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Krizia Joy Borromeo-Galve, MD: Bulacan Medical Center, Department of Pediatrics
Krizia Joy Borromeo-Galve, MD: Bulacan Medical Center, Department of Pediatrics
Herpes
Simplex Epstein Herpes Human
Varicella Virus 1 Virus 6
Barr Virus Cytomegalo Herpes
Zoster
Herpes (type 1 and virus Herpes Virus 8
Virus
Simplex type 2) Virus and 7 (HHV-8)
Virus II
PERIOD OF • 24-48 hours before the rash until the vesicles are
COMMUNICABILITY encrusted (3-7days)
Varicella
Varicella: Pathogenesis
Inoculation of
Replicate in the
VZV to Subclinical
local lymphoid Spread to RES
respiratory viremia
tissue
mucosa
Mononuclear
cells carry Widespread
Second viremic Second viremic
infectious virus cutaneous
phase phase
generating new lesions
cops of lesions
Herpes zoster
Adults- acylclovir
Children with uncomplicated disease –
NO treatment
Varicella: Complications
Bacterial infections
Encephalitis and cerebellar ataxia
Pneumonia
Varicella: Prevention
Active immunization
Post-exposure prophylaxis
○ Immunoglobulin ASAP or within 96hours of
exposure to be given at 125units/10kg (max
625units)
○ Indications
Immunocompromised children
Pregnant women
Newborns
High risk patient in close contact with herpes zoster
PROGRESSIVE
VARICELLA
Highest in children with cellular
immunodeficiency
Clinical manifestation
Visceral involvement, coagulopathy, severe
hemorrhage, Continued development of
lesions
Severe abdominal pain
Hyperkeratotic appearance and
continued new lesion formation for
weeks or months in children with untreated,
late stage HIV
PROGRESSIVE
VARICELLA
PROGRESSIVE VARICELLA
NEONATAL VARICELLA
NEONATAL VARICELLA
Maternal varicella
• Infant has protective antibody to
>5 days Before ameliorate neonatal infecton
• NO treatment except in preterm
Delivery infants <28 weeks of gestation
5 days before to
2 days after • No protective VZV antibody
• Give VZV immunoglobulin
delivery
In adults In children
Localized pain,
The vesicular lesions
hyperesthesias, pruritus and
clustered within one or two
low grade fever are
adjacent dermatomes
infrequent
Genital herpes
Oral acyclovir, famciclovir or valacyclovir
CNS (encephalitis)
IV acyclovir
HSV Infection: Prevention
Prevention
Chemoprophylaxis with acyclovir
Standard methods of infection control
Prevent contact with active lesions
Epstein Barr Virus: Infectious
Mononucleosis: EPIDEMIOLOGY
Low
• Infancy and childhood
socioeconomic
strata
“Deep kissing”
• Fever
• Headache
• Abdominal pain
• Malaise
• Myalgia
• Severe sore throat
EBV: Infectious Mononucleosis:
MANIFESTATIONS: Physical Exam
EBV: Infectious Mononucleosis:
MANIFESTATIONS: Physical Exam
Generalized lymphadenopathy – 90%
Splenomegaly – 50%
Hepatomegaly – 10%
Rashes – 3-15%
EBV: Infectious Mononucleosis:
DIAGNOSIS
Congenital CMV
• Remains a well-recognized cause of disease in the
newborn infant following intrauterine infection
CMV Diseases
• CARDIAC: Associated with Coronary Artery
diseases; Cardiac Allograft Loss
• Transplant vasculopathy
• RENAL: Tubular Sclerosis, Renal Allograft Loss
• GIT: Exacerbations of inflammatory bowel
disease
• CNS: Glioblastoma
Cytomegalovirus: Host Interaction
CMV
•Largest of the Human
herpesvirus
Cytomegalovirus: Host Interaction
CMV
• Largest of the Human herpesvirus
50% Larger than the herpes simplex virus genome and encodes
more than 100 unique virion proteins
• Fatigue
• Occasionally cervical adenopathy
• Heterophile antibody negative
• Mild elevation of ALT, AST
• Decreased platelet
Congenital Cytomegalovirus
Occurs following
intrauterine Transmission
Congenital CMV
transmission of rate: 0.5 to1.0%
CMV
Transmission Hematogenous
Transferred to
rate to fetus: spread of virus to
developing fetus
30% placenta
Cytomegalovirus: Congenital Infections
90% of infected
infants will have no
clinical
manifestations in the
newborn period
Blue berry muffin rash microcephaly
Infants with Symptomatic CMV
11% HEARING LOSS will
Manifestation Laboratory develop in of CMV infected
infants
Hearing Loss:common
long term sequelae Elevated ALT, AST Suspect CMV infection in
hearing loss in older infant
Hepatosplenomegaly and young child
Thrombocytopenia
Petechial Rashes
Anemia
Jaundice
Abnormal findings on Approx 50% of infants with
Microcephaly Cranial UTZ hearing loss is associated
with Congenital CMV
will pass an initial exam
IUGR Increased CSF Protein
BUT develop hearing loss in
infancy and early childhood
Cytomegalovirus: Treatment
Diagnosis requires evidence of primary Infection
HHV-8 contain
Viral proteins Induce expression of
multiple genes that
interfere with p53 Proangiogenesis
impact cell-cycle
and Rb protein factors, vEGF A
regulation
upregulation of
Serves as host cell Encodes IL-6: bind rapamycin pathway:
autocrine growth and activate cytokine instrumental in the
factor receptors control of cell growth
and metabolism
HHV-8: Kaposi Sarcoma
Symptomatic Primary HHV-8
• Fever
• Maculopapular ash
• Mononucleiosis-like sydrome
Immunocompromised Patients
• Fever
• Rash
• Splenomegaly
• Pancytopenia
• Lymphoid hyperplasia
HHV-8: Kaposi Sarcoma Clinical Forms
Classic Kaposi Sarcoma
• Indolent Disorder
• Seen in Elderly men
• Limited involvement of skin of the lower extremities
• Aggressive form
• Occuring in children and young people
• Primarily in Africa
• Include visceral involvement
• Widespread cutaneous lesions (patches, plaques or nodules)
Seroversion
Immunohistochemistry
Multicentric
Exanthem
subitum
(sudden rash)
Roseola: Epidemiology
Most adults • Excrete HHV-6 and HHV-7 in saliva