Congenital Infections Flashcards
TORCH - overview
*an acronym for a group of congenitally acquired infections that may cause significant morbidity and mortality in neonates
TORCH infections
T - toxoplasmosis
O - other (syphilis, HIV, etc)
R - rubella
C - cytomegalovirus (CMV)
H - herpes simplex virus (HSV2)
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
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
toxoplasmosis - causative agent
*causative agent: protozoan and obligate intracellular parasite: Toxoplasma gondii
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
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
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
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
congenital toxoplasmosis - treatment
*pyrimethamine + sulfadiazine + leucovorin for 1 year
syphilis - causative agent
*caused by infection with the gram-negative spirochete Treponema pallidum
syphilis - routes of infection
- direct contact with a spirochete-containing lesion
- sexual contact
- transplacental transmission
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
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)
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
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
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
congenital syphilis - treatment
*penicillin G
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
- eye problems: cataracts, etc
- cardiac manifestations: patent ductus arteriosis (PDA)
- endocrinopathies
- 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
