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Measles

Chapter 246
Wilbert H. Mason
Nelson's Textbook of Pediatrics 20th Edition
Earl Mel Dustin B. Lao
P-3
February 11, 2019
Greetings
• Good day everyone, this will be the second topic to be reported under the Post
Graduate Interns entitled, “Measles”. As of the time of this report, this condition is
currently making headlines throughout the country as the number of victims is now
by the hundreds, and had already claimed a few unfortunate lives. Thus it is
imperrative for us physicians to know the basic behind this disease, especially that
we are already receiving and documenting a few cases from time to time in our
institution.
• With this report, I hope I could share to everyone a good chunk of knowledge
pertaining to this condition and its significance in the overall pediatric setting. Thank
you.
• Earl Mel Dustin B. Lao
Objectives and Outline
To be able to discuss and learn the disease through its various pathologic components
and process.
I. Introduction
II. Etiology and Epidemiology
III. Transmission
IV. Pathology
V. Pathogenesis
VI. Clinical Manifestations
VII. Diagnosis and Differentials
VIII.Complications
IX. Treatment and Prevention
Measles: Introduction
• Measles is a highly contagious viral disease that remains as one of the global health
threats.
• Though this disease is uncommon in developed countries due to widespread
vaccination, it still has a foothold in most underdeveloped nations due to poor health
care.
Measles: Etiology and Epidemiology
• Measles is caused by the Measles Virus
– It is a single stranded, lipid enveloped RNA virus
– Part of the family Paramyxoviridae
– Part of the genus Morbillivirus

• The Measles Virus has 6 major structural proteins


– Out of the 6, the 2 most important in terms of induction of immunity are the
Hemagglutinin (H protein) and the Fusion protein (F protein)
– The neutralizing antibodies are directed against the H protein
– The antibodies directed towards the F protein limit proliferation of the virus
during infection.
Measles: Etiology and Epidemiology
• The introduction of Measles
vaccine had dramatically changed
the epidemiology of measles.
• In the Philippines, it is part of the
EPI
– given subcutaneously at the age of
9 months but can be as early as 6
months in cases of outbreaks
– if monovalent measles vaccine is
unavailable, MMR can be given
Measles: Transmission
• The portal of entry of the measles virus is commonly through the respiratory tract or
the conjunctivae following contact with either large or small droplet aerosols in
which the virus is suspended.
• Measles is considered a higly contagious diseases
– 90% exposed susceptable individuals experience Measles
• Patients are considered infectious 3 days prior to the onset of rashes and 4 - 6 days
after onset.
Measles: Pathology
• Measles infection causes the following problems throughout its course
– Necrosis of the Respiratory epithelium with an accompanying lymphocytic
infiltration
– Produces small vessels vasculitis
– Histology of the rashes and exanthem reveals itracellular edema and dyskeratosis
associated with formation of epidermal syncytial giant cells which can contain
about 26 nuclei
Measles: Pathology
• Warthen-Finkeldey Giant cells:
– These are multinucleated giant cells
that are the result of fusion of
infected cells
– They are pathognomonic for
Measles
Measles: Pathogenesis

• Measles have 4 phases: Incubation, Prodromal, Exanthematous and Recovery phases.

1. Incubation Phase
• Duration of 8 - 12 days
• In this phase, the virus migrates to the regional lymph nodes
• Primary viremia disseminates the virus to the reticuloendothelial systems
• Secondary viremia spreads the virus the body surface

2. Prodromal Phase
• Duration of 3 - 5 days
• This phase begins after the secondary viremia
• This phase is associated with necrosis and giant cell formation
Measles: Pathogenesis

• Measles have 4 phases: Incubation, Prodromal, Exanthematous and Recovery phases.

3. Exanthematous phase
• Begins with the appearance of the Koplik spots, the pathognomonic sign of
measles

4. Recovery phase
• This phase starts upon the onset of rashes, wherein the other manifestations
began to subside.
Measles: Clinical Presentation

• Measles is a serious infection characterized with high grade fever, usually with the
following manifestations:
– 3 Cs: Cough, Coryza and Conjunctivitis
– Enanthem and Exanthem

• The Prodromal phase usually begins with low grade to moderate fever, associated
with the following:
– a prominent cough
– conjunctivitis
– coryza
These symptoms nearly always preceeds the appearance of Koplik spots.
Measles: Clinical Presentation
• The Koplik spots represent the
enanthem and are the pathognomonic
signs of Measles
– appears 1 - 4 days prior to the onset
of rashes
– characterized as discrete red lesions
with bluish white spots in the center
of the inner aspects of the cheeks at
the level of the Premolars
– they can spread involving lips, hard
palate and gingiva
Measles: Clinical Presentation
• The Rashes
– the rashes of Measles are characterized
as red maculopapular eruptions
– they usually begin at the forehead
(hairline) or behind the ears and the
upper neck
– these rashes would later spread
downward towards the trunk and the
extremities and can become confluent on
both the face and trunk
– the onset of rahes heralds the time
wherein the other symptoms begin to
subside
– rashes fades after 7 days in the same
manner as it first appeared
Measles: Clinical Presentation

• In some cases of Measles, lymphadenopathy maybe present.


– The more prominent lymph nodes are usually the ones found in either the Cervical or
Occipital areas.

• Among the major symptoms of measles, the cough is usually the one that last the
longest, usually up to 10 days.

• Inapparent Measles Infection


– This is a subclinical form of measles that usually occurs in individuals that have either
received vaccination while exposed to Measles or those individuals with passively acquired
antibodies such as infants or recipients of blood products.
– Rashes may be brief, indistinct or even absent
– Patients with this infection do not shed the virus thus cannot transmit the infection.
Measles: Diagnosis and Differential

• 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
– lymphocytes decreased more than neutrophils
– absolute neutropenia can also occur
Measles: Diagnosis and Differential

• In the absence of a recognized measles outbreak, confirmation of the clinical


diagnosis is often recommended usually done through serologic confirmation

– serologic confirmation is most conveniently made by identification of


immunoglobulin (Ig) M antibody in serum which appears 1-2 days after the onset
of the rash and remains detectable for about 1 month.
– serologic confirmation can also be made by demonstration of a 4-fold rise in IgG
antibodies in acute and convalescent specimens collected 2-4 wk apart.
Measles: Diagnosis and Differential

• 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
– adenovirus infection
– enterovirus infection
– Epstein-Barr virus infection
– Exanthem subitum (in infants)
– Erythema infectiosum (in older children)
Measles: Diagnosis and Differential

• 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 the
following
– discrete intraoral lesions (Koplik spots)
– severe prodromal cough
– elevations of neutrophils and acute-phase reactants.
– thrombocytosis of Kawasaki syndrome is absent in measles
Measles: Complications

• Complications of measles are largely attributable to the pathogenic effects of the


virus on the respiratory tract and immune system.

• Morbidity and mortality from measles are greatest in patients younger than 5 yr of
age (especially <1 yr of age) and older than 20 yr of age.
Measles: Complications

• Acute otitis media is the most common complication of measles.

• 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.
Measles: Complications

• Other complications of Measles are as follow:


– Croup, tracheitis, and bronchiolitis
– Diarrhea and vomiting
– Appendicitis or abdominal pain may occur from obstruction of the appendiceal
lumen by lymphoid hyperplasia
– Febrile seizures which occur in <3% of children with measles.
Measles: Complications

• 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 central nervous system for several years
– usually, after 7-10 yr the virus apparently regains virulence and attacks the cells in
the central nervous system that offered the virus protection.
– the pathogenic process of this condition is characterized as “slow virus infection”
which results in inflammation and cell death, leading to an inexorable
neurodegeneraive process.
Measles: Treatment and Prevention

• Management of Measles is supportive.


– Antiviral therapy is not effective in the treatment of measles in otherwise normal
patients.
– Prophylactic antimicrobial therapy to prevent bacterial infection is not indicated.
– Maintenance of hydration, oxygenation, and comfort are goals of therapy.
– Antipyretics for comfort and fever control are useful.
– Patients with respiratory tract involvement, airway humidification and
supplemental oxygen may be of benefit.
– Oral rehydration is effective in most cases, but severe dehydration may require
intravenous therapy.
Measles: Treatment and Prevention
• Vitamin A deficiency in children in
developing countries is known to be
associated with increased mortality
from a variety of infectious diseases,
including measles.
• Vitamin A therapy is threfore indicated
for all patients with measles.
– Should be administered once daily for 2
days at doses of 200,000 IU for children
12 mo of age or older
– 100,000 IU for infants 6 mo through 11
mo of age; and 50,000 IU for infants
younger than 6 mo of age.
Measles: Treatment and 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
• Measles Vaccine is given as part of the Expanded Program in Immunization in the
country.
Measles: Treatment and Prevention

• Postexposure Prophylaxis
– Susceptible individuals exposed to measles may be protected from infection by
either vaccine administration or immunization withimmune globulin.
– The vaccine is effective in prevention or modification of measles if given within
72 hr 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).
Quotation for the Day
• “You treat a disease: you win, you lose. You treat a person, I guarentee
you win - no matter the outcome”
-Patch Adams
Thank You!

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