Infectious Disease:

Viral Infections
STANLEY T, AGOR, MD, MPH
Department of Pediatrics
CAGAYAN STATE UNIVERSITY
 RUBEOLA (Measles)
 Highly contagious
 1st described around the 7th century
 1846 by Peter Panum illustrated the incubation period and lifelong
immunity after recovery
 Before the availability of measles vaccine- 90% of children contracted the
disease and they are immune by the age of 15 years
 RUBEOLA (Measles): ETIOLOGY
 Family: Paramyxovirus
 Genus: Morbillivirus
 Enveloped RNA virus, has only 1 serotype
 2 membrane envelop protein: important in the pathogenesis of the disease
F (Fusion) responsible for the fusion of virus and host cell membrane’s
viral penetration and hemolysis, H (Hemeagglutinin) responsible for the
adsorption of the virus to cells
 RUBEOLA (Measles): ETIOLOGY
 Virus is rapidly inactivated by heat light and acidic pH, ether and trypsin
 Short survival time of less than 2 hours in the air or on object and surfaces
 RUBEOLA (Measles): Pathogenesis
 Systemic disease
 Primary site of infection in uncomplicated measles is respiratory: respiratory
epithelium of the nasopharynx and spread to regional lymphatics
 Primary veremia( 2-3 days)- infection of reticuloendothelial system- viral
replication in the regional and distal reticuloendothelial sites- Secondary veremia
(5-7 days after infection ) (generalized measles with infection in respiratory tract and
other organs
 Virus shed from nasopharynx starting with the prodrome until 3-4 days after the onset
of rash
 RUBEOLA (Measles): Epidemiology
 Ranked 3rd leading cause of vaccine preventable death
 Affects very young Filipino children less than 2 years old
 Humans are the only known natural host of the measles virus
 Transmitted primarily by person –to –person contact via respiratory droplets
 Aerosolized droplet nuclei can stay or occur up to 2 hours after a person with measles had
stayed and left the area
 Contagious from 4 days before to 4 days after the onset of rash
 Maximum communicability occurs from the onset of prodrome up to the 1 st 3-4 days of rash
 RUBEOLA (Measles): Clinical
Manifestations
 IP ( EXPOSURE TO PRODROME) about 10 days+/- 2 days
 Rash appears 7-18 days after exposure
 Prodrome: last for 2-4 days average of about 1-7 days
 Onset of clinical measles is characterized by: general malaise, fever, coryza, conjunctivitis
and cough
 Fever is high grade, increases further with the appearance of rash
 Koplik’s spot: pathognomonic of measles, blue white pinpoint – sized dots with reddish
background located in the inner cheeks opposite the lower molar appears 1-2 days before
the rashes appear-- transient
 RUBEOLA (Measles): Clinical
Manifestations
 Maculopapular rash
- appears at the hairline behind the ears- forehead face  upper
neck gradually progresses downward and outward ( centrifugal
distribution)
- branny desquamation of the rash
 RUBEOLA (Measles): Diagnosis
 ELISA test - Measles immunoglobulin (Ig)M antibody serologic test
- the ELISA test use for IgM antibody requires only single serum
specimen
- IgG antibody requires 2 serum specimens diagnosis using
IgG cannot be made until after the 2nd specimen has been
obtained
 RUBEOLA (Measles): Treatment
 Self limiting with no specific antiviral agent
 Antibiotics are given for secondary bacterialcomplications
 Vitamin A : given it once daily for 2 days
- 200,000 IU for 12 months of age or older
- 100,000 IU for 6 months to 11 months
-50,000 IU for < 6 months of age
- another dose should be administered to children 2-4 weeks later if they
have clinical manifestations of Vitamin A deficiency
 RUBEOLA (Measles): Treatment
 Immune globulin (IG) can be given to susceptible infants and children to
prevent or modify the course of measles
- given within 6 days of exposure
- 0.25 ml/kg IM for immunocompetent child
- 0.5 ml/kg IM for immune deficient child
- not recommended for individuals or contacts who have been given
measles vaccine at 12 months or older unless immune- deficient
 RUBEOLA (Measles): Prevention/
Complications
 Live attenuated vaccine ( monovalent, combine)
 Otitis media ( most common)
 Pneumonia
 Encephalitis
 Laryngotracheobronchitis
 Subacute sclerosing panencephalitis (SSPE)
 May cause flare up of an underlying TB infection
 RUBELLA

 Mild communicable disease of infants and children infection among

young women during early pregnancy, cause fetal death, or congenital
rubella virus infection/syndrome
 RUBELLA: Etiology
 Moderately large, single stranded RNA virus
 Familt Togavirus
 Does not require a vector for transmission
 Present in the blood and nasopharyngeal secretions of patient
 Sensitive to heat extremes pH
 Rapidly inactivated at 56 degrees and at 37 degrees, at 4 degrees Celsius
the virus titer is relatively stable for 24 hours
 RUBELLA: Pathogenesis

 Fetal damage is unclear but may include viral cytolysis, chromosomal

breaks, reduced cellular multiplication, alteration of fetal blood supply-
fetal growth may be retarded and defects may develop in multiple organ
systems
 Rubella can persist in the fetus and newborn, it can be excreted for months
to years after birth
 RUBELLA: Epidemiology

 Humans are the nly natural hosts for the rubella virus
 Moderately contagious but less so than measles
 RUBELLA: Clinical Manifestations

 Transmitted by droplets, direct contact with infected fluid, not considered

a truly airborne infection
 Rubella is probably transmissible from just before the onset of the rash
during the prodromal period and during the rash illness phase
 2-3 weeks after IP low grade fever, upper respiratory tract infection,
cough, colds general malaise, lymphadenopathy behind the ears this
may last for a week
 RUBELLA: Clinical Manifestations

 1-3 days after prodromal period: rash lasted for 3 days

 Rash is usually blanchable, maculopapular, occasionally itchy
 Does not usually produce the intensely red conjunctivitis enanthem,
severe cough and branny desquamation
 Causes joint pains
 RUBELLA: Clinical Manifestations of
Congenital Rubella Syndrome (CRS)
 Can result in miscarriage, fetal death or constellation of congenital
anomalies
 Commonly described anomalies: cataracts, pigmentary retinopathy.
Micropthalmos, congenital glaucoma, PDA, pulmonary artery stenosis,
sensorineural hearing impairments neurologic
 Neonatal manifestations: growth restrictions, interstitial pneumonitis,
radioluscent bone disease, hepatoslenomegaly, thrombocytopeniadermal
erythropoiesis “ blueberry muffin” lesiosn
 RUBELLA: Diagnosis

 History taking and physical examination

 Mainly an illness of adolescent and young adults
 Reliable pieces of evidence of acute rubella infection are: positive viral
culture for rubella or detection of rubella virus in PCR, Presence of
rubella-specific IgM antibody, demonstration of significant rise in IgG
antibody from paired and convalescent-phase sera
 RUBELLA: Treatment

 no specific treatment for uncomplicated rubella

 Congenital rubella: supportive care and referral for manageme of
congenital defects monitor hearing impairment
 Gamma globulin replacement therapy for children with low levels of IgG
 Opthalmologic evaluation for infantile glaucoma, cataract, retinopathy
 RUBELLA: Prevention

 Live virus rubella vaccine

 Measles-mumps-rubella (MMR)
 Measles-Mumps-Rubella-varicella (MMRV)
 Measles-containing vaccine (MCV1) monovalent administered at 9-11
months old
 MMR (MCV2) at 12-15 months old
 ROSEOLA:

 Rosealo infantum: aka exanthum subitum, pseudorubella, 6th disease, 3-

day fever
 Acute ill ness frequently seen in young children
 Virus identified from children with roseola: enterovirus, coxsackie virus,
adenovirus, parainfluenza virus type 1 human herpes virus
 HHV 6: major cause of roseola
 ROSEOLA: Pathophysiology

 Unknown pathophysiology
 Not an infection caused by 1 just pathogen
 Rash in roseola may be due to the neutralization of virus in the skin of the
patient at the end of veremia
 Veremia is common in infections with HHV-6 and HHV-7
 ROSEOLA: Epidemiology

 Seen in< 2 years old

 Humans are the only known natural host of HHV6 and HHV7
 ROSEOLA: Clinical Manifestations

 IP: 10-16 days

 Classically manifests as high fever lasting about 3-5 days, followed by the
appearance of rash lasted for 1-2 days
 Irritablity and malaise
 Cough and colds, malaise
 At the lysis of fever- ash appears, maculopapular and discrete.
 Ashes disappears in 1-2 days without desquamation orpigmentataion
 ROSEOLA: Diagnosis

 Made clinically by the presence of FEVER, and the appearance of rash

with the disappearance of fever
 ROSEOLA: Treatment

 No specific treatment for roseola

 Supportive and symptomatic
 Prognosis is generally excellent but maybe guarded if encephalitis occurs
 VARICELLA:

 Varicella zoster virus (VZV)

 It replicates in the nuclei of infected cells where DNA core and capsid are
synthesized
 VARICELLA: Pathogenesis

 IP: 10-23 days, average of 14 days

 VZV establishes latency in the dorsal-root ganglia during primary
infection and/ or breakthrough varicella that may develop despite
immunization
 Reactivation resuls in herpes zoster “shingles”
 VARICELLA:Epidemiology

 Humans are the only source of infection

 Listed 10th leading cause of morbidty
 Transmission via airborne route from direct contact with patient with VZV
lesions
 Highly contagious
 Clinical infection develop in 80-90% of susceptible individuals exposed in
household
 Immunity is lifelong
 VARICELLA: Clinical Manifestations

 Fever
 Generalized pruritic rash lasting for 5 days
 Rash is more intense in the trunk head, extremities
 Rash evolves as a series of “crops” during the course of 1-2 days in a normal host
 250-500 superficial skin lesions, vesicular in varying stages of development and
resolution (crusting)
 Patient is contagious from 1-2 days before the onset of the rush until all lesions
have crusted
 VARICELLA: Clinical Manifestations –
Congenital Varicella Syndrome
 Syndrome occurs after maternal VZV infection develops in the 1st and 2nd
trimester of pregnancy results in fetal death or varicella embryopathy
characterized by limb hypoplasia, cutaneous scarring, eye abnormalities,
CNS damage
 Inapparent varicella and develop zoster early in life without having had
extrauterine varicells
 VARICELLA: Diagnosis

 Polymerase Chain Reaction (PCR) diagnostic test of choice

 Tzank smear
 Direct fluorescent antibody (DFA)assay
 Cell culture using scrapings of vesicle base during first 3-4 days of the
eruptions
 VARICELLA:Treatment

 IV acyclovir therapy is recommended for immunocompromised patiets

including those having chronic corticosteroid treatment
 Oral acyclovis or valacyclovir not recommended
 VARICELLA: Prevention

 Airborne and contact precautions for a minimum of 5 days

 For people without immunity varicella vaccines , ideally administered within 3 days but up to 5
days after exposure
 Varicella –zoster immune globulin (VZIG)
 Passive immunization for immunocompromised patients without immunity, pregnant women,
newborn infants whose mothers had onset of varicella 5 days before delivery or within 48 hours after
delivery
 Hospitalized preterm infants (28 weeks or more of gestation) whose mothers lack evidence of
immunity against varicella
 Hospitalized preterm less than 28 weeks or birthweight of 1,000 g or less regardless of maternal
immunity
 VARICELLA: Prevention

 Active Immunization: Live attenuated varicella zoster vaccine

 Given SQ
 Children 12 months through 15 months  1st dose
 4-6 years old 2nd dose
 Second dose may be given at less than 5 years old with at least 3 months interval between doses
 People 13 years old or older without evidence of immunity should receive 2 doses separated at
least 28 days
 When postpubertal females are immunized , pregnancy must be avoided for at least 1 month
after immunization
 VARICELLA: Prevention

 Breakthrough disease is infection with wild type VZV occurring

morethan 42 days after immunization
 Usually milder , with rash predominantly maculopapular with a median of
fewer than 50 lesions , lower degree of fever and faster recovery