Measles

Dr. Zarghoon Tareen

 Measles is a common and serious childhood
exanthematous illness, which still causes
approximately 350,000 childhood deaths in
developing countries.
 It can affect people of all ages, despite being
considered primarily a childhood illness.
 Measles is marked by prodromal fever, cough,
coryza, conjunctivitis, and pathognomonic
enanthem (ie, Koplik spots), followed by an
erythematous maculopapular rash on the third to
seventh day. Infection confers life-long immunity.
 Maternal antibodies play a significant role
in protection against infection in infants
younger than 1 year and may interfere
with live-attenuated measles vaccination.
 A single dose of measles vaccine
administered to a child older than 12
months induces protective immunity in
95% of recipients.
 Because measles virus is highly
contagious, a 5% susceptible population is
sufficient to sustain periodic outbreaks in
otherwise highly vaccinated populations.
➢ Etiopathogenesis: measles is caused by an RNA
virus belonging to the paramyxovirus family.
➢ The virus is transmitted by droplet spread from
the secretions of the nose and throat usually 4
days before and 5 days after the rash.
➢ Primary viremia occurs resulting in infection of
the RES fallowed by secondary viremia, which
results in systemic symptoms. The IP is around
10 days.
Pathophysiology

 In temperate areas, the peak incidence of

infection occurs during late winter and
spring.
 Infection is transmitted via respiratory
droplets, which can remain active and
contagious, either airborne or on
surfaces, for up to 2 hours.
 Initial infection and viral replication
occur locally in tracheal and bronchial
epithelial cells.
 After 2-4 days, measles virus infects local
lymphatic tissues, perhaps carried by pulmonary
macrophages.
 Following the amplification of measles virus in
regional lymph nodes, a predominantly cell-
associated viremia disseminates the virus to
various organs prior to the appearance of rash.
 Measles virus infection causes a generalized
immunosuppression marked by decreases in
delayed-type hypersensitivity, interleukin (IL)-
12 production, and antigen-specific
lymphoproliferative responses that persist for
weeks to months after the acute infection.
 Immunosuppression may predispose individuals
to secondary opportunistic infections, [15]
particularly bronchopneumonia, a major cause
of measles-related mortality among younger
children.
Etiology

 The cause of measles is the measles virus, a

single-stranded, negative-sense enveloped RNA
virus of the genus Morbillivirus within the
family Paramyxoviridae.
 Humans are the natural hosts of the virus; no
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 the following:
 Children with immunodeficiency due to HIV or
AIDS, leukemia, alkylating agents, or
corticosteroid therapy, regardless of
immunization status
 Travel to areas where measles is endemic or
contact with travelers to endemic areas
 Infants who lose passive antibody before the
age of routine immunization
 Risk factors for severe measles and its
complications include the following:

 Malnutrition

 Underlying immunodeficiency

 Pregnancy

 Vitamin A deficiency
 Clinical features
 The disease is more common in preschool children,
infants are protected by transplacental antibodies,
which gradually decay by 9 m.
 The prodromal phase is characterized by fever,
rhinorrhea, conjunctival congestion and dry hacking
cough.
 Koplik spots considered as pathogonomic of measles
appear on the 2nd or 3rd day of the illness.
 The rash usually appears on the fourth day with rise in
fever as faint reddish macules behind the ears, along
the hairline.
 The rash rapidly becomes maculopapular and spreads
to the face, the neck, chest, arm, trunk thighs and
legs in that order over the next 2-3 days.
 Measles Rash

Hairline • Erythematous papular

Behind Ears eruption

Face
• Travels inferior over 2-3 days

• Coalesces into macular

Trunk “splotches”

• Often desquamates at end of

Limbs illness
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Continue…

 It then starts fading in the same order that it

appeared and leaves behind branny
desquamation and brownish discoloration, which
fades over the next 10 days.
 Modified measles seen in partially immune
individuals is a much milder and shorter illness.
 Hemorrhagic measles is characterized by a
purpuric rash and bleeding from the nose,
mouth or bowel.
Modified and atypical measles

 Modified measles is a milder form of measles

that occurs in individuals who have received
serum immunoglobulin after their exposure to
the measles virus.
 Similar but milder symptoms and signs may
still occur, but the incubation period may be
as long as 21 days.
 Complications

 Widespread mucosal damage and significant

immunosuppression induced by measles account for
the frequent complications seen with this viral
infection. Complications are more frequent in the
very young, the malnourished and the
immunocompromised.
 The most common complications are OM and bacterial
bronchopneumonia.
 Other R complications includes include laryngitis,
tracheitis, bronchitis, broncheictasis and flaring up of
latent M. tuberculosis infection.
 Transient loss of tuberculin hypersensivity reaction is
common following measles.
 GE comp. includes persistent diarrhea, hepatitis and
ileocolitis. Measles can precipitate malnutrition and
can cause noma and gangrene of the cheeks.
 Continue…

 Acute encephalitis occurs in measles at a

frequency of 1-2/1000 cases most commonly
during the period of the rash, consequent to
direct invasion of the brain.
 Post measles encephalitis occurs after recovery
and is believed to be due to an immune
mechanism.
 Measles is also responsible for the almost
uniformly fatal SSPE seen several years after
infection at a frequency of 1:100,000.
 Diagnosis

 The diagnosis is clinical, it may be confirmed by

estimating the levels of IgM antimeasles ab that
is present 3 d after the rash and persists for 1
m.
 Measles needs to be differentiates from other
childhood exanthematous illnesses.
 Differential
Measles Diagnosis
Dengue
Enteroviruses

Rubella Kawasaki
Maculopapular
Rash with Fever
Scarlet
Fever Echoviruses

Reoviruses
Mononucleosis
Roseola Infantum
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 Treatment

 Treatment is mainly supportive and comprises

anti pyretics, maintenance of hygiene,
ensuring adequate fluid and caloric intake,
humidification, etc.
 Vitamin A reduces morbidity and mortality of
measles and a single oral dose of 100,000 units
below 1 y and 200,000 units over the age of 1
y is recommended. Complications should be
managed appropriately.
 Prevention

 Measles is a preventable and potentially

eradicable disease through universal
immunization.
 All children should be given 2 doses of
“Measles vaccine” at the age of 9 and 18
months.
 Measles vaccination resulted in a 80% drop in
measles deaths between 2000 and 2017
worldwide.
 Rubella
(German Measles, Third disease)

28
• Rubella is a mild disease in childhood occurring
in winter and spring
Infectivity
• 7 days pre-rash to 5 days post-rash
• It is spread by droplets

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 Signs and Symptoms
Prodromal phase
• The incubation period is 14–21 days during
which time the child may have a mild illness with
low-grade fever.
Exanthematous phase
• Maculopapular rash starting on the face, then
spreading to cover the whole body, and lasting
up to 5 days.
Other features
• Suboccipital and post-auricular
lymphadenopathy

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Rubella Rash 31
 Congenital rubella syndrome (CRS)
• Mother infected in first 4 months of pregnancy (highest risk).
• Infection in utero, failure of rubella vaccine is <5% and rarely results in CRS.
• Clinical features
▪ Cataracts/congenital glaucoma
▪ Congenital heart disease
▪ Hearing impairment (common)
▪ Purpura ("blueberry muffin baby")
▪ Hepatosplenomegaly
▪ Jaundice
▪ Microcephaly
▪ Developmental delay
▪ Radiolucent bone disease
• Prevention
▪ Routine childhood immunization
▪ Ensure immunity of women of childbearing age with vaccination
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A 4-year-old boy with congenital rubella syndrome with unilateral microphthalmos
and cataract formation in the left eye.
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 Diagnosis
Serology
• If there is a risk of a non-immune pregnant
woman has been exposed to the child, then the
diagnosis should be confirmed by serology.

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Management
• Supportive
Prevention
• MMR (Measles, Mumps, Rubella) vaccine
Prognosis
▪ Excellent prognosis in patients with acquired
disease
▪ Irreversible defects in congenitally infected
patients

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 Complications
• Very rarely children may develop:
▪ Arthritis
▪ Myocarditis
▪ Encephalitis
▪ Thrombocytopenia
Note: When MMR vaccine uptake is reduced, remember
fetal rubella syndrome if a non-immune mother is
infected early in pregnancy

37
Varicella (chicken
pox)
 CP is a mild exanthematous illness in most
healthy children but can be a serious
disease in neonates,
immunocompromized, pregnant women,
and even healthy adults.
 Chickenpox (Varicella)
• Chickenpox results from primary infection with
Varicella-zoster virus (VZV).
• Incubation Period
10–21 days
• Infectivity
1–2 days pre-rash until vesicles have crusted
over.
• Transmission rate is 86% in household contacts.
• Spreads via respiratory secretions (airborne) and
vesicular fluid. 40
 Chickenpox (Varicella)
• Primary infection with virus usually results in life-long
immunity.
• >95% of young adults with varicella are immune.
• Maternal infection in 1st or early 2nd trimester (<2%
risk) can cause congenital varicella syndrome, which
manifests as:
▪ Low birth weight
▪ CNS abnormalities
▪ Digit/limb abnormalities
▪ Cutaneous scarring
▪ Eye defects
• Maternal infection 5 days before to 2 days after
delivery can lead to severe varicella of neonate.
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 Pathophysiology
• Infection is characterized by a generalized pruritic
vesicular rash.
• Children are contagious from 1–2 days prior to the
onset of the rash until the lesions have crusted.
• During primary infection, VZV establishes latency in
dorsal root ganglia.
• Reactivation of virus results in herpes zoster
(shingles).
• The most common complication of chickenpox is
bacterial superinfection with Strep. pyogenes or
Staph. aureus.
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 Pathophysiology (cont.)
• Parents of children who suffer from this complication
often report that children were improving and afebrile
with crusting lesions when they developed a new fever
late in the course of illness.
• Secondary Bacterial Infections (SBIs) include pyogenic
arthritis, osteomyelitis, pneumonia, bacteremia, and
necrotizing fasciitis.
• Nonbacterial complications of chickenpox include
pneumonia, cerebellar ataxia, encephalitis, hepatitis,
hemorrhagic varicella, and arthritis.
• Disseminated VZV infection may cause death in
immunocompromised patients as well as in healthy
patients with a history of recent steroid therapy. 43
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 Clinical Presentation
• Prodrome is 1–3 days, with fever and respiratory
symptoms
• Characteristic polymorphous rash
▪ Very pruritic
▪ Crops of red macules, which quickly become vesicles
surrounded by erythema
▪ “Dewdrop on erythematous base"
▪ Vesicles burst and lesions crust over
▪ On trunk, face, scalp, conjunctivae, oral mucosa,
palms and soles
▪ New crops usually stop forming after 5–7 days
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 Clinical Features
History
• Children with chickenpox have a history of contact
with another infected person within the previous
10 to 21 days.
• Although mild cases of varicella may occur in
children who have been vaccinated against the
disease, children usually have no history of
varicella immunization.
• Prodromal symptoms include fever and malaise.

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 Clinical Features (cont.)
Physical Examination
• Fever is often present.
• The child appears mildly to moderately ill.
• In cases of disseminated chickenpox or bacterial
superinfection, the child may appear very ill.
• The rash begins on the neck, face, or upper trunk and
spreads outward over the next 3 to 5 days.
• Mucous membranes may be involved.
• Lesions initially appear as small papules on an
erythematous base.

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 Clinical Features (cont.)
Physical Examination (cont.)
• The papules evolve into vesicles that eventually form
crusts.
• The rash is often intensely pruritic.
• It is important to inspect the rash for signs of hemorrhage
or infection.
• Lung examination may reveal signs of pneumonia, caused
by VZV or bacteria.
• Careful examination of the bones and joints may indicate
infection caused by Staph. aureus or Strep. pyogenes.
• Neurologic examination may reveal cerebellar ataxia.
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 Laboratory Evaluation
• Diagnosis of varicella is based on clinical findings.
• If the diagnosis is uncertain, it may be necessary to
send scrapings of the bases of vesicular lesions for
direct fluorescent antibody testing specific for VZV.
• A Tzanck smear reveals multinucleated giant cells
▪ It is not specific for VZV and is less sensitive and accurate
than direct fluorescent antibody.
• It is also possible to culture virus from lesions, but
results are not immediately available.
• Blood culture is warranted if bacterial super-infection
is suspected.
• Chest radiograph, CBC, coagulation screen, and liver
enzymes may be appropriate in ill-appearing
children. 50
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 Complications
• Secondary bacterial infection (most common)
▪ Infection with staphylococci, GAS
▪ Presents as impetigo, abscesses, cellulitis, necrotizing fasciitis,
sepsis
• Cerebellar ataxia, pneumonia, hepatitis, encephalitis
• Immunocompromised patients: varicella may be life-
threatening
• Neonates born to mothers who develop varicella from 5
days before to 2 days after delivery are considered high risk
▪ Must administer varicella-zoster immune globulin (VZIG), follow
for signs of infection/sepsis, and consider starting acyclovir
• Virus latent in sensory ganglia and reappears as herpes
zoster in 68/100,000 individuals
▪ Incidence is increased in immunocompromised patients 53
 Treatment
• Supportive (hydration, acetaminophen, anti-pruritics).
▪ AVOID salicylates due to risk of Reye syndrome.
• Proper hygiene, discourage scratching.
• Acyclovir (20 mg/kg/dose QID for 5 days) should be used
for:
▪ Severe disease
▪ Immunocompromised patients
▪ Neonates
• Avoid contact with others until lesions are dry and crusted
and no new ones are appearing.

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 Prophylaxis and Prevention
• Immunization important to prevent complications
(Varicella vaccine subcutaneous at the age of 15
months)
• VZIG (Varicella zoster immunoglobulin) for post-
exposure in high risk susceptible patient (within 4
days of exposure)
• School exclusion: 5 days from start of skin eruption

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Etiopathogenesis

 CP is caused by the VZV, a DNA virus of the herpes virus

family.
 The virus is present in the respiratory secretions and
the skin lesions of an affected child and is transmitted
either by air –borne spread or through direct contact.
 The portal of entry is respiratory tract. During the IP of
10-21 days, the virus replicates in the respiratory
mucosa followed by viremic dissemination to the skin
and various organs.
 The host immune response limits infection and promote
recovery.
 During the later part of the IP, the virus is transported
to the respiratory mucosa and leads to infectivity even
prior to appearance of the rash.
 The period of infectivity lasts from 24-48 h before the
rash until all the vesicles are crusted.
 Features
 CP is rarely subclinical; however, in some children only a few lesions may be
present. The peak age of disease is 5-10 y.
 The prodromal period is short with mild to moderate fever, malaise, headache
and anorexia.
 The rash appears 24-48h after the prodromal symptoms as intensely pruritic
erythematous macules first on the trunk. The rash rapidly to the face and
extremities while it evolves into papules, clear fluid-filled vesicles, and then
crusted vesicles.
 The median number of lesions is around 300 but may be vary from 10-1500.
 Systemic symptoms persist for 2-4 d after appearance of the rash
 The rash lasts 3-7d and leaves behind hypopegmented or hyperpegmented
macules that persist for days to weeks. Scaring is unusual unless lesions are
secondary infected.
Complications

 Secondary bacterial infection of the skin lesions may

occur, occasionally resulting in necrotizing fasciitis.
 Meningoencephalitis, transvers myelitis and optic
neuritis, purpura, ITP.
 CP in pregnancy associated with an increased risk of
severe disease in the mother. Congenital syndrome may
occur following infection in the 1st and 2nd trimester.
Diagnosis

 The diagnosis is clinical and usually not difficult.

 CP should be differentiated from other vesicular
exanthemata such as herpes simplex, enteroviral
infections, insect bites and drug reaction.
 In atypical cases, the diagnosis in made on Tzank smear
of the lesions and presence of anti IgM.
Treatment

 Management is symptomatic and includes antipyretics,

antipruritic agents and good hygiene.
 Aspirin is contraindicated due risk of Raye syndrome.
 The child should not attend the school until all lesions
have crusted.
 Administration of oral acyclovir 20mg/kg/dose four
times a day for 5 days within 24 hr of onset of rash in
healthy children reduces the duration of rash by one
day.
 IV acyclovir 10mg/kg every 8 h for 14-21 days is given to
patients with complicated varicella and illness in high
risk patients( neonates, immunocompromized children,
pregnant women)