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Infectious Disease Flashcards

1
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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2
Q

Causes of atypical lymphocytosis?

A 
EBV
CMV 
Toxoplasmosis 
Mumps 
TB 
Malaria
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3
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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4
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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5
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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6
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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7
Q

What type of organism is gonorrhea?

A

Gram negative diplococcus

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8
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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9
Q

When are patients with chickenpox contageous?

A

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

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10
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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11
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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12
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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13
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 human
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14
Q

Discuss Lyme disease

A
  • Caused by borrelia burgdorferi, transmitted by ticks (IXODES TICK)
  • 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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15
Q

Conjunctivitis with intracytoplasmic inclusion bodies?

A

Chlamydial conjunctivitis

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16
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 organism
  • Treat with IM ceftriaxone, saline irrigation. Need CSF and blood cultures
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17
Q

What is a common gram negative coccobacillus?

A

Haemophilus influenzae

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18
Q

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

A

90% ; R0=18
Airborne or person-to-person
Incubation 6-21 days
Infective -5 to +4 from rash

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19
Q

SIDE EFFECT TB TREATMENT

A
  • Rifampicin: orange body secretions, hepatitis 1%, leukopenia/thrombocytopenia, rash ; CYP450 INDUCER
  • Isoniazid: peripheral neuritis (Rx pyridoxine), hepatitis ; CYP450 INHIBITOR
  • Ethambutol: optic neuritis
  • Pyrazinamide: GI, gout, joint pain, itch ; RASH
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20
Q

Live vaccines in NZ

A

MMR, rotarvirus, varicella, BCG

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21
Q

TB treatment

A

Pulmonary TB (6/12 total)

  • Intensive: 2/12 Rifamp(R) ; Isoniazid(H) ; Pyrazinamide (Z) ; RHZ (add Ethambutol (E) if severe disease)
  • Maintenance: 4/12 Rifampicin and Isoniazid (RH)

If CNS / Miliary / Osteoarticular for 12 months treatment total;
2/12 RHZE ; 10/12 RH

Corticosteroids used for TB meningitis (6-8/52)

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22
Q

What are the main features of Cutaneous leishmaniasis?

A

Found in America, North Africa, Middle East and Asia
Caused by protazoa leishmaniasis
• Acquired through bite of infected sandfly
• Erythematous papule enlarges to nodule to ulcerating lesion months with raised indurated borders
• May spontaneously resolve over months/years
• Biopsy to confirm diagnosis
• Various therapeutic options

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23
Q

What are the main features of Cutaneous larva migrans?

A

AKA “creeping eruption”
• Most frequent skin disease among travellers returning from tropical countries (esp from beaches)
• Animal hookworms (contact with dog/cat faeces)
– Ancylostoma braziliense (cat)
– Ancylostoma caninum (dog)
• Incubation period usually short
• Advancing serpiginous tracts in skin with associated intense pruritus
• Eventually self limiting
• Treatment
– Oral albendazole, or ivermectin

• Complications
– Impetigo
– Local and generalised allergic reactions
– hypereosinophilia

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24
Q

Cerebral malaria associated with which organism

A

Plasmodium Falciparum

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25
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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26
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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27
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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28
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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29
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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30
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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31
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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32
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
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33
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
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34
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
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35
Q

Main cause of cervical cancers?

A

HPV 16 and 18

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36
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
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37
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
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38
Q

Which antibiotics act on cell wall synthesis?

A
  • Beta lactams: penicillin, cephalosporin, carbapenems, monobactams
  • Vancomycin
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39
Q

Which antibiotics act on folate synthesis?

A
  • Sulfonamides

- Trimethoprim

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40
Q

Which antibiotics act on protein synthesis: 50S subunits?

A
  • Macrolides
  • Clindamycin
  • Chloramphenicol
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41
Q

Which antibiotics act on protein synthesis: 3OS subunits?

A
  • Tetracyclines

- Aminoglycosides

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42
Q

Which antibiotics act on DNA gyrase?

A
  • Quinolones (ciprofloxacin)
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43
Q

Enterococci are intrinsically resistant to?

A
  • Cephalosporins
  • Low affinity for enterococcal penicillin binding proteins
  • Need penicillin, amox, or vancomycin
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44
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
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45
Q

Discuss carbapenems

A
  • Very broad spectrum - gram positive, gram negative, ESBL, pseudomonas
  • ADRs: neurotoxicity, lowers seizure threshold esp imipenem
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46
Q

Are beta lactams bactericidal or bacteriostatic?

A

Bactericidal

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47
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
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48
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
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49
Q

What is the mechanism of MRSA resistance?

Treatment options

A
  • Altered receptor binding
  • Resistant to all penicillins and cephalosporins

Rx

  • Cotrimoxazole
  • Clindamycin
  • Vancomycin
  • Linezolid
  • Daptomycin
50
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)
51
Q

Ecthyma gangrenosum is associated with?

A
  • Pseudomonas

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

52
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)

53
Q

Stenotrophomonas maltophilia is resistant to?

A

Universal resistance to beta-lactam antibiotics

Rx Cotrimoxazole

54
Q

Treatment of invasive aspergillus?

A

Voriconazole

55
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
56
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

57
Q

Side effects of antifungals

A
  • Amphotericin B - nephrotoxicity, hypokalaemia
  • Azoles - interact with vincristine
  • Caspofungin - does not penetrate CSF
58
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
59
Q

Treatment of CMV?

A
  • Ganciclovir (IV) - 1st line
  • Foscarnet (2nd line) - nephrotoxic
  • Valganciclovir (oral agent, causes neutropenia)
60
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
61
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
62
Q

Neonate with blueberry muffin rash

A
  • CMV most common
  • Will also have jaundice and hepatosplenomegaly
  • Chorioretinitis, IUGR, anaemia

Extramedullary haematopoiesis
Others rubella, toxo, parvo ; leukaemia, LCH

63
Q

Most common cause of non hereditary congenital deafness?

A

CMV (may not be present from birth)

64
Q

Encapsulated bacteria

A 
S - strep pneumoniae
K - klebsiella 
H - haemophilus influenzae 
P - pseudomonas aeruginosa 
N - neisseria meningitidis 
C - cryptococcus neoformans
65
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
66
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(good PPV and NPV after 18/40), 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%

Only 75%congenitally infected produce detectable IgM

Neonatal infection - Rx until 12 mo with Pyrimethamine, Sulfadiazine, folinic acid. SE neutropenia, monitor FBC

Development, eye, ear FU

67
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
68
Q

Treatment neonatal GBS infection

A
  • Amoxycillin and gentamicin (provides synergy) until blood/CSF sterile
  • Or 10 days bacteraemia,
    14-21 days meningitis, CSF prior to completion Rx
    OA, endocarditis, ventriculitis 4-6weeks Rx
  • 30% have residual neurodisability
  • Can get recurrent infection ~40 days later
69
Q

Signs of neonatal syphillis infection

A

40% petal death/stillbirth
2/3 asymp at birth
2 stages

  1. early (0-2 years)- multi organ infection
  • Snuffles, hemorrhagic rhinitis
  • Skin: vesicobullous lesions, mucous patches, desquamating skin
  • Unexplained large placenta
  • Hepatomegaly +/- spleen, jaundice ; GN
  • Non immune hydrops, ANAEMIA, THROMBOCYTOPENIA
  • Bones- osteochondritis, pseduparalysis
  • lymphadenopathy
  1. late (>2years)
    - eyes/hearing
    - bone/teeth abnormal
    - CNS
70
Q

Mangement of neonatal syphillis

A

risk transmission

  • untreated maternal primary/sec -100%
  • latent - early (80%); late (20%)
  • treated in preg (1-2%)
  • Ix: TPPA (trep), RPR (non-trep) tests, paired with maternal serology
  • 4X RISE RPR consistent congenital infection (non reactive <6mo not CS)
  • TPPA +VE >15mo = CS
  • Long bone x-rays - periosteal reactions
  • LP - CSF VDRL, protein, WCC
  • Spirochetes on placenta
  • Tx: 10days IV benpen, follow up serology 3,6,12m
71
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 3 x vaccine as per imms schedule. Check serology 9m age
72
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
73
Q

VZIg guidelines for neonates?

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

- Any baby <28 weeks gestation if exposure

74
Q

Multiple ringforms in blood cells

A

Falciparum plasmodium

75
Q

Pseudomonas intrinsic resistance to.

A

Cefotaxime low affinity for penicillin binding protein and low permeability

76
Q

Hydatid disease Tx

A

Albenazole

77
Q

Three diseases high risk for yersinia and treatment invasive disease

A

Because pathogenic strains need iron, patients with iron overload
(haemachromatosis, thalassemia, sickle cell) are at high risk.

Treatment: supportive, cotrimoxazole in systemic disease. Resistance to penicillins and cephalosporins due to beta lactamase production.

78
Q

Classification of antifungal agents
• Polyenes –
•Azoles –
• Echinocandins‐

A

All impact cell membrane/wall
• POlyenes – POke holes in cell membranes (Ambisome)
• AzOLes – interfere with cell membrane
function by inhibiting sterOL synthesis (interfere)
• EchINocandins‐ INhibit cell wall synthesis (Caspofungin)

79
Q

Zika mosquito called

A

Aedes aegypti

80
Q

Listeria gram stain result

A

Gram positive rod

81
Q

What are the causes of macular star/neuroretinitis?

A
  • Toxoplasmosis
  • Syphillis
  • Lyme
  • Cat scratch (Bartonella)
82
Q

What is the seafood-associated diarrhoea?

A

Vibrio - supportive management only

83
Q

What does the aedes aegypti mosquito transmit?

A
  • Dengue
  • Zika
  • Chikungunya
  • Yellow fever
84
Q

In SSSS where is the cleavage plane in the skin?

A
  • superficially in the stratum granulosum layer of the skin

- biopsy will show cleaveage in granular layer with no inflammatory cell infiltrate

85
Q

How long does natural immunity to influenza last?

A

4 years

86
Q

Which subtype of influenza is more likely to cause myalgias?

A

B

87
Q

side effects of zidovudine?

A
  • Zidovudine is a NRTI
  • Nausea/vomiting
  • Myopathy
  • Anaemia/granulocytopaenias (e.g. neutropaenia, low basophils/eosinophils)
88
Q

What is the maternal/neonatal treatment for toxoplasmosis?

A
  • Maternal to prevent transmission is spiramycin
  • Maternal if foetal infection is pyrimethamine + sulphadiazine + folinic acid
  • neonatal if infected is 12/12 treatment
    Pyrimethamine, sulfadiazine and leucovorin 5‐10mg 3x weekly
89
Q

What is Gianotti-Crosti Syndrome?

A
  • a.k.a. infantile papular acrodermatitis
  • viral infections and immunizations of all types
  • typically 3-4/7 hx of non itchy 5-10mm dull/dark red spots (first on thighs/bum, then outer arms, then face)
  • evolve from deep red -> purple and become vesicular
  • well/mild fever and mild lymphadenopathy
  • fades in 2–8 weeks with mild scaling.

Associated with viral illnesses
Hepatitis B infection ; EBV; CMV
Enterovirus infections; Echo viruses; RSV

90
Q

What are the HACEK organisms and what is their significance?

A 
H – Haemophilus
A – Aggregatibacter (previously Actinobacilus) 
C – Cardiobacterium 
E – Eikenella 
K - Kingella

Fastidious gram-negatives which cause 5-10% of IE

91
Q

HIV treatment

A

NTRI (nucleoside reverse transcriptor inhibitors) X 2 plus another type of action (lipotrophy) - either NNTRI (CNS s/e) or protease inhibitor (metabolic s/e)

92
Q

What is the mechanism of penicillin resistance in pneumococcal infection?

A
  • Decreased affinity of penicillin binding proteins.

- Resistant pneumococci make altered cell walls.

93
Q

What are the 5 types of malaria and treatment

A

Malaria is a parasitic infection transmitted by Anopheles mosquitoes
The 5 species that infect humans are Plasmodium falciparum, P. vivax, P. ovale, P. malariae, and P. knowlesi

Severe malaria is largely caused by P. falciparum, although children with P. vivax and P. knowlesi malaria can also present seriously ill

Incubation period for P. falciparum infection is usually 14 days (range 7-30)

P. vivax and P. ovale produce liver hypnozoite forms which can cause relapse of the illness months to years later

Uncomplicated malaria is defined as confirmed parasitological diagnosis of malaria without signs of severity (organ dysfunction). Young children (especially <5 years) can deteriorate rapidly and are more likely to have severe and cerebral malaria than adults

Thick and thin film
Malaria antigen/ICT (rapid immunochromatographic assay) - detects P. falciparum with >90% sensitivity - insensitive for other species or low level of parasitaemia

P.Falciparum - Artemether-lumefantrine (Arteminisin combination therapy), x 3/7
Mechanism of action: Act through endoperoxide bridge, this interacts with heme in the parasite. The heme iron cleaves this endoperoxide bridge. Generation of highly reactive free radicals which damage parasite membrane by covalently binding to membrane proteins

P. ovale, P Vivax - chloroquine then primaquine to erradicate it from the liver and prevent relapses (check not G6PD)

P. malaria / P. Knowlesi - chloroquinine ; use Artemether-lumefantrine if resistance

Severe malaria (Falciparum) - IV Artesunate
Signs of serve malaria include prostration, fast deep breathing and impaired consciousness
cerebral malaria, acute lung injury (25% ARDS), acute kidney injury, acidosis

Complications
Haemolytic anaemia ; Hypoglycaemia ; Jaundice
Metabolic acidosis; Increased serum lactate ; Parasitaemia >2% ; Shock
Haemoglobinuria ; Renal impairment ;
Pulmonary oedema, resp distress
Coagulopathy ; Bleeding
Impaired consciousness ; Seizures

94
Q

HIV in children

A

95% through vertical transmission
• Most transmission at delivery 60 - 70%
• Smaller risk of infection in-utero 30-40%
• Breast feeding = 5-20% risk of postpartum transmission

Without intervention, risk of transmission = 25-45%, with intervention (combined ART with viral suppression) <1%

HIV is enveloped RNA virus that destroys CD4 helper T Lymphocytes

Diagnosis
Lab criteria
Children<18 months born to a mother with HIV infection or unknown status
• HIV infected = positive result on at least one specimen(not cord blood) for HIV NAT (DNA or RNA)
• This needs confirmation on repeat testing

Children>18 months
• A positive HIV antibody test and a repeat positive test from a supplemental test different from the first

Clinical: Weight loss (>10%), lymphadenopathy, chronic diarrhoea, prolonged fever, thrush, recurrent VZV
Opportunistic infections (low CD4)

Viral load most predictable of viral transmission
Breastfeeding is risk based, low viral load BF safe

Mx post delivery
Low risk = ADZ (Zidovudine x 1/12)
High risk = HAART (3 drug minimum)

95
Q

TB in children

A

50% children asymptomatic
Infants greatest risk becoming symptomatic

<1 year 50% affected following primary infection

  • 10-20% disseminated TB. ; 30-40% pulmonary TB
  • 50% no disease

1-2 years

  • 2-5% disseminated TB. ; 10-20% pulmonary TB
  • 75-80% no disease

2-5 years

  • 0.5% disseminated TB ; 5% pulmonary TB
  • 95% no disease

Age 5-10 (safe school years)

  • 95% no disease
  • 2% pulmonary, <0.5% disseminated

> 10 years

  • <0.5% disseminated ; 10-20% pulmonary TB
  • 80-90% no disease

Younger children have paucibacillary disease (less infectious)

• In children 50% asymptomatic even with extensive
disease. Cases often found through contact tracing
• Most common presentation cough and fever, systemic symptoms may include malaise, weight loss, night sweats, weakness, decreased appetite
• Infants more likely to be symptomatic - 80%
• TB adenitis typically involves the cervical nodes
• >90% of children who progress to active TB do so within 12 months of primary infection
• Younger children have paucibacillary disease and less infectious

Diagnosis
Recent close contact with an infectious case of TB &
• Positive tuberculin skin test/IGRA
• Suggestive findings on radiology or physical exam
• + culture confirmation (AFB)

96
Q

Persistent generalised lymphadenopathy

A

Infectious
• Tuberculous, infectious mononucleosis, cat scratch disease, cytomegalovirus, toxoplasmosis, other viruses, syphilis, hepatitis, brucellosis, Kawasaki disease, HIV

Noninfectious
• Leukaemia, lymphoma, neuroblastoma, histiocytosis, metastatic tumours, other malignancies, sarcoidosis, stones or tumours of the salivary glands, branchial cleft cyst, dermoid cyst, thyroglossal duct cyst

97
Q

Cat scratch disease

A
  • Bartonella hensalae, fastidious gram negative bacterium
  • Usually benign self-limiting disease: history of contact with kitten/cat (can be absent)
  • Gradual regional L/N enlargement
  • Painful for weeks, most resolve 4-6 weeks
  • May suppurate(approx25%)

• Diagnosis usually by serology, histology, PCR available

Protean manifestations
• PUO, endocarditis
• Encephalitis, aseptic meningitis
• Pneumonitis, hepatitis, osteolytic lesions,
• Loss of vision, Skin rashes
• Parinaud oculoglandular syndrome

Treatment: disease usually self limited, antibiotics usually reserved for severe infections and immunocompromised – azithro, cipro, cotrimox

98
Q

Cutaneous Larva Migrans

A

Most frequent skin disease among travellers returning from tropical countries

Animal hookworms (contact with dog/cat faeces) 
◦ Ancylostoma braziliense (cat)
◦ Ancylostoma caninum (dog)

Incubation period usually short
 Advancing serpiginous tracts in skin with
associated intense pruritus
 Eventually self limiting

Treatment
◦ Oral albendazole, or ivermectin

Complications
◦ Impetigo
◦ Local and generalised allergic reactions
◦ hypereosinophilia

99
Q

Eosinophilic meningitis

A

> 10% eosinophils (20-70%) ; often high opening pressure

Parasites: Angiostrongylus cantonesis meningitis (from eating snails, seen in PI) ; Neurocysticerocis
Malignancy: Eosinophilic leukaemia
Hypereosinophilia syndrome

100
Q

Intestinal parasites requiring treatment

A 
Giardia
Schistosoma
hookworm
Ascaris, Trichiuris, Filaria, 
tapeworms* (Taeniasis, cystercicosis, Hymenopelis nana (dwarf tapeworm), Diplidium caninum, Diphyllobothrium latum, E. granulosus)
Strongyloidiasis, 
Entamoeba histolytica
101
Q

Dengue

A

Most significant mosquito-borne viral disease
 Flavivirus – single stranded RNA virus
 4 serotypes DENV1-4, antigenically distinct
 Spread primarily by Aedes aegypti mosquito, also by Aedes albopictus
 70-80% infections asymptomatic
 Clinical presentation - mild fever to classical dengue
fever with haemorrhage and /or shock
 Classical dengue – high fever, severe headache, retro-orbital pain, malaise, severe joint and muscle pain, N+V, with rash 3-4 days after fever onset
 Severe forms usually seen in secondary infection with different serotype. During defervescence – can rapidly deteriorate with haemorrhage + vascular leak
 Primary infection in young infants may also be associated with severe disease

Clinical signs - tourniquet test, leukopenia, fluid overload, mucosal bleeding, hepatomegaly

Increased vascular permeability differentiates severe infection (haemorrhage, plasma leak with shock or fluid overload ; organ involvement - Hepatitis (ALT>1000, CNS involvement(reduced conscious), cardiac) ; low platelets indicate marrow involvement - warning signs

Diagnosis:
<1week symptoms: Rapid antigen test (NS1) and Viral PCR
>1 week - serological test

102
Q

Antifungals

A

 Polyenes
◦ Amphotericin B, includes liposomal amphotericin compounds, nystatin
SE: Acute reaction (secondary to release cytokines lasts 2-5hours - fever, chills, N+V) ; reduces in intensity with subsequent doses ; Nephrotoxicity, rash, anaemia

 Echinocandins
◦ Caspofungin, micafungin, anidulafungin
SE: GI disturbance, hypotension, rash, fever, chills, headache, hypokalaemia, anaemia, elevated hepatic enzymes, infusion site reactions
 Caspofungin can interact with cyclosporin and rifampicin

 Azoles
◦ Triazoles: fluconazole, voriconazole, itraconazole, posaconazole
◦ Imidazoles: Clotrimazole, econazole, miconazole,, ketaconazole
SE: QT prolongation, electrolyte disturbances, hepatic reactions, exfoliative skin reactions, photosensitivity, acute pancreatitis, visual disturbances
Drug interactions (CYP450 inhibitor)

 Antimetabolite
◦ Flucytosine

 Heterocyclic benzofuran
◦ Griseofulvin

 Allylamine
◦ Terbinafine

103
Q

MIC
MBC

resistance

A

The minimum inhibitory concentration (MIC) is the lowest concentration that, under defined in vitro conditions, prevents the growth of bacteria within a defined period of time.

The minimum bactericidal concentration (MBC) is the lowest concentration of an antibiotic, that under defined in vitro conditions reduces by 99.9%, the number of organisms in a medium containing a defined
inoculum of bacteria, within a defined period of time.

A widely used technique for susceptibility testing is dilution testing. A standard concentration of a microorganism is inoculated into serially diluted concentrations of antibiotic, and the minimum inhibitory concentration (MIC) in μg/mL, the lowest concentration of antibiotic required to inhibit growth of the microorganism, is determined.Dilution testing also permits determination of the minimum bactericidal concentration (MBC), the lowest concentration of antibiotic required to kill the organism.

The MBC is sometimes determined to exclude the possibility of bacterial tolerance (MBC > 4 times the MIC).

104
Q

Typhoid fever

A

• Typhoid fever (also called enteric fever) is an infectious disease caused by Salmonella enterica enterica serovars typhi (commonly called Salmonella typhi) and paratyphi A, B, and C.
• Typhoid occurs in all countries where basic sanitation and food handling is poor, especially Asia, South and Central America, and Africa but also the Pacific.
It occurs in all ages, most commonly children 5-14.
• Transmission is via faecal-oral route via contaminated drinking water and food. 5% of infected individuals develop chronic carriage in gall bladder and act as a reservoir, continuing to shed bacteria in the stool.

  • Incubation 5-21 days.
  • Week 1: fever (100%), abdominal pain, constipation or diarrhoea (60%), headache, dry cough (30%), malaise, myalgia, epistaxis (25%), delirium.
  • Week 2: fever plateaus 39-40oC, symptoms progress, abdominal distention, delirium/neuropsychiatric.
  • Week 3: symptoms progress, complications (intestinal perforation, intestinal haemorrhage, sepsis, myocarditis, abscesses).

Examination: Relative bradycardia (30-50%), dichrotic pulse, abdominal tenderness (60%), hepatosplenomegaly (<40%), rose spots (20%) – week 2 onwards.

  • Investigations of choice are blood and stool cultures.
  • Peripheral white cell count is usually normal or low.
  • Bone marrow biopsy is most sensitive.
  • Empiric therapy is with 10-14 days IV ceftriaxone. Fevers will continue on appropriate antibiotics for 6-7, but the patient will clinically improve. Relapse is 5%.
  • Prevention is through hygiene, detection of carriers, and vaccination.
105
Q

Types of malaria

A

Plasmodium falciparum
◦ high levels of blood stage parasites ◦ Severe disease
◦ Incubation period 10-14 days

P. vivax
◦ Milder disease
◦ Recurrent
◦ Incubation period 2-3 weeks
 - Parasite prefers younger RBC
P. malariae
P. ovale
P. knowlsei
◦ primarily zoonotic in SEA
◦ Can be severe disease
◦ Incubation period 10-14 days

In vivax and ovale infections a proportion of sporozoites become dormant hypnozoites, causing relapse months or years after initial infection. Requires Rx Primaquine (CI in G6PD)

Signs of serve malaria include prostration, fast deep breathing and impaired consciousness
cerebral malaria, acute lung injury (25% ARDS), acute kidney injury, acidosis

106
Q

Chickenpox complications

A
  • Secondary bacterial infection often with group A streptococci
  • Thrombocytopenia with haemorrhage into skin
  • Pneumonia
  • Purpura fulminans
  • Post-infectious encephalitis
  • Immunocompromised patients – severe disseminated haemorrhagic disease
107
Q

Neisseria Meningitis serotypes causing infection

A

A, B, C, X, Y, Z, W135, L

108
Q

Pertussis

A

Caused by Bordatella pertussis (gram -ve encapsulated coccobacilli)

Most common <2 years age ; unimmunised children
Variable presentation especially in older kids
<6mo atypical - apnoea, cyanosis
Most severe <2 years (60% infants require hospitalisation)
Disease epidemic peaks are in February/March

Vaccinated against at 2,4,6 months and booster 4years, adolescence and pregnancy (DTAP)
Protection lasts 5 years, 1 dose no protection, 2doses 75%, 3 doses 95% protection

Highly infectious ; infectivity 1 week before paroxysamal cough to 3 weeks after (maximal in catarrhal stage)
Reduces to 5-10 days with erythromycin / azithro

Incubation period 2 weeks
Duration illness 6-10weeks if uncomplicated

3 stages
1. Catarrhal (coryzal) 1-2 weeks, coryza, cough
At end of catarrhal phase get lymphocytosis
2. Paroxysmal stage 2-4 weeks (coughing paroxysms, severe spasmodic cough +/- whoop or post tussle vomit
young children can get apnoeas
3. Convalescent stage 1-3 weeks (non infectious at this stage), paroxysmal cough, resolving, can take 6months to resolve fully

Clinical cause 
cough x 2 weeks + 1 more of 
one or more of:
- whoop
- cyanosis
- post-tussive vomiting or
- apnoea for which there is no other cause

NPS PCR for diagnosis
IgM +ve from 2-3 weeks ; FBC ++ lymphocytes
Notifiable disease

Macrolides reduce infectivity period but do not alter disease course

Close contacts / household need prophylaxis to protect children in house

  • Aged less than 1 year;
  • Is partially or un-immunised & less than 5 years of age;
  • Has chronic disease or is immunocompromised;
  • In the last trimester of pregnancy;
  • Has daily contact with a high priority contact
109
Q

Pseudomonas

A

gram -ve rod, strict aerobe; can produce bluish green pus(phenzathine pigment)
Opportunistic infections
- Patients CF, ventilated patients, burns/wounds, puncture wounds foot
Rx Tobramycin / Tazocin / Mero / Cefipime / Cipro

SKin manifestation Ecythema Gangrenosum
- pink nodule that becomes haemorrhage and ulcerates, often has gangrenous centre

110
Q

TB children

A

Latent TB = +ve TB but no symptoms and normal CXR, not infectious
Active disease = abnormal CXR +/- complications with +ve Mantoux, sputum may have AFB

Clinical
Active disease (5-10%primary infection, increased in infants)
- Lung - cough, fever, LOW ; upper lobe pneumonia, caveating lesion, Hilar LN
Rare - military TB, effusions
- TB lymphadenitis - cervical (common), painless, matted, unilateral, “cold abscesses”
- TB meningitis - rare but severe, +++protein, low glucose, lymphocyte predominantly ; PCR for AFB
- Renal / GU: Sterile pyruria, haematuria
- Bone: Vertebral collapse (Potts)
- Adrenal (causes Addisons), TB peritonitis

111
Q

Atypical mycobacterial infections

A

Lympadenitis (peak 1-5year olds)
-MAIC most common (Mycobacterium avium complex)
- Unilateral firm, painless, LN, no erythema ; may suppurate over time and develop red/purple discolouration.
Cervical/submandibular most common
Rx Excision

112
Q

VZV

A

Immunised against at 15/12, live attenuated vaccine

Infectious 2 days before rash until all lesions have crusted over.

Complications

  • Secondary infection (GAS > staph aureus)
  • Acute cerebellar ataxia, occurs 2-3 weeks after infection, maximal at onset ; can last 2 months
  • Encephalitis / pneumonia (worse if immunosuppressed)

Congenital varicella - rare
IUGR, microcephaly, limb hypoplasia, cutaneous scarring, choreretinitis/cataracts

Neonatal chickenpox if mum develops VZV 5 days before to 2 days after delivery give baby ZIG.

113
Q

Slapped cheek caused by..

A

Parvovirus B19
school ages kids, infectious until onset of rash

Clinical
slapped cheek with circumoral pallor ;
diffuse macular rash, with central clearing (lacy reticular rash), spares palms and soles

Complications

  • Aplastic crisis in children with chronic hemolysis (SS, thalassemia, HS) ; mostly red cell aplasia
  • Arthropathy
  • Congenital infection - causes fatal loss(1st tri) or hydrops
114
Q

Virsuses that cause hand foot and mouth

A 
Enterovirus 71 (can be comp by mening / encephalitis / myocarditis)
Coxsackie A (Cox A9 assoc petechiae and Purpura, Ddx meningococ)

Clinical
Fever, pharyngitis
Vesicles on hands, feet, buttocks ; resolves over 3-7days

115
Q

UREASE Producing bacteria

A

Urease-producing bacteria (mnemonic PUNCH)

Proteus
Klebsiella - predispose to struvite stone production (UTI)
Ureaplasma urealyticum
Nocardia
Cryptococcus
Helicobacter pylori

However, H pylori depends upon urease (and motility and ability to adhere to gastric epithelium) to allow it to survive and proliferate in the gastric milieu.
Bacterial urease hydrolyses gastric luminal urea to form ammonia that helps neutralise gastric acid and form a protective cloud around the organism, enabling it to penetrate the gastric mucus layer. Urease is produced in abundance, making up >5% of the organisms’s total protein weight. Hence diagnostic tests for H. Pylori include biopsy urease testing, and urea breath testing.

116
Q

MMR efficacy against measles
1st dose
2nd dose

A

1st dose, 95% protection

2 doses 99% protection

117
Q

worms / heminths

A 
Roundworm = Ascariasis lumbricoides (most common worldwide ; large, complications GI, lung, biliary)
Whipworm = Trichuris trichuria
Pinworm = Enterobius vermicularis (small white worms, ++itchy, keep kids wake at night)
Hookworm = Ancylostoma

Rx Mebendazole

118
Q

Post exposure to Varicella

  • immunosuppressed
  • immune competent

Rx and isolation precautions

A

Immune compromised
- Give VZIG / IVIG regardless of prior history
• In 2011 FDA extended period for administering VZIG from 96 hours (4days) to 10 days
• >96 hours, start oral acyclovir 80mg/kg/day in 4 divided doses commencing day 7 following exposure and – in addition to ZIG - continue for 7 days

Immune competent
• Giving vaccine within 3 days may prevent chicken pox
• Giving vaccine within 5 days lessens severity of illness
•Treat with aciclovir if symptomatic

Isolation requirements
• VZIG and acyclovir recipients still need isolation from day 7 –28 post chicken pox exposure VZIG/ IVIG protection lasts approximately 4 weeks
• ZIG administration prolongs isolation time ( increase from 21 to 28 days post exposure)

119
Q

Diagnosis congenital CMV

A

Urine CMV PCR within 2-4weeks after birth to call congenital.
Alternative salivary PCR

Infant blood for PCR (Guthrie has low sense)
Neuroimaging - US if asymptomatic ; MRI if symptomatic
Ophthalmology
Audiology

120
Q

Treatment congenital CMV

A

Start <28days of life for infants with moderate symptomatic disease

PO Valganciclovir or IV ganciclovir
Rx for 6months total (6mo vs 6 weeks, Assoc with better hearing and developmental outcomes in longterm ; no change in short term
SE: Neutropenia

121
Q

Treatment Kerion

A

Terbinafine x 6 weeks

122
Q

Treatment of Stenotrophomonas Maltophilia

A

Co-trimoxazole

Paeds (25 decks)

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