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My Neo Board Quickfacts > ID/Immuno > Flashcards

ID/Immuno Flashcards

1
Q

Treatment for infant born to woman with active TB

A

isoniazid until 3-4 mo of age until PPD can be placed; continued management dependent on results

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2
Q

2 month vaccines

A

2B DR HIP

2 months:
hep B

DTaP (diphtheria, tenanus, acellular pertussis)
Rota (not in NICU)

Hib
IPV (inactivated polio)
Pneumococcal

*diptheria and tetanus are toxoid vaccines

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3
Q

Duration of treatment for infant born to maternal untreated gonorrheal infection

A

tx: both ophthalmic erythro and IV/IM CTX

if disseminated (bacteremia, arthritis) - CTX or cefotax for 7 days

meningitis - 10-14d

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4
Q

most common bacteria a/w osteo in neonates

A

Staph aureus

less common: GBS, E coli, candida, neisseria gonorrheoae

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5
Q

Most common bones for osteo

A

femur > humerus > tibia > radius > maxilla

(femur and tibia in preterm; humerus in term)?

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6
Q

CMV virus type

A

double stranded herpes DNA virus

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7
Q

precautions for CMV+ infant

A

standard

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8
Q

time of CMV maternal infection w/ greater risk of neonatal disease/greater severity of neonatal illness

A

FIRST half of pregnancy

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9
Q

radiographic evidence of osteomyelitis - what and when

A

7-10 days

bony destruction, focal area of metaphysical necrosis, soft tissue swelling

*CT/MR more sensitive but not always possible due to need for transport/sedation

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10
Q

treatment duration for toxo

A

~1 year

pyrimethamine-sulfadiazine and folinic acid*

(supplement with folate b/c sulfadiazine a/w bone marrow suppression –>neutropenia)

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11
Q

symptoms in neonate of toxo

A

usually asymptomatic at birth

80% may develop learning disabilities and visual problems later

*preterm may develop CNS symptoms and eye problems in first 3 months of life (compared to later in term) but both at equal risk in general

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12
Q

MCC of EOS (< 72hr)
- overall
- in term
- in VLBW

A

overall: GBS and E coli

term: GBS

VLBW: E coli (risk of EOS 10x in VLBW than term)

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13
Q

MC serotype of GBS in Late Onset Sepsis

A

Serotype III

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14
Q

Chediak-HIgashi

A

abnormal neutrophil degranulation
leads to partial oculocutaneous albinism
nystagmus
peripheral neuropathy
recurrent infections

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15
Q

Leukocyte adhesion deficiency

A

d/o of neutrophil function despite increased #
defective adhesion and migration
recurrent bacterial infections
poor wound healing
necrotic lesions

*risk of ompholitis
*delayed umbilical cord (sometimes >21d)

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16
Q

Chronic granulomatous disease

A

abnormal phagocytic microbial ability
increased risk of abscesses
poor wound healing
granuloma formation

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17
Q

Hyper IgE aka Job’s syndrome

A

abnormal neutrophil chemotaxis
skin infections
coarse facial features
broad nasal bridge

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18
Q

Kostmann

A

severe congenital neutropenia
frequent infx in first few months

*elastase gene
responds well to rG-CSF

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19
Q

Iso precautions for:
CMV
Rubella
HSV
Toxo
HIV
TB
Varicella
RSV
Parvo
Listeria

A

Standard:
- CMV
- Toxo
- HIV
- Listeria

Contact only:
- HSV
- RSV

Droplet:
- Rubella (+ contact)
- Parvo

Airborn (+ contact)
- TB
- Varicella*

Congenital varicella does not require contact isolation if no active lesions

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20
Q

Rubella virus type

A

RNA

passed through respiratory secretions

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21
Q

HSV virus type

A

double-stranded DNA

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22
Q

Toxo infx type

A

intracellular parasite

passed by poorly cooked meat, cat feces

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23
Q

HIV virus type

A

RNA retrovirus

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24
Q

Varicella virus type

A

DNA herpes

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25
Q

RSV virus type

A

RNA paramyxovirus

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26
Q

ParvoB19 virus type

A

single-stranded DNA

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27
Q

Listeria bacteria type

A

gram-positive rod

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28
Q

Treatment for listeria

A

ampicillin+aminoglycocide
14 d sepsis
21d meningitis

*consider brain imaging to assess for abscess

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29
Q

maternal infections that increase risk of stillbirth or fetal loss

A

Listeria
Parvo B19
Syphilis - 30-40% of congenital syphilis=stillborn

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30
Q

when do symptoms of congenital syphillis typically develop

A

3-14 weeks PNA

(most asymptomatic at birth)

*30-40% chance of stillbirth

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31
Q

CMV hearing loss characteristics

A

MCC (non genetic) of congenital sensorineural healing loss in children
- progressive (may not be detected until after 1 year of life)
- usually bilateral and moderate to profound
- tx w/ gancyclovir* to infants a/w preservation of hearing

*monitor for nephrotoxicity, neutropenia, rising LFTs

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32
Q

Cardiac disease in congenital Rubella

A

(50% chance of heart defect)

PDA
Pulmonary arterial hypoplasia

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33
Q

Salt and pepper chorioretinitis
sensorineural hearing loss
cataracts
insulin-dependent diabetes
thyroid disease

A

Rubella

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34
Q

treatment for congenital rubella

A

supportive only

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35
Q

chance of infant developing HSV i/s/o maternal lesion of primary vs secondary infx

A

primary - 50%
secondary - 2%

*higher risk in prematurity

36
Q

mortality rate of disseminated HSV

A

50-70%

50% HSV- 2
70% HSV - 1

50% w/ encephalitis will have long term sequelae

37
Q

MC presentation of listeria before and after 7d v

A

<7d - pneumonia/sepsis

after first week - meningitis

38
Q

when does all maternal IgG disappear from infant’s circulation

A

9 months

39
Q

How is IgG transported in placenta

A

endocytosis

40
Q

when do IgM levels reach 75% adult levels

A

1 year

(some fetal IgM production)

41
Q

IgA levels reach ____% of adult levels by 1 year

A

20%

*NO fetal IgA production

42
Q

calcifications in CMV vs toxo

A

cmv - PERIventricular

toxo - cortical

43
Q

stain for chlamydia

A

giemsa stain of conjunctival scrapings

44
Q

treatment for congenital TB

A

4 drug regimen:
isoniazid
rifampin
pyrazinamide
aminoglycocide

length depends on sensitivity of organism

note: symptoms present during 2nd or 3rd week of life

45
Q

treatment for neonate born to mother with active TB

A

isoniazid alone if asymptomatic

46
Q

risk of mother to child HIV transmission via breast milk

A

9-15%

47
Q

presumptive vs definitive exclusion of HIV infection in an infant born to HIV+ mom

A

(both need to have no lab or clinical evidence of HIV)

presumptive:
- 2 negative DNA/RNA tests from separate specimens both at least 2 WEEKS and one at least 4 WEEKS of age
- 1 negative DNA/RNA test at least 8 WEEKS of age
- 1 negative Ab test at least 6 MONTHS of age

definitive:
- 2 negative DNA/RNA tests from separate specimens, one at least 1 MONTH of age and one at least 4 MONTHS of age
- 2 negative Ab tests from separate specimens both at least 6 MONTHS of age

48
Q

treatment with POSSIBLE benefit for
Enteroviral sepsis

A

high dose IVIG
—>(Ab to enterovirus from pooled population)
—-> being investigated, no constant benefit

pleconaril
—> antiviral capsid binding drug inhibits viral attachment to host cell
—> experimental; clinical trials

blood products as needed for liver disfunction/coagulopathy

**NOT acyclovir - only works in DNA viral infections; no role in RNA viruses (like enterovirus)

49
Q

treatment for systemic candida infection

A

amphoterocin B

*penetrates blood brain barrier, renal system, ocular orbit

*NOT liposomal form first line (does not penetrate BBB, kidneys and also has liver toxicities); use if renal toxicity

  • could use fluconazole once sensitivities are known but Candida glabarata and Candida kruzii are resisistant
50
Q

most neonates colonized by CONS by ____ day of life

A

3-4 (days of life)

51
Q

bacteria in omphalitis

A

polymicrobial - usually skin flora

staph aureus, Group A strep
e coli

52
Q

MC complication of omphalitis

A

sepsis

53
Q

B cells in fetus

A

pre-B cells in liver starting at 7 weeks (gone by 30)
bone marrow by 12 weeks

mature in bone marrow

higher absolute # of B cells as adult (but same proportion); peaks 3-4 months of age

54
Q

neutrophils in fetus

A

starts at 10-14 weeks gestation

  • defective phagocytosis until term gestation
  • all neonates (term and preterm) have impaired chemotactic response and adhere poorly
  • granulation response in term similar to adults
55
Q

classic complement pathway

A

requires specific Ab against antigen
–>immune complexes (antigen/antibody reaction)

C1
C4
C2
C3*

classic and alternative pathways coverage at C3

56
Q

alternative pathway

A

antibody-independent

C3 is spontaneously cleaved by bacterial cel wall hydroxyl groups (gram pos and gram neg)

cleaved C3 + factor B cause cascade

57
Q

complement - common terminal pathway:
what makes up the membrane attack complex

A

C5,6,7,8,9

58
Q

Most common complement deficiency

A

C2

increases risk of infx (especially pneumococcal) and collagen vascular disease

59
Q

deficiency of early complement components (C1-4)

A

increases risk of infx (especially pneumococcal) and collagen vascular disease

*C2 most common

60
Q

deficiency of lat components (C5-9)

A

increased risk of neisseria infections

61
Q

Clostridium botulinum shape

A

gram+ rod

62
Q

Neisseria gonorrhoeae shape

A

gram neg intracellular diplococcus in pairs

63
Q

streptococcus shape

A

gram positive diplococcus in chains

64
Q

listeria shape

A

gram+ rod

65
Q

treatment for chlamydia conjunctivits

A

14 d oral erythromycin

*a/w pyloric stenosis

66
Q

why does erythromycin eye ointment not work for chlamydia

A

colonization of nasopharynx can still occur

67
Q

when maternal varicella infection highest risk to fetus

A

early (first 20 weeks) - high risk of congenital varicella syndrome (1-2%)

late (5 days before to 2 days after birth) - GREATEST risk; 17% risk of acute infection, 30% mortality

68
Q

maternal varicella infection during 2nd half of pregnancy up to 21 days prior to delivery

A

LOW risk of congenital varicella
may develop varicella zoster early in life

69
Q

placenta of CMV infx

A

villous damage
thrombosis
villitis
some villi w/ inclusion body cells and hemosiderin

70
Q

placenta of syphilis

A

hydros
marked round cell infiltration (maternal)

71
Q
A
72
Q

capsulated bacteria

A

Hflu
Neisseria meningitides
Salmonella typhi
Strep pneumoniae

73
Q

Functions of the spleen

A

site of IgM production
site of complement production
assists in maturation of Ab
supports proliferation of T-cells
scavenges od RBCs and platelets
(recycles iron from hemoglobin for hematopoesis)
reservoir of extra blood

74
Q

SPECIFIC blood cell finding in asplenia

A

Howell-Jolly bodies
(nuclear remnant usually removed by spleen by macrophages)

75
Q

duration of valganciclovir for +CMV screening

A

6 months

76
Q

greatest risk factor for clabsi

A

GA and BW

77
Q

MCC pathogens for EOS (in order)

A

GBS (40%)
E coli (28%)* - leading cause in preterm (38%)
strep other than GBS (10%)
enterococcus (3%)
Staph aureus (2%)
Listeria (<1 %)

78
Q

MC complication of subclinical (asymptomatic untreated) congenital toxoplasmosis

A

chorioretinitis

(other complications not common if not symptomatic)

79
Q

chlamydia acquired during labor will cause late-onset pneumonia at what age

A

2-4 wks of age

*not defined as congenital

80
Q

MCC of early pneumonia

A

GBS
(e coli end)

HSV MC viral pathogen causing early pneumonia

81
Q

white spots on umbilical cord and amniotic membrane

A

candidal chorioamnionitis

82
Q

dose adjustment of zidovudine in preterm infants

A

reduced dose; increase with age

  • cleared via hepatic glucuronidation, which is not fully developed in preterm infants

(still 6 week course)

83
Q

recurrent purulent bacterial and fungal infx
+
nitro blue tetrazolium (NBT) test negative

A

Chronic granulomatous disease

mutations in phocyte NADPH oxidase

84
Q

neutrophil peak in healthy newborns

A

12-24hrs

declines and reaches steady state by ~72hrs

85
Q

collectins

A

host-defense; c-type lectin domain
related in structure to C1q

mannose-binding letin (MBL)
conglutinin
SP-A - do not activate compliment
SP-D - do not activate compliment

86
Q

FGR
direct and indirect hyperbole
coombs-neg hemolytic anemia
thrombocytopenia
lymphadenopathy
mucocutaneous lesions

A

congenital syphilis

lesions are vesicular or bullies, ultimately rupture to form superficial crusted erosions or ulcerations

rash generalized band classically involves palms and soles

87
Q
A

My Neo Board Quickfacts (11 decks)

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