PEDIA 3B- VIROLOGY 2 -Dr.
Mallorca
JAPANESE ENCEPHALITIS
Vector: Culez tritaeniorhynchus summarosus
- night-biting mosquito that feeds
VECTOR/etio
preferentially on large domestic animals
and birds
- Incubation period 4 to 14 days
- A mosquito-borne viral disease of humans as well
as horses, swine, and other domestic animals
- Asia, Northern Japan, Korea, China, Taiwan, the
Philippines, and the Indonesian archipelago and
from Indochina through the Indian subcontinent
EPIDEMIOLOGY
- Infrequently on humans - Summer outbreaks
- The annual incidence in endemic areas ranges 1-10
per 10,000 pop
- Children younger than 15 y/o are principally
affected, with nearly universal exposure by
adulthood
- Pigs serve as an amplifying host --maintain a high
sustained viremia and may be hosts to thousands
of mosquitoes in a single night, thereby producing
an abundant source of infected vectors that can
transmit the infection further
- majority of infections are inapparent or as mild
self-limited illnesses
- Patients who come to medical attention may
have aseptic meningitis or encephalitis, and 5 to
25% die.
- Lethargy, nausea or abdominal pain, headache,
and feverishness
- In 2-3 days, lethargy increases and the child may
exhibit behavior and motor abnormalities
- Sudden convulsion is frequently the initial
symptom
SIGNS AND SYMPTOMS
- Unusual manifestations: acute psychosis and
Guillain-Barré synd
- Signs of meningeal irritation in 2/3 of cases
- Cranial nerve palsies, central facial paralysis
- Muscle weakness, either flaccid or spastic
- With hyperreflexia and ankle clonus
- Focal or generalized convulsions develop in 50 –
75% of patients
- Patients with fulminant infections often die
during the first 5 days of illness
- After virus is introduced by a mosquito bite,
replication locally and within regional lymphatic
tissue  viremia and infection of various organs
and the brain. Neuroinvasion through cerebral
capillaries  infection crosses from the vascular
side of the endothelial cells to the perivascular
PATHOPHYSIOLOGY
space
- Infiltrating T cells elicit a broad inflammatory
response, with B and T cells and macrophages
found in perivascular cuffs and macrophages and
T cells in the parenchyma - The rapidity of the
neutralizing antibody response is the principal
determinant of outcome
- Fatal causes occurring within 5 days after the onset
of illness have no detectable CSF antibody
response while virus is recoverable from the CSF
Famous
MEASLES (Rubeola or Morbilli) / “TIGDAS”
Measles virus SIGNS AND SYMPTOMS
- Family Paramyxovirus Fever (sabay sila nung rash)
- Genus morbillivirus - vs Roseola infantum (Fever muna bago rash) FR
- Has an outer envelope composed of M- protein, H - Temperature rises as rash appears
protein, F-protein, and internal core is RNA - Fever and symptoms subside within 2 days once
- Acute highly contagious rashes are on legs and feet
- single stranded mRNA - If persistent after day 3 – 4 of exanthem, may
– Incubation period: 8 –12 days indicate complication
• Period of communicability
- 1-2 days before the onset of symp. Convalescent stage:
- Brown staining
(3 days before to 4 – 6 days after the onset of rash)
If (+) rashes, antibodies are already formed. - Fine branny desquamation
- Course: 10 – 14 days
• Routes of transmission (DAT)
a. Airborne Other manifestations:
b. Direct contact with infectious droplet Anorexia • Lymphadenopathy • Diarrhea and
c. Transplacentally acquired immunity is protective vomiting • abdominal pain • Slight splenomegaly
for 4 – 6 months; disappear at variable rates COMPLICATIONS
d. Man is the only host. a. Otitis media - most common complication
b. Laryngitis, tracheitis, bronchitis
• Susceptibility of population c. Interstitial pneumonia- 2o to epithelial damage
- 90% of susceptible contact acquire the dse- d. Bronchopneumonia
anything less than 90% can render the whole - Most common cause of death
population still susceptible to the dse - Due to secondary bacterial infection
- Permanent immunity acquired after disease (pneumococcus, streptococcus,
staphylococcus, Hib)
e. Exacerbation of an existing Tuberculous process
Prodrome: - Temporary loss of hypersensitivity
a. 3 – 5 days reaction to tuberculin for 4 – 6 weeks
b. Fever f. Neurologic
c. Cough, colds, conjunctivitis - More common than in any other exanthem
d. Koplik Spot (pathognomonic enanthem) in - Encephalitis: 1-2/1000 cases
the early phase(found near premolars); this - Sub-acute sclerosing panencephalitis
can spread to the vaginal mucosa
ENanthem if found in the buccal mucosa Sub-acute sclerosing panencephalitis
EXanthem if on cutaneous skin (X-Skin) - Rare, degenerative CNS diseases
 Persistent measles virus infection
Rash: Severity of disease is directly related to extent  Infection before 18 months increases risk
and confluence of rash  Boys > girls
1st 24 Faint macules behind ears, along the  Subtle changes in behavior, deterioration of
hours hairline; become confluent school work bizarre behavior frank
DAY 1 maculopapular as it spreads to face, dementia
neck, upper arms and chest  Massive, repetitive, symmetrical myoclonic
2nd 24 Spreads over back, abdomen, entire jerks
hours arms/thighs  True seizures  progresses to stupor and
DAY 2 coma
3rd – Rash reaches legs and feet  fading  High measles antibody titers (HI&CF) in sera
4th day from head to feet  fine branny and CSF
desquamation and brownish  Occur 10.8 years after original infection
discoloration  Others: Guillain-Barré syndrome, hemiplegia,
Nakababa na siya sa L.E and fever cerebral thrombophlebitis, retrobulbar neuritis
usually resolves.
OTHER COMPLICATIONS:
- Myocarditis
- Diarrhea with dehydration
- Idiopathic thrombocytopenia
- Hepatitis
- Appendicitis
Fusion of infected cells results in multinucleated
giant cells, the Warthin-Finkeldey giant cells
that are pathognomonic for measles, with up to
100 nuclei and intracytoplasmic and intranuclear
inclusions
 JAPANESE ENCEPHALITIS MEASLES (Rubeola or Morbilli) / “TIGDAS”
a. Lumbar puncture a. Clinical/epidemiological basis PREVENTION
1. Opening pressures - normal or slightly b. Definitive diagnosis: A. Active immunization
elevated - Measles IgM
2. CSF fluid - lymphocytic pleocytosis fewer 1. Post-exposure immunization
- Increase in measles IgG in paired sera
than 10 cells to several thousand, with a median - Measles vaccine if given within 72 hours
of several hundred per cubic millimeter - Viral isolation (urine, blood, NP after exposure may provide protection in
3. CSF glucose and protein levels are generally secretions) some cases
normal 2. Pre-exposure immunization
b. Electroencephalograms - diffuse theta to delta - 1st dose: at age 6 months
showing wave slowing - 2nd dose: 6 – 9 months after 1st dose, as
c. CT - diffuse white matter edema and non- monovalent vaccine or MMR
DIAGNOSIS

enhancing low-density areas, mainly in the - 3rd dose: monovalent vaccine or MMR at
thalamus, basal ganglia, and pons - Thalamic 4 – 6 years old or 11 – 12 years old
lesions frequently are associated with
hemorrhage B. Passive immunization
d. MRI - similar distribution of abnormalities
- Confirmed serologically by JE virus-specific 1. Immune globulin can be given to prevent or
IgM antibody in serum or CSF by ELISA modify measles in a susceptible person within
- 4-fold titer between acute and convalescent- 6 days of exposure
phase serum 2. Dose: 0.25mL/K IM
- Cross-reactions with dengue virus and other 3. Indications: *remember
flaviviruses are common
- Real-time PCR and T7 promoter-based assays a. Susceptible household contacts especially <1
-- sensitive year old
- JE virus occasionally can be isolated from the b. Pregnant women
blood no later than 6-7 days after onset c. Immunocompromised children - double the
a. No specific antiviral treatment MANAGEMENT dose to 0.5 ml/kg
b. A few patients have been treated with a. Supportive (antipyretics, fluids and electrolytes)
interferon alpha – efficacy has not been b. Appropriate antibiotics for bronchopneumonia
evaluated in wider trials and otitis media DIFFERENTIAL DIAGNOSIS
c. Supportive care and control of intracranial c. Oral Vitamin A • Rubella (German Measles) – more prominent
pressure are critical - 6 months – 1 year old: 100,00 IU cervical L.A
TX AND PREVENTION

d. Mannitol is used routinely - 1 year old and older: 200,00 IU • Roseola infantum
e. Other supportive measures: - Dose repeated the next day and at 4 weeks (Infant Subitum, Exanthem Subitum)
- Control of fever and convulsions if with ophthalmic evidence of vitamin A • Drug rashes
- Fluid balance , Respiratory support deficiency (BITOT’s spots) *remember
- Prevention and treatment of secondary
infections
Prevention :
- Avoidance of vector mosquitoes
- Vaccine:
a. Inactivated
b. Live-attenuated: recommended for
as early as 1yo; 2 doses, 1year apart
 Famous
PARVOVIRUS B 19 ZIKA VIRUS CHIKUNGUNYA VIRUS
ETIOLOGY Mosquito-borne flavivirus (Aedes mosquitoes) - Transmitted by Aedes species and Anopheles
VE
CT
O
R Small, DNA – containing virus spp. ( Similar to dengue)
- Most common in school-aged children 5-15 y/o - Incubation period is unclear - Outbreaks occur
- Incubation period: 4-14 days - Incubation period: 2 – 4 days
- Humans are the only known hosts - First identified in Uganda in 1947 in monkeys
- Transmitted primarily by respiratory secretion - Identified in humans in 1952 in Uganda and the
EPIDEMIOLOGY

- Transmissible in blood/blood products United Republic of Tanzania

- Most adults have been infected - Outbreaks of Zika virus disease have been
- Most infections are subclinical recorded in Africa, the America, Asia and the
- IgG is detectable in most healthy people Pacific
- Sporadic outBreaks, usually among children occur each year
- Transmission from patient to health care staff is not - 2015: Brazil reported an association of
uncommon-Role in nosocomial transmission to other GuillanBarré syndrome and microcephaly
patients
PARVOVIRUS INFECTIONS MOT In infants
1. Fifth Disease (Cutaneous rash)/ Erythema - Can be transmitted through sexual a. Abrupt onset of fever, followed by flushing of
infectiosum,”slapped cheek” intercourse the skin
- Typical lace-like skin rash Contagious - Concern due to an association between b. Febrile convulsion in 1/3 of patients
- Targets red blood cells progenitors before rash Zika virus and adverse pregnancy and c. After 3-5 days of fever, a generalized
- Pain in joints fetal outcomes maculopapular rash and lymphadenopathy
- Results in lysis of cells, thus depleting source of (fever muna bago magrash)
mature red cells d. Conjunctival injection, swelling of the eyelids,
- Anemia ensues pharyngitis, and symptoms and signs of upper
- Rarely fatal and without complications - Symptoms are similar to dengue: respiratory tract diseases are common
 Fever e. No enanthem occurs
2. Transient aplastic crisis (severe acute anemia)  Skin rashes f. some infants have a biphasic fever curve, and
- B19 infection of those with other hemolytic arthralgia may be severe
 Conjunctivitis
anemias Contagious b4  Muscle and joint pain
o Sickle Cell Disease onset of SX In older children
o Thalassemia  Malaise and headache a. Fever, headache, myalgia, and arthralgia
- Can complicate crises  Mild and last for 2-7 days involving various joints (arthralgia more
- Sometimes fatal prominent)
SIGNS AND SYMPTOMS

3. Pure red cell aplasia (chronic anemia) COMPLICATIONS b. Macular blush and a maculopapular rash and
4. Hydrops fetalis (fatal fetal anemia) - microcephaly marked lymphadenopathy precede
5. Infection of immunodeficient patients - Guillain-Barré syndrome defervescence
- Can cause persistent infection in bone marrow c. (+) tourniquet test – rare
- Suppress red cell maturation d. Maculopapular rash, arthralgia or arthritis,
- Leads to anemia and conjunctival injection were more common
6. Infection during pregnancy symptoms symptoms in chikungunya than in
- Can cause fetal anemia dengue
- Usually not fatal to fetus e. Shock and bleeding are rare

OTHER CLINICAL MANIFESTATIONS:

1. Arthritis/Arthralgia
2. Fetal Infections
- Occur with primary infection in mother
- 2nd trimester = most sensitive time
- Non-immune hydrops and/or fetal death
- Lytic infection of erythrocyte precursors red cell aplasia
profound anemia  high output failure  hydrops
- Infected infants in utero born normally at term even with
evidence of hydrops by ultrasound
COMPLICATIONS
1. Persistent arthritis after El
2. Thrombocytopenic purpura
3. Aseptic meningitis
4. Virus – associated hematophagocytic syndrome
a. Laboratory tests not routinely available a. Clinical: travel history and exposure a. Clinical
b. Not isolated by culture b. Nucleic Acid Testing (NAT): b. IgM capture ELISA after 5 days of onset of
DIAGNOSIS

c. Based on observation of Typical Rash and exclusion of whole blood, serum and/or urine collected illness
other conditions from patients presenting with onset of c. PCR
d. (+) IgM anti-B19 – best marker of recent or acute symptoms < 7 days d. Viral culture
infection c. Serology: IgM detection; only done among
e. IgG anti-B19 – past infection or immunity pregnant women or those with GBS

a. No specific antiviral treatment a. No specific treatment a. Supportive

b. IVIg for immunodeficient patients with chronic b. Symptoms are refractory to aspirin or other
Prevention NSAIDs
TX AND PREVENTION

anemia
- Protection against mosquito bites is a c. Chloroquine phosphate (250mg/day) provides
c. Transfusion and supportive care for patients with
key measure to prevent prompt relief from chronic arthralgia in a high
aplastic crisis - Physical barriers such as window proportion of sufferers
d. Intra-uterine blood transfusion in some cases of B- screens or closing d. Analgesics or mild sedation to control pain
19 infected hydrops fetalis e. Febrile convulsions: phenobarbital or diazepam
f. Fluids
PREVENTION : Vaccines: not yet available
Avoidance and Control of mosquitoes
Epidemic measures , Health education
 Famous
RUBELLA (German measles) VARICELLA (Chicken pox) or HERPES ZOSTER (Shingles)
“TIGDAS HANGIN”(internet) ”BULUTONG TUBIG”
- 2 LETTER L, 2 WORDS (german measles) Varicella: zoster virus
Rubella virus of Togaviridae family Herpes viridae family
- German measles: first described by German physicians, Friedrich Hoffman, in the Varicella Zoster Virus
mid-eighteenth century - Acute viral illness, Infectious nature demonstrated in 1875
ETIOLOGY

- Derived from the Latin, meaning little red - Zoster described in premedieval times
- "3-day measles" - Varicella not differentiated from smallpox until end of 19th century
- That starts initially on the face and neck - Herpes virus (DNA)
- Spreads centrifugally to the trunk and extremities within 24 hours - Primary infection results in varicella (chickenpox)
- Begins to fade on the face on the second day - Recurrent infection results in herpes zoster (shingles)
- Congenital rubella syndrome (CRS) described by Gregg in 1941 - Short survival in environment
• Period of communicability: Few days before up to 5 – 7 days after the rash • Period of communicability
• Incubation period: 14 – 21 days - 1 – 2 days before the rash start until 5 – 7 days after the rash and
a. Person to person via respiratory route: the lesions have crusted
- Droplet from nose and throat •Incubation period
- Droplet nuclei (aerosols) - range 10 – 21 days (14 – 16 days)
MOT

- Maintain in human population by chain transmission
b. Acquired during pregnancy – vertical transmission
- Virus can enter via the placenta & infect the fetus in utero (Congenital
Rubella Syndrome)
PATHOGENESIS
- 1 – 16 days in infant born to mother with active varicella (isolate)
• Mode of transmission
- Direct inoculation w/ skin lesions (varicella or herpes zoster)
- Airborne spread (varicella)
- Highly contagious; 80-90% household transmission rate

- Majority (2/3) of infecions are SUBCLINICAL MILD PRODROME 1 – 2 days

- 24 – 48 hours before rash
SIGNS AND SYMPTOMS

a. Lymph nodes - suboccipital, postauricular, and anterior cervical lymph nodes are - Fever, malaise, anorexia, headache and mild abdominal pain
most prominent , 24 hrs before the rashes appear (mauuna muna yung kulani Rash
saka palang magkakarashes) - Generally appear first on the head; most concentrated on trunk
- Appear as very pruritic macules on scalp, face or trunk
b. Rash - first manifestation - Macules rapidly progress to vesicular  pustular  crusting stages
- Begins on the face and neck as small, irregular pink macules that coalesce, (pwede din sila magpakita ng sabay sabay, as in halo halo ang
and it spreads centrifugally to involve the torso and extremities, where it makikita mo)
tends to occur as discrete macules - New crops of lesions daily x 3 – 7 days
- Tends to diasappear by DAY 3 WITHOUT DESQUAMATION OR PEELING - Various stages of evolution
OF THE SKIN (vs MEASLES) - Ulcerative lesions in oropharynx, conjunctivae and genital mucus
membranes
c. Forchheimer spots - Time of onset of the rash, examination of the oropharynx:
tiny rose-colored lesions PROGRESSIVE SEVERE VARICELLA
- Pathognomonic Sign - Continuing eruption of lesions (large, umbilicated and hemorrhagic)
- Fleeting enanthema with high fever unto 2nd week of illness
- Pinpont or larger petechiae that usually occur on the soft palate in 20% - Primary varicella pneumonia, hepatitis, encephalitis
- Similar spots can be seen in measles and scarlet fever - Seen in healthy adolescent and adults, newborn infants and
immunocompromised patients
d. Other signs and Symptoms:
- Eye pain on lateral and upward eye movement (troublesome complaint) COMPLICATIONS
- Conjunctivitis • Sore throat • Headache • General body aches a. Pneumonia - Most common complication in adults
- Low-grade fever- Fever rarely rises above 38°C (100.4°F) VS MEASLES b. Hepatitis - Relatively common; usually subclinical
- Chills • Anorexia • Nausea • Arthritis c. Encephalitis and Cerebellar ataxia
d. Others:
COMPLICATIONS - Thrombocytopenia, nephritis/nephrotic syndrome, hemolytic-uremic
a. May produce transient arthritis, particularly in women syndrome, myocarditis/pericarditis, pancreatitis, orchitis
b. Serious complications: e. Bacterial Superinfection:
- Thrombocytopenic purpura : 1/3000 cases a. Skin:
- Encephalitis : 1/6000 case; progressive rubella encephalitis - Strep. pyogenes or Staph aureus
- range from superficial impetigo to cellulitis, lymphadenitis and
subcutaneous abscesses
IMMUNITY - suspected if with erythema of the base of new vesicle or
a. Antibodies appear in serum as rash fades and antibody titer raise recrudescence of fever 3 – 4 days after initial rash
(pagpawala na yung rash, tumataas na yung antibodies mo) b. More invasive infections:
b. Rapid raise in 1 – 3 weeks - Sepsis , Pneumonia , Arthritis , Osteomyelitis , Varicella gangrenosa ,
c. Rash in association with detection of IgM indicates recent infection Necrotizing fasciitis ,Toxic Shock Syndrome
d. IgG antibodies persist for life
 Continuation…. Famous
CONGENITAL RUBELLA SYNDROME HERPES ZOSTER CONGENITAL VARICELLA SYNDROME
a. Occurs during the 1st trimester of pregnancy a. Reactivation of varicella zoster virus a. Results from maternal infection during
b. Affects the development of the fetus b. Associated with : pregnancy
c. May lead to several birth defects Aging • Immunosuppression • Intrauterine b. Period of risk may extend through first 20
d. Infection may affect all organs exposure • Varicella at <18 month of age weeks of pregnancy
e. May lead to fetal death or premature delivery c. Localized, unilateral vesicular lesions in 1 – 3 c. Atrophy of extremity with skin scarring
f. Severity of damage to fetus depends on gestational dermatomes (Cicatrix- spiral scar), low birth weight, eye and
age d. Infrequently associated with localized pain, neurologic abnormalities
g. Infants: virus is isolated from urine and feces hyperesthesia, pruritus and low grade fever d. Risk appears to be small (<2%)
e. Complete resolution in 1 – 2 weeks
f. Postherpetic neuralgia (pain >1 month)
unusual in children
g. Disseminated cutaneous disease and/or
visceral dissemination in immunocompromised
patients
MATERNAL RUBELLA INFECTION AND RISK OF CRS Stigmata of Varicella-Zoster Virus Fetopathy
Before 11 week of gestation 90% a. Damage to sensory nerves:
11 – 12 weeks 33% Cicatricial skin lesions , Hypopigmentation
13 – 14 weeks 11% b. Damage to optic stalk and lens vesicle:
15 – 16 weeks 24% Microphthalmia • Chorioretinitis • Cataracts •
After 16 weeks of gestation uncommon Optic atrophy
c. Damage to brain/Encephalitis: Microcephaly/
hydrocephaly • Calcifications/aplasia of brain
d. Damage to Cervical or Lumbar cord:
Hypoplasia of extremity • Motor/sensory
deficits • Absent DTRs • Anisocoria/Horner
syndrome • Anal/vesical sphincter dysfunction
a. Sensorineural hearing loss – 58% most common GROUPS AT INCREASED RISK FOR COMPLICATIONS OF VARICELLA
b. Cataract, infantile glaucoma, micro-ophthalmia, 1. Normal adults
pigmentary retinopathy occur in approximately 43% 2. Immunocompromised persons
(“salt and pepper retinopathy”) 3. Newborns with maternal rash onset within 5 days before to 48 hours after delivery (if with
*remember rashes within this period, it implies that the mother is still in the viremic phase no Ab’s from
c. Congenital heart disease PDA and pulmonary the mother yet  the baby is not protected)
artery stenosis - 50%
d. Bone lesions TREATMENT: Acyclovir: DOC for varicella/herpes zoster when indicated
e. Psychiatric disorders
f. T1 Diabetes Mellitus For Zoster: For Varicella:
g. Hypogammaglobulinemia a. Immunocompetent host a. Not routine in healthy children
h. Generalized lymphadenopathy IV: all ages: 30mg/k/day x 7 – 10 days b. Considered in patients at increased risk of
SIGNS AND SYMPTOMS

i. Intrauterine growth restriction Oral: > 12 years old: 4000mg/day in 5 divided moderate to severe varicella
j. Liver and spleen damage doses x 5 – 7 days 1. >12y/o
- Hepatosplenomegaly, hepatitis, jaundice b. Immunocompromised host 2. Chronic cutaneous or pulmonary
- Thrombocytopenic purpura, with IV: disorders
petechiae and "blueberry muffin" lesions <12 years old: 60mg/k/day q8 x 7 – 10 days 3. Long term salicylate therapy
k. CNS >12 years old: 30mg/k/day q8 x 7 days 4. Short, intermittent or aerosolized
- Retardation, microcephaly courses of corticosteroid
- Motor delay, behavioral disorders, autism c. Dose:
- Intellectual disability – 13% 1. Immunocompetent hosts
- A rare complication of panencephalitits can Oral: 80mg/k/day in 4 divided doses x 5
occur in second decade with congenital rubella days (max 3,200mg/day)
syndrome may progress to death 2. Immunocompromised hosts (IV)
a. <1 y/o - 30mg/k/day in 3 divided doses x
7 – 10 days
Classic Triad of Congenital Rubella: CD
b. >1 y/o – 1,500mg/m2/day in 3 divided
- Syempre remember: puti ang mata, maliit ang ulo, doses x 7 – 10 days
may problema sa puso
a. Cataract
b. Cardiac abnormalities
c. Deafness
a. Clinical diagnosis is unreliable DIAGNOSIS
b. Many viral infections mimic Rubella – a. Clinical
c. Specific diagnosis of infection with: Isolation of virus b. Definitive diagnosis:
Evidence of seroconversion - Tissue culture : distinguishes VZV from HSV
DIAGNOSIS

- Direct fluorescent antigen - more rapid/ sensitive than culture

Isolation and Identification of Virus - Tzanck smear - not specific for VZV
a. Nasopharyngeal or throat swabs taken 6 days prior or c. PCR - distinguish wild type strains from vaccine virus
after appearance of rash is a good source or Rubella d. Varicella IgG - retrospective diagnosis
virus
b. Using cell cultured in shell vial antigens can be
detected by immunofluorescent methods
 Post natal Varicella vaccine:
- Mild illness a. Live attenuated wild Oka strain
- Antipyretics and analgesics b. Dose: 0.5mL SQ - 2 doses:
- IVIg or corticosteroids can considered for severe, non- - <13y/o-at 12mos and after 3mos or at 4-6 y/o
remitting thrombocytopenia - 13 y/o and older - 2 dose, 1 month apart
c. Efficacy:
TX AND PREVENTION

CRS (Congenital Rubella Syndrome) - 85-95% effective for prevention of varicella in Children during outbreaks
a. Pediatric, cardiac, audiologic, ophthalmologic, and - 100% effective for prevention of moderate or severe disease
neurologic evaluation
b. Follow-up because many manifestations may not be PREVENTION
readily apparent initially or may worsen with time Passive immunization
c. Hearing screening - Varicella zoster immunoglobulin
- Candidates for VZIG after significant exposure * remember
Prevention 1. Immunocompromised patients without previous infection
a. MMR: live and attenuated; confers lifelong immunity 2. Susceptible pregnant women
b. Given to children 12 – 15 months and again between 3. New born whose mother had chicken pox 5 days before or within 48 hours after delivery
4 – 6 years of age 4. Hospitalized premature (>28wks AOG) whose mother without varicella or negative serostatus
c. Immunization of the young children and teenage 5. Hospitalized premature (<28wks AOG) regardless of maternal history of varicella or serostatus
girls remain the best option to prevent CRS

ROSEOLA INFANTUM /“TIGDAS HANGIN”(in lec)

- Also known as exanthum subitum or sixth disease - Clinically recognized: based on fever, defervescence, and exanthem
- Roseola is a mild febrile, exanthematous illness occuring almost patterns (FED)

DIAGNOSIS
exclusively during infancy - CBC: leukopenia with lymphocytosis
- More than 95% of roseola cases occur in children younger than 3 yr, with - Definite diagnosis (Research labs)
a peak at 6-15 mo of age - Viral isolation (peripheral lymphocytes) – 4 fold rise in Ab titer;
- Transplacental antibodies likely protect most infants until 6 mo. of age implies new infection or reactivation
- Infants with classic roseola exhibit a unique constellation of findings - Detection of HHV – 6 Ag by PCR
displayed over a short period of time
a. Human herpesvirus 6 (HHV-6) - more common 1. Rubella: in Roseola, rashes ALSO disappear without desquamation
- Primary HHV-6 infection occurs early in life 2. Measles
- More than 90% of newborn infants are HHV-6 seropositive, reflecting 3. Roseola-like illnesses i.e. Enteroviruses
DIFFERENTIAL DIAGNOSIS

transplacental transfer of maternal antibodies. 4. Scarlet fever

- By 4-6 mo of age, the prevalence drops significantly (0-60%) 5. Drug hypersensitivity
- Peak acquisition of primary HHV-6 infection, from 6-24 mo of age,
ETIOLOGY

corresponds with peak acquisition of roseola

- Uncommon before 3 months or after 3 years
- can also infect other cells : CD8 (suppressor) T cells, natural killer T cells,
δγ T cells, glial cells, epithelial cells, monocytes, megakaryocytes, and
endothelial cells
b. Human herpesvirus 7 (HHV-7)
- Belong to the β-herpesvirus subfamily of herpesviruses
- The principal target cells for infection in vivo are CD4 T cells
- Sabi ko kanina FR (Fever muna before Rash), oK? a. Supportive care – antipyretic, hydration
- The incubation period averages 10 days (range of 5-15 days). b. Unusual or severe manifestations of primary or presumed reactivated
- The prodromal period is usually asymptomatic HHV-6B infection such as encephalitis, especially in
- mild upper respiratory tract signs e.g.minimal rhinorrhea, slight immunocompromised patients, may benefit from treatment:
pharyngeal inflammation Ganciclovir, Foscarnet, and Cidofovir
- mild conjunctival redness
- Fever – sudden onset, high grade, accompanied by fussiness w/o
apparent cause usually resolves acutely after 72 hrs
- Rash coincident with the appearance of a faint pink or rosecolored,
nonpruritic, 2-3 mm morbilliform rash on the trunk usually lasts 1-3 days,
SIGNS AND SYMPTOMS

but is often described as evanescent and may be visible only for hours,
spreading from the trunk to the face and extremities.
TREATMENT

ASSOCIATED SIGNS AND SYMPTOMS:

- Bulging fontanels: 26 - 30%
- Seizures: 5 - 35%
- Occipital or Cervical Adenopathy: 30-35%
- Respiratory S/Sx: 55 -70%
- Edematous eyelids: 0 -30%
- Mild diarrhea: 55 -70%

- In Asian countries, ulcers at the uvulopalatoglossal junction (Nagayama

spots) are common in infants with roseola
- Exanthems associated with roseola:
- The roseola rash begins as discrete, small (2-5 mm), slightly raised
pink lesions on the trunk and usually spreads to the neck, face, and
proximal extremities

As iron sharpens iron, so one person sharpens another. Prov. 27:17

Tulong-tuong besh! #roadtoJI
Ppt and some lecture notes only