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Intrauterine infections: “TORCH” מציגה : אריאלה קלוטשטיין אופק הנחיה : פרופ ' יחיאל שלזינגר.

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Presentation on theme: "Intrauterine infections: “TORCH” מציגה : אריאלה קלוטשטיין אופק הנחיה : פרופ ' יחיאל שלזינגר."— Presentation transcript:

1 Intrauterine infections: “TORCH” מציגה : אריאלה קלוטשטיין אופק הנחיה : פרופ ' יחיאל שלזינגר

2 Hypothetical case  S.A. female neonate  Has:  Jaundice  HSM  Ptechiae  PDA  Lymphadenopathy  Hearing loss What does she have??

3 Congenital infections:  3 Routs of infection:  Trans placental: TORCH  Ascending/intrapartum: HSV, CMV, HBV, HIV  Breast milk: HBV, CMV, HIV

4 Transplacental infection  May occur at any time during gestation  Signs and symptoms may be present at birth or be delayed for months of even years.  importance of stage of embryonic life in the manifestations of the infection:  1 st trimester: may alter embryogenesis and result in malformations (rubella)  3 rd trimester: often results in active infection at the time of delivery (toxoplasmosis, syphilis)

5 Protection  Maternal antibody is effective for protection of the fetus, in some of the cases (rubella)  transplacental transmission of infection to a fetus is variable because the placenta may function as an effective barrier

6 Clinical signs and symptoms  Maternal- most are asymptomatic  Infant- range from early spontaneous abortion, congenital malformation, intrauterine growth restriction, premature birth, stillbirth, acute or delayed disease in the neonatal period, or asymptomatic persistent infection with sequelae later in life.  In some cases, no apparent effects are seen in the newborn infant.

7 What is TORCH?  T  T - Toxoplasmosis  O  O - others  R  R - Rubella  C  C - cytomegalovirus (CMV)  H  H - Herpes

8 Toxoplasmosis  Caused by the obligate intra-cellular parasite Toxoplasma Gondii  Route of infection:  Fecal-oral: Cat feces  uncooked meet, contaminated water and soil, unpasteurized goat milk.  Usually, the infection causes a mild flu-like illness, or no illness at all.  BUT, in immunocompremised or pregnant women it can be fatal, and cause symtoms such as: encephalitis, myocarditis and pneumonitis.

9 Toxoplasmosis- continue…  Fetal transmission:  in a primary infection, or chronic disease in immunocopremised mother.  The risk of fetal transmission increases with gestational age  The earlier in pregnancy the transmission occurs- the damage is worse.

10  Signs and symptoms:  1 st trimester: death, opthlmologic and CNS sequalea  2 nd trimester: “classic triad”: hydrocephalus, intracranial calcifications, chorioretinitis. Jaundice, HSM, anemia, lymphadenopathy, microcephaly, developemental delay, visual and hearing problems, and seizures.  3 rd trimester: usually asymptomatic at birth. Toxoplasmosis- continue…

11  Treatment:  Pyrimethamine- antimalarian medication  Sulfazidime  Leucovorin- folinic acid

12 Others…  We’ll just come back to it later…

13 Rubella- “The German Measles”  Member of the Togaviridae family.  Route of infection:  Respiratory secretions (both direct contact and droplets)  Transplacentally.

14 Rubella- continue…  Clinical manifestations:  “blueberry muffin” rash  Lymphadenopathy  HSM  Thrmbocytopenia  Interstitial pneumonitis  Radiolucent bone disease  IUGR  Hyperbilirubinenemia  Complications:  Eye problems: micropthalmus, pigmentary retinopathy, cataracts, glaucoma  Cardiac: peripheral pulmonic stenosis, PDA  Endocrine: Diabetes mellitus  Neurologic: developmental delay, encephalitis, sensorineural hearing loss

15 Rubella- continue…  Diagnosis:  Positive infant rubella IgM titer- recent infection  Culture: blood, urine, CSF, oral & nasal secretions  persistently elevated or rising IgG titers over time.  Treatment:  Supportive care only.

16 Cytomegalovirus  Member of the Herpesvirus family  Most common congenital infection in the US (0.5-1% of live births in industrialized nations, approximately annualy in the US)  Route of infection:  Transplacentally  During delivery  Postnatally (breastmilk (causes no clinical sequelae), or direct contact with other body fluids)  Maternal infection before pregnancy significantly reduces the risk of congenital CMV.

17 CMV- continue…  Clinical manifestations:  Most babies are asymptomatic at birth (90%)  Infants to mothers with primary infection- 5-20%: overtly symptomatic.  30% mortality rate  80% of survivors: severe neurologic morbidity  Symptoms include:  IUGR  Microcephaly  Periventricular calcifications  HSM  Petechiae  Hearing loss  Jaundice  Thrombocytopenia  retinitis  Hypotonoia  Lethargy  In preterm infants may present as sepsis

18 CMV- continue…  Complications:  CNS sequelae: retinitis, sensorineural deafness, developmental delay)  Will appear in 20% of asymptomatic neonates  Will appear in 50% (or more!) of symptomatic neonates  Diagnosis:  demonstration of the virus in body fluids (e.g. urine or pharyngeal secretions).  Serology for CMV IgG antibody determination are not useful in this case.  Laboratory abnormalities include: abnormal blood counts (especially thrombocytopenia), hemolytic anemia, elevated transaminases, and elevated direct and indirect serum bilirubin.  Treatment: no approved agent  Ganciclovir- improves hearing loss and neurodevelopmental outcomes

19 Herpes simplex virus  Double-stranded DNA virus of the herpesviridae family  Route of infection:  Primarily: during birth or virus ascending after the rupture of membranes.  Transplacentally- rare  Postnatally  Greatest risk: primery maternal infection during third trimester.

20 HSV- continue…  Clinical manifestations:  SEM disease: skin, eyes, mucosal involvement  CNS disease- temperature instability, respiratory distress, poor feeding, and lethargy (nonspecific)  Disseminated disease with multiple organ involvement  Usually presents in the first 6 weeks.  Most are asymptomatic at birth although many are born prematurely  Complications:  Untreated- high morbidity and mortality  Treated: SEM- best prognosis. 50% will suffer from recurrent skin outbreks. CNS- good survival, significant neurologic sequelae

21 HSV- continue…  Diagnosis:  Serum HSV IgM  HSV PCR of CSF- test of choice, may be false negative in the first 5 days  HSV culture of a lesion/mucosal surface- best for SEM  Treatment: IV acyclovir  improves mortality in all infants  Improves neurologic development in those with SEM and disseminated disease.

22 And…. Back to Others!  HIV  HBV  Parvovirus B19  Syphilis  HCV  VZV  TB

23 HIV  Member of the retroviridae family.  Route of infection to the fetus:  Transplacentally  During labor and delivery- the highest risk (exposure to maternal blood)  Through breastfeeding  Clinical manifestations:  Asymptomatic at birth  T-cell count declines and opportunistic infections take hold: Pneumocystis jiroveci, VZV, CMV, HSV….

24 HIV- continue…  Diagnosis:  The American Academy of Pediatrics and the CDC: HIV screening for all pregnant women in the US.  According to viral load:  HIV drug prophylaxis  C-section before rupture of membranes (viral load greater than 1000 copies/mL at full term delivery)  avoidance of breastfeeding  Early detection in the infant

25 HIV- continue…  Diagnosis:  In the infant: HIV-1 DNA/RNA pcr at:  days after birth  1-2 months  4-6 months  Considered uninfected if:  2 negative tests- one after 1 month, and another at 4 months +  2 negative antibody tests from different specimens obtained at 6 months +  Treatment:  Infants suspected: zidovudine until 6 weeks of age  Infants confirmed: further antiretroviral treatment

26 HBV  DNA virus of the hepadnavirus family  Route of infection:  transplacentally- rare  During delivery with exposure to maternal blood- most cases.  Clinical manifestations:  Most asymptomatic at birth  Rarely- signs of hepatitis: jaundice, thrombocytopenia, elevated transaminase conc., rash.  The risk of morbidity and of progressing to a chronic infection and disease are inversely proportional to gestational age at the initial infection

27 HBV- continue…  So… why are we worried ?  Because- 25% of children chronically infected with HBV will develop hepatocellular carcinoma or cirrhosis!  Diagnosis:  In the US- women are screened for HBsAg  If positive- the infant should receive HBV vaccine and Hepatitis B immune globulin within 12 hrs of birth.  They should complete the regular program of vaccinations to HBV+two more+ HBsAg and anti-HBs testing at 9 months of age

28 HBV- continue…  If the mother’s HBV status is unclear:  Immediate test for HBsAg:  If negative- no further treatment  If positive- the infant should receive HBV immunoglobin within 7 days of birth.  Treatment:  There is no treatment for acute HBV  For chronic HBV- Lamivudine- approved for 2 years of age and older.

29 Parvovirus B19  Single-stranded DNA virus  Usually causes “fifth disease” (“slapped cheek”), and other symptoms.  Route of infection:  Respiratory tract secretions  Contaminated blood  Transplacentally  Clinical manifestations:  Hydrops fetalis (due to severe fetal anemia)  Pleural end pericardial effusions  IUGR  death Hydrops fetalis: a condition in the fetus characterized by an accumulation of fluid, or edema, in at least two fetal compartments. Very high mortality rates

30 Parvovirus B19- continue…  Diagnosis:  IgM titer from the infant serum  PCR of amniotic fluid  Treatment:  Supportive care

31 Hypothetical case  S.A. female neonate  Has:  Jaundice  HSM  Ptechiae  PDA  Lymphadenopathy  Hearing loss What does she have?? Rubella!!

32 Summary  Timely diagnosis of congenital infections is crucial to the initiation of appropiate therapy  High index of suspicion and awareness is required:  Laboratory results obtained from the mother during pregnancy  Clinical manifestations including:  Hydrops fetalis  Microcephaly  Seizures  Cataract  Hearing loss  Congenital heart disease  HSM  Jaundice  Rash  thrombocytopenia

33 The END…


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