Intrauterine infection done under the guidance of my mentor Dr Jagadish S .. Presented in my first year of post graduation.

1. Intrauterine Infections
Moderated By: Dr Jagadish S
Presented By: Dr Ravindra G O

3. IUI:Introduction
• Infections occurring during pregnancy can affect the
fetus and newborn. These infections can be caused by
bacteria, viruses or, in rare cases, parasites and are
transmitted directly from the mother to an embryo, fetus
or baby during pregnancy or childbirth.
• Infection can also be transmitted to the baby during
lactation.

4. IUI:Introduction
• The first described intrauterine infection was congenital
rubella syndrome.
• Subsequently infections due to toxoplasma, syphilis,
cytomegalovirus and hepatitis were given the TORCHES
terminology.

5. IUI:Introduction
• The TORCHES CLAP group of infections can be
symptomatic or asymptomatic and picked up during
routine screening. If diagnosed, not all infections can be
treated.
• The infections that can be treated include toxoplasma,
syphilis, herpes and HIV. Treatment during first trimester
poses a special problem as use of medications may not
be safe.

6. IUI:Introduction
• The original TORCHES group of infections has now
expanded to TORCHES CLAP.

7. IUI:Introduction
• In this context the best way to prevent intrauterine
infections is to protect women of reproductive age group.
• Immunization can be given to prevent Rubella, Hepatitis
B , Varicella and screening can be done for HIV,
Hepatitis B and C, Toxoplasmosis, CMV.

8. IUI:mode of transmission
• Infections during pregnancy can result in fetal or
neonatal infection and transmission can occur through
any of the following routes:
• Antepartum (Intrauterine): Transplacental or ascending
from the genital tract.
• Intrapartum: Contact with infected blood, body
secretions during birth.
• Postpartum: Breast feeding or by direct contact.

9. IUI:OUTCOME
Pregnancy outcome following infections can be any one
of the following depending on the timing of infection.
1. Early pregnancy loss
2. Still birth
3. Preterm
4. IUGR
5. Congenital anomalies
6. Congenital infection
7. Neonatal death
8. Cerebral palsy, neurologic sequelae
9. Behavioural problems.

10. IUI:OUTCOME
• Early pregnancy loss is typical of toxoplasmosis.
• Teratogenic effect is seen commonly with CMV, rubella
,chicken pox infections.
• Coxsackie B3 and B4 infections can cause congenital
heart disease.
• Parvovirus infection causes hydrops fetalis.

12. IUI:OUTCOME
Clinical manifestations of
intrauterine infections
include:-
• Growth restriction,
• Hepatosplenomegaly,
• Jaundice,
• Pneumonia,
• Encephalitis,
• Microcephaly (except in
Toxoplasmosis),
• Intracranial calcification,
• Eye and ear involvement.

13. IUI:OUTCOME
Growth Restriction/ IUGR:-
• About 2/3rd –infants with cytomegalic inclusion disease
and rubella, and about 1/3rd infants with congenital
toxoplasmosis manifest Growth retardation.
• Such babies appear hypo plastic rather than
malnourished.

14. IUI:OUTCOME
Hepatomegaly :-
• The incidence of hepatosplenomegaly is similar to that of
intrauterine growth retardation.
• The enlargement of liver and spleen may persists for
weeks or months.
• In infants with no evidence of hepatits ,extramedullary
hematopoiesis appears to be responsible for
hepatosplenomegally.

15. IUI:OUTCOME
Jaundice :-
• may occur any time during the neonatal period. There is
rise of both indirect and direct reacting bilirubin with
elevation of serum ALP and transaminase enzymes.
• Jaundice is relatively uncommon with rubella infection
but is frequent with toxoplasmosis and cytomegalic
inclusion disease.

16. IUI:OUTCOME
Petechiae and Purpura:-
• Thrombocytopenia is common with rubella and
cytomegalic inclusion disease.
• It is relatively infrequent in infants with congenital
toxoplasmosis.

17. IUI:OUTCOME
Meningoencephalitis:-
Microcephaly( rubella, CMV), hydrocephaly
(toxoplasmosis), cerebral calcification , retinopathy,
cataract( rubella) and abnormal neurologic signs occur in
various combination.

18. IUI:OUTCOME
Radiological abnormalities:-
• Intracranial calcification (rubella , toxoplasmosis, CMV),
osteochondritis , osteochondritis, metaphysitis and
periosteal reaction reaction may be seen.

20. CYTOMEGALO VIRUS(CMV)
• DNA virus and a member of the “herpesvirus group”.
• Most common congenital infection.
• Severe sequelae are more common with infection in the
1st trimester, while the overall risk of infection is greatest
in the 3rd trimester.
• Congenital CMV affects about 0.2-2.5% of babies
worldwide.
• Of these, only 1-10% of the babies born with the CMV
infection will have symptoms at birth and another 10-
15% may not show any symptoms at birth, but still may
have long term affects such as hearing loss(MC
sequelae) and learning disabilities.

21. CMV:Transmission
Secreted in all body fluids
Close contact through saliva, blood, genital secretions ,
urine
Neonatal infection
• Intrauterine or transplacental
• Intrapartum – cervical and vaginal secretions
• 2% to 28% of seropositive pregnant women shed CMV
• Approximately 50% of exposed infants become infected
• Develop clinical signs of CMV disease at about 4 to 6
weeks of age.

22. Transmission
• Postpartum period – Breast Feeding
9% to 88% of seropositive women shed CMV into
their milk.
50% to 60% of infants become infected.
• Blood Transfusions
2 -20% from unscreened or unfiltered blood.
Especially preterms are more prone.

23. Clinical features
• IUGR (60-70%)
• Hepatosplenomegaly and Jaundice (2/3rd of cases)
• Petechiae and bleeding (2/3rd of patients):- “blue berry
muffin spots” on skin due to extramedullary
hematopoiesis.
• Ophthalmic signs:- diffuse white perivascular infiltrates
with haemorrhages and necrosis giving an appearance
of “cottage cheese with ketchup” type of peripheral
chorioretinitis with sparing of macula, micro-ophthalmia ,
uveitis and optic atrophy.
• May develop stabismus and roving eyes in infancy.

24. “Blue berry muffin spots”

25. COTTAGE CHEESE WITH KETCHUP TYPE OF
CHORIORETINITIS
NORMAL ABNORMAL

26. Periventricular calcification
• Neurological features:-
microcephaly,
periventricular
calcification(15%) and
psychomotor retardation.
• CNS manifestations may
appear later.
• Others  Anaemia ,
interstitial pneumonia and
Sensorineural
deafness(MC
SEQUELAE).

27. Diagnosis
• ANTIBODY TITRE
IgG and IgM by ELISA
Not reliable
• VIRAL DETECTION (GOLD STANDARD)
Neonatal body fluids – urine, blood, saliva by PCR or
spin enhanced culture within first 3 weeks of life or
“shell vial” or specific IgM florescent antibody by RIA
or ELISA.

28. Diagnosis
• Cytomegalic inclusion cells in baby`s urine.
-paired maternal and cord sera for complement fixing
antibody.
-repeat at 3-4 months of age
• NEUROIMAGING
Cranial Ultrasound or MRI
• OTHERS
Ophthalmology and audiological evaluation

29. Treatment
• Antiviral therapy should be started if there is CNS
involvement or serious end organ disease, like hepatitis,
pneumonia.
• Ganciclovir 6mg/kg/day IV for 6 weeks or oral
Valganciclovir 16mg/kg/day for 6 weeks is the treatment.

30. Prevention
• Vaccine :- provide limited benefit because re-inections
are known to occur in partially immunised people.
• Two live attenuated vaccines (Towne strain, AD-169)

31. RUBELLA
• Also known as German Measles
• Single stranded RNA virus with a lipid envelope, member
of family Togavirus, and the genus, Rubivirus
• Vaccine preventable disease

32. Epidemiology
• Global estimates of congenital rubella syndrome prior
to introduction of Rubella vaccine varied from 0.8 to
4/1000 live births.
• This has reduced to 0.1 to 0.2/1000 live births in the
post-vaccination era and is likely to be eliminated in
many of the developed countries.

33. Epidemiology
• In India, there is no epidemiologic data, but a recent
literature review suggests that CRS is a significant
problem.
• CRS accounts for 10% to 15 % of childhood cataract,
among children suspected to have intrauterine
infections.
• CRS accounts for 1% to 28 % of cases and among
children with mental sub normality CRS accounts for
7.6% to 13 % of children.

34. Epidemiology
• This study also shows that 10% to 30% of adolescent
girls are susceptible to getting rubella infection.
• The seronegativity of women in the child bearing age
has been reported to be 10% to 15%.

35. Transmission
• During pregnancy, rubella virus can directly infect and
replicate in the placenta .
• Effect on fetus
1st trimester- 80% infection,90% malformation(2-10wk)
2nd trimester- 25% infection, 34% malformation
3rd trimester- 100% infection, 0-10%
malformation(>18 wks).
• Spontaneous abortions occur in up to 20% of cases if
infection occur within 20 wks of gestation.

38. Presentation

40. Congenital Rubella Syndrome
• Congenital rubella syndrome presents a classic triad
• EYE
Cataract
Glaucoma
Chorioretinitis
Microphthalmia
• EAR
Sensorineural hearing loss is the most frequent
sequelae -80% of infected children
Bilateral and progressive

41. Congenital Rubella Syndrome
• HEART
Congenital malformation in ~ 50% of children infected
in first 8 wks of gestation and consist of PDA, Pulmonary
artery stenosis

42. CHORIORETINITIS – Salt and
Pepper type

43. Diagnosis
• ANTIBODY TITRE
-IgG and IgM by ELISA
-Reliable
• VIRAL DETECTION
-Pharyngeal secretions, urine, stool, eye discharge,blood
and CSF upto 1 year of age

44. Treatment
• PRE-PREGNANCY
-Childhood vaccination – MMR
-Vaccination programs for girls in their teens
• PRE-NATAL
-Routine check up of rubella immunity status
at first visit
-Accidental vaccination in early pregnancy
not an indication of termination

45. Specific Treatment
• No specific treatment available
• Supportive management can be provided
• Self limiting disease
• Should be nursed in isolation
• Heart defects and cataracts can be corrected surgically,
but damage to CNS is permanent
• Long term follow up important, as some
abnormalities may develop beyond the first decade of
life

46. TOXOPLASMOSIS
• Caused by Toxoplasma gondii –
an obligate intracellular
protozoan parasite.
• Oocyst, excreted in cat feces –
source of infection to humans.
• In patients with an existing HIV
infection, toxoplasmosis is an
important opportunistic
infection with considerable
morbidity and mortality
especially in the pregnant women.

47. Mode of transmission

48. Clinical presentation (In
mothers)
• In most immunocompetent individuals, including children
and pregnant women, the infection goes unnoticed.
• In approximately 10% of the patients it causes a self limiting
illness, most commonly in the 25-35 years age
group.
• Painless lymphadenopathy(Local or Generalised) is the
most common presenting feature. Cervical lymph nodes
are involved in particular. The mesenteric, mediastinal or
the retroperitoneal nodes may also be involved
• Other features include - Malaise, Fever, Fatigue, Muscle
pain, Sore throat and headache.

49. Congenital Toxoplasmosis
• Clinical features vary widely and can manifest at
different times before and after birth.
• Most infected(70-90%) infants are asymptomatic at
birth but up to 80% may develop learning and visual
disabilities later.
• Classic triad is found in < 10%
Chorioretinitis
Intrcranial calcification
Hydrocephalus
• OTHERS
Strabismus, nystagmus and visual impairment.

50. Presentations
• Chorioretinitis – Central destructive type with
involvement of macula

51. Hydrocephalus

52. Diffuse Cerebral Calcification
Normal Abnormal

53. Diagnosis
• SEROLOGY BY ELISA (Enzyme linked immunosorbent
essay) or ISAGA (Immunoglobulin M immunosorbent
agglutination assay)
Positive toxoplasma IgG in infant at 12 months of age
diagnostic (GOLD STANDARD)
Positive IgM or IgA at 5-10 days of life
ISAGA more sensitive than ELISA.

54. Diagnosis
• CSF analysis
Positive T.Gondii specific IgM in CSF fluid diagnostic
Can produce CSF eosinophilia or extremely high
proteins level (> 1000mg/dl)
• PCR
Positive in CSF, blood, or urine is diagnostic

56. Prevention
• Endemic in cat friendly countries unlike INDIA.
• Cats should be handled with gloves, kept indoors and
hand washed after their handling.
• Meat should be eat after thorough cooking.
• Hands should be washed before and after eating.

57. Herpes Simplex
• DNA Virus
• Two type
– HSV 1
– HSV 2
• Type 1 is responsible for most non-genital infections.
However, more than half of new cases of genital herpes in
adolescents and young adults are caused by HSV-1
infection.
• Type 2 HSV is recovered almost exclusively from the genital
tract and is usually transmitted by sexual contact. Most
recurrences—greater than 90 percent—are secondary to
HSV-2.

58. Transmission
• HSV infection of the neonate can be acquired
intrauterine, intrapartum, or postnatal.
• Most infections are acquired in intrapartum (85%)
period as ascending infections with rupture
membranes or by delivery through an infected
cervix or vagina.
• RISK OF DEVELOPING INFECTION
25 % with HSV1
2% with HSV2

59. Presentations(mother)
• MAY BE ASMPTOMATIC
• Most infected women shed virus intermittently, and
most HSV transmission to a partner occurs during
periods of asymptomatic viral shedding.
• Vesicles on genitilia, labia majora, introitus
• Both partners should be treated.

60. Presentation (neonate)
• Most asymptomatic at birth
• IUGR – Not common
• Peculiar presentation
# If In utero infection
1.SKIN
-Scarring, vesicular lesions
2.EYES
-Keratitis, Microophtalmia, conjuctivitis, chorioretinitis.
3.CNS
-Microcephaly, Menigio-encephalitis, intracranial
calcification(rarely)

61. Presentation (neonate)
• If Intrapartum or Postpartum
1.DISSEMINATED DISEASE
-Involves multiple organs – liver, lungs, skin, eye, brain
etc
-Poor feeding, lethargy, fever, apnea etc
2.CNS
-Seizures, lethargy, bulging anterior fontanelle,
rarely intraccranial calcification.
3.DISEASE LIMITED TO SKIN, EYES, OR MOUTH
- Vesicles, or zoster like eruptions, muco-cutaneous
lesions.

63. Clinical Presenatation

64. Clinical Presenatation
Encephalitis Conjuctivitis

65. Diagnosis
• Viral cultures
-Cultures obtained from conjunctiva, throat, faeces,
urine, nasal, pharynx, and CSF. The virus grows
readily, with preliminary results available in 24-72 hrs.
• Immunologic assays
-To detect HSV antigen in lesion scrapings, usually
using monoclonal anti-HSV antibodies in either an
ELISA or fluorescent microscopy assay, are very
specific and 80-90% sensitive.

66. Diagnosis
• Tzanck smear
-Cytological examination of the base of skin vesicles, looking
for characteristic but nonspecific giant cells is only about 50%
sensitive.
• Serologic tests
-Are not helpful in diagnosis of neonatal infection
• Lumbar puncture
-Should be performed in all suspected cases. Evidence of
hemorrhagic CSF with increased white blood cells and
protein may be found.

67. Treatment of a newborn born to a woman with presumed
active genital herpes simplex virus
(HSV) lesions at delivery in the setting of recurrent genital
HSV infection

68. Treatment
INFANTS
• Acyclovir (DOC)
-20 mg/kg/dose given IV Q8H for 10-14days, for disease
localized to eyes, skin, and mouth .
-For the disseminated or CNS infection given for 21
days.
- has no serious side effects.
• Vidarabine –alternate drug, but has more side effects.

69. • PREVENTION
1.If active genital HSV lesions or prodromal symptoms
at the time of delivery
-Cesarean section should be performed
-Preferably within < 4 hours of rupture of membranes
2.Breast feeding not contraindicated
-Unless active lesions present on breast
3.Mother should wash hands before touching the baby
and should avoid kissing the baby.

70. Congenital Syphilis
• Congenital syphilis, a result of fetal infection with the
spirochete Treponema pallidum, remains a major public
health problem worldwide.
• Infants are infected mostly in utero by a transplacental
route or possibly during delivery by contact with a genital
lesion of an infected mother.
• Early congenital syphilis is when clinical manifestation
occurs before 2 years of age.
• late congenital syphilis is when manifestation occurs at
more than 2 years of life.

71. Syphilis can cause:
1.Preterm delivery
2.Stillbirth
3.Congenital infection
4.Neonatal death

72. Epidemiology
• The World Health Organization estimates that globally,
1.5–1.85 million pregnant women are infected with
syphilis annually, and half of them have neonates with
adverse outcomes, such as
-stillbirth or prematurity in 17%–40%,
-congenital infection including nonimmune hydrops fetalis
in 10%–30%, and
-death in 10%–23% .
• The global burden of congenital syphilis is confounded
further by the high prevalence of infection with HIV, as
syphilis is a known risk factor for acquisition of HIV.

73. Transmission
• Mostly intrauterine during 16th to 28th weeks but may
occuras early as 9th weeks
• If mother has untreated primary or secondary syphilis
Risk of fetal infection 100%.
• In late maternal syphilis of more than 2 years Risk of
infection minimal.
• After infection, it takes 10-45 days for blood tests to
become positive So initial negative test does not rule
out infection.

74. Peculiar Presentation
• MUCOCUTANEOUS
1.Snuffles - Blood tinged nasal discharge
2.Maculopapularrash involving palms and soles
• SKELETAL
-Symmetrical long bone lesions
-Osteochondritis – within 5 weeks of infection
-Periostitis - after 16 weeks of infection
• RETICUOENDOTHELIAL
-Generalized non tender lymphadenopathy
-Anemia , leukopenia.

75. Clinical Features

76. Snuffles and Rash

77. Bony Changes
Osteochondritis and Pericondritis

78. Hutchinson Triad
• MANIFESTATION OF LATE CONGENITAL SYPHILIS
HUTCHINSON INCISORS
INTERSTITIAL KERATITIS
EIGHTH NERVE DEAFNESS

79. Diagnosis
TWO TYPES OF TESTS
A.TREPONEMAL
1.Fluoresent treponemal antobody absortion (FTA-ABS)
2.Traponema pallidum partcile agglutition (TP-PA)
3. Treponemal enzyme immunoassay (EIA)
4. Chemiluminescence immunoassay(CIA)
B.NON-TREPONEMAL
1.Veneral disease research laboratory (VDRL)
2.Rapid plasma reagin (RPR)
3.Automated reagin test (ART)

80. Diagnosis
• VDRL is performed routinely in mothers during antenatal
visits .
• In high risk should be repeated at 28 weeks gestation.
• Any positive non-treponemal test in mother or infant
must be confirmed with a treponemal test.
• Blood, bones and CSF examination in all cases.
• To assess disease activity
Non-treponemal antibodies disappear in unaffected
infants by 6 months of age
Treponemal antibodies disappear by 15-18 months.

81. Diagnosis
• A positive VDRL on CSF is diagnostic of neurosyphilis
-CSF
a. Pleocytosis (more than 18–25 white blood cells per
microliter), and
b. Elevated protein content (>150 mg/dL; >170 mg/dL if
infant is premature).
• However, a reactive CSF VDRL test result in neonates
may be caused by passive transfer of non-treponemal
IgG antibodies from serum into the CSF.

83. Treatment
1. Aqueous penicillin G 50,000 U/kg IV every 12h (1 week
of age), q8 hr (>1 week) or procaine penicillin G 50,000
U/kg IM single daily dose, x 10 days
2.Benzathine penicillin G 50,000 U/kg IM x 1 dose

84. Recommended Treatment for
Syphilis During Pregnancy

85. Recommended Treatment of the Neonate (≤28
Days Old) With Syphilis

86. Follow Up
• Non Treponemal antibody titer should decline by 3
monthsand become negative by 6 months
-If raised at 3 months or positive at 6 months-
Retreatment.
• Infant with neurosyphilis should be followed with CSF
examination every 6 months for 3 years or until cell
count is normal
-If CSF count still elevated at 6 months or VDRL in CSF
is positive – Retreatment.

87. Prevention
• Congenital syphilis is effectively prevented by prenatal
serologic screening of mothers and penicillin treatment
of infected women, their sexual partners, and their
newborns .
• In all pregnant women a serologic test for syphilis should
be performed at the first prenatal visit in the first
trimester, with the test being repeated at 28–32 weeks’
gestation and at delivery in areas with a high incidence
of syphilis.
• All cases of syphilis must be reported to the local public
health department, which performs contact investigation
and identifies core environments and populations.

88. Congenital Malaria
• Caused by Plasmodium
• Defined as presence of malarial parasites (ring forms) in
the peripheral smear of the newborn within 7 days of life
-May be acquired
-In utero or during delivery
• Incidence is low due to
1.Placenta acts as barrier to the parasite
2.IgG antibodies transfer from immune mother
3.Resistance of RBC’s containing fetal Hb to parasite

89. • Two key features play a critical role in the pathogenesis
and natural history of congenital malaria:
1. Maternal and placental parasitemia.
2. Existence of correlation between umbilical cord
parasitemia and neonatal parasitemia.
• Pregnancy itself increases the risk of severe malaria,
resulting maternal– fetal detriment.
• Malaria also increases the risk of adverse pregnancy
outcomes, including prematurity, abortion, and stillbirth.

90. • Malaria in pregnancy also has potentially devastating
effects on the fetus and newborn, including spontaneous
abortion, stillbirth, premature delivery, congenital
infection, low birth weight and neonatal death.
• The most significant consequence of pregnancy-
associated malaria is maternal anemia.
• Clinical features in neonate
- Anemia, hepatosplenomegaly, jaundice, refusal to feed.

91. • Fever (86%)
• Anaemia (36%)
• Splenomegaly (31%)
• Hepatomegaly (20%)
• Thrombocytopenia(15%)
• Jaundice (14%)
• Irritability (10%)
• Anorexia,
• Vomiting,
• Cough , Diarrhea, Lethargy, Hemolysis , Pallor,
• Hyperbilirubinemia ,
• Failure to thrive ,Seizures ,Dyspnea ,Purpura ,Tachycardia
,Monocytosis

92. Diagnosis
1. Diagnostic tests for malaria include
• blood smears,
• rapid antigen detection tests, and PCR.
2. Definitive diagnosis of congenital malaria
is based on the microscopic demonstration of parasites
on stained thick and thin blood films.
3. Rapid diagnostic tests (RDTs) are based on the
immunochromatographic detection of parasite-specific
antigens circulating in the bloodstream.

93. Treatment
• The treatment of patients with malaria consists of
supportive care and antimalarial therapy.
• The treatment regimen is based on the infecting species,
the possibility of drug resistance, and the severity of the
disease.
For mild infections caused by P. vivax, P. ovale and
P. malariae or chloroquine-sensitive P. falciparum
- chloroquine orally (10 mg base/kg initially followed by 5
mg base/kg 6, 24, and 48 hours later)
- Treatment with Primaquine is not necessary .

94. Treatment
• Severe malaria occurs most commonly with P.
falciparum infection and is characterized by one or more
of the following:
(1) parasitemia with more than 5% of red blood cells
infected,
(2) CNS or other end-organ involvement,
(3) shock,
(4) acidosis,
(5) severe anaemia, or
(6) hypoglycemia

95. Treatment
Management of severe malaria involves
1. Parenteral treatment in an intensive care setting.
2. Until recently the only parenteral therapy available in
the United States was quinidine gluconate therapy.
Quinidine is more cardiotoxic than quinine and should
be administered with continuous cardiac monitoring.
3. Artesunates can be given either intravenously or
intramuscularly for 24 hours until oral medication can be
tolerated, at which time combination therapy should be
instituted.
4. Exchange transfusion may be warranted when more
than 10% of red blood cells are infected or if there are
complications at lower parasite densities.

96. Prevention
• The prevention of congenital malaria is based on a
pregnant woman’s avoidance of exposure and use of
chemoprophylaxis.
• The World Health Organization has proposed a three
pronged approach:
(1) Long-lasting insecticidal nets,
(2) Intermittent preventive treatment with an effective
antimalarial agent in pregnancy, and
(3) Prompt diagnosis and effective treatment of malaria
infection.

97. • It has been suggested that neonates born to mothers
with parasitemia at delivery should be treated
presumptively for congenital malaria.

98. Congenital Tuberculosis
• Transmission of M. tuberculosis from the mother to the
neonate can occur
-In utero,
-During birth, or
-After birth.
• The term congenital tuberculosis has historically referred
to infection acquired either in utero or during birth..

99. Congenital Tuberculosis
Congenital TB is transmitted in one of three ways:
1. Haematogenous spread from the infected placenta via the
umbilical vein,
2. In utero aspiration or ingestion of amniotic fluid infected from
the placenta or endometrium, or
3. Ingestion of infected amniotic fluid or secretions from
maternal genital lesions during delivery.
• Postnatal acquisition of M. tuberculosis acquired by airborne
inoculation, either from the mother or from another contagious
adult in the newborn’s environment, is the most common
route of infection of the neonate.
• In addition, postnatal infection can occur from ingestion
of infected breast milk from a mother with a tuberculous breast
abscess.

100. Congenital Tuberculosis
• The criteria required that the infant have proven TB
lesions and one of the following(older) :-
(1) Primary hepatic complex as evidence of dissemination
of the tubercle bacilli via the umbilical vein or
(2) In the absence of a primary complex, the presence of
tuberculous lesions in the first few days of life or the
exclusion of postnatal infection by separation of the
neonate at birth from the mother and other potential
sources of infection.

101. Congenital Tuberculosis
Revised set of diagnostic criteria that became more
applicable to current practice with increased diagnostic
sensitivity.
The neonate must have proven tuberculous lesions
and at least one of the following:
(1) lesions in the first week after birth,
(2) a primary hepatic complex or caseating hepatic
granulomas,
(3) tuberculous infection of the placenta or maternal
genital tract, or
(4) exclusion or postnatal transmission by thorough
investigation of contacts.

102. Congenital Tuberculosis
Complications from TB during pregnancy include
• Stillbirth,
• Recurrent abortion, and
• Infertility.
 The manifestations of the disease resemble those of
neonatal sepsis or other congenital infections.
 The affected neonate is commonly born prematurely.
 Clinical signs may be evident shortly after birth but
typically do not appear until 2–4 weeks of age.

103. Clinical manifestations
• Before the availability of INH, congenital TB was almost
uniformly fatal. Notable signs included failure to thrive,
jaundice , and CNS involvement.
• In the post-INH era, the most commonly described
features of the disease are respiratory distress,
hepatomegaly with or without splenomegaly, and fever.
• Otitis media with aural discharge has been described as
the presenting sign of congenital TB accompanied by
regional lymphadenopathy or facial palsy.

104. Clinical manifestations
• Cutaneous manifestations of congenital TB include
papular, pustular, or vesicular lesions often surrounded
by erythema.

108. Approach to TORCH
• SCREENING
• MATERNAL HISTORY
• NEONATAL PRESENTATION
• WHICH CLINICAL INVESTIGATIONS
• WHICH MICROBILOGICAL TESTING

109. Screening
If suspected exposure in women or with clinical manifestations
• Confirm presence of TORCH specific IgG
• Confirm failure of appearance of IgM
• Reassure patient.
 If maternal infection confirmed serologically
Early Pregnancy
-Termination should be discussed
Late Pregnancy
-Confirmation of fetal infection by invasive procedures
-Fetal growth and well being monitored if infection suspected or
confirmed

110. Screening
Labour, Delivery, and Postnatal
If fetal infection suspected
Blood for serologic investigation
If fetal infection confirmed
Careful pediatric assessment and follow up .

111. Maternal History

114. Relative importance of neonatal viral infections related to the
timing of acquisition of infection.
Viruses are listed in declining relative order of importance
relative to prenatal, perinatal (intrapartum), and
postnatal timing of typical infection.

116. Reference
• INDIAN JOURNAL OF PRACTICAL PEDIATRICS ;
Swarnarekha Bhat; Vol.16 No.3; JUL.- SEP. 2014
• Viral Infections of the Fetus and Newborn;MARK R.
SCHLEISS AND KETZELA J. MARSH; Avery’s Diseases
of the Newborn;10th;2018
• ssss