Infectious, Immunology and Derm Flashcards
Recommended timing and type of testing for HIV-exposed infants
HIV 1/2 DNA PCR at 2 weeks
Due to only 40% being positive in initial 48h, up to 93% if done at 2 weeks
Timing for repeat HIV testing in exposed infants
1-2 months and 4-6 months
Treatment for HIV-exposed infants a) if mother was on PPX and b) if she received no treatment
a) Zidovudine for 6 weeks (start within 12h of birth)
b) Zidovudine for 6 weeks plus Nevaripine for 3 doses
Lymphocytic choriomeningitis virus (LCMV) 1) vector 2) maternal signs 3) neonatal signs 4) longterm sequelae
1) rodents (feces)
2) aseptic meningitis, flu-like illness
3) ventriculomegaly, chorioretinitis, microcephaly, periventricular calcifications,
4) severe delays, seizures, blindness but NOT deafness
Cytomegalovirus (CMV) 1) vector 2) neonatal signs 3) longterm sequelae
1) humans
2) largely asymptomatic…IUGR, microcephaly, thrombocytopenia, chorioretinitis, hepatosplenomegaly, periventricular calcifications, blueberry muffin rash
3) deafness, blindness
Toxoplasmosis 1) vector 2) neonatal signs
1) feline (feces)
2) largely asymptomatic…TRIAD: hydrocephalus, chorioretinitis, scattered intracranial calcifications
Retina has large scars beside acute inflammation
Congenital rubella findings
1) Blueberry muffin rash (extramedullary hematopoesis)
2) PDA or supravalvular pulmonary stenosis
3) Glaucoma, cataracts, and microophthalmia
An increase in transplacental passage of IgG is seen around week ___, but the bulk of IgG is transferred after ___ weeks.
22 and 36 (Relates to both “good” and “bad” antibodies , i.e. immunity purposes and if there’s alloimmunization)
Management of an asymptomatic infant born to a mother with active genital lesion but prenatal h/o HSV
Surface cultures and blood PCR for HSV at 24 hours of age; no treatment (if asymptomatic)
Management of an asymptomatic infant born to a mother with a concerning genital lesion without a prior h/o HSV
Surface cultures, blood and CSF PCR for HSV, LFTs, and acyclovir ALL at 24 hours
If infant symptomatic, do investigation and start treatment earlier
Under what instance might you do HSV surface cultures before 24 hours of age?
If rupture of membranes (ROM) was >6h
Classic test for severe combined immunodeficiency (SCID)
Flow cytometry for lymphocyte subtypes (Demonstrates low T-cell count, can have low B- and NK-cell as well but those can also be normal)
NBS SCID test is “TREC” (T cell receptor excision circles)
Gene mutation most commonly associated with SCID
Interleukin-2 (IL-2)
This form: T-cell/NK-cell deficient, normal number B-cells but dysfunctional 2-2 of T-cell stimulation
Test for chronic granulomatous disease
Dihydrorhodamine oxidation assay, AKA neutrophil oxidative burst
Histology finding for erythema toxicum
Eosinophils
Histology findings on transient neonatal pustular melanosis
Neutrophils (on Wright stain)
Cause of acrodermatitis enteropathica
Zinc deficiency (congenital or acquired) Looks erosive and or crusted mainly on mouth, extremities and diaper when FORMULA FED
What can look like congenital varicella but not dermatomal in distribution
Epidermolysis bullosae (especially junctional)
Classic two mucocutaneous findings in Rubella
Blueberry muffin rash (extramedullary hematopoeisis) and petechiae on hard palate
What’s a fairly distinguishing finding between Rubella and Toxo (since both have blueberry muffin rash)
Chorioretinitis MUCH more prevalent in Toxo, (Rubella’s “buzzword” supravalvular pulmonic stenosis)
Retinitis classically is small focus of acute inflammation beside a huge scar
(AAO.org)
Classic appearance of chorioretinitis from congenital syphillis
“Salt and pepper” (since vasculopathy of the smallest vessels)
(https://webvision.med.utah.edu/)
Characteristics of the most common hemangioma in neonates
Infantile hemangioma:
Benign tumor
Enlarges in first year (flat or raised, red or purple), then involutes
Think of PHACES if on head
What is Kasabach-Merritt
DIC-like process from consumption of factors and platelets in large vascular malformation
Syndromes associated with cafe au lait macules
Tuberous Sclerosis
Neurofibromatosis
McCune-Albright
Think of these if >5
Where do congenital nevi come from and what risk do they confer
Neural crest cells that produce melanin
If large, have risk of melanoma
What is the PC name for hairy epidermal nevi and what risk do large ones confer
Smooth muscle hamartoma, no risk!
Triad for McCune Albright
Cafe au lait spots (coast of Maine)
Polyostotic fibrous dysplasia (fibrous, weak bones)
Precocious puberty
Findings in Peutz-Jegher syndrome
Pigmented macules/“freckles” all around lips GI polyps
Chediak Higashi findings (think of three)
Albinism Granular cell dysfunction—platelet and granulocytes (PMNs etc) Peripheral neuropathy/seizures DIE FROM LYMPHOPROLIFERATIVE DZ See giant granules in cells on a smear
Clinical tetrad for Chediak Higashi and histologic finding
- Albinism (hypopigmentation)
- Infections (dysfunction granulocytes)
- Bleeding (dysfunctional platelets)
- Neurologic degeneration/seizures
HUGE granules in those cells
Dermatologic findings in incontinentia pigmenti
Vesicular, then verrucous, then hyper- or hypopigmented
All follow lines of Blaschko (Christmas tree on back!)
(Have seizures/delay, blindness)
Most common cause of colloidon membrane
Congenital Icthyosiform Erythroderma (CIE)
Colloidon: Thick, parchment-like skin
Mutation: ALOXE3 or ALOX12B
CIE causes ALOXI skin problems
Most severe form of ichthyosis
Harlequin, most die in first few days from sepsis/uncontrollable fluid loss
Mutation: ABCA12
Most benign ichthyosis
Ichthyosis vulgaris
Association: Atopic dermatitis
Most severe form of epidermolysis bullosae and its classic assocation
Junctional and pyloric atresia
This form can affect the mucosa as well (ie. GI)
Two distinguishing features of dystrophic epidermolysis bullosa
- Dystrophic nails
- Blisters heal with scarring and hundreds of milia
What inborn error of metabolism (IEM) should you think of in E. Coli sepsis
Galactosemia
Also have liver failure/hyperbilirubinemia and Fanconi syndrome (PCT HCO3 and nutrient/electrolyte wasting)
Classic findings in Leukocyte Adhesion Deficiency (LAD)
- Delayed (>1 month) separation of the umbilical cord
- Recurrent infections with lack of pus (if infectious sites biopsied/examined, see complete lack of PMNs)
- Usually caused by a beta-integrin mutation
Diagnosis in an infant with: failure to thrive, chronic diarrhea (and/or cough), and eosinophilia
Severe Combined Immunodeficiency (SCID)
IL2RG mutation (most common), common part of all interleukins and those are needed for T-, B- and NK-cell development
What is one of the only “absolute” indications for a cephalosporin in neonates
Gonococcal exposure
(You treat with ceftriaxone x1 IV even if infant asymptomatic)
What are the requirements for an infant to be considered minimal-risk for syphillis transmission
Remember for an antibody titer, it’s a 1:y (if y is higher, the problem is worse)
Maternal penicillin treatment finishing >4 weeks before delivery
AND resulting in a titer decrease of four-fold or greater
One of the only absolute contraindications to breastfeeding
Active tuberculosis (ie. with an abnormal XR)
(Infant must be isolated from mother until both are on treatment)
Diagnosis in an infant with a history of generalized erythema that now has skin blistering and peeling, and sterile bullous fluid
Staphylococcal scalded skin syndrome (SSSS)
S. aureus exotoxin
See “Nikolsky sign” (skin separates with minimal friction)
(emedicine.medscape)
Congenital infection with: large placenta, hepatosplenomegaly, osteochondritis i.e. Wimberger sign
Congenital syphillis
Almost always transplacental, maternal infection at later GA confers GREATER risk of fetal infection
What titer-fold change indicates a POSITIVE non-treponemal test in infant?
Four-fold INCREASE [compared to maternal] is worse
Remember, it’s how many times did you have to dilute serum to get rid of reaction! Non-treponemals are VDRL and RPR
The two bacterial pathogens most likely to transmit transplacentally
Listeria and syphillis
- Which are two bacterial that have birth findings!*
- Listeria: chocolate/”meconium”-stained fluid*
- Syphillis: huge placenta (and IUGR, hydrops)*
Which conjunctivitis presents at 2-5 days (first week)
Neisseria gonorrhea
- Remember the GOO (erythro PPX) helps prevent the GOnorrhea*
- This is the one that’s the most emergent to treat [with 3rd generation cephalosporin]*
The most common infectious conjunctivitis
Chlamydial
- Tends to present after first week which watery drainage that turns purulent*
- Treat with oral erythromycin!*
The most common pathogen for both osteomyelitis and septic arthritis
S. aureus
Both also most commonly acquired via hematogenous spread
