(V) Childhood Exanthems - 9!22!09

Childhood
Exanthems
Myrna DC San Pedro, MD, FPPS

Department of Pediatrics,
Fatima University Medical Center

Exanthem
The medical name given
to a widespread rash or skin eruption
usually accompanied
by systemic symptoms
such as fever, malaise and headache

Classified as
•  Erythematous
•  Maculopapular
•  Vesiculopustular

Caused by
•  Damage to the skin by the
microorganism
•  A reaction to a toxin produced by the
microorganism
•  An immune response
•  Drug reaction (especially antibiotics)
Childhood Exanthems
Historically, 6 "classical" infectious childhood exanthems
recognized in 1905:
–  1st Disease: Measles (Rubeola) -‐ 17th century
–  2nd Disease: Scarlet fever -‐ 17th century
–  3rd Disease: Rubella (German Measles) -‐ 1881
–  4th Disease: Duke’s Disease, no longer considered a
distinct disease, described in 1900
–  5th Disease: Erythema Infectiosum -‐ 1896
–  6th Disease: Roseola Infantum (Exanthem Subitum) – 1809
In addition:
–  Varicella-‐Zoster Infections
–  Hand-‐Foot-‐and-‐Mouth Disease
Childhood Exanthems
Differential Diagnoses:
–  Dengue Fever
–  Infectious Mononucleosis
–  Kawasaki Disease
–  Meningococcal Septicemia
–  Mycoplasma Pneumoniae
(Erythema Multiforme)
–  Rocky Mountain Spotted
Fever
Measles (Rubeola)
Measles (Rubeola)
•  Etiology: Measles virus, RNA virus, genus Morbillivirus of
family Paramyxoviridae
•  Mode of Transmission: Airborne or droplet
•  Age Incidence: Preschool & school-‐aged children
•  Period of Communicability: 3 days before the rash up to 4–6
days after its onset
•  Incubation Period: 8–12 days
•  Clinical Manifestations:
–  Prodromal phase 3-‐5 days
•  Low-‐ to moderate-‐grade fever
•  3 “C’s”: Coryza, Conjunctivitis often with
photophobia & dry, hacking Cough
Measles (Rubeola)
–  Prodromal phase 3-‐5 days
•  Koplik’s spots
–  Discrete red lesions with bluish white spots in the
center on the buccal mucosa at level of premolars
–  Pathognomonic sign, appears 1-‐4 days prior to rash
–  May last only 12 hr
–  Eruptive phase 2-‐3 days
•  Fever peaks
•  Reddish maculopapular rashes appear on the forehead
(hairline), behind ears & on upper neck, spread
cephalocaudally
Measles (Rubeola)
–  Recovery phase
•  Fever subsides
•  Rashes fade same order appeared
•  Leaving branny desquamation
•  Followed by brownish pigmentation lasting 7-‐10 days
–  Other forms: Modified/subclinical & atypical measles
•  Diagnosis:
–  For typical cases, based purely on clinical grounds
–  For atypical cases
•  Serum IgM Ab appears 1–2 days-‐1 mo after onset of rash
•  >4-‐fold rise in IgG Abs by HAI over 2–4 wk
•  Viral culture from blood, urine or respiratory secretions
Measles (Rubeola)
•  Treatment:
–  Supportive
–  Vitamin A therapy
•  Single capsule of 200,000 IU PO for ≥1 yr of age
•  Single capsule of 100,000 IU PO for 6 mo-‐1 yr
•  Repeat next day & 4 wk later if with evident deficiency
•  Prognosis: Death to case ratio fell from 10 to 1/1000 cases
•  Complications:
–  Factors that make complications more likely:
•  <5 yr of age (especially <1 yr of age) & >20 yr of age
•  Crowding
•  Severe malnutrition in children
•  Low serum retinol levels in children
•  Immunocompromised persons
Measles (Rubeola)
–  Pneumonia is the most common cause of death
•  Caused directly by the virus or as superimposed
bacterial infection
•  Most common bacteria: S. pneumoniae, H. influenzae &
S. aureus
–  Croup, tracheitis & bronchiolitis common in infants &
toddlers
–  Acute otitis media is the most common complication
–  Increased rate of activation of pulmonary tuberculosis
–  Hemorrhagic or “black measles” rare, often fatal
–  Myocarditis is a rare complication
Measles (Rubeola)
–  Encephalitis
•  Acute encephalitis during the exanthem
– 1–3/1000 cases, more in adolescents & adults
– Presents with seizures (56%), lethargy (46%),
coma (28%) & irritability (26%)
– About 15% die & 20–40% with sequelae such as
mental retardation, motor disabilities & deafness
•  Subacute measles encephalitis presents 1–10 mo
following measles in immunocompromised patients
•  Subacute sclerosing panencephalitis (SSPE) insidious
onset 7–13 yr after primary measles mainly in children
& adolescents, most die within 1–3 yr
Measles (Rubeola)
•  Prevention:
– Postexposure prophylaxis
•  Measles vaccine within 72 hr of exposure to prevent or
modify disease
•  Immunoglobulin IM >6 days after exposure
– Immunocompetent 0.25 ml/kg
– Immunocompromised 0.5 ml/kg
– Active immunization
•  Live attenuated monovalent measles vaccine SC or IM at
9 mo
•  Live attenuated measles-‐mumps-‐rubella (MMR) vaccine
1 dose each, SC or IM, at 15 mo, 4–6 yr & >11–12 yr
Scarlet Fever
Scarlet Fever
•  Etiology: Erythrogenic exotoxin–producing Group A
Streptococcus (GAS), also known as Streptococcus pyogenes
•  Mode of Transmission: Direct contact, airborne or droplet
•  Age Incidence: Highest in 3–15 yr, especially school-‐aged
•  Incubation Period: Usually 2–5 days
–  Rapid onset of fever, chills, vomiting & headache
–  Rash appears 24–48 hr after onset or with 1st signs of
illness
•  Diffuse, finely papular, erythematous rashes producing
bright red skin discoloration that blanches on pressure
•  Begins around neck, spreads over trunk & extremities,
usually spares face but cheeks may be erythematous
with circumoral pallor
Scarlet Fever
•  Pastia’s lines: Areas of increased erythema in the deep
creases such as antecubital fossae
–  Rashes begin to fade after 3–4 days followed by
desquamation, 1st on the face, then downward, may
include palms & soles, often resembling a mild sunburn
–  Tonsils are hyperemic, often with white exudate &
oropharynx erythematous
–  Tongue is initially white with prominent swollen papillae
but after several days, desquamates, becoming reddened
“strawberry tongue” appearance
•  Diagnosis:
–  Clinically & epidemiologically
Scarlet Fever
•  Diagnosis:
–  Gold standard: Throat culture on a sheep blood agar plate
–  Rapid antigen detection tests, >95% specificity
–  Elevated or increasing streptococcal antibody titer
•  Treatment:
–  DOC: Penicillin V (phenoxyethylpenicillin) 250 mg bid-‐tid
for ≤60 lb & 500 mg bid–tid for >60 lb PO for 10 days
–  A single injection of Benzathine Penicillin G 600,000 IU for
≤60 lb & 1.2 million IU for >60 lb IM
–  DOC for patients allergic to penicillin: Erythromycin
estolate 20–40 mg/kg/day divided bid–qid PO or
erythromycin ethylsuccinate 40 mg/kg/day divided bid–qid
PO for 10 days
Scarlet Fever
•  Treatment:
–  Alternative for patients allergic to penicillin: Narrow-‐
spectrum oral cephalosporin for 10 days
•  Prognosis:
–  Excellent & complete recovery is the rule
–  When therapy provided within 9 days of onset, acute
rheumatic fever is prevented
–  Acute rheumatic fever
–  Acute poststreptococcal glomerulonephritis
–  Cervical lymphadenitis, peritonsillar abscess,
retropharyngeal abscess, otitis media, mastoiditis &
sinusitis still occur in children
Rubella (German Measles)
•  Etiology: Rubella virus, RNA virus, genus Rubivirus of family
Togaviridae
•  Mode of Transmission: Direct contact, droplet or fomite
•  Age Incidence: Most common in preschool & school-‐aged
•  Period of Communicability:
–  Postnatal: 5 days before to 6 days after onset of rash
–  Congenital Rubella Syndrome (CRS): Children with CRS
may excrete virus in respiratory secretions up to 1 yr old
•  Incubation Period: 14-‐21 days
–  Postnatal Rubella
•  Prodrome of low-‐grade fever, sore throat, red eyes
without photophobia, headache, malaise & anorexia
•  One day before rash or 2nd-‐5th day of illness, markedly
tender suboccipital, postauricular & anterior cervical
lymphadenopathy is a characteristic sign
•  In children, 1st manifestation is usually the rash, which is
variable & not distinctive
– Small, irregular pink macules that coalesce & spread
centrifugally to the trunk & extremities
– The rash fades from face as it extends to rest of
body so that whole body may not be involved at any
1 time
– The duration of rash is generally 3 days & usually
resolves without desquamation
•  25–40% of children may not have a rash
•  Forchheimer spots: Tiny, rose-‐colored lesions or
petechial hemorrhages on the soft palate about the
time of onset of the rash
–  Congenital Rubella Syndrome
•  Nerve deafness is the single most common finding
•  “Salt-‐and-‐pepper” retinopathy is the most common
ocular abnormality
•  Unilateral or bilateral cataracts most serious eye
finding, occurring in about ⅓ of infants
•  Neurologic abnormalities common & may progress
•  Cardiac abnormalities occur in ½ of children infected
during 1st 8 wk of gestation
– Patent ductus arteriosus is the most frequently
reported
– Followed by lesions of pulmonary arteries &
valvular disease
•  Other defects are growth retardation, glaucoma,
radiolucent bone disease, hepatosplenomegaly,
thrombocytopenia, jaundice & “blueberry muffin”
skin lesions
•  The risk of congenital defects increases the earlier in
pregnancy the disease occurs:
– At 1-‐2 mo gestation: 40-‐60% risk multiple defects &
spontaneous abortion
– At 3 mo gestation: 30-‐35% risk of single defect
– At 4 mo gestation: 10% risk of single defect
– At 5-‐9 mo gestation: Occasionally associated with
single defect
•  Diagnosis:
–  Most common diagnostic test is rubella IgM enzyme
immunosorbent assay
•  Diagnosis:
–  Viral isolation from throat, blood or urine culture
–  Reverse transcriptase PCR test
•  Treatment: Non-‐specific
•  Prognosis:
–  Postnatal infection excellent prognosis
–  Long-‐term outcomes of CRS less favorable & variable
–  Postinfectious thrombocytopenia in 1:3000 cases, more
frequent among girls, manifests about 2 wk after onset
of rash with petechiae, epistaxis, GIT bleeding &
hematuria
–  Arthritis of small joints of hands within 1 wk of onset of
rash more common among adult women
–  Guillain-‐Barré syndrome & peripheral neuritis
–  Myocarditis is a rare complication
–  Encephalitis is the most serious complication, 2 forms
•  Postinfectious 1/5000 cases, appears within 7 days
following onset of rash, mortality rates of 20%
•  Progressive rubella panencephalitis (PRP), extremely
rare complication of either postnatal rubella or CRS,
onset & course similar to measles SSPE, death occurs
2–5 yr after onset
•  Prevention:
–  Live-‐attenuated rubella vaccine as MMR per SC or IM
•  Given 1 dose each at 15 mo, 4–6 yr & >11–12 yr
•  As postexposure prophylaxis if given within 3 days of
exposure
•  Contraindicated in pregnancy, severely
immunocompromised (e.g., transplant patients) &
those given standard IgG past 3 mo
•  Adverse reactions uncommon in children, include
fever (5–15%), rash (5%), arthralgia (25%), arthritis
(10%), peripheral neuropathies & transient
thrombocytopenia
•  Prevention:
–  Pregnant women
•  As soon as exposed, 2 specimens, 1 for testing, other
saved
– 1st specimen for rubella IgG specific Ab testing
» If (+), mother immune
» If (-‐), obtain 2nd specimen 2–3 wk later & test
concurrently with saved specimen
– 2nd specimen
» If (+), mother seroconverted, recent infection
» If (-‐), obtain 3rd specimen 6 wk after
exposure & test concurrently with saved
specimen
•  Prevention:
–  Pregnant women
– If both 2nd & 3rd specimens (-‐), infection has not
occurred
– A (-‐) 1st specimen & a (+) test result in either 2nd
or 3rd specimen indicate mother has
seroconverted, suggesting recent infection
•  Standard IgG 0.55 ml/kg IM considered if
termination of pregnancy is not an option for
recently infected
– May reduce risk of clinically apparent infection
but does not guarantee prevention of fetal
infection
Erythema Infectiosum
(Fifth Disease)
(Fifth Disease)
•  Etiology: Parvovirus B19, DNA virus, genus Erythrovirus of
family Parvoviridae
•  Mode of Transmission: Droplet, also by blood products
•  Age Incidence: Most prevalent in school-‐aged children
•  Incubation Period: 4–28 days, average of 16–17 days
–  Prodromal phase: Low-‐grade fever, headache &
symptoms of mild URTI
–  Hallmark is characteristic rash in 3 stages, not always
distinguishable
•  1st stage: Erythematous facial flushing giving a
“slapped-‐cheek” appearance
(Fifth Disease)
•  2nd stage: Diffuse macular erythema spreads rapidly or
concurrently to trunk & extremities, spares palms &
soles, sometimes pruritic, followed promptly by central
clearing giving a lacy, reticulated appearance
•  3rd stage: Rash resolves spontaneously without
desquamation but tends to wax and wane over 1–3 wk,
recurs with exposure to sunlight, heat, exercise & stress
–  Duration of rash variable but averages about 10 days
•  Diagnosis:
–  Based on clinical presentation of the typical rash
–  Anti-‐B19 IgM determination best marker of recent infection
on a single serum sample
(Fifth Disease)
•  Diagnosis:
–  Seroconversion of anti-‐B19 IgG Abs in paired sera can also
be used to confirm recent infection
–  The virus cannot be isolated by standard cell culture so
methods to detect viral particles or DNA such as PCR or
nucleic acid hybridization necessary to establish diagnosis
in immunocompromised persons
•  Treatment:
–  Supportive
–  Isolation unnecessary, rash immune-‐mediated
•  Complications: Arthralgia or arthritis in adolescents & adults,
thrombocytopenic purpura & rarely, aseptic meningitis
Roseola Infantum
(Exanthem Subitum or Sixth Disease)
Roseola Infantum
•  Etiology: Human herpesvirus 6 (HHV-‐6) & Human herpesvirus
7 (HHV-‐7), DNA viruses, belong to β-‐herpesvirus subfamily of
Herpesviruses
•  Mode of Transmission: Person to person (from saliva of
healthy persons that enters host through oral, nasal or
conjunctival mucosa)
•  Age Incidence: >95% occur in <3 yr, with peak at 6–15 mo old
•  Incubation Period: 5–15 days, average of 10 days
–  Generally starts with high temperature, usually 37.9-‐40°C,
average 39°C
–  Most behave normally despite high temperatures
Roseola Infantum
–  Seizures may occur in 5–10% during febrile period
–  Infrequent complaints include rhinorrhea, sore throat,
abdominal pain, vomiting & diarrhea
–  Nagayama spots: Erythematous papules or ulcers on soft
palate and uvula common in infants in Asian countries (65%)
–  Fever lasts 3–5 days then typically resolves abruptly (crisis)
but occasionally drops gradually over 24–36 hr (lysis)
–  During defervescence or within 12–24 hr of fever resolution,
diffuse, small, rose-‐colored, maculopapular rash develops
on the trunk then spreads centrifugally
–  The non-‐pruritic rash fades after 1–3 days with no
desquamation nor pigmentation
Roseola Infantum
•  Diagnosis:
–  Primarily on the basis of age, history & clinical findings
–  Specific testing for HHV-‐6 or HHV-‐7 using serology, virus
culture & PCR
•  Treatment:
–  Supportive in healthy persons
–  Antivirals warranted for immunocompromised: ganciclovir
& cidofovir
•  Prognosis: Excellent, no obvious sequelae
–  Hemiparesis & mental retardation, rare, attributable to
brain anoxia during prolonged febrile seizures
–  Encephalitis, hepatitis & pneumonitis, rare
Varicella (Chickenpox)
•  Etiology: Varicella-‐zoster virus (VZV), DNA virus, belong to
α-‐herpesvirus subfamily of Herpesviruses; primary
response of a susceptible host
•  Mode of Transmission: Direct contact, airborne or droplet
•  Age Incidence: Primarily in children <10 yr
•  Period of Communicability: 24-‐48 hr before the rash until
vesicles are crusted, usually 3–7 days after onset of rash
•  Incubation Period: 10-‐21 days
–  Prodrome 1-‐2 days before rash: Moderate fever,
malaise, anorexia, headache & occasionally mild
abdominal pain, which persist 2–4 days after onset of
rash
•  Temperature usually 37.8-‐38.9oC but may be as high as
41.1°C
–  The exanthem starts as intensely pruritic erythematous
macules evolving into papules then into “teardrop” vesicles
then clouding & umbilication of lesions begin in 24–48 hr
then crusting
•  While initial lesions are crusting, new crops form & the
simultaneous presence of lesions in various stages of
evolution is characteristic
•  Lesions appear 1st on the trunk then spread peripherally
•  Crops of new vesicles continue to erupt for 3-‐4 days
•  The severity of illness ranges from <10 to >1500 lesions
with average of 300
–  Neonatal Varicella: Infants whose mothers develop varicella
5 days before to 2 days after delivery, often severe
–  Congenital Varicella Syndrome
•  25% of fetuses may become infected when pregnant
contract varicella early in pregnancy but clinically
apparent disease uncommon
•  Up to 2% of fetuses whose mothers had varicella in the
1st 20 wk of pregnancy demonstrate a VZV embryopathy
– Affects limbs, skin, eyes & brain development
– Characteristic cutaneous lesion: Cicatricial, zigzag
scarring in a dermatomal distribution, often
associated with atrophy of the affected limb
•  Diagnosis:
–  Direct fluorescence assay of cells from cutaneous lesions
–  PCR amplification testing
–  Tissue culture methods
–  4-‐fold rise in IgG Abs also confirmatory of acute infection
•  Treatment:
–  To be most effective, initiate treatment as early as possible,
preferably within 24 hr of the onset of the rash
–  Acyclovir 20 mg/kg/dose, maximum 800 mg/dose, given as
4 doses/day PO for 5 days for
•  Uncomplicated varicella in nonpregnant >13 yr of age
•  Children >12 mo old with chronic cutaneous or
pulmonary disorders
•  Treatment:
•  Receiving short-‐term, intermittent, or aerosolized
corticosteroids
•  Receiving long-‐term salicylate therapy
•  Possibly 2nd cases in household contacts
–  Intravenous therapy acyclovir 500 mg/m2 every 8 hr for
severe disease & for varicella in immunocompromised &
other high-‐risk patients even after 72 hr duration of rash
–  Some experts recommend famciclovir or valacyclovir in
older children who can swallow tablet
–  Treatment is continued for 7 days or until no new lesions
have appeared for 48 hr
•  Prognosis:
–  Mortality rate 2–3/100,000 lowest among 1–9 yr of age
•  Infants 4x greater risk of dying
•  Adults 25x greater risk of dying
–  Mortality rate of
•  Untreated immunocompromised children 7–14%
•  Untreated adults with pneumonia about 50%
–  Pneumonia within 1–6 days after onset of rash, most
common cause of death
–  Secondary skin bacterial infections 5% of children
–  Hemorrhagic conditions
–  CNS complications: Encephalitis 1/50,000 cases & acute
cerebellar ataxia 1/4000 cases
•  Prevention:
–  Postexposure prophylaxis
•  Varicella vaccine to normal children within 3–5 days
after exposure to prevent or modify
•  Oral acyclovir given late in the incubation period may
modify in the normal child, however, its use in this
manner not recommended until further evaluated
•  Human varicella-‐zoster immune globulin (VariZIG) 1
vial (125 units)/10 kg increment (maximum 625 units)
IM within 96 hr after exposure to
immunocompromised children, pregnant women &
newborns exposed to maternal varicella
•  Prevention:
–  Postexposure prophylaxis
•  Intravenous immune globulin (IVIG) 400 mg/kg
administered once within 96 hr of exposure
–  Active immunization
•  Children: Live attenuated monovalent varicella
vaccine SC at 12–18 mo, 4–6 yr & >11–12 yr or
combined with measles-‐mumps-‐rubella vaccines
(MMRV) SC at 15 mo, 4–6 yr & >11–12 yr
•  Children, adolescents & adults without evidence of
immunity: Live attenuated monovalent varicella
vaccine SC 2 doses, at least 4 wk apart
Herpes Zoster (Shingles)
•  Etiology: Varicella-‐zoster virus (VZV), DNA virus, belong to

a-‐herpesvirus subfamily of Herpesviruses; reactivation of a
latent VZV infection
•  Mode of Transmission:
–  Due to stress, trauma, radiation, malignancy &
immunocompromised conditions
–  In children, when infected in utero or in the 1st yr of
life, when receiving immunosuppressives for
malignancy or other diseases & those who have HIV
infection
•  Age Incidence: Very rare in healthy children <10 yr, 75% of
cases >45 yr of age
–  Vesicular lesions clustered within 1 or less commonly 2
adjacent dermatomes
–  Unlike in adults, in children
•  Lesions infrequently associated with localized pain,
hyperesthesia, pruritus & low-‐grade fever
•  The rash is mild, with new lesions appearing for a
few days then complete resolution usually within 1–2
wk
•  Diagnosis:
–  The skin lesions of varicella & herpes zoster have
identical histopathology & infectious VZV is present in
both
•  Diagnosis:
–  Direct fluorescence assay of cells from cutaneous lesions
–  PCR amplification testing
–  Tissue culture methods
•  Treatment:
–  In healthy children
•  Less severe disease & postherpetic neuralgia rare so if
uncomplicated, an antiviral agent not always necessary
•  Some experts would treat with oral acyclovir 20 mg/kg/
dose, maximum 800 mg/dose, to shorten the duration
of illness
•  Corticosteroids not recommended
•  Treatment:
–  In immunocompromised children
•  Can be severe & disseminated, may be life
threatening
•  At high risk for disseminated disease: Acyclovir 500
mg/m2 or 10 mg/kg every 8 hr IV
•  Uncomplicated, at low risk for visceral dissemination:
Oral acyclovir, famciclovir, or valacyclovir are options
–  In healthy adults
•  Acyclovir 800 mg 5x a day PO for 5 days, famciclovir
500 mg tid PO for 7 days & valacyclovir 1000 mg tid
PO for 7 days to reduce the duration of illness & the
risk for postherpetic neuralgia
•  Corticosteroids improve quality of life in the elderly
•  Prognosis: Approximately 4% of patients suffer a 2nd
episode of herpes zoster but 3 or more episodes rare
–  Postherpetic neuralgia very unusual in children but can
be a severe problem in adults, may persist for months,
requiring care by a specialist in pain management
–  Transverse myelitis with transient paralysis is a rare
complication of herpes zoster
–  Immunocompromised patients may experience
disseminated cutaneous disease as well as visceral
dissemination with pneumonia, hepatitis, encephalitis,
and disseminated intravascular coagulopathy
–  Severely immunocompromised children may have
unusual, chronic or relapsing cutaneous disease,
retinitis or CNS disease without rash
•  Prevention:
–  The risk lower after vaccine than after natural VZV
infection among immunocompromised children
–  A new VZV vaccine licensed 2006 as single
immunization for >60 yr of age to prevent reactivation
& to decrease frequency of postherpetic neuralgia
–  Exposure of a high-‐risk patient an indication for VariZIG
–  Passive antibody administration does not reduce risk
for herpes zoster or alter the clinical course
Hand-‐Foot-‐and-‐Mouth Disease
(HFMD)
(HFMD)
•  Etiology: Coxsackie A16 virus, RNA virus, genus Enterovirus of
family Picornaviridae; can also be caused by enterovirus 71,
coxsackie A 5, 7, 9, 10 & coxsackie B 2, 5 viruses
•  Mode of Transmission: Person to person, fecal-‐oral, respiratory
routes, fomites & mother to neonate, prenatally or peripartum
•  Age Incidence: 25% symptomatic infections in children <1 yr
•  Period of Communicability: Respiratory tract shedding <1–3 wk
whereas fecal shedding continues up to 7–11 wk postinfection
•  Incubation Period: 3–6 days
–  Prodrome of 2-‐36 hr: Low-‐grade fever, malaise, cough,
anorexia & abdominal pain
(HFMD)
–  Painful, initially vesicular then ulcerating lesions occur
anywhere in the mouth but most commonly on the hard
palate, tongue & buccal mucosa
–  Maculopapular, vesicular &/or pustular lesions on hands,
fingers, feet, buttocks & groin appears shortly after oral
•  Lesions on hands & feet usually tender vesicles 3-‐7 mm,
more common on dorsal but also on palms & soles
•  Hands more commonly involved than feet
•  Buttock lesions do not usually progress to vesiculation
–  Oral lesions resolve without treatment in 5-‐7 days while skin
lesions gradually disappear over 5-‐10 days without scarring
(HFMD)
•  Diagnosis:
–  Clinical & epidemiological
–  Viral culture using is the gold standard for confirmation
–  Direct testing of patient specimens for enterovirus
nucleic acid more sensitive & faster results
–  Serology generally less useful because requires
presumptive knowledge of infecting serotype
•  Treatment:
–  Supportive for healthy persons
–  IVIG, interferon & oral pleconaril for severe &
complicated cases & immunocompromised
(HFMD)
•  Prognosis:
–  Excellent
–  Increased severity with young age, male sex, poor
hygiene, overcrowding & low socioeconomic status
–  Disseminated vesicular rashes may complicate pre-‐
existing eczema
–  Enterovirus 71 often more severe with increased
neurologic disease: Brainstem encephalomyelitis (90%)
acute flaccid paralysis (10%) & aseptic meningitis (7%)
–  Spontaneous abortion or IUGR with 1st trimester
infection
(HFMD)
–  Other complications include myocarditis, pulmonary
edema, shock & even death especially in young children
•  Prevention:
–  Basic hygiene, such as handwashing
–  Avoidance of shared utensils & drinking containers &
other potential fomites
–  Disinfection of contaminated surfaces
–  Appropriate treatment of drinking water & swimming
pools may be important to prevent transmission
–  Infection control techniques
–  Prophylactic administration of IM or IV IgG
Differential Diagnosis
Infectious mononucleosis (glandular
fever) is a common acute infection
caused by the Epstein-‐Barr virus (EBV),
member of the γ-‐herpesviruses. It is
marked by prolonged fever,
pharyngitis, and generalized
lymphadenopathy. Other findings
include bruising, rashes, an increase in
mononuclear white blood cells & other
atypical lymphocytes & abnormal liver
function. The disease is usually
transmitted by droplet infection but is
not highly contagious. Young people
are most often affected. In childhood,
the disease is mild and usually
unnoticed. The older the person, the
more severe the symptoms are likely
to be. Infection gives permanent
immunity.
Erythema multiforme is an allergic
reaction with many different causes.
The most common are Mycoplasma
pneumoniae, herpes simplex viruses
& drug reactions (sulfa drugs).
Erythema multiforme is not
contagious. It can affect people of
all ages and is often more severe in
children and young adults. It often
starts as a red rash on the palms,
soles, and back of the hands & can
spread to the trunk, face and mouth
in severe cases. Some people have
lesions only in the mouth. As the
skin lesions age they often look like
small targets with purple to dusky
centers surrounded by red rings.
The condition can be associated
with fever, muscle aches and
malaise.
Case 1
An infant with fever and rash
A 7-‐month-‐old infant
presents with 3 days of
fever up to 40OC, a
mildly injected pharynx,
mild cervical
adenopathy and
diarrhea. On the 4th day
of the illness, the fever
ceases and a measles-‐
like rash appears.
Case 2
A 3-‐month-‐old infant with low-‐grade fever and rash
HPI: A week ago, the nurse at the
abandon-‐child-‐home noticed several spots
of skin lesions on the patient. He was also
noted to have low-‐grade fever several
days ago. On the day of admission, he was
less active.
PH: Since he was abandoned by his
parents when he was born, his past history
was unknown.
PE: Body temp was 38OC. Other vital signs
were within normal limits.
Skin: There were 3 crops of
vesiculopapular skin lesions at the chest
wall and back. The 1st crop was the at the
left posterior chest wall, the 2nd at the
right posterior chest wall and the last crop
was at left anterior chest wall.
Other systems: Within normal limits.
Case 3
A boy with a rash
The boy was first seen at the clinic

the day before because of a
widespread rash over the whole
body. He had been treated with
antibiotics for a sore throat 2
weeks before and it was initially
thought that the rash might have
been due to antibiotics even
though he had finished the course
of antibiotics 2 weeks ago.

The next day, the boy's rash got
worse and from the picture the
rash covered almost the whole leg
with just little areas of normal skin:
a ‘sea’ of red with ‘islands of
sparing’ normal skin.
Case 4
An 18-‐month-‐old girl with fever and vesiculopapular rash
HPI: She had been well since birth but 5 days
PTA developed low grade fever, dry cough &
running nose. 2 days PTA, low grade fever
persisted & vesiculopapular lesions were
noted at both palms & soles. 1 day PTA,
although the fever subsided, the skin lesions
increased in number but there was no pain
nor itching.
PH: She has had normal growth &
development & her immunizations has been
up-‐to-‐date.
PE: Body temp was 37.8OC. Other vital signs
were within normal limits.
HEENT: Multiple vesicular lesions on
erythematous bases at the mucosa of the oral
cavity including tongue.
Extremities : Multiple vesiculopapular lesions
on erythematous bases on both palms &
soles. Few papular lesions at both wrists,
spreading from palms.
Other systems: Within normal limits.

(V) Childhood Exanthems - 9!22!09

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Childhood

•  Etiology: Varicella-‐zoster virus (VZV), DNA virus, belong to

The boy was ﬁrst seen at the clinic

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•  Etiology: Varicella-‐zoster virus (VZV), DNA virus, belong to