ROSEOLA INFANTUM

ROSEOLA INFANTUM

ETIOLOGY
HHV-6 and HHV-7
CD46 & CD4 T cells
primary
target cells in vivo

EPIDEMIOLOGY
Early in life
Peak: 6-15mos
2 y.o, 7-10 y.0.

PATHOLOGY
(incubation period)

Saliva, enters the

hostoral, nasal,
conjunctival mucosa
HHV-6 & HHV-7
attach to cellular
receptors
Viral replication,
High level of viremia
develops in PBMCs
Viruses evade immune
system tru
downregulation of MHC I
response

- Enhancement of NK T-cell activity

- Induction of proinflammatory cytokine
response

CLINICAL MANIFESTATIONS

High temp. (37.9-40c) ave. of 39c3-5Days

Roseola rash for 1-3 days
Nagayama spots
Mild conjunctival redness

Rinorrhea
Sore throat
Slight pharyngeal inflammation
Abdl pain
Diarrhea, vomiting

Roseola rash

Nagayama spots

RUBEOLA
(ETIOLOGY):

Measles virus
Remain viable for atleast
34hr at room temp.

ROSEOLA INFANTUM

LABORATORIES

Total WBC (8900/L)

Lymphocyte (3400/L)
Neutrophil (4500/L)
Thrombocytopenia
serum transaminase
Atypical lymphocyte

DIAGNOSIS
High fever (3 days)
blanching maculopapular
rash (trunk)
presence of actively
replicating virus
GOLD STANDARD:
Viral culture

Viral DNA (PCR)

Reverse transcriptase PCR
Serologic methods
Absence of IgG antibody +
replicating virus

COMPLICATIONS

Convulsions
Seizure (peak age: 12-15 months)
post-ictal paralysis
30% - prolonged seizures
29% - focal seizures
38% - repeated seizures
status epilepticus

Encephalitis
Acute disseminated demyelination
Acute cerebellitis
Hepatitis
Myocarditis

 Developmental disabilities
Autistic like features
PALE (posttransplant acute limbic
encephalitis)

TREATMENT

Minimum of 3 weeks

PROGNOSIS

PREVENTION

INFECTIOUS
MONONUCLEOSI
S

ETIOLOGY
Epstein Barr Virus
double-stranded DNA virus
y-herpesvirus
EBV 1 & 2
EBV 1
more prevalent worldwide
Induces growth transformation of B cells

EBV 2 = Africa

EPIDEMIOLOGY
MOT :
oral secretions
> 6 mo after acute infection
intermittently for life
sexual intercourse
PRIMARY INFECTION during childhood
Usually asymptomatic
Mild or indistinguishable
PRIMARY INFECTION in adolescents & adults
30 to 50 %
CLASSIC TRIAD:
fatigue, pharyngitis, generalized lymphadenopathy

PATHOGENESIS
Acquisition in ORAL CAVITY
EBV infects CRYPT EPITHELIAL CELLS >>> pharyngitis
INTRACELLULAR VIRAL REPLICATION & CELL LYSIS (release of
new virions)
VIRUS SPREADS to salivary glands
VIREMIA & INFXN of B lymphocytes , lymphoreticular system
(liver & spleen)
ATYPICAL LYMPHOCYTES ( CD8 T lymphocytes)

CLINICAL MANIFESTATION
INCUBATION PERIOD
30 to 50 days (adolescents)

PRODROMAL PERIOD
1 to 2 weeks

CLINICAL MANIFESTATION

CLINICAL
MANIFESTATION
AMPICILLIN RASH
morbilliform, vasculitic rash

GIANOTTI- CROSTI SYNDROME

symmetric rash on cheeks w/ multiple
erythematous papules
coalesce into plaques
persist 15 to 50 days
appears like atopic dermatitis
appear on extremities & buttocks

DIAGNOSIS: Infectious
mononucleosis
presumptive

presence of typical clinical symptoms with

atypical lymphocytosis

confirmatory

serologic testing

heterophile Abs, or specific EBV Abs

culture (transformation assay)

requires 4-6 weeks

oropharyngeal or genital secretions,
peripheral blood (10-30 mL), or tumor with
human umbilical cord lymphocytes

Laboratory Tests
> 90% of cases
leukocytosis of
10,000-20,000
cells/L (2/3s are
lymphocytes)
atypical
lymphocytes: 2040% of the total
number

Laboratory Tests
Heterophile Antibody Test
transient heterophile antibodies /PaulBunnell antibodies
IgM Abs detected by the Paul-BunnellDavidsohn test for red sheep agglutination
(greater sensitivity) agglutinate in sheep rbc
(+) in 75% cases: 1st week
(+) in 90-95% cases : 2nd week

Laboratory Tests
SPECIFIC EPSTEIN-BARR VIRUS
ANTIBODIES
testing is useful to confirm

acute EBV infection,

in heterophile-negative cases
to confirm past infection
determine susceptibility to future infection

Antigens: EBNA, EA and VCA

Acute IM: VCA (IgG and IgM), EA (IgG)

Treatment
NO specific treatment
Mainstay Management:
rest, encouraging adequate fluid and
nutrition intake
symptomatic treatment with acetaminophen
or NSAIDS (fever, throat discomfort,malaise)

Short courses of corticosteroids (<2 wk)

prednisone 1 mg/kg/day (maximum: 60
mg/day)
airway obstruction, thrombocytopenia with
hemorrhaging, autoimmune, hemolytic
anemia, seizures, and meningitis

Treatment
Antiviral therapy is not
recommended
acyclovir, with or without corticosteroids
decreases viral replication and
oropharyngeal shedding during
it does NOT reduce the severity or duration
of symptoms or alter the eventual outcome

Complications
subcapsular splenic hemorrhage or
splenic rupture
occurs during 2nd week, rate of <0.5%
of cases in adults

Swelling of the tonsils and

oropharyngeal lymphoid tissue
cause airway obstruction
manifest: drooling, stridor, and interference
with breathing

Complication
Airway compromise with progressive symptoms
occurs
<5% of cases
common indication for hospitalization
elevating the head bed, intravenous
hydration, humidified air, and systemic
corticosteroids
Respiratory distress with incipient or actual
airway occlusion
managed by

tonsilloadenoidectomy
endotracheal intubation for 12-24 hr

Complication
Headache (50% of cases)
Headache with severe neurologic
manifestations
seizures and ataxia, in 1-5% of cases

Alice-in-Wonderland syndrome
(metamorphopsia)
Perceptual distortions of sizes, shapes,
and spatial relationships

Complication
Guillain-Barr syndrome or Reye
syndrome
Hemolytic anemia
(+) Coombs test result and with cold
agglutinins specific for red cell antige,
occurs in 3% of cases
1st 2 wk of illness and lasts for <1 mo.

Complication
Aplastic Anemia
3-4 wk after the onset
recovery in 4-8 days
some cases do require bone marrow
transplantation

Mild thrombocytopenia and neutropenia

Myocarditis or interstitial pneumonia
resolving in 3-4 wk

Rare: pancreatitis, parotitis, and orchitis

Prognosis
for complete recovery is EXCELLENT
major symptoms
last 2-4 wk followed by gradual recovery
within 2 mo of onset of symptoms

Cervical lymphadenopathy and

fatigue
resolve slowly

fatigue, malaise, and some disability

may wax and wane for several weeks to
6 mo

Prevention
impractical to prevent
virus is ubiquitous
majority of the population is EBVpositive

CYTOMEGALOVIRUS
INFECTION
ETIOLOGY:
-largest of the herpes virus

CYTOMEGALOVIRUS INFECTION
EPIDEMIOLOGY
Acquired in different settings:
1. Community exposure
2. Nosocomial transmission
3. Intrauterine infection
Transmission: Saliva, Breastmilk, urine,
cervical and vaginal secretions, urine, semen,
stools, blood and tissue or organ transplant
-requires very close or intimate contact

Community exposure
BF is the most common route of CMV
infection in early childhood
Ingestion of BM from Seropositive
mothers- 60-70% of infants infected
Infection common in the 1st 6mos
Adolescents- Inc. infxn dt sexual
contact

Nosocomial Transmission
Exposure to blood product, allograft
transplantation

Congenital CMV infn

Rate of congenital infection (Asia &
Africa)- 2%
Rate of transmission from Mothers
(primary infection) during pregnancy30%
Nonprimary infxn (prev.infected
women)- 1-2%ROT

Pathology

RUBELLA
German measles or 3 day measles
INFANTS AND CHILDREN
ADULTS

ETIOLOGY
Family Togaviridae and is the only species
of the genus Rubivirus.
Single stranded RNA virus
SENSITIVE to heat, UV light, and
extremes of pH
STABLE at cold temperatures
Humans

EPIDEMIOLOGY
PREVACCINE ERA
INTRODUCTION OF THE VACCINE
AFTER SEVERAL YEARS
2 dose recommendation for rubella
vaccine

21st century: decline

PATHOLOGY
Lymphoreticular inflammation and
mononuclear perivascular and
meningeal infiltration.

PATHOGENESIS

CLINICAL MANIFESTATIONS
Incubation period: 14 21 days
Symptoms of:
Low grade fever
Sore throat
Red eyes with or without pain
Headache
Malaise
Anorexia
In older girls and women, polyarthritis may occur with
arthralgia, swelling, tenderness, and effusion bu
Lymphadenopathy
Suboccipital, postauricular and anterior cervical lymph nodes are
most prominent

 RASH
3 days

 Examination of the
oropharynx
tiny, rose-colored lesions
(Forschheimer spots) or
petechial hemorrhages on
the soft palate.

LABORATORY FINDINGS/DIAGNOSIS

Clinical signs and symptoms

Leukopenia
Neutropenia
Mild thrombocytopenia
IgM antibodies are detectable in the first few days
of illness and are diagnostic
Spleen is often slightly enlarged
Culture of Rubella virus from the nasopharynx and
blood

DIFFERENTIAL DIAGNOSES
Measles
Adenovirus infections
Parvovirus infections (erythema
infectiosum)
Eipstein-Barr virus
Enterovirus
Mycoplasma pneumoniae

COMPLICATIONS
Postinfectious thrombocytopenia

Children and girls

Manifests about 2 weeks ff onset of
rash
Petechiae, epistaxis, GI bleeding,
hematuria

COMPLICATIONS
Arthritis
Adults (women)
Begins within 1 week of onset

COMPLICATIONS
Encephalitis
Postinfectious encephalitis

Appears within 7 days after onset of

rash
Headache, seizures, confusion, coma,
focal neurologic signs and ataxia
Non infectious pathogenesis

COMPLICATIONS
Encephalitis
Progressive rubella panencephalitis (PRP)

Infectious pathogenesis
Death occurs 2-5 yrs after onset

TREATMENT
No specific treatment available
Supportive Care

Antipyretics, analgesics
Children with CRS is more complex

PROGNOSIS
Excellent prognosis
Reinfection with wild virus

PREVENTION
Isolation from susceptible individuals
for 7 days after onset of rash
Standard plus droplet precautions
Children with CRS may excrete virus
up to 1 yr of age

VACCINATION
1st at 12 15 months
2nd at 4 6 yrs of age
Postexposure prophylaxis = within 3
days of exposure
Should not be given to severely
immunocompromised px
Should not be given during
pregnancy

Measles/Rubeola

Etiology
Measles Virus
Genus: Morbillivirus
Family:
Paramyxoviridae

Prodromal period:
shed in
Nasopharyngeal
secretions
Blood
Urine

: Neutralizing
antibodies
: Limit
proliferatio
n during
infection

Epidemiology
Endemic throughout the world
90% of children acquire this before 15 years old
before immunizations
Cases have decreased with vaccinations

Resurgence occurred mostly among

Vaccine failure
Low coverage of preschool aged chidren
More rapid waning of maternal Ab in infants

2011: 0.7% per 1,000,000 population

MODE OF
TRANSMISSION
Portal of entry
Respiratory tract
Conjunctivae

Infectious Stage: 3 days

before to 4-6 days after
rash onset
Virus viability: suspended
in air = 1 hour

Pathogenesis
incubation

MV migrates to lymph nodes

Primary viremia
Secondary viremia

Prodromal

Associated with: 1) epithelial necrosis and 2) giant cell

formation in body tissues
Virus shedding

Exanthemat
ous

Onset of rashes
1) Antibody production begins, 2) viral replication 3) subsiding
of symptoms
Infects CD4 T cells

Desquamation of rashes
Recovery

Clinical Manifestations
Pathognomonic Sign: Koplik Spots and
Warthin-Finkeldey Cell
1.
2.
3.
4.
5.
6.

High fever
Enanthem
Cough
Coryza
Conjunctivitis
Prominent exanthem

Clinical Manifestations
Prodromal
Stage

Lasts 3-5days

Conjunctivitis with
photophobia

Appears 1-4 days before

onset of rashes
Location: inner cheeks at

Clinical Manifestations
Final Stage
Increase in
prodromal symptoms
then rashes appear
Rashes appear and
symptoms subside
Rash fade over 7
days
COUGH: lasts longest
Generalized
lymphadenopathy

forehea
d

Behind
ears

Upper
neck

Torso
and
extremit
ies

Palms
and
soles

VELOSO

FIFTH DISEASE/
ERYTHEMA
INFECTIOSUM

ALEGARBES

EPIDEMIOLOGY
PARVOVIRUS B19
Rash and transient aplastic crisis
(school-aged children)
Seasonal peaks: late winter and spring
MOT : respiratory route, blood and
blood products
Transmission rate: 15-30%

 HUMAN BOCAVIRUS
Found in respiratory secretions
Prevalent: <2 years old
Associated with wheezing respiratory
illness
Found as a coinfection:
respiratory syncytial virus
human metapneumovirus
rhinovirus

PATHOGENESIS
PRIMARY TARGET = ERYTHROID CELL LINE
(erythroid precursors near pronormoblast stage)
Viral infection >> CELL LYSIS
Progressive depletion of erythroid precursors &
arrest of erythropoiesis
Endothelial cells, Placental cells, Fetal
myocardial cells

 Biphasic Illness
7 to 11 days after inoculation
Viremia
Decreased reticulocyte counts
Nasopharyngeal viral shedding
Fever
Malaise
Rhinorrhea

Clinical Manifestation:
Parvovirus B19
Erythema Infectiosum (Fifth Disease)
most common
benign, self-limited exanthematous
illness of childhood
incubation period: 4-28 days (average:
16-17 days)
prodromal phase:
mild
low-grade fever in 15-30% of cases,
headache, symptoms of mild URTI

Erythema Infectiosum (Fifth Disease)

Hallmark :
characteristic rash
3 stages
initial stage
face flushing
slapped-cheek
appearance

Erythema Infectiosum (Fifth Disease)

2nd stage
trunk and proximal
extremities

diffuse macular erythema

Central clearing
lacy, reticulated appearance
prominent on extensor
surfaces, (-) palms and soles
afebrile
rash resolves spontaneously
without desquamation
wax and wane over 1-3 wk
recur: sunlight, heat, exercise,
stress

Athropathy
Arthritis and arthralgia
adults and older adolescents
joint symptoms
diffuse polyarthralgia with morning stiffness
to frank arthritis
selflimited
resolve within 2-4 wk

females > males

Transient Aplastic Crisis

transient arrest of erythropoiesis and
absolute reticulocytopenia
sudden fall in serum hemoglobin
occurs in patients with
chronic hemolysis and/or rapid RBC turnover
ill with fever, malaise, and lethargy
s/sx of profound anemia (pallor, tachycardia,
tachypnea)

Rash is rarely present

Immunocompromised
Persons
Chronic anemia
accompanied by neutropenia,
thrombocytopenia, or complete marrow
suppression

cancer chemotherapy or
immunosuppressive therapy
Chronic infections

Fetal Infection
<5% risk for fetal loss after infection
Primary maternal infection: associated
with
nonimmune fetal hydrops
intrauterine fetal demise

mechanism: viral induced RBC

aplasia

 Myocarditis
dx: serologic findings,
B19 DNA in cardiac
tissue

Other Cutaneous
Manifestations
papularpurpuric
gloves-and-socks
syndrome (PPGSS)
fever,
pruritus,painful
edema, erythema
localized to the
distal extremities

self-limited
resolves within a few
weeks

Diagnosis
Based on the clinical presentation of the typical rash
Serologic tests:
B19- specific IgM
Anti-B19 IgG- past infxn
Anti- B19IgM- recent/acute infxn
Seroconversion of anti-B19 IgG AB
Serologic test- not reliable fo IC pxs
PCR/ Nucleic acid hybridization
Immune electron microscopy

Complications
Usually recover fully but with
protracted symptoms
1. Severe pneumonitis with high fatality
rate
if hypoxemia develops