ID & Immunology Flashcards

(44 cards)

1
Q

EOS Pathogens

A

(<72 hr)
vertical transmission or hematagenous .

Preterm: GN 66%, GP 29%
E coli (G-), GBS (G+), Hemophilus, Klebsiella (G-), Enterococcus (G+), Virdans Strep.

Term: GP 79%, GN 19%
GBS, E Coli, Enterococcus, GAS, Strep Bovis.

listeria as EOS pathogen, also cause meningitis

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2
Q

LOS Pathogens

A

Mostly G+ organisms:
Coagulase negative staph.
Staph aureus
Enterococcus
GBS

G- enterics:
Klebsiella
E Coli
Enterobacter
Serratia
Pseudomonas

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3
Q

what bacteria are likely to cause meningitis
which one of them can cause brain abscess

A

Enteric G- (30-40%)
E. coli (dominant)
Klebsieall, Enterobacter
Citrobacter –> Brain abscess
Serratia

GBS (G+ cocci) –> type III
Listeria (G+ rod)

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4
Q

in preterm infant, who is more likely to have UTI, male or female

when UTI occurs

A

MALE (this reverse around 1 year of age)

Never in first 3 days of life. uncommon first week.

E. coli (80%), others include Klebsiella, enterobacter, proteus, citrobacter, salmonella, serratia.

ascending infection or hematogenous spread (1/3 will have bacteremia).

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5
Q

Ophthalmia neonatorum

causative agents

A

conjunctivitis in the first month of life

N gonorrhoeae, Chlamydia
Other:
S. aureus, non-typable H influenzae, pneumococcus, enteric GN, GBS

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6
Q

compare gonococcal vs. chlamydia conjunctivitis

type of bug
time of infection
rate from mom to baby

A

N gonorrhoeae:
* G - intracellular diplococci
* 30-40% + if maternal cervical infection
* 2-5 days of life
* use Thayer-martin media to grow.

erythromycin prophylaxis reduce gonococcal incidence from 10-0.5%.
if baby born to mom with active gonococcal infection, give erythromycin eye ppx AND 1x ceftriaxone.

Tx: 1x ceftriaxone or cefotaxime.

Chlamydia
* Obligate intracelular bacteria
* 20% of infants infected if mom’s infected
* 5-14 days: eye
* 2-8 weeks: pneumonia (cough/congestion w/o fever)

blood tinged discharge
erythromycin ppx not as effective.
Tx: erythromhycine oral for 2 weeks

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7
Q

osteomyelitis/septic arthritis spread and causative agents

A

x-ray SOFT tissue change in 48 hours.
Bony change 7-10 days after infection on X-ray

MRI change in 24-48 hours

hematogenous spread, metaphyses susceptible due to reduced rate of blood flow

staph aurues common cause

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8
Q

what GBS cause meningitis
also rate for GBS disease

A

Type III cause meningitis

early GBS 2-3/1000 -> 0.3-0.4/ 1000
late GBS stay at 0.3 / 1000
(late GBS 7 days to 3 month)

GBS is Strep agalactiae

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9
Q

Staph aureus (what kind of bacteria)

A

anaerobic G+ cocci

more late onset than early onset sepsis

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10
Q

CoNS

A

coagulase negative Staph. -> staph epidermidis (G+ cocci)
ELBW, VLBW. line infection.

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11
Q

what are examples of Gram negative enterics

A

E. coli (capsular polysaccharide, K1 strains, cause most of the meningitis and most sepsis)

Citrobacter species -> brain abscess

Klebeiella -> often ESBL, need meropenum
Enterobacter
Serratia
Pseudomonas species can cause noma neonatorium (gangernous process involving mucocutaneous jxn)

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12
Q

serratia is not transmitted transplanetally in most of the case.
T or F

A

TRUE

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13
Q

Syphilis:

bug, how is it transmitted

symptoms in the following systems:
respiratory, dermatologic, hematologic, renal, orthopedic, neuro, ophtho

A

Troponema pallidum –> spirochete.

Transmitted transplacentally (acquired thorough blood).
Older GA increase risk of infection.
30-40% infected fetus are stillborn.
present with non-immune hydrope and symmetric FGR (2/3 asymptomatic)

Respiratory
*Pneumonitis, rhinitis-”snuffles” (1 wk – 3 mos of age)

Dermatologic
*Cutaneous bullous eruption, pigmented macules, desquamating maculopapular rash (palms soles)

Hematologic
*Hyperbilirubinemia, hemolytic anemia, thrombocytopenia, leukopenia or leukocytosis

Renal
*Nephrotic syndrome

Orthopedic
*Osteochondritis (Wimberger sign = bilateral destruction of proximal medial metaphysis-tibia > humerus), periostitis, bone stippling

*Neurologic
*Erb palsy, leptomeningitis

Ophtho
*Chorioretinitis, uveitis

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14
Q

Wimberger sign

A

bilateral destruction of proximal medial metaphysis-tibia > humerus
in syphillis

periosteo = errosion.

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15
Q

Cutaneous bullous eruption,
pigmented macules,
desquamating maculopapular rash (palms soles)

A

syphillis

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16
Q

HSV:
type of virus

A

ds DNA

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17
Q

RSV:
type of virus

A

ssRNA (two strains)

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18
Q

in the absence of other symptoms, most likely infection causing severe fulminant hepatitis are

A

enterovirus > adenovirus > HSV > CMV

19
Q

Parvovirus (DNA Or RNA)

20
Q

DNA or RNA for:
HBV
what about HAV, HCV, HEV,
HDV

A

ds DNA
HAV, HEV, HCV are ssRNA,
HDV is defective RNA, need HBsAg for its surface coat

21
Q

VZV

22
Q

Chorioretinitis, microcephaly, IC calcifications, HSM, thrombocytopenia;
scarred skin (cicatricial lesions) and limbs with damaged nerves, muscle, and bone

what virus is this? when is the highest risk window for infant?

A

congenital VZV
greatest risk window is: maternal rash 5 days and 2 days after delivery.

23
Q

Tzanck prep

A

VZV, HSV

multinucleated giant cells

24
Q

when to give VZIG or IVIG for VZV

A

premature < 28 weeks.
mom has disease 5d prior up to 2d post birth.
> 28 wk mom with exposure

25
treatment for VZV
acyclovir
26
Rubella (type of gene)
ssRNA Rubella is HUMAN HOST ONLY. Droplet and contact transmission.
27
Risk of fetal rubella infection time pattern
BIMODAL (high first trimester and last 4 weeks) (congenital anomalies rare if infection occurs after 20 weeks) Kid or Adult Rubella infection has rashes.
28
Congenital Rubella Syndrome: symptoms by system
Ophthalmologic: cataracts, **salt and pepper chorioretinitis**, microphthalmos, and congenital glaucoma Cardiac: **PDA, peripheral pulmonary artery stenosis** Auditory: sensorineural hearing loss Neurologic: microcephaly, learning impairment Growth restriction, interstitial pneumonitis, Radiolucent bone disease **celery stalking** hepatosplenomegaly, thrombocytopenia Dermal erythropoiesis (blueberry muffin lesions).
29
Triad of Toxo
chorioretinitis, hydrocephalus, and IC calcification
30
if mom has primary infection of toxo. What’s the management for her?
treat with spiramycin during pregnancy to reduce risk of transmission to fetus
31
infant with toxo need to be treated with what and for how long
pyrimethamine, sulfadiazine, folinic acid for 1 year
32
how is congenital TB acquired?
mostly commonly hematogenous from infected placenta, aspiration of amniotic fluid. airborn disease
33
congenital TB symptoms
Present 2-3rd week of life: Respiratory distress, fever, HSM, poor feeding, lethargy, irritability, abdominal distention, LA, ear drainage, skin lesions, parenchymal infiltrates with hilar adenopathy, only 50% have a miliary pattern on CXR Meningitis – 20% cases
34
Miliary mottling in CXR
TB (congenital TB)
35
Botulism Triad of disease on set type of bug
1) acute symmetric descending flaccidity, 2) no fever, 3) autonomic dysfunction onset 3 week to 6 month. gram + bacilli
36
Can you use antibotics for botulism
no aminoglocoside can increase neuromuscular blockage. toxin in serum or feces
37
Tetanus and Botulism
Both tetanus and botulism may present with progressive diminished feeding, fussiness / crying and decreased movements Both Clostridium tetani and C. botulinum are spore-forming gram + rods, grow anaerobically Neonatal tetanus usually presents early – most commonly after contamination of the umbilical cord Stiffness, rigidity and spasms are characteristic of tetanus vs. Botulism presents with a symmetric, descending, flaccid paralysis
38
micro abscess Granulomatosis infantiseptica
Listeriosis
39
intracrnial lesion difference between Toxo vs. CMV
Toxo: **corticol** calcification. hyrodcephalus, younger cats CMV: **periventricular** calcification Both with mild hepatitis, thrombocytopenia
40
diarrhea, failure to thrive, scaly eruption, frequent illness
SCID
41
eczema, thrombocytopenia, and recurrent infections gender of patients
Wiskott-Aldrich syndrome male
42
x-linked aggamaglobuinemia
Bruton aggamaglobuinemia no B-cells Bruton Tyrosin Kinase defeciency
43
leukocyte adhesion deficiency vs chronic granulomatous disease
LAD: no pus, delayed cord seperation (LAD-1 more common) chronic granulomatous disesae (no oxidative burst function): a lot of pus
44
Kostmann syndrome
Congenital neutropenia Respond to GCSF Mutation in neutrophil elastase gene