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50 Cards in this Set
- Front
- Back
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What diseases causes congenital infections?
TORCHES CLAP |
Toxoplasmosis
Rubella Cytomegalovirus Herpes simplex virus Enteroviruses S yphilis Chickenpox Lyme disease AIDS (HIV) Parvovirus B19 |
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Cytomegalovirus (CMV)
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A member of the Herpesvirus family
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CMV Infection: Epidemiology
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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 |
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CMV infection in Pregnancy
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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 |
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Congenital CMV Infection
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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% |
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Congenital CMV: Pathogenesis
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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 |
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Congenital CMV Infection…. 90% asymptomatic at birth
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Normal appearing at birth
Sequelae: Sensorineural hearing loss At birth (7-15%) Late or delayed-onset (11-18%) |
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Congenital CMV: Diagnosis
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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 |
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Congenital CMV: Treatment
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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) |
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Congential Toxoplasmosis
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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 |
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What is Toxoplasma gondii ??
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obligate intracellular protozoan parasite
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Congenital Toxoplasmosis- what percent of women are seronegative?
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In the US, 80% of women are seronegative and therefore susceptible
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How does maternal infection occurs?
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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 |
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What is the incidence of toxoplasmosis?
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1/10,000 births
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Congenital Toxoplasmosis and gestational age
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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 |
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1st trimester- Congenital Toxoplasmosis
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17% (fetal demise, severe disease)
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2nd trimester- Congenital Toxoplasmosis
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25% (intermediate severity)
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3rd trimester- Congenital Toxoplasmosis
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65% (mild or subclinical disease)
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Toxoplasmosis: Clinical Manifestations
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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 |
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Toxoplasmosis: Classic syndrome
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hydrocephalus, diffuse intracranial calcification and chorioretinits
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Congenital Toxoplasmosis: Hydrocephalus
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more common than other TORCH agents
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Congenital Toxoplasmosis: Signs at birth
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rash, jaundice, hepatosplenomegaly, generalized adenopathy, and thrombocytopenia
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Congenital Toxoplasmosis: Prenatal diagnosis
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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 |
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Toxoplasmosis: Postnatal diagnosis
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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 |
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Congenital Toxoplasmosis: Treatment Regimen
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Symptomatic and asymptomatic congenital infection
Pyrimethamine plus Sulfadiazine Supplement with folinic acid (Leucovorin) Duration of therapy is prolonged (1 year) |
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Acquired Rubella Infection:(German Measles)
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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) |
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Congenital Rubella Syndrome: Clinical Features
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EYES - cataracts, retinopathy
CARDIAC - PDA, PA stenosis AUDITORY - sensorineural deafness (most common manifestation of CRS) NEUROLOGIC - behavioral disorders, meningoencephalitis, mental retardation |
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Congenital Rubella Syndrome: Clinical Features
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Growth retardation
Radiolucent bone disease Hepatosplenomagaly, thrombocytopenia Purpuric skin lesions (“blueberry muffin”) Normal-appearing infants with late-onset sequelae |
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Congenital Rubella: Diagnosis (Serology)
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Most commonly used
Rubella-specific IgM ELISA in neonatal serum (not cord serum) Titers of rubella-specific IgG over months |
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Congenital Rubella: Diagnosis: Virus culture
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difficult (but possible)
nasopharynx most reliable throat, blood, urine, or CSF also useful i nfected infants shed virus for up to 1 year |
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What is the treatment for Rubella Syndrome
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No treatment for congenital rubella syndrome
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Prevention for Rubella Syndrome
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VACCINE
as part of MMR vaccine live-virus rubella vaccine (RA 27/3 strain) |
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How common is Syphilis?
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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 1 0-20% of babies born to untreated mothers become infected |
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How is Congenital Syphilis transmitted?
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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) |
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Is it mainly symptomatic or asymptomatic?
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Asymptomatic > > >
Symptomatic |
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What are the clinical features of fetus in congenital syphillis?
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Stillbirth, hydrops, IUGR
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What are clinic features of neonates in congenital syphillis?
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Asymptomatic or multisystemic disease
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What are the clinical features of a baby who is 4-8 weeks in congenital syphillis?
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Snuffles, ↑LN, ↑liver/spleen, rash, osteochondritis
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What are the clinic features of a baby who is Late (>2 yrs) in congenital syphillis?
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Teeth,* eyes,* 8th nerve,*
nose/face; skeletal |
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What is Hutchington's Triad? What is it pathological for?
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Teeth,* eyes,* 8th nerve,*
nose/face; skeletal Congenital Syphillis |
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Diagnostic Tests for Syphilis
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Non-treponemal serologic tests
VDRL, RPR -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 FTA-ABS, MHA-TP, TPI Reactive forever even after therapy |
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Indications for Therapy for Congenital Syphilis
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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 |
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Therapy for Congenital Syphilis
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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 |
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Neonatal HSV Infection: Epidemiology
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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 |
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Neonatal HSV Infection: Transmission
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Intrapartum (90%-95%)contact with infected maternal genital lesions
I ntrauterine: (5%) congenital defects Postnatal transmission: parent/nursery worker |
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Neonatal HSV Infection: Risk Factors
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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 |
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Neonatal HSV Infection: Clinical Spectrum
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Localized skin, eye, and mouth (40%)
Vesicles, conjunctivitis Central nervous system disease (35%) - Encephalitis, +/- vesicles Disseminated (20%), -Multi-organ disease, +/- vesicles |
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Neonatal HSV Infection: Diagnosis
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Viral culture (vesicles, conjunctiva, mouth, nasopharynx, rectum, urine, blood or CSF)
DFA stain of skin lesions (less sensitive than culture) |
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HSV therapy
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HSV PCR of CSF
Intravenous Acyclovir: 20 mg/kg/Q8h 14-21 Days |
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Human Immunodeficiency Virus Infection
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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 |
