PPS UPEC PIDSP Rashes in Children Module

RASHES IN CHILDREN
Rashes in Children
 ViralExanthems
 Vesiculobullous Lesions
 Purpura/Petechiae
 Diffuse Erythemas with Desquamation
2 Rashes in Children
Viral Exanthems
MACULOPAPULAR
RASH
(red areas of the skin with
small bumps)
VESICULAR RASH
(blisters/fluid-filled)
Maculopapular Rashes
CHILDHOOD VIRAL DISEASES
Rubeola (Measles) Virus
PARAMYXOVIRUS (RNA)
Measles: Disease Review
 Primary viremia 2-3 days after exposure2
 Secondary viremia 5-7 days after exposure with
spread to tissues2
 Morbidity and mortality of measles are greatest in
patients <5y/o and those >20 y/o
1. www.nfid.org, National Foundation for Infectious Disease (accessed Aug 2005)

2. Measles in: William Atkinson, Charles Wolfe eds. Epidemiology & Prevention of Vaccine Preventable Diseases. Dept of Health &
Human Services CDC;7th Edition;2003;96-113
Measles: Disease Review
 Highly contagious virus found throughout
the world1
 Respiratory transmission2
 Incubation period 10-12 days2
 Replication in nasopharynx and regional lymph
nodes2
1. www.nfid.org, National Foundation for Infectious Disease (accessed Aug 2005)

2. Measles in: William Atkinson, Charles Wolfe eds. Epidemiology & Prevention of Vaccine Preventable Diseases. Dept of Health &
Transmission and Immunity
 Transmission
 Droplet infection
 Direct contact
 Period of communicability: 4 days before
and after rashes appear
 Immunity
 Long lasting
 Passive immunity lasts for 5 – 6 months
 Live attenuated vaccine confers lifelong immunity
 Inactivated vaccine 6 – 18 months
Pathogenesis
Upper respiratory passage – nasopharynx or conjunctiva
Epithelial cells infected and virus multiplies
Extension to regional lymphoid tissue
Primary viremia
Multiplication in respiratory epithelium, RES, distant sites
Secondary viremia
Infection in skin and other sites
Virus in blood, respiratory tract, skin and other organs
Viremia, virus in organs

Measles: Clinical Features
Prodrome
 Stepwise increase in fever to >39.5OC or higher
 Cough, coryza, conjunctivitis
 Koplik spots – pathognomonic
 Seen 1 – 2 days before rashes appear
 Whitish pinpoint dots with reddish areola in inner cheeks
opposite lower molars
 Transient
Rash
 2-4 days after prodrome, 14 days after exposure
 Maculopapular, becomes confluent
 Begins on face and head
 Persists 5-6 days
 Fades in order of appearance
 Leaves brawny desquamation
Measles in: William Atkinson, Charles Wolfe eds. Epidemiology & Prevention of Vaccine Preventable Diseases.
Dept of Health & Human Services CDC;7th Edition;2003;96-113
Rash begins around
hairline, on face and
neck, behind ears
Rash spreads
downward to chest
and abdomen
Rash affects arms

and legs last
Measles: Diagnosis
 Clinical picture
 Isolation of measles virus from clinical
specimens
 Serology – IgG, IgM
 Decreased WBC during prodrome and rash
Common Complications
 Life-threatening
 Bronchopneumonia
 Otitis media
 Laryngotracheobronchitis
 Diarrhea
 Blindness
 Flare up of existing TB
Uncommon/Rare Complications
 Myocarditis /Pericarditis – rare
 ITP
 Mesenteric lymphadenitis
 Encephalitis – occurs during rashes, within
8 days from onset
 Convulsions, lethargy, irritability, coma
 20 – 40% with brain damage
 Hemorrhagic/Black measles
 Subacute Sclerosing Panencephalitis (SSPE)
Differential Diagnosis
 Miliaria with acute URTI
 Rubella
 Roseola infantum
 Allergic dermatitis
 Infectious mononucleosis
Inapparent Measles Infection
 Subclinical form of measles
 Individuals with passively acquired antibody:
 infants, recipients of blood products, some
individuals who received the vaccine when
exposed to Measles virus develop some symptoms
 Does not shed the virus and does not transmit
the infection to household contacts
Atypical Measles
 More severe type of measles
 Due to circulating immune complexes that
formed due to an abnormal immune response
to the vaccine
 Occurs in persons vaccinated with an
Inactivated/Killed vaccine (1963-1967)
exposed to natural virus
Treatment and Prevention
 Treatment
 No specific treatment
 Supportive measures – antipyretic, bed rest, fluids
 Vitamin A – reduces morbidity and mortality in
children with severe measles in the developing
world
 Antibiotics for complications
 Prevention
 Live attenuated measles vaccine
 Immune globulin (Ig)
Prevention
 Isolation of patients: from 7th day after exposure until
5 days after the rash appeared
 Measles vaccine: 9 months old
MMR vaccine: (2 doses): 12-15 months old, then 4-
6y/o (minimum interval 4 weeks)
 May be given to 9 months old
 Post-exposure prophylaxis
 Passive immunization with Ig – within 6 days of exposure
(<6 months old or those who are pregnant)
 Vaccine alone within 72 hours from exposure: exposed
children 6 mos. of age or older
Underutilization of Measles Vaccine
The high measles disease burden, despite

an increase in routine measles
immunization coverage,
is attributed mainly to the underutilization
of measles vaccine
These deaths are unacceptable
because measles vaccine is safe,
highly effective and cost-effective
WHO/UNICEF Joint Report: Measles Mortality Reduction And Regional Strategic Plan 2003-2005
Why do we need a 2nd dose of MMR?
 Eradication of measles cannot be achieved with a
single-dose strategy alone
 A second dose of vaccine such as MMR is
recommended by the WHO, to:
 Ensure individuals receive at least one dose
 Ensure immunity to individuals in whom no
immunogenic response occurred with the first dose
 Restore immunity in those whose immunity has waned
World Health Organization, Pan American Health Organization and CDC.MMWR 1997;46(RR-II)
Roseola Infantum
Roseola Infantum
 6th disease, Exanthem subitum
 Etiology
 Human herpesvirus 6 (most cases)
 Human herpesvirus 7
 Echovirus 16
 Transmission
 Probably acquired from saliva of healthy persons and enter
the host through oral, nasal or conjunctival mucosa
Roseola Infantum
 Children < 3 yrs. of age (esp. 6-15mos.)
 Peak incidence Mar – Apr
 Incubation period: 10 -16 days
 Fever – sudden onset, high grade
 subsides after 2 – 3 days
 With lysis of fever – rash appears on face and trunk
 disappears in 1 – 2 days
Roseola Infantum
 Clinical manifestation
 Prodrome period: rhinorrhea, pharyngeal inflammation,
slight conjunctival redness, mild lymphadenopathy
 High-grade fever 3-5 days, may have febrile seizures
 With defervescence maculopapular rash appears
 Trunk, neck, face and proximal extremities for 1 – 3 days
 Diagnosis
 Rashes appear as fever disappears
Roseola Infantum
 PE – normal findings, child active, alert and playful
 Occasionally with full and tense anterior fontanel
 Differential diagnosis
 Measles
 Meningitis
 Treatment
 Symptomatic – antipyretics to lower temperature
 Sedatives or anticonvulsants for seizures
Rose-pink, macular lesions of
Roseola infantum
Erythema Infectiosum
 Fifth disease
 Etiology
 Parvovirus B19
 Transmission
 Respiratory, blood transfusion
Stages of Rash
1. Erythematous and macular – “slapped cheek”
appearance with circumoral pallor and sparing of
nasal bridges
2. Maculopapular rash + pruritus – lacey or reticular
pattern
3. Rash waxes and wanes in 1-3 weeks – rash
recurrence due to heat, cold, exercise, stress
Erythematous and macular

© MEDLibes Online Medical Library
”slapped cheek” appearance
Complications
 Arthropathy – arthritis/arthralgia
 Transient aplastic crisis - arrest in production of red
blood cells may occur in the following conditions:
 Sickle cell disease
 Thalassemia
 Hereditary spherocytosis
 Pyruvate kinase deficiency
 Fetal infection: results in hydrops because of severe
anemia cardiac failure, fetal death, and miscarriage
 Diagnosis
 Serology
 PCR
 Treatment
 Supportive
Rubella Virus
TOGAVIRUS (RNA)
www.med.sc.edu:85/ mhunt/rub1.jpg; accessed in Aug 2005
Rubella Virus: 3-day Measles
 Etiology
 Rubella virus belongs to Rubivirus genus of family togaviridae
 Epidemiology
 Worldwide
 In RP, sporadic
 Highest attack rate in 5 – 9 yrs
 No sex difference
 Transmission
 Respiratory route – droplet infection
 Contact with infected individuals
 Contaminated linen and articles – nasopharyngeal secretion, stool or
urine
German Measles: Pathogenesis
Respiratory transmission of the virus
Replication in the nasopharynx and

regional lymph nodes
Viremia (5-7 days)

Includes placenta and fetus
Signs and Symptoms
 Symptoms (if present) usually mild:
 inflammation of the lymph nodes
 maculopapular rash
 mild catarrhal symptoms
 Adults may feel unwell with fever and loss of
appetite
 Approximately two-thirds of rubella cases not
clinically evident
Clinical features
 Retroauricular, posterior cervical and post-
occipital lymphadenopathy
 most characteristic sign
 appear 24 hours before the rash appears up to the neck
 Rash begins on the face and spreads quickly.
 Evolution is so rapid that the rash may be fading on
the face by the time it appears on the trunk
Rash begins as red spots
on the face
Rash spreads quickly to

trunk and extremities
Rash is highly variable;

often there is no rash
Rubella rash
© Copyright Dr. CW Leung,

Department of Paediatrics and
Adolescent Medicine, Princess
Margaret Hospital, Hong Kong
Clinical Features
 Rash clears by the 3rd day, minimal desquamation
 Fever is low-grade or absent for 1-3 days
© Copyright Dr. CW Leung, Department of

Paediatrics and Adolescent Medicine,
Source: Centers for Disease Control and Prevention Princess Margaret Hospital, Hong Kong
Rubella: Complications
 Rare in childhood or adulthood
 Arthritis or arthralgia in 2% of cases
 Mainly females
 CNS complications (i.e., post-infectious encephalitis)
occur in adults at a rate of 1/6000 cases
 Congenital Rubella Syndrome (CRS)
German Measles (Rubella)
 Reservoir
 Humans
 Transmission
 Respiratory – person-to-person
 Communicability
 7 days before to 5-7 days after rash onset
Congenital Rubella Syndrome
 Up to 85% of infants affected if infection acquired in-
utero during first trimester
 Infection may affect all organs
 May lead to fetal death or premature delivery
 Severity of damage to fetus depends on gestational
age
Rubella in: William Atkinson, Charles Wolfe eds. Epidemiology & Prevention of Vaccine Preventable Diseases. Dept of Health &
Congenital Rubella Syndrome
 Deafness
 Cataracts
 Heart defects
 Microcephaly
 Mental retardation
 Bone alterations
 Liver and spleen damage
Infant with congenital rubella syndrome
Source: Centers for Disease Control and Prevention
CRS: Time of infection
Risk of
Time of Most common
congenital
infection abnormalities
abnormalities
Multiple congenital defects

Up to 8 weeks 40–60%
and/or spontaneous abortion
Single defect e.g. congenital

9–12 weeks 30–35%
heart disease or deafness
12–16 weeks 10% Single defect, usually

deafness
Mandell G, Douglas R, Bennett J eds. Principles and Practice of Infectious Diseases, third edition, 1990
Rubella and CRS in the US and Developing
Countries
 US
 Most reported rubella in the U.S. since the mid-1990s has
occurred among foreign-born Hispanic adults
 Rubella outbreaks have occurred in workplaces where most
employees are foreign-born
 Majority of CRS since 1997 occurred in children
of unvaccinated women born to Hispanic women, most born
in Latin America
 Developing Countries2
 >100,000 CRS cases / year
Treatment and Prevention
 Treatment
 Symptomatic
 Prevention
 Live vaccine
 Recommended in children from 1 yr of age
Why vaccine against MMR?
 To protect children against measles, mumps and
rubella
 To eradicate measles , mumps and rubella from
populations around the world
German Measles Prevention
 MMR vaccine (2 doses):
 12-15 months old
 4-6 years old
 (minimum interval 4 weeks)
 Non-pregnant susceptible contacts of person with
rubella should be vaccinated
Adverse events of MMR vaccine
 Fever 6-12 days after vaccination
 Rash
 Encephalopathy and autism have not been shown to
be causally associated with the MMR vaccine
Rubella Prevention
 For pregnant women exposed to Rubella:
 To diagnose infection, blood specimen is obtained for
Rubella IgG
 If this is positive, the mother is immune. Save
another blood specimen.
 If negative IgG Rubella, 2nd blood specimen taken
2-3 weeks later, tested concurrently with the saved
specimen.
 If negative for IgG Rubella, take a 3rd specimen
6 weeks after exposure and tested concurrently with
the saved specimen
Rubella
 For pregnant women exposed to Rubella:
 If both 2nd and 3rd specimen is negative- infection has not
occurred
 A negative first specimen and a positive 2nd or 3rd
specimen indicate that the mother had recent infection
 Giving immune globulin for susceptible pregnant
woman exposed to Rubella as prophylaxis may reduce
the risk for clinically apparent infection but does not
guarantee prevention of fetal infection
Epstein-Barr Virus
 EBV is shed in oral secretions consistently for > 6
mos after acute infection and intermittently for life
 It establishes lifelong latent infection after the
primary illness
 Immunosupression permits reactivation of latent EBV
 EBV is also found in male and female genital
secretions
Epstein-Barr Virus
 Childhood: inapparent infection (< 4y/o)
 Incubation period: 30-50 days
 Adolescent presentation:
 Triad
 Fatigue
 Pharyngitis
 Generalized lymphadenopathy
 Infectious mononucleosis (IM): most common
presentation in adolescents
EBV: Pathogenesis
Infects oral epithelial cells (pharyngitis)
Intracellular replication and lysis
Salivary glands
Viremia
(infection of B lymphocytes and entire lympho-
reticular system including liver and spleen)
Clinical features
 Generalized lymphadenopathy
 Splenomegaly
 Hepatomegaly
 Marked tonsillar enlargement, occasionally with
exudates
 Ampicillin rash – rash develops 5-10 days after
giving Ampicillin or Amoxicillin to patients with
EBV-associated IM
Laboratory Tests
 Leukocytosis with lymphocytosis
 Atypical lymphocytes: CD8 T lymphocyte
 Heterophile antibody tests
 Specific EBV antibodies
 IgM VCA
 IgG VCA
 Anti EA antibodies
 Anti-EBNA – Last to develop in infectious mononucleosis
 Gradually appears 3-4 mos after the onset of illness and remain
at low levels for life
Laboratory Tests
 IgM VCA - most valuable and specific serologic test
for the diagnosis of acute EBV infection and sufficient
to confirm diagnosis
 Anti EBNA - last to develop in infectious
mononucleosis, gradually appears 3-4 mos after the
onset of illness and remains at low levels for life
Treatment
 Symptomatic treatment
 Rest
 High dose of acyclovir with or w/o corticosteroids
decreases viral replication and oropharyngeal
shedding during period of administration but does not
reduce severity or duration of symptoms or alter
eventual outcome
Oncogenesis
 Nasopharyngeal CA
 Burkitt’s lymphoma
 Hodgkin’s disease
 Leiomyosarcoma (HIV)
Other lymphoproliferative disorders
 Hemophagocytic syndrome
 Oral hairy leukoplakia (HIV)
 Lymphoid interstitial pneumonitis (HIV)
Fever with Vesiculobullous
Lesions
Coxsackie Virus
 A non-polio enterovirus
 Humans – only known reservoir
 Mode of transmission
 Person-to-person by fecal-oral route, respiratory, vertically
(transplacental, intrapartum or postnatal)
Coxsackie Virus
1. Hand, Foot and Mouth Disease (HFMD)
 Most frequently caused by Coxsackie A16
 Oropharynx is inflamed and contains scattered
vesicles on the tongue, buccal mucosa, posterior
pharynx, palate, gingiva and/or lips that ulcerate,
leaving shallow lesions with surrounding erythema
 Same lesions occur on the hands, fingers, feet,
buttocks and groin
Hand, Foot and Mouth
Disease
Lesions in the mouth
Lesions on the hand(s)
Lesions on the feet
Coxsackie Virus
2. Herpangina
 Characterized by fever, sore throat, dysphagia and
characteristic lesion in the posterior pharynx
3. Pleurodynia
 Acute sharp chest pain involving the intercostal
muscles in between the ribs
4. Myocarditis
5. Hemorrhagic conjunctivitis
6. Viral meningitis
Coxsackie Virus
Coxsackie Virus
Mystery Disease Kills 61

Children in Cambodia
July 5, 2012 3:33 PM CDT
Enterovirus 71 causing HFMD
 Affects the lungs and brain
 Meningitis, encephalitis,
 Neurologic, respiratory, cardiac complications
Varicella-zoster virus
Varicella-zoster virus infection
 Public health concern
 Highly communicable
 Etiology: varicella – zoster virus
 Varicella (chickenpox) – result of primary exposure
 Zoster (Shingles) – affects skin and nerves due to
reactivation of latent virus
Varicella-zoster virus infection
VZV or Chicken pox
VZV or Chicken pox
 Self-limiting
 Causes severe complications
 Organ dissemination in adults and <1 yr.
 Women of child-bearing age are immune
 Small percentage susceptible
 Chickenpox in 5/10,000 pregnancies
 Embryopathy
 Life-threatening to newborn
VZV or Chicken pox
 Fatal in persons with immune deficiency
 With previous chickenpox
 Develop herpes zoster
 Reactivation of latent virus
 Increased morbidity and mortality in newborns born
to mothers who develop rash within 5 days before to 2
days after delivery
VZV or Chicken pox
 Affects healthy children 1 –14 years
 1.4 deaths/100,000 population in US (Drwal-Klein
Ann Pharmacother, 1993)
 0.1 deaths/100,000 population based on Philippine
Health Statistics
 10,000/yr. hospitalized due to complications
 100 deaths/year
 Complications higher in >15 years, < 1yr. and
immunocompromised
Seroprevalence rate in Filipino Population
% VZV Positivity
100.00%
90.00%
80.00%
70.00%
60.00%
50.00%
40.00%
30.00%
20.00%
10.00%
0.00%
<5 6-10 11- 16- 21- 26- 31- 36- 41- 46- 51- 56- 61- >65
15 20 25 30 35 40 45 50 55 60 65
Temperate vs Tropical Countries
Tropical Countries
 Median age of VZV infection is delayed
 VZV positivity occurs later in childhood or adulthood
 Adult infections more common
 Thailand, (Misagena et al)
 Urban population – 1/3 adolescents/young adults lacked natural
immunity
Temperate vs Tropical countries
Temperate countries
 Epidemiology differs
 VZV positivity occurs early
 US – 3M/year
 95% in children and adolescents
 Occurs later in childhood or adulthood in tropical
countries
VZV or Chicken pox
 Difference in  Transmission
incidence/prevalence in  Respiratory (airborne)
temperate and tropical  Direct contact with skin
countries attributed to:
lesion
 Virus is heat-labile – delayed
 Incubation period
infection
 14-16 days (10-21 days)
 High humidity - favors
transmission
 Period of Communicability
 1-2 days before to 4-5 days
 No seasonality
 Temperate countries – after onset of rashes
 Usually contagious until
winter/spring
 Peaks in March, April and lesions dry with scab
May formation
Clinical features
 Vesicular rash – characteristic feature
and first manifestation
 4 stages
 Incubation period
 Prodromal phase
 Appearance of varicella rash
 Healing or crusting of vesicular rash
Varicella or
Chicken Pox Lesions
Clinical features
Symptom % Occurrence in Infected
person
Fever 80%
Anorexia 80%
Headache 77%
Cough/Coryza 68%
Sore throat 50%
Varicella
 Mild prodrome of fever, malaise for 1-2 days
 Macules > vesicles in crops > crusted lesions
(simultaneous presence of lesions in various stages of
evolution is characteristic), mucous membrane also
affected
 Umbilication of lesions
 Rashes appear first on head with highest concentration
on the trunk (central/centripetal distribution)
Varicella
Macule PapuleFluid-filled Crusting

Vesicle
Time in days 2 4 6
Varicella or Chicken pox
 Asymptomatic course <5%
 Immunocompromised
 Severe, progressive in 50% especially in leukemics
Bulutong tubig
(Chicken pox)
Complications
Skin
 Most common
 Bullous hemorrhagic, localized gangrene,
necrotizing fascitis, purpura fulminans
 Cellulitis
 Scarring
Complications
Pneumonia
 Rare in children, more in adults
 Viral in etiology
 Secondary infection may ensue
Complications
CNS
 75% of non-suppurative complications
 2 most common
 Encephalitis
 Reye Syndrome – 20% CFR
 Common in 5 – 14 yrs
 1981 – 1990 in US – Among Reye Syndrome cases,
6% of hospitalization due to Varicella
Complications
Rare-induced by viral multiplication in organs
 Glomerulonephritis
 Endocarditis
 Hepatitis
 Gastritis
 Appendicitis
 Pancreatitis
 Orchitis
 Arthritis
Congenital Varicella Infection
 Clinical manifestations of congenital varicella infection
following chickenpox in pregnancy
 Perinatal transmission occurs in 26% of maternal infections
(Drwal-Klein et al, Annals Pharmahother, 1993)
Stage of Infection Sequelae

1st and 2nd Trimester Congenital varicella syndrome
2nd and 3rd Trimester Herpes zoster
Perinatal Disseminated neonatal varicella
Adapted from Miller E. et al Rev Med. Michiot 1993
Neurologic Sequelae of Fetal VZV Infection
Sequelae Manifestation
Damage to Sensory Cutaneous manifestations
e.g. zigzag (cicatricial) skin lesions,
nerves hypopigmentation
Damage to optic Microphthalmia
Optic atrophy
stalk and lens Cataracts
vesicle Choriorerinitis
Damage to cervical Hypoplasia of upper/lower extremities
Motor/sensory deficits
and lumbosacral Absent deep tendon reflexes
cord Anisocoria/Homer’s syndrome
Anal/vesical sphincter dysfunction
Damage to Microcephaly
Calcifications
brain/encephalitis Hydrocephaly
Aplasia of brain

Maternal Antibody Development and
Neonatal
T Varicella P A
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Number of Days Relative to Delivery
f i s
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Rashes in Children
VZV or Chicken pox
 Mortality rate low in Philippines
 Morbidity and cost substantial
 Anti-virals have minimal effect
 Should be given soon after onset
 Prevention of illness alternative approach
 Limited therapeutic measures
 Safe and effective vaccination to control varicella and
complications

Prevention of Varicella
 Vaccine developed in Japan 1974 by Prof. Takahashi
 Oka strain only strain considered suitable by WHO
 Initially for high-risk children in Japan 1987
 1993 administered to healthy children
 Varicella vaccine
 1-13 y/o = 2 doses (12months 4-6y/o or may give at 2
months interval for the 2 doses)
 >13 y/o = 2 doses (1 month apart)

Prevention of Varicella
Post-exposure prophylaxis
 Varicella Zoster Immunoglobulin G: recommended
for immunocompromised children, pregnant women
and newborns exposed to maternal varicella within 96
hours after exposure
 IVIG - if VZIG not available
 Varicella vaccine for healthy children within
3 – 5 days of exposure

Treatment of Varicella
 Supportive therapy
 Antiviral drugs: Acyclovir or Valacyclovir
 Not routinely recommended in healthy children
 Administer within 24 hours after rash onset
 Indications: children >12 yrs without varicella
vaccination; those with chronic skin or pulmonary
disorders, on long term salicylate therapy,receiving
corticosteroid therapy; those with other
immunocompromised conditions

VZV or Chicken pox
Breakthrough Varicella
 Varicella in vaccinated individuals
 Following close exposure to VZV ( household or an
outbreak in school), 1 of every 5 vaccinated children may
develop breakthrough varicella
 Rash is atypical, predominantly maculopapular, less
commonly vesicular, illness is commonly mild with < 50
lesions and little or no fever
 Considered potentially infectious and should be isolated until
lesions have crusted or if there are no vesicles present or until no
new lesions are occurring

Varicella vaccine Recommendation
Susceptible persons at high risk of exposure or
severe illness
 Teachers of young children
 Institutional settings
 Military
 Women of childbearing age
 International travelers
 Health care workers
 Family members of immunocompromised persons

Herpes - Zoster

Herpes – Zoster or Shingles
 Reactivation of a latent VZV infection
 Associated with aging, immunosuppression,
intrauterine exposure, varicella at <18 mos. of age
 Manifested as vesicular lesions clustered within one,
or less commonly 2 adjacent dermatomes

Common Sites for Shingles
Front Back
Complications
 Post-herpetic neuralgia – late protracted pain,
persisting for months to years after the rash has healed

Diagnosis
 Clinical
 Direct fluorescence assay, PCR
 Tzanck smear
 Serology

Treatment
 Self-limiting, supportive therapy
 Antiviral drugs: Acyclovir or Valacyclovir
 Not recommended routinely for healthy children
 Should be started within 72 hrs
 Indications: immunocompromised; with
complications like pneumonia, severe hepatitis,
thrombocytopenia or encephalitis

Prevention
 New formulation VZV vaccine (Zostavax) for persons
> 60 y/o – to prevent reactivation of herpes zoster and
decrease the frequency of herpetic neuralgia
 Not indicated for the treatment of zoster or post-
herpetic neuralgia
 Risk for developing subsequent herpes zoster is lower
after VZV vaccine than after natural Varicella
infection among immunocompromised children and
healthy vaccinees

Herpes Simplex Virus
 Manifested as a primary infection or as a reactivation
 HSV type 1 – commonly seen in skin and mucous
membranes above the waist
 HSV type 2 – seen in the genitals and in neonates
 HSV establishes latent infection in regional sensory
ganglion neurons, but periodically can reactivate and
cause recurrent infection

 Symptomatic recurrent infections tend to be less
severe and of shorter duration than first infections
 Asymptomatic recurrent infections are common
 Recurrent infections are contagious and can transmit
the disease to susceptible individuals

Pathogenesis
Viral infection begins at the cutaneous
portal of entry
(oral cavity, genital mucosa, ocular conjunctiva,
breaks in keratinized epithelia)
virus replicates locally
spreads to neural tissue where replication

also occurs

 Primary infection – occurs in individuals who have
not been infected previously with either HSV 1 or
HSV2
 No pre-existing immunity, infections can be severe

 Non-primary 1st infection – occurs in individuals
previously infected with one HSV type who become
infected for the 1st time with the other HSV type
 Because immunity to one HSV type provides some
cross protection against disease caused by the other
HSV type, non primary 1st infections tend to be less
severe than true primary infections

 Viremia or hematogenous spread does not play a
role in HSV infections in the immunocompetent
host but occurs in neonates, individuals with eczema,
severely malnourished children, HIV, persons on
immunosuppressive therapy, or with defective cell
mediated immunity

1. Acute herpetic gingivostomatitis
 Pain in mouth, salivation, fetor oris, refusal to eat and
fever
 HSV 1 – most common cause of stomatitis
2. Dendritic keratitis
 Eye involvement is unique to HSV
 Presence of herpetic vesicles on the lids
 Steroids will worsen it

Eye involvement
unique to HSV

3. Genital herpes
 Due to HSV2, transmitted by sexual activity
4. Eczema herpeticum
 Most serious manifestation of traumatic herpes, results from
widespread infection of the eczematous skin with HSV
5. Herpes labialis - fever blisters or cold sores
 Most common recurrent HSV 1 infection
6. Herpetic whitlow
 Occurs on the vermilion border of the lips
 Painful, erythematous, swollen lesion that occurs on the
terminal phalanx

most common
Herpes lesions: found on shaft of

penis (male), vagina, vulva, cervix
(female) and around anus
Herpes lesions

7. CNS infection
 HSV1 – most common cause of fatal sporadic
encephalitis
 Fever, altered consciousness, headaches, personality
changes, seizures, dysphasias and focal neurologic signs
 Most common cause of recurrent aseptic meningitis

Diagnosis
 CSF PCR – the only practical test to diagnose HSV
encephalitis beyond the neonatal period, with
sensitivity and specificity >95%
 Brain MRI
 Tzanck smear

Treatment
 Acyclovir – parenteral is recommended treatment for
neonatal HSV infection
 Given to all neonates w/HSV disease
 60 mg/kg/day in 3 divided doses
 14 days for SEM; 21 days for CNS or disseminated disease
 Foscarnet
 Drug of choice for acyclovir-resistant HSV
 Topical Acyclovir
 For oral or genital herpes
 Decreases the period of viral shedding but with little effect on
symptoms

Fever with
Purpura/ Petechiae
Meningococcal infection
 Etiology
 Neisseria meningitidis
 Gram (-) diplococcus
 Commensal colonies of nasopharynx

Micrograph of
Neisseria meningitidis

Acute Meningococcemia
 Initially mimics viral illness with pharyngitis, fever,
myalgia, weakness, vomiting and headache
 Maculopapular rash- petechia/purpura progresses
rapidly to septic shock in a few hours (hypotension,
DIC, acidosis, adrenal hemorrhage, renal failure,
myocardial failure, and coma)

Petechia/purpura of
Meningococcemia

Extensive purpuric lesion of
Meningococcemia
Meningococcal Invasive infection
1. Meningitis
(stiff neck, high fever, headache, petechial rash)
2. Bacteremia/sepsis (meningococcemia)
3. Pneumonia
4. Pericarditis
5. Arthritis

Meningococcal meningitis
 Headache,
 Photophobia,
 Lethargy,
 Vomiting
 Nuchal rigidity
 Other signs of meningeal irritation

Incubation Period
 1-10 days, usually 2-4 days

Mode of Transmission
 Person to person via aerosolized respiratory droplets
or oral secretion from asymptomatic carriers or
individuals with invasive disease
 May also be spread by inanimate objects
contaminated with saliva (e.g. cigarettes, food
utensils, water bottle)
 Human – only known reservoir of Neisseria
meningitidis

Period of Communicability
 Cases remain infective as long as meningococci are
present in oral secretions or until 24 hours after
initiation of effective antibiotic treatment

Meningococcal meningitis
 Remember:
 5-10% of adults are asymptomatic nasopharyngeal
carriers of strain of Neiserria meningitidis, most of
which are not pathogenic

Diagnosis
 Isolation of meningococci from CSF and blood by
culture
 Latex agglutination of CSF

Treatment
 Penicillin G – drug of choice, given for 5-7 days
 Other antibiotics:
 Ceftriaxone
 Cefotaxime
 Chloramphenicol
 Vancomycin

Complications
 Gangrene of extremities  Pneumonia
 Adrenal hemorrhage  Lung abscess
 Endophthalmitis  Peritonitis
 Arthritis  Renal infarcts
 Endocarditis  Deafness – most common
 Pericarditis neurologic sequelae
 Myocarditis

Control of further spread
 Minimum period of isolation of patient: until 24
hours after initiation of appropriate antibiotic
therapy
 Protection of contacts of a case: close contacts of the
patient should be identified for antibiotic
prophylaxis:
 Rifampicin
 Ceftriaxone
 Ciprofloxacin

Definition of ‘close contact’
 Any member of patient’s household or other
individuals who had intimate contact with the
patient’s saliva or oral/nasal secretion
 Health care workers who have intimate contact
with the patient’s oral/nasal secretion (through
unprotected mouth-to-mouth resuscitation,
intubation or suctioning)

Preventive measure
To prevent additional cases:
1. Refer close contacts to health care provider for
appropriate chemoprophylaxis
2. Admit contacts with signs and symptoms of illness
and refer them to their health care provider should
they experience symptoms compatible with invasive
meningococcal disease
3. Practice good hygiene and handwashing

Preventive measure
To prevent additional cases:
4. Avoid sharing food, beverages, cigarettes or eating
utensils
5. Consider immunization in certain circumstances:
 Meningococcal conjugate vaccine
 Meningococcal polysaccharide vaccine

Recommended Chemoprophylaxis
AGE OF INFANTS, DOSE DURATION
CHILDREN AND ADULTS
RIFAMPICIN
< 1 month 5 mg/kg orally q 12 h 2 days
> 1 month 10 mg/kg orally q 12 h 2 days
CEFTRIAXONE
< 15 years old 125 mg IM Single dose
> 15 years old 250 mg IM Single dose
CIPROFLOXACIN
1 month 20 mg/kg orally Single dose
AZITHROMYCIN 10 mg/kg Single dose

Dengue Infection
 Etiology
 Dengue virus 1, 2, 3, 4
 Mode of transmission
 Day-biting female mosquito:
 Aedes aegypti and Aedes albopticus

Dengue Infection

Increasing Global Burden of Dengue

Dengue in the Philippines
 First DHF cases identified
in Manila,
1953/1954/1956
 Subsequent outbreaks
observed in the 1960s and
subsequently at 5-year
intervals
 Nationwide endemicity
 Over 200,000 cases in
2013 Dengue cases continue to increase,
1 Bravo L et al PLoS Negl Trop Dis 2014;8(11):e3027
with highest ever recorded in 2013
2 Carlos CCet al. Am J Trop Med Hyg 2005 Aug;73(2):435–40

In South East Asia, the burden of dengue is higher than
other serious infectious diseases, such as upper respiratory
infections and Hepatitis B

A total of 126,386 suspect dengue cases were reported
nationwide from Jan 1 to September 10, 2016.
This is a 14% higher compared to the same time period last
year (110,828).

In terms of geographic distribution, majority of the cases
were found in the following regions: VI (12.7%), IV-A
(10.4%), VII (10.3%), XII (8.3%), and III (8.1%).

Profile of cases shows age ranged from less than 1 month to
100 years (median is 3 years old).
Majority of cases were male (52.4%). Most (39%) of the
cases belonged to the 5 to 14 years age group.

Dengue is hyper-endemic
Over recent years, highest burden of DEN-1 and DEN-3
Source: ADVA poster, March 2012; Department of Health National Epidemiology Centre; Data kindly provided by Department of
Health National Epidemiology Centre

Dengue: Rapidly spreading, vector-borne, viral
disease
 Dengue is the most rapidly spreading in the tropics and subtropics
mosquito-borne viral disease in the
world
 The dengue virus is a member of the
genus Flavivirus in the family
Flaviviridae
 A genus that also includes yellow
fever, Japanese encephalitis, Zika and
West Nile encephalitis
 The mosquito vector Aedes aegypti,
is found mainly in tropical and sub-
tropical regions
 Dengue is a febrile illness that
affects people of all ages
 Leading cause of illness and death

Dengue mosquito vectors
 Aedes aegypti  Aedes albopictus

 Yellow fever mosquito  Asian tiger mosquito
 Has bright silvery lyre-shaped dorsal  Has a single longitudinal silvery dorsal
pattern and white banded legs stripe and white banded legs
 Sneaky biter  Mostly an outdoor (garden) mosquito
 High preference for taking blood meals  Aggressive biter
from humans and to lesser extent from  Bites humans but also a variety of
domestic mammals, which makes it a available domestic and wild vertebrates
very capable vector of dengue viruses that do not carry the dengue viruses,
 Main dengue vector worldwide which lowers its capacity to transmit
them
Transmission of Dengue infection
Female Aedes Aegypti mosquito acquires dengue
virus by biting infected
human during viremic phase
(4 to 5 days, up to 12 days)
Extrinsic incubation period in the mosquito
Mosquito transmits virus to man during every feeding
Clinical manifestations in man

(2 to 15 days after the bite)
Dengue Transmission

Dengue Transmission

Dengue Transmission

Dengue Transmission

Dengue Transmission

Dengue Transmission

Dengue Transmission

Clinical manifestation
 Incubation
 3-14 days after the bite of an infected mosquito, with an
average of 4-7 days
 Symptoms
 Sudden onset of high  Myalgia
fever (39O to 40O)  Arthralgia
 Maculopapular rash  Retro-orbital pain
(appear 2-5 days after  Prostration
onset of fever)  Malaise
 Severe headache  Nausea

Dengue infection
Dengue infection results in a spectrum of disease
WHO Dengue guidelines for Diagnosis, Treatment, Prevention and Control, 2009.

Dengue Classification
WHO has provided 2 sets of guidelines for Dengue classification

1 WHO, 1997, Clinical diagnosis
2 WHO, 2009, Dengue Guidelines for diagnosis, treatment, prevention and control
Dengue Fever (DF)
Non specific signs and symptoms
 Headache  Abdominal pain
 Conjunctivitis  Myalgia/arthralgia
 Eye pain  Flushed skin
 Sore throat  Lymphadenopathy
 Cough  hepatomegaly
 Anorexia
 Nausea
 Vomiting

Typical DHF Cases: Asian
 High fever
 Hemorrhages
 Hepatomegaly
 Presence of circulatory failure
 Thrombocytopenia with hemoconcentration

Rash in DF and DHF
 Varies with virus strain
 More often seen in upper and lower extremities
 Unusual character of rash
 Flushing or erythematous mottling coincides with
fever maculopaular (2nd – 6th day)
 May start in trunk face extremities
(2-3 days)
 Petechiae or rashes seen during or after
defervescence on lower legs
 Pruritus and desquamation
Character of Chart
Rash Title in DHF
Classic extremities
71%
Classic, generalized
19%
Urticar-
ial
6%
Maculopapular
4%

Character of Rash in DHF

Diagnostic Tests
 Sensitivity of diagnostic tests for dengue is
influenced by the duration of the illness1
 Serotyping of the dengue virus is possible2
 The SIMPLEXATM Dengue RT-PCR assay has been used to serotype
diverse strains in the field
1 Simmons, 2012, N Engl J Med

2 Boaz, 2014, Tials Vaccinol
Dengue diagnosis
VIRUS ISOLATION
Hemagglutination Inhibition (HI)
Plaque Reduction Neutralization test
Mosquito inoculation (intrathoracic)
IgM and IgG ELISA
Toxorhynchites splendens Rapid tests: Dot blot, Immunoblot,
Dipstick, Immunochromatography
Mosquito cell culture
C6/36 (Aedes albopictus)
Anti-dengue Ig
Molecular techniques
Manifestations:
Polymerase chain reaction(PCR)
NS1 antigen detection Shock
Fever Hemorrhage
Encephalitis
Viremia Liver injury
0 2 4 6 8 10 12 14 16
Days after infection

Management of Dengue Infection
 Early and effective replacement of lost plasma with
plasma expanders or fluids and
electrolyte solutions favorable outcome
 Issues on other forms of treatment

Despite decades of research, there is no
Dengue specific treatment available
 Current treatment methods include1
 Acetaminophen for fever and pain
 Oral or intravenous fluid management
 Careful monitoring of patients during
the critical phase around defervescence
is vital for the early detection and
effective management of severe dengue1
 In patients with severe dengue,
management includes1
 Admission to a hospital with access to intensive
care facilities and blood transfusion
 Management of patients’ body fluid volume
 Antiviral treatments are being
investigated, but the field of dengue
drug research is still relatively new1,2
180 1 WHO, 2009, Dengue Guidelines for diagnosis, treatment, prevention and control Rashes in Children
2 WHO, Antiviral Research and Development Against Dengue Virus
Dengue Control and Prevention
Reduce risk for further transmission
 Vector Control
 WHO promotes the strategic approach known as
Integrated Vector Management (IVM) to control
mosquito vectors, including those of dengue
 Vector transmission is reduced through the use or
combination of these three methods:
 Environmental management
 Chemical control
 Biological control

Reduce risk for further transmission
 Individual and household protection
 Self-initiative for course reduction in homes and
community. See “Environmental management”
 Clothing that minimizes skin exposure during daylight
hours when mosquitoes are most active affords some
protection from the bites of dengue vectors
 Repellents may be applied to exposed skin or to clothing
(in strict accordance with label instructions).

Health
Teaching
Posters

Personal Protection
 Clothing
 Wear full sleeves clothes , long dresses
 Screen
 Bednets
 Mosquito repellant
 Contain N, N-diethyl-mtoterosamide (DEET) applied to exposed skin can
prevent mosquito bites
 Avoid DEET at concentration > 30%
 OFF lotion has 28.5% DEET
 In tropical countries, frequent application because of perspiration
 Care when treating small children, not applied to hands or face
 Clothing can be treated with DEET or permethrine
 Mosquito coils and electric vapor prevents mosquito bites

Vaccination Program
 Dengue vaccination program: a major advance for
disease control that could help achieve WHO
objectives1
Vaccination is a critical pillar of the WHO strategy

towards effectively fighting dengue
1 WHO, 2012, Global Strategy for Dengue Prevention and Control
Chikungunya
 Chikungunya is an alphavirus of the family
Togaviridae.
 “Chikungunya” = Means “to become contorted” or “that
which bends up”
 Translated from Bantu language – Tanzania and
Mozambique
 Described the stooped appearance of sufferers with
joint pains.

Chikungunya
 Spread by mosquitoes: Aedes aegypti, Aedes
albopticus
 Causes fever and severe joint pains
 Muscle pain, headache, nausea, fatigue and rashes
 Shares some clinical signs with Dengue and can be
misdiagnosed in areas where Dengue is common

Chikungunya

Clinical features
CLINICAL FEATURES CHIKUNGUNYA DENGUE
Fever (Temp 38.9 C) +++ ++
Myalgia + ++
Arthralgias +++ +/-
Headaches ++ ++a
Rash ++ +
Bleeding dyscrasia +/- ++
Shock - +/-
Leukopenia ++ +++
Neutropenia + +++
Lymphopenia +++ ++
Thrombocytopenia + +++
Note: The mean frequencies of symptoms were determined from studies where the 2 diseases were directly compared among patients symbols indicate
the % of patients exhibiting each feature. +++:70-100%, ++: 40-69%, +: 10-39%, +/-: <10%, -: 0% a - Headache was often retroorbital
190 Clin Infect Dis. (2009) 49 (6) 942-948 Rashes in Children

Symptoms
 Joint pains or arthritis – may be debilitating that
may last for weeks or months.
 The prolonged joint pain associated with
Chikungunya is not typical in Dengue
 Maculopapular rash precedes disappearance of
fever; petechial rash is not common
 Neurological, heart and GI complications have been
reported but rare and is seen in older people

Incubation Period
 2-12 days but is usually 3-7 days
 Chikungunya virus infection is thought to confer
lifelong immunity.
 Fatalities related to Chikungunya are rare

Diagnosis
 Serology (ELISA): IgM and IgG anti-chikungunya
antibodies
 IgM antibody levels are highest 3-5 weeks after the onset
of illness and persist for about two months.
 Should be done after 5 days of illness
 Chikungunya PCR - best done during the first four
days of illness

Treatment
 No specific antiviral treatment
 Symptomatic: rest, fluids
 For fever and joint pains: Ibuprofen, Naproxen,
Acetaminophen or Paracetamol.
 Aspirin should be avoided

Prevention
 No vaccine
 Modify or remove natural and artificial water-filled
container habitats that support breeding of
mosquitoes.
 During outbreaks, insecticide may be sprayed to kill
flying mosquitoes
 Clothing that minimize exposure to day biting
mosquitoes is encouraged.

Prevention
 Repellents can be applied to exposed skin or
clothing: contain DEET, IR 3535 (Ethyl
butylacetylaminopropionate) or Picaridin
 For those who sleep during daytime, insecticide
treated nets should be used
 Mosquito coils or other insecticide vaporizers may
reduce indoor biting.

Diffuse erythema
with Desquamation
Scarlet Fever
 Causative agent
 Group A Beta-hemolytic Streptococcus
 Exanthem
 Finely papular erythematous, “sand-paper” rash on
trunk and extremities with circum-oral pallor
 Presence of Pastia’s lines (petechiae that develop in the
folds of joints)
 Rash fades on pressure and always leads to
desquamation

Scarlet Fever Rash
Pastia’s Line

Scarlet Fever Rash

Scarlet Fever

Scarlet Fever
 Enanthem
 Tonsillopharyngeal congestion
 Palatal petechiae
 Strawberry tongue (swollen red and mottled appearance
that eventually peels)

Strawberry tongue

Tonsillopharyngeal
erythema with tonsillar
exudates

Treatment and Diagnosis
 Diagnosis
 Throat swab culture, ASO
 Treatment
 Penicillin for 10 days

Staphylococcal Scalded Skin Syndrome
 Ritter disease
 Child <5 yo with abrupt onset of generalized diffuse,
tender erythema > blisters and erosions form within
24-48 hrs > exfoliation
 (+) Nikolsky sign – areas of epidermis separate in
response to gentle shear force
 Characteristic facies (periorificial scaling and
superficial erosions)
 Entire skin heals without scarring within 14 days

Staphylococcal
scalded skin
syndrome

Staphylococcal
scalded skin
syndrome

Staphylococcal Scalded Skin Syndrome
 Causative agent
 Staphylococcus aureus, producing toxins (exfoliative
toxin A and B)
 Toxin released by focus of infection
 Nasopharynx, umbilicus, conjunctivae, blood, superficial
abrasion, urinary tract
 Diagnosis
 Blood culture
 Intact bullae are sterile

Treatment
 Anti-staphylococcal antibiotics (e.g. Oxacillin)
 Local skin care
 Dry exfoliating lesion – petrolatum/emollients
 Weeping, crusted lesion – NSS compress for 15 mins
every 1-2 hrs
 Symptomatic and supportive measures

Toxic Shock Syndrome

Toxic Shock Syndrome
1. Major criteria
2. Minor criteria
3. Exclusionary criteria

Major Criteria
ALL REQUIRED
 Acute fever; temperature >38.8OC
 Hypotension
 Rash (erythroderma with late desquamation) –
sunburn like or scarlatiniform

Minor Criteria
ANY THREE (3)
 Mucous membrane inflammation (conjunctivae,
vagina, pharynx, strawberry tongue)
 Vomiting, diarrhea
 Liver abnormalities
 Renal abnormalities
 Muscle abnormalities
 CNS abnormalities
 Thrombocytopenia

Exclusionary Criteria
 Absence of another explanation
 Negative blood cultures (except occasionally for S.
aureus)

Risk Factors
 Use of tampons and other vaginal devices
 Nasal packing
 Wound infections
 Sinusitis, tracheitis, pneumonia, empyema
 Abscesses, burns
 Osteomyelitis
 Primary bacteremia

Staphylococcal Toxic Shock Syndrome
 Etiology:
 S. aureus producing Toxic Shock Syndrome Toxin
(TSST-1) and other enterotoxins

Complications
1. Acute respiratory distress
2. Myocardial dysfunction
3. Renal failure

Outcome
 Recovery in 7-10 days
 Desquamation of palms and soles
 Hair and nail loss in 1 – 2 months

Diagnosis
 No specific laboratory test
 Involvement of several organ systems

Differential Diagnosis
 Kawasaki Disease
 Streptococcal Toxic Shock Syndrome
 Scarlet fever
 Measles
 Leptospirosis
 Toxic Epidermal Necrolysis (TEN)

Treatment
 Anti-staphylococcal antibiotics, e.g. Oxacillin,
Nafcillin, first generation Cephalosporin,
Vancomycin, Clindamycin
 Fluid replacement
 Drainage of vagina or of focally infected sites

Prevention
 Avoid using tampons
 Drainage of abscesses
 Early institution of appropriate systemic
antimicrobial therapy
Kawasaki Disease
 Mucocutaneous lymph node syndrome or infantile
polyarteritis nodosa
 Acute multisystemic vasculitis of infants and
children
 Age of predilection: <5 y.o.
 Etiology
 Unknown

Diagnostic Criteria
 Fever lasting for at least 5 days
 Presence of at least 4 of the following 5 signs:
1. Bilateral bulbar conjunctival infection, generally non-
purulent
2. Changes in mucosa of oropharynx, including injected
pharynx, dry fissured lips, strawberry tongue

Bilateral bulbar
conjunctival infection
Changes in mucosa of
oropharynx
Diagnostic Criteria
3. Changes of the peripheral extremities such as edema
and/or erythema of hands or feet in the acute phase; or
periungual desquamation in the subacute phase

Changes of the
peripheral extremities

Diagnostic Criteria
4. Rash - primarily truncal; polymorphous, erythematous
rash but non-vesicular; can be maculopapular,
morbilliform (measles-like rash), or scarlatiniform
5. Cervical adenopathy, >1.5 cm, usually unilateral
lymphadenopathy; illness not explained by other known
disease process

Polymorphous
erythematous rash
Cervical adenopathy

Kawasaki Disease
 Cardiac involvement – most important
manifestation/sequelae
 Myocarditis, coronary artery aneurysm
 (25% of untreated patients)

Diagnosis
 Clinical
 Laboratory findings:
 Normal to elevated WBC with predominance of
neutrophils and immature forms
 Elevated ESR, CRP
 Platelet count is normal in the 1st week of illness,
increases by 2nd-3rd week
 2D Echo: most useful test to monitor potential
development of coronary artery abnormalities

Treatment
 IVIG – reduces the prevalence of coronary
arterydisease from 20-25% to 2-4%; should be given
within 10 days of the onset of fever
 Aspirin – used for its anti-inflammatory and
antithrombotic activity

Non-infectious causes of
Fever and Rash
 Connective tissue disease
 Malignancies
 Drug Reactions

Children are not things to
be moulded, but are
people to be unfolded.

237
Thank you Rashes in Children

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RASHES IN CHILDREN

1. www.nfid.org, National Foundation for Infectious Disease (accessed Aug 2005)

1. www.nfid.org, National Foundation for Infectious Disease (accessed Aug 2005)

Epithelial cells infected and virus multiplies

Extension to regional lymphoid tissue

Multiplication in respiratory epithelium, RES, distant sites

Infection in skin and other sites

Virus in blood, respiratory tract, skin and other organs

Viremia, virus in organs

Rash affects arms

The high measles disease burden, despite

Erythematous and macular

Respiratory transmission of the virus

Replication in the nasopharynx and

Viremia (5-7 days)

Rash spreads quickly to

Rash is highly variable;

© Copyright Dr. CW Leung,

© Copyright Dr. CW Leung, Department of

Multiple congenital defects

Single defect e.g. congenital

12–16 weeks 10% Single defect, usually

Intracellular replication and lysis

Mystery Disease Kills 61

Macule PapuleFluid-filled Crusting

Stage of Infection Sequelae

Adapted from Miller E. et al Rev Med. Michiot 1993

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virus replicates locally

spreads to neural tissue where replication

117 Rashes in Children

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122 Rashes in Children

123 Rashes in Children

124 Rashes in Children

Herpes lesions: found on shaft of

126 Rashes in Children

127 Rashes in Children

128 Rashes in Children

129 Rashes in Children

131 Rashes in Children

132 Rashes in Children

133 Rashes in Children

134 Rashes in Children

136 Rashes in Children

137 Rashes in Children

138 Rashes in Children

139 Rashes in Children