ID Flashcards
Would the HBsAg be + or - just after vaccination?
Positive! That’s what we inject in the vaccine
GOOD SCREEN: is positive in acute infection
Is HBeAg + or - if vaccinated?
Negative
Tells us how infective the person is!
Releases with replication of the virus ie acute phase of infection - high = more infectious!
Is the HBcAg in the blood regardless of infective state?
No! It is inside the Hep B cell
HBsAb demonstrates what?
Immune response to HBsAg = infection or vaccination!
HBeAb demonstrates what?
Infection!
When the HBeAg - and HBeAb + this means that virus has stopped replicating and patient less infectious due to their good immune response
HBcAb demonstrates what?
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
Viral load of Hepatitis B detects what?
Viral DNA
Th1 cells primarily produce which cytokines?
Interferon gamma
IL-2
– good for intracellular organisms
Th2 cells primarily produce which cytokines?
IL-4, 5, 6, 10, 13
– good for helminths + extracellular parasites
T-helper cells have surface expression of which CD?
CD4
Are T-helper cells antigen presenting cells? Do they have surface expression of MHC?
No + No
T-helper cells recognise antigens presented with which MHC complex?
Type 2
CD8 / cytotoxic T cells recognise antigens presented with which MHC complex?
Type 1
Is MMR vaccine a live vaccine?
Yes, live attenuated
How good is the MMR vaccine?
After 2 doses, most people will have Measles + Rubella Immunity (Mumps not quite as good)
How contagious is Measles if not immunised and exposed to someone who has it?
If in a room with someone with Measles, 90% of those who are unimmunised will get it
What is the key concern with Measles?
Subsclerosing panencephalitis (SSPE)
What is the key concern with Rubella?
Mild febrile illness
Key concern is non-immunised pregnant women - risk of miscarriage + fetal malformations (congenital rubella syndrome: 15% will develop autism)
After what gestation is large amounts of maternal IgG transferred across the placenta?
From 32 weeks
Where does haematopoiesis occur in fetal life?
Yolk sac -> liver -> bone marrow
Which congenital infection is associated with peeling of hands & feet?
Syphilis
What do blueberry muffin spots indicate?
Intra-dermal erythropoiesis - typical of Rubella, but can occur in any infection
DDx: haematological, malignancy, haemolysis, Langerhands cell histiocytosis
Which congenital infection most likely to affect Heart?
Rubella - most commonly PDA + peripheral PA stenosis
Which congenital infection most likely to cause Intracranial Calcification?
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
Which congenital infection most likely to cause Hydrocephalus?
Toxoplasmosis
Which congenital infection most likely to affect Bones & cause peeling of Hands/Feet?
Syphilis
If CMV PCR is positive in urine in the first 3 weeks of life, is this acquired or congenital?
Congenital as incubation period is 2-3 weeks
If Hep B vertical transmission occurs, when can horizontal transmission occur?
Until age 5
If Hep B sAg+, 20% risk of vertical transmission, if Hep B eAg+, what is the risk of vertical transmission?
90%
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)
95% (even if mum eAg+)
Can you have a LUSCS + BF with Hep B?
Yes
If mum is Hep C RNA +, what is the risk of perinatal transmission?
5%
Is maternal Hep C treatment ok during pregnancy?
No, contraindicated
How long can Hep C antibodies from mum still be in baby’s system?
12 months
Thus check Hep C antibodies in babies at 12-18 months
Are HSV infections generally congenital, intrapartum/perinatal from infected secretions or postnatal?
90% intrapartum
- LUSCS reduces risk
- fetal scalp electrode increases risk
Maternal primary HSV and viraemia results in placental infarcts + inflamed umbilical cord.
What is the triad of congenital malformations of HSV & neonatal disease manifestations?
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)
Are most genital HSV infections symptomatic or asymptomatic?
Asymptomatic
- if history of genetil HSV, consider anti-virals from 36 weeks
Primary HSV is higher risk to baby. How many cases of primary HSV in pregnancy are asymptomatic?
70%
– most symptomatic women have RECURRENT disease: lower risk as they pass antibodies to baby, and can plan for LUSCS to reduce risk
What proportion of children who are HIV+ acquired it vertically (pregnancy/birth/BF exposure)?
> 95%
If no preventative strategies, in developed countries risk of transmission in BF and non-BF infants is?
BF: 40%
Non-BF: 20%
Anti-retroviral treatment in HIV+ pregnancy women means transmission rate is now…?
<2%
Highest risk time for vertical HIV transmissions is..?
What are the 2 key preventative strategies?
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%
Does pregnancy increase the risk of inactive TB becoming active?
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
How long can TB positivity be delayed for?
Up to 6 months
What is the risk of parvovirus B19 vertical transmission?
50%
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
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
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
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%
Congenital rubella syndrome (<12 weeks gestation) is characterised by:
- Hearing type?
- CNS?
- Heart?
- Eye?
- Growth?
- Endocrine?
- 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
Rubella infection at 12-18 weeks gestation leads to?
Sensorineural deafness
How long does IgM+ persist after primary rubella infection?
2 months
Toxoplasma gondii is what type of organism & from what zoonotic source?
Protozoan parasite
Oocyst in cat faeces or infected meat
Are most women with toxoplasma symptomatic (flu like illness / LAD) or asymptomatic?
Asymptomatic
When is the highest risk of fetal infection & fetal damage from maternal toxoplasma?
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)
What is the treatment for toxoplasma?
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
What is the most common type of transmission of syphilis? & when?
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
Is syphilis transmitted in breast milk?
No
When is the highest risk period for VZV?
12-18 weeks gestation, 2% risk
What is the timeframe after exposure that we recommend ZIG?
within 96 hours (but can be given up to 10 days later)
What is the highest risk period of transmission to baby?
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
What is the mortality of neonatal varicella?
up to 30%
Zika is a flavivirus transmitted by mosquitos, highest risk with first trimester infection. Unique features are CNS/neuro & EYE:
CNS:
- Severe microcephaly
- Thin cerebral cortices with subcortical calcification
EYE:
- Macular scarring
- Focal pigmentary retinal mottling
NEURO:
- Hypertonia
- Congenital contractures
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)
Leishmaniasis
Raspberries Ingest infected food/water Watery diarrhoea 1 week later Not transmitted faecal-oral, but from infected food/water Oocytes seen on stool specimen
Cyclospora
Different from crypto due to faecal-oral transmission possible
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
Entamoeba histolytica
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
Schistosomiasis
Haem = bladder
Which types of malaria have a dormant stage in liver and can cause illness much later?
Vivax
Ovale
Female mosquito injects into human during bite
To liver first
Then to blood stream
Malaria = Plasmodium (blood parasite)
Where is malaria endemic?
Tropical + subtropical regions
What is the predominant malaria species globally?
Plasmodium falciparum
Fever + chills Headache, myalgia, arthralgia Vomiting, diarrhoea Travel to malaria-endemic region Anaemia, thrombocytopenia
Malaria
Malaria associated with splenomegaly
Falciparum
Vivax
Malaria associated with CNS disease and can be rapidly fatal
Falciparum
Malaria associated with nephrotic syndrome
Malariae
What is the gold standard lab test to diagnose malaria?
Microscopy - thick and thin films stained with Giemsa stain
Microscopy -> Gram stain
Crystal violet stains which cell wall?
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
Gram + coccus in chains / diplococci
Strep
Gram + coccus (not staph or strep)
Enterococcus
Gram + rod/bacillus
Corynebacterium / Bacillus
= Lysteria
Staph + coccus in clusters
Staph aureus
Gram - coccus
Neisseria
Moraxella
Gram - rod/bacillus
E.Coli
Salmonella
Klebsiella
Haemophilus
Gram + rod/bacillus, anaerobe
Clostridium
Parasite faecal OCP = microscopy
Common 4 organisms:
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”
Sensitivities tested by disc diffusion
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
Sensitivities tested by E-test
Bacteria across disc
Antibiotic in graded quantity across test strip - zone of inhibition, read MIC based on where bacteria grows up to
Sensitivities tested by Vitek card
Inferred susceptibility cut off
What is a multi-resistant organism?
Bacteria that is resistant to multiple classes of antibiotics, including first line antibiotics
Can transfer antibiotic resistance by plasmids to other bacteria
What are beta lactamases?
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
What are Carbapenemase producing enterobacteriaceae?
Carried in gut
Have genes that code for enzymes that confer resistance to meropenem and many antibiotics (cephalosporins, tazocin)
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.
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
Neonate with: hepatomegaly, jaundice, ‘snuffles’, rash, lymphadenopathy
Congenital syphilis
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
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
What are Non-treponemal tests for syphilis?
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
How to diagnose syphilis in Australia?
2 confirmatory tests: EIA -> TPPA or TPHA
+ RPR to determine disease activity
How to diagnose congenital syphilis?
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
How to test syphilis cured?
Monitor RPR
Molecular testing (PCR) used for what type of infections?
Viral infections
Pertussis
Qualitative or Quantitative
But doesn’t tell you if organism alive or dead
How does molecular testing work?
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
What does basic reproduction number mean for vaccines?
Number of cases that can occur form a single case
Measles: high (12-18) therefore herd protection required is 94%
Vaccines aim is to have memory antibodies produced?
B cell dependent
Vaccines aim is to have memory B cells. How to measure serum immune response?
Serology: IgG antibody mean concentration/titre
Inactivated vaccines?
- dead parts of virus or bacteria
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
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
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)
Live vaccines?
Rotavirus - virus like particles
MMRV - live attenuated- 18 months
Yellow fever - live attentuated
BCG - live mycobacteria: T cell driven response
Side effect of live-attenuated vaccines?
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
Rabies recommendations?
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
Flu vaccine wanes yes or no?
Yes
Flu vaccine wanes yes or no?
Yes
Thus can give too early
Dravet’s: SCH1A gene defect, epilepsy. Risk with vaccines?
High risk of first seizure with vaccines
Severe B cell immunodeficiency, concern with vaccines?
Live vaccines (BCG, YF, MMRV, rotavirus): contraindicated Inactivated vaccines: ineffective
Severe T cell immunodeficiency, concern with vaccines?
Live: contraindicated
All vaccines: ineffective
When to give vaccines in preterm infants?
Give at chronological age
Risk of apnoea/brady with first vaccine
May need additional boosters: Hep B, Pneumococcal, influenza (after 6 months of age)
If BW <2kg, how many Hep B vaccine doses needed?
4
Birth + 12 months
3 associated with usual vaccines
When on chemo which vaccines can be given during therapy?
Influenza
Live: wait until >3months post treatment
When mum on dmards/mabs during pregnancy, concern about live vaccines crossing placenta - ie not to give BCG
Infants may also need additional boosters
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?
Low recurrence rate
Urticaria post HPV vaccine. Was this allergy?
Majority not allergy and able to have further vaccines
