Professional Documents
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TORCH in Pregnancy
TORCH in Pregnancy
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
: Virus Herpes
Simpleks-2
: Herpesviridae
: 180 - 200 nm
TOXOPLASMOSIS
Source of Toxoplasmosis
infection
Trophoozoit
cyst
Oocyst
Is Toxoplasmosis infection
harmful ?
If infected adult or
children have good immunity,
Usually is not harmful
% (+)
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
Toxoplasma
Toxoplasma gondii
gondii
Mother
Primary infection
Infant
40%
Congenital infection
eye, brain
Asymptomatic
??
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
No treatment
Mothers infected before pregnancy
need no treatment
IgG + / IgM +
IgG - / IgM -
IgG Avidity
High Avidity
Low Avidity
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
- Maternal Treatment
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)
to be diagnosed
12%
45-55%
USA 15-40 %
73 %
31%
Japan 7%
60 %
60 %
45-70%
9%
50%
40-60%
Indonesia 53 %
35%
45%
How we interpret ?
IgG (+) and IgM (-)
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.
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
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.
RUBELLA
Rubella
1941 associated with congenital disease (Gregg)
Today vaccination in developed countries.
Very rare to see cong rubella
Epidemiology
Epidemics every 5 - 7 years
Risk of infection.
During epidemics:
very high of nonimmune women
Epidemic:
Nonepidemic:
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
Rubella
Mother
Child
Before conception
Onset of rash < 11 d. after LMP
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
Diabetes, encephalitis
( permanent damage)
Deafness,
Ocular defects:
cataract, glaucoma, microphthalmia
Cardiac abnormalities: septal defects, pulm stenosis
CNS defects:
mental retardation, microcephaly
3. Delayed defects
Insulin dependent diabetes, thyroid disorder, mental retardation
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
30-50% asymptomatic
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)
IgG +
IgG -
Immune Patient
IgG -
Seroconversion
Not infected
IgM detection
IgM - (?)
IgM +
Testing should
be repeated
recent primary
infection
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%
cervix
urine
breastmilk
Prevention
Hygienic measures
Prenatal screening ?
Ganciclovir
10%
10%
Source of infection
Saliva
Urine
Cervix/Vagina secretion
Sperm
Breast milk
Infected blood/donors organ
Infected pregnant woman
1 - 2%
--------->
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%
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
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
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
Adults
Often asymptomatic
macupapular rash
Polyarthritis
Main reservoir: School aged
children
Parvovirus
Laboratory examination
Direct
Histopathology
Tissue culture
PCR
Indirect
Serologic exam.
IgM, IgG and
IgG Avidity
HSV
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
Laboratory Diagnosis
Tissue culture
Serology examination IgG and IgM
(HSV-1 and HSV-2)
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
*
*
Thank you
&
Success
forever