Far Eastern University – Nicanor Reyes Medical Foundation - There is fever, nonspecific respiratory symptoms (cough,
PEDIA 3B: VIROLOGY B colds), conjunctivitis and photophobia.
Dra. Edna Mallorca
MEASLES/RUBEOLA
- Rubeola / Morbilli
- Common, even before the availability of vaccines.
- HUMANS are the only host
- It is highly contagious. Despite high vaccination rates, there
are still documented cases.
TRANSMISSION
- airborne (cough and droplet) or direct contact with
infectious droplet àmucous membrane or conjunctiva àif
susceptible, you can have the disease.
- 90% chance that a susceptible contact acquires the disease.
- Permanent immunity is acquired after the disease
- Man is the only hoset
PERIOD OF COMMUNICABILITY
- 1-2 days before the onset of symptoms (3 days before to 4-
6 days after the onset of rash) àThe rashes usually appear
on the 3rd day.
- The first manifestation is usually fever.
- 1 day before the appearance of fever or 3 days before the
onset of rash until 4-6 days after the onset of rash, the virus
is communicable.
INCUBATION PERIOD
- 8-12 days
- EXAMPLE: A patient with a history of fever and rashes is
brought to the ER and was eventually diagnosed with
measles.
o There were other patients in the ER during that
time.
o Assuming the patient had a 3- day history of fever
when he came in, and it was the first day of rashes,
he is still contagious.
o The incubation period is significant to the other
patients exposed.
o We will have to monitor the exposed patients from
the 8th to the 12th day from the last time they were
exposed.
o Check the immune status of these patients.
o Observe if they will have an illness from the 8th-
12th day so that appropriate management can be
given.
- In the same way, if a patient comes in with measles we ask
for possible exposure, in the past 1 to 2 weeks.
CLINICAL MANIFESTATIONS
- Prodrome: 3-5 days
PEDIATRICS 3B: VIROLOGY B
o At this time we may already see the pathognomonic
enanthem known as KOPLIK SPOTS
(pathognomonic sign)
§ which are grayish white macules located at the
buccal mucosa in front of the premolars.
§ These may be seen, even in the absence of
rashes. This will be followed by the exanthem.
- 1st 24 hrs: Faint macules behind ears, along the hairline;
become confluent maculopapular as it spreads to face,
neck, upper arms and chest.
- 2nd 24 hrs: Spreads over back, abdomen, entire
arms/thighs
- 3rd – 4th days: Rash reaches legs and feet à fading from
head to feet à Fine branny desquamation and brownish
discoloration
o The rash usually develops within 4 days.
o By the time the rashes reach the sole, the fever
would usually lyse in 24-48 hours.
o If there is persistence or recurrence of fever,
consider possible complications.
- Convalescent stage – branny desquamation with brown
staining of the rashes.
o Darkened rashes confirm the diagnosis
- The whole course of the disease is: 10-14 days
- The rashes are reddish, erythematous, maculopapular and
quite confluent. The child may have conjunctivitis.
OTHER MANIFESTATIONS
- Anorexia à decreased appetite
- Lymphadenopathy
- Diarrhea and vomiting – indication for admission and
provision of IV fluids
- Abdominal pain
- Slight splenomegaly – may have hepatosplenomegaly
MODIFIED MEASLES
- Mother gets measles antibody from prior disease or
complete measles vaccine (acquired and passive)
- Occurs in partially immune hosts
o Partial protection from maternal antibody
o Partial vaccine failure
- Shortened prodrome, cough and coryza are minimal
- Rash w/ same progression pattern w/o confluence
- Koplik spots few and transient, may not occur
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 - Diagnosis not made in the absence of cough
ATYPICAL MEASLES
- Associated with killed measles vaccine (until 1967)
- Less severe cases may follow live attenuated
- Abrupt onset of high fever, headache, myalgia, dry non-
- productive cough, vomiting, pleuritic chest pain &
weakness
- Coryza and conjunctivitis not prominent
- Koplik Spots – rare
- 2-5 days later, maculopapules on palm, wrist, soles and
ankles → centripetal direction → vesicular (w/o scab) →
- purpuric or hemorrhagic
- Lobular/segmental pneumonia w/ pleural effusion is
common
- Other findings:
o Marked hepatomegaly
o Marked hyperesthesia
o Numbness & paresthesia
COMPLICATIONS
- Otitis Media – the most common complication
- Laryngitis, Tracheitis, Bronchitis
- Interstitial Pneumonia secondary to measles virus (damage
to epithelium) or to bronchopneumonia
- Pneumonia – the most common cause of death of patients
with measles
o Due to secondary bacterial infection
- Exacerbation of an existing Tuberculous process
o Temporary loss of hypersensitivity reaction to
tuberculin for 4-6 weeks
- Sub-acute Sclerosing Pan Encephalitis (SSPE) - Long term
complication: indolent illness usually starting 11 years after
the first onset of measles à Gradual deterioration of the
mental status à coma, seizure.
o CSF analysis shows high level of measles antibodies.
Patients who develop measles early on and infants
are at risk.
- Myocarditis
- Diarrhea with dehydration
- Idiopathic Thrombocytopenia
- Hepatitis
- Appendicitis
DIAGNOSIS
- Clinical and Epidemiologic bases
- Definite diagnosis:
o Measles IgM - PCR
o ↑ in measles IgG in paired sera – there should be
an increase in the antibody titer comparing the
acute and convalescent sera.
o Viral isolation (urine, blood, NP secretions) – done
only in reference laboratories.
PEDIATRICS 3B: VIROLOGY B
DIFFERENTIAL DIAGNOSIS
- Rubella – more prominent cervical lymphadenopathy
- Roseola infantum – rashes appear when fever is GONE,
unlike in measles, same onset of rashes and fever
- Drug rashes
MANAGEMENT
- No antiviral used.
- We only give supportive measures (Antipyretics, IV fluids
and electrolytes).
- WHO recommends giving of Oral Vitamin A for 2 days in
developing countries.
o <6 months: 50,000 IU/day
o 6 months to 1 year old: 100,000 IU/day
o >1 year old: 200,000 IU/day
- For patients with ophthalmologic evidence of vitamin A
deficiency (BITOT’S SPOT), the dosage must be repeated
after 2-4 weeks.
PREVENTION
- Active immunization – stimulation of the immune system
- Post-exposure immunization - given to a susceptible
patient to prevent occurrence of measles after an
exposure, given within 72-hours after exposure.
- The patient is already infectious 1-2 days before the onset
of fever.
o If an exposed patient presents with rashes, count at
least 72 hours from the time of exposure.
o If it goes beyond 72 hours, we cannot give the
vaccine anymore since this may worsen the
patient’s condition.
- If the patient is presenting with fever, he is already
contagious.
o Count from the time the patient had fever.
o If the patient presented at the ER and immediately
diagnosed as measles, we can count the 72h.
PRE-EXPOSURE IMMUNIZATION
- Routine immunization
- 1st dose: at 9 months of age
- 2nd dose: MMR at 12 months of age
- 3rd dose: MMR at 4-6 years or 11-12 y/o or at least 1 month
after the second dose.
- Passive Immunization – Immune globulin can be given to
prevent or modify measles in a susceptible person within 6
days after exposure.
o There is a longer golden period.
o Dose: 0.25 ml/k IM
- Indications for passive immunization
o Susceptible household contacts especially < 1year
of age
o Pregnant women – we can’t give active
immunization.
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 § They should be susceptible.
§ No immunization is indicated if she had the
disease before or has received her
immunization since antibodies are already
present.
o Immunocompromised children

RUBELLA / GERMAN MEASLES

- The name “rubella” is from Latin meaning “little red”
- Togaviridae family
- Also known as 3-day measles
- 1st day: Maculopapular rashes start on the face and neck
spreads centrifugally to the trunk and extremities.
- 2nd day: Rashes on the face fade
CLINICAL MANIFESTATIONS
- 3rd day: Rashes disappear throughout body at end of day
- About 2/3 of infections are subclinical
- Rash (exanthema) – the primary symptom of rubella virus
CONGENITAL RUBELLA SYNDROME (CRS)
infection. It appears on the face, which spreads to the trunk
- In general, Rubella acquired after birth is mild. However,
and limbs, and usually fades after three days with no
pregnant women who acquire the infection may develop
staining or peeling of the skin (no desquamation).
this dreaded syndrome. We provide vaccination against
- Lymph Node – tender lymphadenopathy (particularly
Rubella primarily to avoid the development of CRS.
posterior auricular and suboccipital lymph nodes) persist
for days up to a week.
TRANSMISSION
- Low grade fever – rarely rises above 38 OC (100.4 OF)
- mainly through droplets (via respiratory route)
- It can also be acquired during pregnancy via vertical
transmission in which the virus can enter via the placenta &
infect the fetus in utero (Congenital Rubella Syndrome).

PERIOD OF COMMUNICABILITY
- 5 days before up to 6 days after the rash. It is imperative to
determine if there were pregnant women exposed to the
patient. - There is no diarrhea, cough or colds, no branny
desquamation.
INCUBATION PERIOD - Just low grade fever, rashes and lymphadenopathy.
- 14-21 days - FORCHHEIMER’S SPOT – the pathognomonic sign which is
- Significant for those patients exposed. a fleeting enanthem.
- When will you tell a patient that he did not contract the o Pinpoint or larger petechial lesions located at the
disease? 21 days after exposure. soft palate.
o However, these are not that specific.
§ This is also seen in dengue.
§ This is present only in 20% of the patients.
- Other signs and symptoms
o Eye pain on lateral and upward eye movement (a
particularly troublesome complaint), conjunctivitis,
sore throat, headache, general body aches, chills,
anorexia, nausea and arthritis

COMPLICATIONS
- Arthritis (a significant finding), thrombocytopenic purpura,
encephalitis, and Progressive Rubella Panencephalitis

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 IMMUNITY
- Antibodies appear in serum as rash fades and antibody
titers raise
- Rapid raise in 1 – 3 weeks
- Rash in association with detection of IgM indicates recent
infection.
- IgG antibodies persist for life
CONGENITAL RUBELLA SYNDROME
- Results when a susceptible pregnant woman develops
Rubella within the first 8 weeks of gestation.
o It affects the development of the fetus.
o Among infants with CRS, the virus can be isolated
from their urine and the feces until the first year of
age.
o They are contagious while they are shedding the
virus.
- The classic triad or CRS: Cataract, Cardiac Abnormalities,
and Deafness
- Microcephaly and sometimes, hydrocephalus may be
present.
- Patent Ductus Arteriosus is the most common cardiac
abnormality present.
MANIFESTATIONS OF CONGENITAL RUBELLA SYNDROME
- Sensorineural hearing loss – This is the most common
clinical manifestation presenting in 58% of cases.
- Congenital heart disease – PDA (most common) and
pulmonary artery stenosis – presenting in 50% of cases.
- Cataract (most common), infantile glaucoma, micro-
ophthalmia Æ salt & pepper retinopathy – occur in
approximately 43%.
- DM type 1, hypogammaglobulinemia, generalized
lymphadenopathy, IUGR, liver and spleen damage,
hepatosplenomegaly, hepatitis, jaundice,
thrombocytopenic purpura, with petechiae and "blueberry
muffin" lesions and central nervous system à retardation,
microcephaly
MANAGEMENT
- In managing patients with CRS, a multi-organ approach
must be taken.
- Hearing tests must be done; check the heart (may refer
them to cardiologist for clearance); monitor these patients
PEDIATRICS 3B: VIROLOGY B
for possible neurologic problem (warranting referral to a
neurologist); and rule out cataract by examining the ROR
(but better to refer to an ophthalmologist).
- The blueberry muffin lesions may be present at birth and it
is due to thrombocytopenia.
- Eventually some patients may be prone to develop diabetes
mellitus.
DIAGNOSIS
- Mainly Clinical
- Many viral infections mimic Rubella
- Rubella is sometimes misdiagnosed as measles.
- To differentiate Rubella from Measles, the rashes of
Rubella progress faster whereas the rashes of Measles take
longer to progress (4 days) and desquamate later on.
- However in some cases where the patient is partially
immune, there is what we call MODIFIED MEASLES in which
small amount of antibodies are present but insufficient to
protect against full blown measles.
o In these cases, measles is harder to detect due to its
atypical presentation.
- The infection can be specifically diagnosed through viral
isolation and through evidence of seroconversion.
- For example, in a pregnant mother who is exposed to
Rubella, you may get the antibody levels initially as
baseline. If there is seroversion from negative to positive or
there is a fourfold rise in the antibody, then the patient
developed Rubella.
MANAGEMENT
- Post-natal Rubella is a mild illness.
- Supportive measures (antipyretics and analgesics) and rest
are adequate.
- However in cases of non-remitting severe
thrombocytopenia, intravenous immunoglobulin (IV Ig) or
corticosteroids are provided.
- Congenital Rubella Syndrome must be approached in a
multidisciplinary manner.
o Pediatric, cardiac, audiologic, ophthalmologic, and
neurologic evaluations are warranted.
o It is important to follow-up with the patient because
many manifestations may not be readily apparent
initially or may worsen with time.
o Hearing screening must also be done.
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 PREVENTION
- Patients with CRS may secrete virus up to 1 year of age
- Vaccine: MMR - Given to children 12 to 15 months of age.
o The 2nd dose may be given at 4-6 years of age or at
least 1 month from the first dose of MMR
- Immunization - best option to prevent Congenital Rubella
Syndrome.
o Women in their reproductive age group must
receive MMR.
ROSEOLA INFANTUM / EXANTHEM SUBITUM / SIXTH DISEASE
INCIDENCE
- Also known as exanthum subitum or sixth disease; locally
known as tigdas-hangin
- A mild febrile, exanthematous illness occurring almost
exclusively during infancy.
- It is usually seen in children aged 3 months to 3 years.
- More than 95% of Roseola cases occur in children younger
than 3 years of age, with a peak incidence at 6th to 15th
month of age.
- By 4-6 months of age, prevalence drops.
- It is uncommon before 3 months, or after 3 years old.
ETIOLOGIC AGENTS
- HUMAN HERPESVIRUS 6 (HHV-6)
o This is the more common etiologic agent.
o Aside from the CD4 T-cells, this particular virus can
also infect other cells such as the CD8 (suppressor)
T-cells, natural killer T-cells, δγ T cells, glial cells,
epithelial cells, monocytes, megakaryocytes and
endothelial cells.
o Even if it is a mild disease, it can suppress the
immune system.
o The peak acquisition of primary HHV-6 infection is
from 6th to 24th month of age corresponding with
the peak acquisition of Roseola.
- HUMAN HERPESVIRUS 7 (HHV-7) – primarily targets the
CD4 T-cells.
INCUBATION PERIOD
- 10 days (ranging from 5-15 days)
CLINICAL MANIFESTATIONS
- During the prodromal period, the patient is usually
asymptomatic or with mild symptoms.
- He may present with mild upper respiratory tract signs
(mild cold & cough, minimal rhinorrhea, slight pharyngeal
inflammation).
- Some may have a mild conjunctival injections. àFollowed
by a sudden onset high grade fever, accompanied by
“fussiness” lasting for up to three days à Fever lyses à
Rashes appear à nonpruritic, faint pink or rose-colored
PEDIATRICS 3B: VIROLOGY B
and morbilliform, measuring 2-3 mm, initially on the trunk
spreading to the face and extremities.
- If you have a 6th-15th month old patient who presents with
high grade fever and occasional cough, check for the
appearance of rashes on the trunk.
o The rashes usually appear after the fever lyses
(typical of Roseola).
- In Asian countries, infants with roseola can also present
with NAGAYAMA SPOTS which are ulcers at the
uvulopalatoglossal junction.
o These are non-specific.
ASSOCIATED SIGNS AND SYMPTOMS
- Bulging fontanels (26-30%)
- Seizures (5-35%) – Patients are misdiagnosed with
meningitis (high grade fever, bulging fontanel, with seizure)
- Occipital or Cervical Adenopathy (30-35%)
- Respiratory S/Sx (55-70%)
- Edematous eyelids (0-30%)
- Mild diarrhea (55-70%)
- 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.
- The rashes last for around 3-5 days
DIAGNOSIS
- Clinical à based on fever, defervescence and exanthem
pattern.
- CBC result shows leukopenia with lymphocytosis.
- Definitive Diagnosis (epidemiologic studies) à Viral
Isolation, or documentation of fourfold rise in Antibody
titer (seroconversion) and PCR.
DIFFERENTIAL DIAGNOSES
- Rubella, Measles, Roseola-like illnesses
o i.e. Enteroviruses, Scarlet Fever, Drug
Hypersensitivity etc.
MANAGEMENT
- Treatment is primarily supportive.
- Use of antipyretics and hydration indicated.
- Severe manifestations e.g. encephalitis especially in
immunocompromised patients may benefit from antivirals
o i.e. Ganciclovir, Foscarnet, and Cidofovir.
o These are not always indicated.
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 VARICELLA/CHICKENPOX & HERPES ZOSTER/SHINGLES
ETIOLOGIC AGENT
- VARICELLA ZOSTER AND HERPES ZOSTER VIRUS
- Primary infection à Varicella / Chickenpox.
- Latent Infection àleads to reactivation àShingles.
- Herpes viridae family
- Acute viral illness
MODE OF TRANSMISSION
- Direct contact with skin lesions (both varicella & shingles)
- Airborne spread (Varicella)
- VARICELLA
o via airborne, droplet or by contact.
o It is more contagious than Herpes Zoster.
o Likened to measles since there is 90% chance of
acquisition after an exposure to a patients with
Varicella.
- HERPES ZOSTER
o mainly by direct contact.
o If the patient is immunocompromised, the patient
can transmit the disease by airborne
PERIOD OF COMMUNICABILITY
- 1-2 days before until 5-7 days after the appearance of rash
and as long as the lesions haven’t crusted.
- EXAMPLE – A patient presents with “bulutong” and is
asking when he will be able to return to work. There must
be at least 7 days from the onset of the rash AND the lesion
should have all crusted. Even if the 7th day mark has been
reached but there are still lesions that haven’t crusted, we
don’t give clearance.
INCUBATION PERIOD
- 10-21 days.
- To tell a person who is exposed to Varicella that he hasn’t
contracted the disease, there must be at least 3 weeks from
the time of exposure
- 1 – 16 days in infant born to mother with active varicella
PATHOGENESIS
- Varicella gets into the nasopharynxà regional lymph nodes
(viremia) à blood (viremia) à VARICELLA à virus travels
to different tissues, specifically the sensory ganglia and
stays there at the dorsal root ganglia and undergo latency.
- Once re-exposed or immune system is suppressed, it can
reactivate usually at a dermatomal level where the virus
had undergone latency à SHINGLES
CLINICAL MANIFESTATIONS
- Mild Prodrome: 1-2 days.
- There is low grade fever, body malaise, anorexia, headache
and mild abdominal pain à rashes appear, described as
PEDIATRICS 3B: VIROLOGY B
maculopapular and erythematous à rapidly becoming
vesicular and pustular à crusting (final stage).
- Initially located at the head and goes to the trunk
- What we usually see for the first time are vesicles on the
trunk, since lesions at the scalp are not usually noticed.
o The patient would just complain of head itchiness.
o If we have a patient exposed to varicella, initially
inspect the scalp thoroughly for rashes since it starts
there.
- Unlike smallpox, in which the lesions simultaneously
appear, in varicella, the lesions manifest in varying stages
as new crops of lesions appear daily for 3-7 days.
- Ulcerative lesions in oropharynx, conjunctivae and genital
mucosa are also seen.
- Rashes are in different stages but generally follow a pattern
(macularàpapularàvesicularàpustularàcrusting)
- In the middle picture, the rashes seem to coalesce, and are
darker in color.
o This is just a secondary bacterial infection (one of
the most common complications), because lesions
of Varicella DO NOT COALESCE.
o Secondary bacterial infections are more common in
patients who have eczematous lesions (atopic
dermatitis).
PROGRESSIVE SEVERE VARICELLA
- There is continuing eruption of lesions (large, umbilicated
and haemorrhagic) with high fever unto 2nd week of illness.
- Risk factors include immunocompromised patients, those
who are older than 12 years of age and infants younger
than 1 year of age who haven’t received their vaccination.
- Severe varicella can also present with significant swelling
and edema of the face, due to severe inflammation
HERPES ZOSTER
- Reactivation of varicella zoster virus
- Localized, unilateral painful vesicular lesions in 1-3
dermatome àcomplete resolution in 1-2 wks.
- Postherpetic neuralgia à pain at the site of the lesions for
greater than 1 month à unusual in children.
- If children would present with zoster, the lesions will be less
painful.
- There is disseminated cutaneous disease and/or visceral
dissemination in immunocompromised patients.
- Associated usually with aging.
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 o It is not really a disease of children.
o However, among children who develop varicella <1
year of age, and those that contract congenital
varicella, these are the patients that you might see
in your clinic presenting as herpes zoster.
o Other risk factors include immunosuppression, and
intrauterine exposure.
o This is possible if the patient contracts the infection
in an immunocompromised state à no antibody
developed à disseminated infection
CONGENITAL VARICELLA SYNDROME
- Results from maternal infection during pregnancy.
- The period of risk may extend through first 20 weeks of
pregnancy.
- Presentation – Atrophy of extremity with skin scarring
(CICATRIX), low birth weight, cataract and neurologic
abnormalities.

STIGMATA OF VARICELLA ZOSTER VIRUS FETOPATHY

- Damage to Sensory nerves:
o Cicatricial skin lesions
o Hypopigmentation
- Damage to Optic Stalk and Lens Vesicle:
- The lesions are located at a particular dermatomal level. It
o Micropthalmia
may also present as ophthalmic zoster (right image). Zoster
o Chorioretinitis
can also affect the thoracic ganglia (left image).
o Cataracts
o Optic atrroph
HIGH RISK INDIVIDUALS
- Damage to Brain / Encephalitis:
- Adolescent >12years of age
o Microcephaly / Hydrocephaly
- Immunocompromised patients
o Calcifications / Aplasia of brain
- Newborns born to mothers presenting with rash within 5
o Damage to Cervical or Lumbar Cord o Hypoplasia of
days before to 48 hours after delivery à If the child is born
extremity
during this time (5d before or 48h after delivery), there are
o Motor / Sensory deficits
still no maternal antibodies transferred to the child
o Absent DTR’s
o Anisocoria / Horner Syndrome
COMPLICATIONS
o Anal / Vesical Sphincter Dysfunction
- Pneumonia, Hepatitis, Encephalitis and Cerebellar ataxia,
Thrombocytopenia, Nephritis, Nephrotic Syndrome,
DIAGNOSIS
Hemolytic Uremic Syndrome, Myocarditis/Pericarditis,
- Mainly clinical
Pancreatitis, and orchitis
- Definitive Diagnosis – tissue culture (distinguish VZV and
- Bacterial Super infection of the Skin
HSV), direct fluorescent antigen (more rapid and sensitive)
o The most common etiologic agents involved are
and PCR (not specific for VZV).
Streptococcus pyogenes or Staphylococcus aureus.
o Tzanck smear is not specific.
o Manifestations range from superficial impetigo to
o Varicella IgG can be requested for retrospective
cellulitis, lymphadenitis and subcutaneous
diagnosis and determining if one has antibodies to
abscesses.
varicella or is immune
o More invasive infections include sepsis, varicella
gangrenosa, pneumonia, necrotizing fasciitis,
TREATMENT
arthritis, toxic shock syndrome, and osteomyelitis.
- ACYCLOVIR – drug of choice for both.
- Some patients get Varicella, but are asymptomatic.
- For Varicella: It is not routinely given in healthy children.
o Since they weren’t aware of their primary infection,
- It is considered for patients at increased risk of moderate
they get surprised when they already present with
to severe varicella à >12 y/o, <1 y/o, pregnant women
Zoster.
o Chronic cutaneous or pulmonary disorders
o In rare instances, some patients can develop
o Long term salicylate use – may develop Reye’s
Varicella twice.
syndrome
o However, the chance of this happening is
o Short, intermittent or aerosolized courses of
infinitesimal since immunity against Varicella is
corticosteroid
supposed to be for life.
- Dose
o Immunocompetent hosts:

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 § Oral : 80 mg/K/day in 4 divided doses x 5 days
(max 3200 mg / day)
o Immunocompromised hosts:
§ Intravenous :
• <1yr.old: 30mg/K/dayin3 divided
doses x 7-10days
• > 1 yr. old: 1500 mg/m2/day in 3
divided doses x 7-10 days
- For Zoster: (enough to know the drug of choice for exam)
o Immunocompetent host:
§ IV all ages: 30 mkday x 7-10 days
§ Oral: >/= 12 years: 4000mg in 5 divided doses
x 5-7 days
o Immunocompromised host
§ IV < 12y: 60mkd q 8 x 7-10 days
§ IV > 12y: 30mkd q8 x 7 days
PREVENTION
- Live attenuated wild Oka strain
- Dose: 0.5 ml SQ
- <13years – 2 doses at 12 months and after 3 months or at
4-6 years of age
- 13 years and older – 2 doses at 1 month apart
- It will either prevent the disease 100% or if ever you
develop the disease it is usually very mild (presents with 5
lesions).
- If you only receive one dose, there is 67% chance that you
will still develop the disease; you must receive at least 2
doses!
- Passive immunization (enough to know that there is an
immunoglobulin for varicella in the exam)
- Varicella zoster immunoglobulin – not available in PH
- Candidates for VZIG after significant exposure include
o immunocompromised patients w/o previous
infection, susceptible pregnant women, new born
whose mother had chicken pox 5 days before or
within 48 hours after delivery, hospitalized
premature (>28 weeks AOG) whose mother w/o
varicella or negative serostatus, hospitalized
premature (<28 weeks AOG) regardless of maternal
history of varicella or serostatus.
PARVOVIRUS B19
- Small, DNA-containing virus
- Humans are the only host
EPIDEMIOLOGY
- Humans are the only known hosts
- Transmitted primarily by respiratory secretion
- Transmissible in blood / blood products
- Most adults have been infected
o Most infections are subclinical/asymptomatic
o IgG is detectable in most healthy people
- Sporadic outbreaks, usually among children, occur each
year
- Transmission from patient to health care staff is not
uncommon (taken from Yurag trans)
- For Eythema infectiosum- most contagious before rash
- For Hemolytic/Aplastic crisis - contagious before onset of
symptoms through week after onset or longer.
- Most common in school-aged children 5-15 y/o
INCUBATION PERIOD
- 4-14 days
TRANSMISSION
- Primarily by respiratory secretions.
- It can also be transmitted through blood and blood
products.
- Vertical Transmissions have also been reported.
PRESENTATION
- Infection among adults is subclinical.
- Sporadic outbreaks occur usually among children.
CLINCAL MANIFESTATION
- Erythema Infectiosum
o Typical lace-like skin rash
o Facial (slapped cheek) appearance
1ST STAGE - Facial rash
- Intensely red, flushed
- Slapped cheek appearance
2 STAGE
ND
- Rash spread rapidly on trunk and
proximal extremities as diffuse macular
erythema lace-like rash
3RD STAGE - Central clearing of macular lesions giving
lacy, reticular appearance; more
prominent on extensors
- Maybe pruritic
- Resolves w/o desquamation
- Wax & wane for 1 - 3 weeks (heat,
exercise, stress)
OTHER CLINICAL MANIFESTATIONS
- Arthritis / Arthralgia:
- Fetal Infections:
o Occur with primary infection in mother
o 2nd trimester = most sensitive time
o Non-immune hydrops and/or Fetal Death
o Lytic infection of erythrocyte precursors àredcell
aplasiaàprofoundanemia à high output failure à
Hydrops
o Infected infants in utero born normally at term
even with evidence of hydrops by ultrasound

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 DISEASES ASSOCIATED WITH PARVOVIRUS RESPIRATORY VIRUSES
- Fifth disease (cutaneous rash) – Infection can lead to 5th INFLUENZA
disease or Erythema Infectiosum.
- Influenza – 3 Types: A, B & C.
o It manifests as rash characterized as a slapped
- Ones that cause infection among humans are A & B
cheek appearance.
- C (Swine) can also cause infection, but not that frequent.
o We may also appreciate lacy appearance at the
- Types A and B can cause epidemic
extremities.
- ONLY Type A can cause PANDEMIC
- Transient Aplastic Crisis (severe acute anemia) – The virus
- Type A can be subclassified based on its surface antigen à
targets red blood cell progenitors causing lysis of cells and
its ability to produce or react with hemagglutinin (H) and
aplastic anemia.
neuraminidase (N). These can be H1N1, H1N2, or H5N1.
o This results to the exhaustion of sources of mature
red cells. In this regard, anemia ensues.
ANTIGENIC DRIFT
o Arthralgia or pains in joints have also been reported.
- minor variation in Influenza A or B
o This condition is seen in infected individuals with
- The virus can have minor modifications (mutate gradually)
concurrent hemolytic anemia i.e. Sickle cell disease,
à responsible for seasonal epidemics.
Thalassemias etc.
- Pure red cell aplasia – presenting as chronic anemia
ANTIGENIC SHIFT
- Hydrops fetalis (fatal fetal anemia) – infection in utero.
- MAJOR variation in hemagglutinins and neuraminidase à
o May sometimes be mistaken as dengue because of
happens when there is re-assortment of the viral gene
the rashes seen on the extremities, however if the
between two viruses in one individual (co-infection with
slapped cheek appearance of rashes on the face are
two types of viruses, seen only in Influenza A)
seen, Erythema infectiousum becomes the stronger
- Reason why Influenza A à PANDEMICS(world-wide)
diagnosis.
o Since this is a MAJOR variation of the genes, humans
have NO ANTIBODIES yet against this type of virus
SPECIAL CASES
à a lot of individuals can actually develop the
- Infection of immunodeficient patients – This can cause
disease and it can either be a mild or severe
persistent infection in bone marrow à Suppression of red
infection.
cell maturation à Anemia.
- The most severe pandemic (1918) – killed 50M people
- Infection during pregnancy – This can cause fetal anemia
- The most recent pandemic (2009) – H1N1 Influenza A
which is usually not fatal to fetus.
TRANSMISSION
COMPLICATIONS
- mainly by droplet, or by small particle aerosolation à if you
- persistent arthritis, thrombocytopenic purpura, aseptic
suction a patient for secretions, and the secretions
meningitis and virus-associated hemophagocytic
aerosolize, then you can acquire the virus.
syndrome.
INCUBATION PERIOD
DIAGNOSIS
- 12 to 72 hours
- Mainly clinical.
- Peak Season – colder months à In tropical countries, peak
- Laboratory tests are not routinely available and the virus is
season is during the rainy season and colder months --<
not isolated by culture.
starts in June, peaks in August, and goes down again, then
- (+) IGM anti-B19 serves as a marker for recent or acute
peaks again in January to February (2 peaks).
infection while IgG anti-B19 reflects past
infection/immunity.
PATHOPHYSIOLOGY
- Virus gets in the respiratory tract à It will infect the ciliated
TREATMENT
columnar epithelial cells à undergo replication, which
- There is No specific antiviral treatment.
damages the columnar cells (cilia cannot expel the bacteria,
- For Immunodeficient Patients with chronic or severe
and there is no more mucus production) à more prone to
anemia, IV IG is warranted.
develop secondary bacterial infections.
- In cases with aplastic crisis, supportive care and
transfusion (if indicated) are preferred. Intrauterine blood
transfusion is not done in our country.

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 CLINICAL MANIFESTATIONS
- patient may present with abrupt onset of fever, body
malaise, chills, anorexia à followed by coryza, colds,
pharyngitis, and very dry cough.
- Can lead to just an upper respiratory tract infection, croup,
bronchiolitis, or pneumonia.
- In children, there are MORE SYSTEMIC manifestations, like
abdominal pain, diarrhea, vomiting, compared to adults.
- Compared with other respiratory viruses, Influenza has
more of systemic manifestations. à can have DIARRHEA –
other respiratory viruses cannot cause diarrhea.
TRANSMISSIBILITY
- High.
- If the virus is transmitted among members of the family,
and it’s Influenza season,
COMPLICATIONS
- similar to Measles, the most common is Acute Otitis Media.
- Others include pneumonia, either because of the virus
itself, or secondary bacterial infection.
- Unusual manifestations – acute myositis and Reye
Syndrome (more commonly seen in Type B), myocarditis,
toxic shock syndrome (brought about by the virus itself
serving as the super-antigen ≈ Staphylococcus Æ cytokine
crisis), encephalitis, myelitis, & Guillain-Barre Syndrome.
RISK FACTORS FOR SEVERE INFLUENZA
- patients with cardiac problems (cardiomyopathy, valvular
problem); those with bronchopulmonary dysplasia (pre-
term babies who were intubated for a long time); those
with asthma, cystic fibrosis.
- In short, those with chronic pulmonary problems;
neuromuscular problems, pregnant women (seen in
pandemic); those on chemotherapy; those
immunodeficient.
TREATMENT
- Oral Oseltamivir (tablet, suspension) à drug of choice in
pediatrics;
- Inhalational Zanamivir (not available in the country).
- Amantadine and Rimantadine are effective against
Influenza A, but are not approved for children.
- Ideally, should be started within 48 hours from the ONSET
OF ILLNESS to be effective.
o However, among patients who are hospitalized or at
high risk, you may start Oseltamivir anytime, even
after 48 hours.
- Chemoprophylaxis – Oseltamivir, half the therapeutic
dose, given to those unvaccinated;
o those at high risk of severe influenza;
o those for whom the vaccine is contraindicated or
there’s low effectiveness (those who had
PEDIATRICS 3B: VIROLOGY B
anaphylaxis after vaccination, or the patient is
immunocompromised); Residents or patients in
care facilities during institutional influenza
outbreak.
- Vaccine – live attenuated type, given intranasally, but not
available in the country;
o inactivated type, given IM, containing strains of
Types A and B.
o Quadrivalent contains 2 strains of A and B, and the
trivalent contains 2 strains of A, and 1 strain of B.
o Depending whether you belong to the northern or
southern hemisphere, the WHO decides which likely
virus or strain will predominate for a particular year,
because of the antigenic drift and shift.
§ That is why, the vaccine should be given
yearly.
§ Right now, a vaccine is being developed,
wherein it will become universal; meaning, it
will be protective against whatever strain.
PARAINFLUENZA
- 4 types
- This virus usually affects children below 5 years of age.
- Transmission and pathogenesis are similar for influenza.
DIAGNOSIS
- viral isolation, PCR, or direct immunofluorescence staining.
SIGNS AND SYMPTOMS
- similar to influenza, but usually less severe, and less
systemic manifestation.
TREATMENT
- no specific anti-viral regimen.
- For patients with croup, Dexamethasone is recommended
(controversial).
- For obstruction, Racemic epinephrine is used.
o Epinephrine, at a certain dilution, is nebulized.
Supportive measures are also given Æ oxygen and
analgesics.
COMPLICATIONS
- similar to influenza Æ acute otitis media, sinusitis, and
secondary bacterial pneumonia.
PROGNOSIS
- Excellent.
- But there is no vaccine available yet against parainfluenza.
RESPIRATORY SYNCITIAL VIRUS (RSV)
- Major cause of bronchiolitis and pneumonia in children less
than 1 year of age.
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 - Responsible for 40-75% of hospitalized patients with - Associated with wheezing during infancy, and this can be a
bronchiolitis; 40-15% with pneumonia; 15% with croup. risk factor for asthma eventually.

CLINICAL MANIFESTATIONS DIAGNOSIS

- Rhinorrhea, then cough after 1-2 days, then low-grade - RT PCR – not routinely done.
fever, after which, the patient will now have wheezing,
crackles, tachypnea, retractions and difficulty of breathing PREVENTION
on PE. - hand hygiene, cough etiquette.
- Chest X-ray (normal in 30%) may reveal hyper-expansion of
lungs, with peri-bronchial thickening, but the infiltrates are ADENOVIRUS
very mild and minimal (70%), BUT the patient looks toxic. - 50 species
- has tropism capability
DIAGNOSIS - Tropism – ability to target different organs.
- Clinical. o It is able to stay there, so that there are several
- For definitive diagnosis: viral culture, RNA RT-PCR, or check manifestations: respiratory, gastrointestinal,
for antigen. conjunctivitis, cystitis, etc.
- For acute respiratory disease, you can have bronchiolitis,
PROGNOSIS pneumonia, and even pharyngitis.
- good; however, deaths usually happen among high risk o Sometimes, pharyngitis is associated with coryza
infants Æ those with chronic cardiopulmonary problems. and conjunctivitis à pharyngoconjunctival fever –
patient presents with non-purulent conjunctivitis,
TREATMENT pharyngitis, with pre and post-auricular
- mainly supportive. lymphadenopathy
- You can do aerosolized hypertonic saline, epinephrine, and - Ocular manifestations à follicular conjunctivitis, epidemic
β-2 agonist. keratoconjunctivitis (in times when sore eyes is prevalent)
- Ribavirin can be used, but not routinely (not enough à no need for anti-bacterial drops.
evidence to prove its use). - Gastrointestinal à gastroenteritis, which is self-limiting.
- For premature children with chronic lung disease - Genitourinary à hemorrhagic cystitis – patient may
(bronchopulmonary dysplasia), Palivizumab can be used present with hematuria, dysuria, frequency, and on
as a preventive measure, given every 30 days urinalysis, WBC is seen.
o But on culture, negative à no antibiotics.
HUMAN RHINOVIRUS (HRV) o If there are RBC in the urine, first rule out
- Most frequent cause of COMMON COLDS glomerulonephritis and nephron and
- Has more than 100 serotypes à no development of ureterolithiasis, especially if there is associated
immunity à you can have several episodes of common abdominal and back pain.
colds in one season.
DIAGNOSIS
TRANSMISSION - viral culture
- droplet, fomites (it can survive on surfaces).
TREATMENT
INCUBATION PERIOD - supportive
- 1-4 days
HUMAN METAPNEUMOVIRUS
SIGNS AND SYMPTOMS - relatively new virus
- sneezing, nasal congestion, rhinorrhea, sore throat. Lasts - First identified in 2001, and one of the most common virus
longer in children. causing serious lower respiratory tract infection, especially
- It is a major infectious trigger for asthma among children. in children. Humans are the only source.
o It does not cause asthma, but it is an important
trigger. INCUBATION PERIOD
- 3-5 days.
COMPLICATIONS
- sinusitis, asthma exacerbations, bronchitis, and pneumonia
(rare).

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 CLINICAL MANIFESTATIONS o The first infection is usually the most severe.
- Bronchiolitis, pneumonia, croup, but more severe, and may
be associated with colds. DIAGNOSIS
- ELISA to detect antigens, PCR
DIAGNOSIS
- Mainly clinical, but it is very difficult to differentiate it from PREVENTION
other viruses. - Vaccine.
- Also via RT PCR. - 2 types: Monovalent and Pentavalent.
o First given as early as 6 weeks of age à you want to
TREATMENT prevent Rotavirus gastroenteritis in children less
- Supportive. than 2 years of age.
o There has been association of intussusception with
CORONAVIRUS the vaccine if given beyond 8 months, peaks at 5
- also causes common colds and LRTI. months.
- Among infants and neonates, it has also caused diarrhea,
enteritis, and colitis, as well as meningitis and encephalitis. ASTROVIRUS
- 2 epidemics that has caused severe disease in the past few - second most common agent of viral diarrhea in young
years: children.
o SARS-CoV (2003) àcauses severe respiratory - It is milder, compared to rotavirus.
distress and a mortality rate of 60%.
o MERS-CoV (2012) à seen in Middle East among ADENOVIRUS
camels. - also causes gastrointestinal symptoms (longer duration 10-
14 days)
INCUBATION PERIOD
- 10 days. DIAGNOSIS
- has a high case fatality rate, and >65% will have severe - ELISA to detect antigens, PCR
disease, and only 5% will have mild disease.
CALICIVIRUS
TREATMENT
- Norovirus and Sapovirus.
- Supportive.
- They cause gastroenteritis, usually in outbreaks.
- No antiviral or vaccine yet.

NORWALK VIRUS
GASTROINTESTINAL VIRUSES
- similar to Rotavirus, 12 hours
ROTAVIRUS
- It also causes vomiting and diarrhea, and common during
- single most important diarrhea-causing virus among the cold seasons.
children less than 12 years of age. - Causes diarrhea among older individuals.
- Causes severe diarrhea à presents as fever, vomiting, and
explosive diarrheaà patient becomes dehydrated and DIAGNOSIS
needs admission. - mainly clinical
- For those patients who have no access to IV fluids or
hydration, this is a major cause of mortality.
RABIES
- Philippines is highly endemic for Rabies.
INCUBATION PERIOD
- Top 1 is India, followed by China.
- around 48 hours
- FATAL DISEASE – almost always 100% fatal
- Main target of this disease are children less than 2 years of
- Primary host are usually animals.
age.
o Humans are infected through animal bites or
o However, it can also affect children below 5 years of
exposure. >90% are from dog bites.
age.
o Only 6-10% are acquired from cats, cattle, sheep,
o You can have recurrent infections, as much as 3-5
bats.
infections.
- Common in our country are rat bites à rats are not known
o The more infections you have, the milder the
to contain rabies.
disease will be.
o Reptiles also do not contain rabies virus.

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 - In the country, around 300-600 Filipinos die each year, 53%
of which are children less than 14 years of age à children
are at high risk of developing rabies, because of the
characteristics of children. They have small height, easier to
bite the head area, faster to spread to the brain.
- They are very playful, they roam around, they’re helpless,
and most often, they don’t disclose that they were bitten
by a dog, in fear that they will be reprimanded by their
mothers.
TRANSMISSION
- exposure of an infected animal saliva, either through a
scratch or bite, or a contact with a mucus membranes.
- Human-human transmission is very rare.
- Documented also in transplant individuals.
- Aerosolation has been documented in bat caves and in
laboratories (very rare)
INCUBATION PERIOD
- short as 1 day (site of bite is the head), up to 5 years, with
the average at 2 months.
PATHOGENESIS
- after the virus has been inoculated, it will undergo
replication at the site of the bite à ascend through the
peripheral sensory nerves, to the dorsal root ganglion, to
the spinal cord, and to the brain.
- From the brain, it will now go to the different organs of the
body, like the lacrimal duct, salivary glands, an into the
nape.
- Once the virus reaches the brain, the patient will now start
to manifest, during the prodromal phase.
4 STAGES:
- Incubation Period – 1 day to 5 years (Average = 2 mo.)
o The patient may be asymptomatic. The virus may
remain at the site of the bite, and gradually, it will
ascend.
- Prodromal phase – 2-10 days.
o The virus is now seen at the spinal cord. First specific
symptom that the patient may present with rabies
– itchiness, pain or paresthesia at the site of the
bite.
- Acute Neurologic Phase – 2-7days
o Encephalitic / Furious – 80% of cases, “typical
rabies”.
§ The patient becomes hyperactive à
combative, bizarre behavior, with lucid
intervals (Normal – manic state – normal –
manic state, where the patient is more
aggressive than the previous episode).
§ The patient may also have photophobia,
hydrophobia (when they drink water, they
PEDIATRICS 3B: VIROLOGY B
swallow à swallowing is painful because of
contraction of laryngeal muscles upon
drinking), and aerophobia (when you fan the
patient à tendency to swallow Æ pain).
§ Once they present in the ER, the course is very
fast.
§ For example, today, they already present with
hydrophobia and aerophobia. On your next
duty, the patient has already died on the night
of admission. These patients are also very
combative, so they are restrained and
isolated., since they may bite other people.
This is not seen in encephalitic type.
o Paralytic / Dumb / Encephalitic – 20% of cases –
non-specific symptoms, similar to other
encephalitis, with no hydrophobia, aerophobia or
photophobia.
§ Some may not have combative behaviors.
These patient may just present with changes
in sensorium, which is progressive. So in
patients with encephalitis, always ask for
history of bite.
- Coma
o both neurologic types will go into coma eventually,
then respiratory paralysis (cause of death).
DIAGNOSIS
- Mainly clinical.
o Thus, it is more difficult to diagnose the dumb
rabies.
o History of bite, with hydro- and aerophobia is
usually sufficient to diagnose.
- LABORATORY WORK-UPS
o only done if you’re not really sure, usually done for
dumb rabies.
o RT-PCR of saliva (and oral swab) for genomic
detection
- Corneal imprint
- Lumbar tap – will show a “viral picture”
- CSF analysis – can do RT-PCR or detect antibody testing
MANAGEMENT
- almost always 100% fatal, and no specific treatment.
- Some patients are just given Valium to “calm the patient”,
so they would die peacefully.
- Cornerstone of management is prevention.
PREVENTION
- For patients who come in with bites, à proper wound care,
cleaned using soap and water, for at least 10 minutes, then
apply Povidone-Iodine.
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 - DON’T SUTURE à you might introduce the virus into the
deeper layers of the bite site, so it will be more difficult to
infiltrate.
o IF suturing is absolutely necessary (e.g. in the face),
you first have to give immunoglobulin, wait for 2
hours, then you can proceed with suturing.
- Antibiotics – the saliva of animals are teeming with
bacteria, and it might have infiltrated the wound of the
patient.
CATEGORY OF ANIMAL BITES ACCORDING TO EXPOSURE
- Human immune-globulin is expensive, amounting to
around P25K to P50K, depending on the weight of the
patient.
TRANSMISSION
IMMUNIZATION SCHEDULE – (don’t memorize)
- Enough to know that there is an intradermal regimen and
an intramuscular regimen for rabies vaccine.
MOTHER-TO-INFANT TRANSMISSION
- Usually given as post-exposure prophylaxis on days 0, 3, 7,
14, and day 28/30.
o If the dog who bit the patient is still alive on day 14,
you may opt not to give the dose on day 14 and on
day 28/30 à the dog is not rabid at the time of bite.
o If the dog is rabid, and already has the virus in its
saliva at the time of bite, then it should die within
10 days.
o The dog did not die because it bit a person (common
misconception in the provinces).
o It died because the virus has already reached the
brain, and by day 10, it will have respiratory
paralysis.
- If the patient belongs to category III – give either an Equine
or Human Rabies Immune Globulin.
o The dosage is based on the weight of the patient.
o Ideally, this should be introduced at the site of the
bite.
PEDIATRICS 3B: VIROLOGY B
o The rest of the computed dose can be given
intramuscularly.
o Have a skin test first if you’re giving Purified Equine
Rabies Immune Globulin.
- Tetanus Prophylaxis
o Pre-exposure – given to high-risk individuals,
including children with pets at home, veterinarians,
and pet lovers.
§ The benefit is elimination of the use of
immune globulin after a bite, and you only
need to give 2 doses of vaccine after a bite,
instead of 5.
o Regimen of pre-exposure prophylaxis – given at
day 0, 7 and 21/23. If bitten, you only need 2 more
vaccinations, instead of 5, and you don’t give
anymore immune globulin.
HIV
- alarming increase of cases in the country.
- In 2008 à 1 new case per day. In June 2016 à 26 new cases
per day.
- In June 2017 à 29 new cases per day.
- Demographic Data (December 2016) à 40,000 cases;
among these, ~36,000 are still asymptomatic; ~3,600 are
symptomatic à AIDS. 37,000 are males; only 2800 are
females.
- Age range of 25-34 years old are the majority (sexually
active).
- Only less than 100 are in pediatric age.
- Most common mode of transmission – Men having sex with
men
- Primary route of transmission – Vertical transmission
- Other routes: Breast feeding, during delivery.
- Before delivery: 30-40% transmission rate, depending on
the viral load of the mother.
o So, it is very important to treat pregnant mothers
who are HIV positive à to reduce transmission to
her baby.
- Intrapartum transmission: 60-70% transmission rate.
Highest mode of transmission. This usually happens
because of mucosal exposure to blood, and cervico-vaginal
secretions.
o In mothers with high HIV load, it is recommended
that they undergo Cesarean Section.
- Perinatal transmission via Breastmilk: 40%. This is the
reason why breastfeeding is withheld in patients with HIV,
especially in high-income countries. However, in low
income countries, like Africa, EXCLUSIVE BREAST FEEDING
is recommended.
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 o In mixed feeding, there is higher chance of
mortality. If your patient can afford formula-
feeding, then avoid breast feeding.
- For patients born to mothers who are HIV positive, they are
usually asymptomatic, especially if the mother has been
treated. These patients, also, usually become HIV negative,
as long as you give proper prophylaxis.

CLINICAL MANIFESTATIONS
- In patients who acquire HIV during childhood, they usually
present as recurrent bacterial infection, chronic or
recurrent parotid swelling, lymphoproliferative
pneumonitis, or in severe or late cases, progressive
neurologic disorders.
- Infections that you may encounter à patients with TB
(higher rate of TB infections in patients with HIV, especially
among high risk individuals);
- Oral Candidiasis; Esophageal Candidiasis (More AIDS-
defining); or with prolonged chronic symptoms, or a severe
disease, caused by a less virulent organism.

MANAGEMENT
- How to deal with patients when you suspect with HIV à
You test the patient. But first, conduct the three C’s.
o Keep Confidentiality, there should be Counseling,
and there should be Consent.
- In the country, it is usually a physician-initiated test.
o Thus, you maintain confidentiality.
o In hospitals, they have a code for HIV testing.
o You also have to tell the patient that the results will
be confidential.
o The patient should undergo pre-test and post-test
counselling, educating the patient about the
consequences of HIV, and what it means if the
patient has a positive or a negative test. And you
have to prepare the patient for the result. Again,
don’t forget the consent.
- Since we are in Pediatrics, if the child is below 18 and above
12, you have to ask for their assent, aside from the
consent of the parents.

USE AT YOUR OWN RISK!

Notes from Miles Largoza, Benjo Cruz. Stephen Seares Trans

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