This document discusses various perinatal and congenital infections including TORCH infections. It provides details on the causative organisms, modes of transmission, clinical features, diagnosis, and management of toxoplasmosis, rubella, CMV, herpes, HIV, hepatitis B, tuberculosis, varicella zoster virus, syphilis, malaria, and parvovirus infections. Timely diagnosis and treatment of perinatally acquired infections is important. Prevention strategies include maternal screening, vaccination, treatment of infected mothers, and avoiding risk factors during pregnancy and delivery.

1. TORCH INFECTION IN
NEONATES
DR. RAVI KUMAR S
PEDIATRIC RESIDENT
MGMCRI
1

2. DISCUSSION
 Introduction
 Perinatal Infections
 Clinical features
 Diagnosis
 Treatment
 Prevention
2

3. INTRODUCTION
CONGENITAL INFECTIONS
 “Infections acquired in utero or during the birth process”
 The infected newborn may show abnormal growth,
developmental anomalies, or multiple clinical and laboratory
abnormalities
 Severity depends on the gestational age of fetus at the time
of infection & virulence of the organism
 Timely diagnosis of perinatally acquired infections is crucial
the initiation of appropriate therapy.
3

4. PERINATAL INFECTIONS
T = Toxoplasmosis
O = Others
R = Rubella
C = Cytomegalovirus
H = Herpes Simplex virus
The TORCH acronym has now become Obsolete, due to a
large basket of infections in “Others”
4

5. TOXOPLASMOSIS
Causative Organism: Toxoplasma gondii
 Oocyst excreted in cats feces is the source of infection to
humans  Contaminates in soil, water & raw meat
Transmission: Vertical transmission can occur in utero or
during vaginal delivery & risk of fetal transmission is
 25% in 1st Trimester
 75% in 3rd Trimester
 90% during last few weeks prior delivery.
5

6. CLINICAL FEATURES
Most infected newborns are asymptomatic at birth
Few develop
 IUGR
 Fever
 Maculopapular rash
 Anemia
6
• Jaundice
• Seizure
• Hepatospleenomegaly
• Thrombocytopenic purpura

7. Contd.,
Classical Triad
1) Chorioretinitis
2) Diffuse Nodular Intracranial
calcifications
3) Hydrocephalus
7

8. DIAGNOSIS
 Maternal history & Serology
 Clinical Examination
 Laboratory Evaluation - Serology/ CBC / LFT
 Fundus Examination - Chorioretinitis
 Neuroimaging – Intracranial Calcifications/ Hydrocephalus
 Lumbar Puncture – Elevated CSF Protein/ Mononuclear Pleocytosis
 Prenatal Diagnosis- PCR by Amniocentesis is the best method for
prenatal diagnosis of fetal infection.
8

9. CONFIRMED CONGENITAL TOXOPLASMA
INFECTION
Any of the following:
1. Detection of toxoplasma specific IgM (after 5 days of life) or
IgA titres (after 10 days of life) is considered diagnostic of
congenital toxoplasmosis in infants with a positive
Toxoplasma IgG titre
2. Positive for Toxoplasma IgG beyond 12months of age
3. Positive CSF PCR
4. Increase in anti-Toxoplasma IgG titer during the first year of
life or increasing IgG titer compared with the mother's
9

10. MANAGEMENT
WHO & CDC Recommends Combination Therapy for standard
treatment of congenital toxoplasmosis
 Pyrimethamine (1mg/kg/day daily for first 6months &
1mg/kg/day 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)
Prevention
 Avoidance of Exposure- Food hygiene
 Maternal Screening
 Prenatal Treatment - Spiramycin
10

11. RUBELLA
Also known as German 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  CRI
 Maternal infection rate is high, especially at the time of 1st
trimester & last 1 month
 Malformation occurs in 90% of infection during 2-10 weeks of
gestation.
11

12. CLINICAL FEATURES
General: IUGR, Prematurity,
Stillbirth, Abortion
CVS: PDA, PAS, CoA
Eye: Cataracts, Microphthalmia,
Pigmentary 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

13. Blueberry Muffin Rash
13

14. DIAGNOSIS
HISTORY OF MATERNAL INFECTION
 Symptoms - Low-grade fever/Headache/mild coryza and
conjunctivitis occurring 1 to 5 days before the onset of rash.
 Maculopapular exanthem that begins on the face and
the ears and spreads downward over 1 to 2 days.
 The rash disappears in 5 to 7 days from onset,
 Posterior cervical lymphadenopathy is common.
14

15. DIAGNOSIS
ANTENATAL DETECTION
 Specific IgM in Fetal blood obtained by percutaneous
umbilical cord blood sampling.
 Rubella antigen and RNA in a Chorionic villous biopsy
specimen.
POSTNATAL DETECTION OF CONFIRMED CRI
Serology: Detection of Rubella Specific
 IgM below 3months (or)
 IgG between 6months to 12 months.
Virus Isolation: pharyngeal secretions/urine sample upto 1 yr
15

16. MANAGEMENT
 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
16

17. PREVENTION
 Girls should be vaccinated against rubella before entering the
childbearing years.
 Rubella vaccine is a live attenuated vaccine which is available
separately or as triple vaccine (MMR) that contain measles,
mumps and rubella.
 Principal goal of Rubella vaccination is Prevention of CRS.
 As per IAP recommendation – two doses of MMR vaccines -
1st at 15 months and the 2nd at 4–6 years
 Special care should be taken in reproductive females to avoid
pregnancy for 3 months after MMR vaccination.
 Avoidance of Exposure
17

18. CMV
Causative Organism:
 Cytomegalovirus - member of herpes virus family
 It is the most common cause for Non-Hereditary cause of
SNHL worldwide.
Transmission:
 Close contact – young children attending daycare center
 Saliva/ Urine/ Blood & Breastmilk*
 Route – Transplacental/ Intrapartam/ Postnatal
18

19. CLINICAL FEATURES
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At birth, most infants with
congenital CMV are asymptomatic.
Few Develop:
 SGA/Prematurity
 Hepatospleenomegaly
 Microcephaly/Periventricular
Calcifications/SNHL/Seizures
 Petechiae & Jaundice at Birth
 Thrombocytopenia
 Pneumonia

20. DIAGNOSIS
Diagnostic Testing of Urine/Saliva for CMV by
 PCR
 Viral Culture(Shell vial assay)
Detection of CMV IgG antibodies in blood
Post Natal Evaluation Include
 Physical & Neurological Examination
 Laboratory testing (CBC/Coagulation/LFT)
 Hearing assessment (ABR)
 Opthal assessment (Chorioretinitis)
 Neuroimaging (USG Cranium/CT Brain)
20

21. MANAGEMENT
For symptomatic congenital CMV
 Ganciclovir* (12mg/kg/day iv infusion 2 div doses for 6
weeks)
 Valganciclovir
 Close monitoring & Followup of infected infants
Prevention
 Personal protective measures/ Avoidance of unnecessary
blood transfusion & use of leukocyte depleted blood.
 Prenatal diagnosis- By viral culture or CMV DNA detection in
amniotic fluid, or by CMV IgM antibody measurement in fetal
blood of the symptomatic fetus
21

22. HSV
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.
22

23. CLINICAL FEATURES
Inutero Infection:
Skin: Scarring, vesicles, hypo/hyperpigmenation
Eyes: Microphthalmia, retinal dysplasia
CNS: Microcephaly, encephalomalacia, hydranencephaly
Intrapartam/Postpartam Infection:
SEM disease : Vesicular lesions, Conjunctivitis, excessive tearing,
Ulcerative lesions of the mouth, palate & tongue
Disseminated disease : Sepsis, Fever, Respiratory distress, DIC,
Skin lesions, CNS involvement(60 to 75%)
CNS disease+/− Skin : Seizures, Lethargy, Irritability, Tremors,
Poor feeding, Skin lesions(60 to 70%)
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24. LESIONS OF NEONATE WITH
SEM DISEASE
24
NECK VESICLES SCALP LESIONS

25. LESIONS OF NEONATE WITH
SEM DISEASE
25
EYE VESICLES
HYPOPIGMENTED, SCALING, AND
CRUSTED EROSIONS OF THE
TRUNK AND EXTREMITIES

26. DIAGNOSIS
 For SEM disease - Viral Culture by Isolation – Newer vesicular
fluid, Urine & conjunctival smears.
 For Non SEM disease– PCR of CSF
 EEG and Imaging studies of brain also aids in the diagnosis of
HSV encephalitis
 Cytology of vesicular fluid – Presence of Tzanck cells
26

27. MANAGEMENT
Acyclovir Therapy- 60 mg/kg/day 3 div doses
 SEM disease : Duration for 14 days
 CNS / Disseminated disease : Duration for at least 21 days, or
longer if the CSF PCR remains positive.
 Infants with ocular involvement : Ophthalmologic evaluation/
Topical ophthalmic antiviral agents in addition to parenteral
therapy.
27

28. Contd.,
Recent evidence : Suggests to start on suppressive therapy
following parenteral treatment with oral acyclovir 300 mg/m2
per dose three times per day for six months as it reduces
cutaneous recurrences and is associated with improved
neurologic outcomes in infants with CNS disease.
Prevention :
 C-Section for mothers with genital lesions
 Acyclovir for pregnant mothers with primary HSV
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29. PERINATAL HIV INFECTION
Organism:
 Retrovirus
 80% of HIV Infections in children occur during perinatal
period
Transmission:
 35% Risk of Mother to child transmission(MTCT) of HIV
during perinatal period
 30% Vertical
 60% During labor & delivery
 10% Breastmilk
29

30. RISK FACTORS
Maternal:
 High viral load/ Low CD4 count
 Primary infection during pregnancy/Vaginal delivery
 Pronlonged ROM
Fetoplacental:
 Chorioamnionitis
 Prematurity
Postnatal:
 Breastfeeding (viral load)/Cracked nipples/Mastitis
 EBF Infant having oral thrush at less than 6 months
30

31. PREVENTION OF PERINATAL HIV
Risk of MTCT can be reduced by
 ARV Prophylaxis to the mother during pregnancy/ labor & to
the infant after birth.
 Elective C-Section(prior to onset of labor & ROM) &
 Complete avoidance of breastfeeding
 Membranes should not be artificially ruptured unless there is
fetal distress/delay in progress of labor
 Repeated vaginal examinations/instrumental delivery/
invasive procedure on fetus/ routine episiotomy must be
avoided
31

32. ARV REGIME – PREGNANT WOMEN
 Recent WHO guidelines recommends an simplified, optimized
& fixed dose combination of ART
 HIV detected Pregnant women during antenatal period must
be initiated on ART regimen as below throughout the
pregnancy (regardless of clinical stage/CD4 count)
 Tenofovir(TDF) 300mg
 Lamivudine(3TC) 300mg
 Efavirez(EFV) 600mg
 Initiation shouldn’t be delayed for C4 count
 Lifelong ART is initiated as soon as possible
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Alternate Regimen
AZT+3TC+EFV
AZT+3TC+NVP
TDF+3TC+NVP

33. ARV REGIME – INFANTS BORN TO
HIV MOTHER
• If mother received ART adequately/regularly in antenatal
period: Daily NVP prophylaxis at birth till 6 weeks of life.
• If Infected Mother did not receive any ART earlier/ directly
presents in labor without adequate duration of ART(atleast 24
weeks): Daily NVP prophylaxis at birth till 12 weeks of life.
• First dose initiated within 6-12 hrs of delivery
• Dose can be increased to 20mg OD after 6-8 wks of age.
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B.WT NVP DAILY DOSE DAILY DOSE IN SUSP
<2kg 2mg/kg OD 0.2ml/kg
2-2.5kg 10mg OD 1ml OD
>2.5kg 15mg OD 1.5ml OD

34. POSTNATAL DIAGNOSIS OF HIV
INFECTION
34

35. HEPATITIS B VIRUS
Organism:
 HBV- DNA Virus
 Most common cause of acute & chronic Hepatitis
Transmission:
 Exposure of Infected maternal blood via percutaneous or
permucosal routes during delivery.
 Amniocentesis
 Breastfeeding not contraindicated
Clinical Features:
 Affected neonates are mostly asymptomatic.
 Later Develop chronic antigenemia with mild and often
persistent liver enzyme elevations beginning at two to six
months of age
35

36. INFANT BORN TO MOTHER WITH
HEPATITIS-B INFECTION
36

37. Contd.,
37

38. CONGENITAL TUBERCULOSIS
Organism:
Mycobacterium Tuberculosis
Risk factors:
 Tubercular endometriosis
 Miliary TB/Genital TB
Transmission:
 Transplacental spread
 Postnatal exposure from infected mother/healthcare worker
Clinical Features:
 Fever
 Lymphadenopathy
 Lethargy
 Poor feeding
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• HSM
• Tachypnea
• Jaundice

39. INFANT BORN TO MOTHER WITH
TUBERCULOSIS
39

40. OTHER PERINATAL INFECTIONS
DISEASE TRANSMISSION SYMPTOMS DIAGNOSIS TREATMENT
Chickenpox
VZV
1st 20wks of
Pregnancy
• Cicatricial lesions
• Limb hypoplasia
• Microcephaly
• Cataract
PCR of
Vesicular fluid
• Acyclovir
• VZIG
Syphilis
T,Pallidum
Between 1st &
2nd Trimester of
Pregnancy
• Skeletal
abnormalities
• Pseudoparalysis
• Persistent rhinitis
• Maculopapular
rash
Specific IgM
fluorescent
antibody
• Benzathine
Penicillin G
Malaria
P.Vivax &
Falciparum
Infected blood
administration
• Stillbirth/IUGR
• Hemolytic Anemia
• Jaundice
Blood Smear • Chloroquine
Phosphate
Parvo Virus
B19
Within the first
20 weeks
• Abortion/ Anemia
• Hydrops
• Slapped Cheek
rash
PCR of Blood • Supportive
• IVIG
Coxsackie B Intrauterine
exposure
• Carditis
• Orofacial clefts
Cord serum for
specific IgM
Supportive
care
40

41. DIAGNOSTIC TECHNIQUES FOR DIAGNOSIS
OF COMMON PERINATAL INFECTIONS
PATHOGEN TEST OF CHOICE
RUBELLA Isolation – Viral Culture of Urine/ Throat swab
Cord serum for IgM & specific IgM fluorescent
antibodies
HSV PCR of skin lesion, blood, or CSF
CMV PCR urine/saliva
Spin-enhanced urine culture (shell vial)
HIV DNA PCR – Blood if mother is HIV Infected
HBV HBsAg of blood
DNA PCR of blood
VZV PCR of skin lesion
TOXOPLASMA Specific IgM & IgA fluorescent antibody by ELISA/
ISAGA
PCR - CSF
SYPHILIS Specific IgM fluorescent antibody
Paired Maternal & Cord sera for RPR/VDRL 41

42. TAKE HOME MESSAGE
 CMV, Rubella, Toxoplasma are the most common cause of
chronic intrauterine infections in the newborn.
 Congenital TB should be suspected in newborns who have
Non-resolving pneumonia, persistent fever & HSM, in
absence of any of the bacterial pathogen isolated on culture.
 DNA PCR to detect HIV should be conducted in a neonate 6
weeks after cessation of breastfeeding.
 Timely diagnosis of perinatally acquired infections is crucial to
the initiation of appropriate therapy, development of care
plan, prognosis, and family counseling.
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43. THANK YOU
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