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.

1. Dr Md Noor Alam Khan
PG-2 Deptt. Of Paeds
MAMC Agroha
TORCH INFECTIONS

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. • 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
T =Toxoplasmosis
O =Others
R=Rubella
C =Cytomegalovirus
H =Herpes Simplexvirus
The TORCH acronymhasnow become Obsolete

5. TOXOPLASMOSIS

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.  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. 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. 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. 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.

14. 14
Common Clinical Manifestation
Specific Symptoms;
Neurological: Hydrocephalus
Seizure
Motor deficit
Deafness
Cerebral Calcification
Ophthalmological:
Chorioretinitis
Cataract
Microcornea
Necrotising retinitis
Cotton Spots on Fundoscopy

15. • Fever
• Hepatospleenomegaly
• IUGR
• Persistant Conjugate Hyperbilirubinemia
• Anemia
• Thrombocytopenia
• Maculopapular Rash
Other Symptoms

16. 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

17. 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,

18.  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

19. 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

20. RUBELLA

21. 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

22.  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.

23.  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

24. 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

25. 25
Blueberry Muffin Rash Blue berry muffin

26. Rubella Rashes

28. 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.

29. 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

30. 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

31. 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

32. 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 .

33. CYTOMEGALO VIRUS(CMV)

34. 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

35.  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.

36.  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.

37. 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)

38. 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.

39. (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

40. 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

41. 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).

42. 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).

43.  -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.

44.  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

45. 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

46. 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.

47. HERPES SIMPLEX VIRUS
(HSV)

48. 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.

49. 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.

50. LESIONSOFNEONATE WITH SEM
DISEASE
50
NECK VESICLES SCALPLESIONS

51. 51
EYEVESICLES
HYPOPIGMENTED,SCALING,AND
CRUSTEDEROSIONSOFTHE
TRUNKAND EXTREMITIES

52. (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

53. (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.

54. 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

55. Tzanck cell

56. 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.

57. 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).

58. 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

59. SYPHILIS

60.  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

61. 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)

64.  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

65. Interstitial Keratitis
Saddle Nose
Hutchinson’s teeth

66. High Arched Palate
Short maxilla

67. 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)

68. 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

69. 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

70. 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

71. 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)

72. VARICELLA(Chicken Pox)

73.  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

74.  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.

75. 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.

76. (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.

78. 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

79.  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

80.  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

81. THANK YOU
81