TORCH INFECTIONS

INTRODUCTION

TORCH infections (or TORCH syndrome) are a group of infectious diseases that affect a
developing baby (fetus) or newborn baby. If you get a TORCH infection, you can pass it to
your baby during pregnancy, during delivery or after birth.

Since your baby lacks immunity to fight off diseases, TORCH infections can cause
complications to the pregnancy or prevent your baby’s organs from developing properly.
How sick your baby gets depends on the type of infection and how far along they are in
development when they're infected. Typically, infections that occur early in the pregnancy
result in worse outcomes. Prompt medical treatment is needed to reduce the risk of
complications.

TORCH infections Is an acronym for a group of five infectious diseases:

• T=Toxoplasmosis

• O=Other (Hepatitis B)

• R=Rubella (German measles)

• C=Cytomegalovirus (CMV)

• H=Herpes Simplex Virus (HSV)

Each disease may be teratogenic and crosses the placenta ,Each may adversely affect the
developing fetus , The effect of each varies, depending on developmental stage at time of
exposure.

TORCH infection can be a misleading term as it sounds like a single illness. However, the
term is an acronym of five infections caused due to pathogens. These can cause some serious
problems for the unborn foetus and the mother if it is not diagnosed at the right moment.
These pathogens are transferred from the expectant mother to her foetus during pregnancy or
at childbirth. TORCH consists of the following five infections.
TORCH infections are the term given to a group of infectious diseases that can be passed to
your baby during pregnancy, at delivery or after birth. TORCH stands for toxoplasmosis,
rubella, cytomegalovirus, herpes and other agents

COMPONANT

 Toxoplasmosis
Toxoplasmosis is caused by infection with the protozoan Toxoplasma gondii, an
obligate Intracellular parasite.

Transmission
 Ingestion of raw or partially cooked meat, especially pork, lamb
 venison Contact with infected cat feces.
 Transplacentally (if new infection occurs during pregnancy)
 Through organ transplant or transfusion- very rare
 Women with compromised immune systems are at risk for reactivation of a
previous infection. ingestion of toxoplasma eggs from the soil.
Clinical Manifestations
• Most (70-90%) are asymptomatic at birth
• Classic triad of symptoms:
• Chorioretinitis
• Hydrocephalus
• Intracranial calcifications
• Ocular toxoplasmosis (retinochoroiditis)
• Symptoms of retinochoroiditis include the following
• Decreased visual acuity - Other deficits depend on the location of the lesion
• White focal lesions with inflammation of the vitreous humor (the classic "headlight
in the fog" appearance) seen on ophthalmoscopic examination
• Recurrent lesions at the border of the retinochoroidal scarsCongenital toxoplasmosis
• The classic clinical triad of retinochoroiditis, cerebral calcifications, and convulsions
defines

Diagnostic findings
 serologic antibody testing ELISA
 Maternal IgG testing indicates past infection Can be isolated in culture
from placenta, umbilical cord,
 infant serum PCR testing on WBC, CSF, placenta Not standardized
Newborn serologies with IgM/IgA
Treatment
 for pregnant women- Spiramycin 1 g orally every 8 hours
 If the amniotic fluid test result for T gondii is positive: 3 weeks of
pyrimethamine (50 mg/day orally) and sulfadiazine (3 g/day orally in
2-3 divided doses) alternating with a 3-week course of spiramycin 1 g
3 times daily for maternal treatment
 Pyrimethamine (25 mg/day orally) and sulfadiazine (4 g/day orally)
divided 2 or 4 times daily until delivery (this agent may be associated
with marrow suppression and pancytopenia)
 Leucovorin 10-25 mg/day orally to prevent bone marrow suppression
 Immunocompetent, nonpregnant patients typically do not require

Prevention

 Women planning a pregnancy may be tested before pregnancy. If

the test
  positive there is no need to worry about passing a new infection to
the baby.
 Women who test negative can take precautions.
 Wear gloves and wash hands carefully after handling soil.
 Cook meat thoroughly (until no longer pink inside and juices run
clear)
 Wash hands and any equipment or surfaces that raw meat contacts
thoroughly with warm water and soap.
 OTHER (‘O’)

 HIV: A virus spread through sexual contact or direct contact with HIV-infected blood
(like from sharing needles). Most HIV infections in children occur in the third
trimester, during or after delivery when the birthing parent isn't on the appropriate
medications.
 Syphilis: A sexually transmitted infection caused by bacteria. You can get it from
direct contact with syphilis sores during anal, vaginal or oral sex. Congenital syphilis
is on the rise and babies are getting the infection in the birth canal.
 Fifth disease: A mild rash caused by parvovirus B19. It spreads through saliva and
mucus when an infected person coughs or sneezes.
 Chickenpox: A highly contagious disease caused by the varicella-zoster virus (VZV).
In most cases, getting chickenpox once in your lifetime (usually as a child) or getting
vaccinated against the disease gives you immunity for life.
 Zika virus: A virus spread by an infected mosquito in areas where the virus is
common. It can also be passed through sex with an infected person.

 Hepatitis B (HBV)
Hepatitis B (HBV) is a serious viral disease responsible for 4000 to 5000 deaths each
year in the U.S. due to cirrhosis and liver cancer. Acute infection occurs in 1 to 2
pregnancies per 1000. Estimated that 300 million people worldwide are chronically
infected with HBV.
Transmission

 Incubation usually 50-180 days

 Mode of transmission
• Sexual contact • Perinatal • - Transplacental • - Contact with blood, stool and
saliva • - Shared razors, toothbrushes, towels, and other personal items. • At
risk populations • Southeast Asians, Eskimos, Africans, Chinese, Flipinos and
Indonesians

Clinical manifestations

 Physical Findings – Low-grade fever, nausea, anorexia, jaundice,

hepatomegaly, and malaise. Potential Maternal and Neonatal Effects
a. Maternal – Premature labor and delivery, cirrhosis and liver cancer •
b. Neonatal – Stillbirth. Infants infected at birth have a 90% chance of
becoming chronically infected.

Treatment and prevention

Maternal Treatment – Pregnant women who are exposed to HBV should receive

 vaccine and HBIG. Pregnant women who are already infected should eat
 well, get sufficient rest, avoid stress and avoid alcohol. Alpha interferon
 lamivudine are not recommended during pregnancy.

Neonatal - Infants of infected women should receive HBV vaccine and HGIB.
Prevention

 Hepatitis B vaccination is the best prevention.

 The proper and consistent use of latex condoms may prevent sexual
transmission.
 Do not use IV drugs. Never share needles, syringes, water or “works”.
 Do not share personal items that may have blood on them – razors,
toothbrushes.
 Consider the risks before getting a tattoo or piercing.
 Health care workers should use BSP and safe handling of sharps
 RUBELLA
The name rubella is derived from a Latin term meaning "little red." Rubella is
generally a benign communicable exanthematous disease. It is caused by rubella
virus, which is a member of the Rubivirus genus of the family Togaviridae. Nearly
one half of individuals infected with this virus are asymptomatic.
The major complication of rubella is its teratogenic effects when pregnant women
contract the disease, especially in the early weeks of gestation. The virus can be
transmitted to the fetus through the placenta and is capable of causing serious
congenital defects, abortions, and stillbirths.

Transmission And Clinical Features

 Incubation – 2 to 3 weeks .
 Highly contagious .
 Spread through nasopharyngeal secretions .
 Transplacental transmission

Clinical features

• Conjunctivitis
 • Sore throat • Headache

• General body aches

• Low-grade fever • Chills • Anorexia • Nausea • Tender lymphadenopathy

Types of rubella

1. Postnatal Rubella
• Rash in adults may be quite pruritic.
• The synonym "3-day measles" derives from the typical course of rubella
exanthem that starts initially on the face and neck and spreads centrifugally to
the trunk and extremities within 24 hours. It then begins to fade on the face on
the second day and disappears throughout the body by the end of the third day.
• Temperature
• Fever is usually not higher than 38.5°C (101.5°F).
• Lymph nodes
• Enlarged posterior auricular and suboccipital lymph nodes are usually found
on physical examination.
• The Forchheimer sign may still be present on the soft palate.
2. Congenital Rubella Syndrome
• Sensorineural hearing loss is the most common manifestation of congenital
rubella syndrome.It occurs in approximately 58% of patients. Studies have
demonstrated that approximately 40% of patients with congenital rubella
 syndrome may present with deafness as the only abnormality without other
manifestations.
• Ocular abnormalities including cataract, infantile glaucoma, and pigmentary
retinopathy occur in approximately 43% of children with congenital rubella
syndrome. Both eyes are affected in 80% of patients, and the most frequent
findings are cataract and rubella retinopathy. Rubella
• Congenital heart disease including patent ductus arteriosus (PDA) and
pulmonary artery stenosis is present in 50% of infants infected in the first 2
months' gestation.
• Skin manifestations, including blueberry muffin spots that represent dermal
erythropoiesis and dermatoglyphic abnormalities

Diagnostic findings

 ELISA
 Isolation of virus from urine or endocervical secretions.
 Fluorescent antibody (FA)
 complement fixation (CF) test

Management and prevention.

 Maternal – Mild analgesics, rest and support.

 Neonatal - No specific treatment for congenital rubella treatment. Eye or
 cardiac defects may be corrected or improved with surgery. Careful
 screening for problems and special education are indicated.
 Health Education
 Vaccination of non-immune women before pregnancy is the best
 prevention. The rubella and MMR (measles, mumps, rubella) vaccines are not
 recommended during pregnancy. A woman should wait 28 days after
 CYTOMEGALOVIRUS
Cytomegalovirus (CMV) is a double-stranded DNA virus and is a member of the
Herpesviridae family. Risk factors individuals who attend or work at daycare
centers, patients who undergo blood transfusions, persons who have multiple sex
partners, and recipients of CMV mismatched organ or bone marrow transplants.
Transmission
• Incubation – unknown. CMV is in the herpes family and like herpes can reactivate.
• CMV is very common in young children (perhaps 70% of children
• between 1 and 3 years of age in childcare will be excreting (CMV). Transmission
can occur through contact with saliva, urine, feces, blood, and mucous. It can also be
transmitted sexually and through transfusion and organ donation.
• Transplacental transmission tends to be most serious.
• Infants who are infected during birth or from breastfeeding rarely have serious
problems from the infection.

Clinical manifestations

Physical Findings – Sore throat, fever, body aches, fatigue and hepatomegaly. .
Maternal – Most infections are asymptomatic

Neonatal – Infection is most likely to occur with primary maternal

• infection. Approximate congenital infection rate of 1%. Of these, 10 %

• will be symptomatic, of which 25 % will have fatal disease and 90% of the

• survivors will have serious sequelae- IUGR, microcephaly, CNS

• abnormalities, hydrocephaly, periventricular calcification, deafness,

• blindness, and mental retardation. A small percentage of newborns

 • asymptomatic at birth will also develop late sequelae.

Diagnosis

Maternal –

 ELISA, fluorescent antibody (FA), complement fixation (CF)

 seroconversion to +IgM, and isolation of the virus by culture.
 Prenatal - Affected infant’s may demonstrate the following
 ultrasound findings:
• microcephaly, hydrocephalus, necrotic cystic or calcified lesions in the
• brain, liver or placenta, IUGR, oligohydramnios, ascites, pleural or
• pericardial effusion, hypoechogenic bowel and hydrops.
 Amniocentisis with culture or DNA identification.
 Cordocentesis can be used to document presence and severity of disease

Newborn –

 virus isolation is the optimal method of documenting CMV

 infection. Specimens can be taken from urine, nasopharnyx, conjunctiva •
 spinal fluid.

Treatment and prevention

 Maternal – treat symptoms Ganciclovir , Valganciclovir

 Neonatal - no satisfactory treatment available. Infant is contagious and should
be isolated. . Women can reduce their risk of CMV by practicing universal
precautions and careful hand washing, especially after any contact with saliva,
urine, feces, blood and mucous. Avoid sharing glasses or eating utensils.
Medical or day care workers may consider being tested prior to pregnancy to
determine if they have had CMV, as they would then have little cause for
concern.
 Herpes Simplex Virus (HSV)
Herpes is caused by the herpes simplex viruses, which are similar to the viruses that
cause chickenpox and shingles. After the initial infection, the herpes simplex viruses
can hide within nerve cells and later launch new attacks. There are 2 main kinds of
herpes simplex virus (HSV):
• type I→ which is usually associated with cold sores around the mouth
• type 2→ which is usually associated with genital sores. However, either type can
infect either the mouth or genitals and both can be passed on to the newborn.

Clinical features
• Acute herpetic gingivostomatitis
• This is a manifestation of primary HSV-1 infection that occurs in children aged 6
months to 5 years. Adults may also develop acute gingivostomatitis, but it is less
severe and is associated more often with a posterior pharyngitis.
• Infected saliva from an adult or another child is the mode of infection. The
incubation period is 3-6 days.
• Abrupt onset • High temperature (102-104°F)
• Anorexia and listlessness
• Gingivitis (This is the most striking feature, with markedly swollen, erythematous,
friable gums.)
• Vesicular lesions (These develop on the oral mucosa, tongue, and lips and later
rupture and coalesce, leaving ulcerated plaques.) • Tender regional lymphadenopathy
• Perioral skin involvement due to contamination with infected saliva • Course: Acute
herpetic gingivostomatitis lasts 5-7 days, and the symptoms subside in 2 weeks. Viral
shedding from the saliva may continue for 3 weeks or more.
• Acute herpetic pharyngotonsillitis
• In adults, oropharyngeal HSV-1 infection causes pharyngitis and tonsillitis more
often than gingivostomatitis.
• Fever, malaise, headache, and sore throat are presenting features.
• The vesicles rupture to form ulcerative lesions with grayish exudates on the tonsils
and the posterior pharynx.
• Associated oral and labial lesions occur in fewer than 10% of patients.
• HSV-2 infection can cause similar symptoms and can be associated with orogenital
contact or can occur concurrently with genital herpes.
• Herpes labialis
• This is the most common manifestation of recurrent HSV-1 infection. A prodrome
of pain, burning, and tingling often occurs at the site, followed by the development of
erythematous papules• Maximum viral shedding is in the first 24 hours of the acute
illness but may last 5 days.

Types of herpes
a) Primary genital herpes
• Primary genital herpes can be caused by both HSV-1 and HSV-2 and
can be asymptomatic. The clinical features and course of primary
genital herpes caused by both HSV-1 and HSV-2 are indistinguishable,
but recurrences are more common with HSV-2.
• Primary genital herpes is characterized by severe and prolonged
systemic and local symptoms. The symptoms of persons with a first
episode of secondary HSV-2 infection are less severe and of shorter
duration.
• Preexisting antibodies to HSV-1 have an ameliorating effect on
disease severity caused by HSV-2.
• Prior orolabial HSV-1 infection protects against genital HSV-1 but
not HSV-2.
 • Symptoms of primary genital herpes are more severe in women, as
are complications. • Clinical features: The incubation of primary
genital herpes period is 3-7 days (range, 1 d to 3 wk). Constitutional
symptoms include fever, headache, malaise, and myalgia (prominent in
the first 3-4 d). Local symptoms include pain, itching, dysuria, vaginal
and urethral discharge, and tender lymphadenopathy.
• Clinical features in women: Herpetic vesicles appear on the external
genitalia, labia majora, labia minora, vaginal vestibule, and introitus. In
moist areas, the vesicles rupture, leaving exquisitely tender ulcers. The
vaginal mucosa is inflamed and edematous. The cervix is involved in
70%-90% of cases and is characterized by ulcerative or necrotic
cervical mucosa. Cervicitis is the sole manifestation in some patients.
• Clinical features in men: Herpetic vesicles appear in the glans penis,
the prepuce, the shaft of the penis, and sometimes on the scrotum,
thighs, and buttocks. In dry areas, the lesions progress to pustules and
then encrust. Herpetic urethritis occurs in 30%-40% of affected men
and is characterized by severe dysuria and mucoid discharge. The
perianal area and rectum may be involved in persons who engage in
anal intercourse, resulting in herpetic proctitis.
b) Recurrent mucocutaneous HSV infections
• Following the establishment of latency in the corresponding sensory
nerve ganglion cells, HSV can cause recurrent infection that can be
subclinical (manifesting as viral excretion without lesions) or overt
(manifesting as mucosal or cutaneous lesions with viral excretion).
• Oral recurrences are often triggered by recognizable stimuli such as
pyrexia (fever blisters and cold sores), stress, or sunburn. Genital
recurrences are more likely to be linked to stress rather than to pyrexia.
Females may relate a relationship to the menstrual cycle.
• Localized burning or paraesthesias may precede recurrent lesions.
Unlike primary infection, constitutional symptoms are minimal in most
cases. • Recurrences last 3-7 days and can occur numerous times per
year or once or twice in a lifetime. Overall, the number of yearly
recurrences tends to decrease over time.
• Because recurrences can be clinically unrecognizable, transmission to
susceptible individuals can occur in the absence of overt lesions. In
genital HSV infections, barrier protection should be used regardless of
existing lesions, even in the absence of a history of genital HSV
infection.
Diagnostics
 Tissue culture-swab specimen from vesicles
 Pap smear of lesion
 Visualization of a blister or ulcer-like, painful lesion by
experienced clinician.

Treatment and prevention

 Anti-viral drugs can shorten the duration of a herpes attack,

alleviate symptoms and reduce the number of attacks.
 Oral acyclovir is sometimes used in late pregnancy to decrease
the need for cesarean birth.
 Acyclovir and vidarabine are used to treat neonatal HSV –
more successful with localized infection than one that has
spread to brain and
 other internal organs.

Prevention

 Encourage women with a history of genital herpes to avoid

“triggers” (heat, friction, intercourse, peanuts, chocolate,
fever or stress), especially during the later part of
pregnancy.
 Recommend condoms or abstinence in pregnant women
without HSV who have partners with HSV.
 Encourage careful hand washing to prevent spread of HSV
to others or to other parts of the body
 People with active cold sore lesions should avoid kissing
others, especially newborns.
 Educate women of the importance of reporting prodromal
symptoms or lesions to their care providers with suspected
labor or ruptured.