The TORCH complex is a set of perinatal infections that can be transmitted from mother to fetus, including toxoplasmosis, rubella, CMV, and herpes. These infections pose risks for severe fetal anomalies and can cause fetal death. Toxoplasmosis is caused by the parasite Toxoplasma gondii and can be acquired through contaminated food, water, or soil. Rubella virus causes congenital rubella syndrome and poses greater risks the earlier in pregnancy the maternal infection occurs. CMV is the most common congenital viral infection and can cause hearing loss, seizures, or developmental delays in infants. Herpes infection during pregnancy risks transmission to the newborn, potentially causing skin lesions, eye damage

1. ASHLY ALEX

2.  TORCH complex is a medical acronym for a set
of perinatal infections .
 TheTORCH 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 blood stream transplacentally via the
chrionic villi.
 Hematogenous transmission may occur at
anytime 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, ParvovirusB- 19, HEP B)
 R–RUBELLA
 C–CYTOMEGALOVIRUS
 H–HERPES SIMPLEXVIRUS–2

5.  Toxoplasmosis is a disease caused by an
intracellular parasite TOXOPLASMAGONDII.
 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).
Out breaks of toxoplasmosis have also been
linked to the consumption of unfiltered water

7.  •Primary maternal infection in pregnancy–
 Infection rate higher with infection in 3rd
trimester.
 Fetal death higher with infection in 1st
trimester

8. Signs and sympoms
 Infected Pregnant women : usually no clinical
manifestation.
 Although some may have a mild
mononucleosis-like syndrome, regional
lymphadenopathy, or occasionally
chorioretinitis.
 Similarly, infected neonates are usually
asymptomatic at birth.

9.  Manifestations may include :
Prematurity
Intrauterine growth restriction
Jaundice
Hepatosplenomegaly
Myocarditis
Pneumonitis
Various rashes
anemia, thrombocytopenia,
 and abnormal CSF findings (Mononuclear
CSF pleocytosis or elevatedCSF protein)

10. The classic triad of findings :
chorioretinitis,
 hydrocephalus, and
 intracranial calcifications

13. Diagnosis
 Serial IgG measurement (for maternal
infection)
 Amniotic fluid PCR (for fetal infection)
 Serologic testing, brain imaging, CSF analysis
and ophthalmologic evaluation (for neonatal
infection),
 and PCR testing of various body fluids or
tissues

14. Treatment
 •In PREGNANT WOMEN with an established
recent infection, SPIRAMYCIN (3g daily in
divided doses) should be given.
In neonates :
 Pyrimethamine: 50mg twice daily for 2 days
then 50mg daily.
PLUS
Sulfadiazine: 75mg/kg/daily in two divided doses
for 2 days then 50mg/kg/twice daily
PLUS
Folinic Acid: 10-20mg daily

15. Rubella

16.  It is caused by rubella virus,Rubivirus genus and
familyTogaviridae.
 Intrauterine infection with rubella virus is referred
to as congenital rubella infection (CRI) or
syndrome.
 Infection with rubella earlier in pregnancy(1st
trimester ) cause worse prognosis and neonatal
complications.
 The virus can be transmitted to the fetus through
the placenta and is capable of causing serious
congenital defects, abortions, and stillbirths.

17.  In the baby
 Infection in weeks 8-10 of pregnancy results
in damage in up to 90% of surviving infants.
Multiple defects are then common.
 The risk of damage reduces to 10-20% if the
infection is in weeks 11-16 of pregnancy.
 Fetal damage is rare over 18 weeks of
gestation.

18.  Transmission to the fetus occurs via maternal
hematogenous spread to the placenta.
 It typically occurs 5-7 days after maternal
inoculation.
 After the virus invades the placental barrier,
it spreads throughout the fetus via their
vascular system.
 The congenital defects that result from
infection is secondary to the cytopathical
damage ensued to the blood vessels.
 This in turn results in ischemia of the affected
organs .

19. Clinical features
Transient :
 Intrauterine growth restriction.
 Thrombocytopenic purpura (25% - 'blueberry
skin').
 Haemolytic anaemia.
 Hepatosplenomegaly.
 Jaundice (common).
 Radiolucent bone disease (20%).
 Meningoencephalitis (25%) +/- neurological
sequelae

20.  Developmental:
 Sensorineural deafness 80% .
 General learning disability (55%).
 Insulin-dependent diabetes (20%, immune-
mediated but often delayed to adolescence or
adulthood).
 'Late-onset' disease at 3-12 months with rash,
diarrhoea, pneumonitis and high mortality.

21.  Permanent:
 Congenital heart disease (commonly patent
ductus arteriosus or peripheral pulmonary artery
stenosis).
 Eye defects including cataracts, congenital
glaucoma, pigmentary retinopathy (50% - so-
called 'salt and pepper'), severe myopia,
microphthalmia.
 Microcephaly.

23.  The risk of maternal-fetal transmission is the
greatest in the first 10 days after gestation
 cardiac and eye defects typically resulting
when maternal infection occurs prior to 8
week.
 Hearing loss is typically observed in
infections up to 18 weeks of gestation

25. Lab tests :
 Isolation of the rubella virus in culture
 Demonstration of rubella-specific IgM
antibodies
 Demonstration of rubella-specific IgG
antibodies that persist at a higher
concentration or longer duration than
expected from mere passive transfer of
maternal antibodies
 Detection of rubella virus RNA by reverse-
transcriptase polymerase chain reaction

26. Treatment
 Supportive care and surveillance is the only
recommended option available at this time.
 Close monitoring within the first 6 to 12 months of
life is recommended; particularly for the evaluation
of hearing impairment .
 Prevention is considered the most important aspect
as far as the management of CRI concerned.
 Preventive measures include recommended
immunizations, testing of pregnant women for
rubella immunity and proper counseling regarding
avoiding exposure.

28.  CMV is a doubles stranded DNA herpes virus
 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.

29.  Possible routes of transmission include
sexual contact,
organ transplantation,
transplacental transmission,
transmission via breastmilk,and
blood transfusion(rare).

30.  Primary,reactivation,or recurrent CMV infection
can occur in pregnancy and can lead to congenital
CMV infection.
 Approximately 85 percent of newborns with
congenital CMV infection can be asymptomatic
at birth.
 15 percent will develop progressive hearing loss
and visual impairment as they age.

31. Transplacental infection can result in :
 intrauterine growth restriction,
 Sensorineural hearing loss,
 Intracranial calcifications,
 Jaudice
 Petichiae
 microcephaly,
 hydrocephalus,
 hepatosplenomegaly,
 Delayed psychomotor development,
 Thrombocytopenia and/
 Chorioretinitis .

32.  Vertical transmission of CMV can occur at any
stage of pregnancy.
 Severe sequelae are more common with
infection in the 1st trimester.
 The overall risk of infection is greatest in
the 3rd trimester.
 The risk of transmission to the fetus in
primary infection is 30%-40%.

36. Diagosis In foetus
Amniocentisis : viral culture and PCR
Ultrasound

38. Treatment
 Ganciclovir 5mg/kg IV every 12 hours for 14
days
OR

Valganciclovir 900mg PO daily for 3-6
months
OR

CMV-specific hyperimmune globulin (200
units/kg of body weight)

40.  Herpes simplex virus (HSV) infection during
pregnancy can pose a serious threat to the
developing fetus and the newborn infant.
 Transmission typically occurs via direct contact
between the neonate and an infected maternal
genital tract.
 If the primary HSV infection was acquired during
pregnancy, then the risk of transmission is
greater as compared with reactivation of a
previous infection.
 incidence of neonatal HSV infection ranges from
1 in 3200 to 1 in 10,000 births .

41.  HSV is a member of the Herpes viridae family of
viruses
 Enters the host through the inoculation of oral,
genital, or conjunctival mucosa.
 Inoculation also can occur through breaks in the
skin.
 Dissemination of the virus eventually allows the
virus to reach the dorsal root ganglia, where it
remains dormant for the rest of the host’s life.
 Antiviral drugs do not affect latent HSV infection
and therefore infection is life-long

42.  Intrauterine HSV is a rare occurrence and most likely
is caused by maternal viremia associated with
primary infection during pregnancy.
Intrauterine infection is associated with
 hydropsfetalis and
 in-utero fetal demise.
The characteristic triad noted at birth includes
skin lesions consistent of vesicles,
ulcerations or scarring ,
eye damage and
CNS abnormalities, such as hydranencephaly and
microcephaly.

43.  Clinical manifestation can arise any time during
the first six weeks of life, but usually occurs
within the first month of life .
Classic CSF findings include :
 a mononuclear cell pleocytosis,
 normal or slightly low glucose concentration
 and moderately elevated protein level.
Electroencephalogram (EEG) is often abnormal
from early on in the disease and may show focal
or multifocal periodic epileptic form discharges
. Neuroimaging studies may show parenchymal
brain edema, hemorrhage or destructive lesions
in the temporal frontal, parietal or brainstem
regions in the brain

46. Diagnosis
 Diagnosis of neonatal HSV infection can be
established through any of the following
methods:
 Isolation of HSV in culture
 Detection of DNA via PCR assays
 Detection of HSV specific antigens using
rapid direct immunofluorescence or enzyme
immunoassays.

47. Treatment
 Suppressive viral therapy from 36 weeks
until delivery
 Valacyclovir 500 mg orally BD OR
 Acyclovir 400 mg orallyTDS.
Cesarean section is recommended for all
women in labor with active genital lesions
or prodromal symptoms such as vulvar pain

48. Others are :
Disease Trasmission Symptoms Diagnosis Treatment
Varicella zooster Ist 20 weeks of
pregnancy
Cicatricial
lesions ,limb
hypoplasia,micr
ocepaly ,hydrops
etc
Prenatal
Ultrasound
andMRI
Acyclovir
Parvo virus b19 1st 2 trimester of
pregnancy
ProdromalFever,
Slapped cheek
rash anemia etc
Serological
PCR
Symptomatic
relief
Syphilis
(Trepinoma
palidum )
Severe outcome
after 4 weeks
Miscarrage
,prematurity
,still birth,
hepatosplenome
galy,bullous
rash,pneumonia
Serological tests Benzathine
Penicillin G IM
Hep b transmission
specially in the
third trimester.
jaundice ,rashes
PAN ,Vomiting
,dark urine etc
Serological tests Lamivudine
,interferon alpha
entecavir