Congenital Infections Flashcards by Kyra Porter

TORCH - overview

*an acronym for a group of congenitally acquired infections that may cause significant morbidity and mortality in neonates

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TORCH infections

T - toxoplasmosis
O - other (syphilis, HIV, etc)
R - rubella
C - cytomegalovirus (CMV)
H - herpes simplex virus (HSV2)

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s/s in a neonate that should make you think of TORCH infections

*microcephaly
*intracranial calcifications
*rash
*IUGR
*jaundice
*hepatosplenomegaly
*elevated transaminase concentrations
*thrombocytopenia

note - may be silent at birth

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TORCH infections in utero transmission - general points

*if mother experiences a PRIMARY infection while pregnant (as opposed to secondary infection or reactivation), the fetus is MORE LIKELY to be affected
*generally,transmission is more likely if mother is infected during the 3rd trimester compared to during the 1st trimester
*generally, if transmission occurs in the 1st trimester, congenital disease SEVERITY is greater

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toxoplasmosis - causative agent

*causative agent: protozoan and obligate intracellular parasite: Toxoplasma gondii

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toxoplasmosis - route of infection

*spread through fecal-oral route
*oocysts of T. gondii are excreted via CAT FECES and ingested by humans through:
-inadequately cooked meat
-contaminated water and soil
-unpasteurized goat milk

note - this is why pregnant women are advised against cleaning litter box

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congenital toxoplasmosis - risks of in utero transmission & severity of disease

*transmitted to the fetus during a mother’s primary infection (or if mother is immunocompromised & has chronic infection)
*RISK of fetal transmission during a maternal infection INCREASES WITH GESTATIONAL AGE
*however, the SEVERITY of infection is more likely the earlier in pregnancy fetal infection occurs

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congenital toxoplasmosis - classic triad of sx

hydrocephalus (LARGE head; more common than with other TORCH agents)
DIFFUSE intracranial calcifications
CHORIORETINITIS

*note - classic triad presents when fetal transmission occurs during the second trimester

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congenital toxoplasmosis - diagnosis

*diagnosis made by serologies, but is complicated
*diagnosis include:
-organism isolation from placenta, serum, CSF
-positive maternal ELISA
-positive infant toxoplasmosis IgG titer

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congenital toxoplasmosis - treatment

*pyrimethamine + sulfadiazine + leucovorin for 1 year

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syphilis - causative agent

*caused by infection with the gram-negative spirochete Treponema pallidum

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syphilis - routes of infection

direct contact with a spirochete-containing lesion
sexual contact
transplacental transmission

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congenital syphilis - clinical manifestations (overview)

*majority of infants born with congenital syphilis are asymptomatic at bith
*time of onset of clinical manifestations is used to classify

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congenital syphilis - early congenital syphilis clinical manifestations

*early congenital syphilis presents at 1-2 months of age with one or more of:
-MACULOPAPULAR RASH
-SNUFFLES (cold/rhinitis)
-generalized lymphadenopathy
-HEPATOMEGALY
-thrombocytopenia
-anemia
-meningitis
-chorioretinitis
-pneumonia alba
-OSTEOCHONDRITIS (moth-eaten appearance of bone)

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congenital syphilis - late congenital syphilis clinical manifestations

*late congenital syphilis presents after 2 years of age with signs such as:
-Hutchinson teeth (small teeth with an abnormal groove)
-mulberry molars (bulbous protrusions on the molar teeth resembling mulberries)
-eight nerve deafness
-interstitial keratitis
-bony lesions

note: Hutchinson’s triad = Hutchinson’s incisors, interstitial keratitis, 8th nerve deafness; pathognomonic for late congenital syphilis

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congenital syphilis - diagnosis

nontreponemal tests (VRDL, RPR) - used for screening & monitoring treatment
treponemal tests (fluorescent treponemal antibody absorption test or T. pallidum particle agglutination) - used to confirm diangosis

note - treponemal tests are not used alone due to false positives from other infections

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congenital syphilis - screening recommendations

*CDC recommends that all pregnant women be screened for syphilis with a nontreponemal test and, if positive, receive a confirmatory treponemal test
*infected women should be treated with penicillin G

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congenital syphilis - treatment

*penicillin G

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Hepatitis B (HBV) - causative agent

*caused by a DNA virus that hails from the hepadnavirus family

Hepatitis B (HBV) - route of infeciton

*transmission occurs after exposure to contaminated blood or bodily fluids
*transplacental transmission can occur, but is rare

congenital Hepatitis B (HBV) - clinical manifestations

*majority are asymptomatic
*rarely may demonstrate signs of HBV (jaundice, thrombocytopenia, elevated transaminase concentration, rash)

congenital Hepatitis B (HBV) - diagnosis

*essential to know the mother’ status (vaccinated, etc)
*infants born to mothers with a positive HBsAg should receive HBV vaccine and hepatitis B immune globulin within 12 hours of birth

human immunodeficiency virus (HIV) - causative agent

*HIV is an RNA virus belonging to the Retroviridae family
*2 types: HIV-1 and HIV-2
*HIV-1 is the predominant virus in the US

congenital human immunodeficiency virus (HIV) - transmission

*HIV can be transmitted to the infant at any time during the pregnancy:
-transplacentally
-during labor or delivery
-after birth through breastfeeding
*highest risk of neonatal infection is moms with a HIGH HIV RNA load

congenital HIV - clinical manifestations

*asymptomatic at birth *as infection evolves, T-cell function declines

congenital HIV - screening

*CDC recommends routine HIV-1 testing for all pregnant women in the US *measures for decreasing transmission: HIV drug prophylaxis, C-section, avoidance of breastfeeding, early detection in the infant *some practitioners may follow antibodies until 18 months of age because maternally-derived antibodies rarely persist beyond this age

congenital HIV - treatment

*start infant on zidovudine until 6 weeks of age

parvovirus B19 - causative agent

*single-stranded DNA virus

parvovirus B19 - routes of infection

*respiratory tract secretions *exposure to contaminated blood *transplacentally

congenital parvovirus B19 - clinical manifestations

*infants who are infected with congenital parvovirus are at risk for: -hydrops -pleural and pericardial effusions -IUGR -death

rubella - causative agent

*aka German measles *a member of the Togaviridae family

rubella - routes of infection

*contact with respiratory secretions (both direct & droplet) *transplacental transmission

congenital rubella - clinical manifestations

***"blueberry muffin" rash** (dermal erythropoiesis) *lymphadenopathy *hepatosplenomegaly *thrombocytopenia *interstitial pneumonitis *radiolucent bone disease *IUGR ***cataracts, PDA (patent ductus arteriosus)**

congenital rubella - complications

*the earlier during gestation infection occurs, the more severe the disease will be *infection after 12 week s may have no clinical manifestations but is more likely to result in future hearing loss and visual problems 1. eye problems: **cataracts**, etc 2. cardiac manifestations: **patent ductus arteriosis** (PDA) 3. endocrinopathies 4. neurologic sequelae: sensorineural hearing loss

cytomegalovirus (CMV) - causative agent

*part of the herpesviridae family *most common congenital infection in the US

cytomegalovirus (CMV) - routes of transmission

*can be transmitted to an infant during pregnancy (transplacental transmission), during delivery (via contact with infected genital tract secretions) or postnatally (via ingestion of contaminated human milk)

congenital CMV - clinical manifestations

*majority of neonates are asymptomatic at birth *symptomatic infants with CMV may have: -**blueberry muffin rash** -IUGR -**periventricular calcifications** -hepatosplenomegaly -jaundice -thrombocytopenia -retinitis note - the risk of fetal morbidity is increased when the mother has a **primary infection** during pregnancy, especially during the first trimester

congenital CMV - complications

*approximately half of symptomatic neonates will develop CNS sequelae, including: retinitis, **sensorineural deafness,** and developmental delay *there is an increased likelihood of development delay when infants manifest chorioretinitis, microcephaly, and intracranial calcifications

congenital CMV - diagnosis

*demonstration of the **virus in body fluids such as URINE** or pharyngeal secretions in the first 3 weeks after birth *virus usually detected by PCR

congenital CMV - treatment

*tx with **ganciclovir** has been shown to improve both hearing loss & neurodevelopmental outcomes

herpes simplex virus (HSV 1 & 2) - causative agent

*HSV 1 and 2 are **double-stranded DNA viruses from the Herpesviridae family**

HSV - routes of infection

*transmitted primarily through direct contact with infected lesions or mucosa *neonates most often acquire the infection while passing through an infected vaginal canal during birth or from the virus ascending after rupture of membranes ***PRIMARY maternal infection during pregnancy imparts the greatest risk to the fetus**

congenital HSV - clinical manifestations

*infants with congenital HSV usually present in first 6 weeks after birth *early signs include: irritability, poor feeding, lethargy, **skin vesicles, FEVER,** seizures *3 ways to classify manifestations of congenital HSV: 1. primarily skin, eyes, and mucosal involvement (SEM disease) 2. primarily CNS disease 3. disseminated disease with multiple organ involvement

congenital HSV - complications

*untreated: high morbidity and mortality *if treated: -infants with SEM disease have best prognosis, but half will recur -infants with CNS disease have a good prognosis for survival but suffer significant neurologic sequelae

congenital HSV - diagnosis

*HSV PCR is test of choice for evaluation of CSF (high sensitivity); repeat CSF PCR is negative during the first 5 days but still high suspicion

congenital HSV - treatment

*tx with **acyclovir** improves mortality rates for all infants