TORCH (TORCH).pdf

INTRODUCTION
Congenital infections are traditionally referred as TORCH infection
and are significant cause of fetal and neonatal morbidity and
mortality.
Transmission of the pathogens may occur
• Prenatally through transplacental passage of organisms,
• Perinatally from contact with blood and vaginal secretions
AND
• Postnatally; from exposure to breast milk

The original concept of the TORCH perinatal infections was to group five
infections with similar presentations,
These five infections are;
• Toxoplasmosis
• Other(syphilis)
• Rubell
• Cytomegalovirus (CMV)
• Herpes simplex virus (HSV)

This group of infections present with similar clinical and
laboratory findings i.e,
• IUGR,
• Hepatosplenomegaly
• Rash,
• CNS manifestations including calcifications,
• Early jaundice, and
• Low platelets ; hence the usefulness of the TORCH concept

But, now adays The TORCH acronym has become Obsolete,
due to ;
1. The increasing numbers of pathogens responsible for
in utero and perinatal infections grouped in others
2. The validity of indiscriminate screening of neonates or
infants with findings compatible with congenital
infection with “TORCH titers” has been questioned

The “O” acronym has been variably included
• enteroviruses,
• varicella zoster virus,
• parvovirus B19
• hepatitis B, coxsackievirus,
• Epstein-Barr virus,
• Enterovirus/ Parechovirus,
• HIV, and tuberculosis,

So, an alternate approach involves testing of
infants with suspected congenital infections for
specific pathogens based upon their clinical
presentation

Timely diagnosis of perinatally acquired infections
is crucial to the initiation of appropriate therapy.
A high index of suspicion for congenital infection
and awareness of the prominent features of the
most common congenital infections help to
facilitate early diagnosis of congenital infection.

CLINICAL FEATURES OF
TORCH INFECTIONS

APPROACH TO THE INFANT WITH
SUSPECTED INTRAUTERINE INFECTION
• Timely diagnosis of perinatally acquired infections
is crucial to the initiation of appropriate therapy,
the development of a care plan, prognosis, and
family counseling.
• A high index of suspicion for congenital infection
and awareness of the prominent features of the
most common congenital infections can help to
facilitate early diagnosis and tailor appropriate
diagnostic evaluation

Clinical suspicion — In some cases, intrauterine infection may be suspected on the basis of laboratory
results obtained during pregnancy (eg, positive syphilis serology with increasing titers). In the absence
of suggestive maternal laboratory results, intrauterine infection may be suspected in newborns with
certain clinical manifestations, or combinations of clinical manifestations including (but not limited to):
Hydrops fetalis
Microcephaly
Seizures
Cataract
Hearing loss
Congenital heart disease
Hepatosplenomegaly
Jaundice
Rash
• Thrombocytopenia

• These findings are not restricted to TORCH
infections and some of the features above may
occur in other infections (eg, human parvovirus,
Chagas disease) and in conditions other than
intrauterine infection (eg, inborn errors of
metabolism, Rh incompatibility, etc). Thus, the
entire clinical constellation, including maternal
history and exposures must be taken into account
when deciding to evaluate an infant for congenital
infection.

Initial evaluation — The evaluation of a newborn with clinical findings
compatible with intrauterine infection may include :
•
• Review of maternal history (evidence of rubella immunity, syphilis serology,
history of Herpes simplex virus (HSV), exposure to cats, etc)
• Assessment of physical stigmata consistent with various intrauterine infections
• Complete blood count and platelet count
• Liver function tests (particularly important in HSV infection)
• Radiographs of long bbone
• Ophthalmologic evaluation
• Audiologic evaluatio
• Neuroimaging
• Lumbar puncture

• Specific evaluation — The results of the initial
evaluation may help to determine whether
evaluation for a specific pathogen (or pathogens) is
warranted. Findings that are more prominent in
particular infections, and may prompt evaluation
for a specific pathogen

• WHEN TO SUSSPECT TORCH INFECTION????

• HOW TO APPROACH WITH SUSPECTED TORCH
INFECTION???

Toxoplasmosis
Toxoplasma gondii is:-
• An obligate intracellular protozoan,
• Multiplies only in living cells and
• Multiplies all tissue of mammals and birds
 Virulence differs based on parasite genetics

lnfection acquired :-
• Perorally,
• Transplacentally,
• Rarely, parenterally in laboratory accidents;( by transfusion; or from a
transplanted organ.)
Human infection is usually acquired orally by
• eating undercooked or raw meat that contains cysts or
• food or other material contaminated with oocysts from acutely infected
cats

Transmission to the fetus usually follows
• Acquisition of primary infection by pregnant woman
during gestation.
• from immunocompromised women who are chronically
infected.
• But, extremely rarely from immunocompitant mothers
infected before pregnancy

Untreated maternal infections acquired in the
• 1st trimester, approximately 17% of fetuses are
infected, usually with severe disease.
• 3rd trimester, approximately 65% of fetuses are
infected, usually with mild disease or inapparent at
birth

Once infection is acquired will be,
• Asymptomatic and latent encysted organisms persist in
the host throughout life or,
• In immunocompromised persons either initial
acquisition or recrudescence of latent organisms often
causes signs or symptoms

Congenital infection often causes disease
• either perinatally or
• later in life, most frequently chorioretinitis and CNS
lesions.(If untreated)

• Almost all congenitally infected individuals who are
not treated manifest signs or symptoms of
infection, such as chorioretinitis, by adolescence

CLINICAL MANIFESTATIONS
• Most infected newborns are asymptomatic at birth
• Few develop _x0000_
• _x0000_IUGR
•
•  Fever
•
•  Maculopapular rash
•
•  Anemia
• • Jaundice
•
• • Seizure
•
• • Hepatospleenomegaly
•
• • Thrombocytopenic purpura_x0000_

• Classical Triad
•
• 1) Chorioretinitis
•
• 2) Diffuse Nodular Intracranial
•
• calcifications
•
• 3) Hydrocephalus
• _x0000_

DIAGNOSIS
•  Maternal history & Serology
•
•  Clinical Examination
•
•  Laboratory Evaluation - Serology/ CBC / LFT
•
•  Fundus Examination - Chorioretinitis
•
•  Neuroimaging – Intracranial Calcifications/ Hydrocephalus
•
•  Lumbar Puncture – Elevated CSF Protein/ Mononuclear Pleocytosis
•
•  Prenatal Diagnosis- PCR by Amniocentesis is the best method for
•
• prenatal diagnosis of fetal infection.
• _x0000_

CONFIRMED CONGENITAL
TOXOPLASMA
INFECTION
_x0000_
1. Detection of toxoplasma specific IgM (after 5 days of life) or
• IgA titres (after 10 days of life) is considered diagnostic of
•
• congenital toxoplasmosis in infants with a positive
•
• Toxoplasma IgG titre
•
• 2. Positive for Toxoplasma IgG beyond 12months of age
•
• 3. Positive CSF PCR
•
• 4. Increase in anti-Toxoplasma IgG titer during the first year of
•
• life or increasing IgG titer compared with the mother's
• _x0000_

MANAGEMENT_x0000_
Antiparasitic therapy is indicated for infants in
whom a diagnosis of CT is
• confirmed or
• probable based on serology, PCR, or clinical symptoms.

The typical course consists of
• sulfadiazine (50 mg/kg, twice daily),
• pyrimethamine (2 mg/kg/d for 2 days, then 1 mg/kg/d
for 2–6 months, then 1 mg/kg/d 3 times a week), and
• folinic acid (10 mg, 3 times weekly) for a minimum of 12
months.

Corticosteroids in the form of prednisone (1
mg/kg/d in 2 divided doses) should be given
• when CSF protein is >1 g/dL and
• when active chorioretinitis threatens vision.
 Prednisone is continued until resolution of CSF
protein elevation and active chorioretinitis.

• Serial follow-up to gauge the response of the infant
to therapy should include
• neuroradiology,
• ophthalmologic examinations, and
• CSF analysis if indicated.

• Infants treated with pyrimethamine and
sulfadiazine require weekly
• blood counts (complete blood count [CBC]
including platelets) and
• urine microscopy to detect any adverse drug
effects.
• CBC can be spaced to every 2 weeks if counts
remain stable.

Prevention
•  Avoidance of Exposure- Food hygiene
•
•  Maternal Screening
•
•  Prenatal Treatment - Spiramycin
• _x0000_

Chorioretinitis
• Chorioretinitis also called retinochoroiditis, is an
inflammatory process that involves the retina and
the uveal tract of the eye (middle layer of eye),
which consists of the iris, ciliary body, and choroid.
Chorioretinitis is usually caused by congenital viral,
bacterial, or protozoal infections in neonates.

Congenital Infection causes
In immunocompetent children, chorioretinitis is usually associated
with congenital infection; acquired infection is a less likely cause.
Toxoplasma gondii and CMV are the leading causes of congenital
infections associated with chorioretinitis.
• Viral causes include vertical or perinatal infections, including
Herpes Simplex virus (HSV), rubella, varicella, Epstein-Barr virus
(EBV), lymphocytic choriomeningitis virus, and, possibly
flavivirus.

Chorioretinitis Symptoms
The signs and symptoms of chorioretinitis depend on the type of inflammation.
Symptoms of chorioretinitis include:
Vision becoming blurred
“Pink” eye associated with pain
Sensitivity to light sources (photophobia)
Tears being continually produced
• Imagining to see “floaters” – cobweb-like structures that seem to float across
the eyes which are induced because of material in the vitreous gel of the eye

Rubella
• Rubella virus is an enveloped, positive-stranded
RNA virus classified as a Rubivirus in the Togaviridae
family.
• It is capable of causing chronic intrauterine
infection and damage to the developing fetus
(congenital rubella syndrome [CRS]).

• The virus is sensitive to heat, ultraviolet light, and
extremes of pH but is relatively stable at cold
temperatures.
• Of childbearing women, 92% are estimated to be
seropositive (rubella immune).
• It is estimated that >100,000 infants worldwide are
born with CRS each year.

• Humans are the only known host with an
incubation period of 14 to 21 days after contact.
• Virus is spread by respiratory secretions and also
from stool, urine, and cervical secretions.
• Maternal viremia is a prerequisite for placental
infection, which may or may not spread to the
fetus.
• Most cases occur after primary disease, although
few cases (2%) have been described after
reinfection

The fetal infection rate varies according to the timing of
maternal infection during pregnancy.
• at 1 to 12 weeks, 81% risk of fetal infection;
• at 13 to 16 weeks, 54%;
• at 17 to 22 weeks, 36%; at 23 to 30 weeks, 30%.
• at 31 to 36 weeks, rise to 60% and
• to 100% in the last month of pregnancy, but late infection is not
associated with CRS.

The incidence of fetal effects is greater the earlier in
gestation that infection occurs,
• at 1 to 12 weeks, 85% of infected fetuses will have
congenital defects.
• atInfection weeks, 35% of fetuses having congenital defects;
• infection at later gestational ages rarely causes deafness or
congenital malformations.

• Rubella infection can have catastrophic effects on
the developing fetus, resulting in spontaneous
abortion, fetal infection, stillbirth, or intrauterine
growth restriction.

• GIT: HepatoSpleenomegaly
• CNS: Meningoencephalitis,
Microcephaly, Hypotonia, MR
• Skin: Blueberry Muffin Rash,
Dermatoglyphicabnormalities
• Blood: Thrombocytopenia
• Skeletal: Radio-lucenciesof
long bones
CLINICAL FEATURES
• General: IUGR,
Prematurity, Stillbirth,
Abortion
• CVS: PDA, PAS, CoA
• Eye: Cataracts,
Microphthalmia,
PigmentaryRetinopathy
• Ear: Sensory Neural
Deafness

Classic manifestations of CRS
• Deafness,
• cataracts and
• cardiac disease

Diagnosis
• Timely diagnosis of congenital rubella infection is
important both for management of the individual
patient and for prevention of secondary infection
because these infants may remain infectious for 1
year.
• The diagnosis may be suspected clinically but needs
to be confirmed with laboratory tests.

• Laboratory studies
• 1. Open cultures. The virus can be cultured for up to
1 year despite measurable antibody titer.
• The best specimens for viral recovery are from
nasopharyngeal swabs, conjunctival scrapings, urine, and
cerebrospinal fluid (CSF), in decreasing order of
usefulness.
• 2. Serologic studies. These are the mainstay of
rubella diagnosis. detection of rubella-specific IgM
in a serum or oral fluid taken before 3 months of
age.

• Persistance of rubella IgG in sera taken between 6 and
12 months of age
3. Rubella virus PCR. detection of viral RNA in
nasopharyngeal swabs, urine, oral fluid, CSF, lens
aspirate, and ethylenediaminetetraacetic acid (EDTA)-
blood.
4. Cerebrospinal fluid examination. This may reveal
encephalitis with an increased protein and cell count. 5.
Imaging studies. Long-bone films may show
metaphyseal radiolucencies that correlate with
metaphyseal osteoporosis.

• The Centers for Disease Control and Prevention
(CDC) has published an elaborate case definition for
congenital rubella infection
• Cases of CRS are classified as suspected, probable,
confirmed, or infection only, depending on clinical
findings and laboratory criteria for diagnosis.

CDC case definition
• 1. Suspected. An infant who has 1 or more of the
following findings (but does not meet the criteria for a
confirmed or probable case):
• cataracts or congenital glaucoma,
• congenital heart disease
• hearing impairmentor
• pigmentary retinopathy,
• hepatosplenomegaly,
• purpura, jaundice,
• microcephaly, developmental delay, meningoencephalitis, or
• radiolucent bone disease.

2. Probable.
An infant who has at least 2 of the following
findings (but does not have laboratory confirmation
of rubella infection or a more possible etiology):
• cataracts or congenital glaucoma or both (counts as 1),
• hearing impairment, or
• pigmentary retinopathy. OR

An infant who has at least 1 or more of the
following (but does not have laboratory
confirmation or an alternative more plausible
etiology):
• cataracts or congenital glaucoma or both (counts as 1),
• hearing impairment,
• pigmentary retinopathy AND

1 or more of the following of the following:
• purpura,
• microcephaly,
• developmental delay,
• meningoencephalitis, or
• radiolucent bone disease.

3. Confirmed.
An infant with at least 1 symptom (listed
previously) that is clinically consistent with CRS and
laboratory evidence of congenital rubella infection
as demonstrated by:

4. Infection only.
An infant with laboratory evidence of infection but
with no clinical symptoms or signs.
N. B:- If any signs or symptoms are identified later such as
hearing loss, then the diagnosis is reclassified as
confirmed.

MANAGEMENT
Supportive care
Multi disciplinary appapproac
Hearing loss - hearing aids and referral to an early intervention
program
Structural cardiac defects – Surgical correction
Ocular abnormalities – Referral to Ophthalmology expert
CNS abnormalities - special education services, speech,
language, occupational, and/or physical therapy.
Endocrine abnormalities – Expert Followup for Diabetes
Hypothyroidism _x0000_

Prevention
Prevention is considered the most important
aspect as far as the management of CRI concerned.
 Preventive measures include
• recommended imimmunizations
• testing of pregnant women for rubella immunity and
• proper counseling regarding avoiding exposure. _x0000_

CYTOMEGALOVIRUS
• CMV is the largest of the human herpesvirus with
an estimated size of 190 nm.
• The 230-kb double-stranded DNA genome is
approximately 50% larger than the herpes simplex
virus genome and encodes more than 100 unique
virion proteins and an unknown number of
nonstructural proteins

• Human cytomegalovirus (CMV) is ubiquitous in the
population, and once infected, individuals remain
persistently infected for life with intermittent
excretion of infectious virus.
• CMV remains a well-recognized cause of disease in
the newborn infant following intrauterine infection
(congenital CMV) and the allograft recipients
undergoing post transplantation
immunosuppression.

• CMV infections are acquired through several
settings:
• (1) community exposure,(Community acquisition
occurs throughout life and is linked by exposure to
CMV present in saliva and urine.),
• (2) nosocomial transmission, and
• (3) intrauterine infection.

• Breast feeding is the most common route of CMV
infection in early childhood.
• Ingestion of breast milk from seropositive women
results in a rate of infection of approximately 60-
70% in infants.
• Rates of congenital infection between 0.5-1.0%
have been routinely reported in the United
States( 2% in some areas in Asia and Africa)

• The rate of transmission to the fetus is
approximately 30% in women undergoing primary
infection during pregnancy,
• whereas in utero infections also occur in previously
immune women (nonprimary infection) albeit at a
reduced rate on the order of 1-2%

• 1. Subclinical infection. Occurs in 85% to 90% of
cases. Despite being asymptomatic at birth, these
infants are at risk for sensorineural hearing loss
(SNHL) during the first 6 years of life.

• 2. Low birthweight. Maternal CMV infection is
associated with low birthweight and small for
gestational age infants, even when the infant is not
infected.

• 3. Classic cytomegalovirus inclusion disease. Occurs in 10% to 15% of
the cases and consists of
• fetal growth restriction,
• hepatosplenomegaly with jaundice,
• transaminitis,
• thrombocytopenia with or without purpura, and
• severe CNS involvement. ( microcephaly, intracerebral calcifications
(most characteristically in the subependymal periventricular area),
• chorioretinitis, and
• progressive SNHL.
• hemolytic anemia and
• pneumonitis.

• The most severely affected infants have a mortality
rate of approximately 30%.
• Deaths are usually due to hepatic dysfunction,
bleeding, disseminated intravascular coagulation,
or secondary bacterial infection.

classical findings.
Periventricular intracranial calcifications
Microcephaly
Hepatosplenomegaly
Thrombocytopenia
Sensorineural hearing loss

Diagnosis
• A. Laboratory studies
• 1. Culture for demonstration of the virus. The gold
standard for the diagnosis of congenital CMV is urine
or saliva culture obtained before 3 weeks of age.
Most urine specimens from infants with congenital
CMV are positive within 48 to 72 hours, especially if
shell vial tissue culture techniques are used. Shell vial
assay detects CMV-induced antigens by monoclonal
antibodies, allowing for identification of the virus
within 48 hours compared with the standard tissue
culture, which takes 2 to 4 weeks.

• 2. Polymerase chain reaction. PCR for CMV DNA is
as sensitive as a urine or saliva culture for the
detection of CMV infection.

• 3. Serologic tests. Serologic tests based on the
detection of immunoglobulin M (IgM) should not
be used to diagnose congenital CMV because they
are less sensitive and more subject to false-positive
results than culture or PCR. Only 70% of neonates
infected with congenital CMV have IgM antibodies
at birth.

• 4. Other laboratory tests. include CBC, liver
function tests, coagulation panel and CSF,
• B. Imaging and other studies. Ultrasound or
computed tomography scans of the head, Brain
MRI is preferred over other modalities because it is
likely to identify most of the brain anomalies
associated with congenital CMV.

Management
Antiviral agents. Neonates with symptomatic
congenital CMV disease with or without CNS
involvement have improved audiologic and
neurodevelopmental outcomes at 2 years of age
when treated with
• oral valganciclovir (a prodrug for ganciclovir) at 16
mg/kg/dose, given orally twice a day for 6 months, OR
• intravenous ganciclovir at 6 mg/kg/dose is an
alternative.

Significant neutropenia occurs in 20% of infants
treated with oral valganciclovir and in 67% of
infants treated with ganciclovir.
Absolute neutrophil counts should be pperformed
• weekly for 6 weeks
• then at 8 weeks, and
• then monthly for the duration of antiviral treatment;
serum aminotransferase concentration should be
measured monthly during treatment.

Prevention
These include:-
• changes in hygienic behavior for seronegative pregnant
women,
• administration of CMV hyperimmune globulin (CMV-
HIG) to pregnant women with a primary infection,
• administration of antiviral therapy to women with
primary infection, and
• administration of vaccines to girls or women well before
or during pregnancy.??????
• Pasteurization or freezing of donated human milk

Herpes Simplex Viruses
• HSVs contain a double-stranded DNA genome of
approximately 152 kb that encodes at least 84
proteins.
• The 2 closely related herpes simplex viruses (HSVs),
HSV type 1 (HSV-1) and HSV type 2 (HSV-2), cause a
variety of illnesses,

• Common infections involve the skin, eye, oral cavity,
and genital tract.
• Infections tend to be mild and self-limiting, except in
the immunocompromised patient and newborn infant,
• Primary infection occurs in individuals who have not
been infected previously with either HSV-1 or HSV-2. ,
primary infections can be severe.
• Nonprimary 1st infection occurs in individuals previously
infected with 1 type of HSV (e.g., HSV-1) who have
become infected for the 1st time with the other type of
HSV (in this case, HSV-2).

• HSV establishes latent infection in regional sensory
ganglion neurons. Virus is maintained in this latent
state for the life of the host but periodically can
reactivate and cause recurrent infection

• HSV infections are ubiquitous, and there are no
seasonal variations in risk for infection. The only
natural host is humans, and the mode of
transmission is direct contact between
mucocutaneous surfaces.

• Neonatal herpes is an uncommon but potentially
fatal infection of the fetus or more likely the
newborn.
• More than 90% of the cases are the result of
maternal-fetal transmission. The risk for
transmission is greatest during a primary or
nonprimary 1st infection (30-50%) and much lower
when the exposure is during a recurrent infection
(<2%)

Neonatal HSV infection is thought to never be
asymptomatic.
Its clinical presentation reflects timing of infection,
portal of entry, and extent of spread.
Infants with intrauterine infection typically have
• skin vesicles or scarring,
• eye findings including chorioretinitis and keratoconjunctivitis,
and
• microcephaly or hydranencephaly that are present at delivery.
• Few infants survive without therapy, and those who do
generally have severe sequelae. .

Infants infected during delivery or the postpartum
period present with 1 of the following 3 patterns of
disease:
• (1) disease localized to the skin, eyes, or mouth;
• (2) encephalitis with or without skin, eye, and mouth
disease; and
• (3) disseminated infection involving multiple organs,
including the brain, lungs, liver, heart, adrenals, and skin

• 1. Infants with skin, eye, and mouth disease (SEM)
generally present at 5-11 days of life and
typically demonstrate:-
• a few small vesicles, particularly on the presenting part or at
sites of trauma such as sites of scalp electrode placement.
• If untreated, SEM in infants may progress to encephalitis or
disseminated disease.

• 2. Infants with encephalitis typically present at 8-17 days of
life with clinical findings
suggestive of bacterial meningitis, including
• irritability,
• lethargy,
• poor feeding,
• poor tone, and seizures.
Fever is relatively uncommon, and
skin vesicles occur in only approximately 60% of cases
If untreated, 50% of infants with HSV encephalitis die and
most survivors have severe neurologic sequelae.

• 3. Infants with disseminated HSV infections generally
become ill at 5-11 days of life.
Their clinical picture is similar to that of infants with
bacterial sepsis, consisting of
• hyperthermia or hypothermia,
• irritability,
• poor feeding, and vomiting.
They may also exhibit
• respiratory distress, cyanosis, apneic spells,
• jaundice, purpuric rash, and
• evidence of central nervous system infection; seizures are
common.

Skin vesicles are seen in approximately 75% of
cases.
 If untreated, the infection causes
• shock and
• disseminated intravascular coagulation;
approximately 90% of these infants die, and most
survivors have severe neurologic sequelae.

Traids ???
Skin lesions( vesicles, ulcerations or scarring)
Eye damage(conjunctivitis, cataract, retinopathy)
CNS abnormalities( hydranencephaly,
microcephaly)

DIAGNOSIS
• Isolation of HSV in culture
• Detection of DNA via PCR assays
• Detection of HSV specific antigens using rapid direct
immunofluorescence or enzyme immunoassays
• Classical findings in CSF Testing(a mononuclear cell
pleocytosis, normal or slightly low glucose concentration and
moderately elevated protein level)
• On EEG(focal or multifocal periodic epileptic form discharges )
• On neuroimaging(parenchymal brain edema, hemorrhage or
destructive lesions in the temporal, frontal, parietal or
brainstem regions in the brain)

TREATMENT
• 1. Infants born to mothers with a genital lesion. The
American Academy of Pediatrics recommends
• obtaining HSV surface cultures and
• HSV blood PCR in all exposed infants at approximately 24
hours of age. And
• For primary or first episode nonprimary maternal infection ;
start preemptive therapy for those exposed infants with
acyclovir at 60 mg/kg/d for 10 days.
• Infants exposed to active lesions with maternal recurrent
infection ; those infants can be monitored clinically with
education of the family about signs and symptoms of the
disease and treatment only if the infant becomes
symptomatic.

• 2. Infants born to mothers with a history of genital
herpes but no active genital lesions at
delivery. Should be observed for signs of infection
but no surface cultures or parenteral acyclovir is
needed.

• 3. for established herpes simplex virus disease.
 Intravenous acyclovir 60 mg/kg/d, divided every 8
hours (20 mg/kg/dose).
• Duration of therapy is a minimum of
• 21 days for patients with disseminated or CNS disease
and
• 14 days for those with SEM disease.

Infants with ocular HSV involvement should receive
a topical ophthalmic drug (1% trifluridine, 0.1%
iododeoxyuridine, or 0.15% ganciclovir) as well as
parenteral acyclovir.
An ophthalmologist should be involved in the
management.

Oral acyclovir suppressive therapy is recommended
for 6 months after treatment of acute HSV disease

Syphilis
Syphilis is
 a sexually transmitted infection
caused by Treponema pallidum,
• which is a thin, motile spirochete that is extremely fastidious,
• surviving only briefly outside the host.
The CDC issued a case definition of congenital
syphilis (CS) in 2018 as follows:
a condition caused by infection in utero with T pallidum.
 Cases are classified as confirmed (by laboratory
diagnosis) or probable.

Probable CS :-
• a condition affecting an infant whose mother had untreated
or inadequately treated syphilis at delivery, regardless of
signs in the infant, or
• an infant or child who has a reactive nontreponemal test for
syphilis (Venereal Disease Research Laboratory [VDRL], rapid
plasma reagin [RPR], or equivalent serologic methods) and

Any 1 of the following:
1. any evidence of CS on physical examination;
2. any evidence of CS on radiographs of long bones;
3. a reactive cerebrospinal fluid (CSF) VDRL test;
4. an elevated CSF leukocyte (white blood cell [WBC])
count or protein (without other cause) in a
nontraumatic lumbar puncture.

Laboratory criteria for diagnosis entail
demonstration of T pallidum by:
• (1) darkfield microscopy of lesions, body fluids, or
neonatal nasal discharge; or
• (2) polymerase chain reaction (PCR) or other equivalent
direct molecular methods of lesions, neonatal nasal
discharge, placenta, umbilical cord, or autopsy material;
or
• (3) immunohistochemistry or special stains (eg, silver
staining) of specimens from lesions, placenta, umbilical
cord, or autopsy material.

• Suggested parameters for abnormal CSF WBC and
protein values include the following: during the first
30 days of life, a CSF WBC count of >15 WBC/mm3
or a CSF protein >120 mg/dL is abnormal; after the
first 30 days of life, a CSF WBC count of >5
WBC/mm3 or a CSF protein >40 mg/dL is abnormal,
regardless of CSF serology.
• Adequate treatment is defined as completion of a
penicillin-based regimen, in accordance with CDC
treatment guidelines, appropriate for stage of
infection, initiated ≥30 days before delivery.

Treponemes are able to cross the placenta at any
time during pregnancy, thereby infecting the fetus.
Severity and risk of transmission depending on
• the stage of maternal infection and
• duration of fetal infection before delivery.

Untreated infection in the first and second
trimesters often leads to significant fetal morbidity,
whereas with third-trimester infection, many
infants are asymptomatic.

Kassowitz’s law states that the risk of vertical
transmission of syphilis from an infected, untreated
mother decreases as maternal disease progresses.
Thus, transmission ranges from
• 70% to 90% in primary and secondary syphilis,
• 40% for early latent syphilis, and
• 8% for late latent disease.

Clinical presentation
Clinical manifestations after birth are arbitrarily
divided into
A. early CS (<2 years of age) and
B. late CS (>2 years of age).

A. Early manifestations include
• nasal discharge (snuffles) and
• maculopapular or vesiculobullous rash that appears on the palms and soles.
• Other early stigmata include fever,
• abnormal bone radiographs,
• petechiae,
• lymphadenopathy,
• jaundice,
• pneumonia,
• osteochondritis,
• pseudoparalysis,
• hemolytic anemia, leukocytosis, thrombocytopenia, and
• central nervous system (CNS) involvement.

• B. Late manifestations develop in untreated infants
and are characterized by chronic granulomatous
inflammation.
• The sites most often involved include bones and joints,
teeth, eyes, and the nervous system.
• Hutchinson triad (blunted upper incisors, interstitial
keratitis, and eighth nerve deafness) and saddle nose are
distinct complications.
• Some of these consequences may not become apparent
until many years after birth, such as
• interstitial keratitis (5–20 years of age) and
• eighth cranial nerve deafness (10–40 years of age).

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