• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

Card Range To Study



Play button


Play button




Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

50 Cards in this Set

  • Front
  • Back
What diseases causes congenital infections?

Herpes simplex virus
S yphilis

Lyme disease
Parvovirus B19
Cytomegalovirus (CMV)
A member of the Herpesvirus family
CMV Infection: Epidemiology
50-85% of adults are seropositive by age 40

CMV infection is usually asymptomatic

Latency and Reactivation characteristic (“once infected, always infected”)

Virus present in saliva, tears, semen, urine, cervical secretions, blood, breast milk

CMV is spread via direct interpersonal contact with body fluids
CMV infection in Pregnancy
Primary sources of CMV infection in women of child bearing age: young children and sexual contacts

15-45% of pregnant women are susceptible

1-4% will develop primary infection

Most infected women (90%) are asymptomatic
Congenital CMV Infection
Most common congenital viral infection in US

Incidence: 1% of all live births

Primary (first) and recurrent maternal infection can transmit infection to the fetus

Transmission rates:
maternal primary infection: 30-40%

maternal recurrent infection: 0.9-1.5%
Congenital CMV: Pathogenesis
Primary infection during pregnancy - more likely to result in symptoms at birth than recurrent infection

Earlier in gestation fetus infected, greater risk for severe sequelae

Presence of maternal antibody does not prevent transmission

Mechanisms(?): reactivation of latent virus, chronic infection, re-infection with new strain
Congenital CMV Infection…. 90% asymptomatic at birth
Normal appearing at birth

Sequelae: Sensorineural hearing loss

At birth (7-15%)

Late or delayed-onset (11-18%)
Congenital CMV: Diagnosis
VIRAL CULTURE OF URINE (or saliva) of a newborn

Specimen must be collected within the first 3 weeks of life

Usually high titer virus

Serology not useful
Congenital CMV: Treatment
Ganciclovir therapy is not the standard of care and not recommended routinely

May benefit in severe life/sight threatening disease (chorioretinitis or pneumonitis)

Follow-up is critical (hearing, visual and developmental, neurology)
Congential Toxoplasmosis
Toxoplasma gondii - obligate intracellular protozoan parasite

Found in many animal species, but its life cycle involves a sexual stage in cats (primary host)

Like CMV infection, toxoplasmosis is usually asymptomatic in children and adults

Primary infection during pregnancy can cause serious fetal effects
What is Toxoplasma gondii ??
obligate intracellular protozoan parasite
Congenital Toxoplasmosis- what percent of women are seronegative?
In the US, 80% of women are seronegative and therefore susceptible
How does maternal infection occurs?
ingestion of raw or undercooked meat (pork)

ingestion of oocysts from contaminated sources (soil, cat litter, garden vegetables)

Incidence of congenital toxo: 1/10,000 births
What is the incidence of toxoplasmosis?
1/10,000 births
Congenital Toxoplasmosis and gestational age
Rate of transmission is directly related to GA of the fetus at time of infection

Severity of fetal damage, however, is inversely related to gestational age of fetus
1st trimester- Congenital Toxoplasmosis
17% (fetal demise, severe disease)
2nd trimester- Congenital Toxoplasmosis
25% (intermediate severity)
3rd trimester- Congenital Toxoplasmosis
65% (mild or subclinical disease)
Toxoplasmosis: Clinical Manifestations
70-90% of infected infants asymptomatic at birth

“Large” number develop visual impairment, learning disabilities or mental retardation months to years later

Isolated ocular findings (chorioretinitis) in 15% of infants
Toxoplasmosis: Classic syndrome
hydrocephalus, diffuse intracranial calcification and chorioretinits
Congenital Toxoplasmosis: Hydrocephalus
more common than other TORCH agents
Congenital Toxoplasmosis: Signs at birth
rash, jaundice, hepatosplenomegaly, generalized adenopathy, and thrombocytopenia
Congenital Toxoplasmosis: Prenatal diagnosis
Toxo-specific IgM or IgA antibodies in fetal blood (Ref. Lab)

Detecting the parasite in fetal blood or amniotic fluid (PCR or mouse inoculation)

Follow serial fetal ultrasound to look for hydrocephalus
Toxoplasmosis: Postnatal diagnosis
A negative maternal toxo IgG at delivery rules out the diagnosis (no infant work-up)

Toxo-specific antibodies (IgM, IgA, or IgE) in infant serum is diagnostic (Ref. Lab)

Buffy coat or CSF for PCR (Ref. Lab)

T. gondii isolation from placenta, cord, or blood (mouse inoculation) is definitive
Congenital Toxoplasmosis: Treatment Regimen
Symptomatic and asymptomatic congenital infection

Pyrimethamine plus Sulfadiazine

Supplement with folinic acid (Leucovorin)

Duration of therapy is prolonged (1 year)
Acquired Rubella Infection:(German Measles)
Up to 10% of adults are non-immune

Transmission occurs via respiratory droplets

25-50% of cases are asymptomatic

Mild self-limited illness

Fever, maculopapular rash, lymphadenopathy (suboccipital), transient arthralgia/arthritis

Incubation period 14-21 days (mean, 18 days)
Congenital Rubella Syndrome: Clinical Features
EYES - cataracts, retinopathy

CARDIAC - PDA, PA stenosis

AUDITORY - sensorineural deafness (most common manifestation of CRS)

NEUROLOGIC - behavioral disorders, meningoencephalitis, mental retardation
Congenital Rubella Syndrome: Clinical Features
Growth retardation

Radiolucent bone disease

Hepatosplenomagaly, thrombocytopenia

Purpuric skin lesions (“blueberry muffin”)

Normal-appearing infants with late-onset sequelae
Congenital Rubella: Diagnosis (Serology)
Most commonly used
Rubella-specific IgM ELISA in neonatal serum (not cord serum)

Titers of rubella-specific IgG over months
Congenital Rubella: Diagnosis: Virus culture
difficult (but possible)
nasopharynx most reliable
throat, blood, urine, or CSF also useful
nfected infants shed virus for up to 1 year
What is the treatment for Rubella Syndrome
No treatment for congenital rubella syndrome
Prevention for Rubella Syndrome
as part of MMR vaccine

live-virus rubella vaccine (RA 27/3 strain)
How common is Syphilis?
Prevalence among pregnant women varies from < 1% - 5% depending upon risk (e.g.., HIV)

There is a 2.5 fold increased risk of acquiring HIV when syphilis is present

Most cases are from the southern United States
0-20% of babies born to untreated mothers become infected
How is Congenital Syphilis transmitted?
In utero transplacental passage

Placental transfer of organisms occurs > 18 weeks of gestation

↑ rate of transmission as gestation ↑ (90% transmission in 3rd trimester)

Infection can be transmitted at any stage of disease (but highest during secondary phase 60-100% transmission rate)
Is it mainly symptomatic or asymptomatic?
Asymptomatic > > >
What are the clinical features of fetus in congenital syphillis?
Stillbirth, hydrops, IUGR
What are clinic features of neonates in congenital syphillis?
Asymptomatic or multisystemic disease
What are the clinical features of a baby who is 4-8 weeks in congenital syphillis?
Snuffles, ↑LN, ↑liver/spleen, rash, osteochondritis
What are the clinic features of a baby who is Late (>2 yrs) in congenital syphillis?
Teeth,* eyes,* 8th nerve,*
nose/face; skeletal
What is Hutchington's Triad? What is it pathological for?
Teeth,* eyes,* 8th nerve,*
nose/face; skeletal

Congenital Syphillis
Diagnostic Tests for Syphilis
Non-treponemal serologic tests
-Revert to negative 1 – 2 years after therapy
A sustained 4-fold increase in titer suggests successful therapy

A 4-fold ↑ in titer signifies relapse or re-infection

Treponemal serologic tests

Reactive forever even after therapy
Indications for Therapy for Congenital Syphilis
Clinical or radiographic evidence of disease

Quantitative non-treponemal serology (VDRL, RPR) titer > 4 x higher than mother’s

CSF findings are abnormal and CSF-VDRL is positive

Positive Treponemal IgM
Therapy for Congenital Syphilis
Proven or highly probable
- Aqueous penicillin G 50,000U/kg x 10-14d OR
- Procaine penicillin G IM q day x 10-14 d
Asymptomatic infants with RPR < 4-fold less than mother, normal exam, CBC, CSF, X-rays
- Adequate maternal Rx: bicillin IM x 1
- Inadequate maternal Rx: same as for proven infection
Neonatal HSV Infection: Epidemiology
20-30% of US adults are HSV-2 seropositive
5-10% have symptomatic genital HSV infection
Incidence: 1:3,000 - 1:5,000 live births annually
Neonatal HSV Infection: Transmission
Intrapartum (90%-95%)contact with infected maternal genital lesions
ntrauterine: (5%) congenital defects

Postnatal transmission: parent/nursery worker
Neonatal HSV Infection: Risk Factors
Infant born vaginally to a mother with primary genital HSV infection is 33-50%

Infant born vaginally to a mother with recurrent HSV infection is 3-5%

Fetal scalp monitors

Virus types: ~80% HSV-2, 10-15% HSV-1
Neonatal HSV Infection: Clinical Spectrum
Localized skin, eye, and mouth (40%)
Vesicles, conjunctivitis

Central nervous system disease (35%)
- Encephalitis, +/- vesicles

Disseminated (20%),
-Multi-organ disease, +/- vesicles
Neonatal HSV Infection: Diagnosis
Viral culture (vesicles, conjunctiva, mouth, nasopharynx, rectum, urine, blood or CSF)
DFA stain of skin lesions (less sensitive than culture)
HSV therapy
Intravenous Acyclovir:
20 mg/kg/Q8h 14-21 Days
Human Immunodeficiency Virus Infection
Rate of transmission from Mother to Baby:

15-25% (USA/Europe)
25-45% (Africa)

Breastmilk transmission in resource poor countries

Diagnosis by HIV DNA PCR

Zidovudine prophylaxis (pre and intrapartum and to newborn reduces transmission by two-thirds)

Protective role of elective C-section; formula feeding

Year 2003: Maternal HAART

1% transmission