2. 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
3. TORCH Infections
T=toxoplasmosis
O=other (syphilis, Hepatitis, HIV)
R=rubella
C=cytomegalovirus (CMV)
H=herpes simplex (HSV)
Origin was based on 5
infections that presented
similarly, with rash and ocular
findings.
First 4 are acquired antenately
Herpes and hepatitis acquired
prenately or via delivery
Term TORCH somewhat
obsolete as other disease are
important such as HIV
5. Toxoplasmosis - Transmission
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
6. Toxoplasmosis
Acute infection usually asymptomatic
1/3 risk of fetal infection with primary maternal
infection in pregnancy
Infection transmission rate higher with in 3rd
trimester
Fetal death higher with in 1st
trimester
Abnormal growth
7. Clinical Manifestations - Maternal
Most are asymptomatic at birth
Mononucleosis type symptoms:
Fatigue
Headache
Malaise
Lymphadenopathy (7% of infected individual)
Blood test reveals seroconversion
8. Clinical Manifestations - Infant
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
9. 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
10. Prevention andTreatment
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%)
Symptomatic infants
Pyrimethamine (with
leucovorin rescue) and
sulfadiazine
Treatment for 12 months
total
Prevetion
Wash hands before eating,
after handleing raw mean
Wash hands after contact
with cat feces
Wash hands if in contact
with soil
Cook meat adequately
12. Syphilis
Syphilis is a systemic infection caused by the
spirochete Treponema pallidum
Transmitted via sexual contact
Placental transmission as early as 6wks 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
15. Clinical Manifestations
Fetal:
Stillbirth
Neonatal death
Low birth weight
Hydrops fetalis
Congential Malformations
Active congenital syphilis in
the neonate
Long-term sequelae, such as
deafness and neurologic
impairment
SAB after 4th
months when
the spirochetes cross the
placenta
Repeated late abortion
Intrauterine death in 25%
Perinatal mortality in 25-
30% if untreated
17. 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
18. Treatment
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)
20. 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% 1st
month
Risk of fetal infection 22% in 2nd
month
Risk of fetal infection 6-10% in 4th
month
22. Clinical Manifestations
Microcephaly
Cerebral palsy
Sensorineural hearing loss (50-75%)
Cataracts and glaucoma (20-50%)
blindness
Cardiac malformations (20-50%)
Neurologic (10-20%)
Others to include growth retardation, bone
disease, HSM, thrombocytopenia, “blueberry
muffin” lesions
23. 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
24. 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
26. Clinical Manifestations
1:100 babies are born with this congenital infection
90% of newborns are asymptomatic at birth
Symptomatic infection
Small for Gestational dates
Hepatospleenomegaly
Petechiae
Jaundice
>80% develop long term complications
Hearing loss, vision impairment, developmental delay
27. Diagnosis
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
28. 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
30. Herpes Simplex (HSV)
HSV1 or HSV2
Primarily transmitted through infected maternal genital tract
Rationale for C-section delivery prior to membrane rupture
Primary infection with greater transmission risk than
reactivation
31. 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
33. Diagnosis
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
34. Treatment
High dose acyclovir 60mg/kg/day divided q8hrs
X21days for disseminated, CNS disease
X14days for SEM
Ocular involvement requires topical therapy as well
36. 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%
37. Varicella
Maternal
Greater morbidity
Pneumonia
Up 10% of pregnant
women
Severity increases later in
gestion
Encephalatis
Hepatitis
Under 20 weeks gestation
No increase in SAB
Fetal
1-2% of maternal infections
Characterised by skin
scarring
eye defects,
hypoplasia of limbs
neurological
abnormalities
microcephaly
39. 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.
40. 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.
41. 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 U.S.
***Vaccine Contraindicated in Pregnancy***
43. References
Gilbert, R., Gras, L., & European Multicentre Study on
Congenital Toxoplasmosis. (2003). Effect of timing and type of
treatment on the risk of mother to child transmission of
Toxoplasma gondii. BJOG: an international journal of obstetrics
and gynaecology, 110(2), 112.
Editor's Notes
Fale positives
Lores are cracks and fissures around the mouth and hard palette