Measles
Etiology:
Measles is a highly contagious viral illness caused by measles virus which is a
single-stranded, lipid-enveloped RNA virus in the family Paramyxoviridae and
genus Morbillivirus.
Epidemiology:
The measles vaccine has changed the epidemiology of measles dramatically. Once
worldwide in distribution, endemic transmission of measles has been interrupted in
many countries where there is widespread vaccine coverage.
Morbidity and mortality associated with measles decreased prior to the introduction
of the vaccine as a result of improvements in healthcare and nutrition.
Transmission:
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 3days before to up to 4-6 days after the
onset 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 1hr after the patient with the source case leaves a
room. Secondary cases from spread of aerosolized virus have been reported in
airplanes, physicians’offices, and hospitals.
Pathogenesis:
Measles infection 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. Virus shedding begins
in the prodromal phase. With onset of the rash, antibody production begins, and viral
replication and symptoms begin to subside.
Clinical Manifestations:
Measles is a serious infection characterized by high fever, an enanthem, cough,
coryza, conjunctivitis, and a prominent exanthem. 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 1-4 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. 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
exanthema
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. 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.
Modified Measles Infection:
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 a
vaccine, when exposed to measles, may have a rash but few other symptoms. Persons
with modified measles are not considered highly contagious.
Laboratory Findings:
1. The diagnosis of measles is almost always based on clinical and epidemiologic
findings.
2. In the acute phase reduction in the total white blood cell count, with lymphocytes
decreased more than neutrophils. However, absolute neutropenia has been known to
occur.
3. In measles not complicated by bacterial infection, the ESR and CRP levels are
usually normal.
Diagnosis:
In the absence of a recognized measles outbreak, confirmation of the clinical
diagnosis is often recommended.
1. IgM antibody in serum: IgM antibody appears 1-2 days after the onset of the
rash and remains detectable for about 1 mo.
2. Viral isolation from blood, urine, or respiratory secretions can be accomplished
by culture.
3. Molecular detection by polymerase chain reaction is available.
Differential Diagnoses:
Typical measles is unlikely to be confused with other illnesses, especially if Koplik
spots are observed.
*Measles in the later stages or modified or atypical infections may be confused with a
number of other exanthematous immune mediated illnesses and infections, including
rubella, adenovirus infection, enterovirus infection, and Epstein-Barr virus infection.
*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 (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.
Complications:
Morbidity and mortality from measles are greatest in:
= younger than 5 yr of age(especially <1 yr of age) and older than 20 yr of age.
= crowding
=severe malnutrition
=low serum retinol
=immunocompromised persons
The complications of measles include:
1. Pneumonia: is the most common cause of death in measles(manifests as giant
cell pneumonia caused directly by the viral infection or as superimposed
bacterial infection”Streptococcus pneumoniae, Haemophilus influenzae,
and Staphylococcus aureus”.
2. Bronchiolitis obliterans.
3. Croup, tracheitis, and bronchiolitis.
4. Acute otitis media.
5. Sinusitis and mastoiditis.
6. Retropharyngeal abscess.
7. Diarrhea and vomiting, with dehydration as a consequence.
8. Febrile sizures occur in < 3%.
9. Appendicitis or abdominal pain my occur from obstruction of the appendiceal
lumen by lymphoid hyperplasia.
10. Encephalitis (a postinfectious, immunologically mediated process and is
not
the result of a direct effect by the virus. Clinical onset begins during the
exanthema and manifests as seizures(56%), lethargy(46%), coma(28%), and
irritability(26%). Findings in CSF include lymphocytic pleocytosis in 85% of
cases and elevated protein concentrations. Approximately 15% of patients with
measles encephalitis die. Another 20–40% of patients suffer long-term
sequelae, including cognitive impairment, 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.
11. Hemorrhagic measles(black measles)”manifested as a hemorrhagic skin
eruption and often fatal”
12. Thrombocytopenia, myocarditis, cellulitis, and toxic shock syndrome are other
rare complications.
13. Measles during pregnancy is associated with high rates of maternal morbidity,
fetal wastage, and stillbirths, with congenital malformations in 3% of liveborn
infants.
14. Subacute sclerosing panencephalitis (SSPE) is a chronic complication of
measles with a delayed onset and an outcome that is nearly always fatal. After
7-10 yr the virus apparently regains virulence and attacks the cells in the
central nervous system. Measles at an early age favors the development of
SSPE.
Subtle changes in behaviour or school performance appear, including
irritability, reduced attention span, and temper outbursts.
Treatment:
# Management of measles is supportive because there is no specific antiviral therapy.
# Maintenance of hydration, oxygenation, and comfort are goals of therapy.
# Antipyretics for comfort and fever control are useful.
# Oral rehydration is effective in most cases, but severe dehydration may require
intravenous therapy.
# Prophylactic antimicrobial therapy to prevent bacterial infection is not indicated.
# Vitamin A : is indicated for all patients with measles. Vitamin
A 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. In children with signs and symptoms of vitamin A
deficiency, a 3
rd
age appropriate dose is recommended 2-4 wk after the 2
nd
dose.
Prognosis:
With improvements in healthcare and antimicrobial therapy, better nutrition, and
decreased crowding, the death:case ratio fell to 1 per 1,000 cases. Pneumonia and
encephalitis were complications in most of the fatal cases, and immunodeficiency
conditions were identified in 14–16% of deaths.
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.
Vaccination against measles is the most effective and safe prevention strategy.
Postexposure Prophylaxis:
Susceptible individuals exposed to measles may be protected from infection by either
vaccine administration or with Ig. The vaccine is effective in prevention or
modification of measles if given within 72hr of exposure. Ig may be given up to 6
days after exposure to prevent or modify infection. Immunocompetent
children
should receive 0.5 mL/kg (maximum dose in both cases is 15mL/kg) intramuscularly
(IM). For severely immunocompromised children and pregnant woman without
evidence of measles immunity, Ig intravenously is the recommended Ig
at
400mg/kg. Ig is indicated for susceptible household contacts of
measles
patients, especially infants younger than 6mo of age, pregnant women, and
immunocompromised persons.
Rubella
Rubella (German measles or 3-day measles) is a mild, often exanthematous disease
of infants and children that is typically more severe and associated with more
complications in adults. Its major clinical significance is transplacental infection and
fetal damage as part of the congenital rubella syndrome(CRS).
Etiology:
Rubella virus is a single-stranded RNA virus with a lipid envelope and 3 structural
proteins. The virus is sensitive to heat, ultraviolet light, and extremes of pH but is
relatively stable at cold temperatures. Humans are the only known host.
Epidemiology:
Rubella appeared to occur in major epidemics every 6-9 yr, with smaller peaks
interspersed every 3-4yr, and was most common in preschool-age and school-age
children.
Pathogenesis:
Following infection, the virus replicates in the respiratory epithelium and then
spreads to regional lymph nodes. Viremia ensues and is most intense from 10 to 17
days after infection. Viral shedding from the nasopharynx begins approximately 10
days after infection and may be detected up to 2 wk following onset of the rash. The
period of highest communicability is from 5 days before to 6 days after the
appearance of the rash.
Clinical Manifestations:
Postnatal infection with rubella is a mild disease not easily discernible from other
viral infections, especially in children. Following an incubation period of 14-21 days,
a prodrome consisting of low-grade fever, sore throat, red eyes with or without eye
pain, headache, malaise, anorexia, and lymphadenopathy begins.
Suboccipital, postauricular, and anterior cervical lymph nodes are most prominent. In
children, the 1
st
manifestation of rubella is usually the rash, which is variable and not
distinctive. It begins on the face and neck as small, irregular pink macules that
coalesce, and it spreads centrifugally to involve the torso and extremities, where it
tends to occur as discrete macules.
About the time of onset of the rash, examination of the oropharynx may reveal tiny,
rose-colored lesions (Forchheimer spots) or petechial hemorrhages on the soft
palate.
The rash fades from the face as it extends to the rest of the body so that the whole
body may not be involved at any one time.
The duration of the rash is generally 3days, and it usually resolves without
desquamation.
Subclinical infections are common, and 25–40% of children may not have a rash.
Teenagers and adults tend to be more symptomatic and have systemic manifestations,
with up to 70% of females demonstrating arthralgias and arthritis.
Laboratory findings:
Leukopenia, neutropenia, and thrombocytopenia have been described during
postnatal rubella.
Diagnosis:
The most common diagnostic test is rubella immunoglobulin(Ig) M enzyme
immunosorbent assay, which is typically present about 4 days after the appearance
of the rash.
Differential Diagnoses:
1. Measles(in severe cases it may resemble measles but absence of Koplick spots,
absence of severe prodrome, and the shorter course allow differentiation).
2. Adenovirus.
3. Parvovirus B19 (erythema infectiosum).
4. Epstein-Barr virus.
5. Enterovirus.
6. Roseola infantum.
7. Mycoplasma pneumoniae.
Complications: are infrequent and generally not life threatening.
+ Postinfectious thrombocytopenia: manifests about 2wk
following the onset
of the rash as petechiae, epistaxis, gastrointestinal bleeding, and hematuria. It is
usually self-limited.
+ Arthritis: especially in adult women, begins within1wk of onset of the exanthema
and classically involves the small joints of the hands. It is self-limited and resolves
within weeks without sequelae.
+ Encephalitis is the most serious complication of postnatal rubella. It occurs in
2forms: a postinfectious syndrome following acute rubella and a rare progressive
panencephalitis manifesting as a neurodegenerative disorder years following rubella.
+ GuillainBarré syndrome, peripheral neuritis, myocarditis.
Treatment:
There is no specific treatment available.
Supportive Care:
Postnatal rubella is generally a mild illness that requires no care beyond antipyretics
and analgesics. Intravenous immunoglobulin or corticosteroids can be considered for
severe, nonremitting thrombocytopenia.
Prognosis:
Postnatal infection with rubella has an excellent prognosis. Reinfection with wild
virus occurs postnatally in both individuals who were previously infected with wild-
virus rubella and vaccinated individuals.
Reinfection with serious adverse outcomes
to adults or children is rare and of unknown significance.
Prevention: Patients with postnatal infection should be isolated from susceptible
individuals for 7days after onset of the rash. Standard plus droplet precautions are
recommended for hospitalized patients.
Vaccination:
Rubella vaccine is usually administered in combination with measles and mumps
(MMR) or also with varicella(MMRV) in a 2-dose regimen at 12-15mo and 4-6 yr of
age. It theoretically may be effective as postexposure prophylaxis if administered
within 3days of exposure.
Mumps
Mumps is an acute self-limited infection. It is characterized by fever, bilateral or
unilateral parotid swelling and tenderness, and the frequent occurrence of
meningoencephalitis and orchitis.
Etiology:
Mumps virus is in the family Paramyxoviridae and the genus Rubulavirus. It is a
single-stranded pleomorphic RNA virus. Humans are the only natural host.
Epidemiology:
In the prevaccine era, mumps occurred primarily in young children between the ages
of 5 and 9 yr and in epidemics about every 4 yr. Mumps infection occurred more
often in the winter and spring month.
Following the recommendation for routine use
of mumps vaccine in 1977, the incidence of mumps fell dramatically in young
children.
Mumps is spread from person to person by respiratory droplets. Virus appears in the
saliva from up to 7days before to as long as 7days after onset of parotid swelling.
The period of maximum infectiousness is 1-2days before to 5days after onset
of parotid swelling.
Pathology and Pathogenesis:
Mumps virus targets the salivary glands, central nervous system (CNS), pancreas,
testes, and to a lesser extent, thyroid, ovaries, heart, kidneys, liver, and joint synovia.
Clinical Manifestations:
The incubation period for mumps ranges from 12 to 25days but is usually 16-18
days. Mumps virus infection may result in clinical presentation ranging from
asymptomatic or nonspecific symptoms to the typical illness associated with parotitis
with or without complications involving several body systems.
The typical patient presents with a prodrome lasting 1-2days consisting of fever,
headache, vomiting, and achiness. Parotitis follows and may be unilateral initially but
becomes bilateral in approximately 70% of cases. The parotid gland is tender,
and
parotitis may be preceded or accompanied by ear pain on the
ipsilateral
side.
Ingestion of sour or acidic foods or liquids may enhance pain in the parotid area. As
swelling progresses, the angle of the jaw is obscured and the ear lobe may be lifted
upward and outward. The opening of the Stensen duct may be red and edematous.
The parotid swelling peaks in approximately 3days and then gradually subsides over
7days. Fever and the other systemic symptoms resolve in 3-5days.
Submandibular salivary glands may also be involved or may be enlarged without
parotid swelling. Symptoms in immunized individuals are the same but tend to be
less severe, and parotitis may be absent.
Diagnosis:
#In highly immunized populations patients with parotitis lasting longer than 2 days
and of unknown cause, a specific diagnosis of mumps should be confirmed or
ruled out by virologic or serologic means by isolation of the virus in cell culture,
detection of viral antigen by direct immunofluorescence, or identification of nucleic
acid by reverse transcriptase polymerase chain reaction (PCR).
#A significant increase in serum mumps immunoglobulin G antibody between acute
and convalescent serum specimens as detected by complement fixation,
neutralization hemagglutination, or enzyme immunoassay tests establishes the
diagnosis ,an enzyme immunoassay for mumps immunoglobulin
M antibody is
used to identify recent infection.
Differential Diagnoses:
-Parainfluenza1 and parainfluenza 3 viruses,
-Influenza A virus,
-Cytomegalovirus,
-Epstein-Barr
virus,
-Enteroviruses,
-Lymphocytic choriomeningitis virus,
-HIV
-Purulent parotitis (caused by Staphylococcus
aureus, unilateral, extremely
tender, associated with an elevated white blood cell count and may involve purulent
drainage from the Stensen duct),
-Submandibular or anterior cervical adenitis,
-Obstruction of the Stensen duct,
-Collagen vascular diseases (Sjögren syndrome, systemic lupus erythematosus)
-Tumor, and Drugs.
Complications:
The most common complications of mumps are meningitis, with or without
encephalitis, and gonadal (orchitis, oophoritis) involvement.
Uncommon complications include conjunctivitis, optic neuritis, pneumonia, nephritis,
pancreatitis, mastitis, and thrombocytopenia.
Complications can occur in the absence of parotitis especially in immunized
individuals.
Treatment:
No specific antiviral therapy is available for mumps. Management should be aimed at
reducing the pain associated with meningitis or orchitis and maintaining adequate
hydration. Antipyretics may be given for fever.
Prognosis:
The outcome of mumps is nearly always excellent, even when the disease is
complicated by encephalitis, although fatal cases from CNS involvement or
myocarditis have been reported.
Prevention:
Immunization with the live mumps vaccine is the primary mode of prevention. It is
given as part of the MMR 2-dose vaccine schedule, at 12-15mo of age for the 1
st
dose
and 4-6yr of age for the 2
nd
dose. If not given at 4-6yr, the 2
nd
dose should be given
before children enter puberty.