T=toxoplasmosis

O=other (syphilis)
R=rubella
C=cytomegalovirus (CMV)
H=herpes simplex (HSV)
 Each crosses the Placenta
Each may adversely effect the developing
fetus
The effect of each varies, depending on
developmental stage at time of exposure
 When do you think of TORCH infections?
IUGR infants
HSM
Thrombocytopenia
Unusual rash
Concerning maternal history
Classic findings of any specific infection
 Good maternal/prenatal history
Remember most infections of concern are mild
illnesses often unrecognized (flu like syndrome)
Miscarriage history
Thorough exam of infant
Directed labs/studies based on most likely
diagnosis
Again, DO NOT USE TORCH TITERS!
 Retrospective study of 75/182 infants with IUGR
who were screened for TORCH infections
1/75 with clinical findings, 11/75 with abnl lab
findings
All patients screened:
TORCH titers & urine CMV culture
Only 3 diagnosed with infection
NONE by TORCH titer!!
Overall cost of all tests = $51,715
Shotgun screening approach NOT cost effective
nor particularly useful
Diagnostic work-up should be logical and directed
by history/exam findings

Khan, NA, Kazzi, SN. Yield and costs of screening growth-retarded infants for torch
 Caused by protozoan Toxoplasma gondii
Domestic cat is the definitive host with
infections via:
Ingestion of cysts (meats, garden products)
Contact with oocysts in feces
Acute infection usually asymptomatic
1/3 risk of fetal infection with primary
maternal infection in pregnancy
Infection rate higher with infant in 3rd trimester
Fetal death higher with infant in 1st trimester
 Most (70-90%) are asymptomatic at birth
Classic triad of symptoms:
Chorioretinitis
Hydrocephalus
Intracranial calcifications
Other symptoms include fever, rash, HSM,
microcephaly, seizures, jaundice,
thrombocytopenia, lymphadenopathy
Initially asymptomatic infants are still at high risk
of developing abnormalities, especially
chorioretinitis
Chorioretinitis of congenital toxo
 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 : ELISA
 Prenatal testing with varied sensitivity not
useful for screening
Neonatal screening with IgM testing
implemented in some areas
Identifies infected asymptomatic infants who may
benefit from therapy
 Health education
Treatment for pregnant mothers diagnosed with acute toxo
Spiramycin daily
Macrolide antibiotic
Small studies have shown this reduces likelihood of
congenital transmission (up to 50%)
If infant diagnosed prenatally, treat mother
Spiramycin, pyrimethamine (anti-malarial, dihydrofolate
reductase inhib), and sulfadiazine (sulfa antibiotic)
Symptomatic infants
Pyrimethamine (with leucovorin rescue) and sulfadiazine
Treatment for 12 months total
Asymptomatic infants
Course of same medications improved outcomes
 Cause: Treponema pallidum (spirochaete)
Transmitted via sexual contact
Placental transmission as early as 6 wks
gestation
Typically occurs during second half
Mom with primary or secondary syphilis more likely
to transmit than latent disease
Large decrease in congenital syphilis since late
1990s
In 2002, only 11.2 cases/100,000 live births reported
From MMWR
Aug 2004
 2/3 of affected live-born infants are
asymptomatic at birth
Clinical symptoms split into early or late (2
years is cutoff)
3 major classifications:
Fetal effects
Early effects
Late effects
 Fetal:
Stillbirth
Neonatal death
Hydrops fetalis
Intrauterine death in 25%
Perinatal mortality in 25-30% if untreated
 Early congenital (typically 1st 5 weeks):
Cutaneous lesions (palms/soles)
HSM
Jaundice
Anemia
Snuffles
Periostitis and metaphysial dystrophy
Funisitis (umbilical cord vasculitis)
Periostitis of long bones
seen in neonatal syphilis
 Late congenital:
Frontal bossing
Short maxilla
High palatal arch
Hutchinson teeth
8th nerve deafness
Saddle nose
Perioral fissures

Can be prevented with appropriate treatment

Hutchinson teeth late result of
congenital syphilis
 Available serologic testing
RPR/VDRL: nontreponemal test
Sensitive but NOT specific
Quantitative, so can follow to determine disease activity and
treatment response
MHA-TP/FTA-ABS: specific treponemal test
Used for confirmatory testing
Qualitative, once positive always positive
RPR/VDRL screen in ALL pregnant women
early in pregnancy and at time of birth
This is easily treated!!
 Confirmed if T. pallidum identified in skin
lesions, placenta, umbilical cord, or at
autopsy
Presumptive diagnosis if any of:
Physical exam findings
CSF findings (positive VDRL)
Osteitis on long bone x-rays
Funisitis (barber shop pole umbilical cord)
RPR/VDRL >4 times maternal test
Positive IgM antibody
 IgG can represent maternal antibody, not infant
infection
This is VERY intricate and often confusing
Consult your RedBook (or peds ID folks) when faced
with this situation
 Penicillin G is THE drug of choice for ALL
syphilis infections
Maternal treatment during pregnancy very
effective (overall 98% success)
Treat newborn if:
They meet CDC diagnostic criteria
Mom was treated <4wks before delivery
Mom treated with non-PCN med
Maternal titers do not show adequate response (less
than 4-fold decline)
 Single-stranded RNA virus
Incubation period: 2-3 weeks
Spread through nasopharyngeal secretions
Vaccine-preventable disease
Mild, self-limiting illness
Infection earlier in pregnancy has a higher
probability of affected infant
 Reported rubella and CRS: United States, 1966-2004

Meissner, H. C. et al. Pediatrics 2006;117:933-935

Copyright 2006 American Academy of Pediatrics

 Sensorineural hearing loss (50-75%)
Cataracts and glaucoma (20-50%)
Cardiac malformations (20-50%)
Neurologic (10-20%)
Others to include growth retardation, bone
disease, HSM, thrombocytopenia, blueberry
muffin lesions
Blueberry muffin spots representing
extramedullary hematopoesis
 Maternal IgG may represent immunization
or past infection - Useless!
Can isolate virus from nasal secretions
Less frequently from throat, blood, urine, CSF
Serologic testing
IgM = recent postnatal or congenital infection
Rising monthly IgG titers suggest congenital
infection
Diagnosis after 1 year of age difficult to
establish
 Preventionimmunize (Rubella & MMR),
vaccines are not recommended on pregnancy,
should wait at least 28 days before planning of
conception
Breastfeeding may be vaccinated
Supportive care only with parent education
 Virus of herpes family and like herpes can be
reactivated
Incubation: unknown, common in children
(2-3 years old)
Mild, self limiting illness
Transmission can occur with primary
infection or reactivation of virus
40% risk of transmission in primary infxn
Studies suggest increased risk of
transmission later in pregnancy
However, more severe sequalae associated with
earlier acquisition
 Transmissions: saliva, faeces, blood, urine &
mucous
90% are asymptomatic at birth!
Up to 15% develop symptoms later, notably
sensorineural hearing loss
Symptomatic infection
HSM, petechiae, jaundice, chorioretinitis,
periventricular calcifications, neurological deficits
>80% develop long term complications
Hearing loss, vision impairment, developmental
delay
Ventriculomegaly
and
calcifications of
congenital CMV
 Maternal IgG shows only past infection
Infection common this is useless
Viral isolation from urine or saliva in 1st
3weeks of life
Afterwards may represent post-natal infection
Viral load and DNA copies can be assessed
by PCR
Less useful for diagnosis, but helps in following
viral activity in patient
Serologies not helpful given high antibody
in population
 Ganciclovir x6wks in symptomatic infants
Studies show improvement or no progression of
hearing loss at 6mos
No other outcomes evaluated (development, etc.)
Neutropenia often leads to cessation of therapy

Treatment currently not recommended in

asymptomatic infants due to side effects
 HSV1 or HSV2
Incubations: 2-10 days
Primarily transmitted through infected
maternal genital tract
Intimate mucocutaneous exposure
Primary infection with greater transmission
risk than reactivation
 Most are asymptomatic at birth
3 patterns of ~ equal frequency with symptoms
between birth and 4wks:
Skin, eyes, mouth (SEM)
CNS disease
Disseminated disease (present earliest)

Initial manifestations very nonspecific with

skin lesions NOT necessarily present
Presentations of congenital HSV
 Diagnostic findings: tissue culture swab
specimen from vesicles, PAP smear lesions,
visualization of painful blister like ulcer
Culture of maternal lesions if present at
delivery
Cultures in infant:
Skin lesions, oro/nasopharynx, eyes, urine, blood,
rectum/stool, CSF
CSF PCR
Serologies again not helpful given high
prevalence of HSV antibodies in population
 High dose acyclovir 60mg/kg/day divided
q8hrs
X21days for disseminated, CNS disease
X14days for SEM
Ocular involvement requires topical therapy as
well
 Snuffles?
syphilis
Chorioretinitis, hydrocephalus, and
intracranial calcifications?
toxo
Blueberry muffin lesions?
rubella
Periventricular calcifications?
CMV
No symptoms?
All of them
 Rubella

Syphilis