Primary maternal syphilis infection can infect the fetus in utero. Without treatment, fetal infection risks include stillbirth, premature birth, low birthweight, and neonatal death. Fetal infection may also cause deformities of the nose, long bones, and teeth. Diagnosis involves maternal and fetal serology, with treatment of pregnant women and neonates with penicillin to prevent transmission and morbidity.

1. PERINATAL INFECTIONS
DR.SNEHAL PALLOD
DNB PEDIATRICS

2. INTRODUCTION
• Important cause of still births and
morbidity
• Many diseases go undiagnosed
• Appropriate treatment can prevent
morbidity/mortality
• 1971: Andres Nahmias proposed
acronym ToRCH
• 1975: Harold Fuerst added Syphilis to
the acronym

3. ACRONYM:TORCHES CLAP
Toxoplasmosis
Other
(Syphilis,Varicella Zoster,
ParvovirusB- 19, HEP B)
Chickenpox
Rubella Lyme disease
CMV AIDS
Herpes simplex Parvovirus B19
Enterovirus
Syphilis
• Latest addition: Zika virus

4. Toxoplasma
 Toxoplasmosis is a disease caused by an
intracellular parasite TOXOPLASMAGONDII.
 Human acquisition of the infection occurs by:
Oocyst contaminated soil,salads,vegetables.
 Ingestion of raw or undercooked meat
containing tissue cysts (Sheep,pigs and
rabbits are the most common meat sources).
 Out breaks of toxoplasmosis have also been
linked to the consumption of unfiltered wate

6.  Primary maternal infection in
pregnancy–
- Infection rate higher with infection
in 3rd trimester.
- Fetal death higher with infection
in 1st trimester

7. Signs and sympoms
 Infected Pregnant women : usually no
clinical manifestation.
 Although some may have a mild
mononucleosis-like syndrome,
regional lymphadenopathy, or
occasionally chorioretinitis.
 Similarly, infected neonates are
usually asymptomatic at birth.

8. The classic triad of findings :
 chorioretinitis,
 hydrocephalus, and
 intracranial calcifications

10. Diagnosis
 Serial IgG measurement (for maternal
infection
 Amniotic fluid PCR (for fetal infection)
 Serologic testing, brain imaging, CSF
analysis and ophthalmologic
evaluation (for neonatal infection),
and
 PCR testing of various body fluids or
tissues

12. Treatment
•In PREGNANT WOMEN
with an established recent infection,
SPIRAMYCIN (3g daily in divided doses)
should be given.
 In neonates :
Pyrimethamine: 50mg twice daily for 2 days
then 50mg daily. PLUS Sulfadiazine:
75mg/kg/daily in two divided doses for 2 days
then 50mg/kg/twice daily PLUS Folinic Acid:
10-20mg daily

13. Prevention- counselling
 Avoid raw/undercooked meat
 wash hands after gardening
 wash raw vegetables
 minimise contact with young kittens
and their litter

14. RUBELLA

15.  It is caused by rubella virus,Rubivirus genus
and familyTogaviridae.
 Intrauterine infection with rubella virus is
referred to as congenital rubella infection
(CRI) or syndrome.
 Infection with rubella earlier in
pregnancy(1st trimester ) cause worse
prognosis and neonatal complications.
 The virus can be transmitted to the fetus
through the placenta and is capable of
causing serious congenital defects,
abortions, and stillbirth

16.  In the baby
Infection in weeks 8-10 of pregnancy
results in damage in up to 90% of
surviving infants. Multiple defects are
then common.
 The risk of damage reduces to 10-
20% if the infection is in weeks 11-16
of pregnancy.
 Fetal damage is rare over 18 weeks
of gestation.

17.  Transmission to the fetus occurs via
maternal hematogenous spread to the
placenta.
 It typically occurs 5-7 days after
maternal inoculation.
 After the virus invades the placental
barrier, it spreads throughout the fetus
via their vascular system.
 The congenital defects that result from
infection is secondary to the cytopathical
damage ensued to the blood vessels.
 This in turn results in ischemia of the
affected organs

18. Clinical features
 Transient : Intrauterine growth restriction.
Thrombocytopenic purpura (25% - 'blueberry skin').
Haemolytic anaemia.
Hepatosplenomegaly.
Jaundice (common).
Radiolucent bone disease (20%).
Meningoencephalitis (25%) +/- neurological sequelae
 Developmental: Sensorineural deafness 80% .
General learning disability (55%).
Insulin-dependent diabetes (20%,)
'Late-onset' disease at 3-12 months with rash, diarrhoea,
pneumonitis and high mortality.
 Permanent: Congenital heart disease (commonly patent ductus arteriosus or
pulmon ary artery stenosis).
Eye defects ( cataracts, congenital glaucoma, pigmentary
retinopathyand called 'salt and pepper'),
severe myopia,
microphthalmia.
Microcephaly.

20.  The risk of maternal-fetal
transmission is the greatest in the
first 10 days after gestation
 cardiac and eye defects typically
resulting when maternal infection
occurs prior to 8 week.
 Hearing loss is typically observed in
infections up to 18 weeks of gestation

21. DIAGNOSIS
 Isolation of the rubella virus in culture
 Demonstration of rubella-specific IgM
antibodies
 Demonstration of rubella-specific IgG
antibodies that persist at a higher
concentration or longer duration than
expected from mere passive transfer of
maternal antibodies
 Detection of rubella virus RNA by reverse-
transcriptase polymerase chain reaction in
nasopharyngeal swabs, urine, CSF, and
blood at birth
 Avidity testing of IgG

22.  Avidity:
 Strength with which IgG
binds to antigenic epitropes
expressed by a specific
protein.
 Gradually matures over
months.
 IgG produced in first few
months following primary
infection Low avidity (Bind
weakly to Ag)
 Therefore, LOW IgG avidity
is a marker of RECENT
PRIMARY infection.
 High avidity excludes
primary infection in
preceding 3 months.

23.  Treatment
 Supportive care and surveillance is the
only recommended option available at this
time.
 Close monitoring within the first 6 to 12
months of life is recommended; particularly
for the evaluation of hearing impairment .
 Prevention .
Preventive measures include recommended
immunizations, testing of pregnant women for
rubella immunity and proper counseling
regarding avoiding exposure

24. CYTOMEGALOVIRUS

25.  CMV is a doubles stranded DNA herpes virus
 The most common congenital viral infection.
 The CMV seropositivity rate increases with age.
 Geographic location, socioeconomic class, and
work exposure are other factors that influence the
risk of infection.
 CMV infection requires intimate contact through
saliva,urine, and/ or other body fluids.
 Possible routes of transmission include
1. sexual contact, 2. organ transplantation,
3.transplacental transmission,
4. transmission via breastmilk,and
5.blood transfusion(rare)

26.  Primary,reactivation,or recurrent CMV infection can occur in
pregnancy and can lead to congenital CMV infection.
 Approximately 85 percent of newborns with congenital CMV
infection can be asymptomatic at birth.
 15 percent will develop progressive hearing loss and visual
impairment as they age.
 Transplacental infection can result in :
 intrauterine growth restriction
 Sensorineural hearing loss,
 Intracranial calcifications
 Petichiae
 Jaudice
 microcephaly,
 hydrocephalus
 hepatosplenomegaly,
 Delayed psychomotor development,
 Thrombocytopenia and/
 Chorioretinitis

27.  Vertical transmission of CMV can occur at
any stage of pregnancy.
 Severe sequelae are more common
with infection in the 1st trimester.
 The overall risk of infection is greatest
in the 3rd trimester.
 The risk of transmission to the fetus in
primary infection is 30%-40%

28. Diagnosis :
• Virus culture from
urine/saliva
• CMV-DNA PCR in
urine, blood, saliva
and CSF
• CMV IgM antibodies
in blood before 3
weeks of age.
• IgG Avidity testing

29. Treatment
 Ganciclovir 5mg/kg IV every 12
hours for 14 days OR
 Valganciclovir 900mg PO daily for 3-
6 months OR
 CMV-specific hyperimmune globulin
(200 units/kg of body weight)
Foscarnet, Cidofovir for refractory CMV/
Ganciclovir resistance

31. HERPES SIMPLEX VIRUS

32.  Herpes simplex virus (HSV) infection during
pregnancy can pose a serious threat to the
developing fetus and the newborn infant.
 Transmission typically occurs via direct
contact between the neonate and an infected
maternal genital tract.
 If the primary HSV infection was acquired
during pregnancy, then the risk of
transmission is greater as compared with
reactivation of a previous infection.
 incidence of neonatal HSV infection ranges
from 1 in 3200 to 1 in 10,000 births .

33.  HSV is a member of the Herpes viridae family of
viruses
 Enters the host through the inoculation of oral,
genital, or conjunctival mucosa.
 Inoculation also can occur through breaks in the
skin.
 Dissemination of the virus eventually allows the
virus to reach the dorsal root ganglia, where it
remains dormant for the rest of the host’s life.
 Antiviral drugs do not affect latent HSV infection
and therefore infection is life-long
 Intrauterine HSV is a rare occurrence and most
likely is caused by maternal viremia associated
with primary infection during pregnancy.

34.  Intrauterine infection is associated with
 hydropsfetalis and
 in-utero fetal demise.
 The characteristic triad noted at birth includes
 skin lesions consistent of vesicles,
 ulcerations or scarring ,
 eye damage and
 CNS abnormalities, such as hydranencephaly
and microcephaly.
 Clinical manifestation can arise any time during
the first six weeks of life, but usually occurs within
the first month of life

36. Diagnosis
 Isolation of HSV in culture
 Detection of DNA via PCR assays
 Detection of HSV specific antigens using rapid direct
immunofluorescence or enzyme immunoassays.
 Classic CSF findings include :
a mononuclear cell pleocytosis,
normal or slightly low glucose concentration
and moderately elevated protein level.
 Electroencephalogram (EEG) is often abnormal from
early on in the disease and may show focal or multifocal
periodic epileptic form discharges .
 Neuroimaging studies may show parenchymal brain
edema, hemorrhage or destructive lesions in the
temporal frontal, parietal or brainstem regions in the
brain

38.  After completion of parenteral therapy
suppressive course of oral acyclovir for 6
months
 PREVENTION
• 85% neonatal HSV are acquired
perinatally.
• True intrauterine infection 5%
• Careful speculum examination for active
genital HSV
• Caesarean section reduces risk of HSV
transmission

39. SYPHILIS

40.  Infant usually infected in utero by
transplacental passage of Treponema
pallidum from infected mother at any time.
 Infection may also occur from contact with an
infectious lesion during passage through the
birth canal
 It remains unclear what factors determine
which mothers, particularly those in the latent
stage, will pass the disease to the fetuses.
Also unclear why some infants, infected in
utero, are born asymptomatic, but develop
overt dz. In first few wks./mo.

41.  Infection can be transmitted to fetus at any
stage of disease.
Rate of infection 60% - 100% during
second stage.
Transmission rates slowly decreases
with increasing duration of the disease.
 Women, untreated early syphilis: 40% of
pregnancies result in spontaneous
abortion, stillbirth, or perinatal death.

42. Clinical Manifestations
 Damage to fetus depends on the stage of
development at which infection has taken place
and time elapsed before treatment.
a. Early infection, untreated: miscarriage, stillbirth,
neonatal death, IUGR, premature delivery.
a. Survivors :
Early congenital syphilis : clinical manifestations
within first 2 years of life
Late congenital syphilis : clinical manifestations
after 2yo

43. EARLY CONGENITAL SYPHILIS
Early manifestations are varied, with multi-system Involvement
 Hepatosplenomegaly-
diffuse inflammation, scarring
 Jaundice – due to hepatitis
 Generalized
lymphadenopathy –
epitrochclear nodes
 Coombs – hemolytic
anemia, thromobocytopenia,
leukopenia, leukocytosis
 Hydrops fetalis
 Mucocutaneous: rhinitis
(highly infectious) ,
“snuffles”, mucous
patches
 Macuolpapular rash
 Desquamation
 Pemphigus syphiliticus
(vesicular bullous eruptions of
palms and soles)
 Petechial lesions
 Bony lesions,
osteochondritis, periostitis,
pseudoparalysis
 Syphilitc leptomeningitis
 Chorioretinitis, salt and
pepper fundus, glaucoma
 Pancreatitis

45. LATE CONGENITAL SYPHILIS
Results primarily from chronic inflammation of bone, teeth,
and CNS.
 Interstitial keratitis
(inflammatory)
 Nerve deafness
 Clutton’s Joints (synositis,
restricted movement)
 Hutchinson’s triad (teeth,
intersitial keratitis, 8 th nerve
deafness)
 Mulberry molars
 Flaring scapulas
 Hydrocephalus
 Mental retardation
 Frontal bossing
 Saddle nose
 Protruding mandible ,High
arched palate ,Perioral
fissures
 Saber shins Anterior bowing of
tibias
 Rhagades (linear scars that
become fissured or ulcerated)
 Hutchinson’s teeth – peg
shaped upper incisors
 Frontal Bossing
 Gumma: Thin atrophic scar

46. Diagnosis :
• Adequacy of maternal treatment
• Examination of placenta/umbilical cord for pathology
• Dark field microscopy of suspicious lesions/body fluid
• Clinical findings suggestive of syphilis: Non immune
hydrops/ jaundice/hepatosplenomegaly/ rhinitis/ skin
rash
• Quantitative
Nontreponemal test: VDRL, RPR
Quantitative results correlate with disease activity,
therefore helpful in screening.
Titers rise when disease is active, fall when treatment is
adequate
These tests become non- reactive within a few months of
adequate treatment.
Treponemal tests: TPI, FTA-ABS, MHA-TP

47.  Infant Testing Reactive serology in neonate could
be due to IgG passively transferred to newborn
through placenta, and does not indicate active
infection.
 If infant’s titer higher than mother’s congenital
infection
 If decreasing titer in infant passive transfer of
antibodies,
should disappear by 3-4 months of age.
 Persistently reactive VDRL, with rising titer
Active Infection

48. Treatment
 Aqueous crystalline Penicillin G
100,000-150,000U/kg/day (given q8-
q12hrs) IV for 10 days
OR
 Procaine Penicillin G 50,000 U/kg/day
IM for 10days
 If >1 day of therapy missed, entire
course should be restarted

49. CASE SCENARIO S
1.PHYSICAL EXAM
SUGGESTIVE OF
CONGENITAL SYPHILIS
BABY’S VDRL/RPR 4
TIMES HIGHER TITRE
THAN MOTHER
MOTHER NOT
TREATED OR
INADEQUATELY
TREATED
2. PHYSICAL EXAM
NORMAL BABY’S
VDRL/RPR MORE
THAN 4 TIMES
MOTHER’S TITRE
MOTHER NOT TREATED
OR INADEQUATELY
TREATED
 ADDL TESTS: CSF VDRL, LONG BONE
XRAY, OPHTHAL EVALUATION, BERA
 INJ. PENICILLIN G OR PROCAINE
PENICIILIN FOR 10 DAYS
 INJ. PENICILLIN G OR PROCAINE
PENICIILIN FOR 10 DAYS

50. CASE SCENARIO S
3. PHYSICAL EXAM
NORMAL BABY’S
VDRL/RPR LESS THAN 4
TIMES MOTHER’S TITRE
MOTHER NOT TREATED
OR INADEQUATELY
TREATED Syphilis:
4. PHYSICAL EXAM
NORMAL BABY’S
VDRL/RPR LESS THAN 4
TIMES MOTHER’S TITRE
MOTHER ADEQUATELY
TREATED DURING
PREGNANCY
 ADDL TESTS: CSF VDRL,
LONG BONE XRA
 INJ. BENZATHINE PENICILLIN
50000 U/Kg/dose IM SINGLE DOSE
 NO TREATMENT REQUIRED IF
FOLLOW-UP IS CERTAIN ELSE,
INJ. BENZATHINE PENICILLIN
50000 U/Kg/dose IM SINGLE DOSE
NO FURTHER EVALUATION

51. VARICELLA

52.  Neonatal Varicella Infants whose mothers
demonstrate varicella in the period from 5
days prior to delivery to 2 days afterward are
at high risk for severe varicella.
• The infant acquires the infection
transplacentally
• The infant's rash usually occurs toward the
end of the 1st week to the early part of the
2nd week of life
• maternal immunoglobulin G (IgG) is able to
cross the placenta if delivery occurs after 30
wk of gestation

53. Clinical manifestations
1.Congenital varicella syndrome.
include cicatricial skin lesions, ocular defects,limb
abnormalities, CNS abnormalities, IUGR, and fetal demise
or early death.
• The syndrome most commonly occurs with maternal VZV
infection between weeks 7 and 20 of gestation
2. Zoster.
 Zoster is uncommon in young infants but may occur as a
consequence of in utero fetal infection with VZV.
 usually self-limiting, with only symptomatic therapy indicated
in otherwise healthy children.
3.Postnatal varicella.
 mild disease likely due to the presence of maternal antibodies
against the virus.
 Rarely, severe disseminated disease occurs in newborns
exposed shortly after birth following an acute maternal
infection.

56. DIAGNOSIS
 clinical findings and maternal history
 culture of vesicular fluid,
 VZV antibody titer by the fluorescent
antibody to membrane antigen assay
or by ELISA;
 antigen detected from cells at the
base of a vesicle By
immunofluorescent antibody or PCR
detection.

57. TREATMENT
+3-7 -5-6 -4 -3 -2 -1 +1 +2 +4
Newborn will have
protective antibodies
 Likelihood of severe
disease is low
 Do not separate baby
from mother
 Continue breast
feeding
 No VZIG
Acyclovir if baby
develops rash
Newborn will not
have protective
antibodies
Likelihood of severe
disease is high
Separate baby from
mother
 If baby devps rash
stay with mother
VZIG within 72 hours
Acyclovir
 Newborn will not
have protective
antibodies
 But, likelihood of
severe disease is
low
 Separate baby
from mother
 f baby devps
rash stay with
mother
 No VZIG
 Acyclovir if baby
develops ras

58. HEPATITIS

59.  HBV infection during late pregnancy
or near the time of delivery,
however,may result in up to 90%
transmission rate in the absence of
any prophylaxis and is most common
in women who have both HBsAg and
HBeAg detected in blood, indicating
high plasma HBV DNA level.

60.  Risk of vertical transmission
mother
HBsAG +VE BUT HBeAg –VE: 5-20%
HBsAg +ve and HBeAg +ve: 70-90%
• No contraindication for breast feeding
• Hepatitis B vaccine : 90% active immunity
HBIG: additional 5- 10% immunity
• 90% of infected infants become chronic
cases

61. NEONATE BORN TO MOTHER WITH HEPATITIS B
(prenatal testing of all pregnant womens for HBsAG is
recommanded
At birth : Hepatitis B vaccine with HBIG(200 IU IM)
(Perferably within 12 hrs bt not after 48 to 72 hrs)
FOLLOWUP: complete HBV immunization as per schedule
3 dose schedule
Infants<2kg: do not count birth dose and give 3 more dose
Infants>2kg:give total 3 doses
FOLLOW UP TESTING DONE AT 9 TO 18 MONTHS OF AGE FOR
ANTI-HBs and HbsAg

62. FOLLOWUP AT 9 TO 18
MONTHS
Infants with
anti-HB>/10mIU/ml
and HBsAG neg
IMMUNE
NO ACTION
REQUIRED
Infants with
anti HB<10mIU/ml
and HBsAG neg
NO HBV
INFECTION
BUT FAIL TO
RESPOND TO
IMMUNIZATION
REVACCINATION(
3 DOSES)
Infants with
Anti HBs neg
And HBsAG
positive
HBV INFECTION
FOLLOWUP

63. CONGENITAL MALARIA

64.  Malaria during neonatal period occurs
due to administration of infected
blood.
 It appears that placenta act as barrier
to malarial paracite and its
transplacental transmission if futher
blocked if mother is immune.
 Placental malaria is asymptomatic and
it silently causes fetal wasting

65.  Matarnal malaria causes severe anemianand
adversly affect placental circulation interfering
with nutrition and oxygenation--- Leading to
abortion, still birth, prematurity , fetal growth
retardation and neonatal deaths
 Fetal infection occures due to direct
penetration of paracite through chorionic villi,
premature separation of placenta,
maternofetal transfusion during delivery
 Disease manifests around 2-8 weeks with
Fever reticulocytosis
Jaundice thrombocytosis
Hemolytic anemia Hs megaly

66. TREATMENT
 Oral administration
chloroquine 10mg/kg followed by 5mg/kg at 6,24
&48 hrs
(IM injections is unsafe risk of seizures)
• Radical therapy with primaquine is unnessesary as
congenital malaria is form of transfusion malaria
and it has no exoerythrocytic phase
 Chloroquine resistant malaria
oral quinine sulfate 25mg/kg 8th hrly for 3-5 days

67. TUBERCULOSIS

68. • Women with pulmonary TB do not pose any treat to
fetus but may infect after birth
• Congenital TB may occur if mother having
tubercular endometriosis, miliary TB, or placenta
affected by tubercular bacilli.
 Infection may transmit to fetus through umbilical
vein or by aspiration at time of birthInfant may born
with active disease or symptoms may appear in
first 8 weeks of life
 Present with
Features of miliary TB HS megally
LN pathy Tachypnea
Fever Lethargic
Poor feeding Skin papules
Jaundice

70.  Reassure the mother to breast feed the
baby
 Separation of mother & baby required
only if mother –
is sick
 non adherent to treatment
has MDR TB
• BCG vaccination after completion of INH
course