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Congenital Infections TORCH Toxoplasmosis Other (syphilis) Rubella Cytomegalovirus (CMV) Herpes simplex virus (HSV)

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Presentation on theme: "Congenital Infections TORCH Toxoplasmosis Other (syphilis) Rubella Cytomegalovirus (CMV) Herpes simplex virus (HSV)"— Presentation transcript:

1 Congenital Infections TORCH Toxoplasmosis Other (syphilis) Rubella Cytomegalovirus (CMV) Herpes simplex virus (HSV)

2 Varicella zoster (the chickenpox virus). Varicella zoster (the chickenpox virus). Entroviruses Entroviruses Hepatitis B. Hepatitis B. Parvovirus. Parvovirus. HIV (human immune deficiency virus). HIV (human immune deficiency virus). Chlamydia trachomatis. Chlamydia trachomatis. Mycoplasma. Mycoplasma. Group B streptococcus. Group B streptococcus. Malaria Malaria

3 COMMON CLINICAL FEATURES Low birth weight for gestational age Low birth weight for gestational age Prematurity Prematurity Seizures Seizures Chorio-retinitis Chorio-retinitis Cataracts Cataracts Purpura Purpura Cerebral calcification Cerebral calcification Micro-ophthalmia Micro-ophthalmia Jaundice Jaundice Anaemia Anaemia Hepatosplenomegaly Hepatosplenomegaly Pneumonitis Pneumonitis

4 CONGENITAL CMV Caused by a DNA herpesvirus Cytomegalovirus (CMV) Caused by a DNA herpesvirus Cytomegalovirus (CMV) Most common congenital viral infection Most common congenital viral infection The majority of congenital infections are asymptomatic The majority of congenital infections are asymptomatic severe neurologic morbidity occurs in 80 percent of survivors severe neurologic morbidity occurs in 80 percent of survivors sequelae appear to be more severe when infection is acquired earlier in pregnancy sequelae appear to be more severe when infection is acquired earlier in pregnancy

5 PATHOGENESIS Neonatal Neonatal 1. Antenatal (in utero) % of cases Primary Maternal Infection Primary Maternal Infection Recurrent Maternal Infection Recurrent Maternal Infection 2. Perinatal 3. Postnatal Childhood Childhood 1. Horizontal Transmission CMV excreted in saliva, urine, stool, tears CMV excreted in saliva, urine, stool, tears 2. Organ Transplantation kidney, marrow, heart, liver, blood (leukocytes) kidney, marrow, heart, liver, blood (leukocytes)

6 CLINICAL FEATURES: 90% of infants with congenital CMV infection are clinically silent CNS Manifestations CNS Manifestations 70% - microcephaly 70% - microcephaly 60% - intellectual impairment 60% - intellectual impairment 35% - sensorineural hearing loss 35% - sensorineural hearing loss seizures seizures 22% - chorioretinitis 22% - chorioretinitis

7 CLINICAL FEATURES: Systemic Manifestations Systemic Manifestations Reticuloendothelial (Liver) % Reticuloendothelial (Liver) % 70% - hepatomegaly/splenomegaly 70% - hepatomegaly/splenomegaly 68% - jaundice 68% - jaundice 65% - thrombocytopenia (with petechiae and purpura) 65% - thrombocytopenia (with petechiae and purpura) hepatitis hepatitis Others Others 65% - low birth weight (< 2500 gm) 2-5% - pneumonitis

8 INVESTIGATIONS Diagnostic Diagnostic Virology Virology gold standard gold standard of urine, saliva, blood, CSF, nasopharynx of urine, saliva, blood, CSF, nasopharynx Serology Serology ELISA - CMV-specific IgM ELISA - CMV-specific IgM of neonatal blood specimens, cord sampling of neonatal blood specimens, cord sampling Others Others PCR PCR Serum Serum CBC - anemia, thrombocytopenia CBC - anemia, thrombocytopenia conjugated, unconjugated hyperbilirubinemia conjugated, unconjugated hyperbilirubinemia elevated hepatic transaminases elevated hepatic transaminases CSF CSF elevated protein content elevated protein content

9 INVESTIGATIONS: Imaging Studies Imaging Studies CT (Head) periventricular calcifications periventricular calcifications can be identified in 25-50% of symptomatic infants can be identified in 25-50% of symptomatic infants

10 Prognosis Infants with signs of congenital CMV infection Infants with signs of congenital CMV infection 80% have long-term sequelae: 80% have long-term sequelae: sensorineural hearing loss sensorineural hearing loss neuromuscular problems neuromuscular problems motor and intellectual retardation motor and intellectual retardation seizures seizures chorioretinitis with visual deficits chorioretinitis with visual deficits Infants with silent congenital CMV infection Infants with silent congenital CMV infection have a more favourable outcome ® Ganciclovir

11 CONGENITAL TOXOPLASMOSIS caused by the protozoan Toxoplasma gondii caused by the protozoan Toxoplasma gondii ocular, central nervous system (CNS) ocular, central nervous system (CNS) incidence: 0.3-1/1000 live births incidence: 0.3-1/1000 live births

12 Routes of Transmission Routes of Transmission Neonatal (in utero) Primary Maternal Infection Primary Maternal Infection acquired by the ingestion of raw or undercooked meat ( cattle), or of infectious oocysts in feces (cats, birds) acquired by the ingestion of raw or undercooked meat ( cattle), or of infectious oocysts in feces (cats, birds) 1st trimester - 17% - spontaneous abortion 1st trimester - 17% - spontaneous abortion 2nd trimester - 25% - spontaneous abortion or severe disease 2nd trimester - 25% - spontaneous abortion or severe disease 3rd trimester - 65% - subclinical disease 3rd trimester - 65% - subclinical disease

13 CLINICAL FEATURES: 70% of infants with congenital toxoplasmosis infection are asymptomatic Ocular Manifestations (76%) Ocular Manifestations (76%) chorioretinitis chorioretinitis optic nerve atrophy optic nerve atrophy microphthalmias microphthalmias blindness blindness

14 CLINICAL FEATURES: CNS Manifestations (52%) CNS Manifestations (52%) hydrocephaly hydrocephaly motor and intellectual retardation motor and intellectual retardation seizures seizures sensorineuronal hearing loss sensorineuronal hearing loss Systemic Manifestations Systemic Manifestations classic triad of congenital toxoplasmosis : chorioretinitis, hydrocephalus, and intracranial calcifications. classic triad of congenital toxoplasmosis : chorioretinitis, hydrocephalus, and intracranial calcifications.

15 INVESTIGATIONS: Isolation of T. gondii from placenta or cord blood Isolation of T. gondii from placenta or cord blood Serology Serology measures IgG T. gondii antibody measures IgG T. gondii antibody IgM fluorescent antibody test IgM fluorescent antibody test Imaging Studies Imaging Studies CT (Head) CT (Head) intracranial calcifications (33%) intracranial calcifications (33%)

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17 MANAGEMENT combination of : combination of : pyrimethamine pyrimethamine sulphadiazine sulphadiazine folinic acid is added folinic acid is added Spiramycin Spiramycin Spiramycin Prevention

18 CONGENITAL RUBELLA caused by an RNA Togavirus caused by an RNA Togavirus Vaccine-preventable disease Vaccine-preventable disease

19 Routes of Transmission Antenatal (in utero) 1st trimester % 1st trimester % 2nd trimester % 2nd trimester % 3rd trimester % 3rd trimester %

20 CLINICAL FEATURES: Neonatal Manifestations Neonatal Manifestations IUGR low birth weight - prematurity IUGR low birth weight - prematurity stillbirth - spontaneous abortion stillbirth - spontaneous abortion Early Manifestations Early Manifestations cloudy corneas cloudy corneas Cataracts Cataracts microcephaly microcephaly hepatomegaly splenomegaly hepatomegaly splenomegaly jaundice jaundice pulmonary valve stenosis pulmonary valve stenosis patent ductus arteriosus patent ductus arteriosus thrombocytopenia purpura thrombocytopenia purpura

21 INVESTIGATIONS: Virology Virology from urine, naspharynx, CSF from urine, naspharynx, CSF Serology Serology fetal rubella-specific IgM fetal rubella-specific IgM persistence of rubella-specific IgG after 8-12 months of age persistence of rubella-specific IgG after 8-12 months of age


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