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Paediatrics Study > ID > Flashcards

ID Flashcards

1
Q

Would the HBsAg be + or - just after vaccination?

A

Positive! That’s what we inject in the vaccine

GOOD SCREEN: is positive in acute infection

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2
Q

Is HBeAg + or - if vaccinated?

A

Negative

Tells us how infective the person is!

Releases with replication of the virus ie acute phase of infection - high = more infectious!

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3
Q

Is the HBcAg in the blood regardless of infective state?

A

No! It is inside the Hep B cell

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4
Q

HBsAb demonstrates what?

A

Immune response to HBsAg = infection or vaccination!

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5
Q

HBeAb demonstrates what?

A

Infection!
When the HBeAg - and HBeAb + this means that virus has stopped replicating and patient less infectious due to their good immune response

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6
Q

HBcAb demonstrates what?

A

GOOD SCREEN TEST! ?Previous infection

Demonstrate immune response to infection - help us to distinguish between stage of infection! IgM HBcAb = high in ACUTE infection, low in CHRONIC infection
IgG HBcAb = lingers after infection -> MEMORY

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7
Q

Viral load of Hepatitis B detects what?

A

Viral DNA

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8
Q

Th1 cells primarily produce which cytokines?

A

Interferon gamma
IL-2

– good for intracellular organisms

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9
Q

Th2 cells primarily produce which cytokines?

A

IL-4, 5, 6, 10, 13

– good for helminths + extracellular parasites

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10
Q

T-helper cells have surface expression of which CD?

A

CD4

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11
Q

Are T-helper cells antigen presenting cells? Do they have surface expression of MHC?

A

No + No

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12
Q

T-helper cells recognise antigens presented with which MHC complex?

A

Type 2

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13
Q

CD8 / cytotoxic T cells recognise antigens presented with which MHC complex?

A

Type 1

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14
Q

Is MMR vaccine a live vaccine?

A

Yes, live attenuated

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15
Q

How good is the MMR vaccine?

A

After 2 doses, most people will have Measles + Rubella Immunity (Mumps not quite as good)

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16
Q

How contagious is Measles if not immunised and exposed to someone who has it?

A

If in a room with someone with Measles, 90% of those who are unimmunised will get it

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17
Q

What is the key concern with Measles?

A

Subsclerosing panencephalitis (SSPE)

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18
Q

What is the key concern with Rubella?

A

Mild febrile illness
Key concern is non-immunised pregnant women - risk of miscarriage + fetal malformations (congenital rubella syndrome: 15% will develop autism)

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19
Q

After what gestation is large amounts of maternal IgG transferred across the placenta?

A

From 32 weeks

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20
Q

Where does haematopoiesis occur in fetal life?

A

Yolk sac -> liver -> bone marrow

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21
Q

Which congenital infection is associated with peeling of hands & feet?

A

Syphilis

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22
Q

What do blueberry muffin spots indicate?

A

Intra-dermal erythropoiesis - typical of Rubella, but can occur in any infection
DDx: haematological, malignancy, haemolysis, Langerhands cell histiocytosis

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23
Q

Which congenital infection most likely to affect Heart?

A

Rubella - most commonly PDA + peripheral PA stenosis

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24
Q

Which congenital infection most likely to cause Intracranial Calcification?

A

CMV

  • most common congenital infection, in up to 12% of pregnancies
  • maternal infection asymptomatic in >80%
  • highest risk is maternal primary infection (IgG+IgM+) in first 6 months of pregnancy = maternal primary infection has 30% risk of transmission, 10% babies symptomatic with risk of sequalae 50% (SNHL in 5-7years), 90% asymptomatic with risk of sequalae 10% (if late pregnancy, likely to have acute visceral disease: severe thrombocytopenia, hepatitis, pneumonia, purpura)
  • if maternal re-infection or reactivation (IgM+): 1% risk of transmission
  • most common cause of non-hereditary sensorineural hearing loss
  • incidence: 0.2% of births
  • incubation: 3-12 weeks
  • symptomatic baby: petechiae, jaundice, HSM, SGA/microcephaly, SNHL
  • Low avidity = recent infection
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25
Q

Which congenital infection most likely to cause Hydrocephalus?

A

Toxoplasmosis

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26
Q

Which congenital infection most likely to affect Bones & cause peeling of Hands/Feet?

A

Syphilis

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27
Q

If CMV PCR is positive in urine in the first 3 weeks of life, is this acquired or congenital?

A

Congenital as incubation period is 2-3 weeks

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28
Q

If Hep B vertical transmission occurs, when can horizontal transmission occur?

A

Until age 5

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29
Q

If Hep B sAg+, 20% risk of vertical transmission, if Hep B eAg+, what is the risk of vertical transmission?

A

90%

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30
Q

Giving Hep B vaccine and Ig within 12 hours of birth prevents what proportion of Hep B transmission?
(The other aspect of risk reduction is maternal treatment from 30 weeks)

A

95% (even if mum eAg+)

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31
Q

Can you have a LUSCS + BF with Hep B?

A

Yes

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32
Q

If mum is Hep C RNA +, what is the risk of perinatal transmission?

A

5%

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33
Q

Is maternal Hep C treatment ok during pregnancy?

A

No, contraindicated

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34
Q

How long can Hep C antibodies from mum still be in baby’s system?

A

12 months

Thus check Hep C antibodies in babies at 12-18 months

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35
Q

Are HSV infections generally congenital, intrapartum/perinatal from infected secretions or postnatal?

A

90% intrapartum

  • LUSCS reduces risk
  • fetal scalp electrode increases risk
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36
Q

Maternal primary HSV and viraemia results in placental infarcts + inflamed umbilical cord.
What is the triad of congenital malformations of HSV & neonatal disease manifestations?

A

Skin
Eye
CNS

Skin: vesicles, ulcers, scars
Eye: conjunctivitis, excess watering
CNS: microcephaly, hydranencephaly (absent cerebral hemispheres)

CNS disease has 50% mortality (ie HSV meningoencephalitis; seizures, lethargy, irritable, tremors, poor feeding)

Disseminated disease: sepsis like, BM suppression/DIC; has 80% mortality

Presents in the first 6 weeks of life (on average by 1-2 weeks)

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37
Q

Are most genital HSV infections symptomatic or asymptomatic?

A

Asymptomatic

- if history of genetil HSV, consider anti-virals from 36 weeks

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38
Q

Primary HSV is higher risk to baby. How many cases of primary HSV in pregnancy are asymptomatic?

A

70%
– most symptomatic women have RECURRENT disease: lower risk as they pass antibodies to baby, and can plan for LUSCS to reduce risk

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39
Q

What proportion of children who are HIV+ acquired it vertically (pregnancy/birth/BF exposure)?

A

> 95%

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40
Q

If no preventative strategies, in developed countries risk of transmission in BF and non-BF infants is?

A

BF: 40%

Non-BF: 20%

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41
Q

Anti-retroviral treatment in HIV+ pregnancy women means transmission rate is now…?

A

<2%

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42
Q

Highest risk time for vertical HIV transmissions is..?

What are the 2 key preventative strategies?

A

Intrapartum
Risk factors: ROM >4 hours doubles risk; BW <2.5kg doubles risk, prem / vaginal delivery increase risk

(Majority of in utero transmission occurs later in gestation - vascular integrity of placenta weakens)

LUSCS + intrapartum maternal/neonatal zidovudine reduces transmission by 87%

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43
Q

Does pregnancy increase the risk of inactive TB becoming active?

A

No
Airborne spread post delivery is most common but isolation from mother is not recommended
- Mum is infectious if active pulmonary TB (positive sputum smear) or disseminated disease. Not infectious if on/completed anti-TB treatment

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44
Q

How long can TB positivity be delayed for?

A

Up to 6 months

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45
Q

What is the risk of parvovirus B19 vertical transmission?

A

50%

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46
Q

What is the risk of fetal loss if maternal parvovirus infection when <20 weeks gestation?

What is the risk of hydrops if maternal infection from 9-20 weeks?

IgM + +/- IgM+ = recent infection

A

10% fetal loss

3% hydrops (Ix: doppler of fetal MCA peak systolic velocity to screen for fetal anaemia) –> 30% spontaneous resolution, 30% death without intrauterine transfusion, 30% resolution post intrauterine transfusion, 6% death after intrauterine transfusion

NO long-term neurodevelopmental sequelae of infected children

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47
Q

Rubella primary infection in first trimester is most concerning. Infection at 1-12 weeks has what risk of infection & congenital defects?
& at 13-16 weeks?

From 17 weeks, risk of congenital defects is rare

From 31 weeks risk of fetal infection becomes higher again, and from 36 weeks 100% change of fetal infection

A

80% infected, and 85% risk of congenital defects
– Congenital rubella syndrome

50% infection, 35% congenital defects

If asymptomatic reactivation in mum, risk of fetal infection is <10%

48
Q

Congenital rubella syndrome (<12 weeks gestation) is characterised by:

    • Hearing type?
    • CNS?
    • Heart?
    • Eye?
    • Growth?
    • Endocrine?
A
    • Hearing - sensorineural
    • CNS: microcephaly, dev delay, seizures, panencephalitis
    • Heart: PS, PDA
    • Eye: cataracts, retinophathy - progressive retinal damage, glaucoma, cloudy cornea
    • Growth: IUGR
    • Endocrine: diabetes, hypothyroidism
49
Q

Rubella infection at 12-18 weeks gestation leads to?

A

Sensorineural deafness

50
Q

How long does IgM+ persist after primary rubella infection?

A

2 months

51
Q

Toxoplasma gondii is what type of organism & from what zoonotic source?

A

Protozoan parasite

Oocyst in cat faeces or infected meat

52
Q

Are most women with toxoplasma symptomatic (flu like illness / LAD) or asymptomatic?

A

Asymptomatic

53
Q

When is the highest risk of fetal infection & fetal damage from maternal toxoplasma?

A

Fetal infection highest risk 3rd trimester
Fetal damage highest risk 1st trimester
– TRIAD: EYE+EAR (chorioretinitis, deaf), CNS (dev delay, microcephaly/hydrocephalus, seizures, intracranial calcification), HAEM (thrombocytopenia, blueberry muffin spots, LAD, HSM)

54
Q

What is the treatment for toxoplasma?

A

If maternal infection <18 weeks: Spiramycin

If maternal infection >18 weeks: Pyramethamine, sulfadiazine, folinic acid (goal is to treat fetus)

Neonatal treatment: pyrimethamine, sulfadoxine +/- spiramycin for 1 year

55
Q

What is the most common type of transmission of syphilis? & when?

A

Intrauterine transmission of spirochetes in maternal blood stream
– risk of hydrops, prem labour, IUGR, FDIU

Higher risk as gestation advances

Highest risk with primary infection

56
Q

Is syphilis transmitted in breast milk?

A

No

57
Q

When is the highest risk period for VZV?

A

12-18 weeks gestation, 2% risk

58
Q

What is the timeframe after exposure that we recommend ZIG?

A

within 96 hours (but can be given up to 10 days later)

59
Q

What is the highest risk period of transmission to baby?

A

Maternal varicella -7 to +2 days of delivery because IgG from mum takes 5 days to be produced and transmitted transplacentally & because we are infective for 48 hours before rash

– except in preterm neonates as most IgG crosses the placenta in third trimester

60
Q

What is the mortality of neonatal varicella?

A

up to 30%

61
Q

Zika is a flavivirus transmitted by mosquitos, highest risk with first trimester infection. Unique features are CNS/neuro & EYE:

A

CNS:

  • Severe microcephaly
  • Thin cerebral cortices with subcortical calcification

EYE:

  • Macular scarring
  • Focal pigmentary retinal mottling

NEURO:

  • Hypertonia
  • Congenital contractures
62
Q

Sandfly bite to skin
Skin sore, can last months
Parasite phagocytosed by macrophages where it lives in our body
Can cause cutaneous or visceral disease (fever, loss of weight, hepatosplenomegaly)

A

Leishmaniasis

63
Q 
Raspberries 
Ingest infected food/water
Watery diarrhoea 1 week later
Not transmitted faecal-oral, but from infected food/water
Oocytes seen on stool specimen
A

Cyclospora

Different from crypto due to faecal-oral transmission possible

64
Q

Fresh water contaminated with human stool (infected with parasite)
Ingestion
Initially asymptomatic carriage in GIT - shed in stool and infectious
If invade mucosa, severe dysentry
Risk of haematogenous spread, commonly causing liver abscess. Can also spread to lungs and brain
The parasites ingest red blood cells

A

Entamoeba histolytica

65
Q 
Shed from infected human in faeces or urine
Intermediate host: SNAILS
Into water
Penetrates human skin into blood stream
Some species to GIT
One species to GUT 
Shed in faeces and urine respectively 
Appears elongated with spine on one end, like a TALKING SIGN
A

Schistosomiasis

Haem = bladder

66
Q

Which types of malaria have a dormant stage in liver and can cause illness much later?

A

Vivax

Ovale

67
Q

Female mosquito injects into human during bite
To liver first
Then to blood stream

A

Malaria = Plasmodium (blood parasite)

68
Q

Where is malaria endemic?

A

Tropical + subtropical regions

69
Q

What is the predominant malaria species globally?

A

Plasmodium falciparum

70
Q 
Fever + chills
Headache, myalgia, arthralgia
Vomiting, diarrhoea
Travel to malaria-endemic region
Anaemia, thrombocytopenia
A

Malaria

71
Q

Malaria associated with splenomegaly

A

Falciparum

Vivax

72
Q

Malaria associated with CNS disease and can be rapidly fatal

A

Falciparum

73
Q

Malaria associated with nephrotic syndrome

A

Malariae

74
Q

What is the gold standard lab test to diagnose malaria?

A

Microscopy - thick and thin films stained with Giemsa stain

75
Q

Microscopy -> Gram stain

Crystal violet stains which cell wall?

A

Gram + = purple
Washed out with acetone from gram - cell walls

Counter stain with safranin (red stain): taken up by gram - as they still have a cell wall left to stain = pink

76
Q

Gram + coccus in chains / diplococci

A

Strep

77
Q

Gram + coccus (not staph or strep)

A

Enterococcus

78
Q

Gram + rod/bacillus

A

Corynebacterium / Bacillus

= Lysteria

79
Q

Staph + coccus in clusters

A

Staph aureus

80
Q

Gram - coccus

A

Neisseria

Moraxella

81
Q

Gram - rod/bacillus

A

E.Coli
Salmonella
Klebsiella
Haemophilus

82
Q

Gram + rod/bacillus, anaerobe

A

Clostridium

83
Q

Parasite faecal OCP = microscopy

Common 4 organisms:

A

Giardia - most common intestinal parasite and cause of chronic traveller’s diarrhoea. 7% kids in developed countries, 33% people in developing countries. Commonly from infected water ie camping, cysts tolerant to chlorine disinfectant, has outer shell - can survive several months in cold water. Swallow cysts. Intestines. 7-21 days incubation. Diarrhoea for up to several months, weight loss/ malabsorption. Mx: Metronidazole
Cryptosporidia - modified acid fast stain, faecal/oral - animals hosts, infected food/water. 7 days incubation. Small intestine. Diarrhoea
Entamoeba histolytica - Contaminated food/fresh water contaminated with faeces/fecal-oral. Intestinal lumen (asymptomatic), intestinal mucosa (blood diarrhoea), haem spread (liver abscess MOST common, lungs, brain) cysts. 1 nucleus, ground glass granular cytoplasm, ingests red blood cells.
Schistosoma: snail -> penetrate skin -> liver -> intestine or bladder -> stool or urine. Clinical consequences from body’s reaction to eggs after several weeks: fever, cough, abdo pain/diarrhoea, hepsplenomegaly, eosinophilia. “Talking mark shape”

84
Q

Sensitivities tested by disc diffusion

A

Bacteria across disc
Antibiotic disc
Antibiotic diffuses into media and kills bacteria in immediate zone around disc
Zone size diameter tells us how effective the antibiotic is against this bacteria, larger = more effective
Read against susceptibility cut-offs

85
Q

Sensitivities tested by E-test

A

Bacteria across disc

Antibiotic in graded quantity across test strip - zone of inhibition, read MIC based on where bacteria grows up to

86
Q

Sensitivities tested by Vitek card

A

Inferred susceptibility cut off

87
Q

What is a multi-resistant organism?

A

Bacteria that is resistant to multiple classes of antibiotics, including first line antibiotics

Can transfer antibiotic resistance by plasmids to other bacteria

88
Q

What are beta lactamases?

A

Enzymes produced and excreted by bacteria, that break down beta-lactam ring of penicillin rendering them inactive
Also break down cephalosporins

Commonly gram negative
Present on plasmids

89
Q

What are Carbapenemase producing enterobacteriaceae?

A

Carried in gut

Have genes that code for enzymes that confer resistance to meropenem and many antibiotics (cephalosporins, tazocin)

90
Q

Serology testing (performed by enzyme immunoassay; immunochromatographic) for which infections?

ie sample with virus bound to a surface ie bead and antibody with enzyme conjugate attached to viral antigen, add patient’s serum and see if colour change ie binding of antibodies to attached antigen = presence of antibodies in patient’s serum

ie syphilis: PCR of painless chancre on genital region (initial presentation) but at other stages of infection not very sensitive, thus serology best - several weeks later: fever, rash, headache, sore throat - lasts up to 3 months -> then latent syphilis -> decades later: tertiary syphilis - granulomatous nodular lesions through bone / heart /neuro
Most common in MSM. Treponema pallidum, anaerobic spirochete bacteria - can’t culture, can see with dark field microscopy.

A

Viral
Fastidious bacteria that can’t be grown (syphilis, leptospira, rickettsia)
Parasitic infections (toxoplasma, malaria, entamoeba histolytica)

Post vaccine immunity

  • Rubella IgG
  • Hepatitis B sAb
  • IgM first, suggests acute infection; IgG often persists for life
  • IgG avidity: how well it binds to antigens. If binds strongly, been around for a long time ie infection occurred longer time ago; less strongly, likely new IgG
91
Q

Neonate with: hepatomegaly, jaundice, ‘snuffles’, rash, lymphadenopathy

A

Congenital syphilis

92
Q

What are Treponemal tests for syphilis?

Latex beat with antigen and enzyme attached = TPPA (measures IgG)

Red cell with antigen and enzyme attached = TPHA (haemagglutination assay)
Positive is what red cells spread out

FTA: for CSF testing

A

Look for antibodies to syphilis in serum
TPPA, TPHA, EIA, FTA-ABS

Positive earlier (2-4 weeks)
More specific
Positive for life
Useful to screen low prevalence populations

93
Q

What are Non-treponemal tests for syphilis?

A

Look for antibodies to certain substances (anti-lipoidal antibodies) in blood which are released by cells when they are damaged by syphilis

Rapid plasma reagin (RPR), VDRL

Positive at 4-6 weeks
Less specific
Reduce as disease activity reduces

94
Q

How to diagnose syphilis in Australia?

A

2 confirmatory tests: EIA -> TPPA or TPHA

+ RPR to determine disease activity

95
Q

How to diagnose congenital syphilis?

A

TPPA: IgG
RPR: measure of disease load to see if baby’s higher than mum’s. If higher in baby, concern for congenital syphilis
Syphilis IgM (not passed through placenta and confirms congenital syphilis)
Placental syphilis PCR

96
Q

How to test syphilis cured?

A

Monitor RPR

97
Q

Molecular testing (PCR) used for what type of infections?

A

Viral infections
Pertussis

Qualitative or Quantitative
But doesn’t tell you if organism alive or dead

98
Q

How does molecular testing work?

A

Heat sample to separate DNA strands
Extract nucleic acid from sample
Combine primers (combines with strand of interest), probes, nucleotides with sample
Amplification (often PCR: DNA polymerase)
Interpret amplification curves to work out if organism present or not

99
Q

What does basic reproduction number mean for vaccines?

A

Number of cases that can occur form a single case

Measles: high (12-18) therefore herd protection required is 94%

100
Q

Vaccines aim is to have memory antibodies produced?

A

B cell dependent

101
Q

Vaccines aim is to have memory B cells. How to measure serum immune response?

A

Serology: IgG antibody mean concentration/titre

102
Q

Inactivated vaccines?

- dead parts of virus or bacteria

A

Hep B - protein
Pertussis - protein

Prevenar 13 - pneumococcal conjugate (polysaccharide + protein)
Hib - conjugate (polysaccharide + protein)
MenC - conjugate (polysaccharide + protein)

HPV - virus-like particle

Influenza - killed subunit of virus
IPV - killed polio (IV)

Tetanus - toxoid

103
Q

Inactivated vaccines?

Dead parts of virus or bacteria
+
Adjuvants (to help with stimulating the immune system - enhance antigen presentation & co-stimulation)
– example of adjuvants: Toll-like receptors, trigger T and B cell responses

A

Hep B - protein
Pertussis - protein

CONJUGATE VACCINES:

    • T cell dependent, immunogenic for infants, produce immune memory and high levels IgG and reduces carriage ie in nose, helping with broader herd immunity
  • polysaccharides alone don’t provide long-term protection to infants (get IgM, but nil long-term protection) -> conjugation provides long-term protection (IgM, IgG ++ & polysaccharide specific memory B cells-found several days after booster vaccine) using outer capsule of vaccine linked to carrier protein, providing more direct immune stimulus
  • Prevenar 13 - pneumococcal conjugate (polysaccharide + protein). Now 3 doses: 2, 4, 12 months of age (at age 1, better at producing immune memory)
  • Hib - conjugate (polysaccharide + protein)
  • MenACWY - conjugate (polysaccharide + protein)- 12 months & year 10

HPV - virus-like particle
(now for females + males)

Influenza - killed subunit of virus
IPV - killed polio (IV)

Tetanus - toxoid
(6 weeks, 4 months, 6 months, 18 months, 4 years)

104
Q

Live vaccines?

A

Rotavirus - virus like particles

MMRV - live attenuated- 18 months
Yellow fever - live attentuated

BCG - live mycobacteria: T cell driven response

105
Q

Side effect of live-attenuated vaccines?

A

Delayed
Time frame related to incubation period

Fever, rash + febrile convulsion: day 10 for measles

Varicella: rash 3-30 days

Rotavirus: fever + vomiting 2-3 days post vaccine

106
Q

Rabies recommendations?

A

Dog, monkey, bat bites
Intra-dermal or intra-mmuscular vaccine before travel
Not for gluteal region

Pre exposure prophylaxis: ID x3 doses, OR IM x2 doses

Post exposure prophylaxis: if had pre-exposure vaccines, need 2 more vaccine doses. If nil pre, need rabies vaccine and immunoglobulin

107
Q

Flu vaccine wanes yes or no?

A

Yes

108
Q

Flu vaccine wanes yes or no?

A

Yes

Thus can give too early

109
Q

Dravet’s: SCH1A gene defect, epilepsy. Risk with vaccines?

A

High risk of first seizure with vaccines

110
Q

Severe B cell immunodeficiency, concern with vaccines?

A 
Live vaccines (BCG, YF, MMRV, rotavirus): contraindicated
Inactivated vaccines: ineffective
111
Q

Severe T cell immunodeficiency, concern with vaccines?

A

Live: contraindicated

All vaccines: ineffective

112
Q

When to give vaccines in preterm infants?

A

Give at chronological age
Risk of apnoea/brady with first vaccine
May need additional boosters: Hep B, Pneumococcal, influenza (after 6 months of age)

113
Q

If BW <2kg, how many Hep B vaccine doses needed?

A

4
Birth + 12 months
3 associated with usual vaccines

114
Q

When on chemo which vaccines can be given during therapy?

A

Influenza

Live: wait until >3months post treatment

115
Q

When mum on dmards/mabs during pregnancy, concern about live vaccines crossing placenta - ie not to give BCG

A

Infants may also need additional boosters

116
Q

Pale, floppy, unresponsive episodes can occur post vaccine. Can be immediate (vasovagal) or delayed up to 48 hours post vaccine (?vasovagal). Is the recurrence rate of this with subsequent immunisations high or low?

A

Low recurrence rate

117
Q

Urticaria post HPV vaccine. Was this allergy?

A

Majority not allergy and able to have further vaccines

Paediatrics Study (11 decks)

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