal symptoms such as
diarrhea and vomiting

Are more common in infants and small
children (especially if they are
malnourished) than in older children.

Diagnosis
 The diagnosis is usually apparent from the
characteristic clinical picture; laboratory
confirmation is rarely needed
 Testing for measles IgM antibodies is
recommended in some situations
 Measles IgM is detectable for 1 mo after
illness, but sensitivity of IgM assays may be
limited in the first 72 hr of the rash illness.

Diagnosis (cont.)
 Isolation of measles virus from clinical samples is also

useful in identifying the genotype of the strain to
track transmission patterns.
 All suspected measles cases should be reported
immediately to local or health departments.
 During the prodromal stage multinucleated giant
cells can be demonstrated in smears of the nasal
mucosa.

Diagnosis (cont.)
 Antibodies become detectable when the rash

appears;
 testing of acute and convalescent sera
demonstrates the diagnostic seroconversion
or fourfold increase in titer.
 Measles virus can be isolated by tissue
culture in human embryonic or rhesus
monkey kidney cells.

Diagnosis (cont.)
 Cytopathic changes, visible in 5-10 days,

consist of multinucleated giant cells with
intranuclear inclusions.
 The white blood cell count tends to be low
with a relative lymphocytosis
 Cerebrospinal fluid in patients with measles
encephalitis usually shows an increase in
protein and a small increase in lymphocytes.
The glucose level is normal.

The rash of rubeola must be
differentiated from that of:
 Rubella
 Roseola infantum (human herpesvirus 6)
 Infections resulting from:
* echovirus * coxsackievirus * adenovirus
 Infectious mononucleosis
 Toxoplasmosis
 Meningococcemia
 Scarlet fever
 Rickettsial diseases
 Kawasaki disease
 Serum sickness
 Drug rashes

Treatment
 There is no specific antiviral therapy;
 treatment is entirely supportive.
 Antipyretics (acetaminophen or
ibuprofen) for fever
 bed rest
 maintenance of an adequate fluid
intake
are indicated.
Treatment (cont.)
 Humidification may alleviate symptoms of laryngitis

or an excessively irritating cough; it is best to keep
the room comfortably warm rather than cool.
 Patients with photophobia should be protected from
exposure to strong light.
 Bacterial complications of otitis media and
bronchopneumonia require appropriate antimicrobial
therapy.

Treatment (cont.)
 Complications such as encephalitis, subacute

sclerosing panencephalitis, giant cell pneumonia, and
disseminated intravascular coagulation must be
assessed individually.
 Good supportive care is essential.
 Immunoglobulin and corticosteroids are of limited
value.
 Currently available antiviral compounds are not
effective.

Treatment (cont.)
 the American Academy of Pediatrics

recommends consideration of vitamin A
supplementation for:
 children 6 mo to 2 yr of age who are
hospitalized for measles and its
complications
 children older than 6 mo of age with
measles and immunodeficiency;

Treatment (cont.)
 The recommended regimen is a single dose of:

 100,000 IU orally for children 6 mo to 1 yr
 200,000 IU for children 1 yr of age or older
 Children with ophthalmologic evidence of
vitamin A deficiency should be given additional
doses the next day and 4 wk later.

Complications
 The chief complications of measles
are:
 otitis media
 pneumonia
 encephalitis.

Respiratory tract complications
 Interstitial pneumonia may be caused by the

measles virus (giant cell pneumonia).
 Bacterial superinfection and bronchopneumonia are
more frequent, however, usually with
pneumococcus, group A Streptococcus,
Staphylococcus aureus, and Haemophilus influenzae
type b.
 Laryngitis, tracheitis, and bronchitis are common
and may be due to the virus alone

Respiratory tract complications
(cont.)
 Measles may exacerbate underlying

Mycobacterium tuberculosis infection
 There may also be a temporary loss
of hypersensitivity reaction to
tuberculin skin testing.
 Measles pneumonia in HIV-infected
patients is often fatal and is not
always accompanied by rash

Cardiovascular complications
 Noma of the cheeks may occur in rare instances
 Gangrene elsewhere appears to be secondary to :
3. purpura fulminans
4. disseminated intravascular coagulation
following measles
 Myocarditis is an infrequent serious complication,

although transient electrocardiographic changes may
be relatively common.

Neurologic complications
 Are more common in measles than in any of the other
exanthematous diseases.
Encephalomyelitis
 The incidence is estimated to be 1-2/1,000 cases of
measles.
 There is no correlation between the severity of the :
* Rash illness and that of the neurologic involvement
* Initial encephalitic process and the prognosis.

Neurologic complications (cont.)
 Infrequently, encephalitic involvement is manifest in the

pre-eruptive period, but more often its onset occurs 2-5
days after the appearance of the rash.
 The cause of measles encephalitis remains
controversial.
1.Encephalitis early in the course of the disease :
direct viral invasion may be operative for
2. Encephalitis that occurs later is predominantly
demyelinating and may reflect an immunologic reaction.
 Fatal encephalitis has occurred in children receiving
immunosuppressive treatment.

Neurologic complications (cont.)
 Other central nervous system complications,

including:
 Guillain-Barré syndrome
 Hemiplegia
 Cerebral thrombophlebitis
 Retrobulbar neuritis
occur rarely.
Prognosis
 Case fatality rates in the United States have
decreased in recent years to low levels for all
age groups, largely because of:
 Improved socioeconomic conditions
 Effective antibacterial therapy for the

treatment of secondary bacterial infections.
 Despite the decline in measles cases and
fatalities in the United States, the case fatality
rate is still 1-3/1,000 cases.

Prognosis (cont.)
 Deaths are primarily due to pneumonia or

secondary bacterial infections.
 In developing countries measles frequently
occurs in infants; possibly because of
concomitant malnutrition, the disease is very
severe in these locations and has a high
mortality.
 When measles is introduced into a highly
susceptible population, the results may be
disastrous.
Prevention.
 Isolation precautions, especially in
hospitals and other institutions, should
be maintained from the 7th day after
exposure until 5 days after the rash has
appeared.

VACCINE
 The initial measles immunization, usually as

measles-mumps-rubella (MMR) vaccine, is
recommended at 12-15 mo of age
 MMR vaccine may be given for:
1. Measles postexposure
2. Outbreak prophylaxis as early as 6 mo
of age.

VACCINE (cont.)
 A second immunization, also as MMR, is

recommended routinely at 4-6 yr of age
 MMR may be administered at any time during
childhood provided at least 4 wk have elapsed since
the first dose.
 Second measles immunization should be given to :
1. Children who have not previously received the
second dose should be immunized by 11-12 yr of
age.
2.Adolescents entering college or the workforce

VACCINE (cont.)
 A tuberculin test prior to or concurrent

with active immunization against measles
is desirable if tuberculosis is under
consideration.

VACCINE (cont.)
* Measles vaccine is not recommended for:

1. Pregnant women
2. Children with primary immunodeficiency
3. Untreated tuberculosis, cancer, or organ
transplantation
4. Those receiving long-term immunosuppressive
therapy
5. severely immunocompromised HIV-infected
children

VACCINE (cont.)
 HIV-infected children without:

1. Severe immunosuppression
2. Evidence of measles immunity
may receive measles vaccine.

POSTEXPOSURE
PROPHYLAXIS
 Passive immunization with immune globulin is
effective for prevention and attenuation of measles
within 6 days of exposure.
 Susceptible household and hospital contacts who
are:
1. younger than 12 mo of age
2. pregnant
should receive immune globulin (0.25 mL/kg;
maximum: 15 mL) intramuscularly as soon as
possible after exposure, but within 5 days.

POSTEXPOSURE
PROPHYLAXIS (cont.)
 Immunocompromised persons should
receive immune globulin (0.5 mL/kg;
maximum: 15 mL) intramuscularly regardless
of immunization status.
 Infants 6 mo of age or younger born to
nonimmune mothers should receive immune
globulin;
 infants 6 mo of age or younger born to
immune mothers are considered protected by
maternal antibody.

POSTEXPOSURE
PROPHYLAXIS (cont.)
 Susceptible children 6-12 mo of age should
also be vaccinated; this vaccination does not
count as one of the two required measles
vaccinations.
 Susceptible children 12 mo of age or older
should receive vaccine alone within 72 hr.
 Pregnant women and immunocompromised
persons should receive immune globulin but
not vaccine
References
 Centers for Disease Control and Prevention. : Epidemiology of measles –
United States, 2001–2003. MMWR 2004; 53:713-716
 Progress towards measles elimination, western hemisphere, 2002–
2003 : Wkly Epidemiol Rec. 2004; 79:149-151
 Yeung LF, Lurie P, Dayan G, et al: A limited measles outbreak in a highly
vaccinated US boarding school. Pediatrics 2005; 116:1287.
 Parker AA, Staggs W, Dayan GH, et al: Implications of a 2005 measles
outbreak in Indiana for sustained elimination of measles in the United States.
N Engl J Med 2006; 355:447-455
 Centers for Disease Control and Prevention. : Licensure of a combined live
attenuated measles, mumps, rubella, and varicella vaccine. MMWR 2005;
54:1212-1214
 Bellini WJ, Rota JS, Lowe LE, et al: Subacute sclerosing panencephalitis: more
cases of this fatal disease are prevented by measles immunization than was
previously recognized. J Infect Dis 2005; 192:1686-1693.

3 Measles

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3 Measles

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Measles (Rubeola)

Prof. Dr. Saad S Al Ani

It is an acute viral infection

09/18/10 Prof. saad s al ani measles khorfakkan hospital 2

09/18/10 Prof. saad s al ani measles khorfakkan hospital 3

09/18/10 Prof. saad s al ani measles khorfakkan hospital 4

09/18/10 Prof. saad s al ani measles khorfakkan hospital 5

 Individuals born before 1957 are

09/18/10 Prof. saad s al ani measles khorfakkan hospital 6

 Measles is highly contagious;

09/18/10 Prof. saad s al ani measles khorfakkan hospital 7

 Transmission to susceptible contacts

09/18/10 Prof. saad s al ani measles khorfakkan hospital 8

 This immunity is usually complete for

09/18/10 Prof. saad s al ani measles khorfakkan hospital 9

 Most women of childbearing age in

09/18/10 Prof. saad s al ani measles khorfakkan hospital 10

 infants of mothers with measles

09/18/10 Prof. saad s al ani measles khorfakkan hospital 11

 Infants of mothers who are susceptible

09/18/10 Prof. saad s al ani measles khorfakkan hospital 12

cases, by year – United States, 1985 to 2003

09/18/10 Prof. saad s al ani measles khorfakkan hospital 13

rash onset – United States, 2004

09/18/10 Prof. saad s al ani measles khorfakkan hospital 14

09/18/10 Prof. saad s al ani measles khorfakkan hospital 15

09/18/10 Prof. saad s al ani measles khorfakkan hospital 16

 Hyperplasia of lymphoid tissue usually

 Koplik spots consist of serous exudate

09/18/10 Prof. saad s al ani measles khorfakkan hospital 18

 Interstitial pneumonitis resulting

09/18/10 Prof. saad s al ani measles khorfakkan hospital 19

 In fatal cases of encephalomyelitis,

 Measles has three clinical stages:

09/18/10 Prof. saad s al ani measles khorfakkan hospital 21

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 In uncomplicated cases, as the rash appears

09/18/10 Prof. saad s al ani measles khorfakkan hospital 29

09/18/10 Prof. saad s al ani measles khorfakkan hospital 30

 The individual lesions become increasingly

09/18/10 Prof. saad s al ani measles khorfakkan hospital 31

09/18/10 Prof. saad s al ani measles khorfakkan hospital 32

 During the succeeding 24 hr the rash

09/18/10 Prof. saad s al ani measles khorfakkan hospital 33

(Courtesy of J.H. Brien.)

on head with scattered lesions on the trunk. (Courtesy of J.H. Brien.)

09/18/10 Prof. saad s al ani measles khorfakkan hospital 35

 The rash fades downward in the same

09/18/10 Prof. saad s al ani measles khorfakkan hospital 36

 In severe cases the rash is confluent,

 The appearance of the rash may vary

09/18/10 Prof. saad s al ani measles khorfakkan hospital 38

 Complete absence of rash is rare except :

09/18/10 Prof. saad s al ani measles khorfakkan hospital 39

 In the hemorrhagic type of measles

09/18/10 Prof. saad s al ani measles khorfakkan hospital 40

 Itching is generally slight.

09/18/10 Prof. saad s al ani measles khorfakkan hospital 41

 gastrointestinal symptoms such as