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1 Mega Step 1 Deck > Congenital Infections > Flashcards

Congenital Infections Flashcards

1
Q

TORCH - overview

A

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

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2
Q

TORCH infections

A

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

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3
Q

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

A

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

note - may be silent at birth

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4
Q

TORCH infections in utero transmission - general points

A

*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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5
Q

toxoplasmosis - causative agent

A

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

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6
Q

toxoplasmosis - route of infection

A

*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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7
Q

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

A

*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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8
Q

congenital toxoplasmosis - classic triad of sx

A
  1. hydrocephalus (LARGE head; more common than with other TORCH agents)
  2. DIFFUSE intracranial calcifications
  3. CHORIORETINITIS

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

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9
Q

congenital toxoplasmosis - diagnosis

A

*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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10
Q

congenital toxoplasmosis - treatment

A

*pyrimethamine + sulfadiazine + leucovorin for 1 year

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11
Q

syphilis - causative agent

A

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

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12
Q

syphilis - routes of infection

A
  1. direct contact with a spirochete-containing lesion
  2. sexual contact
  3. transplacental transmission
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13
Q

congenital syphilis - clinical manifestations (overview)

A

*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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14
Q

congenital syphilis - early congenital syphilis clinical manifestations

A

*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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15
Q

congenital syphilis - late congenital syphilis clinical manifestations

A

*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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16
Q

congenital syphilis - diagnosis

A
  1. nontreponemal tests (VRDL, RPR) - used for screening & monitoring treatment
  2. 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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17
Q

congenital syphilis - screening recommendations

A

*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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18
Q

congenital syphilis - treatment

A

*penicillin G

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19
Q

Hepatitis B (HBV) - causative agent

A

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

20
Q

Hepatitis B (HBV) - route of infeciton

A

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

21
Q

congenital Hepatitis B (HBV) - clinical manifestations

A

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

22
Q

congenital Hepatitis B (HBV) - diagnosis

A

*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

23
Q

human immunodeficiency virus (HIV) - causative agent

A

*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

24
Q

congenital human immunodeficiency virus (HIV) - transmission

A

*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

25
Q

congenital HIV - clinical manifestations

A

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

26
Q

congenital HIV - screening

A

*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

27
Q

congenital HIV - treatment

A

*start infant on zidovudine until 6 weeks of age

28
Q

parvovirus B19 - causative agent

A

*single-stranded DNA virus

29
Q

parvovirus B19 - routes of infection

A

*respiratory tract secretions
*exposure to contaminated blood
*transplacentally

30
Q

congenital parvovirus B19 - clinical manifestations

A

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

31
Q

rubella - causative agent

A

*aka German measles
*a member of the Togaviridae family

32
Q

rubella - routes of infection

A

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

33
Q

congenital rubella - clinical manifestations

A

*“blueberry muffin” rash (dermal erythropoiesis)
*lymphadenopathy
*hepatosplenomegaly
*thrombocytopenia
*interstitial pneumonitis
*radiolucent bone disease
*IUGR
*cataracts, PDA

34
Q

congenital rubella - complications

A

*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
35
Q

cytomegalovirus (CMV) - causative agent

A

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

36
Q

cytomegalovirus (CMV) - routes of transmission

A

*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)

37
Q

congenital CMV - clinical manifestations

A

*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

38
Q

congenital CMV - complications

A

*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

39
Q

congenital CMV - diagnosis

A

*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

40
Q

congenital CMV - treatment

A

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

41
Q

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

A

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

42
Q

HSV - routes of infection

A

*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

43
Q

congenital HSV - clinical manifestations

A

*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

44
Q

congenital HSV - complications

A

*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

45
Q

congenital HSV - diagnosis

A

*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

46
Q

congenital HSV - treatment

A

*tx with acyclovir improves mortality rates for all infants

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