ID & Immunology Flashcards
EOS Pathogens
(<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
LOS Pathogens
Mostly G+ organisms:
Coagulase negative staph.
Staph aureus
Enterococcus
GBS
G- enterics:
Klebsiella
E Coli
Enterobacter
Serratia
Pseudomonas
what bacteria are likely to cause meningitis
which one of them can cause brain abscess
Enteric G- (30-40%)
E. coli (dominant)
Klebsieall, Enterobacter
Citrobacter –> Brain abscess
Serratia
GBS (G+ cocci) –> type III
Listeria (G+ rod)
in preterm infant, who is more likely to have UTI, male or female
when UTI occurs
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).
Ophthalmia neonatorum
causative agents
conjunctivitis in the first month of life
N gonorrhoeae, Chlamydia
Other:
S. aureus, non-typable H influenzae, pneumococcus, enteric GN, GBS
compare gonococcal vs. chlamydia conjunctivitis
type of bug
time of infection
rate from mom to baby
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
osteomyelitis/septic arthritis spread and causative agents
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
what GBS cause meningitis
also rate for GBS disease
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
Staph aureus (what kind of bacteria)
anaerobic G+ cocci
more late onset than early onset sepsis
CoNS
coagulase negative Staph. -> staph epidermidis (G+ cocci)
ELBW, VLBW. line infection.
what are examples of Gram negative enterics
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)
serratia is not transmitted transplanetally in most of the case.
T or F
TRUE
Syphilis:
bug, how is it transmitted
symptoms in the following systems:
respiratory, dermatologic, hematologic, renal, orthopedic, neuro, ophtho
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
Wimberger sign
bilateral destruction of proximal medial metaphysis-tibia > humerus
in syphillis
periosteo = errosion.
Cutaneous bullous eruption,
pigmented macules,
desquamating maculopapular rash (palms soles)
syphillis
HSV:
type of virus
ds DNA
RSV:
type of virus
ssRNA (two strains)
in the absence of other symptoms, most likely infection causing severe fulminant hepatitis are
enterovirus > adenovirus > HSV > CMV
Parvovirus (DNA Or RNA)
ss DNA
DNA or RNA for:
HBV
what about HAV, HCV, HEV,
HDV
ds DNA
HAV, HEV, HCV are ssRNA,
HDV is defective RNA, need HBsAg for its surface coat
VZV
ds DNA
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?
congenital VZV
greatest risk window is: maternal rash 5 days and 2 days after delivery.
Tzanck prep
VZV, HSV
multinucleated giant cells
when to give VZIG or IVIG for VZV
premature < 28 weeks.
mom has disease 5d prior up to 2d post birth.
> 28 wk mom with exposure
treatment for VZV
acyclovir
Rubella (type of gene)
ssRNA
Rubella is HUMAN HOST ONLY. Droplet and contact transmission.
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.
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).
Triad of Toxo
chorioretinitis, hydrocephalus, and IC calcification
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
infant with toxo need to be treated with what and for how long
pyrimethamine, sulfadiazine, folinic acid
for 1 year
how is congenital TB acquired?
mostly commonly hematogenous from infected placenta, aspiration of amniotic fluid.
airborn disease
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
Miliary mottling in CXR
TB (congenital TB)
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
Can you use antibotics for botulism
no
aminoglocoside can increase neuromuscular blockage.
toxin in serum or feces
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
micro abscess
Granulomatosis infantiseptica
Listeriosis
intracrnial lesion difference between Toxo vs. CMV
Toxo: corticol calcification. hyrodcephalus, younger cats
CMV: periventricular calcification
Both with mild hepatitis, thrombocytopenia
diarrhea, failure to thrive, scaly eruption,
frequent illness
SCID
eczema, thrombocytopenia, and recurrent infections
gender of patients
Wiskott-Aldrich syndrome
male
x-linked aggamaglobuinemia
Bruton aggamaglobuinemia
no B-cells
Bruton Tyrosin Kinase defeciency
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
Kostmann syndrome
Congenital neutropenia
Respond to GCSF
Mutation in neutrophil elastase gene
