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Dr. Athl Humo
Diffuse erythema:
Bacteria: scarlet fever, toxic shock syndrome(staph. aureus),
Staphylococcal scalded skin syndrome(4S).
Virus: EBV, HBV.
Bacteria: mycoplasma.
Virus: measles, rubella, roseola, fifth disease, EBV
Bacteria: scarlet fever(group A streptococcus)
Virus: Herpes simplex, varicella-zoster.
Bacteria: staphyllococcal bullous impetigo.
 Virus: adenovirus, atypical measles.
 Bacteria: meningococcemia
 Mumps
is an acute self-limited infection, now
unusual in developed countries because of
widespread use of vaccination.
 Although no longer common in countries with
extensive vaccination programs, mumps remains
endemic in the rest of the world, warranting
continued vaccine protection.
 It caused by mumps virus which is a singlestranded RNA virus.
Mumps infection occurred more often in the winter and
spring months.
 Mumps is spread from person to person by respiratory
 Virus appears in the saliva from up to 7 days before to as
long as 7 days after onset of parotid swelling. The period
of maximum infectiousness is 2 days before to 5 days
after onset of parotid swelling.
The incubation period is 16-18 days resulting 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 presentation:
 A prodrom 1-2 days and consisting of fever, headache, and vomiting.
 Parotitis then appears and may be unilateral ,then becomes bilateral in about
70% of cases. The parotid gland is tender, and may be accompanied by ear pain
on the ipsilateral side. Sour or acidic foods may enhance pain in the parotid. As
swelling progresses, the angle of the jaw obscured and ear lobe may be lifted
upward and outward.
 The opening of Stensen duct may be red and edematous.
 The parotid swelling peaks in approximately 3 days, then gradually subsides over
7 days. Fever and the other systemic symptoms resolve in 3-5 days.
A morbilliform rash is rarely seen.
Submandibular salivary glands may also be involved or may be enlarged
without parotid swelling.
Edema over the sternum due to lymphatic obstruction may also occur.
Parotid swelling may be caused by many other infectious and
noninfectious conditions.
 Viruses that cause parotitis include: parainfluenza1 & 3
viruses, influenza A virus, CMV, HIV…
 Purulent parotitis, is usually caused by Staphylococcus
aureus, unilateral, extremely tender, and is associated
with an elevated white blood cell count, and may involve
purulent drainage from Stensen duct.
 Submandibular or anterior cervical adenitis due to a
variety of pathogens may also be confused with parotitis.
 Other noninfectious causes of parotid swelling include:
obstruction of the Stensen duct, collagen vascular diseases
such as SLE, and tumor.
 The
most common complications of mumps are
meningitis, with or without encephalitis, and
 Uncommon complications include deafness, optic
neuritis, facial palsy, pancreatitis, pneumonia,
nephritis and thrombocytopenia.
 Maternal infection with mumps during the 1st
trimester of pregnancy results in increased fetal
loss. No fetal malformations have been
associated with intrauterine mumps infection.
 Symptomatic
meningoencephalitis. occurs in only
10-30% of mumps cases, but CSF pleocytosis has
been found in 40-60% of patients as subclinical
more than apparent meningitis.
 The meningoencephalitis is usually benign, may
occur before, along with, or following the
 It most commonly manifests 5 days after the
 Involvement
in young boys is rare, but in
adolescent and after puberty, orchitis occurs in
30-40% of male cases.
 It begins within days following onset of parotitis
in the majority of cases and is associated with
moderate to high fever, chills, and exquisite pain
and swelling of the testes.
 Atrophy of the testes may occur, but sterility is
rare even with bilateral involvement.
 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 12-15 mo of age for the 1st dose and
4-6 yr of age for the 2nd dose.
Measles (rubeola) is highly contagious, owing to
widespread vaccination, endemic transmission is
 It is caused by a single- stranded RNA paramyxovirus.
 Measles virus is transmitted by droplets or the airborne
 Infected persons are contagious from about 3 days
before to 6 days after the appearance of rash and
immunocompromised persons can have prolonged
excretion of contagious virus.
Measles infection is divided into four phases: incubation,
prodromal(catarrhal), exanthematous (rash), and recovery.
The incubation period is 8 to 12 days from exposure to
symptom onset.
The prodromal period (3-day): characterized by cough, coryza,
conjunctivitis, photophobia, and increasing fever. The
pathognomonic Koplik spots (gray-white, sand grain-sized dots
on the buccal mucosa opposite the lower molars) that last 12 to
24 hours, it present in 50-70%. The conjunctiva may reveal a
characteristic transverse line of inflammation along the eyelid
margin (Stimson line).
Symptoms increase in intensity for 2-4 days until the 1st day of
the rash (fever 40° C to 40.5°C).
Koplik spots
The exanthematous phase:
macular rash begins on the head (often above the hairline)
and spreads over most of the body in a cephalad to caudal
pattern over 24 hours. Areas of the rash often are confluent.
The rash fades in the same pattern, and illness severity is
related to the extent of the rash. It may be petechial or
hemorrhagic (black measles). As the rash fades, it undergoes
brownish discoloration and desquamation.
Of the major symptoms of measles, the cough lasts the
longest, often up to 10 days.
Cervical lymphadenitis, splenomegaly, and mesenteric LAP
with abdominal pain may be noted with the rash. Otitis
media, pneumonia, and diarrhea are more common in
infants. Liver involvement is more common in adults.
The diagnosis of measles is almost always based on
clinical and epidemiologic findings.
 Laboratory findings in the acute phase include
 Serologic confirmation is most conveniently made by:
identification of immunoglobulin IgM antibody in serum.
IgM antibody appears 1-2 days after the onset of the rash
and remains detectable for about 1 mo.
 demonstration of a 4-fold rise in IgG antibodies in
acute and convalescent specimens.
 Viral isolation from blood, urine, or respiratory
secretions can be accomplished by culture.
Otitis media is the most common complication of measles infection.
Interstitial (measles) pneumonia or may result from secondary
bacterial infection. Persons with impaired cell-mediated immunity
may develop giant cell (Hecht) pneumonia, which is usually fatal.
Myocarditis and mesenteric lymphadenitis are infrequent
Encephalomyelitis (1 to 2 per 1000 cases) usually occurs 2 to 5 days
after the onset of the rash. Early encephalitis probably is caused by
direct viral infection of brain tissue, whereas later onset
encephalitis is a demyelinating and probably an immunopathologic
Subacute sclerosing panencephalitis is a late (after 8 to 10 years)
neurologic complication of slow measles infection that is
characterized by progressive behavioral and intellectual
deterioration and eventual death.There is no effective treatment.
 Routine
supportive care includes maintaining
adequate hydration and antipyretics.
 The
WHO recommends routine administration of
vitamin A for 2 days to all children with acute
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.
 Live measles vaccine prevents infection and is
recommended as measles, mumps, and rubella (MMR)
for children at 12 to 15 months and 4 to 6 years of age.
 Susceptible household contacts with a chronic disease
or who are immunocompromised should receive
postexposure prophylaxis with measles vaccine within
72 hours of measles exposure or immunoglobulin within
6 days of exposure.
 Rubella,
also known as German measles or 3-day
 It is caused by a single-stranded RNA virus.
 Rubella virus is most contagious through direct or
droplet contact with nasopharyngeal secretions
from 2 days before until 5 to 7 days after rash
 Rubella usually occurs in the spring.
 Transplacental antibody is protective during the
first 6 months of life.
The incubation period for postnatal rubella is typically 16 to 18 days
(range, 14 to 21 days).
The mild catarrhal symptoms of the prodromal phase of rubella may
go unnoticed.
The characteristic signs of rubella are retroauricular, posterior
cervical, and posterior occipital LAP accompanied by an
erythematous, maculopapular, discrete rash. The rash begins on the
face and spreads to the body, lasting for 3 days and less prominent
than that of measles, usually resolves without desquamation. Rosecolored spots on the soft palate, known as Forchheimer spots,
develop in 20% of patients and may appear before the rash.
Other manifestations of rubella include mild pharyngitis,
conjunctivitis, anorexia, headache, malaise, and low-grade fever.
Polyarthritis, usually of the hands, may occur, especially among adult
females, but usually resolves without sequelae. Paresthesias and
tendinitis may occur.
Diagnosis is confirmed by serologic testing:
 IgM antibodies (typically positive 5 days after
symptom onset)
 Fourfold increase in specific IgG antibodies in
paired acute and convalescent sera.
 There
is no specific therapy for rubella.
 Routine supportive care includes maintaining
adequate hydration and antipyretics.
Live rubella vaccine prevents infection and is
recommended as MMR for children at 12 to 15
months and at 4 to 6 years of age.