Fever and Rash by xfpXVUwB

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									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
‫پوستو‬
‫(طاول)‬   ‫بول‬
   ‫ندول‬
‫(اریتم ندوالر)‬
 ‫اولسر‬
‫نکروتیک‬
‫گانگرن (پدیده ی‬
‫اکسفولیاسیون یا‬
     ‫پوسته ریزی‬
‫واسکولیت‬
‫کهیر‬
 ‫توزیع‬
‫محیطی‬
Classic Childhood
Exanthems
1.   Measles
2.   Scarlet fever
3.   Rubella )“German measles”(
4.   Atypical scarlet fever
5.   Erythema Infectiosum
6.   Roseola
Today, dozens of exanthems
are recognized:
   Adenovirus               Rocky Mountain
   Anthrax                   spotted fever
   Mononucleosis            Relapsing fever
   Colorado tick fever      Meningococcemia

   Mumps                    Typhus
   Cat-scratch fever        Hand-foot-mouth
                              disease
   Rat-bite fever
                     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       Respiratory
                       Airborne

   Temporal pattern Peak in late winter–
    spring

   Communicability   4 days before to 4 days
    after
                      rash onset
#1 Measles
Rash and Disease
 Enanthem: Koplik spots = gray
  pinheads, ring of erythema, buccal
  mucosa. 0.5–2d.
 Exanthem: erythematous blanching
  macules.
     Startsforehead, 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).
            laryngo-tracheobronchitis,
     Rarely,
      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 immuno-
  compromised
 VZIG if pregnant, premature, or
  immunocompromised
Measles Vaccine

 Composition   Live virus
 Efficacy      95% (range,
  90%-98%)
 Duration of
  Immunity      Lifelong
 Schedule      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
#2- Scarlet Fever
   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:
   Scarlet fever (scarlatina) is an exotoxin-
    mediated 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
   Strawberry tongue
   Exudative pharyngitis
   Generalized; spares palms and soles
   Pinpoint papules
   Desquamation of the tips of the fingers and toes
Sex:
   Males and females are affected
    equally.
Age:
   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:
   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:
   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.
   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.
       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.
     Kitsare 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.
   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:
    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 first-
    generation 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
   Rheumatic fever
   Acute renal failure from poststreptococcal
    glomerulonephritis
Prognosis:
 The prognosis is excellent; most
  patients fully recover.
 Attacks may recur.
    Rubella (German Measles)
   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

   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
   Exanthem:
     Startsface, 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.

   Low-grade fever, pruritus possible.
             Congenital Rubella

   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
          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
           Laboratory Diagnosis

   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


   Attenuated live vaccine (MMR)
   Seroconversion occurs in over 95%
   Protection persists for more than 20 years
   Administration in pregnancy is contra-
    indicated
   Pregnancy should be avoided for the month
    following vaccination
#3 Rubella
   Diagnosis
     Acute  and convalescent titers
     rubella IgM antibody (esp. for exposed
      pregnant women)
   Treatment
     Symptomatic.
     NSAIDs   for arthritis.
#3 Rubella
   Complications
                 polyarthritis in girls, young
     Self-limiting
      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

   “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
     IgMand IgG serologies, acute and
     convalescent antibody titers, DNA
     hybridization
   Treatment
     Symptomatic.
         and transfusions if hematologic
     IVIG
     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.
             IgM and IgG for acute and
     Specific
     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
   Picornavirus

   Icosahedral, positive sense, linear, ssRNA

   Two groups: A and B

   Group A:
      Herpangina (vesicular pharyngitis)
      Hand – Foot – and – Mouth disease
      Acute hemorrhagic conjunctivitis


   Group B:
      Pleurodynia (epidemic myalgia)
      Myocarditis
      Meningoencephalitis
Hand, Foot, and Mouth disease

 Virus: Enteroviruses
 Demographics
     Summer
    6   mo to 13 yr
   Prodrome Brief. Sore throat, anorexia,
    malaise, low-grade fever.
Hand, Foot, and Mouth
disease
   Diagnosis
     Clinical
     Specificserotype 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
   Enanthem:
     Oral mucosal vesicles that erode to form
      ulcers 2 mm to 2 cm in diameter.
     Painful!

   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


   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

   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

   Incubation period: 14 – 15 days

   The patient is infectious for 2 days before and up to
    5 days after onset

   The rash is most dense on the trunk and head

   Macules ---- Papules ---- Vesicles ----
    Pustules
                 Complications

   Secondary bacterial infection (commonest)

   Pneumonia

   CNS
      cerebellar ataxia syndrome
      acute encephalitits
          Varicella in pregnancy
   Varicella virus can cross the placenta following
    viremia and infect the fetus

   Two types of intra-uterine infection

   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)

   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

   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.
   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
   Purulent   parotitis, 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.
Parotitis .
                 Complications
   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
 Inthe 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

								
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