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TORCH Infection in neonate (newborn)

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TORCH Infection in neonate (newborn)

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This slide contains clinical features, perinatal and post natal diagnosis of congenital torch infection in fetus and neonates, and management of congenital toxaplasma, rubella, CMV, Herpes simplex, varicella, and other infections.

This slide contains clinical features, perinatal and post natal diagnosis of congenital torch infection in fetus and neonates, and management of congenital toxaplasma, rubella, CMV, Herpes simplex, varicella, and other infections.


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TORCH Infection in neonate (newborn)

  1. 1. Dr Md Noor Alam Khan PG-2 Deptt. Of Paeds MAMC Agroha TORCH INFECTIONS
  2. 2. INTRODUCTION 2 Vertically transmitted (mother-to-child) infections of the fetus and newborn can generally be divided into two major categories. Congenital infections: Infections which are transmitted to the fetus in utero. Perinatal infections: which are acquired intrapartum or in the postpartum period.
  3. 3. • Congenital infections can have manifestations that are clinically apparent antenatally or postnatally. Whereas • Perinatal infections may not become clinically obvious until after the first few days or weeks of life.
  4. 4. 4 T =Toxoplasmosis O =Others R=Rubella C =Cytomegalovirus H =Herpes Simplexvirus The TORCH acronymhasnow become Obsolete
  6. 6. 6 • CausativeOrganism:Toxoplasmagondii • Transmission:Oocystexcretedincatsfecesisthe sourceof infectiontohumen. • Contaminatesinsoil,water&rawmeat. • Verticaltransmissioncanoccur inuteroor during vaginal delivery • The riskofcongenitalinfectionincreaseswithgestational age. o 6%- 1st trimester o 22%-2nd trimester o 72%- 3rd trimester
  7. 7.  The fetal disease severity, however, is inversely proportional to gestational age. o 61% - 1st trimester (mostly die in utero or postnatally/ Severe CNS & opthalmological Disease) o 30% - 2nd Trimester (Mostly subclinical/mild) o 9% - 3rd trimester (almost all subclinical/mild)  Highest risk period- 10 to 24 week gestation
  8. 8. Clinical Manifestation  Four recognized patterns of presentation for congenital toxoplasmosis. 1. Subclinical Infection: 80-90% 2. Neonatal symptomatic disease 3. Delayed Onset 4. Sequelae or Relapse
  9. 9. 1. Subclinical infection: 80-90% o Asymptomatic o May have retinal and CNS abnormality 2. Symptomatic Disease: Usually severe Classical Triad of toxoplasmosis: • Chorioretinitis • Diffuse Nodular Intracranial calcifications • Hydrocephalus
  10. 10. 3. Delayed Onset: a. In preterm Infants b. within 1st 3 months c. like Neonatal Symptomatic Disease 4. Sequelae or relapse: a. Occurs in 24-85% cases b. Mainly ophthalmological & neurological symptoms.
  11. 11. 14 Common Clinical Manifestation Specific Symptoms; Neurological: Hydrocephalus Seizure Motor deficit Deafness Cerebral Calcification Ophthalmological: Chorioretinitis Cataract Microcornea Necrotising retinitis Cotton Spots on Fundoscopy
  12. 12. • Fever • Hepatospleenomegaly • IUGR • Persistant Conjugate Hyperbilirubinemia • Anemia • Thrombocytopenia • Maculopapular Rash Other Symptoms
  13. 13. Diagnosis 1-Maternal Infection  Sreening;- Serum IgG & IgM  Confirnatory: IgM; immunoglobulin A (IgA); immunoglobulin, E (IgE). Rising titer Avidity Testing  Foetal Testing  USG  Amniotic Fluid PCR
  14. 14. 2-In Suspected Neonate  Maternal History  Clinical examination  Lab oCBC- thrombocytopenia, Leucocytosis/Cytopenia, Anemia oCSF- Elevated protein, Xanthochromia,  CT Imaging- Calcifications, hydrocephalus, Cortical Atrophy  Pathology- Cyst or trophozoits in tissue, placenta & body fluids  Fundoscopy- Chorioretinitis,
  15. 15.  Serological Test-  IgG- Appear within 1-2 week Peak at 1-2 months, Persists life long  IgM- Not crosses placenta Useful to detect cong infection Low sensitivity  IgA- Rises rapidly, disappear by 7 months More sensitive than IgM
  16. 16. MANAGEMENT 19 Medications- • Pyrimethamine (1mg/kg 12 hourly for 2 days, F/B daily for 6months F/B thrice a week for second 6 months) • Sulfadiazine (100mg/kg/day in 2 divided doses for 1 year) • Leucovorin (Folinic Acid; 5-10mg thrice a week) •Prednisolone ( 0.5 mg/kg 12hourly) in active CNS disease Surgery- ventricular Shunting
  17. 17. RUBELLA
  18. 18. 21 Also known asGerman Measles Organism: RNA virus, a member of the Togavirus family Transmission: • Direct droplet contact from nasopharyngeal secretions • virus replicates in the lymph tissue of the upper respiratory tract • spreads hematogenously across the placenta
  19. 19.  Cause self limited infection in adult  Effect on fetus is devasting  Fetal infection can occur at anytime, but early gestation infection results in multiple organ anomalies.  Gestational age is direct proportional to infection rate and inversely proportional to disease severity.
  20. 20.  Infection at 10 week- 100% of infected have cardiac defect and deafness. • 13-16 weeks-33% deafness • after 20 week – no anomaly  Triad of CRS: o Cataract o SNHL o Cardiac Anomaly - PDA>PS
  21. 21. CLINICAL FEATURES General: IUGR, Prematurity, Stillbirth, Abortion CVS:PDA, PAS, CoA Eye:Cataracts, Microphthalmia, Pigmentary(salt -pepper ) Retinopathy Ear:Sensory Neural Deafness GIT: HepatoSpleenomegaly CNS: Meningoencephalitis, Microcephaly, Hypotonia, MR Skin: Blueberry Muffin Rash, Dermatoglyphic abnormalities Blood: Thrombocytopenia Skeletal: Radio-lucencies of long bones 12
  22. 22. 25 Blueberry Muffin Rash Blue berry muffin
  23. 23. Rubella Rashes
  24. 24. DIAGNOSIS 28 HISTORY OF MATERNAL INFECTION • Symptoms - Low-grade fever/Headache/mild coryza and Conjunctivitis occurring 1to 5 days before the onset of rash. • Maculopapular exanthem that begins on the face and the ears and spreads downward over 1to 2days. • The rash disappears in 5 to 7 days from onset, • Posterior cervical lymphadenopathy iscommon.
  25. 25. 29 ANTENATAL DETECTION • Specific IgM in Fetal blood obtained by percutaneous umbilical cord blood sampling. • Rubella antigen and RNA in a Chorionic villous biopsy specimen. POSTNATALDETECTION • Serology: Detection of Rubella Specific IgM in cord or neonatal blood • Persistent IgG titer over time • Virus Isolation: pharyngeal secretions/urine sample upto 1 yr
  26. 26. Treatment  No specific therapy to halt the progression of complicated CRS.  Close follow up if early gestation infection is suspected or timing of infection is unknown.  If maternal infection is confirmed: If Gestation <20 weeks Discussfor MTP If Gestation >20 Reasssure parent No risk of abnormalities
  27. 27. 31 • Supportive care • Multi disciplinary approach • Hearing loss - hearing aids and referral to an early intervention program • Structural cardiac defects – Surgical correction • Ocular abnormalities – Referral to Ophthalmology expert • CNS abnormalities - special education services, speech, language, occupational, and/or physical therapy. • Endocrine abnormalities – Expert Followup for Diabetes/ Hypothyroidism If Baby Born With Rubella Infected Mother
  28. 28. PREVENTION 32 • Girls should be vaccinated against rubella before entering the childbearing years • Avoid contact to any known or susceptible Rubella infected person. • Avoid conception for 3 months following immunization. • Hyperimmunoglobulin if infected pregnant female don’t want to terminate pregnency .
  30. 30. 34 Causative Organism: • Cytomegalovirus – DNA virus • member of herpes virus family Transmission: • Only Human reservoir, lifelong infection • Present in saliva, urine, genital secretion, breast milk and blood products. • Close contact transmission • Route – Transplacental/ Intrapartam/ Postnatal
  31. 31.  Primary infection (acute infection)- usually asymptomatic in older infants, children, and adults, may present with mononucleosis like symptoms eg. prolonged fever and a mild hepatitis.  Latent infection- Asymptomatic unless host become immunocompromised.  Very common, with seroprevalence 50-85% by 40 yrs age.
  32. 32.  Primary CMV infection occurs in 1-3% of pregnant women, with a fetal attack rate of 30-40%.  80% of infants with congenital CMV infection will remain asymptomatic.  Vertical transmission can occur at any time, infection during early gestation carries higher risk of severe fetal disease.  More common among HIV-1 infected infants, so screening for CMV in HIV exposed infants is advised.
  33. 33. Clinical Feature (A) Symptomatic congenital disease- 1. Acute fulminant infection- 30% mortality Signs- petechiae/ purpura, Hepatosplenomegaly, juandice, prematurity, IUGR(1/3), and “blueberry muffin spots” reflecting extra-medullary hematopoiesis. Lab- CBC(anemia, thrombocytopenia), LFT(↑transaminases and bilirubin)
  34. 34. Without life-threatening complication-  IUGR or disproportionate microcephaly with or without intracranial calcification (periventricular area) and chorioretinitis.  Other CNS- ventricular dilation, cortical atrophy, develo- pmental abnormalities and neurological dysfunction.  SNHL most common sequele (60% symptomatic and 5% asymptomatic infants at birth), so any infant failing newborn hearing screening should be screened for CMV infection.
  35. 35. (B) Asymptomatic congenital infection- • Present in later infancy • Developmental abnormalities, hearing loss, MR, motor spasticity and acquired microcephaly. (C) Perinatally acquired CMV- can be acquired from- • Intrapartum exposure within the maternal genital tract • Postnatal exposure to infected breast milk • Infected blood or blood products • Nosocomially urine or saliva
  36. 36. Almost all full term- remain asymptomatic In preterm infants - acute infection syndrome (neutropenia, anemia, HSM, lymphadenopathy, hearing loss). (D) CMV pneumonitis- In preterm infants <4 months old
  37. 37. DIAGNOSIS 20 • CMV infection diagnosis is made if CMV is identified in urine, saliva, blood or respiratory secretion. • Congenital infection- if found in first 2 wks. • Perinatal infection- if negative in first 2wks and positive after 4 wks of life. • Blood is the earliest specimen to become positive and urine- highest sensitivity for diagnosis of CMV (as CMV is concentrated in urine).
  38. 38. Neurological outcomes of congenital CMV infection. Examples of computed tomography (A) and magnetic resonance imaging (B and C) of three infants with severe symptomatic congenital CMV infection with CNS involvement are shown. The classical pattern of injury described with congenital CMV infection involving the CNS is characterized by periventricular calcifications (panel A, arrow). Other consequences of fetal brain infection include abnormalities of neuronal migration, leading to polymicrogyria (panel B, arrows) and, in extreme cases, profound structural defects such as porencephalic cysts with associated schizencephaly (panel C, arrow).
  39. 39.  -ve blood can’t rule out CMV but –ve urine test in an untreated symptomatic infant for 4 wks or more rule out infection  Diagnostic techniques: 1.CMV PCR- in urine or blood. Sensitivity is high for urine, but –ve PCR in blood doesn’t rule out infection. 2. CMV IgG and IgM:- IgG -ve in both maternal and infant sera, excludes congenital CMV infection.
  40. 40.  If IgG +ve in infant sera… Uninfected infant Infected infant IgG declined within 1 month and not Detectable by 4-12 months Continue to produce The IgG through out the same period • CMV specific IgM have limited specificity
  41. 41. MANAGEMENT 45 For symptomatic congenital CMV • Ganciclovir (12mg/kg/day iv infusion 2 div doses for 6 weeks) • Valganciclovir-oral and less toxic. • Close monitoring & Followup of infectedinfants
  42. 42. Prevention • Personal protective measures(hand washing etc) • Avoidance of unnecessary blood transfusion & use of leukocyte depletedblood. • If Mononucleusis like illness during pregnency, screen for CMV Infection. • Prenatal diagnosis- Byviral culture or CMV DNA detection in amniotic fluid, or by CMV IgM antibody measurement in fetal blood of the symptomatic fetus.
  44. 44. 48 Organism: • Herpes Simplex Virus(HSV) - DNA virus with two virologically distinct types: 1 and 2 • The virus can cause localized disease of the infant's skin, eye, or mouth (SEM)or may be Disseminated disease or CNS disease. Transmission: • Contact with genital lesions during delivery: Common • Transplacental : Rare.
  45. 45. Clinical Manifestation (A)Localised SEM (skin, eye and mouth infection) 50% • Vesicles typically appear on the 6th to 9th day of life • Cluster of vesicles on the presenting part of the body (extended direct contact). • Significant morbidity despite in the absence of signs of disseminated disease. • Up to 10% later shows neurologic impairment and infants with keratoconjunctivitis can develop chorioretinitis, cataract and retinopathy.
  48. 48. (B) CNS infection- • 1/3 of neonates with HSV present with encephalitis in the absence of disseminated disease. • Symptomatic at 8-17 days of life • Hematogenous spread to CNS • lethargy, seizures, temperature instability, hypotonia. • 2/3 have impaired nurodevelopment
  49. 49. (C) Disseminated disease- • Most severe form of neonatal HSV, accounts for 22% of all neonatal HSV. • Mortality >50%, pneumonitis and fulminant hepatitis are associated with greater mortality. • Present with shock, seizures, respiratory distress, respiratory failure, DIC.
  50. 50. DIAGNOSIS 54 • For SEMdisease - Viral Culture by Isolation –Newer vesicular fluid, Urine & conjunctivalsmears. • For Non SEMdisease– PCR ofCSF,oral,nasopharyngeal,conjuctival secretion, stool&urine • EEG and Imaging studies of brain also aids in the diagnosis of HSV encephalitis • Cytology of vesicular fluid – Presence of Tzanck cells
  51. 51. Tzanck cell
  52. 52. MANAGEMENT 56 Acyclovir Therapy- 60 mg/kg/day 3 div doses • SEMdisease :Duration for 14 days • CNS/ Disseminated disease :Duration for at least 21 days, or longer if the CSFPCRremainspositive. • Infants with ocular involvement :Ophthalmologic evaluation/ Topical ophthalmic antiviral agents in addition to parenteral therapy.
  53. 53. Prevention • Known HSV-2 seronegative woman should avoid sexual intercourse with known HSV-2 seropositive partner in the third trimester. • HSV- 2 primary infection during pregnancy- 10 days course of acyclovir to woman. • Women with HSV-2- test for HIV (as HSV-2 seropositive person have two fold greater risk for acquisition of HIV).
  54. 54. Delivery- offer acyclovir near term until delivery to women with clinical or serological evidence of HSV-2, establishing vaginal route of delivery if no visible lesions  Csection in mothers with visible genital lesion
  55. 55. SYPHILIS
  56. 56.  Causative Agent- Spirochete, Treponema pallidum  Transmission-horizontal- Sexually Vertical – to fetus through Placenta Congenital Syphilis- Transplacental passage of T.Pallidum or contact with infectious lesion during birth. More recent maternal infection, more likely transmission
  57. 57. Clinical Features  May result in still birth, hydrops fetalis, prematurity.  Mostly Asymptomatic at birth  Common signs in <2 years child: Hepatospleenomegaly Condylomata lata Jaundice Snuffles(watery nasal discharge) Anemia Edema Skeletal abnormalities (Osteochondritis, periostitis)
  58. 58.  Common signs in >2 years old child Sensorineural hearing loss Interstitial keratitis Hutchinsons teeth Saddle nose Bony Changes Frontal bossing Short maxilla High palatal arch
  59. 59. Interstitial Keratitis Saddle Nose Hutchinson’s teeth
  60. 60. High Arched Palate Short maxilla
  61. 61. Approach Routine Serological testing for syphilis in all pregnant female Mother with Syphilis( reactive VDRL/RPR and confirmed by reactive TPHA/FTA-ABS Evaluate the infant 1. Assess adequacy of maternal treatment 2. Pathological examination of placenta/umblical cord 3. Darkfield microscopy 4. Clinical examination of infant 5. Quantitative VDRL/RPR on infant serum(no need of TPHA/FTA-ABS)
  62. 62. S N Scenario Additional Evaluation Treatment 1 Proven/Highly probable disease: Presence of any one 1. Physical abnormalities S/O cong. syphilis OR 2. VDRL/RPR: 4 X high titers than mother’s titer OR Positive darkfield test of body fluids 1. CSFF(VDRL, Cell, protein) 2. CBC, Differential and platelet Count 3. Other test as clinically indicated(long bone and chest X- rays, LFT, neuroimaging, ophthalmologic examination and BERA Penicillin G (1-1.5 lac unit/kg/day) as 50,000 umits/kg/dose IV for 10 days •q 12 h during first 7 days of life • q 8 h there after OR Procain Penicillin G 50,000 unit/kg/dose IM OD for 10 days
  63. 63. S N Scenario Additional Evaluation Treatment 2 Possible congenital syphilis: Presence of all 3 1. Normal physical examination 2. VDRL/RPR ≤ 4 X of maternal titer 3. Mother: not treated/inadequatel y treated/treated with non Peniciliin regimen/treated <4 week before delivery As above(scenario 1) As above(scenario 1) If complete evaluation not done or uncertain follow up OR Benzathinepenicillin G 50,000 unit/kg/dose IM single dose if Normal complete evaluation and follow up is certain
  64. 64. S N Scenario Additional Evaluation Treatment 3 Congenital syphilis less likely: Presence of all three 1. Normal physical examination 2. VDRL/RPR ≤ 4 X of maternal titre 3. Mother: adequately treated during pregnancy and >4 week before delivery And no reinfection or relapse No evaluation required No treatment required if follow up is certain. Benzathine penicillin G 50,000 unit/kg as a single IM injection if follow up is uncertain
  65. 65. S N Scenario Additional Evaluation Treatment 4 Congenital syphilis unlikely:Presence of all three 1. Normal physical examination 2. VDRL/RPR ≤ 4 X of maternal titre 3. Mother: adequately treated before pregnancy and her VDRL/RPR titre remain low and stable before and during pregnency and at delivery No evaluation required As above (scenario 3)
  66. 66. VARICELLA(Chicken Pox)
  67. 67.  Causative agent- Varicella zoster virus, DNA virus of herpervirus family.  Primary infection- Chicken pox  Reactivation of latent virus(in sensory ganglia)- Zoster  Transmission- o Horizontal- Droplet, contact to vesicular lesion o Vertical- Mother to fetus through placenta
  68. 68.  Risk of congenital varicella syndrome (CVS) is o 0.4 % if maternal infection in first 12 weeks of pregnancy o 2% for infection in 13-20 weeks. • Peripartum Varicella in mother: • 25% of newborn develop varicella • Severe disease if maternal varicella occurs 5 days before and 2 days after delivery.
  69. 69. Clinical Features (A)Congenital varicella syndrome- o Cicatrical skin scarring (cicatrix) o Limb hypoplasia o Ocular defects o CNS abnormalities (cortical atrophy) o IUGR o Early death.  Most commonly occurs with maternal V-ZV infection in 7- 20 wks of gestation.
  70. 70. (B) Postnatal varicella-  post natal exposure in newborn period, generally mild disease.  Varicella has been detected in breast milk, so it may be prudent to defer breastfeeding at least during the period, mother is likely viremic or infectious.
  71. 71. Approach  If maternal rash earlier than 5 days before delivery: Likely hood of infection Isolation Treatment Infant has protective antibodies AND low likely hood of severe disease Do not separate baby from mother, continue breastfeeding, isolate from other infants No VZIG Acyclovir if baby develop rashes
  72. 72.  If maternal rash appear with 5 days prior to and 2 days after delivery: Likely hood of infection Isolation Treatment Infant do not have protective antibodies AND likely hood of severe neonatal disease is high Separate mother and baby until maternal lesion dried up If baby develop rash: Baby to stay with mother, isolate both from other infants and mothers VZIG within 72 hours of exposure, Acyclovir
  73. 73.  If maternal rash appears after 2 days of delivery: Likely hood of infection Isolation Treatment Infant do not have protective antibodies BUT likely hood of severe neonatal disease is low Separate mother and baby until maternal lesion dried up If baby develop rash: Baby to stay with mother, isolate both from other infants and mothers No VZIG Acyclovir if baby develop rashe
  74. 74. THANK YOU 81

Editor's Notes

  • When congenital or perinatal infections are suspected, the diagnosis of each of the possible infectious agents should be considered separately and the appropriate
    most rapid diagnostic test requested in order to implement therapy as quickly as possible.
  • 1-an obligate, intracellular protozoan parasite
  • 1IgG is detectable in 1 to 2 weeks, peaks in 3 to
    6 months, and persists at low titers for life.
    2-IgM appears within 2 weeks after infection, peaks at 1 month, and
    usually declines to undetectable levels within 6 to 9 months. IgM may persist for more than 1 year after initial infection