TORCH Infection in Pregnancy

dr. Eddy Tiro, SpOG(K)

Social Obgyn Division
Obstetric and Gynecologic Department
Medical Faculty of Hasanuddin University
Dr. Wahidin Sudirohusodo Hospital
Makassar

What is TORCH INFECTION?

A group of infectious diseases that causes
congenital and perinatal infection
TORCH is abbreviation of 4 infectious
disease (Toxoplasmosis, Rubella, CMV
dan HSV)

T.O.R.C.H.
BV
GBS
Varicella
Listeria
MALARIA
SYFILIS
OTHERS

TOXOPLASMOSIS

COMPLEX

CHLAMYDIA

R
RUBELLA

H
HERPES
genitalis

CYTOMEGALO
VIRUS

HP B19
HPV
HIV
HEPATIT B,C..

Toxoplasmosis
Protozoa Parasit T. gondii
Family : Sarcocystidae
Tachyzoite 2-4 & 4-8 m
Oocyst
12,1 x 11 m
Cyst
200 m

Rubella
Antigen : Virus Rubella
Family : Togaviridae
Size
: 60 - 70 nm

TORCH
Cytomegalovirus

Herpes Genitalis

Antigen : Virus Cytomegalovirus Antigen

Family : Herpesviridae
Size
: 180 - 200 nm
Family
Size

: Virus Herpes
Simpleks-2
: Herpesviridae
: 180 - 200 nm

TORCH infection have

a few resemblance:
- infected pregnant woman usually asymptomatic
- infection to the fetus gives a various effect:
* no infection
* mild to heavy infection or death of the fetus
* the baby born with symptoms: brain, lungs, eyes, or
ear damage

Who can be infected by

TORCH ?
Every one can be infected by
TORCH

What is TORCH examination?

Examination to know or to diagnose

TORCH infection

TOXOPLASMOSIS

 Toxoplasma gondii cause congenital infection

in 1/10.000 until 80/10.000 pregnancy
Congenital toxoplasmosis infection correlate
with primary infection of the mother during
pregnancy
Transmission of mother to fetus more common
in pregnant women who was infected at the end
of gestation

 Infection in early gestation make more heavy

defect
Overall, 30-40% of infected pregnant women
result congenital infection of neonates

Source of Toxoplasmosis
infection

Cats feces (contain oocyst)

Infected meat (contain cyst)

Infected pregnant woman

Infected Donors Organ/ Blood

3 shape of Toxoplasmosis gondii:

Trophoozoit

cyst

Oocyst

How is the transmission of

Toxoplasmosis ?
Food : vegetable and fruit that polluted by
cats feces (source of oocyst)
Fresh and uncooked meat (contain cyst)
Mucous contaminated (mouth & eye)
vertically from mother to child
Blood transfusion
Organ transplantation

Is Toxoplasmosis infection
harmful ?
If infected adult or
children have good immunity,
Usually is not harmful

The Positivity of Toxoplasma IgG and IgM in Women

Area

% (+)
IgG (+)

IgM (+)

Jakarta

50,1

4,9

West Java

68,3

8,6

East Java

43,2

4,9

Central java

57,9

6,1

Bali

39,8

1,0

West Nusa Tg

53,8

3,8

Sumut + Aceh

48,5

4,4

Riau

55,9

1,1

North Sulawesi

46,3

2,1

South Sulawesi

44,6

2,3

S. Kalimantan

48,6

53,0

5,4

Total

Source : Prodia, Jan-August, 2001

Toxoplasma
Toxoplasma gondii
gondii
Mother
Primary infection

Infant
40%

Congenital infection
eye, brain

Asymptomatic

90% Asymptomatic at birth

at 18 years

??
With antibodies

Mental retardation
Visual affection

Protected

20%
45%

44%
71%

Congenital toxoplasmosis
Ultrasonographic Findings
Calcification
Intrahepatic
Intracranial

Splenomegaly
Hydrocephalus
Classical triad: hydrocephalus, intracranial
calcification and chorioretinitis

Toxoplasmosis

Liver calcification

Cerebral calcification

Hydrocephalus

Recommendation of maternal treatment

Infected mother:

Treat placental infection

Minimum 3 weeks with
Spiramycin 9 MIU/day or
Azithromycin 0.5 g 3 days /week

Treat fetal infection

until birth
Spiramycin (alternating with P/S/ F)
Fansidar 2 tablets once per week untill birth
Not necessary to follow maternal serology

Criteria for congenital infected infant

IgG at birth reflects the mother
Follow-up needed.
IgG positive at 1 year of age: infected infant
IgM positive in 55%
dependent on gestational age at infection
and maternal treatment
Parasites / antigen identified in amniotic fluid,
placenta. cordblood

No treatment
Mothers infected before pregnancy

need no treatment

Future Recommendation for Indonesia

Frequency of Toxoplasma infection varies

from area to area.
In most places so high that serological testing is
justified
Any testing has to be combined with
correct treatment and
follow-up of the children to 1 year of age.

Remember: IgM neg infants may be infected

Serological Monitoring of Toxoplasmosis in Pregnant Women

Sample 1

IgG + / IgM immune

patient

IgG + / IgM +

IgG - / IgM -

- recent primary infection ?

- old infection with residual IgM ?
Ask the laboratory to
continue with IgG Avidity

Non Immune patient *

Patient Education and Serologic Follow up
continued untill the end of pregnancy

IgG Avidity
High Avidity

Low Avidity

Infection acquired > 4

months ago

Infection most likely

acquired <4mos ago

If the tests is taken in

2nd half of pregnancy,
look on the titer of IgG

IgG - / IgM -

IgG + / IgM +

IgG - / IgM + **

Non immune
patient *
Follow up
until the end of
pregnancy

Low IgG

High IgG

Old
infection

Probable
Recent
infection

Recent
Primary
infection

confirmatory tests needed

3 weeks later (IgG, IgM)
- Prenatal Diagnosis

- Maternal Treatment

- Follow up the Mother and Newborn

Additional Guidelines :
First sample should be collected early in pregnancy and preferably tested with both IgG & IgM
* if IgG-/IgM- : non immune patient, education and serologic follow up (every trimester; in high risk areas every 6-8 weeks)
** If IgM + without IgG, it may be the beginning of infection, retest 2-3 weeks later, if the result unchanged : unspecific IgM
Babill Stray-Pedersen

Dangerous! for.
Fetus, if pregnant woman is being primarily
infected (the 1st infection for the life time) or
The person with bad immune system
(AIDS, cancer, person who undergo organ
transplantation)

What happen to the baby

if mother infected when she was
Pregnant?
Can be:
spontaneous abortion
still birth
Hydrocephalus, eye disorder,
ear (listening disorder),
brain calcification, convulsion

If the mother infected,

will the fetus be infected too?
Not always. As pregnancy getting older
when the mother primarily infected,
The more possibility the fetus get infected

What is the effect for the fetus ?

More young gestational age when the

mother primarily infected,
more bad effect will appear.

What is the symptom of this

infection ?

Commonly asymptomatic, the symptom

is usually unspecific (flu like)

So the doctor or the patients usually
didnt recognize it.

Clinical diagnosis hard

to be diagnosed

Is there any other way to diagnose

This infection ?
Yes, the diagnosis of this infection
Depends on laboratory examination

What are the laboratory exam.?

Protozoa parasite Identification

(tissue culture, inoculation on mice,

DNA-PCR detection).
These exam. are complicated, and
need a lot of time and expensive
Toxoplasmosis antibody exam:

IgM, IgG, IgA and IgG Avidity

What are IgM, IgG, IgA and

IgG Avidity ?

IgM, IgG and IgA are

Immunoglobulin that will rise
If these is an infection

IgG Avidity is binding strength of

IgG antibody and antigen

Purpose of IgG Avidity exam.

To predict the time of infection

In assumption of primer infection

(IgG (+) and IgM (+)) on the same serum,
If there is hesitation :
IgM (-), and IgG stabile or
IgM (-) and IgG rise significantly
High level : prediction of infection

> 4 months before exam.

Low level : prediction of infection
< 4 months before exam.

Toxoplasma-antibodies in pregnant women

12%
14 %

12%
45-55%

USA 15-40 %

73 %

31%
Japan 7%

60 %
60 %

45-70%

9%

50%
40-60%

Indonesia 53 %
35%

45%

Incidence of primary infection in pregnancy: 0.1 - 1 per 100

How we interpret ?
IgG (+) and IgM (-)

Have been infected before (long time

infection) and now is Immune.
The mother didnt need to be examined again
except high level of IgG (+)
There is possibility that doctor will ask for
IgG Avidity exam.
Or if there is other consideration doctor will ask
for this exam. 1 more time (3 weeks later)
to eliminate the presence of primary infection

How we interpret ?
IgG (+) and IgM (+)
Possibility of new primary infection
or long time infection but IgM
is still detected (slowly disappear) = persistent.
Need IgG Avidity examination
directly on the same serum
to predict the time of infection, before
or after pregnancy.

Infection that occur before pregnancy

Didnt need attention, only primary
Infection when the mother pregnant
Is harmful, especially on 1st TM
we need to know
When the examination done
In pregnancy

How we interpret ?
IgG (-) and IgM (-)
Never been infected. If the woman are
Pregnant, we need to exam. on the next
trimester, until the 3rd trimester,
If the result remain negative

How we interpret ?
IgG (-) and IgM (+)
This case is rare. May be
A beginning of infection. Must be
examined again 3 weeks later
is the IgG become positive/not?.
If not, means non specific IgM,
means that the mother is not infected

Primary infection diagnosis

Conversion of IgG from negative

to positive or significant rising IgG titer
(> 2 x) on serial examination
after 3 weeks

IgM positive and/or IgA positive

Low level of IgG Avidity

Congenital infection diagnosis

IgM positive and/or IgA positive

Persisting positive IgG on

The first year after born
(serial examination)

Interpretation of serologic examination

of Congenital Toxoplasmosis
''Cord Blood'

Interpretation of congenital
Toxoplasmosis Serologic
IgM from mother Serum vs. Neonates

Who needs
Toxoplasmosis exam.?
The woman that will pregnant (ideal)
Pregnant woman
(if the previous exam negative or unknown,
minimally checked every TM
The new born baby whose mother infected
When she was pregnant
Suspected patients

Is Toxoplasmosis infection
Can be cured ?
Therapy is not 100% cure
but can prevent more damage.
So we need an immediate therapy
after diagnosed.
If the baby infected, give therapy
until 1 year old.

TOKSOPLASMOSIS Therapy
Sulfonamida
Pyrimethamine
Administration: Adult dose of pyrimethamine: 50-75
mg/oral 1x/day, Combine with sulfonamida 1 - 4 gr for
1-3 weeks => and reduce half of doses of each drugs for
4-5 weeks.
Side effect: damage of blood cell if given in high doses.
Lack of folic acid stimulate agranulositosis. Urtikaria
can appear in therapy

 Spiramycin (Rovamycine)
The most active makrolide antibiotic to Toxoplasmosis
as Bakterioside
Concentration in placenta is very high (6.2 mg/L), so can
prevent maternal infection infiltrate to the fetus.
Safe for fetus
Well tolerated for pregnant woman
Spiramycin dose for congenital Toxoplasmosis infection:
3 x1gr/day, for 3 weeks and repeated after an interval of 2
weeks until labor.

 Spiramycin doses for congenital toxoplasmosis

prophylaxis: 3x daily 3 MIU or 3x1 gr for 3
weeks than repeat after 2 weeks interval until
labor
Remington:
Acute toxoplasmosis in pregnant women:
Spiramycin 3gr/day for 3 weeks, 2 weeks interval
until labor
Pregnancy 24 weeks: sulfadiazin 50-100 mg/kg +
pyrimethamine 0,5-1 mg/kg/day every 2-4 days
until labor

RUBELLA

Rubella
1941 associated with congenital disease (Gregg)
Today vaccination in developed countries.
Very rare to see cong rubella

In developing countries Without vaccination 70 - 80% of women are

already infected by childbearing age.

Yes: 110 countries: 57%

No
52 countries 43%

Epidemiology
Epidemics every 5 - 7 years
Risk of infection.
During epidemics:
very high of nonimmune women
Epidemic:
Nonepidemic:

Infection risk : 1 % in 3 months

Infection risk : 0.1 % in 3 months

Rubella infection in Indonesia 1996

T Rachimhadhi 1997

Center

No

Jakarta
Bandung
Semarang
Yogya
Surabaya
Denpasar

Total

73
102
100
92
101
100

568

IgG

IgM

% pos

% pos

67.1
77.5
78.0
79.3
77.2
78.0

76.6

1.4
0
0
0
0.9
3.0

0. 9

Source of infection
Nasopharyngeal infection
Infected pregnant woman

How is the transmission ?

Through airway
Through placenta, from mother to fetus

Rubella
Mother

Child

Before conception
Onset of rash < 11 d. after LMP

Maternal reinfection I trim

Maternal vaccination

Prevention
vaccination

No risk

8%

Theoretical risk
never proven

Rubella
Mother
First trimester

Child
20%

Miscarriage

Congenital defects
Symptomatic
Asymptomatic

90 %
90 %

Ear affection
Heart /eye defects

13-16 weeks
17-20 weeks

17 %
6%

> 20 weeks

No

Retinopathy
Learning defect
Late sequelae >17yrs

After first trimester

Diabetes, encephalitis

Congenital Rubella Syndrome

Incidence of Fetal Infection
In 1st trimester occurred in 81% at 0-12
weeks
based on LMP
In 2nd trimester decresed from 67% at
13-14
weeks to 25% at 23-26 weeks
In 3rd trimester 35% at 27-30 weeks
60% at 31-36 weeks
100% in 8 infants
exposed > 36
weeks

 The term Congenital Rubella Syndrome (CRS) is used

to denote any combination of the findings known to result
from gestasional rubella
Birth defects almost exclusively result from infection in
the first 16 weeks of gestation
The main defects :
Deafness
Eye defects (cataracts),
Cardiovascular defects (Patent Ductus Arteriosus)
CNS damage leading to mental retardation

Congenital rubella syndrome

1. Developmental defects

( permanent damage)

Deafness,
Ocular defects:
cataract, glaucoma, microphthalmia
Cardiac abnormalities: septal defects, pulm stenosis
CNS defects:
mental retardation, microcephaly

2. On going viral infection at birth

(not permanent damage)

Low birthweight, trombocytopenia,

hepato-splenomegaly,

3. Delayed defects
Insulin dependent diabetes, thyroid disorder, mental retardation

Pathogenesis of Fetal defects

Many of defects are at the interface of malformations and
disruptions
Placental involvement
During the period of maternal viremia, the placental
may become infected damaged endothelial cells
the virus entered the fetal circulation by embolic
transport

 Heart Defects
Once the virus has entered the early embryo, a
chronic nonlytic infection is established the
virus can infect virtually any organ
Cardiac malformations occur after infection at any
time in the first 12 weeks of gestation but rare
after this time

 Eye Defects
Lenses from 1st trimester rubella-infected
abortuses showed pyknotic nuclei, cytoplasmic
vacuoles, and inclusion bodies in the primary lens
cells and retardation of lens development
For the cataract formation the virus reach the
lens from the amniotic fluid gain access to the
lens as long as the invagination and detachment
of the lens vesicle from the surface ectoderm was
incomplete

 Deafness
Sensorineural deafness is the most common
defect and mainly result when infection occurs in
the first 16 weeks gestation
It can progress after birth
It is caused by direct viral damage of the
epithelium of the cochlear duct or to the stria
vascularis causing changes of the endolymph
and structure of cochlear duct

Congenital rubella

Outcome of Congenital Rubella syndrome

1/3 will lead normal independent lives

1/3 will live with parents
1/3 will be institutionalised
The only effective way to prevent cong.rubella
is to
- detect infection in I trimester
- terminate pregnancy

The effects to fetus :

Fetal death abortion
Still birth
Heart, eye, and hearing disorder,

with/without mental retardation and

microcephaly

What are the symptoms ?

Usually mild fever, headache,

Fatigue and feeling not well,
Sore throat, cough

30-50% asymptomatic

Rash 16 to 18 days after exposed

In adult, usually accompanied by pain

on joints

Laboratory exam.
Viral isolation on tissue culture
(urine, Nasopharyngeal secretion)
RNA detection (PCR)
Antibody detection serologic exam.)
: IgM, IgG, IgA of
Rubella and IgG avidity

Immune response
IgM
Appear 2 -3 days after rash
Peak level after 1 to 4 weeks
can be detected on the 3rd to 8th week
remain until 6 - 12 month

Immune response
IgG
Detected 5 to 10 days after the rash
(can appear earlier)
Peak level after 15 to 30 days
Slowly decreases until a few years
until a low level and constant

Prevention
Antenatal screening / postpartum vaccination
All pregnant women should be tested for
rubella immune status IgG
Non-immune women
Should be offered rubella vaccination
in the immediate post partum period.

Recommendation of today :
Serologic testing for antibodies of women of
childbearing age
Vaccination of nonimmune( seronegative) women
Young women caring for children:
teachers, health care providers etc

Infertility patients
(part of routine examination)

Pre pregnancy counseling

Vaccination by accident in first trimester:

No indication for medical termination

Serological Monitoring of Rubella in Pregnant Women

Prenatal Screening (first half of Pregnancy)
Determination of IgG

IgG +

IgG -

Immune Patient

Non Immune patient

second sample should
be collected at 17-20 th
week of pregnancy
IgG +

IgG -

Seroconversion

Not infected

IgM detection
IgM - (?)

IgM +

Testing should
be repeated

recent primary
infection

Primary infection is harmful to the fetus before 17 th week of pregnancy

Abortion is today only option
Babill Stray-Pedersen

Is immunity after vaccination can

Remain for a lifetime ?
Adult

: remain > 8 years (if the titer is

high)
children : 25% will lose the antibody after
5 years
So need to be reexamined
IgG Rubella when the woman have a plan to
pregnant (3 to 6 months before)

Who need to be examined ?

The woman before pregnant (ideally)
In early gestation on 20 weeks

gestation (for the seronegative

woman)
Neonates whose mother primarily
infected when she was pregnant
Suspected patient
After vaccination

CMV

CMV
Population Survey CMV may be found in
40-100% of people, depending on
socioeconomic conditions
In developing countries infection earlier
in life
50% young adults are
seronegative

Mother

CMV

Primary infection

40-50%

Recurrent infection

1-2%

asymptomatic
1

Seropositivity:
20 -100%

Infant
Viral excretion 0,5-2%

10%

Congenital disease < 0,2%

10% Symptomatic 90% sequelae
90% Asympt
15% sequelae

cervix
urine
breastmilk

Prevention
Hygienic measures
Prenatal screening ?

Brain / ear / eye

35%

Ganciclovir

10%

10%

Congenital CMV infection

Clinical symtoms:
Ptechie (71%)
Icteric (67%)
Microcephaly (53%)
Small for gestational age (50%)
Most deafness in children caused by
CMV infection

Congenital CMV infection

Abnormal laboratory result:
Hyperbilirubinemia (81%)
Elevated transaminase (83%)
Trombositopenia (77%)
Elevation of CSF protein level (77%)

Source of infection

Saliva
Urine
Cervix/Vagina secretion
Sperm
Breast milk
Infected blood/donors organ
Infected pregnant woman

The way of transmission

Respiratory droplets
contact with source of infection (saliva,
urine, cervix and vaginal secretion,
sperm, breast milk, tears)
Transfusion & organ transplantation
Vertically from mother to fetus:
* prenatal (placenta)
* perinatal (in labor)
* postnatal (breast milk, direct contact)

The risk of transmission from

Mother to fetus
If the mother primarily infected,
in pregnancy, transmission to fetus is
40%
If the mother secondary infected
(have been infected before pregnancy),
So the risk of transmission to fetus 1 to 2%

Prevalence of CMV infection

Newborn:

1 - 2%

--------->

1 year: 15- 40%

Women working small children: annual acquisition rate 8- 20%

General population:

annual acquisition rate 3- 5%

Pregnant population
Europe

Other

England:

25%

Canada

44%

Denmark

52%

USA

50-80%

Norway

70%

Chile

98%

Finland

85%

Africa

98-100%

Russian

70%

Asia

98-100%

Congenital infection : 0.5 - 2 %

Identification of Primary CMV in pregnancy

Mother
Serologic testing
CMV - IgG pos.
Iow IgG avidity
CMV - IgM pos.
or seroconverter

Fetus Amniocentesis
Viral / antigen detection CMV - PCR
Viral load : Severe infection

Ultrasound
Newborn
CMV-IgM pos
Virus / PCR pos in body fluids (urin)
CMV IgG pos at 1 year

CMV: Ultrasonographic Findings

Best diagnostic clue:
Calcification
Intracranial
Hepatic
Hepato spleno megaly
Amniotic fluid volume disorder

CMV
Calcifications

Liver

Brain

CMV
Ascites and Echogenic bowel

Ascites

23 gest week

37 gest week

CMV- amniocentesis
At least 6-7 weeks after
maternal infection
Mat.viremia: 2-3 weeks post infection
Fetal infection 4-6 weeks later

After 21-23 gest week

Fetal diuresis >21 week

Lisnard et al, Obst Gynecol 2000,95,881

Gouarin et al, J Clin Micr 2002 ,1767

CMV Recommendation
App 90 % IgG positivity
10% of pregnant women can acquire the
primary infection in this high risk area.
Testing of pregnant women working with
children may be justified
Give hygienic advise

CMV Treatment
Medical Care
Ganciclovir treatment
The drug of choice for CMV disease
Nucleoside analogue that inhibits DNA synthesis
in the same manner as acyclovir
The length of treatment is variable and depends
on the disease and the host
Induction dose: 5mg/ kg twice daily.
Later, the dose is decreased from twice daily to
once daily and continued as maintenance therapy

 Ganciclovir treatment
Also been used to treat CNS disease, including
encephalitis and neuropathy
For pregnancy C
Safety for use during pregnancy has not been
established

Prognosis
Symptomatic neonates
Mortality rate up to 30%
70- 90% have some neurologic impairment,
including hearing loss, mental retardation, and
visual disturbances
Asymptomatic neonates
10% develop neurologic sequele

Prevention
Nonimmune pregnant women should attempt to limit
exposure to the virus
Pregnant women should always wash hands after
exposure to urine and respiratory secretions from
children
Development of a vaccine against CMV is under
investigation

The 5th children disease

Butterfly rash in children
Mild febrile illness
Upper respiratory symptoms

Adults
Often asymptomatic
macupapular rash
Polyarthritis
Main reservoir: School aged
children

Fatal foetal hydrops due to B19

Parvo virus. The fulminant ascites is typical

Parvovirus

What is the symptoms ?

90 % primary infection on
Immunocompetent adult and children are
asymptomatic

Laboratory examination
Direct

Histopathology
Tissue culture
PCR

Indirect

Serologic exam.
IgM, IgG and
IgG Avidity

When and who need to be

examined ?

Blood / tissue donor

Transplanted tissue recipient
Woman, before pregnant (ideal),
If negative, exam. on early pregnancy,
And on late pregnancy
Neonates of infected mother

HSV

Herpes Simplex Virus (HSV)

Both HSV types, HSV-1 dan HSV-2 can cause
oral and genital infection
HSV-1 cause gingivostomatitis,
herpes labialis, and herpes keratitis
HSV-2 cause genital lesion
After initial infectio HSV dormant in
ganglia nerve and can cause periodic
symptoms

 Recurrent herpes eruption precipitated by

Excessive exposure to the light

Disease accompanying with fever
Physic and physical stress
Immunosuppresion
Unknown stimulation

Recurrent erruption usually not too sever, and

didnt usuallny appear

Neonatal and Congenital

HSV
Type of Infection

Timing of
acquisition

Mode of acquisition

Congenital

In Utero
( antepartum)

Transplasental

Neonatal

At or near birth
(intrapartum)

Genital exposure

Neonatal

Postnatal

Nosocomial (staff or
family direct skin
contact)

Epidemiology
The incidence of Genital HSV infection rise in
developing county
From the study in Canada, seropositive HSV-2
in pregnant women about 17 %
Canada Neonatal HSV 1 : 17.000
newborn
US Neonatal HSV 1 : 3500 newborn

Clinical Manifestation
Manifestation of congenital and neonates HSV
classified into 3 levels:
1. Infection of skin, eye, and mouth (38% can cause
neurological sequale)
2. Central nervous system disorder ( ensephalitis with
or without infection of skin, eye, and mouth)
3. Systemic spreading (in serious infection, mortality
rate can reach 90% if didnt get therapy)

HSV in pregnancy
Primary infection in 1st and 2nd trimester
infection increase the risk of abortion,
premature, and small for gestational age
Primary infection in the 3rd trimester Ig G
hasnt completely developed fetus didnt get
protection 30-50% risk of neonates herpes
infection

Source of infection

Saliva
Vesicle liquid
Infected pregnant woman

HSV transmission

contact with lesion

Indirect contact
Vertically from mother to fetus
* Prenatal (placental rare
1 : 200.000 pregnancy)
* Perinatal
* Postnatal

What are the symptoms ?

Primary infection
Fever, headache, malaise, neuralgia
broad lesion
lymphadenopaty
asymptomatic (8%)
Recurrent infection
The symptoms are milder and healing time
is shorter

Laboratory Diagnosis
Tissue culture
Serology examination IgG and IgM
(HSV-1 and HSV-2)

Who and when, we need

to exam.?

Suspected patient
Woman before pregnant
If (-), examine in early pregnancy
* If (-), examine her couple
* If (-), her couple (+) with previous
Herpes Genital, examined his wife
toward the end of pregnancy
Infected mothers neonates

Prevention strategy
Dont
do
sexual
intercourse
during
*
Active lesions are present
Better use condom

*
*

Born by Caesarean section,

If there are lesions
(prevent mother to fetus transmission)

Thank you
&
Success
forever