Transcript Fever and Rash

Fever and Rash
DR.Rezai MS
Pediatrics infectious disease sub specialist
‫ماکول( اکیموز )‬
‫بثورات ماکولوپاپولر‬
‫پاپول‬
‫بثورات‬
‫ماکولوپاپولر با‬
‫توزیع محیطی‬
‫بثورات ماکولوپاپولر‬
‫با توزیع مرکزی‬
‫وزیکول‬
‫پوست‬
‫بول‬
‫(طاول)‬
‫ندول‬
‫(اریتم ندوالر)‬
‫اولسر‬
‫نکروتیک‬
‫گانگرن (پدیده ی‬
‫اکسفولیاسیون یا‬
‫پوسته ریزی‬
‫واسکولیت‬
‫کهیر‬
‫توزیع‬
‫محیطی‬
Classic Childhood
Exanthems
1.
2.
3.
4.
5.
6.
Measles
Scarlet fever
Rubella )“German measles”(
Atypical scarlet fever
Erythema Infectiosum
Roseola
Today, dozens of exanthems
are recognized:
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Adenovirus
Anthrax
Mononucleosis
Colorado tick fever
Mumps
Cat-scratch fever
Rat-bite fever
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Rocky Mountain
spotted fever
Relapsing fever

Meningococcemia
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Typhus
Hand-foot-mouth
disease
Measles
 Measles virus is a paramyxovirus
 Paramyxoviruses :
 Enveloped virus, ssRNA genome as a single piece.
 The family includes parainfluenza virus, mumps virus, measles
virus and respiratory syncytial virus.
 Parainfluenza and mumps virus have a surface hemagglutinin
and neuraminidase, while measles have a hemagglutinin, but
not neuraminidase.
 The virion structure includes:
 Spikes
 F protein
 Matrix protein M, below the envelope
 Only one serotype
#1- Measles
Virus: Rubeola
 Demographics Winter or spring Infancy
to young adulthood 8- to 12-day
incubation Epidemics until 96%
immunized
 Prodrome 2–4 days. High fever, cough,
coryza, conjunctivitis, photophobia, Koplik
spots, lethargy, sneezing.

Measles Epidemiology

Reservoir
Human

Transmission
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Temporal pattern Peak in late winter–
spring
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Communicability
after
Respiratory
Airborne
4 days before to 4 days
rash onset
#1 Measles
Rash and Disease
Enanthem: Koplik spots = gray
pinheads, ring of erythema, buccal
mucosa. 0.5–2d.
 Exanthem: erythematous blanching
macules.

 Starts
forehead, spreads downward
 Confluent by 72 hr
 Spares palms, and soles, 4–6 days.
 Toxic appearance.
#1- Measles
Diagnosis Leukopenia, IgG and IgM
serologies, acute and convalescent titers
 Treatment Symptomatic. Antipyretics.

 In
severe disease, vitamin A.
#1- Measles

Complications Otitis media, diarrhea,
pneumonia (common in atypical rubeola).
 Rarely,
laryngo-tracheobronchitis,
myocarditis, encephalitis. Subacute sclerosing
panencephalitis
Complications
 Giant cell pneumonia, more common in adults
 Post-measles encephalitis
 Subacute sclerosing panencephalitis (SSPE):
progressive and fatal degenerative disease
within the infected cells, there is a defective form
of the virus which because it can not produce
functional M protein, is not released as complete
virus from the cells.
#1- Measles
Prevention
Vaccinate all at 12–18 mo.
 Two doses for 13 years and older.
 Post-exposure vaccine if immunocompromised
 VZIG if pregnant, premature, or
immunocompromised

Measles Vaccine
 Composition
 Efficacy
90%-98%)
 Duration of
Immunity
 Schedule
Live virus
95% (range,
Lifelong
2 doses
MMR Vaccine
Contraindications and Precautions
Severe allergic reaction to vaccine
component or following prior dose
 Pregnancy
 Immunosuppression
 Moderate or severe acute illness
 Recent blood product
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#2- Scarlet Fever
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Streptococcal, erythrogenic toxin.
Demographics 1 to 10 yr
Prodrome 2 to 4 days
Pathophysiology:

Streptococci are gram-positive cocci that grow in
chains. They are classified by their ability to
produce a zone of hemolysis on blood agar and
by differences in carbohydrate cell wall
components.

Streptococci may be alpha-hemolytic (partial
hemolysis), beta-hemolytic (complete hemolysis),
or gamma-hemolytic (no hemolysis). Most
streptococci excrete hemolyzing enzymes and
toxins. Erythrogenic toxins cause the rash of
scarlet fever.
Background:
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Scarlet fever (scarlatina) is an exotoxinmediated disease arising from group A
beta-hemolytic streptococcal infection.
Ordinarily, scarlet fever evolves from a
tonsillar pharyngeal focus,

Exotoxin-mediated streptococcal
infections range from localized skin
disorders (eg, bullous impetigo) to the
systemic rash of scarlet fever to the
uncommon but highly lethal streptococcal
toxic shock syndrome.
#2- Scarlet Fever
Rash and Disease
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Strawberry tongue
Exudative pharyngitis
Generalized; spares palms and soles
Pinpoint papules
Desquamation of the tips of the fingers and toes
Sex:
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Males and females are affected
equally.
Age:
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Peak incidence of scarlet fever occurs in
persons aged 4-8 years.
By the time children are 10-years-old,
80% have developed lifelong protective
antibodies against streptococcal pyrogenic
exotoxins.
Scarlet fever is rare in children younger
than 2 years, because of the presence of
maternal antiexotoxin antibodies and lack
of prior sensitization.
History:
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The incubation period of streptococcal
pharyngitis is usually 2-4 days.
Prodrome
 Sore throat
 Headache
 Vomiting
 Abdominal pain
Fever
The rash appears 12- 48 hours after onset of
illness, first on the trunk and then extending
rapidly over the entire body to finally involve
the extremities.
Fever abates within 12-24 hours after
initiation of antibiotic therapy.
Physical:
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The patient usually appears moderately ill.
Fever
Tachycardia
Tonsils - Edematous, erythematous, and
covered with a yellow, grey, or white
exudate
Petechiae on the soft palate
Tender anterior cervical lymphadenopathy
Face - Flushed with perioral pallor

The exanthem is diffusely erythematous;
but, in some patients, it is more palpable
than visible.
 Exanthem
usually has the texture of coarse
sandpaper, and the erythema blanches with
pressure.
 The skin can be pruritic but usually is not
painful.
A
few days following generalization of
the rash, it becomes more intense along
skin folds and produces lines of
confluent petechiae known as the Pastia
sign. These lines are caused by
increased capillary fragility.
 The rash begins to fade 3-4 days after
onset, and the desquamation phase
begins. This phase begins with flakes
peeling from the face. Peeling from the
palms and around the fingers occurs
about a week later and lasts for about a
month after onset of the disease.
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The appearance of the tongue also
has a characteristic course in scarlet
fever.
 During
the first 2 days of the disease,
the tongue has a white coat through
which the red and edematous papillae
project. This is referred to as a white
strawberry tongue.
 After 2 days, the tongue also
desquamates, resulting in a red tongue
with prominent papillae called the red
strawberry tongue.
Lab Studies:

Throat culture remains the criterion standard for
confirmation of group A streptococcal upper
respiratory infection.
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American Heart Association guidelines for prevention
and treatment of rheumatic fever state that group A
streptococci virtually always is found on throat culture
during acute infection.
Throat cultures are approximately 90% sensitive for
presence of group A beta-hemolytic streptococci in the
pharynx. However, because a 10-15% carriage rate
exists among healthy individuals, the presence of group
A beta-hemolytic streptococci is not proof of disease.
To maximize sensitivity, proper obtaining of specimens
is crucial.
Vigorously swab the posterior pharynx, tonsils, and any
exudate with a cotton or Dacron swab under strong
illumination, avoiding the lips, tongue, and buccal
mucosa.

Direct antigen detection kits (ie,
rapid antigen tests [RATs], strep
screens) have been proposed to
allow immediate diagnosis and
prompt administration of antibiotics.
 Kits
are latex agglutination or a costlier
enzyme-linked immunosorbent assay
(ELISA).
 Several trials of RAT kits report results
of 78-100% specificity and 44-100%
sensitivity compared to throat cultures.
These studies usually were performed
under laboratory conditions.
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Streptococcal antibody tests are used
to confirm previous group A
streptococcal infection.
 The
most commonly available
streptococcal antibody test is the
antistreptolysin O test (ASLO test:
antibodies to streptococcal extracellular
products) .
 Currently, streptococcal antibody tests
during acute illness are not indicated.
 These tests can provide confirmatory
evidence of recent infection but have no
value in acute infection.
 They may be of value in patients
suspected of having acute renal failure

Complete blood count
 White
blood cell (WBC) count in scarlet
fever may increase to 12,000-16,000 per
mm3, with a differential of up to 95%
polymorphonuclear lymphocytes.
 During the second week, eosinophilia, as
high as 20%, can develop.
Treatment:
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The goals when treating scarlet fever are to
(1) prevent acute rheumatic fever
(2) reduce the spread of infection
(3) prevent supportive complications
(4) shorten the course of illness.
Penicillin remains the drug of choice (there are
still no documented cases of penicillin-resistant
group A streptococci infections). A firstgeneration cephalosporin may be an effective
alternative, as long as the patient does not have
any documented anaphylactic reactions to
penicillin. If this is the case, erythromycin can be
considered as an alternative.
Complications:

Suppurative complications
 Cervical
adenitis
 Otitis media/mastoiditis
 Ethmoiditis
 Sinusitis
 Peritonsillar abscess
 Pneumonia
 Septicemia, meningitis, osteomyelitis, and
septic arthritis
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Rheumatic fever
Acute renal failure from poststreptococcal
glomerulonephritis
Prognosis:
The prognosis is excellent; most
patients fully recover.
 Attacks may recur.
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Rubella (German Measles)
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Rubella Virus
Classified as togavirus
ssRNA virus with an envelope
pleomorphic in appearance, 50 – 60 nm in
diameter
nucleocapsid is icosahedral in symmetry
ssRNA is infective and replication occurs in the
cytoplasm
three major polypeptides: C and envelope
glycoproteins E1 and E2
single serotype
Postnatal Rubella
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Incubation period: 12 – 21 days
Macular rash, appears first on the face, then
spreads to the trunk and limbs
Minor pyrexia, malaise and lymphadenopathy
with suboccipital nodes most commonly
enlarged and tender
Arthralgia is uncommon in children, but may
occur in up to 60% of adult females,
involving the fingers, wrists, ankles and
knees
Encephalitis and thrombocytopenia are rare
complications
#3 Rubella
Rash and Disease
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Exanthem:
 Starts
face, spreads by 24 hr to trunk,
extremities.
 Day 1: 1- to 4-mm macules, usually distinct,
sometimes reticular.
 Day 2: pinpoint papules.
 Day 3: clears. Sometimes mild desquamation.
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Low-grade fever, pruritus possible.
Congenital Rubella
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Congenital rubella syndrome involves eyes, ears
and heart
Eyes: cataracts, micro-ophthalmia, glaucoma,
retinopathy
Ears: sensorineural deafness
Heart: patent ductus arteriosus, pulmonary
artery and valvular stenosis and ventricular
septal defect
Low birth weight, thrombocytopenia,
hepatosplenomegaly
Intrauterine death with abortion or stillbirth
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If maternal infection occurs:
in the first trimester, > 70% of babies will
be affected
 in the fourth month, the risk is reduced to
20% and only involves sensorineural
deafness
 after 16 th week, no increased risk
 before conception, no harm to the fetus

Pathogenesis
Virus is transmitted by air-borne route
URT
Viremia
 Skin, joints, placenta
cross the
barrier
 Infect fetal differentiating cells
 Early in pregnancy: this will cause
congenital abnormalities
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Laboratory Diagnosis
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Clinical diagnosis is unreliable
Investigation by virus isolation is not indicated
(unreliable and time-consuming)
Serological diagnosis is the method of choice,
detecting rubella specific IgG and rubella specific
IgM. These tests are also used for screening to
ascertain susceptibility and whether rubella
immunization is indicated.
Congenital rubella syndrome: serological testing for
specific IgM. Maternal IgM does not cross the
placenta so detection of specific IgM is diagnostic of
intrauterine infection
Control
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Attenuated live vaccine (MMR)
Seroconversion occurs in over 95%
Protection persists for more than 20 years
Administration in pregnancy is contraindicated
Pregnancy should be avoided for the month
following vaccination
#3 Rubella
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Diagnosis
 Acute
and convalescent titers
 rubella IgM antibody (esp. for exposed
pregnant women)

Treatment
 Symptomatic.
 NSAIDs
for arthritis.
#3 Rubella
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Complications
 Self-limiting
polyarthritis in girls, young
women. Hands and wrists, large joint
effusions.
#3 Rubella
Prevention
Vaccine at 12–15 mo
 Second dose at 18 mo.
 Immune globulin not indicated.

#5- Erythema Infectiosum
Virus: Parvovirus B19
 Demographics:

 Spring
 5–17
yr
 4- to 21-d incubation

Prodrome

Low-grade fever, headache, malaise.
#5- Erythema Infectiosum
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“Slapped cheeks” facial erythema with
abrupt onset
Circumoral and perioral pallor, sparing of
nasal bridge.
Body develops pale maculopapular
exanthem; may involve palms and soles.
Lasts 3–5 days
Atypically, Papular-Purpuric
Gloves and Socks syndrome (only hands
and feet affected)
#5- Erythema Infectiosum

Diagnosis
 IgM
and IgG serologies, acute and
convalescent antibody titers, DNA
hybridization

Treatment
 Symptomatic.
 IVIG
and transfusions if hematologic
complications
#5- Erythema Infectiosum
Complications

In anyone:
 Henoch-Schonlein
purpura,
 Polyarteritis nodosa
 Infectious mononucleosis.

In HIV+ or those with hemolytic anemia:
 aplastic

anemia.
In pregnancy: fetal hydrops or stillbirth.
#5- Erythema Infectiosum

No vaccine.

No isolation once symptomatic (not
contagious);
 Pregnant women should avoid
outbreak sites for 3 wk and get
serologic testing.
#6- Roseola
Virus: HHV-6 /HHV-7
 Demographics 0–3 yr
 Prodrome:

 3–5
d intermittent fever to 40.5°C.
 Child appears well.
#6- Roseola

Exanthem:
 0–2
d after defervesces
 1- to 5-mm rose macules with pale areola densest on
neck and trunk.
 Can get confluent.
 Lasts 1–3 d.

Enanthem: pinpoint papules or streaks on
uvula, soft palate. LAD, periorbital edema,
cough, headache, coryza, abdominal pain.
#6- Roseola

Diagnosis
 Clinical.
 Specific
IgM and IgG for acute and
convalescent titers not widely available.

Treatment
 Symptomatic.
Antipyretics for fever.
#6- Roseola
Complications
Febrile seizures.
 More rarely:

 mononucleosis
 neonatal
hepatitis
 fatal hemophagocytic syndrome
 encephalitis
 thrombotic thrombocytopenic purpura

Prevention: none
Coxsackie viruses
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Picornavirus

Icosahedral, positive sense, linear, ssRNA

Two groups: A and B

Group A:
 Herpangina (vesicular pharyngitis)
 Hand – Foot – and – Mouth disease
 Acute hemorrhagic conjunctivitis
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Group B:
 Pleurodynia (epidemic myalgia)
 Myocarditis
 Meningoencephalitis
Hand, Foot, and Mouth disease
Virus: Enteroviruses
 Demographics
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 Summer
6
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mo to 13 yr
Prodrome Brief. Sore throat, anorexia,
malaise, low-grade fever.
Hand, Foot, and Mouth
disease

Diagnosis
 Clinical
 Specific
serotype testing should clinician
suspect a particular enterovirus

Treatment
 Symptomatic.
Analgesia to help child with
oral intake, steroids for itch
Hand, Foot, and Mouth
disease Rash and Disease
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Enanthem:
 Oral
mucosal vesicles that erode to form
ulcers 2 mm to 2 cm in diameter.
 Painful!
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Exanthem:
 3-
to 7- mm vesicles on dorsal hands, feet,
and sometimes palms, sole.
 Tender, pruritic, or asymptomatic
Varicella Zoster Virus

Two forms

Primary infection is a generalized eruption (chicken
pox)

Reactivation is localized to one or few dermatomes
(shingles, Varicella Zoster)

Only one antigenic type
Pathogenesis of Chicken
Pox
 Children, vesicular skin eruption
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Virus enters through URT or conjunctiva

The virus causes viremia

The vesicles lie in the middle of the epidermis. The
fluid becomes cloudy with the influx of leucocytes.
These pustules dry up, scabs form and desquamate.

Lesions in all stages are present at any time while
new ones are appearing.
Pathogenesis of Varicella
Zoster
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VZV stays latent in the sensory ganglia

Reactivation can occur at any age but the rate is
much increased in persons aged 60 years or over.

Zoster is usually limited to one dermatome; in adults
most commonly in the thoracic or upper lumbar
region.
Clinical Features
Chicken Pox
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Incubation period: 14 – 15 days

The patient is infectious for 2 days before and up to
5 days after onset
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The rash is most dense on the trunk and head

Macules ---- Papules ---- Vesicles ---Pustules
Complications
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Secondary bacterial infection (commonest)
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Pneumonia
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CNS
 cerebellar ataxia syndrome
 acute encephalitits
Varicella in pregnancy

Varicella virus can cross the placenta following
viremia and infect the fetus
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Two types of intra-uterine infection
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Fetal varicella syndrome
 In the first half of pregnancy
 Skin scarring
 Limbs hypoplasia
 Chorioretinitis
 Silent intrauterine infection can also occur

Neonatal Varicella
 Within
the first two week of life
 Disseminated disease with pneumonitis and
encephalitis
 The infant is at serious risk if varicella occurs 6
days or less before delivery
Herpes Zoster

Reactivated VZV infection

Localized eruption, unilateral, typically confined to
one dermatome

Prodromal paraesthesia and pain in the area
supplied by affected nerve are common before skin
lesions develop

Postherpetic neuralgia
 Most common complication of zoster
 50% risk in patients aged over 60 years
 pain persisting for 1 month or more after the rash
Mumps (parotitis)
Mumps (parotitis)
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Inflammation of the salivary glands.
Mainly the parotid glands are affected.
There are three pairs of salivary glands.
Two parotid glands, the largest, one in each cheek, over
the angle of the jaw , in front of the ear.
Two sub mandibular glands at the back of the mouth.
Two sub-lingual glands, under the floor of the mouth.
Salivary glands .
Viral etiology
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Caused by mumps virus.
Family: paramyxoviridae.
Genus: parainfluenza virus.
Pleomorphic, enveloped with helical nucleocapsid.
The viral genome is ss-RNA, with negative polarity.
The viral envelope is covered with two glycoprotein
spikes, the HN which posses both hemagglutinine and
neuraminidase activities , and the fusion glycoprotein.
Viral etiology
 The
fusion protein enables the
virus to form multinucleated giant
cell by fusing infected cells
together.
 Mumps virus exists as a single
immunotype, and humans are the
only natural host
EPIDEMIOLOY
Endemic in the rest of the world
 Virus appears in the saliva from up to 7 days
before to as long as 7 days after onset of
parotid swelling.
 Maximum infectiousness is 1-2 days before to
5 days after parotid swelling.

Transmission
Mumps infection occurred more often in
the winter and spring months.
 By inhalation of respiratory droplets,
during sneezing and coughing.
 The virus sheds in saliva.
 The virus can be transmitted by direct
contact with saliva.

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Mumps virus causes necrosis of infected cells
and is associated with a lymphocytic
inflammatory infiltrate.
CLINICAL MANIFESTATION
Incubation period for mumps ranges from
12 to 25 days, but is usually 16 to 18 days
 Prodrome lasting 1-2 days consisting of
fever, headache, vomiting, and achiness.
Parotitis then appears and may be
unilateral initially but becomes bilateral in
about 70% of cases

The opening of the Stensen duct may be red
and edematous.
 The parotid swelling peaks in 3 days then
gradually subsides over 7 days.
 Fever resolves in 3 to 5 days along with the
other systemic symptoms.

 Submandibular
salivary glands
may also be involved or may be
enlarged without parotid
 A morbilliform rash is rarely seen.
 Edema over the sternum due to
lymphatic obstruction may also
occur.
Mumps
is a highly infectious
child-hood disease.
The swelling appears in front
of the ear.
DIAGNOSIS

When mumps was highly prevalent, the
diagnosis could be made based on history
of exposure to mumps infection, an
appropriate
incubation
period,
and
development of typical clinical findings.
Confirmation with elevated amylase level
 Leukopenia with a relative lymphocytosis was a
common finding
 Today, in patients with parotiditis of >2 days 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.

 IgG
antibody tests may cross react
with antibodies to parainfluenza virus
 More commonly, an EIA for mumps
IgM antibody is used to identify
recent infection.
 Skin testing for mumps is neither
sensitive nor specific and should not
be used.
DIFFERENTIAL DIAGNOSIS
parainfluenza 1and 3
 influenza A
 Cytomegalovirus
 Epstein-Barr virus
 enteroviruses,
 lymphocytic choriomeningitis virus
 HIV

usually
caused
by
Staphylococcus aureus, is unilateral, extremely
tender, and associated with an elevated white
blood cell count, and may have purulent
drainage from the Stensen duct.
 Submandibular or anterior cervical adenitis
 collagen vascular diseases such as Sjogren
syndrome, systemic lupus erythematosis
 tumor.

Purulent
parotitis,
Parotitis .
Complications
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Aseptic meningitis
Encephalitis
Orchitis, Oophoritis
Pancreatitis
Thyroiditis
Cardiac Involvement (endocardial fibroelastosis.)
Arthritis:monoarthritis, and migratory polyarthritis
usually occurs within 3 weeks of onset of parotid
swelling.
It is generally mild and self-limited
Meningitis
Meningoencephalitis
The most common complications of
mumps are meningitis, with or without
encephalitis, and gonadal involvement.
 Symptomatic CNS involvement occurs in
10-30% of infected individuals, but CSF
pleocytosis has been found in 40-60% of
patients with mumps parotitis.

The meningoencephalitis may occur before,
along with, or following the parotitis. It most
commonly will present 5 days after the
parotitis.
 Infants and young children will have fever,
malaise, and lethargy, while older children,
adolescents, and adults will complain of
headache and demonstrate meningeal signs.
 symptoms resolve in 7-10 days

Mumps meningitis
Pleocytosis of 200-600/mm3 with a
predominance of lymphocytes.
 The glucose is normal in most patients, but a
moderate hypoglycorrhachia (20-40 mg/dL)
may be seen in 10-20% of patients.
 Protein is normal or mildly elevated.

Transverse myelitis
 Aqueductal stenosis
 Facial palsy.
 Sensorineural hearing loss

Orchitis and Oophoritis
In adolescent and adult males, epidymoorchitis
is 2nd only to parotitis as a common finding in
mumps.
 following puberty it occurs in 30-40% of males

 Moderate
to high fever, chills, and
exquisite pain and swelling of the
testes.
 In ≥1/3of cases the orchitis is
bilateral.
 Atrophy of the testes may occur, but
sterility is rare even with bilateral
involvement.
 Oophoritis is uncommon
Pancreatitis
May occur in mumps with or without parotid
involvement.
 Severe disease is rare, but fever,epigastric pain
, and vomiting are suggestive
 May be associated with the subsequent
development of diabetes mellitus

Thyroiditis
Rare following mumps.
 It has not been reported without parotitis
and may occur weeks following the acute
infection.
 Most cases resolve, but some become
relapsing and result in hypothyroidism.

Treatment
There
is no specific anti-viral
drug therapy.
Treatment is supportive by
treating symptoms, using
antipyretics and analgesics.
Child care







The child must rest in bed until the fever goes away.
Isolate the child, to prevent spreading the disease to
other.
Use analgesics and anti-pyretic to ease symptoms.
Avoid food that require chewing.
Avoid sour foods that stimulate saliva production.
Drink plenty of water.
Use cold compress to ease the pain of swelling
glands.
Prognosis
 In
the absence of complications
recovery is usual.
Prevention
A live attenuated vaccine is available
(MMR)..
 The vaccine is protective. Immunity appears
to be long lasting, with existing serologic
and epidemiologic evidence indicating
protection for >25 yr
