TOXOPLASMOSIS IN

PREGNANCY
HM Sulchan Sofoewan
Departement of Obstetrics and
Gynecology Faculty of Medicine
Gadjah Mada University
TOXOPLASMOSIS
Parasitic infection
Caused by protozoa: Toxoplasma Gondii
Toxoplasma Gondii exists oin three forms:
1. Trophozoite/Tachyzoite
2. Tissue cysts/Bradyzoite
3. Oocysts/Sporozoite



FREQUENCY OF TOXOPLASMA
ANTIBODY IN WOMEN IN IND
Year No IgG % pos IgM % pos

1996 568 52,3 12,9
2000 3236 51,3 5,2
2001 8565 53,0 5,4
TOXOPLASMA GONDII
Trophozoite:
Requires in intracellular habitat to survive
and multiply
Reproduction is endogenous
During the acute phase, it invades every
type of cell
After invasion the organisms multiply until
cell cytoplasm is so filled that the cell is
disrupted
TOXOPLASMA GONDII
Tissue cysts:
Formed within the host cells as early as
eight day of an acute infection
Probably persist throughout the life of the
host
Skeleton, heart muscle and brain are the
most common sites for latent infections

TOXOPLASMA GONDII
Oocyst:
Produced in the small intestine of the cat
One shed, the oocyte sporulates in 1 to 5 days
and become infectious
Under appropriate condition it remain infectious
for more than 1 year
The parasite transmitted by direct handling of
contaminated soil and cat feces
All form of parasite are destroyed by adequate
freezing and heating
MATERNAL INFECTION
Transmission of toxoplasma to human occurs
through the ingestion of under-cooked meat
Through other foods contaminated with oocyte,
or by transfusion of whole blood.
Syndrome including: fatigue, malaise, cervical
lymphadenopathy and atypical lymphocytosis
Placental and fetal infection occur during the
spreading phase of the parasitemia
Fetal infection 30-40%, increase with gestational
age
FETAL INFECTION
During 1
st
trim, the rate of transmission is
approximately 15%, the rate of 2
nd
trim is
approximately 30 % and 3
rd
trim is 60 %
Fetal morbidity and mortality rate are higher
after early transmission
Infected neonates often have evidence of
disease: LBW. Hepatosplenomegaly, icterus,
anemia, hydrocephalus, intracranial calcification
Sequelae vision loss, psychomotor and mental
retardation, hearing loss and chorioretinitis
PREVENTION
Primary prevention: information about the
way of infection (cat, raw meet) to avoid
ingestion, inhalation, important for all
pregnant women areseronegative
Secondary prevention: detection of
infected women during pregnancy to start
treatment before fetus gets infected
Tertiary prevention: treatment of infected
children to reduced/avoid symptom
HYGIENIC AND DIETITIC
EDUCATION
There is no vaccine for toxoplasmosis, but many
cases of congenital infection could be prevented
Avoid eating raw or uncooked meat
Wash salads, vegetables, fruits and berries
Have good kitchen hygiene
Avoid contact with cat feces (kittens)
Wash hands after contact with sand and soil
Use gloves when gardening
DIAGNOSIS OF CONGENITAL
TOXOPLASMOSIS
Search for the parasite: seldomly used
Serological test: measure antibodies
Detection of the symptoms:
- prenatal ultrasound
- cranial ultrasound
Amniocentesis: to look for DNA of parasite
by PCR-technique
SEROLOGICAL TEST
Being infected leads to some weeks of
parasitemia, can be passed on to the fetus
The body starts to produced antibodies
They fight againt the parasite, control the
disease, no more parasite circle in blood
Some group of Ig: IgG, IgM, IgA, IgE
For diagnosis of toxoplasmosis usually IgG
dan IgM are measured

Continue
Before happened an infection IgG -, IgM
When an infection happens, IgG +, IgM +
IgM + during acute infection and stay + in limited
time 6 months 1 year
IgG rise during acute infection, sink slowly
again, but stay +, protect against another
parasitemia, protect to the fetus
If stable IgG and no IgM: infection long ago,
protection, latent infection
Early pregnancy and + testing later
seroconversion acute infection
If IgG+ IgM +,infection happened short time ago
SEROLOGICAL TEST
Interpretation of toxoplasmosis serology
results:
IgM IgG Interpratation
+ - Possible acute infection, IgG
titers reassed in several weeks
+ + Possible acute infection
- + Remote infection
- - Susceptible, uninfected
Continue
When fetal infection is diagnosed by
prenatal testing, pyrimethamine,
sulfonamides and folinic acid are added to
spiramycine to eradicate parasites in the
placenta and fetus.
DIAGNOSTIK PRENATAL
Menyadari besarnya dampak toksoplasmosis
kongenital pada janin, bayi serta anak disertai
kebutuhan konfirmasi infeksi janin prenatal pada
ibu hamil, maka para obstetrikus
memperkenalkan metode baru yang merupakan
koreksi atas konsep dasar pengobatan
toksoplasmosis kongenital yg lampau.
Konsep lama hanya bersifat empiris dan
berpedoman pada hasil uji serologis ibu hamil.
Lanjutan
Saat ini pemanfaatan tindakan kordosentesis
dan amniosentisis dengan panduan
ultrasonografi guna memperoleh darah janin
atau cairan ketuban sebagai pendekatan
diagnostik merupakan ciri para obstetrikus pada
dekade 90-an.
Selanjutnya segera dilakukan pemeriksaan
spesifik dan rumit yang sifatnya biomolekuler
atas komponen janin tsb (darah atau air
ketuban) dalam waktu relatif singkat dengan
ketepatan yg tinggi.

Lanjutan
Bahkan diagnostik prenatal dipandang
lebih efektif utk menghindari atau
menekan risiko toksoplasmosis kongenital
karena upaya prevensi primer pada ibu
hamil berupa nasihat menghindari
makanan/minuman yg kurang dimasak
kurang berhasil. Sehingga upaya
diagnostik prenatal disebut sebagai
prevensi sekunder.
AKTIVITAS DIAGNOSIS
PRENATAL
Diagnosos prenatal umumnya dilakukan
pada usia kehamilan 14-27 minggu,
aktivitasnya sbb:
1. Kordosentesis dan amniosentesis
2. Pembiakan darah janin dan air ketuban,
atau inokulasi kedlam ruang peritoneum
tikus, diikuti isolasi parasit.
3. Pemeriksaan PCR utk mengidentifikasi
DNA T.Gondii.

Lanjutan
4. Pemeriksaan dgn tehnik ELISA pada darah
janin guna mendeteksi antibodi IgM dan IgA
janin spesifik (anti toksoplasma).
5. Pemeriksaan tambahan berupa menetapkan
kadar enzim liver, platelet, leukosit (monosit dan
eosinofil) dan limfosit khususnya rasio CD4 dan
CD8
Diagnosis toksoplasmosis kongenital ditegakkan
berdasar hasil pemeriksaan adanya IgM dan IgA
dari darah janin, ditemukan parasit pada kultur
atau inokulasi dan DNA dari T.Gondii pd PCR
darah janin atau air ketuban.
AGAR HASILNYA TERPERCAYA
1. Didahului oleh skrining serologik maternal,
terjadi serokonversi.
2. Ketrampilan klinis melakukan kordosentesis /
amniosentesis
3. Ketrampilan melakukan kultur dan inokulasi,
ELISA dan PCR
4. Diagnosis prenatal berdasar amniosentesis
juga untuk diagnosis infeksi janin kongenital
paling sering digunakan utk Dx infeksi janin
kengenital.
Lanjutan
Amniosentesis dapat dikerjakan sejak
umur kehamilan 14 minggu, kordosentisis
setelah umur kehamilan 20 minggu.
Amniosentesis kurang berbahaya
dibanding kordosentesis karena kurang
invasive.
PCR dg air ketuban sensitifitas 97,4% dan
spesifisitas 100%.
Lanjutan
PCR air ket tunggal sensitifitas 81%, spesifisitas
96%.
Bila inokulasi mencit dikombinasi dg air ket dgn
PCR, sensitifitas 91%.
Untuk pemeriksaan IgM dan IgA spesifik darah
janin sensitifitas berturut-turut 47% dan 38%
Sensitifitas dan spesifisitas IgM spesifik dalam
cairan ketuban adalah 73,3% dan 100%.
Adapun IgM spesifik dlm air ket adalah produksi
janin terinfeksi, karena IgM ibu tidak dapat
melewati barier plasenta.
Lanjutan
Pemeriksaan USG hendaknya dilakukan
dalam diagnosis prenatal untuk mengukur
rasio ventrikel-hemisphere, deteksi
kalsifikasi intrakranial dan adanya asites,
Pemeriksaan USG dianjurkan tiap 3 bulan
sekali sejak diagnosis prenatal.



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