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Aisha > Dunedin-ID > Flashcards

Dunedin-ID Flashcards

1
Q

What is the mechanism of MRSA?

A

Modified penicillin-binding protein (altered target site of beta-lactam binding)

mecA gene encodes for PBP2a which has an altered terminal amino acid resulting in hugely reduced affinity for beta-lactam drug binding

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2
Q

Discuss PVL genes regarding community acquired MRSA and hospital-acquired MRSA

A

Community acquired MRSA- many carry PVL genes

hospital-associated MRSA: PVL expression less common

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3
Q

Define multi-resistant MRSA

A

Either two or more of the non-beta-lactam antibiotics e.g. erythro/clinda,* co- trim, genta, rifampicin, fusidic, mupirocin, tetracycline, chloramphenicol

Or ciprofloxacin (marker for the EMRSA-15)

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4
Q

What is PVL (Panto-valentine leucocidin)?

A

a pore-forming necrotising exotoxin that causes leucocyte destruction and tissue necrosis, with marked neutrophil activation and release of pro-inflammatory cytokines

seen in MRSA

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5
Q

Treatment of non-multi-resistant MRSA

A

Non-severe: cotrimoxazole, clindamycin, erythromycin, doxycycline, rifampicin, fusidic acid, gentamicin
linezolid

Severe: vancomycin, teicoplanin, daptomycin

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6
Q

What is a S/E of linezolid

A

reversible bone marrow depression with prolonged use
irreversible neuropathy
optic neuropathy

serotonin syndrome

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7
Q

What is the MOA of linezolid?

A

bacteriostatic, inhibits bacterial proteins synthesis, binds to both 30s and 50s ribosomal subunits

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8
Q

What is the MOA of daptomycin

A

cyclic lipopeptide bactericidal antibiotic that causes depolarisation of the bacterial cell membrane

ineffective in respiratory tract infections due to inactivation by pulmonary surfactant

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9
Q

What are S/E of daptomycin?

A

myopathy, peripheral neuropathy, eosinophilic pneumonia

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10
Q

What is the MOA of tigecycline?

A

protein synthesis inhibitor, binding at the 30s ribosomal subunit

limited in UTIs

active against acinetobacter and stenotrophomonas

NOT active against pseudomonas, proteus, Providencia

not suitable for treatment of ventilator-associated pneumonia or CNS infections

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11
Q

How to treat enterococci?

A

penicillin, amoxicillin/ampicillin or vancomycin

inherently resistant to cephalosporins

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12
Q

What is the difference between E.faecalis and E.Faecium?

A

E.Faecalis –> more virulent, sensitive to penicillin/amoxicillin

E.Faecium –> less virulent, usually resistant to penicillin/amoxicillin
Vanc resistant

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13
Q

What is the MOA of vancomycin?

A

Inhibits synthesis of bacterial cell wall by binding to “D- alanyl-D-alanine terminus of the pentapeptide side-chain” preventing cross-linking.

active against gram POSITIVE bacteria, cant penetrate outer lipid membrane of gram negatives

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14
Q

What are S/E of vancomycin

A

Nephrotoxicity, ototoxicity, “Red Man” syndrome, neutropenia, thrombocytopenia, rash

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15
Q

What is teicoplanin?

A

glycopeptide antibiotic, similar to vancomycin

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16
Q

How do you get vanc resistance?

A

D-Ala D-Ala –> D-Ala D-Lac

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17
Q

What gene clusters give rise of Vancomycin resistance?

A
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18
Q

What are VRE Treatment options?

A

penicillin/amoxicillin/ampicillin
teicoplanin- only for Van B/ Van C
linezolid
daptomycin +/- beta-lactam
tigecycline
ceftaroline

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19
Q

What is the mechanism of pneumococcal resistant to penicillin and cephalosporin?

A

alteration of penicillin-binding proteins (transpeptidase enzyme)

therefore clavulanic acid (e.g. augmentin) adds nothing

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20
Q

What is IV penicillin MIC break points?

A

Non-meningeal infections:
- susceptible: <0.06 mg/L
- resistant >2mg/L

Meningeal infection
- susceptible <0.06mg/L
- resistant: >0.06 mg/L

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21
Q

What is the mechanism of macrolide resistance for S.Pneumonia?

A

Macrolide resistance occurs via either mefA gene (efflux pump, low level resistance) or ermB gene (alteration of binding site, high level resistance)

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22
Q

What is the difference between gram +ve and gram-ve bacteria?

A

Gram +ve: 2 layer cell wall (thick peptidoglycan layer), cytoplasmic membrane

Gram -ve: three layer cell wall (outer membrane is outer lipid bilayer), cell wall (thin peptidoglycan layer), cytoplasmic membrane

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23
Q

What is the mechanisms of beta-lactam resistance

A

1) altered porins (only in gram -ve bacteria)

2) beta-lactamases

3) prevention of binding

4) efflux pumps

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24
Q

What is the mechanism of resistance for ESCHAPPM organisms?

A

AmpC Beta-lactamse genes which may be found on bacterial chromosomes or plasmids

resistant to cephalosporins (apart from cefepime)

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25
Q

How to treat ESCHAPPM organisms?

A

Carbapenems - empiric abx of choice
cefepine
possibly tazocin

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26
Q

What are extended spectrum beta-lactamases (ESBL) resistant to?

A

Most commonly found on e.coli and klebsiella

Treatment: carbapenem
outpatient ESBL UTI: nitrofurantoin (useful for lower UTI), ciprofloxacin, cotrimoxazole, gentamicin, fosfomycin

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27
Q

List some carbapenem-resistant enterobacteriaceae (CRE)

A
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28
Q

What is the treatment for CRE?

A

note in Australia mainly NDM rather than KPC

Colistin no longer first line but can be used. tigecycline not useful for bacteraemia

CRE urine: nitrofurantoin, cotrimoxazole, ciprofloxacin, fosfomycin, stat dose IM amino glycoside

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29
Q

What is avibactam and what is the mechanism of action?

A

avibactam is a second generation beta-lactamase inhibitor

normally beta-lactamase inhibitors bind to the beta-lactamase inhibitor and undergo hydrolysis

Avibactam binds to the beta-lactamase enzyme and inactivates it through a process of “reversible cyclisation”. it is released/regenerated to continue to inhibit other molecules.

Can inhibit Class A enzymes (ESBL, KPCs) and Class C (AmpC producers) and Class D (OXA-48)

No activity against the metal-beta lactamases (NDM, VIM, IMP)

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30
Q

What are the most common organisms in meningitis?

A

strep pneumoniae, neisseria meningitis, listeria with age>50

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31
Q

Risk factors for meningitis?

A
  • Abnormal communication between nasopharynx and subarachnoid space due to trauma or anatomic abnormality
  • Anatomic or functional asplenia or immunoglobulin deficiency are risk factors for infection from encapsulated organisms (Pneumococci, Meningococci)
  • Complement deficiency
  • Terminal complement inhibitory - Eculizumab (2000 fold risk)
  • HIV
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32
Q

What is the difference between Kernig sign and Bruzinski sign

A

Kernig sign: inability to full knee flexion when hip flexed
to 90 degree angle

Brudzinski: spontaneous flexion of hips during passive flexion of the neck

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33
Q

What are the indications for CT prior to LP?

A
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34
Q

Interpretation of CSF

A
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35
Q

What is the empiric treatment of bacterial meningitis?

A
  1. Dex 10mg IV q6hrly (maximum 4 days)
  2. ceftriaxone 2g IV BD

If pneumococcal risk, add IV vancomycin e.g. gram +ve cocci on initial stain, pneumococcal antigen +ve, suspected otitis, sinusitis, or mastoiditis

If listeria risk, add benpen 2.4g IV q4hrly

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36
Q

What is streptococcal Suis associated with?

A

common cause of meningitis in SE Asia. Hearing loss +++. Associated with pigs & handling pork

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37
Q

Describe LP findings of aseptic meningitis and causes

A

CSF: lymphocyte-predominant pleocytosis, typically <500cells/uL, normal glucose concentration, normal or slightly elevated protein, negative bacterial antigen tests/ culture

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38
Q

Describe LP findings fo TB meningitis

A

*Predominant lymphocytic CSF >50%, with low CSF:blood glucose ratio (<0.5) and a high protein conc. >1.0 g/L

  • Low numbers of bacilli in CSF - yield of ZN staining & culture adequate only if large volume of CSF is examined (>5 ml)
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39
Q

What sort of meningitis is common in HIV?

A

cryptococcal meningitis:
Two species: Cryptococcus neoformans (immunocompromised) and Cryptococcus gattii* (immuno-competent)

May be associated with cerebral mass lesion e.g. cryptococcoma.

typically raised ICP

no role of steroids

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40
Q

What is the most common valvular lesion associated with IE?

A

mitral valve prolapse with regurg

previously was mitral stenosis secondary to RHD

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41
Q

What is a determinant of IE caused by streptococci?

A

the amount of dextran

42
Q

What is the other name with streptococcus gallotyicus?

A

AKA strep bovis
associated with colon pathology such as cancer

43
Q

What are HACEK organisms?

A

Oral gram negative bacilli that are slow to grow in traditional culture media

44
Q

What are examples of culture-negative endocarditis?

A

*Bartonella
* Coxiella burnetii (Q fever)
* Brucella
* Legionella
* Tropheryma whipplei

45
Q

What is empiric therapy for IE?

A

Native valve:
Benpen + fluclox + gent IV daily
OR
gent IV daily + vanc

Prosthetic valve:
Fluclox + vanc + gent
OR
Vanc + Gent

46
Q

How to treat streptococcal IE specific therapy?

A

Depends on penicillin MIC

47
Q

How to treat enterococcal IE?

A
48
Q

What are some oral options for Infective endocarditis?

A

Many thing, but can trial linezolid + rifampicin

49
Q

What are indications for surgery in infective endocarditis?

A

Heart failure

Uncontrolled infection (root abscess, persisting fevers and positive blood cultures despite >10d therapy, fungal or MDRO)

Prevention of embolism (Vege >15mm, large vege _ embolic episodes)

50
Q

When to use prophylaxis for infective endocarditis?

A

high risk cardiac condition (prosthetic heart valve, rheumatic valvular heart disease, previous endocarditis, unrepaired cyanotic congenital heart disease)

PLUS
high risk procedure (dental procedure, tonsillectomy or adeniodectomy, surgery at site of an established infection)

51
Q

What is the IE prophylaxis?

A
52
Q

What is the CURB-65 score?

A
53
Q

When can you use steroids with pneumonia?

A
54
Q

What is Multi-drug resistant tuberculosis?

A

TB resistant to isoniazid and rifampicin.

note isolated rifampicin every rare, usually indicated MDR

55
Q

What are risk factors for MDR TB?

A
  • migrants from high risk areas such as china, Eastern Europe, India, PNG, Russia, SEAsia, sub-saharan and south africa

patients who treatment previously failed

failure to response to treatment within 2-3 months

contacts of MDR TB cases

56
Q

What are CXR findings in HIV and TB?

A

CXR findings commonly less typical – may be lower zone, diffuse infiltrate, cavitation unusual, and less mediastinal adenopathy

57
Q

Describe TB therapy:

A

Initiation phase: 2 months
- isoniazid, rifampicin, pyrazinamide, ethambutol

Continuation phase: 4 months
- isoniazid, rifampicin

usually total of 6 months but can extend to 9 months if cavitary disease, pulmonary TB still positive at 2 months, bone or joint ,TB meningitis

58
Q

Is Q.gold affected by BCG vaccine?

A

NO

unlike mantoux test

59
Q

What are treatment regimens for latent TB?

A

Isoniazid 300mg PO daily x 6 – 9 months

Isoniazid 300mg/Rifampicin 600mg daily x 3 months

Rifampicin 600mg PO daily x 4 months

Rifapentine 900mg + Isoniazid 900mg weekly x 12 weeks

60
Q

Why is oral doxycycline 100mg BD the recommended first-line treatment option for chlamydia urogenital infection in non-pregnant females?

A

increasing neisseria gonorrhoea and mycoplasma genitalum azithromycin-resistance

61
Q

Compared to standard pyogenic infection, mycobacterial bone and joint infections are typified by?

A

subacute presentation

62
Q

Regarding HSV encephalitis, describe MRI findings

A

Unilateral temporal lobe involvement on MRI is more common than bilateral involvement

HSV1 is most common cause
HSV meningitis can be self limiting but NOT HSV encephalitis.

63
Q

Regarding pregnancy and varicella exposure in someone without previous vaccination and no detectable serum VZV IgG

A
  • should offer varicella-zoster immunoglobulin up to 10 days after exposure (BUT HAS TO BE BEFORE THE RASH)
  • if she develops chickenpox, she has 10% risk of developing varicella pneumonia
64
Q

In the treatment of a severe, complex intra-abdominal infection, metronidazole should be combined with which abx?

A

Cefepime

65
Q

Prosthetic joint infections are often treated with surgery + rifampicin. Why?

A

anti-biofilm activity

66
Q

Describe the likelihood of strep species causing IE

A
67
Q

What factor is considered most potent at generating infectious aerosols?

A

Forceful coughing

68
Q

How does aspergillus appear on bronchoalveolar lavage?

A

branching filamentous fungi with septate hyphae

69
Q

How do you treat aspergillus infection?

A

Voriconaozle
aspergillus is a mould

70
Q

What is an example of a granulomatous change in skin without acid-fast bacilli?

A

myocobacterium marinum

risk factor: tropical fish tank cleaning

71
Q

What is sporothrix schenckii (sporotrichosis) ?

A

Sporotrichosis (“rose gardener’s disease”) is a fungal skin infection caused by Sporothrix, a fungus that lives in soil and on plants

71
Q

What is the main benefit of the new recombinant zoster vaccine (Shingrix)?

A

it can be used in immunocompromised patients

72
Q

Compare monkeypox and chicken pox

A

*monkey pox is spread predominately by skin to skin contact whereas chicken pox is airborne
*the incubation for both diseases is up to 21 days
* monkey pox vesicles may be concentrated on the hands and feet which is rare for chicken pox
* chicken pox vesicles evolve in various stages and erupts in several crops, whereas monkey pox the lesions are mostly at the same stage
* lymphadenopathy is more common in monkey pox than in chickenpox

73
Q

Describe the life cycle of HIV

A
74
Q

What indicates abacavir hypersensitivity?

A

HLAB5701

75
Q

List antiretroviral medications in HI

A
76
Q

What is the basic treatment of HIV?

A

Integrase inhibitor + 1or 2 NNRTI

if prior use of cabotegravir use darunavir (protease inhibitor) + 2NNRTI as there may be integrate resistance

77
Q

What is a common S/E of efavirenz?

A

Mental health stuff

78
Q

List some live vaccines

A

BCG
Oral Typhoid
MMR
Varicella (chickenpox Shingles)
Yellow Fever
Rotavirus
Intranasal Influenza
Oral Polio

79
Q

What are some HIV associated pulmonary disorders?

A

Common: pneumococcus, pneumocystis, TB

Uncommon: aspergillus, staphylococcus, toxoplasma

Rare: CMV, MAC

80
Q

When do you need to give PJP prophylaxis?

A

Prednisone > 20 mg /day for > 4 weeks

81
Q

What is the best prognostic indicator for survival with PJP?

A

level of oxygenation at diagnosis
if PaO2 >70mm Hg, addition of pred is needed

82
Q

What is the treatment of cryptococcus meningitis?

A

Induction: liposomal amphotericin, flucystosine

Consolidation: fluconazole

chronic maintenance: 12 months of fluconazole

control of ICP: daily LP until <25cm H2o

83
Q

At what CD4 cell count does CNS toxoplasmosis usually occur?

A

<100 or even <100

84
Q

How to diagnose CNS toxoplasmosis?

A

Toxo IgG + serum
PCR of CSF for toxo
imaging; ring enhancing lesions

85
Q

How to treat CNS toxoplasmosis

A

Bactrim

86
Q

What is the treatment for CMV retinitis?

A

sight-threatening lesion: ARV, IV ganciclovir, intravitreal ganciclovir

Small-peripheral lesion
- ARV, Oral valganciclovir

87
Q

What are common drugs that impact T cells?

A

Purine analogues: Fludarabine, cladribine, antithymocyte globulin

88
Q

Describe step mitis

A

lives in mouth
gram +ve in cocci in clusters
alpha haemolytic

89
Q

Describe viridans streptococci in neutropenic patients

A

Fevers, rash and stomatitis

often neutropenia, mucositis, high dose cytarabine

associated with VGS shock syndrome, ARDS

90
Q

Describe neutropenic enterocolitis (Typhlitis)

A

usually mixed infection- GN, GP, anaerobic

91
Q

What is sweet syndrome?

A

febrile neutrophilic dermatosis
a skin reaction to a systemic disease like RA
“intense neutrophilic dermal infiltrate in the reticular dermis)

92
Q

What is the MOA of classes of anti fungal agents?

A

echinocandins: inhibits the enzyme that synthesises B-glucans, called the “penicillin of antifungals”

Polyenes (eg amphotericin B): bind ergosterol, weaken the membrane, cause pore formation, leakage of K+ and Na+, fungal cell death

Azoles: inhibit the enzyme that synthesis ergosterol

5-Flucytosine (5-FC)- is converted to F-FU to inhibit DNA synthesis as a pyrimidine analog. can cause myelosuppression

93
Q

Describe fungal testing

A

blood culture- only good for candida

Cell wall test:
- galactomannan - for aspergillus and histoplasma, fusarium, cryptococcal
- b-glucan- fungal cell wall eg candida, aspergillus, pneumocystis, fusarium
- cyptococcus antigen
- histoplasmosis antigen

PCR tests
- pneumocystis, aspergillus

94
Q

How to treat candidaemia in a neutropaenic patient?

A

caspofungin 70mg IV load, then 50mg IV daily

95
Q

What do we NOT use for cryptoccous ?

A

Caspofungin

CRAP- cryptococcus and caspofungas

96
Q

What organism is most likely to cause hepatosplenic candidiasis syndrome?

A

Candida albicans

97
Q

Which malignancy is invasive mould infections most commonly seen in?

A

AML

98
Q

What is the treatment of choice for invasive aspergillosis?

A

Voriconazole

99
Q

What is nocardia and how do we treat it?

A

Treat with Bactrim!

100
Q
A

Aisha (33 decks)

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