Hi everyone This presentation explains details about intrauterine infections also called TORCH. Thank you

1.  You are taking care of a term newborn male with birth
weight/length <10th %ile. Physical exam is normal
except for a slightly enlarged liver span. A CBC is
significant for low platelets
 What, if anything, do I worry about?

2. DR ANKIT GUPTA
KIMS KARAD

3.  The original concept of the TORCH perinatal
infections was to group five infections with similar
presentations, including rash and ocular findings
 These five infections are:
 Toxoplasmosis
 Other (syphilis)
 Rubella
 Cytomegalovirus (CMV)
 Herpes simplex virus (HSV)
 Also described as STORCH

4.  VIRUSES
 Varicella, Parvovirus B19,
 Hep B and C, HIV
 Enteroviruses (coxackie)
 BACTERIA
 Listeria, Neisseria
 Mycobacterium tuberculosis, salmonella, campylobater
 PARASITES
 Trepenoma pallidum, plasmodium
 FUNGAL
 Candida

5. ASYMPTOMATIC IN MOTHER
HAVOC IN OFFSPRING

6.  Fetus may get infected
 In utero
 During delivery
 Severity of manifestation depends on gestational age
 Less the age more the morbidity
 May lead to fetal loss or congenital malformations
 Neonate may be even asymptomatic at birth and may
manifest symptoms later anytime during infancy or
even upto first decade of life
 Therefore it is very important to recognize and manage
the neonate at the earliest

7. WRONG CONCEPTS
BASIC NOT CLEAR
UNNECESSARY TREATMENT
IMPROPER MANAGEMENT

8.  COMMON PRESENTATION
1. Premature delivery
2. IUGR or intrauterine death
3. Jaundice, petechia or purpura
4. Hepatosplenomegaly,
anemia,thrombocytopenia
5. Hydrocephaly,
microcephaly,intracranial calcification
6. Chorioretinitis
7. Myocarditis & cardiac abnormalities
 But each infection have its peculiar
presentation and management
 So, very important to differentiate
and identify the particular
infection

9.  DNA virus and a member of the “herpesvirus group”.
 Most common congenital infection
 Severe sequalae 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 and
learning disabilities

10.  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.

11.  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
 Source - Stehel EK and Sanchez PJ. Cytomegalovirus
Infection in the Fetus and Neonate. NeoReviews
2005;6;e38-e45

12. MOSTLY
ASMPTOMATIC

13.  PERIVENTRICULAR CALCIFICATION

14.  BLUEBERRY MUFFIN SPOTS

15.  COTTAGE CHEESE WITH KETCHUP TYPE OF
CHORIORETINITIS
NORMAL ABNORMAL

16.  SENSINEURAL DEAFNESS
 Most commonly seen if infection occurs in first or
second trimester
 Usually progressive, unilateral or bilateral and may even
manifest later in life

17.  ANTIBODY TITRE
 IgG and IgM by ELISA
 Not reliable
 VIRAL DETECTION (GOLD STANDARD)
 Neonatal body fluids – urine, blood, saliva by PCR or
culture within first 3 weeks of life
 NEUROIMAGING
 Cranial Ultrasound or MRI
 OTHERS
 Ophthalmology and audiological evaluation

18.  PREVENTION IS BETTER THAN CURE
 Mother should wash hands before and after handling
the baby
 No donor breast milk
 High chances of transmission through breast milk especially
in preterms
 Mother can continue breast feeding
 Avoid unnecessary blood transfusion

19.  WHEN TO GIVE
 Specific indication
 Chorioretinitis
 Relative indication
 Hepatitis, menigioencephalitis,
 Rx
 Ganciclovir
 Induction - 5mg/kg/dose 12 hourly for 2-3 weeks
 Maintainence – 5mg/kg/dose once daily for 8-10 weeks
 Very toxic – Daily monitoring of blood counts and platelets
 Should be stopped if Neutrophils < 500/mm3 or platelets <
25000/mm3
 May lead to testicular atrophy

20.  Also known as German Measles
 Single stranded RNA virus, member of family
Togavirus, and the genus, Rubivirus
 Vaccine preventable disease
 Effect on fetus
 1st trimester- 80% infection, 90% malformation
 2nd trimester- 25% infection, 30% malformation
 3rd trimester- 100% infection, 10% malformation
 Spontaneous abortions occur in upto 20% of cases if
infection occur within 20 wks of gestation.

21.  MAY BE ASMPTOMATIC
 May present as acute viral illness
 Low grade fever, headache, swollen lymph nodes, joint
pain runny nose and rash
 Contagious one week before and after the rash

22.  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
 HEART
 Congenital malformation in ~ 50% of children infected in first 8
wks of gestation and consist of PDA, Pulmonary artery stenosis

24.  CHORIORETINITIS – Salt and Pepper type

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

26.  PRE-PREGNANCY
 Childhood vaccination – MMR
 Vaccination programs for girls in their teens
 PRE-NATAL
 Routine checkup of rubella immunity status at first visit
 Accidental vaccination in early pregnancy not an
indication of termination

27.  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

28.  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

30.  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

31.  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
 Srabismus, nystagmus and visual impairment

32.  Chorioretinitis – Central destructive type with
involvement of macula

33.  Hydrocephalus

34.  Diffuse cerebral calcification
NORMAL ABNORMAL

35.  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
 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

36.  MOTHER
 SPIRAMYCIN
 2gm/day throughout pregnancy
 After 20 weeks gestation add sulfadiazine and pyrimethamine
 INFANT
 FIRST 6 MONTHS
 Sulfadiazine 100 mg/kg/day in 2 divided doses
 Pyrimethamine 1 mg/kg/day single dose
 NEXT 6 MONTHS
 Same therapy for 1 month alternated with spiramycin for 1 month(100
mg/kg/day in 2 divided doses)
 Precaution
 Sulfadiazine not to be used during 1st week
 Folinic acid (5mg twice weekly) to be given along with
pyrimethamine

37.  CORTICOSTEROIDS
 When toxoplasmosis associated with acute
inflammatory response ( chorioretinitis, raised CSF
proteins etc)
 Given for 8-12 weeks
 Eyes to be examined every 3 months till the age of 18
months and then yearly
 NEITHER MOTHER NOR INFANT IS INFECTIOUS
AND CAN BE HANDLED NORMALLY

38.  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

39. • 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.

40.  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

41.  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

42.  Most asymptomatic at birth
 IUGR – Not common
 Peculiar presentation
 If In utero infection
 SKIN
 Scarring, vesicular lesions
 EYES
 Keratitis, Microophtalmia, conjuctivitis, chorioretinitis
 CNS
 Microcephaly, Menigio-encephalitis, intracranial
calcification(rarely)

43.  If Intrapartum or Postpartum
 DISSEMINATED DISEASE
 Involves multiple organs – liver, lungs, skin, eye, brain etc
 Poor feeding, lethargy, fever, apnea etc
 CNS
 Seizures, lethargy, bulging anterior fontanelle
 DISEASE LIMITED TO SKIN, EYES, OR MOUTH
 Vesicles, or zoster like eruptions

44.  Presentations of congenital HSV
PRESNTATION OF CONGENITAL HSV

45. ENCEPHALITIS CONJUCTIVITIS

46.  Viral cultures
 Cultures obtained from conjunctiva, throat, faeces, urine, nasal
pharynx, and CSF. The virus grows readily, with preliminary results
available in 24-72 h
 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
 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

47.  PREVENTION
 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
 Breast feeding not contraindicated
 Unless active lesions present on breast
 Mother should wash hands before touching the baby
and should avoid kissing the baby

48.  TREATMENT
 ACYCLOVIR – Drug of choice
 Dose – 20 mg/kg/dose 8 hourly
 Disease localized to eyes, skin and mouth
 For 14 days
 Disseminated disease or CNS involvement
 For 21 days
 No serious side effects
 VIDARABINE – Alternative but more side effects
 Prevention and management of complications

49.  Sexually transmitted disease caused by the spirochete,
Treponema pallidum
 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
 As per WHO, in 2009
 2.6 million stillbirths and 3.1 million neonatal deaths
due to congenital syphilis
 Syphilis can cause:
 Preterm delivery
 Stillbirth
 Congenital infection
 Neonatal death

50.  Mostly intrauterine during 16th to 28th weeks but may
occur as 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

51.  If adequate treatment taken
 Mostly asymptomatic at birth
 If untreated may lead to
 Stillbirths
 Hydrops fetalis
 Premature delivery
 May develop symptoms between 3 weeks and 14 weeks
after birth
 Early congenital syphilis – first 2 years
 Late congenital syphilis – after 2 years

52.  MUCOCUTANEOUS
 Snuffles - Blood tinged nasal discharge
 Maculopapular rash 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

53. SNUFFLES AND RASH

54. PERIOSTITISOSTEOCHONDRITIS

55.  MANIFESTATION OF LATE CONGENITAL SYPHILIS
 HUTCHINSON INCISORS
 INTERSTITIAL KERATITIS
 EIGHTH NERVE DEAFNESS

56.  TWO TYPES OF TESTS
 TREPONEMAL
 Fluoresent treponemal antobody absortion (FTA-ABS)
 Traponema pallidum partcile agglutition (TP-PA)
 NON-TREPONEMAL
 Veneral disease research laboratory (VDRL)
 Rapid plasma reagin (RPR)
 Automated reagin test (ART)
 VDRL is performed routinely in mothers during
antenatal visits
 In high risk should be repeated at 28 weeks gestation

57.  Any positive non-treponemal test in mother or infant
must be confirmed with a treponemal test
 Blood, bones and CSF examination in all cases
 A positive VDRL on CSF is diagnostic of neurosyphilis
 To assess disease activity
 Non-treponemal antibodies disappear in unaffected
infants by 6 months of age
 Treponemal antibodies disappear by 15-18 months

58.  Aqueous or crystalline penicillin G
 Dose - 50000 IU/kg/dose
 Duration
 Without evidence of CNS infection – 10-14 days
 With evidence of CNS infection – 21 days
 Dosing
 < 1 week age – 12 hourly
 > 1 week age – 8 hourly
 Patient become non infectious after 24 hours of
therapy

59.  Non Treponemal antibody titer should decline by 3
months and 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

60.  Cause chicken pox – usually a mild disease
 If occurs in pregnancy may cause severe disease in mother
and baby
 Congenital Varicella Syndrome
 Skin scarring, malformed extremities, cataracts and brain
abnormalities
 If disease occurs in mother 5 days before or 2 days after
delivery severe fatal neonatal disease may occur
 Management
 Vaccination of the neonate with varicella vaccine
 Varicella IVIG (25 IU/kg) for passive immunity within 96
hours
 Inj Acyclovir in affected neonates (doubtful utility)

61.  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 aquired
 In utero or during delivery
 Incidence is low due to
 Placenta acts as barrier to the parasite
 IgG antibodies transfer from immune mother
 Resistance of RBC’s containing fetal Hb to parasite

62.  Effect on fetus
 Abortion, still birth, prematurity, low birth weight
 Clinical features in neonate
 Anemia, hepatosplenomegaly, jaundice, refusal to feed
 Treatment
 Oral Chloroquine phosphate
 10 mg/kg loading
 5 mg/kg at 6, 24 and 48 hours
 Intravenous chloroquine unsafe
 Radical therapy with primaquine unnecessary
 In chloroquine resistant oral quinine sulfate
recommended

63.  Tuberculosis continues to be a major health problem
 Congenital tuberculosis is fortunately rare (340 cases)
 Route of transmission
 Pulomonary tuberculosis not a threat to fetus
 Tubercular endometriosis, miliary Tb and genital Tb
 Post natal exposure from infected mother
 Clinical features
 Poor feeding, lethargy, skin papules, jaundice
 Hepatosplenomegaly, lymphadenopathy, tachypnea
 Meningitis or sudden death

64.  Diagnosis
 Mantaux test is usually negative
 Chest X ray may show evidence of miliary Tb
 CSF should be examined for CNS involvement
 Acid fast stains and cultures of gastric aspirate

65.  Treatment
 Rifampicin (10mg/kg/day), pyrizinimide (30mg/kg/day),
isoniazid(INH) (5mg/kg/day)
 Pyrizinimide for first 2 months and rifampicin and
isoniazid for 9- 12 months
 INH should be supplemented with pyridoxine
 Corticosteroids if CNS involvement
 Aminoglycosides for 2 months in HIV infected
newborns
 INH for 3 months in asmptomatic infants of mother
with active Tb

66.  25-35%risk of mother to child transmission(MTCT)
during perinatal period
 30% occur during pregnancy and 70% during labor and
delivery
 Risk of infection through breast milk is 10-15%
 Risk factors
 Advanced disease, high viral load, low CD4 count
 Vaginal delivery, PROM, chorioamnionitis
 Breast feeding

67.  Diagnosis
 ELISA AND WESTERN BLOT MAY BE FALSE POSITIVE
 Because of presence of maternal IgG antibodies
 Persistence beyond 15 months indicate infection
 Early detection can be done by
 HIV specific IgM antibodies
 Viral culture, p24 core anigen
 HIV DNA by PCR

68.  Vertical transmission can be reduced to <2% by
administration of antiretroviral therapy (ART) to
mother
 NEWBORN BABY (NVP prophylaxis)
 <2kg – 2mg/kg
 2-2.5kg – 10mg once daily
 > 2.5 kg – 15mg once daily
 Nevirapine – each ml = 10 mg
 Duration – 6 weeks
 After 6 weeks – Start Clotrimazole prophylactic
therapy

69.  Breastfeeding
 Should be avoided if formula feeding is acceptable,
feasible, affordable, sustainable and safe (AFASS)

70.  SCREENING
 MATERNAL HISTORY
 NEONATAL PRESENTATION
 WHICH CLINICAL INVESTIGATIONS
 WHICH MICROBILOGICAL TESTING

71.  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
 Labour, Delivery, and Postnatal
 If fetal infection suspected
 Blood for serologic investigation
 If fetal infection confirmed
 Careful pediatric assessment and follow up
 SOURCE- Dk james , infection in pregnancy in High Risk Pregnancy Management Option, 4th edition,
elsevier , uk , 2011, pp-556.

72.  ROUTINE SCREENING IN EVERY WOMAN NOT
RECOMMENED
 Cost of the investigations
 Difficult to differentiate between primary infection and
reinfection
 Sensitivity and specificity of the serological test variable
 Create unnecessary confusion and treatment

73. HISTORY INFECTION
EXPOSURE
1. Handling or ingestion of raw meat
2. Contact with diapered children
3. Travel to certain regions
4.Kitten or cat at home
5. No of sexual partners, illicit drug use
6. Unimmunized
Toxoplasmosis
Cytomegalovirus
Tuberculosis, malaria
Toxoplasmosis
Syphilis, herpes simplex, HepB, HIV
Rubella
ILLNESS
1. Rash
2. Arthritis
Syphilis, rubella, parvovirus B19
Rubella
Mononucleosis like fatigue,
lymphadenopathy
Toxoplasmosis, HIV
Screening in pregnancy or previous
history
HBV, rubella, syphilis, HIV
Fetal ultrasonography Variable

74.  GENERAL FEATURES
1. Premature delivery
2. IUGR or intrauterine death
3. Jaundice, petechia or purpura
4. Hepatosplenomegaly, anemia,thrombocytopenia
5. Hydrocephaly, microcephaly,intracranial calcification
6. Chorioretinitis
7. Myocarditis & cardiac abnormalities
With suggestive maternal history
SUSPECT TORCH

75.  CATARCT, MICROPHTALMIA, GLAUCOMA
 CONGENITAL HEART DISEASE
 DEAFNESS
RUBELLA

76.  BLUEBERRY MUFFIN SPOTS
 COTTAGE CHEESE IN KETCHUP
CHORIORETINITIS
 PERIVENTRICULAR CALCIFICATION
CYTOMEGALOVIRUS

77.  HYDROCEPHALUS
 OCULAR DEFECTS
 CENTRALLY DESTRUCTIVE CHORIORETINITIS
 DIFFUSE CEREBRAL CALCIFICATION
TOXOPLASMOSIS

78.  SNUFFLES
 PERIOSTITIS OR OSTEOCHONDRITIS
 KERATITIS
 MACULOPAPULAR RASH
SYPHILLIS

79.  SKIN LESIONS
 CONJUCTIVITIS
 DISSEMINATED DISEASE
HERPES SIMPLEX

80.  PHYSICAL EXAMINATION
 Gestational age, height, weight, head circumference
 Liver/spleen size
 Skin lesions (petechie, purpura, rash etc)
 Ophthalmologic examination (pediatric expert)
 LABORATORY
 Complete blood count and smear with platelet count
 Liver function tests and bilirubin (direct and indirect)
 CSF examination ( as relevant)
 Maternal and infant sera for microbiological testing (
not cord blood)
 Hold pretransfusion blood for additional tests

81.  OTHER INVESTIGATIONS
 Cranial ultrasound, Computed Tomographic (CT) scan
or Magnetic resonance imaging (MRI) as relevant
 Long bone X-rays (if suspecting syphilis or rubella)
 Placenta pathology
 FOLLOW UP
 Audiology assessment
 Serology
 Prevention and management of complications

82. SPECIMEN TESTS INTERPRETATION
Urine Viral culture or detection
(CMV, HSV, Rubella)
For CMV within 3 weeks
should be done. If
positive, diagnostic
Throat swab Viral detection
(CMV, HSV, Rubella)
If positive, diagnostic
Blood Viral detection If positive, diagnostic
Serology of baby and
mother
IgG and IgM antibody
detection
Diffrentiates past and
recent infection
CSF Culture or detection
(CMV, HSV,
toxoplasmosis)
Rubella sepcific IgM
antibody
VDRL
If positive, diagnostic
Nasopharngeal secretions Dark field for T pallidum If positive, diagnostic

83. Skin lesions Culture or detection of
herpes, varicella zoster or
dark field for T pallidum
If positive, diagnostic
Stool Culture for enterovirus If positve, diagnostic
Placenta Patholgy Variable
DETECTION REFERS TO CULTURE OR POLYMERASE CHAIN REACTION

84.  The TORCH test is used to screen pregnant women and
newborns for antibodies to the infectious diseases included
in the panel, if either the mother or new born has
symptoms
 The blood test can determine if the person has had a recent
infection, a past infection, or has never been exposed.
 The test is ordered when a pregnant woman is suspected of
having any of the TORCH infections
 These infections can be serious if they occur during
pregnancy because they can cross the placenta from the
mother to the developing fetus and can cause congenital
defects in the newborn

85.  TEST DONE - ELISA
 Results are usually given as positive or negative, indicating
the presence or absence of IgG and IgM antibodies for each
of the infectious agents tested for with the panel
 A "normal“ result is negative (undetectable) IgM antibody in
the blood of the mother or newborn
 IgM antibodies produced in the mother cannot cross the
placenta, so presence of this type of antibody strongly
suggests an active infection in the infant
 Presence of IgG and absence of IgM antibody in an infant may
reflect passive transfer of maternal antibody to the baby and
does not indicate active infection in that infant

86.  If IgG positive in neonate
 Compare with mother’s IgG titer
 > 4 times indicates recent infection
 Repeat after 3 months
 Same or rising titer indicates recent infection
 Presence of IgM and absence of IgG indicates false
positive

87.  Likewise, the presence of IgM antibody in a pregnant
woman suggests a new infection with the virus or parasite
 Further testing must be done to confirm these results since
IgM antibody may be present for other reasons
 IgG antibody in the pregnant woman may be a sign of past
infection with one of these infectious agents. By testing a
second blood sample drawn two weeks later, the level of
antibody can be compared
 If the second blood draw shows an increase in IgG
antibody, it may indicate a recent infection with the
infectious agent

88.  Acute maternal infection doesn’t imply fetal infection
 Early diagnosis and treatment can make a difference
 TORCH doesn’t cause recurrent abortion
 ELISA is not the only diagnostic test
 All infected neonates should be followed up closely for
delayed sequalae
 Reconfirmation of the positive test must be done from
a reference laboratory
 Counselling is important

89.  PIYUSH GUPTA
 CARE OF THE NEWBORN – MEHERBAN SINGH
 O P GHAI
 VARIOUS SOURCES FROM INTERNET