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dr. Ulynar Marpaung, Sp. A

Written by:
Raras Mayang Kencono

Department of Pediatrics
Bhayangkara Tk. I R. Said Sukanto Hospital
Yarsi University Jakarta

Name : Child M.A.R
Birth Date : April 14th, 2017
Age : 10 months
Gender : Male
Address : Batu Ampar street, number V,East Jakarta
Nationality : Indonesian
Religion : Islam
MR No. : 940132
Date of admission : February 17th, 2018
Date of examination : February 18th, 2018

Father Mother
Name Mr. F Mrs. A
Age 30 years old 27 years old
Job Entrepreneur Housewife
Nationality Indonesian Indonesian
Religion Islam Islam
Education Diploma 3 S1
Address Batu Ampar street, number V,East Jakarta

The anamnesis was taken on February 18th, 2018 using alloanamnesis
method. It was taken at room Hardja 2A, Bhayangkara Tk.I R. Said Sukanto
Hospital, Jakarta.
Chief complaint : Fever since 5 days before admission to the
Additional Complaint : Eritema all over the body, cough and diarrhea
History of Present Illness :
Since 5 days before admission to the hospital, the patient had fever.
Fever felt suddenly, rising and down throughout the day. The temperature
is measured at home between 38-39ºC. The patient had already
consumed paracetamol and the temperature is lower but increase soon
after. Fever accompanied with diarrhea. Diarrhea occur >3x per day with
watery consistency and a little bit of solid consistency. The faeces colour
is yellow with acidic odor. There is no blood nor slime in the faeces. Patient
also had cough. Cough with sputum but the sputum can’t be excreted.
Since 2 days before admission to the hospital, the patient had
erythema. Erythema starts from the back of the ears and grow to the

History of Past Illness

There is no history of past illness

Allergic History
The patient have no allergy to medicine and food.

Birth History
Mother’s Pregnancy History
The mother routinely checked her pregnancy at local clinic with a midwife
since she knew she got pregnant and every months until she gave birth.
She also said that she consumed vitamins during pregnancy.

Child’s Birth History

- Labor : Hospital
- Birth attendants : Doctor
- Mode of delivery : Sectio Caesaria
- Gestation : 39 weeks
- Infant state : Healthy
- Birth weight : 2850 grams
- Body length : 49 cm
- According to the mother, the baby cried, there was no shortness of
breathing, sianotic, and jaundice.

Development History
• First dentition : 7 months
• Psychomotor development
• Smile : 4 months
• Slant : 4 months
• Speech initiation : 6 months
• Prone position : 6 months
• Sitting : 6 months
• Crawling : 7 months
Conclusion : Growth and developmental is still in the normal limits
and was appropriate according to the patient’s age.

History of Eating
- Breast milk : Exclusively 6 months
- Formula milk : Bebellove
- Baby biscuit : Milna
- Fruit and vegetables : Banana, papaya

History Immunization
According to the mother, patient has not got measles immunisation.

Family History : None

History of Sibling
- The patient is the 1st child of the family
- The patient’s siblings: none
- Born died : (-)
- Child dies : (-)
- Miscarriage : (-)

PHYSICAL EXAMINATION (January 19th, 2018)

General Status
- General condition : Mildly ill
- Consciousness : Compos Mentis
- Pulse : 110 x/min, regular
- Breathing rate : 24 x/min
- Temperature : 38.5 °C per axilla
Anthropometry Status
- Weight : 8.3 kg
- Height : 70 cm
Nutritional Status based on CDC :
- WFA (Weight for Age) : 8.3/10 x 100 % = 83 % (normal weight)
- LFA (Length for Age) : 70/75 x 100 % = 93 % (normal length)
Conclution : The patient has a good noutritional status

Head to Toe Examination

- Head
Normocephal, hair (black, normal distribution, not easily
removed), no sign of trauma
- Eyes
Scleral icterus (-), pale conjunctiva (-), lacrimation +/+, pupil
3mm/3mm, isocor, direct light response +/+, indirect light
response +/+
- Ears
Normal shape, no wound, no bleeding, no secretion, no cerumen
- Nose
Normal shape, midline septum.
- Mouth
Lips : moist
Mucous : moist
Tongue : Not dirty
Tonsils : T1/T1, hyperemia (-)
Pharinx : Hyperemia (+)
- Neck
Lymph node enlargement (-).
- Thorax
Inspection : Symmetric when breathing, retraction (-), ictus
cordis is not visible
Palpation : Fremitus tactile +/+, mass (-)
Percussion : Sonor on both lungs
Auscultation :
Cor : S1S2 reguller, murmur (-), gallop (-)
Pulmo : Vesicular +/+, rhonchi -/-,
wheezing -/-
- Abdomen
Inspection : Relax
Palpation : Abdominal mass(-), skin pinch goes back fast
Percussion : tympanic, shifting dullness (-)
Auscultation : Increased bowel sound
- Vertebra
There is no scoliosis, kyphosis, lordosis, and any mass along the
vertebral line.
- Extremity
Warm, capillary refill time <2 second, edema -/-
- Skin
Erythema macular rash all over the body
- Genitalia
Eritema natum (-)

Neurogical Examination
Meningeal Sign
- Nuchal rigidity (-)
- Kernig sign (-)
- Lasegue sign (-)
- Brudzinski I (-)
- Brudzinski II (-)

Motoric Examination
- Hand 5555/5555
- Feet
- Hand Normotonus/ Normotonus
- Feet
Normotonus / Normotonus
- Hand Normotrophy /
- Feet
Normotrophy /
Physiologic Reflex
Upper extremities
- Biceps +2 / +2
- Triceps
+2 / +2
Lower extremities
- Patella
+2 / +2
- Achilles
+2 / +2

Physiologic Reflex
Upper extremities
- Biceps +2 / +2
- Triceps
+2 / +2
Lower extremities
- Patella
+2 / +2
- Achilles
+2 / +2
Pathologic Reflex
Upper extremities
- Hoffman -/-
- Trommer
Lower extremities
- Babinsky
- Chaddock
- Oppenheim -/-
- Gordon
- Schaeffer
- Patella -/-
- Achilles

Hematology (February 18th, 2017)
Results Normal Value
Hemoglobin 9.6 13 – 16 g/dl
White blood cells 7.600 5.000 – 10.000 u/l
Hematocrit 30 40 – 48 %

Platelet count 222.000 150.000 –400.000 /ul

Acute diarrhea without dehydration

- IVFD RL 800cc/24hours
- Paracetamol 3 x 0.8 cc PO
- Ambroxol 3 x 0.8 cc PO
- Vitamin A 1 x 100.000 IU
- Lacto B 2 x 1 sacchet PO
- Zinkid 1 x 10 mg PO
- Quo ad vitam : Bonam
- Quo ad functionam : Bonam
- Quo ad sanationam : Bonam

February 18th 2018, 1st day of hospitalization, 6th day of illness
Fever (+)
Erythema all over the body (+)
Cough (+)
Diarrhea (+)
O Consciousness : Compos Mentis
General condition: Midly ill
Temperature :38.5 °C
Pulse :110 x/min
Respiratory rate : 24 x/min
Head : Normocephal
Eyes : Pale conjungtiva (-), icteric sklera (-), sunken eyes
Mouth : Wet lips, wet mucous, tonsils T1/T1, hyperemia
pharynx (+)
Pulmonary: Vesicular +/+, rhonchi -/-, wheezing -/-
Cardio : S1S2 regullar, murmur (-), gallop (-)
Abdomen : Distention (-), bowel sound (+) increase,
shifting dullness (-)
Extremity: Warm, CRT <2 seconds, macular erythema all
over the body

Laboratory Investigation
Haemoglobin 9,6 13-16 g/dl
Leukocyte 7.600 5.000-10.000 u/dl
Haemotocrite 30% 37-43%
Thrombocyte 222.000 150.000-
400.000 /uL
Natrium 136 135-145 mmol/l
Kalium 3,5 3,5-5,0 mmol/l
chlorida 99 98-108

A Acute diarrhea without dehydration
- IVFD RL 700cc/24hours
- Paracetamol 3 x 0.8 cc PO
- Ambroxol 3 x 0.8 cc PO
- Vitamin A 1 x 100.000 IU
- Lacto B 2 x 1 sacchet PO
- Zinkid 1 x 10 mg PO

February 19 th 2018, 2nd day of hospitalization, 7th day of illness

Erythema all over the body (+)
Cough (+) decrease
Consciousness : Compos Mentis
General condition: Midly ill
Temperature :36.5 °C
Pulse :105 x/min
Respiratory rate : 24 x/min
Head : Normocephal
Eyes : Pale conjungtiva (-), icteric sklera (-), sunken eyes (-),
Mouth : Wet lips, wet mucous, tonsils T1/T1, hyperemia pharynx
Pulmonary: Vesicular +/+, rhonchi -/-, wheezing -/-
Cardio : S1S2 regullar, murmur (-), gallop (-)
Abdomen : Distention (-), bowel sound (+) increase, shifting
dullness (-)
Extremity: Warm, CRT <2 seconds, macular erythema all over the

Laboratory Investigation
Examination Results Normal range
Haemoglobin 9,4 13-16 g/dl
Leukocyte 7.600 5.000-10.000 u/l
Haemotocrite 29% 40-48%
Thrombocyte 222.000 150.000-400.000/ul

A Acute diarrhea without dehydration
- IVFD RL 700cc/24hours
- Paracetamol 3 x 0.8 cc PO (prn)
- Ambroxol 3 x 0.8 cc PO
P - Vitamin A 1 x 100.000 IU
- Lacto B 2 x 1 sacchet PO
- Zinkid 1 x 10 mg PO
- Salisil powder

February 20 th 2018, 3rd day of hospitalization, 7th day of illness

Erythema all over the body (+)
Cough (+) decrease
Consciousness : Compos Mentis
General condition: Midly ill
Temperature :36 °C
Pulse :110 x/min
Respiratory rate : 24 x/min
Head : Normocephal
Eyes : Pale conjungtiva (-), icteric sklera (-), sunken eyes (-),
Mouth : Wet lips, wet mucous, tonsils T1/T1, hyperemia pharynx
Pulmonary: Vesicular +/+, rhonchi -/-, wheezing -/-
Cardio : S1S2 regullar, murmur (-), gallop (-)
Abdomen : Distention (-), bowel sound (+) increase, shifting
dullness (-)
Extremity: Warm, CRT <2 seconds, macular erythema all over
the body

A Measles
Acute diarrhea without dehydration
Normal nutritional and development status
- IVFD RL 700cc/24hours
- Paracetamol 3 x 0.8 cc PO (prn)
- Ambroxol 3 x 0.8 cc PO
P - Vitamin A 1 x 100.000 IU
- Lacto B 2 x 1 sacchet PO
- Zinkid 1 x 10 mg PO
- Salisil powder


2.1 Introduction
Measles is a highly contagious, serious disease caused by a virus.
Before the introduction of measles vaccine in 1963 and widespread
vaccination, major epidemics occurred approximately every 2–3 years
and measles caused an estimated 2.6 million deaths each year.
The disease remains one of the leading causes of death among
young children globally, despite the availability of a safe and effective
vaccine. Approximately 89.780 people died from measles in 2016 –
mostly children under the age of 5 years.
Measles is caused by a virus in the paramyxovirus family and it is
normally passed through direct contact and through the air. The virus
infects the respiratory tract, then spreads throughout the body.
Accelerated immunization activities have had a major impact on
reducing measles deaths. During 2000–2016, measles vaccination
prevented an estimated 20.4 million deaths. Global measles deaths have
decreased by 84% from an estimated 550 100 in 2000 to 89 780 in 2016.

Clinical definition
Measles, or rubeola, is a viral infection of the respiratory system.
Measles is a very contagious disease that can spread through contact with
infected mucus and saliva. An infected person can release the infection
into the air when they cough or sneeze.
The measles virus can live on surfaces for several hours. As the
infected particles enter the air and settle on surfaces, anyone within close
proximity can become infected. Drinking from an infected person’s glass,
or sharing eating utensils with an infected person, increases the risk of
Since measles is caused by a virus, there is no specific medical
treatment for it and the virus has to run its course. But a child who is sick
should drink plenty of fluids, get lots of rest, and be kept from spreading
the infection to others.

2.2 Epidemiology
The epidemiology of measles is variable across the globe and is
related to immunization levels achieved in a particular region. Prior to the
implementation of widespread vaccination programs, measles accounted
for an estimated 2.6 million deaths. The World Health Organization (WHO)
reported that approximately 134200 deaths (15 deaths/hour) occurred in
2015 due to measles. Unvaccinated young children and pregnant women
are at high risk to contract measles. Measles virus has no animal
reservoirs and occurs only in humans.
In 2013–14 there were almost 10,000 cases in 30 European
countries. Most cases occurred in unvaccinated individuals and over 90%
of cases occurred in the five European nations: Germany, Italy, the
Netherlands, Romania, and the United Kingdom. Between October 2014
and March 2015, a measles outbreak in the German capital of Berlin
resulted in at least 782 cases.
United States
The United States was declared free of circulating measles in 2000
with 911 cases from 2001 to 2011. The CDC states that endemic measles,
rubella, and congenital rubella syndrome has not returned to the United
States. Occasional measles outbreaks persist because of cases imported
from abroad, of which more than half are the result of unvaccinated U.S.
residents who are infected abroad and infect others upon return to the
United States.
Southeast Asia
In the Vietnamese measles epidemic in spring of 2014, an estimated
8,500 measles cases were reported as of April 19, with 114 fatalities; as of
May 30, 21,639 suspected measles cases had been reported, with 142
measles-related fatalities.
Every year through surveillance, reported >11.000 of suspect
measles cases, and with laboratory confirmation stated 12-39% are
measles. From 2010 until 2015, approximately 23.164 cases of measles
reported. This number expected to be much lower than the real cases,
because there are still a lot of cases which are not reported, especially
from private health facility also the low number of complete surveillance
2.3 Etiology
Measles is caused by the measles virus, a single-stranded, negative-
sense, enveloped RNA virus of the genus Morbillivirus within the family
Paramyxoviridae. The virus was first isolated in 1954 by Nobel Laureate
John F. Enders and Thomas Peebles, who were careful to point out that the
isolations were made from patients who had Koplik's spots. Humans are
the only natural hosts of the virus, and no other animal reservoirs are
known to exist. This highly contagious virus is spread by coughing and
sneezing via close personal contact or direct contact with secretions. Risk
factors for measles virus infection include immunodeficiency caused by
HIV or AIDS, immunosuppression following receipt of an organ or a stem
cell transplant, alkylating agents, or corticosteroid therapy, regardless of
immunization status; travel to areas where measles is endemic or contact
with travelers to endemic areas; and the loss of passive, inherited
antibodies before the age of routine immunization.

The measles virus is a non-segmented, negative-sense RNA virus
and a member of the Morbillivirus genus in the family of Paramyxoviridae.
The genome of about 16.000 nucleotides encodes six structural proteins,
the nucleoprotein, phosphoprotein, matrix, fusion, haemagglutinin, and
large protein, and two non-structural proteins V and C encoded within the
phosphoprotein gene. The haemagglutinin protein is one of two
transmembrane glycoproteins on the surface of the virion and binds to
cellular receptors, including the signaling lymphocyte activation molecule
(SLAM or CD150) on lymphocytes, monocytes, macrophages, and
dendritic cells, and nectin-4, a component of epithelial cell adherens
junctions. The distribution of these receptors determines the broad cell
types and tissues infected with measles virus.
The lifelong immunity that follows measles is due to neutralising IgG
antibodies to the haemagglutinin protein that block binding to host cell
receptors. The fusion protein, the second viral glycoprotein exposed on
the viral surface, is responsible for fusion of the viral envelope with the
host cell membrane, enabling entry of viral ribonucleoproteins into the cell
Recent evidence suggests detailed measles virus transmission
networks can be identified by sequencing larger segments of the measles
virus genome, such as the haemagglutinin and phosphoprotein genes, or
sequencing the whole viral genome through Sanger or next generation
sequencing techniques. An important characteristic of measles virus is
that it is an antigenically monotypic virus, despite its genotypic diversity
and the fact that RNA viruses have high mutation rates.
Consequently, attenuated measles vaccines derived from a single
measles virus genotype isolated in the 1950s, including the Schwarz and
Moraten measles vaccine strains, remain protective worldwide. Thus, new
measles vaccines do not need to be developed to counter evolving
measles virus strains because the neutralising epitopes on the
haemagglutinin protein that confer protection are highly conserved,
probably because of functional constraints on the amino acid sequence
and tertiary structure of the surface proteins.

2.4 Pathophisiology
The highly contagious virus is spread by coughing and sneezing,
close personal contact or direct contact with infected nasal or throat
secretions. The incubation period is 10 to 14 days, although longer periods
have been reported.
The virus remains active and contagious in the air or on infected
surfaces for up to 2 hours.
Measles commonly affects young children. However, there has been
a shift to older children and adolescents due to increasing levels of
immunization coverage and alterations in the levels of population
immunity at different ages. Young infants born to mothers with acquired
immunity are protected from measles due to passive antibody transfer,
but as these antibodies wane, they become susceptible. The infectivity is
maximal in the peri-rash period (4 days before and 4 days after rash),
which coincides with peak levels of viremia and the development of a
cough and coryza.
Measles outbreaks can result in epidemics that cause many deaths,
especially among young, malnourished children. In countries where
measles has been largely eliminated, cases imported from other countries
remain an important source of infection.
Measles virus acquired through respiratory droplets or aerosolised
particles initially infects lymphocytes, dendritic cells, and alveolar
macrophages in the respiratory tract. The virus replicates and spreads
during the incubation period, first to local lymphoid tissue and is then
disseminated throughout the blood stream by infected lymphocytes,
infecting epithelial and endothelial cells primarily through direct
transmission across cells in almost all organ systems. Infected dendritic
cells and lymphocytes transfer measles virus to epithelial cells of the
respiratory tract using the nectin-4 receptor. Measles virus buds from the
apical surface of respiratory epithelial cells or is shed through damaged
epithelium, enabling respiratory transmission to susceptible hosts.
Although the infectious period for measles extends from several
days before to several days after start of the rash, measles virus RNA can
be detected in clinical samples for at least 3 months after rash onset.
Measles virus RNA declined rapidly as infectious virus was cleared,
followed by a rebound in measles virus RNA by as much as ten-fold that
slowly declined to undetectable levels over 10 weeks. Measles virus RNA
remained detectable in lymphoid tissue after it was no longer detectable
in blood.

Immune responses
Immune responses to measles virus are crucial for viral clearance
and the establishment of protective immunity but also are the
pathological basis of the clinical signs and symptoms that contribute to
measles morbidity and mortality. The rash of measles, for example, is
characterised histologically by perivascular, lymphocytic infiltrates. The
earliest, innate immune responses occur during the prodromal phase
before the onset of rash. Two non-structural viral proteins (V and C)
suppress host interferon production, facilitating virus replication. The
adaptive immune response follows and consists of cellular and humoral
responses, which are essential for recovery and the establishment of long-
term, protective immunity, respectively. The initial humoral response
consists of IgM antibodies that arise at the time of the rash and persist for
6–8 weeks. Detection of IgM antibodies by enzyme immunoassay is the
most commonly used laboratory method of confirming measles virus
infection, but IgM antibodies might not be detectable early in the disease
course shortly after rash onset. Subsequently, IgG antibodies are
produced, the most abundant of which are against the nucleoproten.
The efficacy of antibodies alone in preventing measles is shown by
the protection conferred by passively acquired maternal antibodies and
post-exposure administration of antimeasles virus immune globulin.
Cellular immune responses to measles virus are important for viral
clearance and recovery, as shown by the fact that children with
agammaglobulinaemia recover from measles, but children with T-cell
deficiencies develop severe or fatal disease.
Plasma interferon-γ levels, consistent with a predominant Th1
immune response, are increased during the acute phase of infection.
During convalescence, a Th2 response promotes the development of
protective measles virus-specific antibodies and is characterised by high
concentrations of interleukin 4, interleukin 10, and interleukin 13.
Measles was the first immunosuppressive infection to be described.
Deficiencies of both innate and adaptive immune responses can render
individuals with measles more susceptible to secondary bacterial and viral
infections. Transient lymphopenia occurs in the blood during measles but
is likely due to the redistribution of lymphocytes from peripheral blood to
lymphatic tissues. The Th2 response during convalescence might inhibit
Th1 responses, increasing susceptibility to intracellular pathogens. Plasma
interleukin 10 concentrations are increased for weeks in children with
measles and also might contribute to immune suppression.

2.5 Clinical Features

The classic signs and symptoms of measles include four-day fevers
(the 4 D's) and the three C's—cough, coryza (head cold, fever, sneezing),
and conjunctivitis (red eyes)—along with fever and rashes. Fever is
common and typically lasts for about one week; the fever seen with
measles is often as high as 40 °C (104 °F). Koplik's spots seen inside the
mouth on the buccal mucosa as small white papules are pathognomonic
(diagnostic) for measles, but are temporary and therefore rarely seen, it
provides an opportunity to clinically diagnose measles a day or two before
the rash. Recognizing these spots before a person reaches their maximum
infectiousness can help physicians reduce the spread of the disease.
The characteristic measles rash is classically described as a
generalized red maculopapular rash that begins 3–4 days after the onset
of fever, coinciding with development of the adaptive immune response. It
starts on the back of the ears and, after a few hours, spreads to the head
and neck before spreading to cover most of the body, often causing
itching. The measles rash appears two to four days after the initial
symptoms and lasts for up to eight days. The rash is said to "stain",
changing color from red to dark brown, before disappearing. Overall, the
disease from infection with the measles virus usually resolves after about
three weeks. The fever and catarrhal symptoms typically peak with the
rash, which persists for 3–4 days.
The rash might be minimal in children with vaccine-modified
measles who have previous immunity following vaccination, and these
children might not have cough, coryza, or conjunctivitis. Malnourished
children can develop a deeply pigmented rash that desquamates during
recovery. As the rash represents a perivascular lymphocytic infiltration,
children with impaired cellular immunity, such as those infected with HIV,
might not develop the characteristic rash or the rash might be delayed.
Recovery typically occurs within 1 week of rash onset in people with
uncomplicated measles.

2.6 Diagnosis
Measles is readily recognised by clinicians familiar with the disease
in people presenting with fever and generalised rash, particularly during
outbreaks or in patients with a history of travel to endemic areas. Other
acute viral infections that might be confused with measles include
infection with rubella virus, human herpes virus type 6, parvovirus B19,
and dengue viruses. The medical history and physical examination should
focus on the clinical features of measles as well as potential
complications, including pneumonia, otitis media, keratoconjunctivitis, and
diarrhea. Assessment of nutritional and immune status, most importantly
vitamin A deficiency and HIV infection, will identify individuals at highest
risk of mortality. Health-care personnel should take appropriate measures,
including prompt isolation of infectious cases using airborne precautions,
to prevent transmission within health-care settings. The clinical diagnosis
of measles is more challenging to clinicians unfamiliar with the disease,
before the onset of rash, in immunocompromised and undernourished
children in whom the rash might be absent or altered, and in individuals
with pre-existing antibodies from maternal immunity, immune globulin, or
previous vaccination who can have a longer incubation period, milder
prodromal illness, and a less apparent rash than typical cases.
The most common laboratory method for confirming measles virus
infection is detection of measles virus specific IgM antibodies in serum or
plasma. However, measles virus-specific IgM antibodies might be low or
undetectable until 4 days or more after rash onset, resulting in false
negative results if samples are collected early. About 75% of people with
measles will have detectable measles virus-specific IgM antibodies within
the first 72 h after rash and almost all people with measles will have
detectable measles virus-specific IgM antibodies after 4 days. Measles
virus-specific IgM antibodies peak within 1–3 weeks after the onset of rash
and decline to undetectable levels within 4–8 weeks. Acute infection also
can be confirmed serologically by measuring a fourfold or greater increase
in measles virus-specific IgG antibody levels between acute and
convalescent sera. The presence of IgG antibodies to measles virus in a
single serum specimen is evidence of previous infection or immunisation.
Measles virus infection also can be confirmed by detection of viral RNA
through RT-PCR using throat, nasal, nasopharyngeal, and urine samples
before measles virus-specific IgM antibodies are detectable.

2.7 Management
The management of patients with measles consists of supportive
therapy to correct or prevent dehydration and nutritional deficiencies,
prompt recognition and treatment of secondary bacterial infections, and
provision of vitamin A. WHO recommends administration of once daily
doses of 200 000 IU of vitamin A for 2 consecutive days to all children with
measles older than 1 year of age. In younger children, lower doses are
recommended, specifically 100 000 IU per day for children 6–12 months of
age and 50 000 IU per day for children younger than 6 months. For
children with clinical evidence of vitamin A deficiency, a third dose is
recommended 2–4 weeks later. This treatment restores low vitamin A
levels during measles that occur even in well-nourished children and can
help prevent eye damage and blindness. Two doses of vitamin A, but not a
single dose, has been associated with a reduction in the risk of mortality
in children younger than 2 years and a reduction in the risk of pneumonia-
specific mortality.
No specific antiviral therapies exist for measles, although ribavirin,
interferon alfa, and other antiviral drugs have been used to treat severe
measles. Evidence supporting the use of prophylactic antibiotics for
children with measles is limited and such use is not recommended, but
antibiotics are indicated for people with measles who have clinical
evidence of bacterial infection, including pneumonia and otitis media.
There is no specific treatment for measles. Most people with
uncomplicated measles will recover with rest and supportive treatment.
Severe complications from measles can be avoided through supportive
care that ensures good nutrition, adequate fluid intake and treatment of
dehydration with WHO-recommended oral rehydration solution. This
solution replaces fluids and other essential elements that are lost through
diarrhea or vomiting. Antibiotics should be prescribed to treat eye and ear
infections, and pneumonia.

2.8 Complications
Complications with measles are relatively common, ranging from
mild complications such as diarrhea to serious complications such as
pneumonia (either direct viral pneumonia or secondary bacterial
pneumonia), bronchitis (either direct viral bronchitis or secondary
bacterial bronchitis), otitis media, acute brain inflammation (and very
rarely SSPE—subacute sclerosing panencephalitis), and corneal ulceration
(leading to corneal scarring). Complications are usually more severe in
adults who catch the virus.
People that are at high risk for complications are: Infants and
children aged <5 years, adults aged >20 years, pregnant women, and
people with compromised immune systems, such as from leukemia and
HIV infection, particularly children with vitamin A deficiency. The
respiratory tract is a frequent site of complication, with pneumonia
accounting for most measles-associated morbidity and mortality.
Pneumonia is most often caused by secondary viral or bacterial pathogens
but can be due to measles virus itself resulting in Hecht’s giant cell
pneumonia. Bacterial and viral pathogens associated with pneumonia in
children with measles are not well characterised, particularly in children
vaccinated against pneumococcus and Haemophilus influenzae type b.
Other complications of the respiratory tract include
laryngotracheobronchitis (croup) and otitis media. Diarrhoea can result in
considerable morbidity and mortality, and is often due to secondary
infections with bacteria or protozoa. Keratoconjunctivitis, another serious
complication of measles, was a frequent cause of blindness before the
widespread use of measles vaccine and vitamin A supplementation.
Measles in pregnancy is associated with an increased risk of low
birthweight, spontaneous abortion, intrauterine fetal death, and maternal
Three rare but serious CNS complications of measles were a major
motivating factor to prevent infection through vaccination in countries
where case fatality was low. First, acute disseminated encephalomyelitis
(ADEM) is a demyelinating autoimmune disease that is triggered by
measles virus and occurs within days to weeks in approximately one in
1000 cases. ADEM is characterised
by fever, seizures, and other neurological deficits. Second, measles
inclusion body encephalitis (MIBE) is a progressive measles virus infection
of the brain that results in neurological deterioration and death in
individuals with impaired cellular immunity within months of the acute
illness. MIBE has been described in children who are immunosuppressed
following organ transplants and in HIV-infected persons. Third, subacute
sclerosing panencephalitis (SSPE) is a delayed complication of measles
that occurs in about 1:10 000 to 1:100 000 cases 5–10 years after the
acute illness, caused by the host response to production of mutated
virions with defective assembly and budding. SSPE most often occurs in
people infected with measles virus before 2 years of age and is
characterised by seizures, progressive deterioration of cognitive and
motor function, and death. A recent report of SSPE in the USA identified a
much higher incidence than previously described, including an incidence
of 1:1367 cases in children who acquired measles younger than 5 years of
age and 1:609 cases in children with measles before 1 year of age.
Measles vaccination reduces the incidence of SSPE.

2.9 Prevention
The most important thing to protect kids from measles is to have
them vaccinated according to the immunization schedule. For most,
measles protection is part of the measles-mumps-rubella vaccine (MMR)
or measles-mumps-rubella-varicella vaccine (MMRV) given when they're
12 to 15 months old and again when they're 4 to 6 years old.
Measles antibodies are transferred from mothers who have been
vaccinated against measles or who have been previously infected with
measles to their children while they are still in the womb. Such antibodies
will usually give newborn infants some immunity against measles, but
such antibodies are gradually lost over the course of the first six months
of life. Infants under one year of age whose maternal anti-measles
antibodies have disappeared become susceptible to infection with the
measles virus. Infants are generally protected from measles for 6 months
after birth due to immunity passed on by their mothers.
The measles vaccine sometimes causes side effects in kids who
don't have underlying health problems. The most common reactions are
fever 6-12 days after vaccination (in about 15% of kids vaccinated) and a
measles-like rash, which isn't contagious and fades on its own (in about
5% of vaccinated kids).
For Adults
Anyone born during or after 1957, who has never had measles or
has never been vaccinated, is at risk for measles. They should get at least
one dose of the MMR vaccine. Two doses are recommended for adults at
increased risk, such as students in college, trade school, and training
programs, international travelers, and health care professionals. There is
no harm in getting another dose of MMR vaccine if you may already be
immune to measles.
Women who are planning to become pregnant should make sure
they are protected against measles before they get pregnant. Most
women of childbearing age were vaccinated as children with the MMR
vaccine, but they should confirm this with their doctor. If they need to get
vaccinated for measles, they should avoid becoming pregnant until one
month (28 days) after receiving the MMR vaccine.

The measles vaccine should not be given to these at-risk groups:

 pregnant women
 kids with untreated tuberculosis, leukemia, or other cancers people
whose immune systems are weakened for any reason
 kids who have a history of severe allergic reaction to gelatin or to
the antibiotic neomycin, as they could have serious reactions to the

Because certain people cannot receive the measles vaccine for health
reasons, it's all the more important to make sure that children who can
get the vaccine get it on schedule. At-risk children depend on "herd
immunity." This means a high percentage of people have been immunized
against a disease, which prevents the disease from spreading in a
population and helps prevent outbreaks.

2.10 Prognosis
The majority of people survive measles, though in some cases,
complications may occur. Possible consequences of measles virus
infection include bronchitis, sensorineural hearing loss, and—in about 1 in
10,000 to 1 in 300,000 cases—panencephalitis, which is usually fatal.
Acute measles encephalitis is another serious risk of measles virus
infection. It typically occurs two days to one week after the breakout of
the measles rash and begins with very high fever, severe headache,
convulsions and altered mentation. A person with measles encephalitis
may become comatose, and death or brain injury may occur.

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