This document discusses TORCH infections that can affect pregnancy. It covers Toxoplasmosis, Rubella, CMV, and Herpes infections. For each infection, it describes transmission, clinical manifestations, effects on pregnancy like risk of transmission and fetal anomalies, diagnosis, and treatment approaches. For toxoplasmosis, it highlights risks increase with gestational age and treatments include pyrimethamine and spiramycin. For rubella, congenital rubella syndrome can cause fetal defects if acquired early in pregnancy. CMV and herpes infections also pose risks of fetal transmission and growth restriction. Diagnosis involves serology and PCR testing of amniotic fluid. Treatment may include antivirals and monitoring for complications.

1. TORCH IN PREGNANCY
Mukesh Sah
Post graduate Medical Intern

2. TORCH
Torch Complex is a medical acronym for a set of perinatal
infections, that can lead to severe fetal anomalies or even death.
They are a group of viral, bacterial and protozoan infections that
gain access to the fetal blood stream tranplacentally via chrionic
villi.

3. TORCH
T- toxoplasmosis
O- other infections
R-rubella
C-cytomegalovirus
H-herpes simplex virus.
Other infections-syphilis, varicella zoaster, parvo virus.

4. TOXOPLASMOSIS
Toxoplasmosis is a protozoan infestation caused by Toxoplama
gondii.
Human acquisition of the infection occurs by:
feco-oral route.
Oocyte contamination soil, salads, vegetables.
Ingestion of raw or undercooked meat containing tissue cysts
(sheep, pigs and rabbits are the most common meat sources).

5. Outbreaks of toxoplasmosis have also been linked to
the consumption of unfiltered water.

6. CLINICAL MANIFESTATIONS (1/2)
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 23-35 years age group.

7. CLINICAL MANIFESTATIONS (2/2)
Painless lymphadenopathy (local or generalized) is
the most common presenting feature.
Other features include- malaise, fever, fatigue.
Muscle pain, sore throat and headache

8. EFFECTS ON PREGNANCY (1/2)The fetal risk of infection increases with duration of pregnancy and is
approximately 15%, 30% and 60% in the first, second and third trimester of
pregnancy.
Risks of fetus includes:
 intrauterine death.
 Low birth weight.
 Enlarged liver and spleen.
 Jaundice

9. EFFECTS ON PREGNANCY (2/2) Anemia
 Intracranial calcifications.
 Hydrocephalus
 Macular lesions.
 Infected neonates may be asymptomatic at birth, but can develop retinal
and neurological disease.

10. DIAGNOSIS
Serological test is done for toxoplasma specific IgM antibodies.
Amniocentesis and cordocentesis for detection of IgM
antibodies in the amniotic in the amniotic fluid and fetal blood.
If the fetus is infected and hydrocephalus is present, counselling
for termination is to be done.

11. MANAGEMENT
Toxoplasmosis is a self limited illness in an immunocompetent
adult and does not require any treatment.
Pyrimethamine 25mg orally daily and oral sulfadiazine 1gm four
times a day is effective.
Luncovorin is added to minimize toxicity.
Pyrimethamine is not given in the first trimester.

12. MANAGEMENT
Spiromycin (3gm orally daily) has also been used as an
alternative.
Acute toxoplasmosis during pregnancy is treated with
spiromycin.
Extended courses is needed in an immunocompromised patient
to cure infection.
Treatment to the mother reduces the risk of congenital infection
and the late sequelae.

13. PREVENTION
Appropriate information includes advising women
about washing kitchen surfaces following contact
with uncooked meats, avoiding cat and dog faeces

14. VARICELLA ZOSTER
Varicella zoster is a member of the herpes virus family.
It is also known as chickenpox.
Varicella zoster virus (VAV) is a highly contagious, self-limiting
disease of childhood that is transmitted by respiratory droplets or
close contact.
Incubation period-15 days and is infectious for 48hours before the
rash appears until vesicles crust over.

16. VARICELLA ZOSTER
It is usually acquired by 90% of the population before the
reproductive age, thus most women are immune before they
become pregnant .
After the primary infection the virus remains dormant in the
sensory nerve root ganglia and with any recurrent infection can
result in herpes zoster (shingles).

18. EFFECTS ON PREGNANCY(1/3)
Primary infection during pregnancy can result in serious adverse
outcome.
Varicella zoster virus does cross the placenta and may cause
congenital or neonatal chickenpox.
Maternal mortality is high due to varicella pneumonia.
During the first 20 weeks of pregnancy baby has about a 2% risk of
fetal varicella syndrome (FVS).

19. EFFECTS ON PREGNANCY(2/3)
Congenital varicella syndrome is characterized by:
 Hypoplasia of limp
 Limb deformity
 Choroidoretinal scarring
 Cataracts.
 Microcephaly and cutaneous scarring.
The risk of congenital malformations is nearly absent when maternal infection
occurs after 20 weeks.

20. EFFECTS ON PREGNANCY(3/3)
About 30% of babies born with skin lesions die in the first months of
life.
Maternal infection after 36 weeks, and particularly in the week before
the birth (when cord blood VZV IgG is low) to 2 days after, can result
in infection rates upto 50%.
About 25% of those infected will develop neonatal clinical varicella.

21. DIAGNOSIS
It is primarily clinical, by recognition of the rash. If necessary,
it can be confirmed by detection of antigen (Direct
Immunofluorescence), PCR or by viral culture of the aspirated
vesicular fluid.

22. TREATMENT
Oral acyclovir (800mg 5 times daily for 5 days) or IV acyclovir
10 mg/kg every 8 hours, although higher doses (12–15 mg/kg)
are sometimes used for life-threatening infections, especially in
immunocompromised patients.
Women infected during the first 20 weeks may request
termination of pregnancy.

23. PARVOVIRUS INFECTION
It is caused by parvovirus B-19.
Incubation period- 14-21 days.
Parvovirus infection is a common
and highly contagious childhood
ailment — sometimes called
slapped-cheek disease because of
the distinctive face rash that
develops

24. 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 cause 10-15% of non-immune (Non-Rhesus related) Hydrops
fetalis.

25. TREATMENT (1/2)
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 B-19
infection.
If exposed, serology should be done to establish whether they are non-
immune.

26. TREATMENT(2/2)
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

27. RUBELLA(1/3)
It is disease caused by the rubella virus.
Rubella or German measles is transmitted by respiratory droplet
exposure. The virus may also be present in the urine, faeces and
on the skin.
For most immunocompetent children and adults (including
pregnant women), the rubella virus causes a mild, insignificant
illness spread by droplet infection.

29. RUBELLA(2/3)
During pregnancy the virus can have potentially devastating effects on
developing fetus.
Congenital rubella syndromes (CRS) in the newborn however remains a major
cause of development anomalies that include blindness and deafness.
The child may be born with CRS if the mother is infected within the 1st 16
weeks of pregnancy.
The virus has teratogenic properties.

30. RUBELLA(3/3)
After infecting placenta, virus spreads through vascular system of the
developing fetus, causing cytopathic damage to blood vessels and
ischemia in the developing organs.
Incubation period- 2-3 weeks.
Primary rubella infection is most likely to cause problems if it is acquired
in the first 12 weeks of pregnancy and in this situation maternal-fetal
transmission rates are as high as 80%.

31. CLINICAL FEATURES (1/2)
The primary symptom of rubella virus infection is the
appearance of a rash (exanthema) 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.

32. CLINICAL FEATURES (2/2)
Others symptoms include low grade fever, swollen glands (sub
occipital and posterior cervical lymphadenopathy, joint pains,
headache and conjunctivitis.
The rash disappears after a few days with no staining or peeling of the
skin.

33. CONGENITAL RUBELLA SYNDROME
CRS characterized by;
- Intrauterine growth restriction.
- Intracranial calcifications
- Microcephaly
- Cataracts
- Cardia defects
- Neurologic disease
- Osteitis and hepatosplenomegaly

34. EFFECTS ON PREGNANCY
First trimester infection can result in spontaneous abortion and
in surviving babies, a number of serious and permanent
consequences.
These includes cataracts, sensorineural deafness, congenital
heart defects, microcephaly, meningocephalitis, dermal
erythropoiesis, thrombocytopenia and significant developmental
delay.

35. DIAGNOSIS
Detection of Rubella virus specific IgM antibodies.
Rubella specific IgG antibodies are present for life after natural
infection or vaccination.
Prenatal diagnosis of rubella virus infection using PCR can be
done from chorionic villi, fetal blood and amniotic fluid
samples.

36. TREATMENT (1/4)
Rubella vaccine are given at 9 and 15months.
Rubella vaccine are not recommended in pregnant women.
When giving during the childbearing period, pregnancy should be
prevented within three months by contraceptive measure.
However, If pregnancy occurs during the period, termination of
pregnancy is not recommended.

37. TREATMENT (2/4)
There is no specific treatment for rubella; however, management
is a matter of responding to symptoms to diminished discomfort.
Treatment of newly born babies is focused on management of
the complications.
Congenital heart and cataracts can be corrected by direct
surgery.

38. TREATMENT(3/4)
Management for ocular congenital rubella syndrome (CRS) is similar to
that for age-related macular degeneration, including counselling, 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.

39. TREATMENT(4/4)
Active immunization programs using live, disabled virus vaccines
All girls should be vaccinated against rubella before entering the
child bearing years.
Women wishing to conceive should be counselled and encouraged
to have their antibody status determined and vaccinated if needed.

40. CYTOMEGALOVIRUS INFECTION (1/2)
Cytomegalovirus (CMV) is a common viral infection.
It is estimated that 50% of the adult population has had the infection at
some point in their life.
The virus causes the flu like illness and pregnant women have an
increased susceptibility to infection during pregnancy.
However, primary infection in pregnancy is low, at around 1%.

41. CYTOMEGALOVIRUS INFECTION (2/2)
Possible route of transmission include sexual contact, organ
transplantation, transplacental transmission, transmission via
breast milk, and blood transfusion (rare).

42. EFFECTS ON PREGNANCY (1/2)
There is 40% chance of transmission to the fetus.
Transplacental infection can result in intrauterine growth
restriction, sensorineural hearing loss, intracranial calcifications,
microcephaly, hydrocephalus, hepatosplenomegaly, delayed
psychomotor development, thrombocytopenia and/or optic
atrophy.

43. EFFECTS ON PREGNANCY (2/2)
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.

44. DIAGNOSIS
Serological testing in women with suspected cytomegalovirus
(CMV).
Amniocentesis
Ultrasonography
PCR for viral DNA in amniotic fluid.

45. TREATMENT
Intravenous treatment with CMV-hyperimmune globulin
Ganciclovir: The usual dose of intravenous ganciclovir for the initial
treatment of CMV is 5 mg / kg every 12 hours for 14 to 21 days.
- To prevent a relapse of CMV, the usual dose is 5 mg / kg once daily
every day of the week, or 6 mg / kg once daily 5 days a week

46. HERPES SIMPLEX VIRUS INFECTION
HSV is an ubiquitous enveloped and double stranded DNA virus
(family Herpesviridae)
During pregnancy the major concern of maternal HSV infection
is transmission of the fetus.
HSV-1 predominate orofacial lesion (trigeminal ganglia)
HSV-2 found in the genital lesions lumbosacral ganglia.

47. CLINICAL MANIFESTATION(1/2)
Vary depend on the stage of infection and prior immune status.
First episode primary infection, describes cases in which HSV is
isolated from genital secretions in the absence of HSV
antibodies.
Present with severe painful genital ulcers, pruritus, dysuria,
fever, tender inguinal lymphadenopathy and headache.

48. CLINICAL MANIFESTATION(2/2)
Recurrent episodes of HSV infection are characterized by the
presence of antibody against the same HSV type and the herpes
outbreaks are usually mild (7-10days) with less severe symptoms
than the first episode.
Preceded by prodromal symptoms such as pruritus, burning or pain
before lesion are visible
Mild symptoms and few lesions or no symptoms at all.

50. VERTICAL TRANSMISSION
Occurs during labor and delivery as a results of direct contact with
virus shed from infected sites (cervix, vaginal, perianal area)
Viral shedding can occur in the absence of maternal symptoms
and lesions.
The frequency of shedding is higher in HSV-2 versus HSV-1
infection.

51. DIAGNOSIS
Presence of vesicular or ulcerated lesion
PCR
Viral culture
Direct fluorescent antibody test.

52. MANAGEMENTACOG recommends that women with active recurrent genital herpes
should be offered.
Suppressive viral therapy from 36weeks until delivery.
- Valacyclovir 500mg orally bd or
- Acyclovir 400mg orally tds.
C/S is recommended for all women in labor/rupture of membrane with
active genital lesions or prodromal symptoms such vulvar pain, burning.

53. MANAGEMENT
Sitz bath to relieve vulvar pain, dysuria and other local symptoms
Analgesia e.g. acetaminophen
Avoid transcervical procedure (cerclage, chorionic villus sampling)
in women with genital lesions.

54. PREVENTION
Avoidance of sexual activity during disease
Use of barrier protection.
Chronic suppressive therapy to reduce risk of transmission to an
uninfected partner
Patient education.

55. REFERENCES
 Https://www.Slideshare.Net/barakmsumi/torch-s-in-pregnancy
 Https://www.Webmd.Com/children/what-is-torch-syndrome#1
 https://hivclinic.ca/main/drugs_fact_files/ganciclovir.pdf
 Annamma Jacob. A comprehensive textbook of midwifery and gynecological
nursing. 4th edition. New Delhi: Jaypee brothers; 2015. p. 641-643
 DC Dutta’s. Textbook of obstetrics including perinatology and contraceptive.
7th. New Delhi: Jaypee brothers; Nov2013. p. 297.
 Myles. Textbook for midwives. 16th edition. New York: Elsevier; 2014. p. 676-
678.