Vous êtes sur la page 1sur 27

HERPES SIMPLEX VIRUS

Viral infections
comprehensive review 2 SEROTYPES

DR. MA. ANNA BANEZ


HSV 1 – mouth and skin above the waist
PEDIATRIC INFECTIOUS DISEASES

HSV 2 – genital organs

2 TYPES of INFECTION 2 TYPES of INFECTION


1. Primary Infection 2. RECURRENT INFECTION
• mostly subclinical
• otherwise,local superficial lesions w/                      • reactivation of latent infection in an immune 
varying degrees of systemic reaction host w/ circulating antibodies
• w/ serious systemic reaction w/o lesions in  • follows non‐specific stimuli: cold, uv light, 
NB and severely malnourished menstruation, fever, emotional stress
• circulating antibodies and CMI response in  • asymptomatic or localized lesions w/o 
non‐fatal cases                                          systemic reactions

3 Distinct Times of
Epidemiology
Acquisition
• risk of transmission from pregnant women to 
fetus/newborn
44% after primary infection Congenital
3% after recurrence
• neonatal disease more commonly acquired from 
Perinatal
maternal GUT during parturition Postnatal
• HSV2 account >/ 75% neonatal infections
• majority of women w/ HSV infection are 
asymptomatic
• genital lesions present at parturition <10%
of cases

1 | PEDIA-VIRO
CONGENITAL INFECTION PERINATAL INFECTION
• Very rare; 1 in 250,000 live births • acquired from primary or recurrent HSV 
infected cervicovaginal secretions
• due to transplacental maternal viremia or as 
• 1/2,000 births
ascending infection after  rupture of 
• presents either as:
membranes – Disseminated disease
• Classis TRIAD at birth:  – Encephalitis
skin vesicles or scars           – Skin,Eye,Mouth lesions
chorioretinitis/keratocojunctivitis, 
hydranencephaly or microcephaly
• Poor neurodevelopmental outcome

PERINATAL INFECTION PERINATAL INFECTION


Disseminated (20%) Encephalitis
– onset:4‐11 days of life • Onset: 16‐17 days of life
– irritability,respiratory • Fever,irritability,lethargy,focal/generalized 
distress,jaundice,shock seizures,poor feeding
seizures,DI • Suspect in any neonate w/ aseptic meningitis or focal 
– skin lesions‐80% signs
– meningoencephalitis‐60‐75% • Isolated(30%), w/ skin lesions(60%),disseminated
– sepsis‐like picture • Mortality:15‐50%, neurodevelopmental sequelae
– mortality:70=90% common

PERINATAL INFECTION POSTNATAL INFECTION


SKIN,EYE and/or Mouth(SEM) (40%)
• Onset:10‐11 days of life
• Discrete clusters of vesicles on skin/scalp – Acquired from close contact after birth
• SEM alone,part of encephalitis(30%) or disseminated  – Majority asymptomatic
disease
– Usually SEM, may progress to encephalitis 
• Cutaneous recurrences during 1st yr of life
or disseminate
• Mortality: rare
• may progress to encephalitis,pneumonitis,dissemination
• Suspect in neonate w/ rash,conjunctivitis,oral
lesions,unexplained stridor.
• Greatest opportunity for intervention

2 | PEDIA-VIRO
POSTNATAL INFECTION *Primary Herpetic
Gingivostomatitis Gingivostomatitis
– most common form of primary infection
Herpes labialis(cold sores)
• Enanthem:
– painful vesicles on lips,
– Most common form of reactivation
gums, buccal mucosa, 
Genital herpes
anterior tongue and hard   palate
– Most common form in adolescent/adults
– Primary or recurrent – vesicles rapidly become
Eye Infection shallow tan‐yellow  ulcers   
– Primary or recurrent with erythematous halo
– Superficial conjunctivitis/chorioretinitis
Herpetic Whitlow – gingivitis        
– Single/multiple vesicles on distal fingers

Primary Herpetic Gingivostomatitis


POSTNATAL INFECTION
Meningoencephalitis
‐ predilection for frontal/parietal lobes
‐ unusual cause of aseptic meningitis
‐ most common cause of fatal focal encephalitis;75%mortality
‐ fever,altered sensorium,headache.personality
changes,seizures,dysphasia,focal neurologic signs 
Herpes Labialis Erythema multiforme
‐ HSV implicated as the most common etiology of EM
‐ classic lesion:target or bull’s eye‐lesion
Immunocompromised patient
– Severe local lesions/disseminated

DIAGNOSIS TREATMENT
Based on any 2 of the following: Acyclovir
1)compatible clinical picture • Drug of choice
• Dose:15‐20 mg/k/dose q 8 hrs x14‐21days,IV
2)Isolation of the virus:vesicles,urine,stool,blood, csf,swabs
for all infants w/ neonatal infection irrespective of 
3)Development of specific antibodies presentation, herpes encephalitis
4)Demonstration  of characteristic cells, histologic changes, viral  • Topical treatment for oral/genital herpes: decrease viral 
antigens or HSV DNA in scrapings, CSF or biopsy shedding but not symptoms;not recommended
CSF PCR for HSV DNA: • Topical trifluorothymidine,vidarabine,idoxuridine for 
‐ diagnostic method of choice for HSV encephalitis keratitis
‐ sensitivity:75%  neonatal CNS infection; 95% beyond neonatal  • Gingivostomatitis:15m/k/dose 5x/day, w/in
period 72 hr of onset   x 7 days
Serology not useful  for rapid dx in neonates • Genital infection:
1st episode:  40‐80 mkdy q6‐8 x 5‐10 days
Positive cultures beyond 48 hrs after birth indicate true infection
recurrence  >/=12y : 1000‐1200mg/day q8 x3‐5 days

3 | PEDIA-VIRO
PREVENTION
• Stat CS delivery for a woman with ruptured membranes and 
active genital lesions at term
• For exposed asymptomatic infants who were born vaginally 
to mothers with active genital lesions (10, recurrent or 
unknown status) CYTOMEGALOVIRUS
– Obtain cultures:eyes,mouth,urine,stool
– Empiric acyclovir therapy after cultures are done
– Acyclovir therapy after culture is POSITIVE
• Since infection rate for infants whose mothers have active 
recurrent genital herpes infection is <5%, most experts do 
not recommend empiric treatment. Family education about 
s/sx

Cytomegalovirus Cytomegalovirus
• Source:  • Incidence: 
saliva • Worldwide distribution 
breastmilk • Congenital infection: 0.2 – 2.4% of live births
cervical and vaginal secretions • Perinatal infection: 10‐60% by 6 months old
urine • After 1st year of life: 50‐80% infection rate
semen
blood

Cytomegalovirus Cytomegalovirus
• Mode of Transmission:
Predisposing factors:
Vertical
‐ In utero: transplacental passage
• immunocompromised patients
‐ At birth: passage through infected maternal genital tract • seronegative premature infants
‐ Postnatal: ingestion of CMV‐positive breastmilk • seronegative recipients of organs
Horizontal
‐ salivary contamination
‐ contact with infected urine
‐ sexual contact
‐ blood transfusion
‐ organ transplantation

4 | PEDIA-VIRO
Cytomegalovirus Clinical Manifestations
• Incubation Period: • Congenital
1. Asymptomatic infection 
3- 12 weeks after blood transfusion ‐ 90% of cases
1-4 months after tissue transplantation ‐ 5 to 10% develop sensorineural hearing  loss later
unknown for horizontal transmission
2. Cytomegalic inclusion disease 
‐ 10% of cases
‐ IUGR, jaundice, purpura, hepato‐ splenomegaly, 
microcephaly, intracerebral calcifications &/or chorioretinitis

Clinical Manifestations Clinical Manifestations


• Perinatal infection • Infection in older children, adolescent and 
‐ majority are asymptomatic adults
‐ in infants & young children:   1. Mononucleosis‐ like syndrome: fatigue, malaise, myalgia, 
pneumonitis, hepatomegaly,  hepatitis,&  headache, fever, hepatosplenomegaly, increased liver 
petechial rashes enzymes and atypical lymphocytes;       milder
2. Persistent fever
3. Hepatitis
4. Morbilliform rash
5. Combination of above conditions

Infection in
Immunocompromised Patient: DIAGNOSIS
‐increased risk of  disease  whether primary or recurrent • Active CMV infection
1. Viral isolation
1. pneumonitis 2. Rapid detection of CMV antigens
2. hepatitis 3. Detection of CMV antibodies
IgG- primary or recurrent
3. chorioretinitis
IgM-acute phase of symptomatic/
4. GIT disease asymptomatic patient, rare in recurrent
4. Examination of urine for intranuclear inclusions
5. fever with leucopenia                   5. Detection of pp 65 antigen in WBC of
immunocompromised hosts

5 | PEDIA-VIRO
DIAGNOSIS Prevention
• Blood product, human milk, & transplant donor selection
• Congenital Infection • Passive immunoprophylaxis
1. Positive viral culture – usually urine; the use of IVIG/CMV IVIG for prophylaxis in solid 
organ/BM transplant recipients reduces risk of 
within 3 weeks of birth symptomatic disease not prevent infection
2. Strongly positive IgM anti- CMV • Prophylaxis and early preemptive therapy with antiviral 
agents
antibody • Active immunization
Adult study:Towne strain vaccine doesn’t protect against 
natural infection
• Behavioral strategies to prevent primary CMV infection

Treatment Prognosis
• Ganciclovir • 90% with congenital infection demonstrate CNS
-combined with IVIG or CMV IVIG for life-threatening infections in the
immunocompromised & hearing defects in later years
-not routine in congenital infections; insufficient efficacy data,with adverse 30% - death rate of symptomatic congenital
side effect cytomegalovirus infection
-Randomized phase III study for syptomatic congenital infection:
12 mg/k/dy x 6 wk; • infants with subclinical infection
prevents hearing deterioration, improves/maintains normal
hearing at 6 mos old, prevent hearing deterioration at 5-10% - sensorineural hearing loss
>/1 yr old
3-5% - chorioretinitis
• Alternative drugs: less frequent:developmental abnormalities,
– Foscarnet
– Cidofovir microcephaly,neurologic defects
– Fomivirsen

Care of exposed persons Epstein Barr Virus


• Hand hygiene, especially after changing • Causes 80 to 95% of mononucleosis syndrome
diapers • Epidemiology:
• Pregnant personnel must be educated Source: Man – sole source
about the risk of acquisition and practice Mode of transmission:
standard precautions. 1. oral- salivary spread
2. close intimate contact - kissing
3. blood transfusion

6 | PEDIA-VIRO
Epstein Barr Virus Clinical Manifestations
• Incidence: predominantly in children and young Infectious Mononucleosis:
adults – Prodromal period: 2‐5 
days malaise, fatigue 
• Period of communicability:
with or without fever
Indeterminate; may be months after infection
– Triad: 
• Incubation Period: 30 to 50 day lymphadenopathy
• Majority of primary infections in infants and splenomegaly
young children are silent exudative pharyngitis

Clinical Manifestations Occasional Signs and Symptoms


– Signs and symptoms:  Erythematous and maculopapular rash; 80% w/   
Fever – usually rises to 39?C ‘ampicillin rash’ if treated w/ ampicillin or 
Adenopathy‐90%;usually in the anterior ,  amoxicillin
posterior cervical , & submandibular  Enanthem
nodes;suggestive if epitrochlear  Edema of eyelids
Splenomegaly – 50%   Jaundice
Hepatomegaly – 10%  Guillain‐ Barre syndrome
Tonsillopharyngitis‐  Myelitis
Palatal petechiae  Bell’s palsy
 Acute cerebellar ataxia

Diagnosis
• Other distinct disorders associated to EBV: Absolute lymphocytosis : total leukocytes  > 5,000/mm3 
‐ atypical lymphocytes >10% of  total leukocytes
– Lymphoproliferative disorders 
– Burkitt’s lymphoma Serologic Tests:
– Nasopharyngeal carcinoma 1. Paul‐Bunnel heterophil test and slide agglutination 
reaction (Monospot test)
– Undifferentiated B‐cell lymphoma of the CNS ‐ negative in children <4 years old
2. EBV specific serological test
‐ eg. IgM anti‐ VCA (viral capsid antigen)
3. Viral isolation

7 | PEDIA-VIRO
Diagnosis Complications
Infection VCA IgG VCA EA (D) EBNA • Hematologic
IgM
No previous infection 1. Splenic rupture
- - - - 2. Thrombocytopenia, ITP
Acute infection + + +/- - 3. Agranulocytosis
Recent infection + +/- +/- +/-
4. Hemolytic anemia
5. Hemophagocytic syndrome
Past infection + - +/- +

Complications Other Complications


• CNS • Pneumonia
1. Aseptic meningitis • Orchitis
2. Encephalitis • Myocarditis
3. Myelitis
4. Optic neuritis
5. Cranial nerve palsies
6. Transverse myelitis
7. Guillain- Barre syndrome

Treatment
Treatment
3. Steroids (1 mkday; max 20 mg/day) x 7 days
1. Bed rest - rarely needed
- considered in the following conditions:
2. No contact sports or activities that can
cause rupture of spleen until it is not
1. marked tonsillar inflammation with
palpable impending airway obstruction
2. Massive splenomegaly
3. Myocarditis
4. Hemolytic anemia
5. Hemophagocytic syndrome

8 | PEDIA-VIRO
Enterovirus (Nonpoliovirus)
Infections
Enteroviruses • Epidemiology
(NonPoliovirus) Infections – Source: feces and oropharyngeal secretions
Group A&B – Mode of Transmission: 
Coxsackieviruses,Echovirus person to person by fecal‐ oral route
and Numbered Enteroviruses possibly oral‐ oral (respiratory) route
• Incubation period: 3‐6 days except for acute 
hemorrhagic conjunctivitis

Clinical Syndromes Clinical Syndromes


– Noteworthy virus/ disease associations
‐common to most enteroviruses
1. Non specific febrile illness ‐ >90% of cases Hand, foot and mouth Coxsackievirus A16
2. Respiratory – common colds, pharyngitis,  disease Enterovirus 71
herpangina, stomatitis, pneumonia,      Acute hemorrhagic Coxsackievirus A24
pleurodynia conjunctivitis Enterovirus 70
3. GIT – vomiting, diarrhea, abdominal pain, hepatitis Encephalitis and polio- Enterovirus 71
4. Skin – macular, maculopapular, vesicular,  like paralysis
petechial rashes
5. CNS – encephalitis and paralysis Aseptic meningitis with Echovirus 9
petechial exanthem
Myopericarditis Coxsackievirus B1- B5

Clinical Syndromes Clinical Syndromes


– Noteworthy virus/ disease associations

Non specific febrile Echovirus 9 Herpangina


illness with rash ‐ anorexia, dysphagia, 
Herpangina salivation, sore throat,
Pleurodynia or Bornholm’s Coxsackieviruses B3 and B5
vesicles and ulcers on anterior 
disease
Orchitis and epidydimitis Coxsackievirus B5, B2 and
pillars (most    common site), 
B4 soft palate, uvula, tonsils, 
Myositis Coxsackievirus A2 pharyngeal wall, posterior 
Polymyositis Coxsackievirus A & buccal surfaces
Echovirus 18
Neonatal infections Coxsackievirus B1- B5

9 | PEDIA-VIRO
Hand, Foot and Mouth Syndrome Clinical Syndromes
– Pleurodynia or Bornholm’s Disease
‐ sudden onset of fever and muscular pain 
(chest or abdomen), spasmodic and 
excruciatingly severe with profuse 
sweating
‐ usually lasts 1‐2 days
‐ may be biphasic

Clinical Syndromes Clinical Syndromes


Non‐specific febrile illness with rash Neonatal infections
 Echovirus 9 • asymptomatic to sepsis‐like illness,fatal
 rubelliform or petechial rash encephalitis & myocarditis w/in 2 wks of        
 rash & fever usually at the same time life
 mimics meningoccocemia • transplacental transmission immediately 
prior to delivery 

Diagnosis Treatment
– Viral isolation:  – No specific therapy
stool,throat,csf,blood,biopsy;
less specific in stool alone since viral 
– Immune Globulin Intravenous (IgIV)
shedding x6‐ 12 wks in asypmtomatic ‐ may be beneficial for chronic 
patients enteroviral meningoencephalitis
– PCR – for enterovirus RNA in CSF
– Rise in neutralizing antibody titer from an 
acute and convalescent specimen

10 | P E D I A - V I R O
Poliovirus Infections
• Epidemiology
WHO Polio Global Eradication Program 
Poliovirus Infections ‐ launched in 1988 with the following 
strategies:
(Poliomyelitis) 1. Routine immunization
2. National Immunization Days (NID)
3. Active Acute Flaccid Paralysis (AFP) 
Surveillance
4. “Mopping Up”: extra immunization 
rounds when a wild virus is found

Poliovirus Infections Poliovirus Infections


• Epidemiology • Epidemiology
Remaining Polio‐ endemic countries : Based on active WHO AFP Surveillance
1. India ‐ last case of wild poliovirus in America:
in Peru (1991), and by 1994‐ declared polio‐
2. Pakistan
free
3. Afghanistan ‐ In Philippines‐ last case of wild poliovirus:
4. Nigeria in Cebu (1993);last case in WPR 1997
‐ Philippines and the rest of the Western Pacific    
Region  were certified polio‐ free by 2000

Poliovirus Infections Poliovirus Infections


• Circulating vaccine‐ derived poliovirus ( c VDPV)
• Epidemiology
‐ dependent of sabin virus
2001 – type 1 circulating vaccine‐ derived 
‐ accumulation of small spot mutations over a 
poliovirus ( c VDPV) was isolated from 3  period of >/= 6 months resulting in 
children in 3 places:  virologically different strain
Cagayan de Oro ‐ recovers properties of wild virus like 
Cavite neurovirulence, recombination and 
transmissibility
Laguna
‐ ocurs only where there is no wild virus
‐ with accumulation of susceptibles

11 | P E D I A - V I R O
Poliovirus Infections Poliovirus Infections
• Source • Period of Communicability
‐ feces and possibly, oropharyngeal secretions  ‐ Patients are potentially contagious for as 
of man long as fecal excretion persists
• Mode of Transmission: ‐ OPV recipient: virus persists in throat for 1‐2 
‐ fecal to oral weeks and excreted in feces for several weeks
‐ possibly oral to oral (respiratory) routes • Incubation period:
3‐6 days – abortive poliomyelitis
7‐21 days – paralysis in paralytic poliomyelitis

Clinical Forms
Clinical Forms
Inapparent illness – account for 90- 95% of cases
Abortive Cases (4‐8%) Non paralytic or aseptic  Paralytic (0.1‐ 2%)
meningitis (1‐5%) Post‐polio syndrome
Non specific febrile  Signs & symptoms of  Signs & symptoms of 
illness minor illness non‐ paralytic illness
• Occurs 30‐40 years later as muscle pain,
Malaise + + & exacerbation of weakness or new weakness 
Nausea/ vomiting Nuchal/ spinal skeletal   Weakness of >1 muscle
rigidity Or cranial (spinal, 
or paralysis among 30‐40% of
Headache
Sorethroat
+ bulbar, bulbospinal or 
encephalitic)
• Patients w/ childhood poliomyelitis
Increase/ decrease in 
Constipation superficial/ or deep 
Diffuse abdominal pain tendon reflexes Flacid paralysis w/o 
sensory loss (hallmark)

Absent DTRs

Difference between virus in VAPP &


Clinical Forms VDPV
Vaccine‐Associated Paralytic Poliomyelitis Features Virus in VAPP VDPV
• VAPP Structure Identical to sabin >3% different from 
vaccine virus sabin vaccine virus 
• a paralytic disease in OPV recipient /close  (mutant)
contact Virus circulation in a  None Circulates or is 
community transmissible
• incidence: 1 case in >/3 million doses  Occurrence Wherever OPV is  Occurs only where 
distributed used there is no wild 
virus and there is an 
accumulation of 
susceptibles

12 | P E D I A - V I R O
Complications Diagnosis
• GIT: gastric dilatation, hemorrhage, melena,  • Clinical
paralytic ileus • Laboratory
1. viral isolation from 2 stool specimen taken 24‐ 48 hours 
• Hypertension, occ pulmonary edema apart within 14 days of onset of paralysis
• Skeletal decalcification 2º to immobilization  2. serology: acute & convalescent sera
leading to hypercalcemia, hypercalciuria,  3. with CNS involvement: CSF examination
nephrocalcinosis ‐ pleocytosis with early PMN predominance followed by 
shift to mononuclears
‐ protein: normal or slightly elevated
‐ normal glucose
4. DNA sequence analysis – distinguish wild virus from vaccine 
virus 

Treatment: Influenza
• No specific treatment;symptomatic & 
supportive ‐Types A,B and C
‐Epidemic disease: Type A and B
‐ Influenza A subclassified by 2 surface antigens:
Control Measures: Hemagglutinin (HA) & Neuraminidase (NA) ;
• OPV:vaccine of choice for global eradication in  examples: H1N1, H1N2, & H3N2
areas w/ VDPV,developing countries where  ‐Antigenic drift: minor variations in influenza B or A; 
inadequate sanitation necessitates optimal  seasonal epidemics
mucosal barrier ‐Antigenic shift: major variations in HA or NA; only w/ 
influenza A; pandemics
• IPV:areas not at risk to wild type,
immunodeficient patients

Influenza Influenza
‐predominantly respiratory Diagnosis:
‐abrupt onset of coryza,conjunctivitis.pharyngitis, dry cough viral culture, immunofluorescent, or rapid diagnostic tests
‐localize as URI, croup, bronchiolitis or pneumonia for antigens, direct fluorescent antibody(DFA) and   indirect 
‐commonly associated w/ high fever(2‐4 days), myalgia,  immunofluorescent antibody(IFA) staining for 
malaise & headache Influenza A and B antigens in NP specimens
‐close contacts often have similar illness
‐indistinguishable from RSV, parainfluenza viruses & 
adenovirus

13 | P E D I A - V I R O
Antiviral Drugs for Influenza * Influenza Vaccine
Admini- Treatment Prophylaxis Prophylaxis
Drug Virus stration Indications Indications Adverse Effects Recommended in:
Central nervous
system, • Children 6mos‐5 yo
Amantadine A Oral =1 y of age =1 y of age anxiety,
gastrointestinal • High‐risk children:chronic heart 
Central nervous /lung/metabolic diseases,renal disorders 
=13 y of system,
Rimantadine A Oral
age
=1 y of age
anxiety, &hemoglobinopathies
gastrointestinal
Zanamivir
A&B Inhalation =7 y of age =5 y of age Bronchospasm
• Children on long  term aspirin tx
Oseltamivir A&B Oral =1 y of age =1 y of age Nausea, vomiting

Influenza Vaccine * 2009 Flu pandemic


• Global outbreak of a novel influenza AH1N1 identified 
Children 6mos‐8yo: 2 doses, 4 weeks apart then  April 2009
yearly • Infects and transmissible between humans
Preferably  given Feb to June • A re‐assortment of 4 known strains of influenzae A virus 
subtype H1N1: 1 endemin in humans, 1 endemic in birds 
Healthy children>5 yo who want to be protected  and 2 endemic in pigs
against influenza can be given the  • WHO data as of July 6,2009 : 94,512 cases, 429 deaths
vaccine • Symptoms similar to other forms of influenzae: fever, 
cough, sorethroat, headache, myalgia, chills diarrhea , 
vomiting

Flu vaccine for 2009, Southern strain Avian influenza (H5N1)


‐mainly in birds; deadly
‐doesn’t usually infect people but human infections
have resulted from direct or close contact with     
H5N1 infected poultry

14 | P E D I A - V I R O
Parainfluenza viruses Respiratory Syncitial Virus

‐members of paramyxoviridae family ‐major cause of bronchiolitis and pneumonia in children <1 yr 


‐types 1‐4 old
‐account for 50% of hospitalizations for croup, 15% of  ‐the most important respiratory pathogen of early childhood
bronchiolitis and pneumonia ‐initially,rhinorrhea and pharyngitis, cough ,low grade 
‐not associated with fever; systemic complaints rare feverwheezing
‐diagnosis is based only clinical and epidemiologic criteria ‐if progressive: cough and wheezing increase,(+)air hunger, 
tachypnea, retractions, hyperexpansion of chest, restlessness, 
‐”Steeple sign” or progressive narrowing of the subglottic region 
cyanosis
on xray : characteristic of parainfluenza virus
‐CXR: normal(10%), air‐trapping(50%), interstitial pneumonia(50‐
respiratory tract infection
80%), segmental cosolidation(10‐25%)

Respiratory Syncitial Virus Respiratory Syncitial Virus

‐association of RSV bronchiolitis early in life and  Diagnosis:


reactive airway disease remains poorly understoood;  detection of viral antigen by EIA , immunofluorescence,viral
underlying predisposition to reactive airway disease  isolation
rather than a direct consequence of RSV infection Treatment:
Ribavirin aerosol treatment not routine; small studies show increase O2 
‐almost all children infected once by 2 yrs old ;  saturation; consistent decrease for mechanical ventilation, decrease 
reinfection common  length of PICU stay, decrease hospitalization days among recipients
Prevention: Palivizumab, humanized mouse monoclonal antibody given 
IM, reduces risk of RSV hospitalization in high‐risk children (chronic lung 
disease of prematurity,preterm, CHD): q 30 days starting early november
x 5 doses

Adenovirus Adenovirus

Acute Respiratory Disease Pharyngoconjunctival fever‐type 3; high fever x 


‐most comon manifestation in children & adults 4‐5 days, pharyngitis, non‐purulent 
‐not clinicaly distinctive; types 1‐6 conjunctivitis, preauricular & cervical 
‐primary infections w/ fever & respiratory symptoms 
complicated by otitis media in > half of patients;with diarrhea.
lymphadenopathies & rhinitis + headache, 
pharyngitis malaise & weakness
pneumonia: types 3,7,& 21 cause severe type w/ 10%   
mortality; residual airway damage: bronchiectasis; 
bronchiolitis obliterans, rarely pulmonary fibrosis
pertussis‐like syndrome

15 | P E D I A - V I R O
Adenovirus Adenovirus
Other manifestations: Infections in the Immunocompromised:
Follicular conjunctivitis Chronic meningoencephailtis in B‐cell deficiency
Myocarditis Prolonged diarrhea in T‐cell deficiency
GIT Infections‐ diarrhea, intussuception
Hemorrhagic cystitis‐ suden onset bacteriologically
sterile hematuria,dysuria, frequency & urgency x 1‐2  Diagnosis: immunohistology in biopsy ,viral culture 
weeks; types 11 & 21 or PCR, serology
Reye Syndrome and Reye‐like Syndrome Treatment: posssible role of Cidofivir

Viral Gastroenteritis DIARLEX ROTA-ADENO


Rotavirus • The latex reagent is composed of either anti‐
‐single most important cause of severe  rotavirus antibodies(rabbit) or anti‐adenovirus 
dehydration diarrhea in early childhood antibodies (rabbit) bound to red latex particle
Astrovirus
• When a fecal extract containing rotavirus or 
‐2nd most important agent of viral diarrhea in 
adenovirus particles(antigen) is mixed with 
young children
the test latex reagent, an antigen‐antibody 
Enteric adenovirus
reaction occurs resulting in visible 
Caliciviruses
agglutination (red color)of the latex particles.
‐ most common cause of gastroenteritis outbreaks 
on older children & adults

Rotavirus Vaccine
Monovalent human RV: 2‐dose series
1st dose: 6 wks old, 4 weeks apart 
2nd dose: not later than 24 weeks
Pentavalent human‐bovine reassortant RV: 
THE END
1st dose:6‐12 weeks old, 4‐10 wk intervals
final dose :not later than 32 weeks  •
May be given with OPV or 2 weeks apart
With a potentially higher risk of intussuception if 1st
"Lord, thank you for everything, I can’t name them all
dose given beyond recommended age but it all comes from You, everyday I am very grateful
for everything!"

16 | P E D I A - V I R O
RABIES
• Primarily a disease of animals
• Dogs account for >90% of reported human 
RABIES & HIV cases
• 6‐10% ‐ cats, cattle, horse, sheep, bats,  exotic 
pets
• Small rodents, birds & reptiles are NOT 
KNOWN to serve as reservoir of infections

Rabies • Variation: 
Rabies
– Severity of the bite
• Transmission: bites of rabid animals or by  – Site of bite in relation to nerve supply 
licking of the mucosa or open wounds – Size of inoculum, protection offered by clothing & other 
factors
• Period of communicability: 
– Age and immune status of host
– Dogs & cats‐ 3‐5days before the onset of 
• Incidence:
symptoms until the entire course of illness
WHO:  11th major killer diseases
– Person to person‐ NOT DOCUMENTED
60,000 deaths worldwide
• Incubation period: 1day to 5 years (8 WEEKS – >30,000 die yearly in Asia
average) about 10M exposed annually
DOH: 2006(219 cases)
2007(281 cases)

Rabies
• Infected patients go through 4 stages
– Incubation period
• Usually 20‐90 days
• >95% will present with s/sx within 6 months
• Virus remains at the site of the bite
• The only time when vaccination is effective
– Prodrome
• 2‐10 days
• Virus reaches the spinal cord
• 1st rabies specific sx‐pain or itching or paresthesia at 
bite site

17 | P E D I A - V I R O
Rabies Rabies
Acute neurologic phase‐2‐7days
2 TYPES:
• Diagnosis
1. Encephalitic or furious rabies ‐80% – CBC‐ wbc 20,000‐30,000/mm3 with 
– Hyperactive episodes(combative,bizarre behavior,apprehensive) polymorphonucleosis
– Hydrophobia( agitation,cringing,due to painful contractions of 
laryngeal muscles upon drinking)  – CSF‐ mononuclear cells may increase 100/mm3, 
– aerophobia protein is slightly elevated
2. Paralytic or dumb rabies‐20%
– Paralysis of bitten area  respiratory paralysis – PREMORTEM DIAGNOSIS
– Often missed;hydrophobia & aerophobia absent • Fluorescent microscopy of skin biopsies from nape
– Rabies suspected if with paralysis or encephalitis
• Isolation of virus
Coma ‐ 4‐10 days • Detection of antibody‐serum & CSF in unvaccinated 
‐complications: myocarditis, diabetes insipidus,SIADH persons
‐outcome: death due to respiratory paralysis
• Detection of viral nucleic acid (PCR) in infected tissues

Rabies Rabies
• Diagnosis: • PROGNOSIS: fatal
– POSTMORTEM DIAGNOSIS‐ fluorescent  • TREATMENT: intensive symptomatic or 
microscopy of brain and salivary glands supportive care
– ANIMAL BRAIN 
• ISOLATION: strict throughout the illness; 
• Fluorescent antibody stain of brain tissue
caution against contamination of open wound 
• Positive for negri bodies
or mucous membrane with patient’s saliva

Therapeutic Management of Local wound care


Patients Exposed to Rabies
• Immediate vigorous washing & flushing w/ soap & water
• General principles of post‐exposure treament
• Apply alcohol or Povidone Iodine
• Suturing avoided  or delayed as it may inoculate virus deeper. If 
‐minimize amount of virus at the site of inoculation unavoidable, suturing done loosely. RIG must be instilled deep into 
the wound before suturing

‐develop a high titer of neutralizing antibody early • Do not apply ointment, cream or occlusive dressing to the bite site

• Anti‐tetanus prophylaxis should be initiated or boosted as indicated
• Antibiotics for all category III cat bites, category III dog bites that 
are on the hand or  deep,multiple & extensive
‐amoxycillin as propjylaxis
‐cloxacillin or amoxyclav if infected
• Antibiotics for category I & II only if wound is infected

18 | P E D I A - V I R O
Vaccination Vaccination
CARE OF EXPOSED PERSONS:
• ACTIVE IMMUNIZATION  • STANDARD INTRAMUSCULAR SCHEDULE
– Purified vero cell rabies vaccine 0.5ml/vial
– Purified chick embryo cell vaccine 1ml/vial Day of PVRV PDEV/ Site of
• PASSIVE IMMUNIZATION immunization PCECV injection
‐ for all Category III exposures + anti‐rabies vaccine
‐RIG should be inflitrated around and into the wound as  
Day 0 0.5ml 1ml One deltoid
anatomicaly feasible even if lesion has begun to heal, the       Day 3 0.5ml 1ml One deltoid
rest IM Day 7 0.5ml 1ml One deltoid
‐may be given until 7days after the 1st dose
– Human  rabies immune globulin (PREFERRED)
Day 14 0.5ml 1ml One deltoid
20IU/K   Day 28 0.5ml 1ml One deltoid
– Hyper immune equine rabies immune globulin(Fab2):
40IU/K IM, needs skin testing

SUMMARY SCHEDULE OF ACTIVE


IMMUNIZATION AGAINST RABIES

Postexposure Rabies Prophylaxis

Category I Category I
• Feeding/touching an animal • Wash exposed skin immediately with soap 
• Licking of intact skin (with reliable history and  and water
thorough physical examination) • No vaccine or RIG needed
• Exposure to patient with S/Sx of rabies by  • May opt to give pre‐exposure prophylaxis
sharing of eating or drinking utensils
• Casual contact to patient with signs and 
symptoms of rabies

19 | P E D I A - V I R O
Category II Category II
• Nibbling of uncovered skin • Start vaccine immediately
• Complete vaccination regimen until day 28/30 if:
• Minor scratches/abrasions without bleeding*
– Animal is rabid, killed, had died or unavailable for 14‐day 
• Licks on broken skin observation or examination
– Animal under observation died within 14 days and was 
FAT‐positive or no FAT testing was done or had signs of 
rabies

* Includes wounds that


are induced to bleed
OLD: Complete vaccination regimen until day 90

Category II Category III


• Complete vaccination regimen until day 7 if: • Single or multiple transdermal bites or scratches
– Animal is alive and remains healthy after 14‐day  – Puncture wounds, lacerations, avulsions, deep abrasions
observation period
– Animal under observation died within 14 days, was FAT‐
• Contamination of mucous membrane with saliva (i.e. 
negative and without any signs of rabies licks)
• Handling of infected carcass or ingestion of raw 
infected meat
• All Category II exposures on head and neck area

OLD: Complete vaccination regimen until day 30

Category III Category III


• Exposure to a rabies patient* through bites,  • Start vaccine and RIG immediately
contamination of mucous membranes with  • Complete vaccination regimen until day 28/30 if:
saliva/fluids through splattering, through  – Animal is rabid, killed, had died or unavailable for 14‐day 
mouth‐to mouth resuscitation, licks of eyes,  observation or examination
– Animal under observation died within 14 days and was 
lips, vulva, sexual activity, exchanging kisses  FAT‐positive or no FAT testing was done or had signs of 
on the mouth or other direct mucous  rabies
membrane contact with saliva

* does not include sharing of food/ drink/


utensils and casual contact with rabid patient OLD: Complete vaccination regimen until day 90

20 | P E D I A - V I R O
Category III Passive Immunization
• Complete vaccination regimen until day 7 if: • to neutralize rapidly the virus locally in the wound 
– Animal is alive and remains healthy after 14‐day  before it reaches the local nerve endings
observation period
– Animal under observation died within 14 days,  • To provide the immediate availability of neutralizing 
was FAT‐negative and without any signs of rabies Ab at the site of the exposure before it is 
physiologically possible for the patient to begin 
• Give anti‐tetanus prophylaxis producing his or her own Ab after vaccination 
(usually 7 to 14 days later)

• 3 kinds: HRIG, ERIG, Fab2
OLD: Complete vaccination regimen until day 30

National Rabies Prevention and


Anti-Rabies Act of 2007 Control Program, Philippines
• Republic Act No. 9482 GOAL: 
• An Act providing for the control and elimination of human 
and animal rabies To eliminate human rabies and declare the 
• Signed into law on May 25,2007; IRR signed in March 2008
• Provisions:
Philippines RABIES FREE by 2020
– Mass dog registration/vaccination
– Dog population control
– Provision of PEP to bite victims
– Information‐education
– Responsible pet ownership
– Provision of free PreP to high risk individuals and children 5 – 14 yrs in 
high incidence areas (IR>2.5/M pop)

Pre-exposure Prophylaxis Regions with IR > 2.5/M pop


2007 N=281 2006 N=216
Day 0 Day 7 Day 21/28 5 (7.76/M) 2 (8.65/M)
2 (7.37/M) 12 (5.2/M)
8 (4.61/M) 5 (4.16/M)
3 (4.55/M) 8 (4.16/M)
IM dose = 0.5 ml PVRV or 1.0 ml PCECV 9 (4.42/M) 1 (3.11/M)
7 (3.38/M) 3 (2.36/M)
ID dose = 0.1 ml PVRV, PCECV
12 (3.9/M) 7 (2.92/M)
4A (3.2/M) 4A (1.01/M)
Into the deltoid muscle or
anterolateral thigh in infants 1 (2.67/M)

21 | P E D I A - V I R O
Guidelines for subsequent exposure following
primary immunization(PreXP :D0,7,28 0r
PEP:D0,3,7)
HIV
‐no RIG needed
• Broad spectrum of disease
‐any exposure,regardless of severity,after completion of the  • Varied clinical course
primary immunization should be given as follows: • AIDS‐most severe end of the clinical spectrum
• Target cells
<1month                          no booster
1‐6 months                     1 booster
– T‐helper CD 4+ lymphocyte
>6mos‐3 yrs                   2 boosters on D0 & D3  – Monocytes
> 3 years                        repeat full course  of vaccine without  – Macrophages
RIG  – CNS cells with CD4 + receptors

Reported modes of Transmission Mother to infant transmission


HIV/AIDS registry
Jan 1984-Aug 2008 (vertical)
• Primary route of transmission
Reported modes of N=3358 • Rate: 12‐30% in US & Europe
transmission
• Time of transmission
Heterosexual contact 1,934
Homosexual contact 727 – Before delivery
Bisexual contact 303 • 30‐40%, (+) PCR within 1st week
Blood/blood product 19 – Intra‐partum transmission
Injecting drug use 8 • 60‐70%, no detectable virus before 1 week of age
Needle prick injuries 3 – Via breast feeding
Perinatal 46 • WHO recommend breastfeeding in developing countries
No exposure reported 318 • 14% risk of transmission in women with HIV before pregnancy
• 29% risk in women with HIV postnatally

• Mother‐to‐Child Transmission(n=46)
‐25 M,21 F
‐1‐11 yo
‐30 asymptomatic
‐16 AIDS cases,7 deaths
‐last MTCT wasin FEB 2008
In 2007, 8 cases reported
4 –Region IV
3 –Region III
1 – Region I 

22 | P E D I A - V I R O
Clinical manifestations Infections
• Vary widely  20%  of  AIDS‐defining  illnesses  recurrent  bacterial  infections 
caused by encapsulated organisms(pneumococcus, salmonella)
• PE at birth may be normal  Most  common  serious  infections:  bacteremia,  sepsis, 
• Initial symptoms may be subtle/ non‐specific pneumonia
 Opportunistic infections with severe depression of CD4 count
• Symptoms more common in children than adults  PCP  pneumonia:  most  common  opportunistic  infection 
– Recurrent bacterial infections children; peak: 3‐6 months;44‐47%  mortality
– Chronic parotid swelling  Tuberculosis‐higher  prevalence  of  TB  &  HIV  co‐infection  in 
– Lymphoproliferative interstitial pneumonitis developing countries
 Oral candidiasis‐most common fungal infection in HIV infected 
– Early onset of progressive neurologic disorder patients
 Viral infections with Herpes viruses pose a significant problem

• GI
• CNS – Oral candidiasis, gingivitis, parotitis
– occurs in 50‐90 % of perinatally infected children in developing  – Most common symptoms: chronic or recurrent 
countries as progressive encephalopathy, loss of developmental  diarrhea with malabsorption, abdominal pain, 
milestone cognitive deterioration and impaired brain growth. dysphagia, failure to thrive, chronic hepatitis
• RESPIRATORY TRACT – Pathogens: salmonella, campylobacter,MAC, giardia, 
– Recurrent otitis media and sinusitis are common
cryptosporidium, CMV, HSV, rotavirus, candida
– LIP – the most common chronic lower respiratory tract  • Renal
abnormality; affects 30‐40% of HIV infected children; maybe an  – uncommon
exaggerated response to EBV & HIV, non‐productive cough,  • Skin
insidious hypoxia, bronchiectasis, pulmonary decompensation, 
clubbing – Severe & unresponsive seborrheic dermatitis or 
eczema
• CARDIOVASCULAR SYSTEM
• Hematologic
– Rhythm disturbances; dilated cardiomyopathy & LVH
– Anemia, leukopenia, thrombocytopenia
– Malignant diseases infrequent in children
– Common reported neoplasms: NHL, primary CNS 
lymphoma, leiomyosarcoma

Diagnosis of HIV Infection Steps to HIV Testing

• Initial clues to consider possibility of HIV infection: A.Pre‐test Counseling
1. Having multiple sex partners(MSP) ‐important because of the profound psychosocial 
2. Unprotected sex w/a person who has MSP impact of an HIV(+) antibody test
3. Hx of STI ‐assess person’s risk for HIV infection
4. Hx of  IV drug use ‐provide adequate & correct info  about HIV 
5. Unprotected sex w/ an HIV infected person antibody test and HIV/AIDS
6. (+) clinical conditions suggestive of HIV infection  not  ‐assess how the person would cope with a (+) test
explaned by other causes ‐promote behaviors that will prevent transmission
7. Children below 13 years born to HIV infected 
mothers

23 | P E D I A - V I R O
Steps to HIV Testing Steps to HIV Testing
B.Request for HIV Ab Test C.Post‐test Counseling
‐provide intitial emotional support in case of a (+) 
‐informed CONSENT prior to test HIV antibody test
‐request for HIV Ab testing must be  written on the  ‐provide adequate medical info about HIV/AIDS
chart using a code name for the test ‐identify other medical and social support system
‐all hospital personnel with whom the patient may  ‐re‐emphasize behaviors that will prevent HIV 
interact for the conduct of HIV testing should act  transmission to other people
professionally and responsibly to ensure  ‐if (‐), explain the meaning of a (‐) test and re‐
CONFIDENTIALITY of the test emphasize  prevention

Case definition for HIV infection


Diagnosis of HIV infection
age <18months (CDC, 1999)
• Serologic test • Positive result on 2 separate determination from 1 or 
– ELISA more of the ff, HIV virologic test, HIV culture, HIV 
PCR, HIV p24 antigen (definite)
– Western blot assay
• Positive result on only 1 specimen using any HIV 
• Definitive virologic diagnosis virologic test and no subsequent negative HIV 
– Viral culture virologic or negative antibody test (presumptive)
– HIV DNA PCR • Any condition that meets criteria for AIDS (clinical)
– HIV p24 antigen

Case definition for HIV infection


age >18months (CDC, 1999)
• HIV antibody positive by repeatedly reactive 
EIA and confirmatory test (western blot or 
IFA)
• Positive result on any HIV virologic test, HIV 
culture, HIV PCR, HIV p24 antigen
• Any condition that meets criteria for AIDS

24 | P E D I A - V I R O
Clinical Categories for Children with Human
Immunodeficiency Virus (HIV) Infection

CATEGORY N: NOT SYMPTOMATIC
• Children who have no signs or symptoms considered to be the result of 
HIV infection or who h we only one of the conditions listed in Category A.

CATEGORY A: MILDLY SYMPTOMATIC
• Children with two or more of the conditions listed bel )W but none of the 
conditions listed in Categories B and C.
• Lymphadenopathy (>0.5 cm at more than two sites; bilateral= one site)
• Hepatomegaly
• Splenomegaly
• Dermatitis
• Parotitis
• Recurrent or persistent upper respiratory infections, sinusitis, or otitis
media

CATEGORY B: MODERATELY SYMPTOMATIC CATEGORY B: MODERATELY SYMPTOMATIC

• Herpes simplex virus (HSV) stomatitis, recurrent (more than two episodes 
• Children who have symptomatic conditions other than those listed for  within 1 year)
Category A or C that are attributed to HIV infection. Examples of conditions  • HSV bronchitis, pneumonitis, or esophagitis with onset before 1 month of age
in clinical Category B include but are not limited to: • Herpes zoster (shingles) involving at least two distinct episodes or more than 
• Anemia (<8 gm/dL), neutropenia (<1000/mm3), or thrombocytopenia  one dermatome
(<100,000/mm3) persisting >30 days • Leiomyosarcoma
• Bacterial meningitis, pneumonia, or sepsis (single episode) • Lymphoid interstitial pneumonia (LIP) or pulmonary lymphoid hyperplasia 
• Candidiasis, oropharyngeal (thrush), persisting (>2 months) in children >6  complex
months of age • Nephropathy
• Cardiomyopathy • Nocardiosis
• Cytomegalovirus infection, with onset before 1 month of age • Persistent fever (lasting >1 month)
• Diarrhea, recurrent or chronic • Toxoplasmosis, onset before 1 month of age
• Hepatitis • Varicella, disseminated (complicated chickenpox)

CATEGORY C: SEVERELY SYMPTOMATIC CATEGORY C: SEVERELY SYMPTOMATIC


Serious bacterial infections, multiple or recurrent (i.e., any combination of at least two cul‐ture‐ Histoplasmosis, disseminated (at a site other than or in addition to lungs or cervical or hilar lymph 
confirmed infections within a 2‐year period), of the following types: septicemia, pneumonia,  nodes)
meningitis, bone or joint infection, or abscess of an internal organ or body cavity (excluding otitis Kaposi's sarcoma
media, superficial skin or mucosal abscesses, and indwelling cathe‐ ter‐related infections) Lymphoma, primary, in brain
Candidiasis, esophageal or pulmonary (bronchi, trachea, lungs) Lymphoma, small, noncleaved cell (Burkitt’s), or immunobiastic or large cell lymphoma of B‐ceii or 
Coccidioidomycosis, disseminated (at site other than or in addition to lungs or cervical or hilar unknown immunologic phenotype
lymph nodes) Mycobacterium tuberculosis, disseminated or extrapulmonary
Cryptococcosis, extrapulmonary Mycobacterium, other species or unidentified species, disseminated (at a site other than or in 
Cryptosporidiosis or isosporiasis with diarrhea persisting >1 month addition to lungs, skin, or cervical or hilar lymph nodes)
Cytomegalovirus disease with onset of symptoms at age >1 month (at a site other than liver,  Mycobacterium avium complex or Mycobacterium kansasii, disseminated (at site other than or in 
spleen, or lymph nodes) addition to lungs, skin, or cervical or hilar lymph nodes)
Encephalopathy (at least one of the following progressive findings present for at least 2 months in  Pneumocystis carinii pneumonia
the absence of a concurrent illness other than HIV infection that could explain the findings): a)  Progressive multifocal leukoencephalopathy
failure to attain or loss of developmental milestones or loss of intellectual ability, verified by 
standard developmental scale or neuropsychological tests; b) impaired brain growth or acquired  Salmonella (nontyphoid) septicemia, recurrent
microcephaly demonstrated by head circumference measure‐ments or brain atrophy  Toxoplasmosis of the brain with onset at >1 month of age
demonstrated by computerized tomography or magnetic resonance imaging (serial imaging is  Wasting syndrome in the absence of a concurrent illness other than HIV infection that could 
required for children <2 years of age); c) acquired symmetric motor deficit manifested by two or  explain the following findings: a) persistent weight loss >10% of baseline OR b) downward crossing 
more of the following: paresis, pathologic reflexes, ataxia, or gait disturbance of at least two of the following percentile lines on the weight‐for‐age chart (e.g., 95th, 75th, 50th, 
Herpes simplex virus infection causing a mucocutaneous ulcer that persists for >1 month; or  25th, 5th) in a child 21 year of age OR c) <5th percentile on weight‐for‐height chart on two 
bronchitis, pneumonitis, or esophagitis for any duration affecting a child >1 month of age consecutive measurements, 230 days apart ELLIS a) chronic diarrhea (i.e., at least two loose stools 
per day for 230 days) OR b) documented fever (for 230 days, intermittent or constant)

25 | P E D I A - V I R O
Management Treatment

Antiretroviral therapy Antiretroviral therapy does not eradicate 
– Prevention of infection virus nor cure
• Prophylaxis against specific infections – Indicated for HIV‐infected children with 
• Vaccination symptoms or immunosuppressed regardless of 
• IVIg viral load
– Provision of psychosocial support – Triple drug therapy: 1 protease inhibitor 
(Nelfinavir, ritonivir, indinavir) + 2 nucleoside 
analogue reverse transcriptase inhibitors 
(zidovudine + dideoxynosine or lamivudine)

• Early diagnosis/aggressive treatment of opportunistic  • Early diagnosis/aggressive treatment of opportunistic 
infections infections
• Prophylaxis • Prophylaxis
Tuberculosis
PPD (+) 5 mm induration or exposure to open case of     – IVIG
TB • To prevent serious bacterial infection for HIV 
Pneumocystis jiroveci pneumonia infected children with: at 2 lab documented serious 
• Trimetoprim sulfa, aerosolized pentamidine, dapsone bacterial infections
‐at 4‐6wks‐1 yo unless hiv excluded • Lab‐documented inability to make antigen‐specific 
‐CD4+T cell count <200 cells or (+) oral thrush  or AIDS‐defining  antibodies
conditions
MAC prophylaxis • Hypogammaglobulinemia
• Clarithromycin or azithromycin • 400mg/kg every 4 weeks
‐CD4 + T cel l  <100 cells  or clinical condition(marked wasting, alopecia, 
skin dicoloration

Recommendations for Routine Immunization of Prevention


HIV-Infected Children in US
A. Abstinence
B. Be faithful (mutual monogamy)
C. Careful sex/correct and consistent condom 
use
D. Do not take prohibited drugs/do not share 
contaminated needles
E. Education/Early detection and treatment of 
STI

26 | P E D I A - V I R O
Zidovudine Regimen for decreasing the Prevention of Mother-to-Child
rate of peri-natal transmission of HIV Transmission of HIV (PMTCT)
Period of time 1)Primary prevention of HIV‐infection among women 
Route Dosage
of reproductive age(HIV info and voluntary 
During pregnancy, initiate Oral 200 mg tid or counseling and testing(VCT) of ANC
anytime after 14 wk AOG
& throughout pregnancy 300 mg BID 2)Prevention of unintended pregnancies among HIV‐
infected women thru family planning
During labor and delivery IV 2mg 1st hr, 3)Prevention of vertical transmission thru ARV 
1mg/k/hr until prophylaxis
delivery
4)Provision of Tx, care and support for HIV‐women and 
For newborn, within 6-12 Oral 2mg’k qid, for
hr of birth children
1st 6 wk of life

Monitoring of Pediatric HIV


Infection Monitoring of Pediatric HIV
CD4+ Cell Count/C4+ %:
Infection
– Obtained once (+) virologic test for HIV, then 
every 3 months Quantitative RNA Assay:
– Declines as HIV infection progresses – Indicates viral burden in peripheral blood
– Lower counts associated with poorer prognosis – Best single prognostic indicator
 CD4+ Cell Count: – Higher levels(>100,000 copies/ml) associated 
o Identifies a specific level of immune suppression that  with high risk for disease progression and 
changes with age mortality, particularly if also with CD4+ 
 CD4+ %: lymphocyte of < 15%
o Not affected by age
o A better marker of disease progression

THE END

"Lord, thank you for everything, I can’t name them all
but it all comes from You, everyday I am very grateful
for everything!"

27 | P E D I A - V I R O