Toxoplasmosis in pregnancy dr. Wulan M. Soemardji, SpOG

TOXOPLASMOSIS • Parasitic infection • Caused by protozoa: Toxoplasma Gondii Toxoplasma Gondii exists oin three forms: 1. Trophozoite 2. Tissue cysts 3. Oocysts

FREQUENCY OF TOXOPLASMA ANTIBODY IN WOMEN IN INDO 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 infectiousfor 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, cervicallymphadenopathy and atypical lymphocytosis • Placental and fetal infection occur during thespreading phase of the parasitemia • Fetal infection 30-40%, increase with gestational age

FETAL INFECTION • During 1st trim, the rate of transmission is approximately 15%, the rate of 2nd trim is approximately 30 % and 3rd trim is 60 % • Fetal morbidity and mortality rate are higher afterearly transmission • Infected neonates often have evidence of disease: LBW. Hepatosplenomegaly, icterus,anemia, hydrocephalus, intracranial calcification • Sequelae vision loss, psychomotor and mentalretardation, hearing loss and chorioretinitis

MOTHER INFANT 1st trimester 15% miscarriage severe disease 2nd trimester 40% severe+ subclinical 3rd trimester 80% subclinical infection  mental retardation 20% visual affection 45%

Primary infection 40% congenital infc asymptomatic (eye, brain) MOTHER INFANT Primary infection 40% congenital infc asymptomatic (eye, brain) 90% asymp at birth at 18 years with antibodies protected Mental retardation 20% Visual affection 45%

PREVENTION • Primary prevention: information about the way of infection (cat, raw meet) to avoid ingestion, inhalation, important for all pregnant women are”seronegative” • 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 • 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

Diagnosis on primary infection Seroconversion Significant rice of IgG titer & IgM positive High titer of IgG & IgM positive, Low IgG avidity

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 and IgM are measured

Before happened an infection IgG -, IgM – • When an infection happens, IgG +, IgM + • IgM + during acute infection and stay + in limitedtime 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

The problem of interpretation High titer of IgG may persist for several years Not all primary infections give a high IgG titer IgM may persist fir more than 6 months (sometimes even for years)

Management of primary Toxoplasma infection in pregnancy 1st trimester 2nd trimester 24weeks 3rd trimester 38weeks Serologic screening repeated testing repeated testing IgM + seroconverter amniocentesis IgG avidity low  toxo PCR, USG treatment until birth examination of baby at birth : serologic/parasitologic treatment and follow up until 1 year of life

Recommendation of maternal treatment Infected mother : Treat placental infection Minimum 3 weeks with Spiramycin 9 MIU/day Treat fetal infection Until birth Spiramycin Not necessary to follow maternal serology

European multicenter study Complication in 144 infants born to seroconverting mothers related to treatment in pregnancy in pregnancy no treatment treatment total no of mother 25 119 Cong. Infected infants 7 (28%) 12 (10%) p=0.03 with sequelae Cong. Infected infants 5 (20%) 4 (3%) p<0.01 with severe sequelae at 1 year of age

PRINSIP ULTRASONOGRAFI

CHORDOCYNTHESIS

AMNIOSENTESIS