Congenital and

Perinatal
Infections

Department of Faculty and

Hospital Paediatrics

Definition
Congenital (intrauterine) infection is
an infection acquired in utero that
causes fetal loss or can result in
intrauterine growth restriction,
congenital anomalies, prematurity, or
postnatal infection any of which is
obvious at birth
Perinatal infection refers to the
infectious process which originates
from intrapartum or postpartum period

Definition
Vertical infection any infection of a newborn
acquired from a mother
Congenital infections may be broadly summarized
by acronym TORCH: T Toxoplasmosis, O
Others, R Rubella, C Cytomegalovirus (CMV),
H Herpes simplex viruses (HSV) I and II
The term TORCH is a misnomer because
the others category continues to expand;
several infections are rarely truly congenital - they are
usually perinatally acquired with clinical onset within the
first month of age.
screening tests only assesses maternal exposure, but
not necessarily antenatal or perinatal infection in the
fetus

Incidence
Approximately 1% of newborn infants
excrete CMV
Up to 15 % of infants are infected with
Chlamydia trachomatis
about one third of these infants develop
conjunctivitis and
one sixth develop pneumonia

1 to 8 infants per 1000 live births develop

bacterial sepsis
Regional incidences of congenital rubella
and syphilis very much depend on the
prevention programs

Incidence
In utero a perinatal infection with HSV,
Toxoplasma gondii and VZV occurs in
about 1 infant per 1000 live births (1 ),
but the sequelae of infection are usually
severe
The incidence of perinatally HIV-infection
is still uncertain. In the absence of any
prevention measures about 25% of
infants born to infected mothers develop
this disease

Consequences
Infection acquired in utero may result
in
resorption of the embryo,
abortion,
stillbirth,
malformation,
intrauterine growth retardation
prematurity and
the untoward sequelae of chronic postnatal
infection

Consequences
Infection acquired during the birth
process or soon after birth may result in
severe systemic disease that leads to
death or
persistent postnatal infection

Both in utero infection and infection

acquired during the birth process may
lead to late-onset disease

Consequences
The infection may be inapparent at birth
but may present with signs of disease
weeks, months or years later, as
exemplified by the chorioretinitis of
T.
gondii, the hearing loss of CMV or rubella
virus and the immunologic defects that
result from HIV
The immediate as well as the long-term
effects of these infections are a major
problem throughout the world

Relative Frequency of
Congenital and Perinatal
Infections According to
Pathogen

Pathogen
Toxoplasma
Treponema
VZV
HIV Type I
Rubella virus
CMV
HSV

Congenital

Perinatal

+++
+++
++
+
+++
++
+

+
+
++
+++
+
++
+++

Pathogenesis of haematogenous
transplacental infections

Pathogenetic mechanisms
Because of their relatively low virulence, the
organisms involved seldom lead to fetal death
beyond the earliest stages of embryogenesis
Since the fetus is essentially a graft of foreign
tissue in the uterus, the placenta constitutes a
protective immunologic barrier that shields the
fetus from the mother's humoral and cellmediated immune responses
This makes the fetus especially susceptible to
infection during the first trimester and the
perinatal period.

Pathogenetic mechanisms
Early in pregnancy the most complex events
in embryogenesis take place, making sensory
organs such as the eyes and ears vulnerable.
The immature fetus lacks the immunologic
mechanisms necessary to completely
eliminate an infecting organism
Therefore, a state of immunologic tolerance is
often established, which results in persistence
of organisms that ordinarily would be
eliminated by a normal child or adult

The degree of severity is

dependent on ...
Gestational age of the fetus when
infected
Virulence of the organism,
Damage to the placenta,
Severity of maternal disease
Primary maternal infection (the
highest risk of fetal injury)

Clues to the diagnosis of

possible infection
Congenital growth retardation
symmetrical type
Microcephaly

//
Petechiae/ purpura / blue
berry muffins
Cranial calcificates,

Brain edema,
, ,
Hydrops foetalis

Congenital heart disease

, ,

/


()

, ,

Congenital syphilis
Syphilis is a sexually transmitted disease
caused by Treponema pallidum.
Early congenital syphilis is when clinical
manifestations occur before
2 years of age
Late congenital syphilis is when
manifestations occur at >2
years of age

Congenital syphilis
Untreated maternal syphilis can result in
stillbirth/ perinatal death/ premature delivery
congenital infection
about half of survivors have long-term
neurological sequelae

Untreated infection in the first and second

trimesters often leads to significant fetal
morbidity
With third-trimester infection many infants
are asymptomatic

Congenital syphilis
Infection can also be acquired via contact of
infectious lesions during passage through the
birth canal
Virtually all infants born to untreated women
with primary and secondary syphilis have
congenital infection
50% are clinically symptomatic
The infection rate is only 40% with early latent
disease and 6-14% with late latent stages.
The mortality rate may be as high as 54% in
infected infants

Clinical presentation
The most common findings in the
neonatal period include hepatosplenomegaly, jaundice, and osteochondritis
Other signs include generalized lymphadenopathy, pneumonitis, myocarditis,
nephrosis, pseudoparalysis (atypical
Erb's palsy), rash (vesicobullous,
especially on the palms and soles),
hemolytic anemia (normocytic or
normochromic), leukemoid reaction, and
hemorrhagic rhinitis (snuffles)

Clinical presentation
Late congenital syphilis manifests by
Hutchinson's teeth, healed retinitis,
eighth nerve deafness, saddle nose,
mental retardation, arrested
hydrocephalus, and saber shins
Other clues to the diagnosis of
congenital syphilis include
placentomegaly and congenital
hydrops

Diagnosis
Laboratory studies - Nonspecific
reagin antibody tests
Venereal Disease Research Laboratory
(VDRL) slide test
A VDRL titer at least 2 dilutions (4-fold)
higher in the infant than in the mother
signifies probable active infection
Titers should be monitored and repeated.
If liters decrease in the first 8 months of life,
the infant is probably not infected

Diagnosis
Laboratory studies - Nonspecific
reagin antibody tests
Rapid plasma reagin test
This is an NTA test that detects antibodies to
cardiolipin and is a screening test for syphilis
It should not be used on spinal fluid
A normal test result is negative, and any
positive test should be followed up with a
specific treponemal test
Titers can also be reported as for the VDRL
test

Diagnosis
Laboratory studies - Specific
treponemal tests (FTA-ABS test, Micro-

hemagglutination test for T. pallidum (MHTPA)

Specific STA tests verify a diagnosis of current
or past infection
These tests should be performed if NTA test
results are positive
These antibody tests do not correlate with
disease activity and are not quantified
They are useful for diagnosing a first episode of
syphilis and for distinguishing a false-positive
result of NTA tests

Diagnosis
Direct antigen tests for T. pallidum, including
an ELISA that uses monoclonal antibody to
the organism's surface proteins, as well as a
PCR test that can detect the organism in
CSF, amniotic fluid, and other specimen
Microscopic dark-field examination
Complete blood cell count with differential
Monocytosis is typically seen
look for hemolytic anemia or a leukemoid
reaction

Diagnosis
Lumbar puncture. CNS disease may be
detected by positive serologic tests, darkfield examination positive for spirochetes,
elevated monocyte count, or elevated spinal
fluid protein levels
The VDRL test is the only one approved for
use on CSF
PCRs on CSF may prove useful
X-ray studies of the long bones may show
sclerotic changes of the metaphysis and
diaphysis, with widespread osteitis and
periostitis

Management
Symptomatic infant should be treated
The infant should be treated if
maternal treatment was inadequate, unknown,
or given during the last 4 weeks of pregnancy
or
if a drug other than penicillin (eg,
erythromycin) was used

Infants with positive VDRL tests, even if this

is only an indication of maternal transfer of
IgG, should be treated if adequate follow-up
cannot be obtained

Treatment
Aqueous crystalline penicillin G - 100,000150,000 units/kg/24 h IV, or alternately
50,000 units/kg/day of procaine penicillin IM;
The duration of therapy should be 10-14
days in both instances
Asymptomatic infants born to mothers
whose treatment for syphilis may have been
inadequate should be fully evaluated,
including CSF examination

Treatment
Some experts would treat them with
aqueous crystalline or procaine penicillin G
However, if CSF is normal, as well as
normal X-ray films of long bones, platelet
count, and liver functions, many experts
would treat with a single IM dose of 50,000
units/kg of penicillin G benzathine
However, if the mother is infected with HIV1, a complete 10- to 14-day course of
therapy is recommended

Prevention
Screening at the initial antenatal visit is
part of routine obstetric care since women
may have asymptomatic latent disease
(28 wks, before birth)
Prevention of vertical transmission
Any newborn should not be discharged
without the result of mothers investigation

Toxoplasmosis
Congenital Toxoplasmosis occurs in
between 0,2 to 10 per thousand pregnancies
T. gondii is a parasitic organism. The
domestic cat is the primary host. Infection
can be contracted by
ingesting oocytes present in faecal material of infected
hosts
eating pseudocysts present in undercooked meat

Most women have no symptoms. Although

15% of women report acute flu-like illness
with lymphadenopathy

Toxoplasmosis
Risk of fetal infection is lowest in early
pregnancy but most fetuses infected early have
severe consequences
Risk of fetal
infection

Severe
consequences of
infection

1st trimester

10%

70%

3rd trimester

60%

<1%

Clinical features
Infants congenitally infected with
Toxoplasmosis can be
completely asymptomatic
unaffected at birth and manifest
problems later
severely affected in-utero and at birth

Clinical features
Infection usually affects the neurological
and haemopoietic systems. The classical
tetrad described by Sabin in 1942 includes

hydrocephalus/microcephaly
chorioretinitis
convulsions
other evidence of CNS involvement (including
calcification)
2 clinical forms: infection of the CNS or the
eyes, or infection of the CNS and eyes with
disseminated infection

Clinical features
Haematological

hydrops due to
anaemia
rash due to
thrombocytopenia
-purpura
blueberry muffin
appearance (seen in
25% of generalised
infection)
lymphadenopathy
hepatosplenomegaly

Neurological

convulsions
hydrocephalus with
bulging fontanelle

microcephaly
chorioretinitis can be
present early or
develop later

Generalised features
include

lethargy and malaise

poor feeding
vomiting
diarrhoea
temperature instability
jaundice

Diagnosis - Serologic tests

Toxoplasma-specific IgM antibodies can be measured by
indirect fluorescent antibody (IFA) test, ELISA, or IgM
immunosorbent agglutination assay (IgM-ISAGA)
Usually become positive within 1-2 weeks of infection; and
persist for months or years, especially when very sensitive
assays such as double-sandwich IgM enzyme
immunoassay (DS-IgM EIA) or IgM-ISAGA are used.
If IgM titers are high and accompanied by high specific IgG
titers of >1:512, as measured by IFA or Sabin-Feldman dye
test, this suggests acute infection
IgA antibodies are found in >95% of patients with acute
infections
Toxoplasma-specific IgE antibodies are found
in almost all women who seroconvert during pregnancy

Diagnosis
Perinatal diagnosis can be made by using
polymerase chain reaction (PCR) amplification of
the B gene of T. gondii in a sample of amniotic
fluid. DS-IgM EIA and ISAGA detect Toxoplasma
IgM in >75-80% of infants with congenital
infection
CSF examination should be performed in
suspected cases. The most characteristic
abnormalities are xanthochromia, mononuclear
pleocytosis, and a very high protein level.
Tests for CSF IgM to toxoplasmosis may also
be performed

Diagnosis
A cranial ultrasonogram or CT scan of the head
may demonstrate characteristic intracranial
calcifications (speckled throughout the CNS,
including the meninges)
Long-bone films may show abnormalities,
specifically, metaphyseal lucency and irregularity
of the line of calcification at the epiphyseal plates
without periosteal reaction.
Other studies. Ophthalmologic examination
characteristically shows chorioretinitis. Other
ocular features are often present at some stages

Management
In cases of an infected child with
symptoms, spiramycin 100 mg/kg/day
for 2 weeks, followed by alternating 1
month of pyrimethamine 1 mg/kg/day
and sulfadiazine 100 mg/kg/day, and
1 month of spiramycin 100 mg/kg/day
is recommended.
This regimen should continue for 1
year

Management
Asymptomatic neonates with serologically-proven infection should also
be treated for the first 2 weeks with
spiramycin and then by sulfadoxinepyrimethamine 1 + 20 mg/kg/week for
the first year of life
In all cases close clinical observation
is suggested

Prevention
Many European countries have instituted
compulsory testing for anti-T. gondii
antibody during pregnancy, and others are
preparing the legislature for such tests.
Avoidance of contact with cat feces and
consumption of only cooked or pickled
meat, and careful handling of raw meat and
meat products should be part of health
education preceding pregnancy

Cytomegalovirus
infection
CMV is a DNA virus and a
member of the herpes virus
family

CMV infection

Epidemiology
CMV is a ubiquitous virus that may be
transmitted in secretions, including saliva,
tears, semen, urine, cervical secretions,
blood (white blood cells), and breast milk
Both primary and recurrent maternal CMV
can lead to transmission of virus to the
fetus
When primary maternal infection occurs
during pregnancy, virus is transmitted to
the fetus in about 35% of cases

Epidemiology
The risk does not appear to vary
significantly with gestational age at time of
maternal infection
During recurrent infection, transmission
rate is only 0,2-1,8%
More than 90% of infants born with CMV
have subclinical infection
Symptomatic infants are usually born to
women with primary infection.

Epidemiology

Clinical presentation
Subclinical infection is 10 times
more common than clinical illness
Low birth weight. Maternal CMV
infection is associated with low birth
weight and small for gestational age
infants even when the infant is not
infected

Classic CMV inclusion

disease

Intrauterine growth retardation, hepatosplenomegaly

with jaundice, abnormal liver function tests, thrombocytopenia with or without purpura, and severe CNS
disease (CNS and sensory impairments are seen in
50-90% of symptomatic newborns), including
microcephaly, intracerebral calcifications, chorioretinitis, and progressive sensorineural hearing loss (1020% of cases)
Other symptoms include hemolytic anemia and
pneumonitis
By 2 years of age, 5-15% of infants who are
asymptomatic at birth may experience serious
sequelae, such as hearing loss or ocular abnormalities

Late sequelae
With subclinical infection, late sequelae such as
mental retardation, learning disability, and
sensorineural hearing loss have been attributed to
CMV
Studies have now shown for children with
asymptomatic congenital CMV infection a
prevalence of sensorineural hearing loss of 7-15%
Approximately one half had bilateral loss, and 50%
of affected children had progressive deterioration
Repeated auditory evaluation during the first 3
years is strongly recommended

Diagnosis
Culture for demonstration of the virus.
The "gold standard" for CMV
diagnosis is urine or saliva culture
Most urine specimens from infants with
congenital CMV are positive within 48-72 h
Shell vial tissue culture technique
detection of CMV-induced antigens
by monoclonal antibodies, allowing for
identification of the virus within
18 h.

Diagnosis
PCR may also be used; however, it does
not appear to offer any advantage over
culture-based methods
Serologic tests based on detection of IgM
should not be used to diagnose congenital
CMV because they are less sensitive and
more subject to false-positive results than
culture or PCR
Radiological studies. Skull films or CT
scans of the head may demonstrate
characteristic intracranial calcifications

Postdiagnosis evaluation
CT scan of the brain, ophthalmologic
examination, brainstem evoked responses
(BER) hearing evaluation, complete blood
cell count, platelet count, liver enzyme
levels, bilirubin level, CSF for cell
count, protein and glucose, CSF CMV
culture, or test for CMV DNA

Treatment and prevention

Under life-threatening circumstances
Ganciclovir 6 mg/kg/dose every 12 hrs
6 wks
Specific intravenous immunoglobulin
Prevention
A phase II clinical trial of a recombinant
subunit vaccine in young women
is underway
Standard precautions, especially good hand
washing after diaper changes, is particularly
important for pregnant personnel

Perinatal Herpes
Infection

HSV-II infection

Epidemiology
Two serologic subtypes can be distinguished by antigenic and serologic tests:
HSV-1 (orolabial) and HSV-2 (genital)
Three quarters of neonatal herpes
infections are secondary to HSV-2;
HSV-1, however, is the cause of 7-50% of
primary genital herpes infections.
HSV infection of the neonate can be
acquired at one of three times: intrauterine,
intrapartum, or postnatal

Epidemiology
Most infections (80%) are acquired in the
intrapartum period as ascending infections
with ruptured membranes (4-6 h is
considered a critical period for this to
occur) or by delivery through an infected
cervix or vagina
Only 25-33% of cases have signs or
symptoms of genital herpes at the time of
labor and delivery despite having active
infection

Epidemiology
The primary infection may be "active" for
as long as 2 months.
Many neonatal infections occur because of
asymptomatic cervical shedding of virus,
usually after a primary episode of HSV
infection
The usual portals of entry for the virus are
the skin, eyes, mouth, and respiratory tract

Epidemiology
Infection in a newborn
33% because of primary maternal
infection
3% - because of recurrent infection
(virus load, longer viral excretion,
lower antibody level)

Clinical presentation
Localized infections involving the skin,
eyes, or oral cavity usually manifest at 1011 days of age and account for 40% of
neonatal herpes
Infants with disseminated HSV infection
account for 25% of all neonatal herpes
patients. Usually, they present at 9-11 days
of age
Infants with encephalitis usually present at
15-17 days of age (30-40% will have no
herpetic skin lesions)

Disseminated disease
Signs and symptoms of localized disease as well
as anorexia, vomiting, lethargy, fever, jaundice
(with abnormal LFTs), rash or purpura, apnea,
respiratory distress, bleeding, and shock
Presentation with bleeding and cardiovascular
collapse may be sudden and rapidly fatal
CNS involvement is present in two thirds of these
patients
Without antiviral therapy, 80% or more die, and
most go on to have serious neurologic sequelae
The mortality rate remains as high as 55%, even
with appropriate treatment; however, 40-55% of
survivors suffer longterm neurologic impairment

Diagnosis
Viral cultures. The virus grows readily, with
preliminary results available in 24-72 h.
Cultures are usually obtained from conjunctiva,
throat, feces, urine, nasal pharynx, and CSF
Immunologic assays to detect HSV antigen in
lesion scrapings, usually using monoclonal antiHSV antibodies in either an ELISA or
fluorescent microscopy assay, are very specific
and 80-90% sensitive
Serologic tests are not helpful in the diagnosis
of neonatal infection, until a test for HSV IgM is
readily available

Diagnosis
PCR to detect HSV DNA is a very sensitive
method, as high as 100% in diagnosing
HSV within CSF. Contamination, however,
can frequently occur with this technique
Lumbar puncture should be performed in
all suspected cases. Evidence of
hemorrhagic CNS infection with increased
white and red blood cells and protein is
found. PCR should also be performed on
CSF

Diagnosis
CT scan of the head may be useful in the
diagnosis of CNS disease, but magnetic
resonance imaging (MRI) and an electroen
cephalogram (multiple independent foci of
periodic slow and sharp wave discharge) are
probably better for detecting earlier disease.
In the neonate, CNS disease is more diffuse
than in older patients
Brain biopsy may be needed in certain
cases to confirm the diagnosis; however,
PCR testing of CSF may make this obsolete

Management
Studies are ongoing to determine whether acyclovir
therapy should be given to pregnant women who have
a primary episode of genital HSV as well as to women
with active infection (primary or secondary) near or at
time of delivery
If there are no visible lesions at the onset of labor or
prodromal symptoms, vaginal delivery is acceptable
Deliver by cesarean section (C-section) in women
who have clinically apparent HSV infection (definitely
for primary infection and most experts also recommend
in secondary infection as well). Debate exists if
membranes have already been ruptured for >6 h. Most
experts still recommend C-section.

Management
Infants with known infection or exposure to HSV
be placed in contact isolation
Infants born to mothers with a genital lesion. If
it is a known recurrent lesion and the infant is
asymptomatic, the infection rate is 1-3%. Con
sider surface screen cultures of the infant at 2448 h of age. Treat if symptoms develop or if the
culture is positive
If maternal infection is primary, the risk to the
infant is 33-50%; therefore, most clinicians
recommend empiric acyclovir at birth after
cultures have been obtained

Treatment
The first-line drug of choice is acyclovir
with current recommendations for highdose therapy of 60 mg/kg/day for 21
days for CNS and disseminated
disease
The second choice being vidarabine
(which requires 12-h infusion with a
large volume of fluid)
Trifluridine is the treatment of choice
for ocular HSV infection in the neonate

HIV infection
HIV is an enveloped RNA virus that is a
member of the Lentivirus subfamily of
retroviruses. Infection is most
commonly secondary to HIV-1

Estimated Number of People

Living with HIV
Total: 39,5 (34,1 47,1) million
Western &
Central Europe

0,74 million

North America

1.4 million

[0,88 2.2 million]

Caribbean

Eastern Europe
& Central Asia

[0,58 0,97 million]

North Africa & Middle East

0,25 million

[0,19 0,32 million]

Latin America

1.7 million

[1.3 2.5 million]

0,46 million

[0,27 0,76 million]

Sub-Saharan Africa

24.7 million

[21.8 27.7 million]

1.7 million

[1.2 2.6 million]

East Asia

0,75 million

[0,46 1.2 million]

South & South-East Asia

7.8 million

[5.2 12.0 million]

Oceania

0,081 million

[0,05 0,17 million]

UNAIDS/WHO, 2006

Risk of infants infection

63

15
15
7

63 infants will
not be
infected
37 infants will
be infected with
HIV

Number HIV negative

Number infected during two years of breast feeding
Number infected during labour
Number infected during pregnancy

PMTCT Intervention and

MTCT Risk
No ART + 2 years breastfeeding

45%
ART + 2 years breastfeeding
35%
No ART + breastfeeding replacement
25%
ART + breastfeeding replacement
8%
ART + C-Section + breastfeeding replacement

2%

Features of the infection

Vertically infected children experience
more rapid disease progression
than those infected at an older age or
adults
More than 80% of vertically infected
children manifest HIV-1-related symptoms
or CD4 T-cell depletion by 2 years of age
An AIDS-defining condition developed in
-23% by 1 year and in -40% by 4 years of
age in vertically infected infants

Clinical presentation
The newborn may be asymptomatic or may have
low birth weight, weight loss, or failure to thrive
Recurrent upper respiratory tract infections, otitis
media, sinusitis, and invasive bacterial infections are
common
Recurrent oral thrush is common, and Candida
esophagitis may become particularly troublesome
Other infections that increase in frequency and
difficulty to control include acute and recurrent VZV
infections, measles, CMV, and gastrointestinal
infections (eg, Salmonella, Giardia, Campylobacter,
rotavirus, and Cryptosporidium)

Clinical presentation
Nonspecific features of infection can include
hepatosplenomegaly, lymphadenopathy, and
fever
Neurologic disease may be either static (delayed
attainment of milestones) or progressive, with
impaired brain growth, failure to reach milestones,
and progressive motor deficits
Common CT scan findings include basal ganglia
calcification and cortical atrophy. Cardiac
abnormalities, pericardial disease, myocardial
dysfunction, dysrhythmias, and cardiomyopathies
are common, particularly in advanced disease

Diagnosis
Diagnosis is based on
(1) suspicion of infection because of
epidemiologic risk or clinical presentation
and
(2) confirmation by different virologic assays
in infants <18 months old or serologic tests
if the infant is >18 months old
Surrogate markers for disease. Immunologic
abnormalities, including hypergammaglobulinemia, a low CD4+ T-lymphocyte count, or a
decreased CD4+ percentage OR marker
diseases

Elective Caesarean Section

Could Reduce MTCT by
50%
Elective caesarean section should be
recommended to HIV-positive women and
performed at:
38 weeks of pregnancy
Prior contractions
If the rupture of membranes is less than 4
hours

Safe Vaginal Delivery

Practices
Use partogram to monitor labour
Avoid unnecessary frequent cervical
examinations
Prevent long rupture of membranes (>4
hours increases MTCT by 50%)
Avoid invasive obstetric interventions and
procedures during labour
Promote free position for women during
delivery

Avoid prolonged labour

WHO, CDC, 2004

ARV prevention in labour

Assess ARV drugs taken during pregnancy, thus select
the ARV regimen based on obstetric scenario and prior
ARV treatment

Woman treated from 24-28 weeks by ZDV

Labour: Zidovudine (ZDV) until delivery + Lamivoudine

(3TC) + Nevirapine (NVP) at onset of labour
Caesarean section: continue ZDV

Woman treated for less than 4 weeks by ZDV

Zidovudine (ZDV) + Lamivoudine (3TC) + Nevirapine

(NVP)
Independently of the mode of delivery

Woman did not receive ARV during pregnancy

Zidovudine (ZDV) + Nevirapine (NVP) + Lamivoudine

(3TC)
Independently of the mode of delivery
WHO EURO, 2006

Specific Care for Infant

Born to HIV-Positive
Mother

Prevent carefully blood splashing during

umbilical cutting
ART prophylaxis depending on mother's ART
Mothers ART since 24-28 weeks
If mother received NVP - give the infant Zidovudine
(ZDV) + Lamivoudine (3TC) + Nevirapine (NVP)
If mother did not received NVP - give the infant
Zidovudine (ZDV) only

Mothers ART less than 4 weeks during

pregnancy
Zidovudine (ZDV)

Mother not treated by ART

Zidovudine (ZDV) + Lamivoudine (3TC) +WHO
Nevirapine
EURO, 2006

ARV prevention

WHO, 2006

Infant care
Infant HIV testing
Polymerase Chain Reaction - PCR DNA HIV
Could be done after 48 hours
HIV ELISA test
Only after 12 to 18 months

Prophylactic of Pneumocistic carinii

pneumonia starting after 4 weeks:
Cotrimoxazole syrup (240 mg/5ml)
0,5 ml/kg/24h
3 times a week until confirmation of HIV-negative
status