2. AN OVERVIEW OF TORCH INFECTIONS
THE TORCH COMPLEX
TORCH complex is a medical acronym for a set of
perinatal infections (i.e. infections that are passed from a
pregnant woman to her fetus). The TORCH infections can
lead to severe fetal anomalies or even fetal loss. They are
a group of viral, bacterial, and protozoan infections that
gain access to the fetal bloodstream transplacentally via
the chrionic villi. Hematogenous transmission may occur
at any time during gestation or occasionally at the time of
delivery via maternal-to-fetal transfusion.

3. The capitalization "TORCH” consists of :
T – TOXOPLASMOSIS
O – Other infections (Syphilis, Varicella Zoster, Parvovirus B-19, Listerosis & Coxsackie Virus)
R – RUBELLA
C – CYTOMEGALOVIRUS
H – HERPES SIMPLEX VIRUS – 2
Hepatitis B may also be included among "other infections",
but the hepatitis B virus is a large virus and does not cross
the placenta, hence it cannot infect the fetus unless there
have been breaks in the maternal-fetal barrier, such as
can occur in bleeding during childbirth or amniocentesis.

4. TOXOPLASMOSIS
Toxoplasmosis is a disease caused by an intracellular
parasite TOXOPLASMA GONDII.
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).
•Outbreaks of toxoplasmosis have also been linked to the
consumption of unfiltered water.

6. •Sera from randomly selected 345 pregnant Nepalese women
aged 16-36 years and 13 women with bad obstetric history
(BOH) were tested for the presence of Toxoplasma antibodies
using microlatex agglutination (MLA) and ELISA methods.
•The overall prevalence was 55.4% (191/345).
•Prevalence was slightly higher (59.0%) in older age-group
(27- 36 years) compared with younger age-group (16-26
years) (52.2%).
•In patients with an existing HIV infection, toxoplasmosis is
an important oppurtunistic infection with considerable
morbidity and mortality especially in the pregnant women.

7. CLINICAL FEATURES :
• 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.

8. • Complete resolution usually occurs within a few months,
although symptoms and lymphadenopathy tend to
fluctuate unpredictably and some patients do not
recover completely even for a year or more.
•Sometimes the patient may also develop encephalitis,
hepatitis, pneumonitis and myocarditis.
•Retinochoroiditis is nearly always the result of congenital
infection.

9. CONGENITAL TOXOPLASMOSIS
•Acute toxoplasmosis, mostly subclinical, affects 0.3-1% of
pregnant women, with an approximately 60% transmission
rate to the fetus which increases with increasing gestation.
•Primary maternal infection in pregnancy –
Infection rate higher with infection in 3rd trimester.
Fetal death higher with infection in 1st trimester.
•Congenital disease affects approximately 40% of
infected fetuses, and is more likely to be severe with
infection early in gestation.
•Many fetal infections are also subclinical at birth but the
long-term sequelae include hydrocephalus, microcephaly
and retinochoroiditis.

10. INVESTIGATIONS:
• In the immunocompetent patient – Serology is often
done while in the immunocompromised the diagnosis
often requires the direct detection of parasites.
•SABIN-FELDMAN DYE TEST (Indirect Fluorescent Antibody
Test) – detects the IgG –Antibody.
Recent infection is indicated by a four-fold increase in titre
while peak titres of 1/1000 or more are reached within 2
months of onset of infection.
•The detection of Toxoplasma specific IgM-Antibody may
be useful in confirming acute infections. However, false
positives or persistence of IgM-Antibodies for years after
infection make interpretation difficult. Negative IgM-
Antibody virtually rules out acute infection.

11. Toxoplasma Gondii in
fluorescent stain

12. • During pregnancy it is highly critical to differentiate
between recent and past infection - the presence of high-
avidity IgG-Antibodies excludes infection acquired in the
preceding 3-4 months.
•If necessary , the presence of Toxoplasma Organisms in a
lymph node biopsy can be sought for by staining sections
histochemically with T. Gondii- Antiserum or by the use of
PCR to detect Toxoplasma-specific DNA.

13. TREATMENT:
• In immunocompetent subjects, uncomplicated
toxoplasmosis is self-limiting and responds poorly to anti-
microbial therapy.
•In PREGNANT WOMEN with an established recent
infection, SPIRAMYCIN (3g daily in divided doses) should
be given until term.
• Once fetal infection is established, treatment with
SULFADIAZINE AND PYRIMETHAMINE plus CALCIUM
FOLINATE is recommended as SPIRAMYCIN does not cross
the placental barrier.

14. OTHER INFECTIONS
VARICELLA ZOSTER
• Varicella Zoster is a member of the herpes virus family.
•Varicella also known as Chickenpox, is the acute primary
disease.
•Incubation Period – 15 days and is communicable 2 days
before and 5 days after the onset of rash.
•After an initial episode of infection with Varicella Zoster
leading to Chickenpox , the virus may persist in a latent
state in the posterior root ganglia of the spinal cord for
year. Reactivation results in Herpes Zoster.

15. • It is highly contagious, self-limiting disease of childhood
that is transmitted by respiratory droplets or close contact.
•It is usually acquired by 90% of the population before the
reproductive age, thus most women are immune before
they become pregnant.
•The incidence of Varicella in pregnancy is 0.7/1000.
•CLINICAL FEATURES include vesicular eruptions often on
mucosal surfaces first followed by a rapid dissemination in
a centripetal pattern. New lesions appear every 2-4 days
and each crop is associated with fever. The rash
progresses from macules to vesicles and then to pustule in
24 hours.

17. •Maternal varicella infection in the first 20 weeks of
pregnancy can cause VARICELLA EMBRYOPATHY also
called Congenital Varicella Syndrome in approximately
1-2% of cases characterised by hallmark cicatricial lesions
in dermatomal pattern, limb hypoplasia, contractures and
can also involve the eye and central nervous system. The
prognosis is poor if an infant be infected.Diagnosis is by
Prenatal Ultrasound and MRI may show Oligohydramnios,
IUGR, hydrops, limb deformities and microcephaly.
•However, the risk of congenital varicella syndrome is
negligible because antibodies in the maternal blood
prevent the virus from crossing the placenta and infecting
the fetus.
•In 1994, Enders and colleagues showed no clinical evidence of infection in infants born to 366
women with Varicella Zoster in pregnancy.

18. DIAGNOSIS :
Is primarily clinical, by recognition of the rash. If necessary,
it can be confirmed by detection of antigen (Direct
Immunofluroscence), PCR or by VIRAL CULTURE of the
aspirated Vesicular Fluid.
TREATMENT :
ACYCLOVIR (800mg 5 times daily at 4 hourly intervals for 7
days) or ACYCLOVIR 5mg/kg 8 hourly IV until patient is
improving is a Class-C antiviral agent used in the treatment
of Varicella Zoster. Oral Acyclovir has been shown to
significantly reduce symptoms, duration and intensity.
•Many studies have showed the safety of Acyclovir use in pregnancy. In 1993,
Center for Disease Control published data showing no risk of fetal
abnormalities in patients exposed in the first trimester receiving Acyclovir.
•The newer drugs like VALACYCLOVIR and FAMCYCLOVIR have a better bio-availability
and a less frequent dosing than Acyclovir with similar efficacy.

19. PARVOVIRUS B-19 INFECTION :
•Parvovirus B-19 virus is a small single stranded DNA virus
and has a predilection for rapidly dividing cells
particularly the erythroblasts. Many infections are sub-
clinical.
•Incubation Period – 14-21 days.
•CLINICAL FEATURES : Prodromal Fever, Coryzal
Symptoms, and a characteristic “Slapped-cheek rash”,
Impaired Erythropoiesis causing mild anemia and
polyarthropathy.
•Trans-placental fetal infection can occur during the first
two trimesters of pregnancy with an impact on the fetal
bone marrow. It causes 10-15% of non-immune (Non-
Rhesus related) HYDROPS FETALIS.

21. TREATMENT :
•Infection is usually self-limiting.
•Symptomatic relief from Arthritic symptoms may be
required by the use of analgesics.
•Pregnant women should avoid contact with cases of
Parvovirus-B19 infection.
•If exposed, SEROLOGY should be done to establish
whether they are non-immune.
•Passive prophylaxis with NORMAL IMMUNOGLOBIN has
been suggested .
•The pregnancy should be monitored closely by USG, so
that Hydrops Fetalis can be treated by Fetal Transfusion.

22. SYPHILIS :
• Syphilis is caused by infection, through abrasions in the
skin or mucous membranes with the spirochaete
TREPONEMA PALLIDUM.
•In adults the infection is usually sexually acquired,
however transmission by kissing, blood transfusion and
percutaneous injury have also been reported.
•Infection may remain latent throughout or clinical
features may develop at any time.
•All women should have syphilis serology carried out in
the first trimester of pregnancy or at the first antenatal
visit.
•Women at a risk of acquiring syphilis should have a
further test in the 3rd trimester preferably at 28-30 weeks.

23. CONGENITAL SYPHILIS –
• Congenital Syphilis is rare where antenatal serological
screening is practised.
•Treponemal infection may give rise to a variety of
outcomes after 4 months of gestation when the fetus
becomes immunocompetent:
1. Miscarriage or Still-birth, Premature or at term.
2. Birth of a syphilitic baby (very sick baby with
hepatosplenomegaly, bullous rash and perhaps
pneumonia).
3. Birth of a baby with latent infection who either remains
well or develops Congenital Syphilis later in life.

24. • Syphilis may be divided as Early or Latent Syphilis.
•CLINICAL FEATURES :
• Incubation period of Early Syphilis is usually 14-28 days
with a wide range of 9-90 days.
• The primary lesion or chancre develops at the site of
infection usually on the genital area and may also develop
on the vaginal wall and the cervix.
•After 6-8 weeks the treponemes disseminate to produce a
multi-system disease. Constitutional features such as fever,
malaise and headache are common. Over 75% patients
present with a rash on the trunk and limbs that later
involves the palms and soles.
•Generalised non-tender lymphadenopathy is present in
over 50% patients.

25. •Often features such as meningitis, cranial nerve palsies,
hepatitis, gastritis, glomerulonephritis and anterior/posterior
uveitis are seen.
INVESTIGATIONS :
SEROLOGICAL TESTS FOR SYPHILIS
Non-treponemal ( Non-specific) tests:
•Veneral Diseases Research Laboratory ( VDRL ) Test
•Rapid Plasma Reagin Test
Treponemal (Specific) antibody tests:
•Treponemal antigen-based enzyme immuno assay
(EIA) for IgG and IgM
•T. Pallidum haemagglutination assay (TPHA)
•T. Pallidum Particle agglutination assay (TPPA)
•Fluorescent treponemal antibody-absorbed (FTA-
ABS) test

27. TREATMENT :
•In early latent stage: single dose of 2.4 Million units
Benzathine Penicillin G IM
In late latent stage: 3 doses of 2.4 million units of Benzathine
Penicillin G IM is given. It is given once in a week.
•ERYTHROMYCIN STEARATE can be given if there is
Penicillin hypersensitivity, but it crosses the placenta
poorly. The treatment of syphilis can be considered
adequate if it is completed by at least 30 days before
delivery or there is a documentef 4-fold drop in RPR titre.

28. •The newborn baby must therefore be treated
with a course of Penicillin and consideration
given to re-treating the mother.
•Success has also been achieved with
CEFTRIAXONE 250mg IM for 10 days in many
cases.
All pregnant women testing positive for Syphilis
should also be screened for HIV.

29. COXSACKIE VIRUS INFECTION :
• The virus is a member of the Picornaviridae and have a
single-stranded RNA. It may cause clinically inapparent
infection in the mother but may prove fatal to the fetus or
the infant by increasing congenital malformations.
•Infection is spread from person to person. The virus is
present in secretions and body fluids of infected people.
•Fetal death may be caused by viraemia resulting in
Hepatitis, Myocarditis and Encephalomyelitis due to
placentitis and clinical chorioamnionitis.
•The virus may be grown from the amniotic fluid or the
neonatal spinal fluid.PCR can detect 66-90% of the
infection.

30. CLINICAL FEATURES : Common Cold, Rash, diarrhoea,
sore throat. Severe manifestations include meningitis,
encephalitis, severe chest pain, myopericarditis.
TREATMENT :
•There is no specific medication known to kill the
Coxsackie virus.
•Fortunately, the body’s immune system is usually able to
destroy the virus.
•Some reports suggest that there might be a benefit to IV
Immunoglobulin which is made from human serum and
contains antibodies.
•Treatment for Myocarditis is supportive.

32. LISTEROSIS :
• Recent surveys have shown that 4% of pregnant women
harbor LISTERIA MONOCYTOGENS, a Gram-positive
bacteria in the cervix.
•Trancplacental infections can occur from an infected
mother.
•Such patients have Influenza like symptoms, premature
delivery and dirty brown amniotic fluid, fever, myalgia,
choriamnionitis and abortions.
•Babies born to these mothers may get infected
transplacentally or during delivery with a high morbidity
and mortality due to Pyogenic Meningitis.

33. INVESTIGATIONS :
• Diagnosis is made by Blood/CSF Culture, a positive
fluoroscent antibody test and culture of stomach content,
liquor .
TREATMENT :
•The most effective regimen consists of IV AMINOPENICILLIN
(AMOXYCILLIN/AMPICILLIN) + AN AMINOGLYCOSIDE.
•Patients allergic to Penicillin may be given a combination
of Sulfamethoxazole/Trimethoprim.
• Dietary precaution : Pregnant women are advised to
avoid high-risk products like undercooked chicken, fish, raw
vegetables and soft cheese.

34. RUBELLA :
•Rubella, commonly known as German measles, is a
disease caused by the rubella virus a togavirus that is
enveloped and has a single-stranded RNA genome.
•This disease is often mild and attacks often pass
unnoticed. The disease can last one to three days.
Children recover more quickly than adults.
•Infection of the mother by Rubella virus during pregnancy
can be serious; if the mother is infected within the first 20
weeks of pregnancy, the child may be born with
congenital rubella syndrome (CRS), which entails a range
of serious incurable illnesses. Spontaneous abortion occurs
in up to 20% of cases. The virus has teratogenic properties
and is capable of crossing the placenta and infecting the
fetus where it stops cells from developing or destroys
them.

35. •Acquired (i.e. not congenital) rubella is transmitted via
airborne droplet emission from the upper respiratory tract
of active cases and replicates in the nasopharynx and
lymph nodes.
•The virus may also be present in the urine, Faeces and on
the skin. There is no carrier state: the reservoir exists entirely
in active human cases.
•The disease has an incubation period of 2 to 3 weeks.
•In most people the virus is rapidly eliminated. However, it
may persist for some months post partum in infants
surviving the CRS. These children are a significant source of
infection to other infants and, more importantly, to
pregnant female contacts.

36. CLINICAL FEATURES :
•German measles causes symptoms that are similar to the
flu. The primary symptom of rubella virus infection is the
appearance of a rash (exanthem) on the face which
spreads to the trunk and limbs and usually fades after three
days.
•The facial rash usually clears as it spreads to other parts of
the body. Other symptoms include low grade fever,
swollen glands (sub occipital & posterior cervical
lymphadenopathy), joint pains, headache and
conjunctivitis.The swollen glands or lymph nodes can
persist for up to a week and the fever rarely rises above 38
degrees centigrate . The rash disappears after a few days
with no staining or peeling of the skin.
•.

37. CONGENITAL RUBELLA SYNDROME
•Congenital rubella syndrome (CRS) is characterized by:
 Intrauterine growth restriction
 Intracranial calcifications
 Microcephaly
 Cataracts
 Cardiac defects (most commonly patent ductus arteriosus
or pulmonary arterial hypoplasia).
 Neurologic disease (with a broad range of presentations,
from behavior disorders to meningoencephalitis)
Osteitis and hepatosplenomegaly

39. •Most of these complications develop in infants born to
mothers who acquire rubella infection during the first 16
weeks of pregnancy.
• 90% of infants present with some finding of congenital
rubella if infection occurs within the first 12 weeks, and 20%
present with congenital disease if the infection occurs
between weeks 12 and 16.
•Cataracts results when infection occurs between the third
and eighth week of gestation, deafness between the 3rd
and 18th week, and heart abnormalities between the 3rd
and 10th week.

40. DIAGNOSIS :
•Rubella virus specific IgM antibodies are present in
people recently infected by Rubella virus but these
antibodies can persist for over a year and a positive test
result needs to be interpreted with caution.
• The presence of these antibodies along with, or a short
time after, the characteristic rash confirms the diagnosis.

41. TREATMENT :
•Rubella infections are prevented by active immunisation
programs using live, disabled virus vaccines. Two live
attenuated virus vaccines, RA 27/3 and Cendehill strains,
are effective in the prevention of adult disease.
•The vaccine is now usually given as part of the MMR
vaccine. The WHO recommends the first dose is given at 12
to 18 months of age with a second dose at 36 months.
Pregnant women are usually tested for immunity to rubella
early on. Women found to be susceptible are not
vaccinated until after the baby is born because the
vaccine contains live virus.

42. •There is no specific treatment for Rubella; however,
management is a matter of responding to symptoms to
diminish discomfort.
•Treatment of newly born babies is focused on
management of the complications.
•Congenital heart and cataracts can be corrected by
direct surgery.
•Management for ocular congenital rubella syndrome
(CRS) is similar to that for age-related macular
degeneration, including counseling, regular monitoring,
and the provision of low vision devices, if required.
•Rubella infection of children and adults is usually mild, self-
limiting and often asymptomatic. The prognosis in children
born with CRS is poor.

43. CYTOMEGALOVIRUS INFECTION :
•CMV is a double-stranded DNA herpes virus and
represents 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 sexual contact,
organ transplantation, transplacental transmission,
transmission via breast milk, and blood transfusion (rare).

44. •Primary, reactivation, or recurrent CMV infection can
occur in pregnancy and can lead to congenital CMV
infection.
•Transplacental infection can result in intrauterine growth
restriction, sensorineural hearing loss, intracranial
calcifications, microcephaly, hydrocephalus,
hepatosplenomegaly, delayed psychomotor
development, thrombocytopenia and/or optic atrophy.
•Vertical transmission of CMV can occur at any stage of
pregnancy; however, severe sequelae are more common
with infection in the 1st trimester, while the overall risk of
infection is greatest in the 3rd trimester.
•The risk of transmission to the fetus in primary infection is
30%-40%.

46. •The transmission rate to the fetus is between 30-50%
according to the Organization of Teratology Information
Service (OTIS).
•Of those babies who become infected, only 10-15% show
signs of congenital CMV after primary maternal infection.
• 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.

48. DIAGNOSIS & MANAGEMENT :
•Serologic testing in women with suspected
Cytomegalovirus (CMV)
•Amniocentesis
•Ultrasonography
• Quantitative polymerase chain reaction (PCR) for viral
DNA in amniotic fluid
•Fetal magnetic resonance imaging (MRI) (considered
but not recommended)
•Intravenous treatment with CMV-hyperimmune globulin
•Ganciclovir treatment.

49. HERPES SIMPLEX VIRUS -2 INFECTION :
•Herpes simplex virus (HSV) infection is one of the most
common viral sexually transmitted diseases worldwide. The
primary infection of the mother may lead to severe illness
in pregnancy and may be associated with virus
transmission from mother to foetus/newborn.
•Since the incidence of this sexually transmitted infection
continues to rise and because the greatest incidence of
herpes simplex virus infections occur in women of
reproductive age, the risk of maternal transmission of the
virus to the foetus or neonate has become a major health
concern.

50. •A pregnant woman who acquires genital herpes as a
primary infection in the latter half of pregnancy, rather
than prior to pregnancy, is at greatest risk of transmitting
these viruses to her newborn.
•Additional risk factors for neonatal HSV infection include
the use of a foetal-scalp electrode and the age of the
mother < 21 years.
• Herpes Simplex Virus-2 is a DNA virus that belongs to
Alphaherpesvirinae family.
• HSV-2 is most commonly found in the lumbosacral
ganglia.
•The most important HSV infection during pregnancy is the
primary genital HSV infection.

51. •Primary HSV infections in pregnant women can result in
more severe diseases than that in non-pregnant ones.
• In particular, gingivostomatitis and vulvovaginitis
herpetica tend towards dissemination. As a result, women
can develop disseminated skin lesions associated with
visceral involvement such as hepatitis, encephalitis,
thrombocytopenia, leucopoenia and coagulopathy.
• Although disseminated HSV infection is uncommon in
pregnancy, the mortality is about 50%. In particular,
pregnant women with primary mucous membrane
infection during the 3rd trimester, have an increased risk for
dissemination and they could transmit HSV to their babies
during vaginal delivery.

52. •The great majority of recurrent genital herpes is due to
HSV-2 because this virus reactivates more frequently than
HSV-1.
•Recurrent episodes of HSV infection are characterized by
the presence of antibody against the same HSV type and
the herpes outbreaks are usually mild (7–10 days) with less
severe symptoms than the first episode.
•Prodromal symptoms (itching, tingling, neuralgia) may
occur hours or days before a recurrent herpes episode.
•The apparently asymptomatic phases between clinical
outbreaks of genital herpes are important, since HSV can
reactivate periodically in latently infected cells of sensory
ganglia travelling via the neuronal axons back to the
genital mucosa, without clinical signs or symptoms. This
mechanism is known as asymptomatic virus shedding.

53. •Asymptomatic shedding has been shown to be higher in
women with HSV-2 infection compared with those with
HSV-1.
•Although there is a small risk of vertical transmission,
recurrent genital herpes must be regarded as the most
common cause of neonatal infections and the passage
through an infected birth canal is the most probable
route of transmission .
•In recurrent infections associated with clinical symptoms,
the risk of neonatal disease is reduced dramatically by
Caesarean section.

55. DIAGNOSIS :
•Clinical diagnosis of genital herpes is limited in accuracy.
First, HSV is only one of several diseases characterized by
genital ulcers. More importantly, many persons are
unaware that their symptoms are those of herpes.
•The typical lesions may not appear, and recurrences may
be at different locations along a dermatome. Women may
experience only prodromal symptoms, such as burning or
tingling; have single ulcers, fissures, or erosion; or
experience erythema or edema as the primary symptom.
•Available tests for herpes include both culture and PCR-
DNA testing for viral shedding, and the use of blood tests to
screen for previous exposure.

56. MANAGEMENT :
•The American Congress of Obstetricians and
Gynecologists (ACOG) recommends that women with
active recurrent genital herpes should be offered –
•Suppressive viral therapy from 36 weeks until delivery
Valacyclovir 500 mg orally BD OR
Acyclovir 400 mg orally TDS.
•Transplacental infection of the fetus is rare during
pregnancy. Intrauterine HSV infection has uncommonly
been associated with skin lesions, chorioretinitis,
microcephaly, hydranencephaly , and microphthalmia.

57. •While primary HSV infections in the first trimester are
associated with higher rates of spontaneous abortion and
stillbirth, infection later in pregnancy appears more likely to
be associated with preterm labor or growth restriction.
•Of greatest concern is the risk of primary infection
acquired at birth which could lead to herpetic
meningitis. The infection rate is 34 to 80% for infants born
vaginally during a primary infection.
•Cesarean section is recommended for all women in labor
with active genital lesions or prodromal symptoms such as
vulvar pain.
For patients with preterm premature rupture of membranes remote
from term complicated by recurrent maternal HSV infection, the risks of
prematurity should be weighed against the risk of neonatal HSV
disease in considering expectant management. Prophylactic
treatment with antiviral agents (eg, acyclovir) may be considered if
expectant management is chosen.

59. THE TORCH TEST :
•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 newborn 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.

60. •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.
•Presence of IgM antibodies indicates either a current or
recent infection. A positive IgM result in a newborn
indicates high likelihood of infection with that organism.
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.

61. •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.

62. REFERENCES
• Davidson’s Principles & Practice of MEDICINE -21st edition
•Novak’s Textbook of Obstetrics – 10th edition
•TORCH Infections in Pregnancy – Veena Gupta – Jaypee
Publication – 2nd edition.
•William’s Textbook of Obstetrics – 23rd edition
•Article on Torch infections in Pregnancy – THE BRITISH
MEDICAL JOURNAL (BMJ)
•Article on TORCH INFECTIONS in Pregnancy – AMERICAN
COLLEGE OF OBSTETRICS & GYNAECOLOGY (ACOG)