

TORCH
Infections
 Background

 Infections acquired in utero or during the birth process

are a significant cause of fetal and neonatal mortality.
 Most fetus if infected during the first trimester will
suffer congenital malformation
 Perinatal infections account for 2% - 3% of birth defects
which arise form a spectrum of organisms & have
varying modes of transmission
 Not all birth defects are routinely screened for
during prenatal care
 TORCH Infections

 T=toxoplasmosis  Origin was based on 5

infections that presented
 O=other (syphilis, Hepatitis, similarly, with rash and
HIV) ocular findings.
 R=rubella
 First 4 are acquired
 C=cytomegalovirus
antenately
(CMV)  Herpes and hepatitis
 H=herpes simplex
acquired prenately or via
(HSV) delivery
Term TORCH somewhat
obsolete as other disease
are important such as HIV
Toxoplasmosis
 Toxoplasmosis - Transmission

 Caused by protozoan –
Toxoplasma gondii
 Domestic cat is the
definitive host
with
 Ingestioninfections
of
via:cysts (meats,
garden
 products)
Contact with oocysts
in feces
 Toxoplasmosis

 Acute infection usually asymptomatic

 1/3 risk of fetal infection with primary
maternal
 Infectioninfection in pregnancy
transmission rate higher with in 3rdtrimester
 Fetal death higher with in 1st trimester
 Abnormal growth
Clinical Manifestations - Maternal
 Most are asymptomatic at
birth
 Fatigue
 Mononucleosis
Headach type
 e
symptoms:
 Malaise
Lymphad
enopathy
 Blood test reveals
(7% of
seroconversion
infected
individual
)
 Clinical Manifestations -
Infant
 Most (70-90%) are asymptomatic at
birth
 Chorioretinitis
Classic
  triad of symptoms:
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
 Toxo Screening

 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
 Prevention and
Treatment
 Treatment for pregnant  Prevetion
mothers diagnosed with
acute toxo  Wash hands before
 Spiramycin eating, after handleing
daily
 Macrolide antibiotic  raw mean
 Small studies have shown this
reduces likelihood of Wash hands after
congenital transmission (up  contact with cat feces
to 50%)
Wash hands if in
 Symptomatic  contact with soil
 Pyrimethamine (with
infants Cook meat adequately
leucovorin rescue)
and sulfadiazine
 Treatment for 12
months total
Syphilis
 Syphilis

 Syphilis is a systemic infection caused by

the spirochete Treponema pallidum
 Transmitted via sexual contact
 Placental transmission
 Typically occurs duringas earlyhalf
second as 6wks
gestation
 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
 Clinical Manifestations
 SAB after 4thmonths when  Fetal:
the spirochetes cross the  Stillbirth
placenta  Neonatal death
 Low birth
 Repeated late
 weight Hydrops
abortion
 Intrauterine death in  fetalis
25%  Congential
 Perinatal mortality in Malformations
25- 30% if untreated  Active congenital syphilis
in the neonate
Long-term sequelae, such
as deafness and neurologic
impairment
 Clinical Manifestations

•2/3 of affected live-born infants are

asymptomatic at birth
•Clinical symptoms split into early
or late
Congenital syphilis Hutchinson Teeth Lores
 Diagnosing Syphilis
Maternal

 Available serologic testing

 RPR/VDRL: nontreponemal
test
 Sensitive but NOT specific
 RPR/VDRL screen in ALL pregnant women
early in pregnancy and at time of birth
 This is easily
treated
 Treatment

 Penicillin G is THE drug of choice for ALL

syphilis infections
 Maternal treatment during pregnancy
very effective (overall 98% success)
 Treat
 newborn
They meet CDCif: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)
Rubella
 Rubella
 Single-stranded RNA virus, spread via
respiration
 Vaccine-preventable disease
 No longer considered endemic in the
U.S.
 Mild, self-limiting
illness
 Infection earlier in pregnancy has a higher probability of
affected infant within the first 16 weeks
 Risk of fetal infection 50-60% 1stmonth
 Risk of fetal infection 22% in 2ndmonth
 Risk of fetal infection 6-10% in 4th
month
 Clinical Manifestations
 Microcephal
y
 Cerebral
palsy
 Sensorineural hearing loss (50-
75%)
 Cataracts and glaucoma (20-
 blindness
50%)
 Cardiac malformations (20-
50%)
 Neurologic (10-
20%)
 Others to include growth retardation, bone
disease, HSM, thrombocytopenia,
“blueberry muffin” lesions
 Diagnosis
 Maternal IgG may represent immunization or
past infection

 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
 Treatment

 Acute infection – droplet

precautions
 Prevention…immunize, immunize, immunize! (before or
after pregnancy)
 20% of women of child bearing age do not possess
rubella anitbody
 Avoid pregnancy for 3 months after
vaccination
 Supportive care only with parent
education
Cytomegalovirus (CMV)
 Clinical Manifestations
 1:100 babies are born with this congenital
infection

 90% of newborns are asymptomatic at birth

 Small for Gestational
Symptomatic
  dates infection
 Hepatospleenomegaly
 Petechiae
 Jaundice
>80% develop long term
complications
 Hearing loss, vision
impairment, developmental
 Diagnosis
 Maternal IgG shows only past infection
 Infection common – this is
useless
 Viral isolation from urine or saliva in 1st3weeks
of life
 Afterwards may represent post-natal
infection
 Viral load and DNA copies can be assessed by
 Less useful for diagnosis, but helps in following
PCR viral activity in patient

 Serologies not helpful given high antibody

in population
 Treatment

 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
Herpes Simplex
(HSV)
 Herpes Simplex
(HSV)
 HSV1 or HSV2

 Primarily transmitted through infected maternal genital

 Rationale for C-section delivery prior to membrane
tract rupture
 Primary infection with greater transmission risk
than reactivation
 Clinical Manifestations

 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
 Diagnosis

 Culture of maternal lesions if present at

delivery
 Skin lesions, oro/nasopharynx, eyes, urine,
 Cultures
blood,inrectum/stool,
infant: CSF

 CSF PCR

 Serologies again not helpful given high prevalence

of HSV antibodies in population
 Treatment

 High dose acyclovir 60mg/kg/day divided

 X21days for disseminated, CNS
q8hrs
 disease X14days for SEM

 Ocular involvement requires topical therapy as

well
Varicella Zoster
 Varicella Zoster
 Herpes Virus in a DNA
virus
 Highly contagious & transmitted by respiratory droplets & by
direct personal contact with vesicle fluid.
 Complicates 3 in 1,000
pregnancies
 Incubation period-10-21 days. Infectious 48 hrs before the rash -
vesicle crust over.
 If primary infection occurs in the first trimester 4.9% risk of
congenital vaircella
 Infection acquired in the last 10 days of pregnancy result in
variable congential infection with neonatal mortality as high as
34%
 Varicella

Maternal Fetal
 Greater morbidity  1-2% of maternal
 Pneumoni infectionsby
 Characterised
a
 Up 10% of skin scarring
pregnant women
 eye defects,
 Severity increases later
in gestion  hypoplasia of
 Encephalati  limbs
 s Hepatitis neurological
 abnormalitie
 Under 20 weeks
s
gestation
 No increase in
microcephal
SAB
y
Fetal Varicella
 Varicella

 Serology (IgG and IgM).

 Screening: Routine screening generally not recommended

 Prevention: If pregnant woman (with no history of previous

chickenpox) is exposed, perform STAT Varicella IgG.
Exposed neonate should receive VZIG prophylaxis.
 Treatment and Prevention

 In non-immune adult who plans to become pregnant - Live

attenuated varicella vaccine is safe & effective in
preventing chickenpox
 If nonimmune - Give VZIG within 10 days of
exposure
 Avoid contact with susceptible
individual.
 Symptomatic
treatment
 Oral acyclovir reduces the duration of symptoms if
started within 24 hours of development of rash.
 Herpes
Zoster (Shingles)
 Caused by reactivation of a latent varicella zoster
virus infection

 Can occur years or decades after illness with

chickenpox

 Generally associated with normal aging and with anything

that causes reduced immunocompetence

 Lifetime risk of 32% in the United States

 Estimated 1 million cases zoster diagnosed annually in the

Questions
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