Torch Infection in Pregnancy: Neha Barari Assistant Professor SNSR

TORCH INFECTION IN
PREGNANCY
NEHA BARARI
ASSISTANT PROFESSOR
SNSR
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.
 T- toxoplasmosis
 O- other infections
 R- rubella
 C- cytomegalovirus
 H- herpes simplex II virus
Other infections- syphilis, varicella zoaster,

parvo virus.
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.
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.
 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.

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.

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.)
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 non-
suppurative.
Other symptoms are flu like illness such as-
 fever
 fatigue
 Headache
 Muscle pain, sore throat.
Severe and rare symptoms are-
 Polymyositis (skeleton muscles)
 Dermatomyositis
 Chorioretinitis (choroid)
 Chorioretinitis Polymyositis
DERMATOMYOSITIS

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.
HYDROCEPHALUS INTRACRANIAL CALCIFICATION
Other symptoms –
 Fever
 Rash
 Microcephaly
 Siezures
 Jaundice
 Thrombocytopenia (platelets)
 Lymphoadenopathy
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.
Two classes of Toxoplasma antibodies may be
found in the blood: IgM and IgG. IgM antibodies
are the first to be produced by the body in
response to a Toxoplasma infection.
Sabin- feldman dye test- indirect fluorescent

antibody test detects the level of IgG antibody.
ELISA- to detect IgM
 Lymph node biopsy
 Ultrasound.
Investigation for detecting the fetal
transmission-
 Cordocentesis
 Amniocentesis
 USG for fetal triad ( Chorioretinitis, cerebral
calcifications, and hydrocephalus.)

Treatment
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.

PREVENTION
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• Wear gloves and thoroughly clean hands and nails when
handling material potentially contaminated by cat feces (sand,
soil, gardening).
• Reduce the exposure risk of pet cats by (1) keeping all cats
indoors (2) giving domestic cats only cooked, preserved, or dry
food.
• Disinfect emptied cat litter tray with near-boiling water for 5
minutes before refilling.
• Eat only well-cooked meat ( > 67°C/153°F).
• Freezing meat to at least −20°C/−4°F also kills T. gondii cysts.
• Clean surfaces and utensils that have been in contact with raw
meat.
• Do not consume raw eggs or raw milk.
• Wash uncooked fruits and vegetables before consumption.
• Prevent cross-contamination: thoroughly clean hands and utensils
after touching raw meat or vegetables.
• Do not drink water potentially contaminated with oocysts.
RUBELLA
 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.
 Spontaneous abortions occur upto 20% of cases. If
infection occur within 20 wks of gestation.

CLINICAL MANIFESTATIONS
Maternal symptoms-
Same as other flu-
1. Rashes
2. Low grade fever
3. Lymphoadenopath
y
4. Joint pain
5. Headache
6. Conjunctivitis
Congenital rubella syndrome
It is characterized by-
 Cardiac – septal defects, PDA, pulmonary arterial
hypoplasia.
 Neurological diseases- with a broad range of
presentation from behaviors to meningoencephalitis.

 Ostitis
 Hepatosplenomegaly.
 Microcephaly
 IUGR
 Cataracts
 Thrombocytopenia – blue berry muffin
lesions.
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.
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.
Symptomatic treatment- analgesic and antipyretics.
Newborn should be managed for complications.
CYTOMEGALOVIRUS
 CMV is a member of the herpes virus species.

 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).
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.
Clinical manifestations
Maternal symptoms- Fetal symptoms-

 Fever 90% are asymptomatic at birth
 Weakness  Petechiae, jaundice
 Swollen glands  Chorioretinitis
 Joint stiffness  IUGR, hearing loss
 Muscle ache  Microcephaly
 Loss of appetite.  Delayed psychomotor
development
 Heart block
Diagnostic evaluations
 Serological testing- IgM are detected

 Amniocentesis
 Cordocentesis
 USG
 Fetal MRI ( rarely)
Treatment
 No definitive Rx.
 Pregnancy termination
 Antiviral drugs-
1. Gangciclovir
2. Foscarnet
3. Cidofovir
Most effective drugs- hyper immune globulin.
HERPES SIMPLEX VIRUS
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.
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 there.
 IUGR if infection acquired in 3rd trimester.
Neonatal infections-
 Chorioretinitis
 MR
 Seizures
 Microcephaly
 Deaths.
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)
Thank you

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TORCH INFECTION IN

They are a group of viral, bacterial, and protozoan

 H- herpes simplex II virus

Other infections- syphilis, varicella zoaster,

 Caused by protozoan intracellular parasite-

by eating infected raw or cocked meat, or

 Trophozytes develop and multiply within the

cells causes cell rupture and death.

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.

 Acute toxoplasmosis is mostly subclinical.

 Affects 0.3-1% of pregnant women, with an

approximately 60% transmission rate to the

 Risk Increases with gestation age.

 Fetal death higher with infection in 1st trimester

 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 non-

 If acute toxoplasmosis is acquired during pregnancy,

the infant is at the risk of developing congenital

toxoplasma infection is-

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

Sabin- feldman dye test- indirect fluorescent

 USG for fetal triad ( Chorioretinitis, cerebral

calcifications, and hydrocephalus.)

Once fetal infection is established-

4-6 weeks course is given to the mother.

 Caused by rubella virus ,a togavirus has single

stranded RNA genome.

 Virus has teratogenic properties can cross the

associated with maternal gestational age.

 Spontaneous abortions occur upto 20% of cases. If

infection occur within 20 wks of gestation.

presentation from behaviors to meningoencephalitis.

 Thrombocytopenia – blue berry muffin

 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

 Prevention by active immunization.

 CMV is a member of the herpes virus species.

 Primary vertical cmv infection caries a 30% - 40%

Maternal symptoms- Fetal symptoms-

 Serological testing- IgM are detected

 Most common STD worldwide.

 Transplacental infection is not usual.

 CS indicated in primary HSV infection.

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