ARBAMINCH UNIVERISITY

COLLEGE OF MEDICIN AND HEALTH SCIENCES

SCHOOL OF NURSING POST GRADUATE PROGRAM ON NEONATAL
NURSING.
COURSE TITLE- Advanced Neonatal Nursing I
Individual Assignment on TORCHS infection
PREPARED BY: Bishaw Mebreku………PRMSH/023/15

Submitted to: Nega D. (BSc, MSc, Ass. Prof. of PACHN )

Submitted date: 11/27/2023

ARBAMINCH ETHIOPIA
12/19/2023 By Bishaw M.
Presentation out line

• Introduction. • Diagnosis

• Epidemiology • Treatment

• pathophysiology • Prevention of TORCH infection.

• Clinical feature • References.

Objectives

• At the end of this presentation , you will able to:

Define “TORCH”
Elaborate the epidemiology and etiology of TORCH infections.
Discuss the way of transmission TORCH infections.
Explain the clinical features of TORCH infections.
Discuss the diagnosis, and treatment of TORCH infections
 Introduction

 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 or TORCHS infections are a group of infections that in a pregnant

woman can lead to severe fetal anomalies or even fetal loss.

 Vertical transmission is passage of an infectious agent from the mother to

her fetus through the placenta, during labor or delivery,or by breastfeeding.
 Cont..,

 The mother often has a mild infection with few or no symptoms.

 TORCH is an acronym

T – Toxoplasmosis

O – Other agents (parvovirus, HIV, HBV)

R – Rubella

C – Cytomegalovirus

H – HSV

S – Syphilis
Pathophysiology
Cont..,

Mode of transmition Transplace Perinatal

ntal
Toxoplasmosis Yes No
HBV Yes Yes
Syphilis Yes No
Rubella Yes No
CMV Yes Yes
HSV Yes Yes
 TORCH Infections - Common Clinical Manifestations

Fetus: abortion, still birth, IUGR, congenital anomalies

Neonate:

General: SGA, prematurity, failure to thrive

Vital Signs: hypo/hyperthermia, apnea, tachypnea

Skin: petechiae , purpura , pallor, maculopapular rash, jaundice

Head: microcephaly, large fontanelle, hydrocephalus

 Cont..,

Eyes: chorioretinitis, cataracts, glaucoma , microphthalmia

Respiratory: pneumonia

Cardiovascular: structural defects , CHF

Abdomen: hepatosplenomegaly

CNS: hypo/hypertonia, seizures, microcephaly

All TORCH infections are associated with varying degrees of pregnancy

loss.
 Congenital Toxoplasmosis

If a woman becomes newly infected with Toxoplasma during or just before
pregnancy, she can pass the infection to her unborn baby (congenital
transmission).

Congenital transmission from immunologically normal women infected

before pregnancy is extremely rare.

Transmission to the fetus usually occurs when infection is acquired by an

immunologically normal mother during gestation.
Epidemiology

The damage to the unborn child is often more severe the earlier in
pregnancy the transmission occurs.

untreated maternal infections acquired in the first trimester,

approximately 25% of fetuses are infected, usually with severe
disease.

 Of untreated maternal infection acquired in the second trimester

approximately 25% fetus infected.
 Cont..,

untreated maternal infection acquired in the third trimester, approximately

65% of fetuses are infected, usually with disease that is mild or inapparent
at birth.

These different rates of transmission and outcomes are most likely related
to placental blood flow, virulence and amount of T. gondii acquired, and
immunologic capacity of the mother to limit parasitemia.
Transmission and pathogenesis

The cat is the only definitive host, but other mammals can be

infected incidentally.

 Farm animals (cattle, pigs, sheep) can acquire infection after

ingestion of food or water contaminated with infected cat feces that
contain oocysts.
Cont..,

Humans can acquire infection by ingestion of raw or poorly cooked

meat containing the Toxoplasma cysts or by ingestion of food or water

contaminated with oocysts

Congenital toxoplasmosis occurs almost exclusively as a result of

primary maternal infection during pregnancy
 Etiology

protozoan, Toxoplasma gondii.

o Oral intake of raw/ not well cooked meat or

o Of contamination with cats feces could lead to human infection

(Acquired).

o Congenital Toxoplasmosis results from transplacental infection during

pregnancy.
 Clinical manifestation

• more than 75% of infected newborns are asymptomatic in early infancy.

• Almost all congenitally infected individuals manifest signs or symptoms of

infection, such as chorioretinitis, by adolescence if they are not treated in the
newborn period.

• More than half of congenitally infected infants are considered normal in the
perinatal period, but almost all such children will have ocular involvement
later in life.
 Cont..,

the four most common presentations include

1. A healthy-appearing term infant with subclinical infection in whom

symptoms develop later in childhood,

2. A healthy-appearing term infant in whom clinical evidence of disease

develops in the first few months of life,

3.An infant with generalized disease at birth, and

4. An infant with predominantly neurologic involvement at birth

 Cont..,

Possible Signs and Symptoms of Congenital Toxoplasmosis in infancy

or later in life;

• Jaundice

• Anemia Thrombocytopenia

• Maculopapular rash

• Convulsions

• Mental retardation
Cont..,

• Hydrocephalus Microcephaly

• Chorioretinitis -Intracranial calcifications

• Learning disabilities -Abnormal CSF

• Visual impairment -Growth retardation

Diagnosis

• Isolation of organism (histology, tissue culture)

• Serologic tests:

– IgG

– IgM cannot pass the placenta.

• PCR
Complication

 Blindness or severe visual disability

 Severe mental retardation

 Other neurological manifestations

 Management
Treatment of prenatally infected children with overt (symptomatic) disease
• 6 months: Combination of:
– Pyrimethamine
– Sulfadiazine
– Folinic Acid
• 6 months: alternating to the first birthday
– 4 weeks Spiramycine
– 4 weeks Pyrimethamine, Sulfadiazine, Folinic Acid
• In case of signs of acute inflammation:
– Corticosteroids (Prednisolone)
 Cont..,
Treatment of prenatally infected children with subclinical infection (no
symptoms)
• 6 weeks: A Combination of:
– Pyrimethamine
– Sulfadiazine
– Folinic Acid
• 6 weeks: B
– Spiramycine
• alternating A and B to the first birthday
– 4 weeks Pyrimethamine, Sulfadiazine, Folinic Acid
– 6 weeks Spiramycine
 Prognosis

A normal outcome was documented for 100% of infants treated with pyrimethamine
and sulfadiazine for 1 year when there was not evidence of substantial neurologic
disease at birth.

Cognitive, neurologic, and auditory outcomes all were normal for these children.

Normal neurologic or cognitive outcomes were also observed in greater than 72% of
infants who did have moderate or severe neurologic disease at birth.

None had sensorineural hearing loss, and most children in each group did not
develop new eye lesions.
 Hepatitis B virus (HBV)

Hepatitis B virus (HBV) is a double-stranded DNA virus belonging to the

family of hepadnaviruses.

HBV infection is a global public health problem.

Hepatitis means inflammation of the liver.

When the liver is inflamed or damaged, its function can be affected.

 Heavy alcohol use, toxins, some medications, and certain medical

conditions can cause hepatitis.
Epidemiology

Hepatitis B is one of the most common infectious diseases globally.

It has been estimated that there are (HBV) 96 million HBV carriers,
1.5 million new infections per year on the worldwide.

For a newborn born to a HBsAg positive mother, there is a risk of

vertical transmission as high as 90 per cent, if no prophylaxis is given.
 Symptoms and Signs of Neonatal HBV Infection

 They develop jaundice,

 lethargy,

 failure to thrive,

 abdominal distention, and

 clay-colored stools.

Occasionally, severe infection with hepatomegaly,

 ascites, and hyperbilirubinemia.

Prevention:

• For known HepBsAg positive mother: There is evidence to suggest that

hepatitis B immunoglobulin alone, hepatitis B vaccine alone.

• Give hepatitis B immune globulin and hepatitis B vaccine 100 IU given

by intramuscular injection to their infants within 12 hours of birth.

• Hepatitis B vaccine alone starting at birth will prevent transmission of

the virus in 70%–95% of infants born to chronically infected mothers.
 Congenital rubella

Rubella virus, the cause of rubella, is an RNA virus of the genus Rubivirus in the

family Togaviridae.

 The risk for congenital defects and disease is greatest with primary maternal

infection during the first trimester.

 Congenital defects occur in about 90% of infants whose mothers acquire maternal

infection before the 11th week of pregnancy, diminishing to about 10–20% by the

end of the first trimester.

 with an overall risk for the trimester being about 70%

Symptoms in the infant may include

• Cloudy corneas or white appearance to pupil

• Deafness

• HSM

• Anemia, thrombocytopenia

• Developmental delay
Cont..,

• Low birth weight

• Mental retardation

• Seizures

• Small head size

• Skin rash at birth

diagnosis

 The diagnosis is confirmed by finding rubella-specific IgM antibody

in the neonatal serum, or

 by culturing rubella virus from the infant (nasopharynx, urine, tissues).

 Virus can be shed in the urine for 1 yr or longer.

 complication

Eyes:
Central nervous system:
• Cataracts
• Mental retardation
• Glaucoma
• Motor retardation
• Retinitis
• Microcephaly(a)
Heart:
• Encephalitis
• Patent ductus arteriosus(a)
• Meningitis
• Pulmonary artery stenosis
• Deafness
• Other heart defects
Prevention

 Active immunization programs using live, disabled virus vaccines

 All girls should be vaccinated against rubella before entering the child
bearing years.

 Women wishing to conceive should be counseled and encouraged to

have their antibody status determined and vaccinated if needed.
 Congenital CMV

The cytomegaloviruses are the largest viruses in the herpesvirus family

and are noted for their worldwide distribution among humans and
animals.

The virus is highly species specific, and humans are the only known
reservoir for disease among humans.

Most CMV infections are inapparent, but the virus can cause a variety of
clinical illnesses that range in severity from mild to fatal.
Cont..,

Cytomegalovirus (CMV) is a ubiquitous DNA herpesvirus.

CMV is the most common cause of congenital infection, which

occasionally causes the syndrome of cytomegalic inclusion disease
(hepatosplenomegaly, jaundice, petechiae, purpura, and microcephaly).

Disease may result from primary or recurrent CMV infection, but the
former is a more common cause of severe disease.
 Epidemiology

CMV is currently the most common intrauterine infection.

birth prevalence of 0.67 percent in of worldwide studies .

Approximately 90% of newborns with congenital CMV infection are

asymptomatic at birth

 10 percent are symptomatic.

of newborns, and it is a leading cause of deafness and learning disability.

 in developed countries, where crowding and poor hygiene are more common.
Symptomatic congenital CMV infection

Only 5% of all congenitally infected infants have severe cytomegalic

inclusion disease,

Another 5% have Mild involvement, and

90% are born with subclinical, but still chronic, CMV infection.
 The characteristic signs and symptoms:

– IUGR

– prematurity

– hepatosplenomegaly and jaundice

– thrombocytopenia and purpura

– microcephaly and intracranial calcifications.

• Other neurologic problems: chorioretinitis, sensorineural hearing loss, and

mild increases in cerebrospinal fluid protein.
 Diagnosis
Antenatal diagnosis

o most women remain asymptomatic with CMV infection, screening for primary
CMV IgG, which has high sensitivity and specificity.

Neonatal diagnosis

o Active CMV infection is best confirmed by culture virus isolation from: urine,
saliva, bronchoalveolar washings, breast milk, cervical secretions, or tissues
obtained by biopsy.

o PCR
Treatment

1.Prevention method

• Prevention is the most important available means to avoid infection.

• hand washing procedures, as do women health care workers,

particularly in nurseries.

2.Pharmacological method

• ganciclovir oral solution

Neonatal HSV Infection

• HSV are a group of large double-stranded DNA viruses within an

icosahedral nucleocapsid and a lipid envelope.

• There is considerable cross-reactivity between the two serotypes,

HSV-1 and HSV-2.

• Most cases of neonatal herpes occur due to maternal infection during

delivery, and approximately 75% are HSV type 2.
Epidemiology

Maternal primary or first episode genital herpes (no antibody present

against the type of virus shed) has an infant attack rate of 33–50%.

Recurrent maternal disease has an infant attack rate of only 1–3%.

Girls have a higher seroprevalence than boys.

Black children have a 35% seroprevalence by age 5 compared with

18% in white children.
 Clinical presentation

Perinatal infection manifests in the first month of life, with 9% on the first
day, and in 40% by the first week.

• There are 3 major categories:

1. localized skin, eye, and mouth infection

2. Disseminated infection and

3.CNS infection involvement; found in 48–79% and include lethargy, poor

feeding, irritability, poor tone, and seizures.
Cont..,
 Diagnosis

The diagnosis is based on any two of the following:

1. a compatible clinical pattern

2. isolation of the virus

3. development of specific antibodies; and

4. demonstration of characteristic cells, histologic changes, viral antigen, or

HSV DNA in scrapings, CSF, or biopsy material.
 Cont..,

o The use of PCR analysis of CSF and perhaps blood is critical to

diagnose neonatal HSV infection, especially in the absence of skin
lesions.

o The sensitivity of CSF PCR in neonatal CNS infection is 75%.

o Microscopic examination of scrapings from lesions (Tzanck stain)

reveals multinuclear giant cells and intranuclear inclusions
approximately 50% of the time.
 Management

 Vidarabine was the first antiviral agent used to treat HSV that was
efficacious despite the toxicity.

 A low-dose acyclovir (30 mg/kg per day in three divided doses)

 High-dose intravenous acyclovir (60 mg/kg per day in three divided

doses) a longer treatment duration (21 days for disseminated or CNS
disease and 14 days for disease localized to skin, eyes, or mouth.
Congenital syphilis

Congenital syphilis occurs when the spirochete Treponema pallidum

is transmitted from a pregnant individual to the fetus.

Severe, disabling, and often life-threatening infection seen in infants.

 About half of all infected fetuses die shortly before or after birth.
 Epidemiology

• untreated early syphilis, 40 percent of pregnancies result in spontaneous

abortion.

• Approximately 60 to 90 percent of live-born neonates with congenital syphilis

are asymptomatic at birth.

• Incidence – Congenital syphilis is a significant public health problem,

complicating an estimated one million pregnancies per year throughout the
world.
pathogenesis and pathology

 congenital syphilis is most frequently results from transplacental

transmission of spirochetes.

 Transmission can occur at any stage of pregnancy.

 Pregnant women with primary and secondary syphilis and

spirochetemia are more likely to transmit infection to the fetus than are
women with latent infection.
Cont..,

 syphilis during pregnancy than if she acquired syphilis.

 Rate of transmission is almost 100% during the whole period of

Pregnancy.

 The incidence of congenital infection in the offspring of untreated

infected women remains highest during the first 4 yr after acquisition
of primary infection, secondary, and early latent disease.
Etiology of Congenital Syphilis

 Treponema pallidum, a long, slender, tightly coiled, motile spirochete

 The pathogenic members of this genus include

T. pallidum (venereal syphilis),

T. pertenue (yaws),

T. pallidum subsp. endemicum (endemic syphilis), and

T. carateum (pinta).
 Clinical manifestation of congenital Syphilis

Fetal or perinatal death ( 40%)

Among survivors, manifestations are:

1. Early signs- appear during the first 2 yrs of life

2.late signs- appear gradually b/n 2-20yrs of age

 Early manifestations result from transplacental spirochetemia and are

analogous to the secondary stage of acquired syphilis.
Cont.,

Approximately two thirds of infected infants are asymptomatic at the

time of birth.

if untreated, symptoms develop within weeks or months.

 The early manifestations of congenital infection are varied and

involve multiple organ systems.

 Hepatosplenomegaly, jaundice, and elevated liver enzymes

(common).
 Cont..,

• Nonimmune hydrops fetalis

• Intrauterine growth restriction

• Failure to thrive

• Generalized lymphadenopathy

• Bone abnormalities Periostitis

• Osteochondritis (Wimberger sign)

• Osteitis
Cont..,

• Hepatosplenomegaly (with or without elevated jaundice)

• Mucocutaneous lesions

• Maculopapular eruption

• Mucous patches of palate

 Cont..,

• Persistent rhinitis (snuffles, contagious)

• Pneumonitis (pneumonia alba)

• Nephrotic syndrome

• Neurologic abnormalities

• Syphilitic leptomeningitis
 Cont..,
Hematologic abnormalities

• Leukocytosis

• Leukopenia

• Anemia, Coombs-negative hemolytic

• Thrombocytopenia

Ocular abnormalities

• Chorioretinitis

• Uveitis
Cont..,

Clinical Manifestations of Late Congenital Syphilis

DENTAL
• Hutchinson teeth (notched, peg-shaped upper central incisors)
• Mulberry molars
(multiple small cusps)
 Cont..,
BONE

o Frontal bossae of Parrot

o Saddle nose deformity

o Short maxillae

o High-arched palate

o Higouménakis sign (sternoclavicular thickening)

o Flaring scapulae

o Saber shins (anterior bowing of tibia)

o Clutton joints (painless synovitis, hydrarthrosis)

 Cont..,

CUTANEOUS

• Rhagades (linear scars radiating from mouth, nares, and anus)

OCULAR

• Interstitial keratitis
 Cont..,
NEUROLOGIC

• Eighth cranial nerve deafness

• Mental retardation

• Hydrocephalus

• Cranial nerve palsies

• Seizure disorder
 Diagnosis of Congenital Syphilis

• Dark-field microscopy or direct immunofluorescence

• serologic tests for syphilis are the principal means for diagnosis.

• Nontreponemal tests

– VDRL and

– rapid plasma regain (RPR)

• In congenital infection, these tests become nonreactive within a few months

after adequate treatment.
Treatment of congenital syphilis

Aqueous crystalline penicillin G (100,000–150,000U/kg/24hr, given as

50,000U/kg IV BID for the first 7 days and TID thereafter) for 10–14
days OR

Alternatively, procaine penicillin G 50,000 U/kg IM single daily dose

for 10 days can be given.

Benzathine penicillin G 50,000 U/kg IM.

 Reference
• FANAROFF AND MARTIN’S neonatal-perinatal medicine Diseases of the fetus and infant 9th
Edition.

• Neonatal Intensive Care Unit (NICU) Training Participants’ Manual 2014 and 2021.

• Tahotná A, Brucknerová J, Brucknerová I. Zika virus infection from a newborn point of view.
TORCH or TORZiCH? Interdiscip Toxicol. 2018 Dec;11(4):241-246. [PMC free article]
[PubMed]

• Marsico C, Kimberlin DW. Congenital Cytomegalovirus infection: advances and challenges in

diagnosis, prevention and treatment. Ital J Pediatr. 2017 Apr 17;43(1):38. [PMC free article]
[PubMed]

• UpToDate 2023
12/19/2023 By Bishaw M.