SECTION I

Case Report
IDENTITY
Patient
Name
Birth Date
Age
Gender
Address
Nationality
Religion
MR No.
Date of admission
Date of examination

: L.A
: May 4th, 2005
: 10 years 3 months
: Male
: Kp Tangsi RT3/RW6 Cikarang, East Jakarta
: Indonesia
: Moslem
: 60-77-xx
: August 25th 2015
: August 25th 2015
Father

Mother

Name

Mr. S

Mrs. M

Age

40 years old

35 years old

Job

Employee

Housewife

Nationality

Indonesian

Indonesian

Religion

Moslem

Moslem

Education

High School

High School

Earning/month

Rp.5.000.000,-

Address

Kp Tangsi RT3/RW6 Cikarang, East Jakarta

ANAMNESIS
The anamnesis was taken on August 25th 2015, using alloanamnesis method.
The anamnesis taken at room no.6 Anggrek II Ward, RS POLRI R Said Sukanto
Chief complain
Additional complains
abdominal pain

: Fever since four days prior to admission at hospital.

:Rash, cough, flu, headache, nausea, vomiting, diarrhea,

History Of Present Ilness

A 10 years 3 months old boy with body weight 26 kg, came to Raden Said
Sukanto Police Center Hospital ER at 07.30 am, with a chief complain of fever. The
fever lasts from 4 days before admission to the hospital. The mother says that the
fever are sudden became high and wont goes down. The fever came up high at noon.
The mother gave panadol to decrease the temperature. This complains also followed
by rash all over his body, cough, flu, headache, nausea, vomiting, diarrhea, abdominal
pain since 4 days and swallowing pain since 1 day before admission.
History Of Past Illness
1

Pharyngitis/Tonsilitis
Bronchitis
Pneumonia
Morbilli
Pertussis
Varicella
Diphteria
Malaria
Polio
Enteritis
Bacillary Dysentry
Amoeba Dysentry
Diarrhea
Thypoid
Worms
Surgery
Brain Concussion
Fracture
Drug Reaction

+
+
-

Allergic History
The patient didnt have allergy to medicine
The patient didnt have allergy to food, or pollen
The patient didnt have allergy to weather
Birth History
Mothers Pregnancy History
The mother routinely checked her pregnancy at local clinics with a doctor ever since
she knew shes pregnant and every months until she gave birth. She also said she
consumed vitamins, iron supplement, and folic acid during pregnancy.
Childs Birth History
Labor

: Clinic

Birth attendants

: Doctor

Mode of delivery

: Pervaginam

Gestation

: 38 weeks

Infant state

: healthy

Birth weight

: 3400 grams

Body length

: 50 cm

According to the mother, the baby started to cry and the baby's skin is red, no
congenital defects were reported

Development History
First dentition: 6 months old
Psychomotor development

Smile

: 1 month old

Slant

: 2 months old

Speech Initation

: 2 months old

Prone Position

: 4 months old

Sitting

: 6 months old

Crawling

: 8 months old

Standing

: 10 months old

Walking

: 12 months old

Conclusion: growth and developmental is still in the normal limits and was
appropriate according to the patients age
Post Natal History
After birth, the baby checked at local doctor and the infant state is healthy.
History of Eating

Breast Milk

: 6 months.

Formula milk : SGM since 7 months old

Baby biscuits : Milna, Regal

Fruit and vegetables : Banana, papaya

Solid foods and side dishes : Baby porridge

Immunization History
Immunization
BCG
Hepatitis B
DPT
Polio
Hib
Measles

Frequency
1 time
3 times
3 times
4 times
4 times
1 time

Time
1 month old
0, 1, 6 months old
2, 4, 6 months old
0, 2, 4, 6 months old
2, 4, 6, months old
9 months old

Family History
Patients father didnt have hypertension nor diabetes mellitus

Patients mother didnt have hypertension nor diabetes mellitus

The patient has 1 sister, and he is the first child of 2 siblings.

Born died : ( - )
Child dies : ( - )
Miscarriage : ( - )

History of Disease in Other Family Members / Around the House

Her neighbors son had measles a week ago.
PHYSICAL EXAMINATION (August 25th 2015)
General Status
-

General condition
Consciousness
Pulse
Breathing rate
Temperature

: Mildly ill
: Compos Mentis
: 100x /min, regular, full, strong.
: 20x /min
: 38.3o C (per axilla)

Anthropometry Status
- Weight
- Height

: 26 kilogram
: 131 cm

Nutritional Status based NCHS (National Center for Health Statistics) year 2000:
WFA (Weight for Age): 26/31 x 100 % = 83 % (good nutrition)
HFA (Height for Age): 131/137 x 100 % = 95 % (good nutrition)
WFH (Weight for Height): 26/26 x 100 % = 100 % (good nutrition)
Conclusion: The patient has good nutritional status.

Head to Toe Examination

Head
Normocephaly, hair (black, normal distributon, not easily removed ) sign of
trauma (-), large fontanelle closed. Rash (+)

Eyes
Icteric sclera -/-, pale conjunctiva -/-, hyperaemia conjunctiva +/+,
lacrimation -/-, sunken eyes -/-, pupils 3mm/3mm isokor, Direct and indirect
light response ++/++

Ears
Normal shape, no wound, no bleeding ,secretion or serumen. Rash (+)

Nose
Normal shape, midline septum, secretion -/-. Rash (+)

Mouth

Lips: dry
Teeth: no caries
Mucous: moist
Tongue: Not dirty
Tonsils: T1/T1, No hyperemia
Pharynx: hyperemia

Neck
Lymph node enlargement (+), scrofuloderma (-), Rash (+)

Thorax
i. Inspection
ii.
iii.
iv.
1.
2.

:
: symmetric when breathing , no retraction, ictus cordis is not

visible. Rash (+)

Palpation
: mass (-), tactile fremitus +/+
Percussion
: sonor on both lungs
Auscultation :
Cor
: regular S1-S2, murmur (-), gallop (-)
Pulmo : vesicular +/+, Wheezing -/- , Rhonchy -/-

Abdomen
i. Inspection

:
: Convex, epigastric retraction (-), there is no a widening of the

veins, no spider nevi. Rash (+)

ii. Auscultation : bowel sound normal , bruit (-)
iii. Palpation
: supple, liver and spleen not palpable, fluid wave (-),
abdominal mass (-)
iv. Percussion
: The entire field of tympanic abdomen, shifting dullness (-)

Vertebra

: There does not appear scoliosis, kyphosis, and lordosis, do not

look any mass along the line of the vertebral

Ekstremities

: warm, capillary refill time < 2 second, edema(-) rash (+)

Skin

: Good turgor.

Neurological Examination
Meningeal Sign

Motoric Examination
Power
Hand
Feet
Tonus
Hand
Feet
Trophy
Hand
Feet
Physiologic Reflex
Upper extrimities
Biceps
Triceps

5 5 5 5/ 5 5 5 5
5 5 5 5/ 5 5 5 5
Normotonus / Normotonus
Normotonus / Normotonus
Normotrophy / Normotrophy
Normotrophy / Normotrophy
+/+
+/+

Lower extrimities
Patella
Achilles

+/+
+/+

Pathologic Reflex
Upper extrimities
Hoffman
Trommer

-/-/-

Lower extrimities
Babinsky
Chaddock
Oppenheim
Gordon
Schaeffer

-/-/-/-/-/-

Clonus
Patella
Achilles

-/-/-

Autonom Examination
Normal ( 1 times daily, normal consistency )
Normal ( 4-5 times daily )
Normal

Defecation
Urination
Sweating
Laboratory Investigation
Hematology August 25th 2015
Hematology

Results

Normal Value

Hemoglobin

12.8 g/dL

13-16 g/dL

Leukocytes

4.900/L

5,000 10,000/L

Hematocrits
Thrombocytes

35 %
274.000/ L

40 48 %
150,000 400,000/L

Erythrocytes

4.68 million/L

4 5 million/L

WORKING DIAGNOSIS
Morbilli
Differential Diagnosis : Dengue Fever
MANAGEMENT
IVFD RL, macro drip, 22 dpm 1650cc / 24 Hours.
Inj. Cefotaxime 2x1g IV
Sanmol 3x1 tab
Lacto B 2x1 sach
Zinc 1x1 cth
Domperidone 2x1 cth
Ambroxol syrup 3x1 cth
Vit A 1x200.000 units

PROGNOSIS
Quo ad vitam
Quo ad functionam
Quo ad sanactionam

: dubia ad bonam
: dubia ad bonam
: dubia ad bonam

August 26th 2015, second day of hospitalization, 6th day of illness

S
Cough (+)
Fever (+)
Rash (+)
Coryza (+)

General condition: Compos Mentis

Heart rate
= 100x /min
Respiratory rate = 26x /min
Temperature = 37.5C
Cardio : S1/S2, reguler, no murmur, no gallop
Pulmonary : vesiculer +/+, rhonchi -/-, wheezing -/Abdomen : distention (-), bowel sound (+) normal
Rash (+)

A
P

Morbilli
IVFD RL 1650cc 22dpm

Inj. Cefotaxime 2 x 1 g i.v.

Ambroxol 3 x 1 c
Sanmol 3 x 1 c
Lacto B 2 x 1 sach
Zinkid 1 x 1 c
Domperidone 2 x 1 c
Vit A 1x200.000 units
Salicyl talc

August 27th 2015, third day of hospitalization, 7th day of illness

S

Cough (+)
9

A
P

Fever (-)
Rash (+)
Coryza (+)
General condition: Compos Mentis
Heart rate
= 110x /min
Respiratory rate = 24x /min
Temperature = 36C
Cardio : S1/S2, reguler, no murmur, no gallop
Pulmonary : vesiculer +/+, rhonchi -/-, wheezing -/Abdomen : distention (-), bowel sound (+) normal
Rash (+)
Morbilli
IVFD RL 1650cc 22dpm

Inj. Cefotaxime 2 x 1 g i.v.

Ambroxol 3 x 1 c
Sanmol 3 x 1 c
Lacto B 2 x 1 sach
Zinkid 1 x 1 c
Domperidone 2 x 1 c
Vit A 1x200.000 units
Salicyl talc

August 28th 2015, third day of hospitalization, 8th day of illness

S

A
P

Cough (+)
Fever (-)
Rash (+)
Coryza (-)
General condition: Compos Mentis
Heart rate
= 106x /min
Respiratory rate = 22x /min
Temperature = 35.7C
Cardio : S1/S2, reguler, no murmur, no gallop
Pulmonary : vesiculer +/+, rhonchi -/-, wheezing -/Abdomen : distention (-), bowel sound (+) normal
Rash (+)
Morbilli
IVFD RL 1650cc 22dpm

Inj. Cefotaxime 2 x 1 g i.v.

Ambroxol 3 x 1 c
Sanmol 3 x 1 c
Lacto B 2 x 1 sach
Zinkid 1 x 1 c
Domperidone 2 x 1 c
Vit A 1x200.000 units
Salicyl talc

10

11

SECTION II
LITERATURE OF REVIEW
MEASLES/ MORBILLI
Prevalence
A nationwide indigenous measles outbreak occurred in 1989-1991, resulting in
55,000 cases, 11,000 hospitalizations, and 123 deaths, demonstrating that the
infection had not yet been conquered. This resurgence was attributed to vaccine
failure in a small number of school-aged children, low coverage of preschool- aged
children, and more rapid waning of maternal antibodies in infants born to mothers
who had never experienced wild-type measles infection. Implementation of the 2-dose
vaccine policy and more intensive immunization strategies resulted in interruption of
endemic transmission in the USA in 1993. The current rate is 1 case/1,000,000
population. Meanwhile, prevalence of measles in Indonesia occurs in about
3.14/100,000 total populations in year 2014.
Etiology
Measles virus is a single-stranded, lipid-enveloped RNA virus in the family
Paramyxoviridae and genus Morbillivirus. Other members of the genus Morbillivirus
affect a variety of mammals, such as rinderpest virus in cattle and distemper virus in
dogs, but humans are the only host of measles virus. Of the 6 major structural proteins
of measles virus, the 2 most important in terms of induction of immunity are the
hemagglutinin (H) protein and the fusion (F) protein. The neutralizing antibodies are
directed against the H protein, and antibodies to the F protein limit proliferation of the
virus during infection. Small variations in genetic composition have also been
identified that result in no effect on protective immunity but provide molecular
markers that can distinguish between viral types. These markers have been useful in
the evaluation of endemic spread of measles.
Pathogenesis and Pathology
The portal of entry of measles virus is through the respiratory tract or conjunctivae
following contact with large droplets or small-droplet aerosols in which the virus is
suspended. Patients are infectious from 3 days before to up to 4-6 days after the onset
12

of rash. Approximately 90% of exposed susceptible individuals experience measles.

Face-to-face contact is not necessary, because viable virus may be suspended in air for
as long as 1 hour after the patient with the source case leaves a room. Secondary cases
due to spread of aerosolized virus have been reported in physicians offices and in
hospitals.
Measles infection causes necrosis of the respiratory tract epithelium and an
accompanying lymphocytic infiltrate. Measles produces a small vessel vasculitis on
the skin and on the oral mucous membranes. Histology of the rash and exanthem
reveals intracellular edema and dyskeratosis associated with formation of epidermal
syncytial giant cells with up to 26 nuclei. Viral particles have been identified within
these giant cells. In lymphoreticular tissue, lymphoid hyperplasia is prominent. Fusion
of infected cells results in multinucleated giant cells, the Warthin-Finkeldey giant
cells that are pathognomonic for measles, with up to 100 nuclei and intracytoplasmic
and intranuclear inclusions.
Measles consists of 4 phases: incubation period, prodromal illness, exanthematous
phase, and recovery. During incubation, measles virus migrates to regional lymph
nodes. A primary viremia ensues that disseminates the virus to the reticuloendothelial system. A secondary viremia spreads virus to body surfaces. The prodromal illness
begins after the secondary viremia and is associated with epithelial necrosis and giant
cell formation in body tissues. Cells are killed by cell-to-cell plasma membrane fusion
associated with viral replication that occurs in many body tissues, including cells of
the central nervous system (CNS). Virus shedding begins in the prodromal phase.
With onset of the rash, antibody production begins, and viral replication and
symptoms begin to subside. Measles virus also infects CD4T cells, resulting in
suppression of the Th1 immune response and a multitude of other immunosuppressive
effects.

13

Clinical Manifestations
Measles is a serious infection characterized by high fever, enanthem cough, coryza,
conjunctivitis, and a prominent exanthema. After an incubation period of 8-12 days,
the prodromal phase begins with a mild fever followed by the onset of conjunctivitis
with photophobia, coryza, a prominent cough, and increasing fever. Koplik spots
represent the enanthem and are the pathognomonic sign of measles, appearing 1 to 4
days prior to the onset of the rash. They first appear as discrete red lesions with bluish
white spots in the center on the inner aspects of the cheeks at the level of the
premolars. They may spread to involve the lips, hard palate, and gingiva. They also
may occur in conjunctival folds and in the vaginal mucosa. Koplik spots have been
reported in 50-70% of measles cases but probably occur in the great majority.
Symptoms increase in intensity for 2-4 days until the 1st day of the rash (Eruption
phase). The rash begins on the forehead (around the hairline), behind the ears, and on
the upper neck as a red maculopapular eruption. It then spreads downward to the torso
and extremities, reaching the palms and soles in up to 50% of cases. The exanthem
frequently becomes confluent on the face and upper trunk.
With the onset of the rash, symptoms begin to subside. The rash fades over about 7
days in the same progression as it evolved, often leaving a fine desquamation of skin
in its wake (Convalescents/ Recovery Phase) . Of the major symptoms of measles, the
cough lasts the longest, often up to 10 days. In more severe cases, generalized
lymphadenopathy may be present, with cervical and occipital lymph nodes especially
prominent
In individuals with passively acquired antibody, such as infants and recipients of
blood products, a subclinical form of measles may occur. The rash may be indistinct,
brief, or, rarely, entirely absent. Likewise, some individuals who have received
vaccine, when exposed to measles, may have a rash but few other symptoms. Persons
with inapparent or subclinical measles do not shed measles virus and do not transmit
infection to household contacts.
Children who had received the original formalin-inactivated measles vaccine at times
demonstrated a more severe form of disease called atypical measles. Such patients
had onset of high fever and headache followed by the appearance of a maculopapular
14

rash on the extremities that become petechial and purpuric and progressed in a
centripetal direction. Pneumonia and pleural effusions frequently complicated the
illness. It is thought that atypical measles was caused by development of circulating
immune complexes that formed as a result of an abnormal immune response to the
vaccine.

Laboratory Data
The diagnosis of measles is almost always based on clinical and epidemiologic
findings. Laboratory findings in the acute phase include reduction in the total white
blood cell count, with lymphocytes decreased more than neutrophils. Absolute
neutropenia has been known to occur, however. In measles not complicated by
bacterial infection, the erythrocyte sedimentation rate and C-reactive protein level are
normal.
Antibody Assays
The measles virus sandwich-capture IgM antibody assay, is the
quickest method of confirming acute measles. Because IgM may not be
detectable during the first 2 days of rash, obtain blood for measles-specific
IgM on the third day of the rash or on any subsequent day up to 1 month after
onset to avoid a false-negative IgM result.
Among persons with confirmed measles infection, the seropositivity
rate for first samples is about 77% when collected within 72 hours; the rate
rises to 100% when collected 4-11 days after rash onset. Although the measles
serum IgM level remains positive 30-60 days after the illness in most
individuals, the IgM titer may become undetectable in some subjects at 4
weeks after rash onset. False-positive results can occur in patients with
rheumatologic

diseases,

parvovirus

B19

infection,

or

infectious

mononucleosis.
Immunoglobulin G
Laboratories can confirm measles by demonstrating more than a 4-fold

15

rise in IgG antibodies between acute and convalescent sera, although relying
solely on rising IgG titers for the diagnosis delays treatment considerably. The
earlier the acute serum is drawn, the more reliable the results. IgG antibodies
may be detectable 4 days after the onset of the rash, although most cases have
detectable IgG antibodies by about a week after rash onset.
Accordingly, it is recommended that specimens be drawn on the
seventh day after rash onset. Blood drawn for convalescent serum should be
drawn 10-14 days after that drawn for acute serum, and the acute and
convalescent sera should be tested simultaneously as paired sera.
Virus Culture
Throat swabs and nasal swabs can be sent on viral transport medium or
a viral culturette swab to isolate the measles virus. Urine specimens can be
sent in a sterile container for viral culture.
Viral genotyping in a reference laboratory may determine whether an
isolate is endemic or imported. In immunocompromised patients, who may
have poor antibody responses that preclude serologic confirmation of measles,
isolation of the virus from infected tissue or identification of measles antigen
by means of immunofluorescence may be the only feasible method of
confirming the diagnosis
Tissue analysis and histologic findings
A skin biopsy from a lesion of the morbilliform eruption shows
spongiosis and vesiculation in the epidermis with scattered dyskeratotic
keratinocytes. Occasional lymphoid multinucleated giant cells ( 100 nm in
diameter) can be identified in biopsies of Koplik spots, in dermal or epithelial
rashes, in hair follicles and acrosyringium and in lung or lymphoid tissue.
These findings are not specific, but they are suggestive of a viral exanthem.
Brain biopsies of patients with measles encephalitis can reveal
demyelination, vascular cuffing, gliosis, and infiltration of fat-laden
macrophages near blood vessel walls.

16

Diagnosis
In the absence of a recognized measles outbreak, confirmation of the clinical
diagnosis is often recommended. Serologic confirmation is most conveniently made
by identification of immunoglobulin M (IgM) antibody in serum. Serologic
confirmation may also be made by demonstration of a fourfold rise in IgG antibodies
in acute and convalescent specimens collected 2-4 weeks later. Viral isolation from
blood, urine, or respiratory secretions can be accomplished by culture at the CDC or
local or state laboratories. Molecular detection by polymerase chain reaction (PCR) is
possible but is a research tool.
Supporting Examination
Chest radiography
If bacterial pneumonia is suspected, perform chest radiography. The frequent
occurrence of measles pneumonia, even in uncomplicated cases, limits the predictive
value of chest radiography for bacterial bronchopneumonia.
Lumbar puncture
If encephalitis is suspected, perform a lumbar puncture. CSF examination reveals the
following:

Increased protein

Normal glucose

Mild pleocytosis with a predominance of lymphocytes

Differential Diagnosis
Typical measles is unlikely to be confused with other illnesses, especially if
Koplik spots are observed. Measles in the later stages or inapparent or subclinical
infections may be confused with a number of other exanthematous immune-mediated
illnesses and infections, including rubella, adenoviruses, enteroviruses, and EpsteinBarr virus. Exanthem subitum (in infants) and erythema infectiosum (in older
children) may also be confused with measles. Mycoplasma pneumoniae and group A
streptococcus may also produce rashes similar to that of measles. Kawasaki syndrome
can cause many of the same findings as measles but lacks discrete intraoral lesions
17

(Koplik spots) and a severe prodromal cough, and typically leads to elevations of
neutrophils and acute-phase reactants. In addition, the characteristic thrombocytosis
of Kawasaki syndrome is absent in measles. Drug eruptions may occasionally be
mistaken for measles.
The diagnosis of measles is usually determined from the classic clinical
picture, including the classic triad of cough, coryza, and conjunctivitis; the
pathognomonic Koplik spots; and the characteristic cephalocaudal progression of the
morbilliform exanthem.
It is worthwhile to be mindful of the syndrome known as atypical measles,
which has been described in individuals who were infected with wild measles virus
several years after immunization with a killed measles vaccine (a vaccine used in the
United States from 1963-1967). This syndrome tends to be more prolonged and
severe than regular measles and is marked by a prolonged high fever, pneumonitis,
and a rash that begins peripherally and may be urticarial, maculopapular,
hemorrhagic, and/or vesicular.
The assumed pathogenesis of atypical measles is hypersensitivity to measles
virus in a partially immune host. Laboratory tests reveal a very low measles antibody
titer early in the course of the disease, followed soon thereafter by the appearance of
an extremely high measles immunoglobulin G (IgG) antibody titer (eg, 1:1,000,000)
in the serum.
Other diagnoses to be considered include the following:

Kawasaki disease

Dengue

Serum sickness

Syphilis

Systemic lupus erythematosus

Toxic shock syndrome

18

Treatment
Management of measles is supportive. Antiviral therapy is not effective in the
treatment of measles in otherwise normal patients. Maintenance of hydration,
oxygenation, and comfort are goals of therapy. Antipyretics for comfort and fever
control are useful. For patients with respiratory tract involvement, airway humidification and supplemental oxygen may be of benefit. Respiratory failure due to croup
or pneumonia may require ventilatory support. Oral rehydration is effective in most
cases, but severe dehydration may require intravenous therapy. Prophylactic antimicrobial therapy to prevent bacterial infection is not indicated.
Measles infection in immunocompromised patients is highly lethal. Ribavirin
is active in vitro against measles virus. Anecdotal reports of ribavirin therapy with or
without intravenous gamma globulin suggest some benefit in individual patients.
Vitamin A
Vitamin A deficiency in children in developing countries has long been known
to be associated with increased mortality from a variety of infectious diseases,
including measles. The American Academy of Pediatrics suggests vitamin A therapy
for selected patients with measles

19

Complications
Complications of measles are largely attributable to the pathogenic effects of
the virus on the respiratory tract and immune system Several factors make
complications more likely. Morbidity and mortality from measles are greatest in
patients 5 years of age (especially 1 years of age) and 20 years of age. In
developing countries, higher case fatality rates have been associated with crowding,
which are possibly attributable to larger inoculum doses after household exposure.
Severe malnutrition in children results in suboptimal immune response and higher
morbidity and mortality with measles infection. Measles infection lowers serum
retinol concentrations, so subclinical cases of hyporetinolemia may be made
symptomatic during measles. Measles infection in immunocompromised persons is
associated with increased morbidity and mortality. Among patients with malignancy
in whom measles develops, pneumonitis occurs in 58% and encephalitis in 20%.
Pneumonia is the most common cause of death in measles. It may manifest as
giant cell pneumonia caused directly by the viral infection or as superimposed
bacterial infection. The most common bacterial pathogens are Streptococcus
pneumoniae, Haemophilus influenzae, and Staphylococcus aureus. Following severe
measles pneumonia, the final common pathway to a fatal outcome is often the
development of bronchiolitis obliterans. croup, tracheitis, and bronchiolitis are
common complications in infants and toddlers with measles. The clinical severity of
these complications frequently requires intubation and ventilatory support until the
infection resolves.
Measles infection is known to suppress skin test responsiveness to purified
tuberculin antigen. There may be a higher rate of activation of pulmonary
tuberculoses in populations of individuals infected with Mycobacterium tuberculosis
who are then exposed to measles.
Diarrhea and vomiting are common symptoms associated with acute measles,
and diffuse giant cell formation is found in the epithelium the gastrointestinal tract.
Dehydration is a common consequence, especially in young infants and children.
Appendicitis may occur from obstruction of the appendiceal lumen by lymphoid
hyperplasia.

20

Febrile seizures occur in 3% of children with measles. Encephalitis

following measles has been a long-associated complication, often with an unfavorable
outcome. Rates of 1-3/1,000 cases of measles have been reported, with greater
numbers occur- ring in adolescents and adults than in preschool or school-aged
children. Encephalitis is a post-infectious, immunologically mediated process and is
not due to a direct effect by the virus. Clinical onset begins during the exanthem and
manifests as seizures (56%), lethargy (46%), coma (28%), and irritability (26%).
Findings in cerebrospinal fluid (CSF) include lymphocytic pleocytosis in 85% of
cases and elevated protein concentration. Approximately 15% of patients with
measles encephalitis die, and 20-40% suffer long-term sequelae, including mental
retardation, motor disabilities, and deafness.
Measles encephalitis in immunocompromised patients results from direct
damage to the brain by the virus. Subacute measles encephalitis manifests 1-10 mo
after measles in immunocompromised patients, particularly those with AIDS,
lymphoreticular malignancies, and immunosuppression. Signs and symptoms include
seizures, myoclonus, stupor, and coma. In addition to intracellular inclusions,
abundant viral nucleocapsids and viral antigen are seen in brain tissue. Progressive
disease and death almost always occur.
A severe form of measles rarely seen now is hemorrhagic measles or black
measles. It manifested as a hemorrhagic skin eruption and was often fatal. Keratitis,
appearing as multiple punctate epithelial foci, resolved with recovery from the
infection. Thrombocytopenia sometimes occurred following measles.
Myocarditis is a rare complication of measles. Miscellaneous bacterial
infections have been reported, including bacteremia, cellulitis, and toxic shock
syndrome. Measles during pregnancy has been associated with high maternal
morbidity, fetal wastage and stillbirths, and congenital malformations in 3% of live
born infants.
Subacute sclerosing panencephalitis (SSPE) is a chronic complication of
measles with a delayed onset and an outcome that is nearly always fatal. It appears to
result from a persistent infection with an altered measles virus that is harbored
intracellularly in the CNS for several years. After 7-10 years the virus apparently

21

regains virulence and attacks the cells in the CNS that offered the virus protection.
This slow virus infection results in inflammation and cell death, leading to an
inexorable neurodegenerative process.
The pathogenesis of SSPE remains enigmatic. Factors that seem to be
involved include defective measles virus and interaction with a defective or immature
immune system. The virus isolated from brain tissue of patients with SSPE is missing
1 of the 6 structural proteins, the matrix or M protein. This protein is responsible for
assembly, orientation, and alignment of the virus in preparation for budding during
viral replication. Immature virus may be able to reside, and possibly propagate, within
neuronal cells for long periods. The fact that most patients with SSPE were exposed at
a young age suggests that immune immaturity is involved in pathogenesis. In
addition, the intracellular location of the virus sequesters it from the immune system,
especially from humoral immunity.
Clinical manifestations of SSPE begin insidiously 7-13 years after primary
measles infection. Subtle changes in behavior or school performance appear,
including irritability, reduced attention span, and temper outbursts. This initial phase
(stage I) may at times be missed because of brevity or mildness of the symptoms.
Fever, headache, and other signs of encephalitis are absent. The hallmark of the
second stage is massive myoclonus, which coincides with extension of the
inflammatory process site to deeper structures in the brain, including the basal
ganglia. Involuntary movements and repetitive myoclonic jerks begin in single muscle
groups but give way to massive spasms and jerks involving both axial and
appendicular muscles. Consciousness is maintained. In the third stage, involuntary
movements disappear and are replaced by choreoathetosis, immobility, dystonia, and
lead pipe rigidity that result from destruction of deeper centers in the basal ganglia.
Sensorium deteriorates into dementia, stupor, and then coma. The fourth stage
is characterized by loss of critical centers that support breathing, heart rate, and blood
pressure. Death soon ensues. Progression through the clinical stages may follow
courses characterized as acute, subacute, or chronic progressive.
The diagnosis of SSPE can be established through documentation of a
compatible clinical course and at least 1 of the following supporting findings:

22

(1) measles antibody detected in CSF,

(2) characteristic electroencephalographic findings,
(3) typical histologic findings in and/or isolation of virus or viral antigen from brain
tissue obtained by biopsy or postmortem examination.
CSF analysis reveals normal cells but elevated IgG and IgM antibody titers in
dilutions 1:8. Electroencephalographic pat- terns are normal in stage I, but in the
myoclonic phase, suppression-burst episodes are seen that are characteristic of but not
pathognomonic for SSPE. Brain biopsy is no longer routinely indicated for diagnosis
of SSPE.
Management of SSPE is primarily supportive and similar to care provided to
patients with other neurodegenerative diseases
Virtually all patients eventually succumb to SSPE. Most die within 1-3 years
of onset from infection or loss of autonomic control mechanisms. Prevention of SSPE
depends on prevention of primary measles infection through vaccination. SSPE has
been described in patients who have no history of measles infection and only
exposure to the vaccine virus. However, wild-type virus, not vaccine virus, has been
found in brain tissue of at least some of these patients, suggesting that they had had
subclinical measles previously.
Prevention
Patients shed measles virus from 7 days after exposure to 4-6 days after the
onset of rash. Exposure of susceptible individuals to patients with measles should be
avoided during this period. In hospitals, standard and airborne precautions should be
observed for this period. Immunocompromised patients with measles will shed virus
for the duration of the illness, so isolation should be maintained throughout the
disease.
Vaccine
Currently available in Indonesia are measles itself or measles-mumps- rubella
(MMR) vaccine, the last of which is the recommended form in most circumstances.

23

The current recommendations include a first dose at 9 months old followed by a

second dose at 24 moths old and 6 years old for measles and first dose at 15 months
old and followed by second dose at 5-6 years old.
Adverse events from the MMR vaccine include fever (usually 6-12 days
following vaccination), rash in about 5% of vaccines, and, rarely, transient
thrombocytopenia. Children prone to febrile seizures may experience an event
following vaccination, so the risks and benefits of vaccination should be discussed
with parents. Encephalopathy and autism have not been shown to patients with HIV
who are not severely immunocompromised should be immunized. Because measles
virus may suppress the cutaneous response to tuberculous antigen, skin testing for
tuberculosis should be performed before or at the same time as administration of the
vaccine. Individuals infected with M. tuberculosis should be receiving appropriate
treatment at the time of administration of measles vaccine.
Postexposure Prophylaxis
Susceptible individuals exposed to measles may be protected from infection
by either vaccine administration or immunization with immune globulin. The vaccine
is effective in prevention or modification of measles if given within 72 hours of
exposure. Immune globulin may be given up to 6 days after exposure to prevent or
modify

infection.

Immunocompetent

children

should

receive

0.25

mL/kg

intramuscularly, and immunocompromised children should receive 0.5 mL/kg

(maximum dose in both cases is 15 mL/ kg). Immune globulin is indicated for
susceptible household contacts of measles patients, especially infants 6 months old,
pregnant women, and immunocompromised persons.
Prognosis
In the early 20th century, deaths due to measles varied between 2,000 and
10,000, or about 10 deaths per 1,000 cases of measles. With improvements in health
care and antimicrobial therapy, better nutrition, and decreased crowding, the death-tocase ratio fell to 1/1,000 cases. In 2014, WHO estimated that there were 350 deaths
caused by measles in Indonesia, with a death-to-case ratio of 1.8-2.5/100,000 cases of
measles. Pneumonia and encephalitis were complications in most of the fatal cases,
and immunodeficiency conditions were identified in 14-16% of deaths.
24

References
1. Kliegman RM, Stanton BF, Schor NF, Behrman RE, St.Geme JW (2011)
Nelson Textbook of Pediatrics, 19th ed., United States of America: Elsevier
Inc.
2. Kenneth Todar University of Wisconsin-Madison Department of Bacteriology.
2006. Measles. Online, www.bact.wisc.edu/themicrobialworld/Measles.jpg,
(Accessed 12th may 2015).
3. American Academy of Pediatrics. Measles. In: Pickering L, Baker C,
Kimberlin D, Long S, eds. Red Book: 2009 Report of the Committee on
Infectious Diseases. 28th ed. Elk Grove Village, IL: American Academy of
Pediatrics, 2009:44455.
4. William, W. 2002. Current Pediatric Diagnosis & Treatment 16

th

edition.

USA: MacGraw-Hill Education

5. Silver HK, Kempe CH, Bruyn HB. Handbook of Pediatric, 14 th ed. Singapore:
Lange Medical Publications; 1990.
6. Burnett M., 2007. Measles, Rubeola. http://www.e-emedicine.com. (Accessed
12th May 2015).

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