2. Background
๏ฌ Infections acquired in utero or during the birth process are
a significant cause of fetal and neonatal mortality.
๏ฌ Most fetus if infected during the first trimester will suffer
congenital malformation
๏ฌ Perinatal infections account for 2% - 3% of birth defects
which arise form a spectrum of organisms & have varying
modes of transmission
๏ฌ Not all birth defects are routinely screened for during
prenatal care
3. TORCH Infections
๏ฌ T=toxoplasmosis
๏ฌ O=other (syphilis, Hepatitis, HIV)
๏ฌ R=rubella
๏ฌ C=cytomegalovirus (CMV)
๏ฌ H=herpes simplex (HSV)
๏ฌ Origin was based on 5
infections that presented
similarly, with rash and ocular
findings.
๏ฌ First 4 are acquired antenately
๏ฌ Herpes and hepatitis acquired
prenately or via delivery
๏ฌ Term TORCH somewhat
obsolete as other disease are
important such as HIV
5. Toxoplasmosis - Transmission
๏ฌ Caused by protozoan โ
Toxoplasma gondii
๏ฌ Domestic cat is the
definitive host with
infections via:
๏ฌ Ingestion of cysts
(meats, garden
products)
๏ฌ Contact with oocysts in
feces
6. Toxoplasmosis
๏ฌ Acute infection usually asymptomatic
๏ฌ 1/3 risk of fetal infection with primary maternal
infection in pregnancy
๏ฌ Infection transmission rate higher with in 3rd
trimester
๏ฌ Fetal death higher with in 1st
trimester
๏ฌ Abnormal growth
7. Clinical Manifestations - Maternal
๏ฌ Most are asymptomatic at birth
๏ฌ Mononucleosis type symptoms:
๏ฌ Fatigue
๏ฌ Headache
๏ฌ Malaise
๏ฌ Lymphadenopathy (7% of infected individual)
๏ฌ Blood test reveals seroconversion
8. Clinical Manifestations - Infant
๏ฌ Most (70-90%) are asymptomatic at birth
๏ฌ Classic triad of symptoms:
๏ฌ Chorioretinitis
๏ฌ Hydrocephalus
๏ฌ Intracranial calcifications
๏ฌ Other symptoms include fever, rash, HSM,
microcephaly, seizures, jaundice, thrombocytopenia,
lymphadenopathy
๏ฌ Initially asymptomatic infants are still at high risk of
developing abnormalities, especially chorioretinitis
9. Toxo Screening
๏ฌ Prenatal testing with varied sensitivity
not useful for screening
๏ฌ Neonatal screening with IgM testing
implemented in some areas
๏ฌ Identifies infected asymptomatic
infants who may benefit from
therapy
10. Prevention andTreatment
๏ฌ Treatment for pregnant
mothers diagnosed with acute
toxo
๏ฌ Spiramycin daily
๏ฌ Macrolide antibiotic
๏ฌ Small studies have shown this
reduces likelihood of
congenital transmission (up to
50%)
๏ฌ Symptomatic infants
๏ฌ Pyrimethamine (with
leucovorin rescue) and
sulfadiazine
๏ฌ Treatment for 12 months
total
๏ฌ Prevetion
๏ฌ Wash hands before eating,
after handleing raw mean
๏ฌ Wash hands after contact
with cat feces
๏ฌ Wash hands if in contact
with soil
๏ฌ Cook meat adequately
12. Syphilis
๏ฌ Syphilis is a systemic infection caused by the
spirochete Treponema pallidum
๏ฌ Transmitted via sexual contact
๏ฌ Placental transmission as early as 6wks gestation
๏ฌ Typically occurs during second half
๏ฌ Mom with primary or secondary syphilis more likely to
transmit than latent disease
๏ฌ Large decrease in congenital syphilis since late
1990s
๏ฌ In 2002, only 11.2 cases/100,000 live births reported
15. Clinical Manifestations
๏ฌ Fetal:
๏ฌ Stillbirth
๏ฌ Neonatal death
๏ฌ Low birth weight
๏ฌ Hydrops fetalis
๏ฌ Congential Malformations
๏ฌ Active congenital syphilis in
the neonate
๏ฌ Long-term sequelae, such as
deafness and neurologic
impairment
๏ฌ SAB after 4th
months when
the spirochetes cross the
placenta
๏ฌ Repeated late abortion
๏ฌ Intrauterine death in 25%
๏ฌ Perinatal mortality in 25-
30% if untreated
16. Clinical Manifestations
Congenital syphilis Hutchinson Teeth Lores
โข2/3 of affected live-born infants are
asymptomatic at birth
โขClinical symptoms split into early or late
17. Diagnosing Syphilis
Maternal
๏ฌ Available serologic testing
๏ฌ RPR/VDRL: nontreponemal test
๏ฌ Sensitive but NOT specific
๏ฌ RPR/VDRL screen in ALL pregnant women
early in pregnancy and at time of birth
๏ฌ This is easily treated
18. Treatment
๏ฌ Penicillin G is THE drug of choice for ALL syphilis
infections
๏ฌ Maternal treatment during pregnancy very
effective (overall 98% success)
๏ฌ Treat newborn if:
๏ฌ They meet CDC diagnostic criteria
๏ฌ Mom was treated <4wks before delivery
๏ฌ Mom treated with non-PCN med
๏ฌ Maternal titers do not show adequate response
(less than 4-fold decline)
20. Rubella
๏ฌ Single-stranded RNA virus, spread via respiration
๏ฌ Vaccine-preventable disease
๏ฌ No longer considered endemic in the U.S.
๏ฌ Mild, self-limiting illness
๏ฌ Infection earlier in pregnancy has a higher probability of affected
infant within the first 16 weeks
๏ฌ Risk of fetal infection 50-60% 1st
month
๏ฌ Risk of fetal infection 22% in 2nd
month
๏ฌ Risk of fetal infection 6-10% in 4th
month
21. Copyright ยฉ2006 American Academy of PediatricsMeissner, H. C. et al. Pediatrics 2006;117:933-935
Reported rubella and CRS: United States, 1966-2004
22. Clinical Manifestations
๏ฌ Microcephaly
๏ฌ Cerebral palsy
๏ฌ Sensorineural hearing loss (50-75%)
๏ฌ Cataracts and glaucoma (20-50%)
๏ฌ blindness
๏ฌ Cardiac malformations (20-50%)
๏ฌ Neurologic (10-20%)
๏ฌ Others to include growth retardation, bone
disease, HSM, thrombocytopenia, โblueberry
muffinโ lesions
23. Diagnosis
๏ฌ Maternal IgG may represent immunization or
past infection
๏ฌ Can isolate virus from nasal secretions
๏ฌ Less frequently from throat, blood, urine, CSF
๏ฌ Serologic testing
๏ฌ IgM = recent postnatal or congenital infection
๏ฌ Rising monthly IgG titers suggest congenital infection
24. Treatment
๏ฌ Acute infection โ droplet precautions
๏ฌ Preventionโฆimmunize, immunize, immunize! (before or after
pregnancy)
๏ฌ 20% of women of child bearing age do not possess rubella
anitbody
๏ฌ Avoid pregnancy for 3 months after vaccination
๏ฌ Supportive care only with parent education
26. Clinical Manifestations
๏ฌ 1:100 babies are born with this congenital infection
๏ฌ 90% of newborns are asymptomatic at birth
๏ฌ Symptomatic infection
๏ฌ Small for Gestational dates
๏ฌ Hepatospleenomegaly
๏ฌ Petechiae
๏ฌ Jaundice
๏ฌ >80% develop long term complications
๏ฌ Hearing loss, vision impairment, developmental delay
27. Diagnosis
๏ฌ Maternal IgG shows only past infection
๏ฌ Infection common โ this is useless
๏ฌ Viral isolation from urine or saliva in 1st
3weeks of
life
๏ฌ Afterwards may represent post-natal infection
๏ฌ Viral load and DNA copies can be assessed by PCR
๏ฌ Less useful for diagnosis, but helps in following viral
activity in patient
๏ฌ Serologies not helpful given high antibody in
population
28. Treatment
๏ฌ Ganciclovir x6wks in symptomatic infants
๏ฌ Studies show improvement or no progression of hearing
loss at 6mos
๏ฌ No other outcomes evaluated (development, etc.)
๏ฌ Neutropenia often leads to cessation of therapy
๏ฌ Treatment currently not recommended in
asymptomatic infants due to side effects
30. Herpes Simplex (HSV)
๏ฌ HSV1 or HSV2
๏ฌ Primarily transmitted through infected maternal genital tract
๏ฌ Rationale for C-section delivery prior to membrane rupture
๏ฌ Primary infection with greater transmission risk than
reactivation
31. Clinical Manifestations
๏ฌ Most are asymptomatic at birth
๏ฌ 3 patterns of ~ equal frequency with symptoms
between birth and 4wks:
๏ฌ Skin, eyes, mouth (SEM)
๏ฌ CNS disease
๏ฌ Disseminated disease (present earliest)
๏ฌ Initial manifestations very nonspecific with skin
lesions NOT necessarily present
33. Diagnosis
๏ฌ Culture of maternal lesions if present at delivery
๏ฌ Cultures in infant:
๏ฌ Skin lesions, oro/nasopharynx, eyes, urine, blood,
rectum/stool, CSF
๏ฌ CSF PCR
๏ฌ Serologies again not helpful given high prevalence of
HSV antibodies in population
34. Treatment
๏ฌ High dose acyclovir 60mg/kg/day divided q8hrs
๏ฌ X21days for disseminated, CNS disease
๏ฌ X14days for SEM
๏ฌ Ocular involvement requires topical therapy as well
36. Varicella Zoster
๏ฌ Herpes Virus in a DNA virus
๏ฌ Highly contagious & transmitted by respiratory droplets & by direct
personal contact with vesicle fluid.
๏ฌ Complicates 3 in 1,000 pregnancies
๏ฌ Incubation period-10-21 days. Infectious 48 hrs before the rash - vesicle
crust over.
๏ฌ If primary infection occurs in the first trimester 4.9% risk of congenital
vaircella
๏ฌ Infection acquired in the last 10 days of pregnancy result in variable
congential infection with neonatal mortality as high as 34%
37. Varicella
Maternal
๏ฌ Greater morbidity
๏ฌ Pneumonia
๏ฌ Up 10% of pregnant
women
๏ฌ Severity increases later in
gestion
๏ฌ Encephalatis
๏ฌ Hepatitis
๏ฌ Under 20 weeks gestation
๏ฌ No increase in SAB
Fetal
๏ฌ 1-2% of maternal infections
๏ฌ Characterised by skin
scarring
๏ฌ eye defects,
๏ฌ hypoplasia of limbs
๏ฌ neurological
abnormalities
๏ฌ microcephaly
39. Varicella
๏ฌ Serology (IgG and IgM).
๏ฌ Screening: Routine screening generally not recommended
๏ฌ 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
๏ฌ In non-immune adult who plans to become pregnant - Live
attenuated varicella vaccine is safe & effective in preventing
chickenpox
๏ฌ If nonimmune - Give VZIG within 10 days of exposure
๏ฌ Avoid contact with susceptible individual.
๏ฌ Symptomatic treatment
๏ฌ Oral acyclovir reduces the duration of symptoms if started
within 24 hours of development of rash.
41. Herpes Zoster (Shingles)
๏ฌ Caused by reactivation of a latent varicella zoster virus
infection
๏ฌ Can occur years or decades after illness with chickenpox
๏ฌ Generally associated with normal aging and with anything that
causes reduced immunocompetence
๏ฌ Lifetime risk of 32% in the United States
๏ฌ Estimated 1 million cases zoster diagnosed annually in the U.S.
๏ฌ ***Vaccine Contraindicated in Pregnancy***
43. References
๏ฌ 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