TORCH

INTRODUCCION

TORCH infections classically include:

• Toxoplasmosis
• Other Infections (Varicella, syphilis and Parvovirus B19)
• Rubella
• Cytomegalovirus (CMV)
• Herpes simplex virus (HSV)
TORCH infections have also been known to include Treponema pallidum, Hepatitis viruses, and
human immunodeficiency virus (HIV).[3]
DEVELOPMENT

In addition to passing horizontally (from person to person), TORCH infections can also transmit
vertically (from mother to infant). When a pregnant woman becomes infected, the infection can
spread to her unborn fetus. Generally, the earlier the exposure to the teratogen, the more
deleterious its effects. Infection during the first trimester is likely to cause a more severe version
of the congenital defects in the growing embryo. The later in pregnancy that an infection occurs,
the more likely that the fetus will develop a neonatal infection rather than develop congenital
abnormalities.
ETIOLOGY

• The TORCH infections include causative organisms Toxoplasma gondii, rubella virus,
cytomegalovirus, HSV 1 and 2, hepatitis B virus, HIV, and others like syphilis, parvovirus, and
varicella. Transmission of the pathogens may occur prenatally by the transplacental route,
perinatally by blood or vaginal secretions. Postnatal infections tend to be less impactful.
Others, such as HIV, hepatitis B, and syphilis, can be transmitted via sexual contact to a
susceptible mother. Rubella and varicella can be prevented by properly immunizing mothers.
TOXOPLASMOSIS

Results from infection with the parasite Toxoplasma gondii. This parasite goes through its
reproductive stages in the intestines of the Felidae family and then gets expelled as an oocyst into
the environment. Then, these oocysts cause toxoplasmosis through inhalation of fecal particles or
by the ingestion of infected tissue. After infection of the mother, there is a transplacental
transmission of the parasite to the fetus causing congenital toxoplasmosis. The likelihood of
infection is the highest in the third trimester but the earlier in the pregnancy that the infection
occurs, the more severe the manifestation of the congenital birth defects
TESTING

• requires proving the presence of either the parasite itself, through PCR, microscopy or
inoculation, or by identifying the toxoplasma gondii specific IgG, IgM or IgA humoral
response. Brain imaging (calcifications, hydrocephaly, and microcephaly) and retinal exams
(chorioretinitis) can be used to determine the severity of symptoms but are not
considered diagnostic.
CLINICAL

• A perinatal, or more rarely prenatal, initial infection of Toxoplasma gondii classically causes a
baby to be born with retinal lesions, hydrocephalus, and intracranial calcifications but is also
associated with anemia, jaundice, hepatosplenomegaly, and thrombocytopenia. Approximately
75% of those infected in utero will be asymptomatic at birth, but as they grow, they will be at
significant risk for developing motor dysfunction, cerebellar dysfunction, microcephaly,
seizures, chorioretinitis, intellectual disabilities, and sensorineural hearing loss.[26]
Toxoplasmosis in healthy adults is typically asymptomatic.[3] The prevalence of congenital
toxoplasmosis is approximately 0.1 to 0.01 per 1000 live births and is attributable to pregnant
women eating undercooked meat and cleaning cat litter boxes.[
TREATMENT

• observational studies have demonstrated an effective reduction in transplacental transmission

and/or severity of clinical manifestations in symptomatic infants. The two regimens often used
are spiramycin (fetal prophylaxis preventing intrauterine infection) and combined
pyrimethamine/sulfadiazine/ folinic acid (treatment of evolving fetal infection)
OTHER

Varicella-zoster virus (VZV) is an airborne DNA virus of the herpesvirus group that spreads by
sneezing, coughing, or contact with active lesions.[8] It also passes from mother to fetus
transplacentally.[9] There is an estimated 2% chance that an infant will develop congenital
varicella syndrome if the mother contracts VZV during the first two trimesters.[10]
TESTING

• The mother’s history of chickenpox clinically confirms congenital varicella syndrome (CVS)
during the pregnancy and the presence of congenital skin lesions following dermatomes in the
infant. It is also diagnosable by detecting VZV DNA in either amniotic fluid or fetal blood
CLINICAL

• Despite there being 60 million new cases of varicella infection each year, CVS is rather rare,
only 130 cases reported since 1947, but mortality rates are 30% in the first few months. CVS
often causes skin lesions, limb hypoplasia, neurological abnormalities, and developmental
delay. There is no evidence that infants born asymptomatic will develop symptoms in the future
OTHER

• Syphilis is an infection of the spirochete Treponema pallidum and spreads by sexual exposure
or vertical transmission. Vertical transmission most commonly occurs transplacentally but can
also occur due to peripartum exposure to vaginal fluid. In women recently infected with
syphilis, the probability of transmission is more than 80%.
TESTING

• Congenital syphilis diagnosis is by a combination of serology and the presence of clinical

symptoms. Often this diagnosis is presumptive, and an infant will need to be periodically
checked by a physician if it is at risk for congenital syphilis
CLINICAL

• Syphilis infects 5.6 million people per year.[11] Pregnancies where the woman contracts
syphilis and is not treated result in stillbirth 25% of the time, neonatal death 14% of the time
and in 41% of cases the infant is born with congenital syphilis. Congenital syphilis can result in
neurodevelopmental deficits, musculoskeletal deformities as well as renal and gastrointestinal
issues. The classical Hutchinson triad described in infants with congenital syphilis consists of
Hutchinson teeth (small, peg-shaped, notched upper incisors), interstitial keratitis and
sensorineural hearing loss. There is only a 20% chance that an untreated affected mother will
have a healthy infant. The longer the fetus is exposed to T. pallidum in utero the bleaker the
outcome. Pregnant women can be treated with benzathine penicillin G to diminish the bacterial
load and decrease the likelihood of complications during pregnancy
TREATMENT

• Syphilis must be diagnosed and treated immediately. Expectant mothers should be tested during
pregnancy and, if positive, treated.[25] Treatment of the neonate will depend on whether the
mother was treated appropriately during pregnancy. Normal neonates born to mothers adequately
treated during pregnancy and greater than four weeks before delivery or have a non-reactive RPR
but were born to mothers not treated properly should receive a single intramuscular injection of
benzathine penicillin G (50,000 U/kg), although no evaluation is required or recommended.
Infants with serologic tests that confirm congenital syphilis should receive aqueous penicillin
g (200,000 to 300,000 units/kg/day IV, administered as 50,000 units/kg every 4 to 6 hours for ten
days). If the child has a negative evaluation for clinical and laboratory evidence of syphilis,
treatment with up to 3 weekly doses of benzathine penicillin G (50,000 U/kg IM) can be
considered
OTHER

Parvovirus B19, a single-stranded DNA virus, is the only member of the Parvoviridae family that
is pathogenic in humans. It passes through respiratory droplets, blood exposure, or vertically
transmitted through the placenta.
TESTING

• Congenital parvovirus B19 is most accurately diagnosed using a PCR assay to isolate
parvovirus B19 DNA in the amniotic fluid or fetal blood. Clinicians can measure it with IgM
antibody serology
CLINICAL

• Parvovirus B19 only affects 1 to 5% of pregnant women, but the consequences can be
devastating. This infection can lead to spontaneous abortion, severe neurodevelopmental
deficits, and hydrops fetalis but 67 to 76% of infants are born to mothers infected with
parvovirus B19 are unaffected
RUBELLA

• Rubella is a single-stranded, positive-sense RNA virus that gets transmitted from infected
individuals through aerosols. It also passes from the infected mother to the fetus
transplacentally
TESTING

• To diagnose a patient with congenital rubella, the virus itself can be isolated, through PCR or
culture, or the virus’ RNA can be isolated through reverse transcriptase PCR of bodily fluids.
The presence of rubella specific IgM and IgG is also enough to base a diagnosis of congenital
rubella
CLINICAL

• Infants perinatally infected with rubella are often asymptomatic but may later develop hearing
loss, blindness, heart defects, encephalitis, endocrinopathies as well as behavioral and
intellectual deficits. Children suspected of having congenital rubella must be surveilled
carefully for the onset of new symptoms. The prevalence of congenital rubella is as high as
approximately 175 per 100000 live births in the developing Americas.[29][30][31] In general,
the earlier the fetus is infected with rubella during pregnancy, the more severe the congenital
deficits are. Up to 85% of babies born to mothers infected with rubella during the first trimester
may develop the congenital rubella syndrome which consists of sensorineural deafness,
cataracts, congenital heart problems, central nervous system deficits, impaired mental
development, bone defects, and hepatosplenomegaly.
TREATMENT

• Congenital rubella, once developed, cannot be treated. But it is the most common vaccine-
preventable neonatal disease. A single dose of rubella vaccine to mother can produce life long
immunity.[16] Mothers should have their immunity checked at the beginning of a pregnancy
CITOMEGALOVIRUS

• CMV is a human-specific double-stranded DNA virus of the Herpesviridae family. Horizontal

transmission is via the mucous membrane, blood transfusions or, organ transplants. It can pass
from mother to fetus transplacentally but also from contact with cervical or vaginal secretions
during the birthing process or by breastmilk postnatally. Though rarer, a woman with a latent
CMV infection can infect her fetus if she becomes infected with an additional strain during
pregnancy.
TESTING

• Despite the high disease burden, there are still no screening programs for mothers or infants to
detect CMV infections. In infants, clinical symptoms can go absent or can be ambiguous
enough not to suspect congenital CMV. In the past, testing for congenital cytomegalovirus
involved using urine or saliva samples to isolate the virus in tissue cultures.[22] More recently,
real-time PCR, which gets repeated if positive, is being used to detect the virus, which is less
resource-intensive and could potentially support more widespread screening in the future.[23]
In pregnant women, CMV diagnosis can also be through CMV specific IgM and IgG serology.
CLINICAL

• Though commonly asymptomatic in healthy adults, CMV affects an estimated 60% of people in
the United States (age-adjusted).[32] Additionally, CMV is the number one cause of infection-
induced birth defects. Congenital CMV affects one in every 150 live births globally.[33] CMV is
also the leading cause of nongenetic congenital hearing loss. Approximately 7 to 10% of infants
with congenital CMV develop clinical manifestations. These include petechiae, jaundice,
hepatosplenomegaly, chorioretinitis as well as neurological deficits, which consists of physical
and mental retardation, deafness, and even death in about 10% of patients. Many of these infants
are born asymptomatic and lack proper screening for congenital CMV. They are likely to develop
these issues later in life. It is common practice to treat symptomatic CMV positive infants with six
months of valganciclovir. Asymptomatic infants customarily receive no treatment
• Patients with symptomatic cytomegalovirus infections should be treated with ganciclovir and
valganciclovir. The primary reason for this therapy is to preserve hearing. Neonates with
symptomatic congenital CMV disease with or without central nervous system (CNS)
involvement show better outcomes at two years when treated with oral valganciclovir (16
mg/kg/dose, administered orally twice daily) for six months. Dosing should be adjusted as the
infant grows.
HSV

HSV-1 and HSV-2 are large, enveloped double-stranded DNA viruses. These viruses are passed
from direct contact with mucous membranes, saliva or sores and can occur despite a lack of active
infection. Once acquired, the virus often is asymptomatic or non-specific, which leads to the spread
of the infection due to a lack of proper precautions. HSV-1 is more commonly found orally, while
HSV-2 is more often a genital infection, but infection of either virus can occur anywhere on the
body. This virus is primarily passed to the infant during delivery when the mother has an active
infection with sores but has been known to occur during latent infections. While episodes of active
HSV can be relatively rare after initial infection, pregnancy often triggers active infection in
approximately 75% of HSV positive women. Infants born to mothers initially infected with HSV in
the third trimester of pregnancy are at the highest risk for contracting neonatal HSV
TESTING

• Congenital HSV is detected by either HSV isolation on culture or by PCR. Today, PCR is
becoming a more common test due to its more accurate and precise ability to diagnose an HSV
infection. Screening for HSV antibodies is problematic as it is not type-specific, and oral HSV-
1 infections are prevalent and do not pose the same risk as a genital HSV-2 infection
CLINICAL

• Approximately 50 to 70% of people in developed countries and nearly 100% of those in

developing countries are seropositive for oral herpes simplex virus (HSV-1). Genital herpes
simplex virus (HSV-2) is present in approximately 10 to 40% of the population and about 22% of
pregnant women.[16][25] These viruses affect a huge percentage of the population and are
incurable and require lifetime management. Neonatal herpes is uncommon, but symptoms are
severe and can be deadly. Symptoms include viral sepsis, organ failure (lung, liver), disseminated
intravascular coagulation, encephalitis, vesicular rash, seizures, bulging fontanelle, and death.
Acyclovir, an anti-viral treatment, is available for affected infants but must be administered
promptly to afford the most protection to the infant. If an HSV infection is suspected, a cesarean
delivery is the recommended approach as 85% of neonatal HSV infection is peripartum.
TREATMENT

• Patients with neonatal HSV should be treated aggressively. Clinical trials have demonstrated
that high-dose intravenous acyclovir (60 mg/kg/day intravenously divided three times daily)
for acute therapy. The length of this therapy varies from fourteen to twenty-one days depending
on the severity of disease (10 for SEM/21 for disseminated and CNS) followed by long-term
oral acyclovir suppressive therapy (300 mg/m/dose, given orally three times daily for six
months is best for the management of neonatal herpes infection. This work has dramatically
reduced morbidity and mortality from neonatal HSV.[23] Complete blood counts and renal
function should be monitored. Dosing should be adjusted as the infant grows.
COMPLICACIONES

• Complications are intrauterine and postnatal. In utero complications include intrauterine

growth retardation, hydrops fetalis, and intrauterine death. Postnatal complications include
failure to thrive, ophthalmologic disease, developmental delay, paralysis, seizure disorders,
hearing loss, congenital heart diseases, and death.[36] Congenital infections are the number one
cause of sensorineural hearing loss in children.
PATIENT EDUCATION

• Maternal education and early in utero diagnosis is very important in diagnosing a child with a TORCH infection. Early
intervention may allow for the treatment during pregnancy (toxoplasmosis and syphilis) or prophylaxis at delivery
(HSV) to help eliminate risk to the newborn. Regular prenatal care and maternal health are key elements for any
pregnancy. All women of childbearing age should ensure that they have their immunizations up to date as this can
prevent any possibility of congenital rubella syndrome.[37]
• Safe sexual practices can help eliminate the risk of the acquisition of syphilis, HIV, and HSV during
pregnancy. Expectant mothers who have a febrile illness during pregnancy should be sure to report that illness to their
physicians. Safe eating practices such as the avoidance of processed foods (deli meats) and eating thoroughly cooked
foods can help prevent the transmission of toxoplasmosis. Similarly, expectant mothers should refrain from cleaning
the cat litter boxes during pregnancy to prevent the transmission of toxoplasmosis. [38] The prevention of
cytomegalovirus has focused on the area of hygiene, encouraging expectant mothers to avoid situations such as child
care settings or nursing care when possible. When not possible, hand hygiene is essential. Some recent reports have
looked at the use of immunoglobulin to prevent the transmission of CMV to the fetus and show some promise.
• EQUIPO ENTRE OBSTETRA Y NEONATOLOGO (RADIOLOGO)
BIBLIOGRAFIA

• Jaan A, Rajnik M. TORCH Complex. [Updated 2023 Jul 17]. In:

StatPearls [Internet]. Treasure Island (FL): StatPearls
Publishing; 2023 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK560528/
• Belanger BG, Lui F. Embryology, Teratology TORCH. [Updated 2023
Jul 24]. In: StatPearls [Internet]. Treasure Island (FL):
StatPearls Publishing; 2023 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK545148/