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ID Flashcards

1
Q

EOS, LOS, VLOS

A

eos: 0-7d (sometimes 3), Ecoli, GBS, +/- listeria, entorococcus, haemopholus. Greatest mortalitity, filminant and multisystem. Greater risk of pna. los: 7-90d, Ecoli, GBS, Listeria, enterococcus, CONS, staph, pseudomonas. More focal infections. Greater risk of meningitis. vlos: 90d - discharge, GBS, candida, cons

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2
Q

gbs prophylaxis

A

screening vaginal-rectal at 35-37 weeks. adequately treated = >4hrs prior to delivery

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3
Q

normal CSF values

A

wbc <10; protein: 60-80 T, 150 PT; glucose 50T, 65 PTIt:

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4
Q

predictors of sepsis

A

I:T >0.2, WBC <5, CRP or procalcitonin >10

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5
Q

duration of abx therapy

A

bacterial sepsis: 10 days meningitis: 14-28d

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6
Q

emperic abx treatment

A

eos: amp/gent, eos meningitis: amp/ 3rd or 4th gen cephalosoporin los: vanc/gent… naf/gent los meninigitis: vanc/3-4 gen ceph

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7
Q

antifungals

A

amphotericin B deoxycholate - emperic for fungal infection 21d fluconazole - good cns and uti penetrance, not as potent micafungin - not good for cns or uti

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8
Q

antiviral treatment

A

acyclovir 14-21d, nothing for enterovirus

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9
Q

meningitis

A

mc cause: GEL consider brain abscess with citrobacter, cronobacter sakazakii (certain gram negatives) tx: amp + 3/4th ceph or carpanem (avoid 3rd gen cephalosporin that binds to protein b/c may displace bilirubin or interact with IV Ca2+) gbs/listeria: 14-21d of amp ecoli/gram-: 21-28d of ceph/meropenem f/u hearing and dvlpt, higher chance of sequelae after gbs meningitis

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10
Q

congenital syphillis

A

dx: serologic tests b/c difficult to identify, cannot culture spirochetes. Earlier transmission, worse it is. rash: looks like postdate peeling skin, moist lesions in mucous membranes or hands/feet; bone changes, hpmgly; jaundice; lymphadenopathy/ pseudoparalysis of Parrot (mimic erbs palsy), rhinitis/snuffles dx: (can start with EIA enzyme immuno assay) –> start with nontreponemeal (RPR or VDRL) –> if (+) confirm with T pallidum Ab (TPPA) or FTA Ab (will be positive for life once infected). all babies need at least RPR. tx: pcn

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11
Q

listeria

A

gram (+) rod, food borne acquired vertically intracellular, may be mistaken as diptheriod deli style meat, unpasteurized milk, soft cheese, poultry can have granulomatosis infantisepticum (small papular rash) tx: amp, 14d for bacteremia, 21d for meningitis

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12
Q

HSV

A

rash: grouped/single dewdrop on erythematous base vesicle on skin/eye/mouth Most infections are through genital tract. Primary maternal infection is most likely to cause HSV transmission to fetus. Consider outbreak if previously had HSV1 or 2 and now has the other. Consider recurrence if repeat of prior infection with Ab. Treat with suppressive therapy once diagnosed and then again after 36 weeks to prevent recurrent lesions. Csection if lesions or prodromal symptoms (burning/itching) present during labor. Breastfeeding not contraindicated unless lesions on breast.

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13
Q

treatment for impetigo/boils/abscesses

A

likely Group A strep pyogenes or s. aureus treat with 1st ceph or augmentin if extensive consider mrsa, treat with vanc or clinda

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14
Q

treatment for S aureus scalded skin syndrome

A

cefazolin, if mrsa: clinda/vanc

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15
Q

treatment for listeria

A

amp, add gent

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16
Q

UTI

A

uncommon in first week of life as primary source (not bacteremia. If fungal, fluc is best for penetration. Look for fungal balls. Frequently gram neg reds, enterococcus, cons.

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17
Q

Describe the various etiologies of conjunctivitis

A

d1-3: chemical, presents iwith erythema b/l and resolves in 48h d3-7: gonnorhea: severe, purulent –> x1 ceftriaxone, if disemminate x7d cefotaxime. Can progress to involve cornea - emergent. Very serious, so evaluate for this when evaluating for chlamydia. PPx erythromycin is to prevent this. d5-14: chlamydia: minimal watery discharge: tx with oral azithro or erythromycin x14d. HSV: 6-14d with SEM disease (40% present with SEM), mucocutaneous conjunctivitis can be only presentation. 90% will present with clusters of vesicles. Tx with systemic and topical acyclovir For all conjunctivitis diagnose with gram stain, culture, and Giemsa stain and NAAT for chlamydia

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18
Q

omphalitis

A

staph aureus, strep pyogenes, gbs, ecoli, gram - stage 1: funisitis, stage 2: cellulitis at insertion, stage 3: abd wall cellulitis st4: nec fasciitis consider syphillis for isolated funisitis tx: cefazolin (1st gen ceph)/clinda if mrsa/ + gent

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19
Q

oseteoarticular infection

A

osteomyeitis vs septic arthritis s.aureus/gbs: cefazolin or naf, consider 3rd gen cephalosporin

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20
Q

gbs

A

gram (+) cocci, pairs/chains tx: amp/penG +/- gent for synergy. or + cefotax for LOS (better for meningitis?) GBS meningitis: high dose amp/penG + 3d with gent x14-21d GBS bacteremia/cellulitis: 10d amp or penG septic arthritis/osteo: 3-4w

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21
Q

s aureus

A

gram (+) cocci, clusters, coag (+) skin infections, + staph scalded skin syndrome is toxin mediated (red painful peeling skin (nikolsky sign)) tx: naf/cefazolin, if mrsa –> clinda/vanc

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22
Q

CONS

A

like staph epi have bio film, lots from catheters most resistent to antistaph pcns –> use vanc.

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23
Q

gram negs, ecoli

A

ecoli more cause of meningitis. tx: amp + gent initially. replace gent with 3rd gen cephalosporin for better cns penetration if suspecting meningitis. Non fermenting gram neg (pseudomonas, acinetobacter) –> antipseudomonal pcn (zosyn) or carbepnem

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24
Q

How is congenital TB acquired? How is perinatal TB acquired?

A

Congenital TB can be acquired from aspiration of infected amniotic fluid or from infected placenta via hematogenous spread. Perinatal TB is acquired through airdroplets.

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25
Q

chlamydia trachomatis

A

conjunctivitis, pneumonia. Tx: azithro x3d/erythrom x14d transmission in 50% of infected mothers topical erythro is geared at preventing gonnorheal conjunctivitis, only partially ppx for chlamydia

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26
Q

candida

A

can be on skin, eyes, renal, cns fungemia: 14d meningitis 21d

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27
Q

rubella: what are the manifestations

A

rna virus congenital rubella syndrome: embryopathy if mother infected <17w. sga, congenital cataracts*, pigmented retina, petechia w/ blueberry muffin rash*; bone defects with longitudinal bands of demineralization (celery stalking); CV malformations* (pda, peripheral PA stenosis); SNHL*, fetal hydrops

28
Q

CMV: what are the common manifestations? diagnosis and treatment?

A

microcephaly, periventricular calcifications, choreoretinitis, petechia, thrombocytopenia, jaundice, #1 cause of SNHL. iugr dx: pcr or culture in first month of life. tx: oral valgancyclovir x 6m - follow anc

29
Q

HSV

A

disseminated: 25% mc affecting liver and lungs tx: 21d CNS: 30% +/- skin tx: 21d SEM: 45% tx: 14d onset 1-2 weeks for SEM/disseminated, 2-3rd for CNS skin vesicles, keratoconjunctivitis, acute CNS findings like szs, hepatits, pneumonitis, sepsis like picture need optho and cns evaluation, need test of cure for LP oral acyclovir suppressive therapy for 6m after treatment

30
Q

parvo b19

A

hydrops, ascites, hpmgly, ventriculomegaly, hypertrophic cardiomyopathy, anemia low chance of seroconversion but high chance of mortality (5%) if infected before 20 w.

31
Q

What is the difference between congenital and neonatal varicella? How do you treat an exposed neonate?

A

congenital varicella very rare - from maternal vzv in first 20 weeks -> embryopathy (GI/urinary tract abnormalities 10%), LIMB HYPOPLASIA 50%, rash. Neonatal varicella if mom has vzv near delivery (5days prior to delivery to 2d after) –> presents after 5-10 d, fever, rash, severe disease. –> iv acyclovir. If mild (outside this time window, oral acyclovir is okay) dermatoral scarring If exposure to VZV, treat with ivig or VariZIG if <28w, ELBW, >28w but no maternal hx of immunity, mother had checkenpox within pre5-post2 day window - give w/i 10d of exposure VZV vaccine not appropriate for children <1 y/o

32
Q

lymphcytic choriomeningitis virus

A

hydrocephalus, chorioretinitis, intracranial calcifications, negative CMV and toxo

33
Q

hiv

A

can be transmitted during pregnancy, peripartum or breastfeeding –> c/i. Mother should be treated, baby receive ppx x6w zidovudine and avoid bf. Dx: serial pcr at +/- birth, 2 wk, 1m, 4-6m. Ab not helpful, will be maternal. text naat at 2-3w, 4-6w and 4-6m. Test additionally at birth and 8-10w if high risk pt.

34
Q

hep B

A

high rate of transmission B. increases risk of hepatocelluluarm carcinomal and cirrhosis. Dx: HGB surface antigen. pos: everyone gets hbig and hep b within 12h of life. don’t count birth series if <2k. unknown: <2k get both within 12h, >2k get hep B, consider hbig at 7d

35
Q

hep C

A

low transmission. higher if coinfected with HIV. Dx: PCR at 3-4m or Ab at 18m

36
Q

toxo

A

certical transmission ~25%, if primary infection during pregnancy. congenital toxo is severe, visual/hearing impairment, intracranial calcification*, MR, chorioretinitis*, hydrocephalus* tx: pyrimethamine + sulfadizene for 1 yr. leucovorin (foliniic acid) to decrease hematologic adverse effects spiramycin may prevent transmission, does not cross the placenta though - give if dx before 18w. If baby is (+) on amnio, switch to pyrimethamine

37
Q

neonatal alloimmune neutropenia

A

like NAIT but against paternal neutrophils. sx: delayed umbilical cord separation, mild infections. usually resolves by 7 wks. Can give IVIG. Dx: granulocyte agglutination test

38
Q

immune system review

A

innate: NK cells (go after cells without MHC1) - absent in xlinked recessive SCID adaptive: Tcells (cd4 helper, activate b cells and cd8/ CD8 cytotoxic) and B cells (make ab via plasma cells after activation with Ag and CD4) APC: digest Ag and present to T cells (I involved in innate, 2 involved in b cells) neonate: decrease efficacy of cd4 helper, less cytokine release, less complement, less PMN recruitment

39
Q

lactoferrin

A

iron dependent, helps with phagocytosis. Helps kill entrapped bacteria and fungi. secreted into phagosomes, produce lethal peroxidase, lyse microorganism

40
Q

collectin

A

include Surfactant Protein A and D. Recognize and bind to certain patterns of carbs on virus, bacteria and fungi –> facilitates phagocytosis and can activate complement

41
Q

defensins

A

help kill entraped microorganisms are create lethal holes in envelopes and cell membranes

42
Q

fibronetctin

A

facilitate adhesion between cells, component of ECM. Help immobilize microorganisms. Low in newborns.

43
Q

selectin

A

slow down neutrophils, involved in chemotaxis

44
Q

acyclovir

A

Acyclovir is a synthetic acyclic purine nucleoside analog that selectively inhibits viral DNA replication of herpes simplex virus. requires phosphorylation by a viral enzyme (thymidine kinase) to acyclovir monophosphate.. After repeated phorphorylation, acts as substrate for viral dna polymerase –> suicide inactivation. Most active against HSV1 > HSV2 > VZV > CMV. Causes neutropenia, nephrotoxicity. Renal excretion.

45
Q

How do you diagnose HSV in a neonate, and when is it indicated?

A

Increased risk to neonate if genital lesions w/ >4h ROM and primary maternal infection. If maternal hx (+), 12-24h after birth baby should have surface cultures mouth, nares, rectum, conjunctivae. If (+), consider not a contaminant. If suspected to have HSV, isolate from other infants.

46
Q

How do you manage a neonate with suspected TB?

A

If suspected TB –> Treat with INH and chemo If mother is (+) but baby is negative –> 9 months of INH and keep away from treated mother until started on INH

47
Q

what is parrot pseudoparalsysis

A

a refusal to move a painful swollen extremity affected by metaphyseal osteochondritis, due to congenital syphillis. Wimberger sign refers to demineralization of of proximal tibial metaphysis.

48
Q

when does congenital syphillis present? what are early symptoms?

A

2/3 asymptomatic at birth. early symptoms present by 3w-3m: 1st sx usually snuffles (blood tinged), rash (peeling, vesicles, on palms/soles), osteochondritis –> pseudoparalysis (Wimberger sign refers to demineralization of of proximal tibial metaphysis.), fissures. Non specific: hepatomegaly, jaundice, lymphadenopathy.

49
Q

what are late manifestations of syphillis?

A

2-20y: cns, bones, teeth: neurosyphillis, saber shins (bowing of tibia), keratitis, hutchinson teeth, 8th nerve deafness, perf of hard palate, saddle nose, clutton joints (synovial painless effusions) hutchinson triad: deafness, interstitial keratits, notched incisors

50
Q

how is VAP defined? what measures are recommended to decrease VAP rates?

A

ventilator associated pneumonia, changes in CXR findings.

To decrease rates: recommend clearing condensate from vent tubing, some sort of oral hygiene regimen, and not changing humidified circuits until visibily needed

51
Q

when do you get congenital vzv vs neonatal vzv

A

congenital is extremely rare - when mother is infected early in pregnancy. presents with eye, cns, and limb findings.

Neonatal VZV most common when mother is infected <5d prior or <2d after delivery. Treat baby with acyclovir.

Equally transmitted ante/intra/post partum.

52
Q

which HSV manifestation is most common?

A

SEM 45%, CNS 30%, disseminated 20%. SEM presents around 10-14d, CNS presents around 15-21d. Treat SEM with 14d acyclovir, CNS with 21d.

53
Q

what is the difference between HSV1 vs 2 infection

A

HSV1 25% of neonatal infections, HSV 2 75%. HSV1 has less severe CNS disease.

54
Q

what type of maternal hsv disease is most likely to be transmitted and when

A

maternal primary infection in third trimester is most likely to transmit. Most common to transmit during delivery. Mothers frequently asymptomatic.

55
Q

what is acyclovir dosing and therapy for hsv

A

20mg/kg q8 for 14-21d depending on presentation (SEM vs CNS). Continue 6m oral acyclovir for suppression. Repeat LP if had CNS disease after treatment and ct if still (+).

56
Q

what is CMV presentation, diagnosis, and treatment

A

presentation:

thrombocytopenia (blueberry muffin rash, petechia)

CNS: microcephaly, periventricular calfications, chorioretinitis, lower IQ, SNHL

hepatic: hepatomegaly, elevated lfts and d.bili and jaundice
diagnosis: PCR <3w for congenital. otherwise might be acquired. IgG is okay but just tells maternal infection. No IgM.
treatment: 6m valgancyclovir po. monitor for neutropenia. if cannot take po, IV gancyclovir.

57
Q

what is the appropriate gbs ppx regimen?

A

PCN or amp if able (load with 5mu, then 3mu q4 OR load with 2g then 1g q4).

If low risk of anaphylaxis –> cephalosporin. if hx of anaphylaxis –> erythromycin or clinda if susceptibilites known. If not, vanc.

58
Q

what are the most common bugs causing EOS? LOS?

A

EOS: gbs, ecoli, streptococcus

LOS: cons, ecoli, staph, enterococcus, klebsiella

59
Q

how does ecoli work?

A

has a polysaccharide capsule, k1 strain

60
Q

how does listeria present, how is it diagnosed

A

maternal history of flu like illness.

placenta can have abscesses, amniotic fluid can be chocolate colored.

diptheroid, gram (+) rod on stain. CSF elevated protein normal glucose. (+) monocytes (listeria monocytogenes)

61
Q

what is the derm manifestation of listeria?

A

granulomatosis infantiseptica

62
Q

what is follow up for cmv?

A

serial biannual hearing testing until 3 y

63
Q

most common causes of neonatal hepatitis?

A

enterovirus > adenovirus > hsv > cmv

64
Q

how does chlamydia conjunctivitis present

A

5-10d, can have bloody eye discharge. Intracellular inclusions so you have to diagnose with scraping of conjunctiva. Tx with irrigation and ceftriaxone.

65
Q

what do you do for infants exposed to VZV?

A

give VZV ig to susceptible infants:

those who have mothers who are susceptible (non vaccinated), those who are <28w, those who were exposed to <5d to <2d after delivery.

VZV vaccine only after 1y old.

66
Q

how are ureaplasma and mycoplasma transmitted

A

most likely by sexual contact. colonize lower GU tract. no association between uti.

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