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Paediatrics RACP written exam > Infectious Disease > Flashcards

Infectious Disease Flashcards

1
Q

A child returns from travelling with suspected cerebral malaria, which organism are you likely to find?

A

All species of Plasmodium can cause Malaria but only P. Falciparum causes cerebral malaria.

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2
Q

Causes of cervical lymphadenopathy?

A 
Abscess/lymphadenitis 
Atypical TB
Cat scratch
Mumps
Malignancy e.g. lymphoma
EBV
Toxopasmosis
Brucellosis
Salivary stones
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3
Q

Causes of atypical lymphocytosis?

A 
EBV
CMV
Toxoplasmosis
Mumps
TB 
Malaria
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4
Q

Causes of eosinophilia?

A

Atopy (asthma, eczema, EO)
Parasitic disease (hookworm, amoebiasis, schistosomiasis)
Psoriasis
Hodgkin’s lymphoma + eosinophilic leukaemia
Drug sensitivity

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5
Q

Causes of hydrops fetalis?

A
  • 10-15% “immune” - fetal anaemia due to anti-D/anti-Kell
  • 85-90% “non-immune” - parvovirus, toxo, syphilis, aneuploidy, SVT, congenital heart block, TTT syndrome, muscular dystrophy, alpha thalassaemia major
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6
Q

Prognostic markers in HIV?

A
  • HIV viral load is most important predictor of progressive disease in early stages of HIV infection
  • CD4 count is important prognosticator in late stage disease
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7
Q

India ink stain with halo indicates which organism?

A
  • Cryptococcus neoformans - commonest cause of fungal meningitis in immunocompromised patients.
  • Onset may be insidious.
  • India ink stain is the classic stain for this organism and the halo is due to the stain being unable to penetrate the capsule of the organism.
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8
Q

What type of organism is gonorrhea?

A

Gram negative diplococcus

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9
Q

What are the contraindications for BCG vaccination?

A
  • Immunocompromised
  • HIV or suspected HIV
  • Generalised infected skin condition
  • Positive IGRA or mantoux and <8m age
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10
Q

When are patients with chickenpox contageous?

A

From 24-48 hours before the rash appears and until all the vesicles have crusted over

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11
Q 
Describe the antigen/antibodies in these situations:
A: Acute hepatitis B infection
B: Chronic hepatitis B infection 
C: Hepatitis D superinfection
D: Past hepatitis B vaccination
E: Previous hepatitis B infection
A

A: Acute hepatitis B infection - HBsAg positive, anti-HBc positive, IgM anti-HBc positive

B: Chronic hepatitis B infection - HBsAg positive, anti-HBc positive, IgM anti-HBc negative

C: Hepatitis D superinfection - this should be suspected in a patient with chronic hepatitis B whose condition suddenly worsens

D: Past hepatitis B vaccination - HBsAg negative, anti-HBc negative, anti-HBs positive

E: Previous hepatitis B infection - HBsAg negative, anti-HBc positive, anti-HBS positive

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12
Q

Which antibiotic is most likely to cause oesophageal ulceration if not taken with fluids or food and at least 1 hour prior to going to sleep?

A

Doxycycline

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13
Q

What are the blood film freatures in HUS?

A
  • Schistocytes/helmet cells = fragmented cells
  • Microangiopathic anaemia
  • Thrombocytopenia
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14
Q

What is the mechanism of weakness in infantile botulism?

A
  • Inhibition of neurotransmitter release by neurotoxins produced by the Clostridium botulinum bacterium
  • Symmetric descending paralysis beginning with cranial nerves/bulbar palsy
  • It presents with: constipation, poor feeding, drooling, choking, weak cry, increasing weakness and floppiness and breathing difficulties
  • Medical emergency. Needs ventilation, IVF, antitoxin early
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15
Q

Cut off values for mantoux test?

A

> 5mm or more is considered positive in:
A recent contact with TB, HIV +ve, fibrotic x-ray changes, immunosuppressed

>10mm or more is considered positive in:
Recent immigrants (<5 years) from high prevalence countries, <4y/o, high risk exposure

> 15mm or more is considered positive in:
Any person

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16
Q

Describe the mechanism behind tick paralysis

A
  • Holocyclus = tick causing paralysis in Australia
  • Toxin released by the tick blocks acetylcholine at the neuromuscular junction
  • Results in dilated pupils, lethargy, weakness, ataxia, slurred speech, ascending paralysis, depressed deep tendon and gag reflexes
  • Sensory symptoms absent (differentiates from Guillain Barre which has frequent prodromal sensory symptoms).
  • Can resemble botulism.
  • Treatment: remove tick, although this may create short term worsening in symptoms. Toxin antidote can cause serum sickness in humans
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17
Q

Discuss Lyme disease

A
  • Caused by borrelia burgdorferi, transmitted by ticks
  • Erythema migrans (red, circular rash with central bullseye) at site of bite
  • Malaise, lymphadenopathy, paresthesia, headaches, myalgia, difficulties with memory and concentration
  • 21 day course of doxycycline, majority of patients recover
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18
Q

What are the risk factors for cerebral abscess?

A
  • Congenital heart disease
  • Trauma
  • Surrounding infection (e.g. ocular, ear)
  • Surgery
  • Immunocompromised patients
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19
Q

What is the steeple sign?

A
  • Narrowing of the trachea on x-ray (looks like a church steeple)
  • Seen in croup
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20
Q

What are the risks of neisseria gonorrhoeae conjunctivitis?

A
  • Severe keratitis
  • Endophthalmitis (purulent inflammation of intraocular fluid)
  • Disseminated infection (ophthalmia neonatorum)
  • Gram -ve diplococci
  • Treat with IM ceftriaxone, saline irrigation. Need CSF and blood cultures
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21
Q

Conjunctivitis with intracytoplasmic inclusion bodies?

A

Chlamydial conjunctivitis

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22
Q

What is a common gram negative coccobacillus?

A

Haemophilus influenzae

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23
Q

What is the attack rate, spread, and incubation period of measles?

A

90%
Airborne or person-to-person
Incubation 6-21 days
Infective -5 to +4 from rash

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24
Q

Describe the presentation of parechovirus in young infants

A
  • Severe sepsis-like presentation
  • Diffuse erythematous maculopapular rash
  • May have diarrhoea
  • Shocked, extreme tachycardia and tachypnoea
  • Can develop encephalitis with long term white matter injury
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25
Q

Describe HSV infection in a neonate

A
  • Rash, lethargy, fever
  • Neonatal encephalitis with prolonged focal seizures
  • Characteristic T2 hyperintensity in temporal and basal frontal lobes
  • Surviving infants have lifelong epilepsy and intellectual disability, especially if treatment is delayed
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26
Q

Describe subacute sclerosing panencephalitis (SSPE)

A
  • Late onset after measles infection
  • Progressive neurological disorder with memory loss, dementia, behavioural change, myoclonus, pyramidal and extrapyramidal signs
  • Leads to vegetative state and death in 1-3 years
  • MRI: signal change in PV white matter
  • EEG: Radermecker complex
  • CSF: high titre measles IgM and IgG antibodies
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27
Q

What is the mechanism of resistance in the SPACE group organisms?

A
  • Serratia, pseudomonas, acinetobacter, citrobacter, enterobacter
  • May produced AmpC beta-lactamase, which rapidly hydrolyses penicillins and cephalosporins
  • If low levels of AmpC, can become resistant with prolonged treatment courses (inducible resistance)
  • Therefore, even if reported as susceptible, cephalosporins not recommended as 1st line therapy for serious infections caused by SPACE organisms
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28
Q

What type of vaccine is the HPV-9 vaccine?

A
  • Recombinant subunit vaccine containing virus-like particles
  • Covers 6, 11, 16, 18, 31, 33, 45, 52, 58
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29
Q

What are examples of an inactivated vaccine?

A

Influenza, cholera, plague, polio

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30
Q

What are examples of an attenuated vaccine?

A

Yellow fever, MMR, TB

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31
Q

What are examples of a toxoid vaccine?

A

Tetanus, diphtheria, snake bites

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32
Q

What are examples of a subunit vaccine?

A

Hepatitis B, HPV

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33
Q

What are examples of a conjugate vaccine?

A

Haemophilus influenza

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34
Q

What organisms can be present after animal bites?

A
  • Cat - pasteurella multocida, staph aureus
  • Dog - pasteurella canis, staph aureus, bacteroides, fusobacterium
  • Monkey - herpes B virus (monkeypox, herpes simia)
  • Rabies
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35
Q

A child who has a known diagnosis of HIV develops massive splenomegaly. Splenic aspirate reveals multiple amastigotes.

A
  • Leishmani donoavani
  • Visceral Leishmaniasis can present with massive splenomegaly, hepatomegaly, lymphadenopathy
  • Can test on urine antigen, gold standard is identifying amastigote
  • Small spherical or oval bodies which are transmitted by sandflies. Splenic aspirate is >95% sensitive.
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36
Q

A child from East Africa has been diagnosed with scabies which has been resistant to treatment. A skin snip reveals multiple microfilariae.

A
  • Onchocerca volvulus
  • Filarial worm responsible for river blindness, transmitted by simulium flies who breed in rapidly flowing water
  • Intensely itchy rash which can be misdiagnosed as scabies
  • Presence of microfilariae on skin snip
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37
Q

What are the alternative names for human herpes virus 1-8?

A
  • HSV1 and HSV2
  • HSV 3 = VZV/varicella
  • HSV 4 = EBV
  • HSV 5 = CMV
  • HSV 6 and 7 = roseola
  • HSV 8 = kaposi-associated herpes virus
38
Q

What antibiotics are protein-synthesis inhibitors?

A

Aminoglycosides, tetracyclines, chloramphenicol and macrolides.

  • Tetracyclines and aminoglycsides inhibit binding of tRNA at the ribosome
  • Aminoglycosides also stuff up the reading of mRNA
  • Chloramphenicol inhibits peptidyltransferase activity at the ribosome
  • Erythromycin inhibits translocation
39
Q

Side effect of ribavirin (for Hep C)

A

Haemolytic anaemia

40
Q

Conjugate vs polysaccharide vaccines

A
  • Conjugate (polysaccharide + protein = more potent) more effective in infancy, don’t develop response to polysaccharide vaccines
  • Conjugate gives higher antibody response and more effective protection
  • Polysaccharide (e.g. pneumovax) doesn’t provide herd immunity, no booster response, T-cell independent
41
Q

Discuss meningicoccal disease

A
  • Men B most common cause in industrialised countries
    • Poorly immunogenic therefore vaccine development difficult (as polysaccharide capsule similar to fetal nerve cells)
    • Very reactogenic vaccine - give paracetamol pre dose as high risk fever
  • Men W increasing - covered by quadrivalent vaccine (A, C, W, Y)
  • New 4cMenBV vaccine - also covers MenB
  • Men A - bad in Sub-Saharan Africa
42
Q

Rotavirus vaccine and intussusception

A
  • Aim to start and complete course early (6w + 3m) as risk of intussusception increases from 6-12m age
  • Elevated risk day 1-7, decreased after 2nd dose
43
Q

Main cause of genital warts?

A

HPV 6 and 11

44
Q

Main cause of cervical cancers?

A

HPV 16 and 18

45
Q

Time-dependent killing

A
  • Beta lactams, macrolides, vancomycin
  • Most important factor is the time above MIC i.e. dosing interval
  • Reach maximum kill rate at 2-4x MIC
  • No post antibiotics effect
46
Q

Concentration-dependent killing

A
  • Aminoglycosides, fluoroquinolones (ciprofloxacin)
  • Most important factor is peak concentration
  • Max bactericidal activity achieved when levels much higher (10x) than MIC
  • Significant post-antibiotic effect also concentration dependent, so better with a larger peak
  • Once daily dosing means large doses given less frequently
  • CMax/MIC = aminoglyc, fluoro
  • AUC/MIC = vancomycin, aminogly, azithro
47
Q

Which antibiotics act on cell wall synthesis?

A
  • Beta lactams: penicillin, cephalosporin, carbapenems, monobactams
  • Vancomycin
48
Q

Which antibiotics act on folate synthesis?

A
  • Sulfonamides

- Trimethoprim

49
Q

Which antibiotics act on protein synthesis: 50S subunits?

A
  • Macrolides
  • Clindamycin
  • Chloramphenicol
50
Q

Which antibiotics act on protein synthesis: 3OS subunits?

A
  • Tetracyclines

- Aminoglycosides

51
Q

Which antibiotics act on DNA gyrase?

A
  • Quinolones (ciprofloxacin)
52
Q

Enterococci are intrinsically resistant to?

A
  • Cephalosporins
  • Low affinity for enterococcal penicillin binding proteins
  • Need penicillin, amox, or vancomycin
53
Q

Pseudomonas is intrinsically resistant to?

A
  • Cefotaxime

- Low affinity for pseudomonal penicillin binding proteins

54
Q

Penicillin is good for treating?

A
  • Streptococci
  • Enterococci
  • Neisseria
  • Listeria
  • Syphilis
  • > has poor penetration into CSF, so lower threshold for defining penicillin resistance in meningitis than at other sites
55
Q

Flucloxacillin is good for treating?

A
  • Staph
  • Strep
  • Not enterococcus
56
Q

Augmentin is good for?

A
  • Beta lactamase inhibitor
  • Restores activity against staph aureus
  • Improved activity against gram -ve bacteria
57
Q

Discuss cephalosporins

A
  • Same mechanism as penicillins but with differing affinity for penicillin binding proteins
  • No activity against enterococci
  • Resistant to beta lactamase
  • As you go to newer generations, have better gram negative cover, poorer gram positive cover (until get to 4-5th generation)
58
Q

Discuss carbapenems

A
  • Very broad spectrum - gram positive, gram negative, ESBL, pseudomonas
  • ADRs: neurotoxicity, lowers seizure threshold esp imipenem
59
Q

Are beta lactams bactericidal or bacteriostatic?

A

Bactericidal

60
Q

Mechanisms of beta lactam resistance

A
  • Beta-lactamase production - E.Coli, staph aureus
  • Altered penicillin binding proteins i.e. altered binding site e.g. MRSA
  • Reduced drug entry - reduces susceptibility but not usually resistant
  • Removal of drug (efflux pumps) - pseudomonas
61
Q

Extended spectrum beta lactamases (ESBLs)

A
  • Confer resistance to penicillins, cephalosporins, monobactam
  • Retain susceptibility to carbapenems (eg meropenem)
  • Hydrolyse beta lactam rings, some only do this to penicillin so may still be able to use augmentin/cephalosporin
  • e.g. Klebsiella, E.Coli
  • Important amongst travellers esp SE Asia
  • Can still use nitrofurantoin for lower UTI
62
Q

What is the mechanism of MRSA resistance?

A
  • Altered receptor binding

- Resistant to all penicillins and cephalosporins

63
Q

MRSA treatment options?

A
  • Cotrimoxazole
  • Clindamycin
  • Vancomycin
  • Linezolid
  • Daptomycin
64
Q

Discuss clindamycin

A
  • Protein synthesis inhibitor
  • Limits exotoxin production and improves outcome in toxic shock syndrome with strep, ? same effect in staph toxin
  • If erythromycin resistance than risk of inducible clindamycin resistance, therefore don’t use
  • Good in MRSA, increasing literature for use in pneumonia, empyema, bone/joint (not for infective endocarditis alone)
65
Q

Ecthyma gangrenosum is associated with?

A
  • Pseudomonas

- Bacterial invasion of walls or blood vessels in skin and subcut tissue

66
Q

Early transplant infection (first 30 days) likely to be caused by?

A

Gram -ve bacteraemia, especially hospital acquired - E.Coli, pseudomonas, Klebsiella
(after day 30 get aspergillosis, invasive fungal infections)

67
Q

Stenotrophomonas maltophilia is resistant to?

A

Universal resistance to beta-lactam antibiotics

68
Q

What drugs can you use to treat pseudomonas?

A

Gentamicin, ceftazidime, tazocin, meropenem

69
Q

Treatment of invasive aspergillus?

A

Voriconazole

70
Q

Discuss aspergillus

A
  • Pathogen after first 30 days post HSCT
  • Usually causes pulmonary disease (80%)
  • CT - halo sign, air crescent (once develop neutrophils cavitation will occur). Infarcted lung tissue full of hyphae
  • Diagnosed on BAL
  • Treated with voriconazole, 2nd line caspofungin
  • Is resistant to fluconazole
71
Q

Which antifungal would you use:

1) prolonged fever and neutropenia
2) candidemia or invasive candidiasis
3) invasive aspergillosis

A

1) amphotericin B
2) fluconazole (if sense) or amphotericin B
3) voriconazole

72
Q

Side effects of antifungals

A
  • Amphotericin B - nephrotoxicity, hypokalaemia
  • Azoles - interact with vincristine
  • Caspofungin - does not penetrate CSF
73
Q

Discuss invasive candida infection

A
  • immunocompromised
  • Can involve any site, multiple focal liver or spleen lesions
  • Can be in eyes and skin
  • Unexplained fever or signs of severe sepsis while on antibiotics - suspect candida
  • Can be rapidly fatal
  • Treat with amphotericin B
74
Q

Treatment of CMV?

A
  • Ganciclovir (IV) - 1st line
  • Foscarnet (2nd line) - nephrotoxic
  • Valganciclovir (oral agent, causes neutropenia)
75
Q

Post-transplant lymphoproliferative disorder

A
  • EBV, B lymphocyte proliferation
  • Spectrum of disease from fever/LAN to high grade lymphoma
  • High risk: child, first 2 yrs post transplant, EBV+ve transplant in EBV-ve patient, heavy immune suppression, amount of lymphoid tissue transplanted (lung/liver/heart > renal)
  • Worse if associated CMV
  • Tx: reduce immunosuppression, rituximab (anti CD20), low dose chemotherapy
76
Q

Discuss antiretrovirals for HIV treatment

A
  • Need combination of 3 drugs: 2 x NRTI + 1 x NNRTI or 1 x protease inhibitors
  • Multiple drug interactions
  • ADRs: N+V, diarrhoea, pancreatitis, hepatitis, osteopenia, hyperlipidaemia , SJS
77
Q

Side effects of TB treatment?

A
  • Rifampicin - red/orange tears/secretions, P450 induction
  • Isoniazid - sideroblastic anaemia, peripheral neuritis, hepatitis
  • Pyrazinamide - inc uric acid
  • Ethambutol - eyes, optic neuritis, decr visual acuity
78
Q

Discuss cat scratch disease

A
  • Bartonella henselae
  • Regional lymphadenopathy, commonly axillary, 25% suppurate
  • Can have: PUO, encephalitis, pneumonitis, hepatitis, loss of vision, skin rashes
  • Tx: self-limiting unless immunosuppressed - then use azithromycin, ciprofloxacin, cotrimoxazole
79
Q

Neonate with blueberry muffin rash

A
  • CMV
  • Will also have jaundice and hepatosplenomegaly
  • Chorioretinitis, IUGR, anaemia
80
Q

Most common cause of non hereditary congenital deafness?

A

CMV

81
Q

Encapsulated bacteria

A 
S - strep pneumoniae
K - klebsiella
H - haemophilus influenzae
P - pseudomonas aeruginosa
N - neisseria meningitidis 
C - cryptococcus neoformans
82
Q

Discuss congenital CMV

A
  • Primary maternal CMV infection - 30-50% transmission
  • Only 10% symptomatic at birth: jaundice, blueberry muffin, HSM, microcephaly, retinitis, 50% deaf
  • Another 10% develop SNHL within 5-7yrs
  • Ix: urine CMV culture/PCR, paired maternal and infant serology - if IgM+ve baby then confirmed CMV
  • MRI, opthal
  • Tx: if <28d old, mod symptomatic disease: PO valganciclovir (improves ID and SNHL) for 6/12 total (can cause neutropenia)
  • Universal antenatal screening not currently recommended. No evidence that treating maternal primary infection will decrease risk congenital CMV
83
Q

Discuss toxoplasmosis infection

A
  • Self limiting non specific illness
  • Cats, kitty litter, gardening, raw veges
  • Highest risk transmission in 3rd trimester, but risk of congenital abnormalities highest in 1st trimester
  • Ix: maternal + fetal IgG and IgM, amniotic fluid PCR, neonate PCR CSF
  • Tx: maternal spiramycin 3g/day to reduce fetal transmission (doesn’t treat fetus as doesn’t cross placenta)
    If confirmed fetal infection then pyrimethamine + sulfadiazine + folinic acid AN and PN until 12m old
  • 85% babies normal at birth. Most develop chorioretinitis, hearing loss 30%, GDD 20-75%
84
Q

Tx neonatal HSV

A
  • IV acyclovir 14 days (mild) or 21 days (CNS/disseminated)
  • Then 6m PO aciclovir post above to improve neurodevelopmental follow up
  • 30% mortality with disseminated disease, 6% with CNS infection
  • Oral aciclovir poor bioavailability and poor CNS penetration
85
Q

Treatment neonatal GBS infection

A
  • Amoxycillin and gentamicin (provides synergy) until blood/CSF sterile
  • Or 10 days bacteraemia, 14-21 days meningitis
  • 30% have residual neurodisability
  • Can get recurrent infection ~40 days later
86
Q

Signs of neonatal syphillis infection

A
  • Snuffles, hemorrhagic rhinitis
  • Skin: bullous lesions, mucous patches, desquamating skin
  • Unexplained large placenta
  • Hepatomegaly +/- spleen, jaundice
  • Non immune hydrops
87
Q

Mangement of neonatal syphillis

A
  • Ix: TPPA (trep), RPR (non-trep) tests, paired with maternal serology
  • Long bone x-rays - periosteal reactions
  • LP - CSF VDRL, protein, WCC
  • Spirochetes on placenta
  • Tx: 10days IV benpen, follow up serology 3,6,12m
88
Q

Outcome of neonatal Hep B infection

A
  • 90% become chronically infected
  • 25% develop cirrhosis or HCC in adult life
  • Higher risk transmission if maternal HBeAg positive, and if untreated (up to 90% risk, decr. to 30% treated)
  • Neonate Hep B vaccine and HBIG within 12hrs birth, then 2 x vaccine as per imms schedule. Check serology 9m age
89
Q

Risk of parvovirus in pregnancy?

A
  • 1st trimester - 10% risk fetal loss
  • 9-20 weeks, high risk of fetal hydrops - can give IU transfusion
  • No medication to prevent fetal infection
90
Q

Discuss congenital rubella

A
  • Highest risk preconception or 1st trimester (50%)
  • SNHL (60%), cataracts/retinopathy/microphthalmia, cardiac (PA stenosis and PDA), ND disability
  • High infectious
91
Q

VZIg guidelines for neonates?

A
  • Maternal VZV 7d before to 7d after delivery - VZIg or IVIG

- Any baby <28 weeks gestation if exposure

92
Q

Multiple ringforms in blood cells

A

Falciparum plasmodium

Paediatrics RACP written exam (18 decks)

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