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Toxoplasmosis in pregnancy. Introduction . A zoonoziz , caused by T.gondii , an intracellular protozoan parasite Its more common in tropical & coastal regions is less common in regions that are either cold ,warm or at high elevation 1 of every 900 pregnancies in the USA. Transmission.
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Introduction • A zoonoziz , caused by T.gondii , an intracellular protozoan parasite • Its more common in tropical & coastal regions • is less common in regions that are either cold ,warm or at high elevation • 1 of every 900 pregnancies in the USA
Transmission • Cats • host for T. gondii • They acquire infection by eating infected wild rodents and birds • A week after infection, the cat begins to shed oocystsin its feces • Shedding of the oocysts persists for about 2 weeks • within days to weeks these oocystssporulate and become extremely infectious
Transmission • Food • ingestion of contaminated food is an important cause of toxoplasmosis • Meat is the most common infected food • unpasteurized milk and unfiltered water sources also are at risk • Organ transplantation
Pathophysiology • Acute toxoplasmosis generally is well tolerated in immunocompetent adults • may result in vertical infection to the fetus and • lead to potentially serious consequences • In immunocompetent adult, symptoms usually are mild or inapparent • In about 10%: • fever • fatigue • Malaise • headache • myalgias • lymphadenopathy These symptoms will resolve in weeks to months without specific therapy
Pathophysiology • In immunosuppressed : • signs and symptoms often will be more pronounced • can result in significant ocular and CNS abnormalities • Reactivation infection in immunosuppressed pregnant women also can cause fetal infection
T. gondii • three forms • trophozoites or proliferative • tissue cysts • Oocytes • Trophozoite is seen in the acute phase of the infection in the human
Utero Transmission • Newborns become infected in uteroby transplacental passage of the parasite when the mother has acute infection • Chronic infections (onset precedes pregnancy) do not lead to congenital infection • except in the rare circumstance of an immunocompromised host with reactivation • likelihood of fetal infection increases with each trimester of pregnancy • Fetal infection is : • 15% in the first trimester, • 25% second, • 60% in third trimester
Utero Transmission • The severity of damage associated with timing of maternal infection • the risks decrease toward term • Severe fetal disease or fetal death: • occurs in about 10% of cases when infection occurs during the first trimester • extremely rare with infection during the third trimester • Mild damage is more frequent in the second and third trimesters (about 5%)
Utero Transmission • Subclinical infections increase from about 2% with first-trimester infections to 50% with third-trimester infections • acute infection could be associated with preterm delivery and stillbirth but not with spontaneous abortion
Diagnosis in Pregnancy 1. Maternal Infection • usually is asymptomatic • 10% to 20% of infected mothers have lymphadenopathy (Posterior cervical is the most frequent ) • The infection also can result in a mononucleosis like syndrome with: • fatigue • assitude and • rarely, can cause encephalitis • The clinical picture can be much more severe in immunocompromised adults.
Maternal Infection • clinicians are forced to rely on serologic tools for the diagnosis of toxoplasmosis in pregnancy • diagnosis of primary infection : • demonstration of a seroconversion to this organism • significant rise in antibody titer obtained from maternal sera taken at two different times • detection of toxoplasma-specific IgM antibody
Maternal Infection • Adults with primary infection develop IgG and IgM antibody to toxoplasma rapidly • Toxoplasma-specific IgG antibody: • develops within after infection • peaks in 6 to 8 weeks2 weeks • drops down over the subsequent several months • then persists for life • Toxoplasma-specific IgM • develops within 10 days after infection • remains elevated for 6 months to more than 6 years
Maternal Infection • IgM titers may not provide useful information to document recent primary infection in pregnant women • The IFA test frequently is more useful than ELISA in differentiating remote from recent primary infection of a pregnant woman • In any case, the presence of IgG and the absence of IgM suggest an infection that is probably at least a year old
Maternal Infection • Up to 40% of positive toxoplasma-specific IgM are false positives • Avidity testing is a newer type of testing • Approximately 50% of placentas of congenitally infected infants will show T. gondii cysts on histologic slides • Additional cases can be detected by the presence of parasites in the cord blood
Maternal Infection • The organism also has been isolated from placental tissue of acutely infected mothers in 2% to 25% of cases • Isolation of organisms from • tissue specimens, • buffy coat heparinized blood • body fluids
Prenatal Diagnosis • Antenatal diagnosis of fetal toxoplasmosis • culture of amniotic fluid • fetal blood • The main difficulties with culture techniques: • some assays may take up to several weeks • few laboratories are able to perform the assay • amniocentesis performed too early in gestation occasionally can be falsely negative
Prenatal Diagnosis • Toxoplasma-specific IgM, when present in fetal blood from cordocentesis, also has been used to diagnose fetal infection prenatally • fetal-specific IgM antibody • frequently does not develop until after 21 to 24 weeks gestation • is positive in only about 50% of infected cases • Additionally, cordocentesis is a procedure that entails some risk.
Prenatal Diagnosis • the PCR has been used to detect T. gondii in amniotic fluid and has been shown to be useful in the detection of in utero infections • Prenatal ultrasound also may demonstrate abnormalities • Ventriculomegaly and hydrocephalus as well as microcephaly will be poor prognosticators • Intracranial calcifications, placentomegaly, hepatomegaly cataracts, and hydrops may be other signs
Neonatal Infection • Most congenitally infected newborns are asymptomatic at birth • Literature has shown that detection of toxoplasma-specific immunoglobulin A (IgA) may be a reliable method for the diagnosis of toxoplasmosis in the newborn • Demonstration of toxoplasma-specific IgM infection may be diagnostic, although in newborns • approximately 20% of infections are not detectable by toxoplasma-specific IgM at birth • A number of these asymptomatic, untreated infants will go on to have delayed and potentially serious manifestations
Neonatal Infection • 20% with clinically obvious symptoms at birth will exhibit multiple findings • The most frequent clinical findings are : • Chorioretinitis • jaundice • Fever • Hepatosplenomegaly • in severe cases : • Hydrocephaly • microcephaly • cerebral calcifications
Treatment • Treatment of acute toxoplasmosis in immunocompetent, nonpregnant adults is primarily supportive • the prognosis following acute infection is good, except in cases of profound immunosuppression • The treatment in pregnancy is a bit more complex
Treatment • In Europe spiramycin is the first-line agent used • agent generally does not cross the placenta, and if fetal infection is detected, women also are treated with a combination of • pyrimethamine • folinic acid • sulfonamide
Treatment • Although not definitive, treatment with these regimens may prevent maternal-to-fetal transmission of the infection or improve the outcome among infected fetuses • The standard dosage is : • 25 mg of pyrimethamine by mouth given daily • 1 g of sulfadiazine by mouth four times daily for 1 year • Folinic acid, 6 mg given intramuscularly or by mouth every other day ***Pyrimethamine is a folic acid antagonist and therefore may have teratogenic effects when given in the first trimester
Prevention • avoid eating raw or undercooked meat • Fruits and vegetables should be peeled and washed before eating • proper hand hygiene • Gloves should be used for gardening and during any contact with soil or sand • Pregnant women should avoid close contact with cat feces • need for obstetricians to educate pregnant patients about these important preventive steps
Prevention • routine serologic screening programs • screening of newborns and the institution of treatment during the neonatal period to minimize the morbidity • Many infections in children that otherwise would be missed on routine clinical examination can be detected with IgM assays • Treatment of these infected infants has been associated with very low rates of subsequent neurologic or retinal disease