Measles

1. MEASLES (RUBEOLA)
It is an acute viral infection characterized by a final stage with a maculopapular rash erupting successively
over the neck and face, trunk, arms, and legs, and accompanied by a high fever.
Etiology
 Measles virus, the cause of measles, is an RNA virus of the genus Morbillivirus in the family
Paramyxoviridae.
 Only one serotype is known.
Epidemiology
 Measles is endemic throughout the world.
 In the past, epidemics tended to occur irregularly , appearing in the spring in large cities at 2-4-yr
intervals as new groups of susceptible children were exposed.
 It is rarely subclinical .
 Prior to the use of measles vaccine, the peak incidence was among children 5-10 yr of age.
 Individuals born before 1957 are considered to have had natural infection and to be immune
TRANSMISSION
 Measles is highly contagious ; approximately 90% of susceptible household contacts acquire the disease.
 Maximal dissemination of virus occurs by droplet spray during the prodromal period ( catarrhal stage ).
 Transmission to susceptible contacts often occurs prior to diagnosis of the index case
 Infants acquire immunity transplacentally from mothers who have had measles or measles immunization.
 This immunity is usually complete for the first 4-6 months of life and wanes at a variable rate.
 Some protection persists that may interfere with immunization administered before 12 months of age.
 Most women of childbearing age in the United States now have measles immunity by means of
immunization rather than disease.
 Infants of mothers with measles vaccine-induced immunity lose passive antibody at a younger age than
infants of mothers who had measles infection.
 Infants of mothers who are susceptible to measles have no measles immunity and may contract the
disease simultaneously with the mother before or after delivery.
Pathogenesis
 The essential lesion of measles is found in the skin, conjunctivae, and the mucous membranes of the
nasopharynx, bronchi, and intestinal tract.
 Serous exudate and proliferation of mononuclear cells and a few polymorphonuclear cells occur around
the capillaries.
 Hyperplasia of lymphoid tissue usually occurs, particularly in the appendix, where multinucleated giant
cells of up to 100 μm in diameter ( Warthin-Finkeldey reticuloendothelial giant cells ) may be found.
 In the skin, the reaction is particularly notable about the sebaceous glands and hair follicles.
 Koplik spots consist of serous exudate and proliferation of endothelial cells similar to those in the skin
lesions.
 A general inflammatory reaction of the buccal and pharyngeal mucosa extends into the lymphoid tissue
and the tracheobronchial mucous membrane.
 Interstitial pneumonitis resulting from measles virus takes the form of Hecht giant cell pneumonia.
 Bronchopneumonia may occur from secondary bacterial infection.
 In fatal cases of encephalomyelitis, perivascular demyelinization occurs in areas of the brain and spinal
cord.
 In subacute sclerosing panencephalitis (SSPE), there may be degeneration of the cortex and white matter
with intranuclear and intracytoplasmic inclusion bodies.
Clinical Manifestations
 Measles has three clinical stages:
1. an incubation stage

2. 2. a prodromal stage with an enanthem (Koplik spots) and mild symptoms.
3. a final stage with a maculopapular rash accompanied by high fever.
The incubation period
 lasts approximately 10-12 days to the first prodromal symptoms and another 2-4 days to the appearance
of the rash; rarely, it may be as short as 6-10 days.
 Body temperature may increase slightly 9-10 days from the date of infection and then subside for 24 hr
or so.
 The patient may transmit the virus by the 9th-10th day after exposure and occasionally as early as the
7th day, before the illness can be diagnosed.
The prodromal phase
 Usually lasts 3-5 days and is characterized by:
 low-grade to moderate fever
 dry cough
 coryza
 conjunctivitis
 These symptoms nearly always precede the appearance of Koplik spots , the pathognomonic sign of
measles, by 2-3 days.
 The conjunctival inflammation and photophobia may suggest measles before Koplik spots appear.
 In particular, a transverse line of conjunctival inflammation, sharply demarcated along the eyelid margin,
may be of diagnostic assistance in the prodromal stage. As the entire conjunctiva becomes involved, the
line disappears.
 Occasionally, the prodromal phase may be severe , being ushered in by a sudden high fever , sometimes
with convulsions and even pneumonia .
 Usually the coryza, fever, and cough are increasingly severe up to the time the rash has covered the body.
 The temperature rises abruptly as the rash appears and often reaches 40°C (104°F) or higher.
 In uncomplicated cases, as the rash appears on the legs and feet, the symptoms subside rapidly within
about 2 days , usually with an abrupt drop in temperature to normal.
 Patients up to this point may appear desperately ill, but within 24 hr after the temperature drops, they
appear well.
 Otitis media
 bronchopneumonia
 gastrointestinal symptoms such as diarrhea and vomiting
are more common in infants and small children (especially if they are malnourished) than in older children.
Koplik spots
 An enanthem or red mottling is usually present on the hard and soft palates
 the pathognomonic sign of measles are greyish white dots, usually as small as grains of sand, that have
slight, reddish areolae; occasionally they are hemorrhagic.
 Tend to occur opposite the lower molars but may spread irregularly over the rest of the buccal mucosa.
 Rarely they are found within the midportion of the lower lip , on the palate , and on the lacrimal caruncle
.
 They appear and disappear rapidly , usually within 12-18 hr .
 As they fade , a red , spotty discoloration of the mucosa may remain.
The rash
 Usually starts as faint macules on the:
 upper lateral parts of the neck
 behind the ears
 along the hairline

3.  posterior parts of the cheek.
 The individual lesions become increasingly maculopapular as the rash spreads rapidly over the:
 entire face
 neck
 upper arms
 upper part of the chest
within approximately the first 24 hr.
 During the succeeding 24 hr the rash spreads over the back, abdomen, entire arm, and thighs.
 As it finally reaches the feet on the 2nd-3rd day, it begins to fade on the face.
 Typical rash on day 2–3 of measles.
 Rash on day 5 of measles showing typical confluence and density on head with scattered lesions on the
trunk.
 The rash fades downward in the same sequence in which it appeared.
 The severity of the disease is directly related to the extent and confluence of the rash.
 In mild measles the rash tends not to be confluent , and in very mild cases there are few, if any, lesions
on the legs.
 In severe cases the rash is confluent , the skin is completely covered, including the palms and soles, and
the face is swollen and disfigured.
 The rash is often slightly hemorrhagic ; in severe cases with a confluent rash, petechiae may be present
in large numbers, and there may be extensive ecchymoses.
 The appearance of the rash may vary markedly.
 Infrequently a slight urticarial , faint macular , or scarlatiniform rash may appear during the early
prodromal stage, disappearing in advance of the typical rash.
 Complete absence of rash is rare except :
1. in patients who have received immunoglobulin (Ig) during the incubation period
2. in some patients with HIV infection
3. occasionally in infants younger than 9 months of age who have appreciable levels of maternal antibody.
 In the hemorrhagic type of measles ( black measles ), bleeding may occur from the mouth, nose, or
bowel.
In mild cases the rash may be less macular and more nearly pinpoint , somewhat resembling that of scarlet
fever or rubella.
 Itching is generally slight .
 As the rash fades , branny desquamation and brownish discoloration occur and then disappear within 7-
10 days.
Diagnosis
 The diagnosis is usually apparent from the characteristic clinical picture ; laboratory confirmation is
rarely needed.
 Testing for measles IgM antibodies is recommended in some situations.
 Measles IgM is detectable for 1 months after illness , but sensitivity of IgM assays may be limited in the
first 72 hr of the rash illness.
 Isolation of measles virus from clinical samples is also useful in identifying the genotype of the strain to
track transmission patterns.
 All suspected measles cases should be reported immediately to local or health departments.
 During the prodromal stage multinucleated giant cells can be demonstrated in smears of the nasal
mucosa.
 Antibodies become detectable when the rash appears ;
 testing of acute and convalescent sera demonstrates the diagnostic seroconversion or fourfold increase
in titer.
 Measles virus can be isolated by tissue culture in human embryonic or rhesus monkey kidney cells.

4.  Cytopathic changes , visible in 5-10 days, consist of multinucleated giant cells with intranuclear
inclusions .
 The white blood cell count tends to be low with a relative lymphocytosis
 Cerebrospinal fluid in patients with measles encephalitis usually shows an increase in protein and a small
increase in lymphocytes . The glucose level is normal.
The rash of rubeola must be differentiated from that of:
 Rubella
 Roseola infantum (human herpesvirus 6)
 Infections resulting from: echovirus, coxsackievirus, adenovirus
Infectious mononucleosis
 Toxoplasmosis
 Meningococcemia
 Scarlet fever
 Rickettsial diseases
 Kawasaki disease
 Serum sickness
 Drug rashes
Treatment
 There is no specific antiviral therapy;
 treatment is entirely supportive .
 Antipyretics (acetaminophen or ibuprofen) for fever
 bed rest
 maintenance of an adequate fluid intake
are indicated.
 Humidification may alleviate symptoms of laryngitis or an excessively irritating cough; it is best to keep
the room comfortably warm rather than cool.
 Patients with photophobia should be protected from exposure to strong light .
 Bacterial complications of otitis media and bronchopneumonia require appropriate antimicrobial
therapy.
 Complications such as encephalitis, subacute sclerosing panencephalitis, giant cell pneumonia, and
disseminated intravascular coagulation must be assessed individually .
 Good supportive care is essential.
 Immunoglobulin and corticosteroids are of limited value.
 Currently available antiviral compounds are not effective.
 The American Academy of Pediatrics recommends consideration of vitamin A supplementation for:
 children 6 months to 2 years of age who are hospitalized for measles and its complications
 children older than 6 months of age with measles and immunodeficiency.
 The recommended regimen is a single dose of:
 100,000 IU orally for children 6 months to 1 year
 200,000 IU for children 1 year of age or older
 Children with ophthalmologic evidence of vitamin A deficiency should be given additional doses the
next day and 4 week later.
Complications
The chief complications of measles are: otitis media, pneumonia, encephalitis.
Respiratory tract complications
 Interstitial pneumonia may be caused by the measles virus ( giant cell pneumonia ).
 Bacterial superinfection and bronchopneumonia are more frequent, however, usually with
pneumococcus , group A Streptococcus , Staphylococcus aureus , and Haemophilus influenzae type b .
 Laryngitis , tracheitis , and bronchitis are common and may be due to the virus alone.

5.  Measles may exacerbate underlying Mycobacterium tuberculosis infection.
 There may also be a temporary loss of hypersensitivity reaction to tuberculin skin testing.  Measles
pneumonia in HIV-infected patients is often fatal and is not always accompanied by rash.
Cardiovascular complications
 Noma of the cheeks may occur in rare instances.
 Gangrene elsewhere appears to be secondary to :
 purpura fulminans
 disseminated intravascular coagulation following measles
 Myocarditis is an infrequent serious complication, although transient electrocardiographic changes may
be relatively common.
Neurologic complications
 Are more common in measles than in any of the other exanthematous diseases. Encephalomyelitis
 The incidence is estimated to be 1-2/1,000 cases of measles.
 There is no correlation between the severity of the:
 Rash illness and that of the neurologic involvement
 Initial encephalitic process and the prognosis.
 Infrequently, encephalitic involvement is manifest in the pre-eruptive period , but more often its onset
occurs 2-5 days after the appearance of the rash .
 The cause of measles encephalitis remains controversial .
1. Encephalitis early in the course of the disease : direct viral invasion may be operative for
2. Encephalitis that occurs later is predominantly demyelinating and may reflect an immunologic reaction
.
 Fatal encephalitis has occurred in children receiving immunosuppressive treatment.
 Other central nervous system complications, including:
 Guillain-Barré syndrome
 Hemiplegia
 Cerebral thrombophlebitis
 Retrobulbar neuritis
occur rarely.
Prognosis
 Case fatality rates in the United States have decreased in recent years to low levels for all age groups,
largely because of :
 Improved socioeconomic conditions
 Effective antibacterial therapy for the treatment of secondary bacterial infections.
 Despite the decline in measles cases and fatalities in the United States, the case fatality rate is still
1-3/1,000 cases.
 Deaths are primarily due to pneumonia or secondary bacterial infections.
 In developing countries measles frequently occurs in infants ; possibly because of concomitant
malnutrition, the disease is very severe in these locations and has a high mortality .
 When measles is introduced into a highly susceptible population , the results may be disastrous.
Prevention
 Isolation precautions , especially in hospitals and other institutions, should be maintained from the 7th
day after exposure until 5 days after the rash has appeared.
VACCINE
 The initial measles immunization, usually as measles-mumps-rubella (MMR) vaccine, is recommended
at 12-15 months of age.
 MMR vaccine may be given for:
1. Measles postexposure

6. 2. Outbreak prophylaxis as early as 6 months of age.
 A second immunization , also as MMR, is recommended routinely at 4-6 years of age
 MMR may be administered at any time during childhood provided at least 4 wk have elapsed since the
first dose .
 Second measles immunization should be given to :
1. Children who have not previously received the second dose should be immunized by 11-12 years of
age.
2.Adolescents entering college or the workforce.
 A tuberculin test prior to or concurrent with active immunization against measles is desirable if
tuberculosis is under consideration.
 Measles vaccine is not recommended for:
1. Pregnant women
2. Children with primary immunodeficiency
3. Untreated tuberculosis, cancer, or organ transplantation
4. Those receiving long-term immunosuppressive therapy
5. severely immunocompromised HIV-infected children.
 HIV-infected children without :
1. Severe immunosuppression
2. Evidence of measles immunity
may receive measles vaccine .
POSTEXPOSURE PROPHYLAXIS
 Passive immunization with immune globulin is effective for prevention and attenuation of measles within
6 days of exposure.
 Susceptible household and hospital contacts who are:
1. younger than 12 months of age
2. pregnant
should receive immune globulin (0.25 mL/kg; maximum: 15 mL) intramuscularly as soon as possible after
exposure, but within 5 days.
 Immunocompromised persons should receive immune globulin (0.5 mL/kg; maximum: 15 mL)
intramuscularly regardless of immunization status.
 Infants 6 months of age or younger born to nonimmune mothers should receive immune globulin ;
 Infants 6 months of age or younger born to immune mothers are considered protected by maternal
antibody.
 Susceptible children 6-12 months of age should also be vaccinated; this vaccination does not count as
one of the two required measles vaccinations.
 Susceptible children 12 months of age or older should receive vaccine alone within 72 hr.
 Pregnant women and immunocompromised persons should receive immune globulin but not vaccine.