The TORCH complex refers to a group of perinatal infections - Toxoplasmosis, Other (syphilis, varicella, parvo virus), Rubella, Cytomegalovirus, and Herpes simplex virus type 2. These infections can cross the placenta and infect the fetus, potentially causing severe anomalies or death. Toxoplasmosis is caused by the protozoan Toxoplasma gondii which can infect fetuses during acute maternal infection via the placenta. Rubella virus infection during pregnancy increases risks of fetal anomalies, especially in the first trimester. Cytomegalovirus is a herpes virus that commonly infects fetuses, with 30

1. NIDHI SHUKLA JUGLAN
TORCH INFECTION IN
PREGNANCY

2. 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
transplacentally via the chorionic villi.

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

4. TOXOPLASMOSIS
 Caused by protozoan intracellular parasite-
toxoplasma gondii.
 Modes of transmission – feco-oral route
by eating infected raw or cocked meat, or through
contact with infected cat faeces.
Or through placenta.

5. Organism and transmission
 T. gondii has three different
forms
 The definitive host is cat.
 The oocytes produced the
sporozites in the
enteroepithilial cells of cat
and passed into the faeces.
 Sporozites become infected
after 21 days of shedding.
 Excystation in the human
gut after ingestion of
infected sporozytes.

6.  Sporozytes circulates in maternal blood stream.
 Trophozytes develop and multiply within the cells
causes cell rupture and death.
 Host immune response activated and begins third
stage.
 Host antibody formation reaction converts the
parasites from the trophozites into tissue cyst form,
and no longer circulate in blood to cause infection.
 Fetal infections occurs only in acute phase of
infection, when T. gondii in maternal blood
transported to placenta and fetus.

8. Clinical manifestations
 Acute toxoplasmosis is mostly subclinical.
 Affects 0.3-1% of pregnant women, with an
approximately 60% transmission rate to the fetus.
 Risk Increases with gestation age.

9. Primary maternal infection in pregnancy-
 Fetal death higher with infection in 1st trimester
 Infection rate is higher with infection in 3rd
trimester.
Risk of fetal infection-
1st trimester- 15% ( decreases the incidence of
infection but serious diseases are common,
including abortion).
2nd trimester- 25%
3rd trimester- 65% ( 90% newborns are without
clinical signs of infection.)

10. Maternal clinical manifestations
 Most women are asymptomatic. Only about 10% of
women have s/s during acute infection-
1. lymphoadenopathy- indicates recent infection,
these are generally non tender, and
nonsuppurative.
2. Other symptoms are flu like illness such as-
 fever
 fatigue
 Headache
 Muscle pain, sore throat.

11. Severe and rare symptoms are-
 Polymyositis
 Dermatomyositis
 chorioretinitis

12. Fetal clinical manifestations
 If acute toxoplasmosis is acquired during pregnancy,
the infant is at the risk of developing congenital
toxoplasmosis.
 Clinical triad of signs associated with congenital
toxoplasma infection is-
 Chorioretinitis
Hydrocephalus
Intra cranial calcification.

14. Other symptoms –
 Fever
 Rash
 Microcephaly
 Siezures
 Jaundice
 Thrombocytopenia
 Lymphoadenopathy

15. Diagnostic evaluation
 Serological testing-
is done in the immunocompetent patient. Screening
for the absence or presence of IgG or IgM specific
antibodies is vital to make the diagnosis of acute
toxoplasmosis in pregnancy.
Sabin- feldman dye test- indirect fluorescent
antibody test detects the level of IgG antibody.
ELISA- to detect IgM.
 Lymphnode biopsy
 Ultrasound.

16. Investigation for detecting the fetal
transmission-
 Cordocentesis
 Amniocentesis
 USG for fetal triad.

17. Treatment
 Self limiting.
 Poorly respond to anti- microbial therapy.
Pregnant women-
 Spiramycin 3 gm daily untill term.
Once fetal infection is established-
 Sulfadiazine 1gm qid
 Pyrimethamine 25 mg Po od (not in 1st trimes.)
 Calcium folinate.
4-6 weeks course is given to the mother.

18. Prevention ??????????

19. RUBELLA
 AKA german measels.
 Caused by rubella virus ,a togavirus has single
stranded RNA genome.
 Transmitted by droplet infection.
 Virus has teratogenic properties can cross the
placenta where it stops cell development and leads
cell death.
 Risk of developing fetal anomalies is directly
associated with maternal gestational age.

20. Incidences
 1st trimester- 50% major fetal anomalies.
 2nd trimester- 25%
 3rd trimester- 10%
Spontaneous abortions occur upto 20% of cases. If
infection occur within 20 wks of gestation.

21. Clinical manifestations
 Maternal symptoms-
Same as other flu-
1. Rashes
2. Low grade fever
3. Lymphoadenopathy
( suboccipital, posti cervical)
1. Joint pain
2. Headache
3. Conjunctivitis

22. Congenital rubella syndrome
It is characterized by-
 Cochlear- sensorineural defects.
 Cardiac – septal defects, PDA, pulmonary arterial
hypoplasia.
 Neurological diseases- with a broad range of
presentation from behaviors to memingoencephalitis.
 Ostitis
 Hepatosplenomegaly.
 Microcephaly
 IUGR
 Cataracts
 Thrombocytopenia – blue berry muffin lesions.

24. Diagnostic evaluation
 Serological test to detect rubella specific antibodies.
 Routine rubella IgG is done in the first trimester
 Rubella IgM is done in suspected case.
 Presence of antibodies + rash = confirm the
diagnosis.

25. Treatment
 Prevention by active immunization.
 No such treatment available.
 Self limiting disease.
 Maternal screening should be performed in early
pregnancy.
 In infection is present in pregnancy, mother could not be
vaccinated because the rubella vaccine contained live
virus which can cross the placenta and affect the fetus.
 Infact women should not be vaccinated 28 days before
conception.

26.  Symptomatic treatment- analgesic and antipyretics.
 Newborn should be managed for complications.

27. CYTOMEGALOVIRUS
 CMV is a member of the herpes virus species.
 Double strained DNA virus.
 The virus most frequently passed on to fetus during
pregnancy.
 Acc to American academy of pediatrics about 1% of
babies are born with the infection, a condition called
congenital CMV.
 Transmission- direct person to person contact
(saliva, milk, urine, semen, tears, stools, blood,
cervical and vaginal secretions).

28. Incidences
 Primary vertical cmv infection caries a 30% - 40%
risk of vertical transmission.
 Among 30-40% , 2-4% develop severe
malformations.
 40000 infant per year in the US.

29. Clinical manifestations
Maternal symptoms-
 Fever
 Weakness
 Swollen glands
 Joint stiffness
 Muscle ache
 Loss of appetite.
Fetal symptoms-
90% are asymptomatic at birth
 Petechiae, jaundice
 Chorioretinitis
 Periventricular calcifications.
 IUGR, hearing loss
 Microcephaly
 Delayed psychomotor
development
 Heart block

30. Diagnostic evaluations
 Serological testing- IgM are detected
 Amniocentesis
 Cordocentesis
 USG
 Fetal MRI ( rarely)

31. Treatment
 No definitive Rx.
 Pregnancy termination
 Antiviral drugs-
1. Gangciclovir
2. Foscarnet
3. Cidofovir
 Most effective drugs- hyper immune globulin.

32. HERPES SIMPLEX VIRUS-2
INFECTION
 Most common STD worldwide.
 DNA virus belongs to alpha herpes virinae family
 Primary infection to mother can lead severe illness to
mother in pregnancy.
 The most common infection during pregnancy is
primary genital HSV infection.

33. Effect on pregnancy
 Transplacental infection is not usual.
 Fetus become infected by virus shed from the cervix
and vagina during vaginal delivery.
 In utero transmission may occur in rupture of
membraines.
 Increased risk of abortion is inconducive.
 IUGR if infection acquired in 3rd trimester.

34. Neonatal infections-
 Chorioretinitis
 MR
 Seizures
 Microcephaly
 Deaths.

35. Treatment
 CS indicated in primary HSV infection.
Suppressive viral therapy from 36 weeks untill
delivery, it includes-
 Valacyclovir 500 mg PO bd
 Acyclovir 400mg po tds. ( drug of choice)

36. Thank you