Infectious Disease Flashcards

1
Q

The classic triad of congenital HSV

A
  • cutaneous
    • skin vesicles or scarring (hypopigmented) present at birth
  • neurologic
    • microcephaly
    • abnormal brain computed tomography findings identified within the first week after birth
  • ophthalmologic
    • chorioretinitis identified within the first week after birth
    • microphthalmia

HSV is a double stranded DNA virus just like CMV, EBV, varicella, HHV6

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2
Q

What is most common intrauterine infection

A

CMV

  • Most asymptomatic
  • Symptoms 10%
    • Jaundice, petechiae, hepatosplenomegaly,
    • microcephaly,
    • sensorineural hearing loss
    • Chorioretinitis
  • Gold standard dx: Urine CMV culture
  • Treat if symptomatic with ganciclovir x 6 wks or valacyclovir x 6 mos
    • SE: neutropenia
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3
Q

What are the most common congenital infections

A
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4
Q

What is the source of infection of rubella

A

Humans

  • Transmission: direct or droplet contact from nasopharyngeal secretions.
  • Replicates in the respiratory mucosa and cervical lymph nodes before reaching the target organs via systemic circulation.
  • Infectious period: 8 days before to 8 days after the rash onset.
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5
Q

How can a baby with congenital rubella spread the virus

A
  • continue to spread the virus in nasopharyngeal secretions and urine for a year or more.
  • recovered from lens aspirates in children with congenital cataracts for several years.
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6
Q

Incidence of fetus acquiring congenital rubella based on gestational age

A

85%: during the first 12 weeks of gestation,

50%: during the first 13 to 16 weeks of gestation

25%: latter half of the second trimester

  • has a U-shape distribution
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7
Q

Findings of congenital rubella

A
  • Congenital heart defects: PDA, PPAS, VSD, ASD
  • Auditory: sensorineural hearing impairment (most common)
  • Ophthalmologic: cataracts, pigmentary retinopathy, microphthalmos, chorioretinitis
  • Neurologic: microcephaly, cerebral calcifications, meningoencephalitis, behavioral disorders, mental retardation
  • Hematologic: thrombocytopenia, hemolytic anemia, petechiae/purpura, dermal erythropoiesis causing “blueberry muffin” rash
  • Neonatal manifestation: low birth weight, interstitial pneumonitis, radiolucent bone disease leading to “celery stalking” of long bone metaphyses, hepatosplenomegaly)
  • Delayed onset of insulin-dependent diabetes and thyroid disease.
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8
Q

Fetal Diagnosis of rubella

A

Detection of viral genome in amniotic fluid, fetal blood or chorionic villus biopsies (PCR).

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9
Q

Postnatal diagnosis of congenital rubella syndrome

A
  • RV-IgG antibodies in neonatal serum using ELISA.
    • sensitivity and specificity of nearly 100% in infants less than three months of age.
  • Confirmation: detection of rubella virus in nasopharyngeal swabs, urine and oral fluid using PCR
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10
Q

Strongest predictors of EOS with greatest clinical utility

A
  1. gestational age
  2. Intraamniotic infection (Maternal temp 102.2F, or 100.4-102 with additional clinical factor)
  3. Neonatal clinical illness
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11
Q

Most common pathogenesis of EOS

A

ascending colonization of the uterine compartment with maternal GI/GU organism (ie ureplasma)

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12
Q

Predominant pathogen for EOS in (1) term, (2) preterm

A

(1) GBS
(2) E coli

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13
Q

Factors associated with near zero-risk EOS

A

Elective CS not in labor (no attempts in induction)

ROM at delivery

No signs of fetal distress

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14
Q

True or False- Maternal IAP exposure affects on reliability of blood CS or time to positivity

A

False

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15
Q

True or false- Ampicillin and gentamicin is not enough coverage for EOS

A

False

  • Despite increasing resistance, Amp and gent provide optimal coverage for >90% of EOS
  • Broad spectrum antibx later inc risk for NEC, fungal infxn, dysbiosis
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16
Q

It is sepsis accompanied by BP

A

Septic shock

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17
Q

Major risk factor for LOS (late onset sepsis)

A

Preterm birth

Critical Illness

  • central cath
  • mech vent
  • prolong TPN
  • surgical intervention
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18
Q

Pathogen of LOS

A
  • High income countries: Gm Pos
    • 50% CoNS
  • Mid-low income: Gm neg
  • 3-10% Fungal (candida)
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19
Q

LOS pathogen associated with higher illness severity, higher mortality, short and long term morbidities

A

Gm Neg

  1. E coli
  2. Klebsiella
  3. Pseudomonas
  4. Enterobacter
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20
Q

Role of CRP or procalcitonin in sepsis management

A
  • serial measurements result in a higher sensitivity and negative predictive value
  • assist in discontinue antibiotics
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21
Q

Best practice for blood culture collection and volume requirement

A
  1. Disinfect with chlorhexidine (the longer- >30sec and allow to dry)
  2. Culture from peripheral site
  3. Blood volume: at least 1 ml (63% detection)
  • 0.5 ml 39%
  • 3 ml 95%

only 9% Bld Cs would be positive

betadine can be systemically absorbed- hypothyroidism

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22
Q

Preventive measures for LOS

A
  1. hand hygiene
  2. aseptic protocol
  3. antimicrobial stewardship
  4. care protocol: enteral feeds, breastmilk
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23
Q

Sepsis attributable mortality risk based on pathogen

A

higher mortality: fungal and Gm neg

31% fungal

20% Gm Neg: Pseudomonas

15% Gm Pos

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24
Q

Major sequela of LOS

A

Neurodevelopmental impairment

  • from direct bacterial cytotoxicity, adverse systemic inflammation, altered brain perfusion
  • White matter injury (oligodendrocyte injury)
  • Noted as intellectual impairment on culture pos LOS

Postnatal growth failure- persists until NICU d/c

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25
Q

True or false prolonged empiric antibiotics is associated with LOS

A

True

empiric antibiotics >4 days at birth associated with 1.25-2.5 fold higher odd for LOS and mortality

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26
Q

Most common causative org of UTI

A

E coli (80%)

-Klebsiella and enterobacter

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27
Q

Condition associated with E coli sepsis

A

Galactosemia

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28
Q

Predisposing Factors for UTI in infants

A

Neonatal:

  • Male (<3 months)
  • Uncircumcised
  • Prematurity
  • Renal and urinary tract malformation
  • high temperature (>102.2F)

Maternal characteristics

  • History of UTI
  • PROM
  • Exposure to antibiotics
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29
Q

Etiology of UTI associated with VUR

A

Klebsiella

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30
Q

Hyperbilirubinemia and UTI

A

Elevated direct bilirubin- screen for UTI

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31
Q

True or false

Bacteremia with UTI is directly related to age

A

False

  • Its inversely proportional
32
Q

Diagnosis of UTI

A
33
Q

What are the preventive strategies of perinatal HIV (4)

A
  1. Universal opt-out HIV testing for preg women or for postive HIV ART during pregnancy & labor
  2. Planned CS before labor and ROM for HIV viral load >1000 copies/ml
  3. Provision of antiretroviral prophylaxis to HIV exposed infants for 4-6 wks
  4. Complete avoidance of BF
34
Q

Who are high risk for HIV

A
  • incarcerated
  • communities with HIV 1/1000 per yr
  • injected drugs
  • exchange sex for money
  • live with someone with HIV
  • > 1 sex partner during pregnancy

advised 2nd test at 3rd TM

35
Q

Testing of infant when mom’s HIV status unknown at time of labor and delivery

A

Expedited HIV testing on either the mom or infant
(HIV antigen and antibody)

If positive: treat as presumptive HIV and send for supplemental test

  • prophylaxis within 6-12 hours
  • no BF
  • If supplement test negative d/c ART and start BF
36
Q

What supplemental HIV test can be sent

A
  1. HIV-1 and HIV-2 antibody
  2. HIV RNA testing
37
Q

What is the maternal HIV treatment during pregnancy

A

at least 3 ART regardless of viral load or CD4 count

38
Q

What intervention during labor and delivery for HIV mom

A
  • Continue ART during labor
  • If >1000 copies/ml: AZT, planned CS before labor and ROM at 38 wks
  • If 50-999 copies/ml: consider AZT
  • < 50 copies: none

If less than 1000, CS not recommended due to low risk of transmission and inc complication

39
Q

What is (1) HIV prophylaxis and (2) who should receive it?

for neonates

A
  1. AZT for 6 weeks
  2. Term infant to women with HIV received ART and low viral load
40
Q

What is (1) HIV presumptive therapy and (2) who should receive it?

for neonates

A
  1. 6 week 3 drug combo- AZT + lamivudine (3TC), nevirapine/raltegravir
  2. high risk cases: a. suboptimal viral suppression b. only antepartum antiviral , c. no meds (antepartum and intrapartum), d. drug resistant virus

discuss with peds ID or national clinician consultation center

prescribe full course prior to d/c

41
Q

Why is BF contraindicated for HIV mom in the US

A
  1. Risk of passing HIV with potential for drug resistant virus
  2. Risk for drug toxicity (unpredictable concerntration in BM)
  3. Alternative feeds readily available
42
Q

HIV diagnostic test is used for neonates

A
  1. <18 mos: HIV DNA/RNA PCR (NAAT)
  2. > 18 mos: HIV Ab present

  • Cord blood should not be used: high false positive rate
  • NAAT positive:
    within 48 HOL- in utero
    after 1 wk- intrapartum
  • If HIV Ab initial neg, then at 24 mos pos- after infancy via BF, premastication, sex abuse
43
Q

Timing of HIV diagnostic testing

A
  1. Birth: high risk infants
  2. 14 d: exposed to HIV-1
  3. 1-2 mos
  4. 4-6 mos
  5. 12-18 mos: for antibody to HIV-1

negative:
1. 2 neg NAAT at 2wks and 1 mo
2. 1 neg NAAT at 4 mos
3. neg HIV Ab at 6 mos (preferably 18 mos)

44
Q

True or false: For HIV pos infant, CD4 and HIV RNA copy can reliably predict risk for progress

A

False

Only used after the 1st bday for CD4

45
Q

Who needs to received PCP prophylaxis?

A

Neonates with HIV infection diagnosed at 4-6 weeks

Duration of prophylaxis: until 1st bday then need will based on CD4

46
Q

Which vaccine is contraindicated with children with HIV

A

BCG

risk for disseminated disease

47
Q

What test is done to monitor toxicity for HIV drug exposure

A

CBC

done at birth, 4 or more weeks for therapy

  • due to risk for anemia and neutropenia
  • will resolved after d/c meds
48
Q

what screen should be done to determine need for HCV antiviral treatment

A

hepatits C NAAT at 3 yrs

  • because HCV meds start at 3 yrs
  • associated dec liver inflam and Ca
49
Q

Which bacteremia requires removal of central catheter (catheter sterilization)

A
  1. Nonenteric gram-negative bacteria (Alcaligenes, Pseudomonas, Stenotrophomonas)
  2. Methicillin-resistant S aureus
  3. Candida species

due to risk of more complications

50
Q

When to remove central line with CoNS

A
  1. blood cultures remain positive for more than 3 to 5 days after initiation of antimicrobial therapy
  2. patient fails to improve

  • evaluate for metastatic foci of infection
  • No foci, BCx neg, 5 days appropriate
51
Q

Antibiotic of choice for CoNS

A

Vancomycin

90% of health care related CoNS is methicillin resistant

52
Q

Clinically significant CoNS includes:

A
  1. bacteremia 2 or more cultures resulting positive with the same Staphylococcus species from different collection sites
  2. growth within 15 hours of incubation
  3. clinical findings of infection
  4. intravascular catheter in place for 3 days or more.
53
Q

Which malaria parasite is responsible for the majority of adverse outcomes during pregnancy

A

P falciparum

the most common and the deadliest, and is transmitted throughout the tropics,

54
Q

What factors increase risk of acquiring malaria parasites during pregnancy (4)

A
  1. younger patients
  2. first or second pregnancy
  3. malnourished
  4. with human immunodeciency virus
55
Q

What are the consequneces of malarial infection during pregnancy

A
  1. LBW infants
  2. IUGR
  3. preterm birth: greater in women infected before 24 weeks’ gestation

70% of IUGR cases
36% of preterm births

56
Q

An IUGR newborn born to immigrant mother from Africa presents with
fever, hepatosplenomegaly, hemolysis, anemia, thrombocytopenia, and poor feeding

What is the diagnosis?

A

Congenital malaria

defined as “the presence of asexual P falciparum parasites in the cord blood or in the peripheral blood during the first week of life.

57
Q

what bone is most common site of GBS osteo

A

Humerus
- presents at 3-4 wks

58
Q

What test and when will a baby be presumptively exclude HIV infection

A
  1. 2 neg HIV RNA/DNA NAAT done >2 weeks and one at >4 weeks
  2. 1 neg HIV RNA/DNA NAAT done at >8 weeks
  3. 1 neg HIV antibody test at >6 mos
59
Q

What and when HIV test can definitely exclude HIV

A
  1. 2 neg HIV RNA/DNA NAAT at >1 month and >4 month
  2. 2 neg HIV antibody test at > 6 mos
60
Q

How is congenital TB acquired

A
  1. In utero: transplacentally, apiration of infected amniotic fluid
  2. Perinatal: immediate postpartum - inhalation/ingestion of infected droplet or direct contact with infected materal genital tract

MORTALITY: 53% increased due to HIV co infection

61
Q

A 2 week old newborn that presents with sepsis that is not improving with broad spectrum antibiotics. Mom recently migrated from India. What is diagnosis should be suspected?

A

Congenital TB

  • Presents usually 2-3 weeks
  • Common sx: RDS, fever, HSM, lethargy with periods of irritability, abd distension, lymphadenopathy
  • High risk maternal characteristics: foreign born in high prevalence countries (India, SE asia, South africa), illicit drug user, unprotected health care workers in high risk setting, homeless, contact with contagious TB
62
Q

Mom has active TB, baby is asymptomatic. What is the management

A

If the initial evaluation findings of the newborn are negative, - isoniazid for 3 months and then reevaluate with a repeat TB skin test at 3 to 4 months.

  • If the subsequent TB skin test is negative, stop treatment.
  • If the subsequent TB skin test is positive, further evaluation (chest radiography, aspirate testing, laboratory studies)
63
Q

Mom has active TB, baby is PPD positive but negative active TB. What is the management

A
  • isoniazid monotherapy for 9 months
  • if the mother has multi–drug-resistant TB, add rifampin
64
Q

Which TB med is bacteriostatic and bactericial at the same time

A

Isonaizid

Adverse effect: hepatitis and peripheral neuritis
Add Vit B6- competative inhibitor for neuritis

65
Q

Which TB med turn secretions orange

A

Rifampin

66
Q

Which TB med has optic neuritis as side effect

A

Ethambutol

67
Q

In relation to TB, when do you separate Mother-Infant

A
  1. Mom has active disease (symptomatic, postive CXR) for at least 2-3 weeks from start of tx
  2. Mom has latent (pos PPD but neg sx)- no need to separate, can breastfeed

Breastfeed: TB meds low in breastmilk
Isolation for TB: contact and airborne

68
Q

Long bone xray of a neonate showed:
- localized demineralization of the proximal medial tibia (Wimberger sign)
- sawtooth metaphyseal serration (Wegener sign)
- diaphyseal periosteal reaction with new bone formation. Irregular areas of rarefaction and increased density (moth-eaten appearance)

What is the diagnosis

A

Congenital syphillis

69
Q

Newborn presents with:
* limb hypoplasia
* cutaneous scarring
* eye abnormalities (optic nerve atrophy, cataracts, chorioretinitis)
* CNS: microcephaly, hydrocephalus, seizures

What the diagnosis

A

Congenital varicella syndrome

70
Q

What are the encapsulated bacterias

A

Strep pneumonaie
H. influenzae
Neiserria meningitidis
Salmonella

SHINS (encapsule- protected)

71
Q

when does maternal IgG disappear in neonates

A

9 months

placental transfer via endocytosis
IgA: no fetal IgA production

72
Q

what is used to screen for SCIDs

A

T-cell receptor excision circles (TRECs)
confirmatory: Lymphocyte subset evaluation (via flow cytometry)

  • Cure: Bone marrow transplate if done by 3 months or before infection
  • No live vaccines
  • Prophylaxis: acyclovir (herpes), bactrim (Pneumocystis)
73
Q

A newborn presentes with delayed umbilical separation and omphalitis
-Diagnosis:

Delayed UC separation: 21 days

A

Leukocyte adhesion deficiency

inc neutrophils but defective adhesion and migration
- No pus, recurrent bacterial infxn

74
Q

What infection can cross breast milk

A
  • CMV
  • HIV
  • Hepatitis B
  • Rubella
  • HSV

CMV is inactivated by holder pasturization, freezing decreases it

75
Q

Facts on Toxoplasmosis
* Source of infection
* Transmission to fetus
* Presentation
* Treatment

A
  • Source of infection: poorly cooked meat, feces from kitten feces
  • Transmission: greater with increasing GA, severe disease early in pregnancy
  • Presentation: chorioretinitis, cortical brain calcification, hydrocephalus, microcephaly, IUGR
  • Treatment: pyrimethamine + sulfadizine x 1yr

SE: neutropenia, supplement with folinic acid

76
Q

Facts in CMV
* Source of maternal infection:
* Transmission
* Presentation
* Diagnosis
* Treatment

A
  • Source of maternal infection: secretions (pregnant mom working as preschool teacher/daycare)
  • Transmission: close contact (greatest early preg, severe if early), human milk
  • Presentation: asymptomatic, IUGR, HSM, petechiae, chorioretinitis, periventricular calcification, progressive sensorineural hearing loss
  • Diagnosis: urine CMV PCR (within 3 weeks for congenital)
  • Treatment: Valcyclovir x 6 mos

SE: neutropenia, transaminitis

77
Q

In addtion to the routine 2 month vaccine, what other vaccine is recommended for children with asplenia

A

Meningococcal vaccine

  • can be given at 2,4,6, 12 months
  • Meningococcal (groups A, C, Y, and W135) Oligosaccharide Diphtheria CRM197 Conjugate Vaccine (MenACWY CRM)