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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

acts against gram +ve

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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

high volume of distribution

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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 but longer half life

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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 (ampC, EBSL, CRE)

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

note cefepime is still effective

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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

HSV meningits- CSF often has many red cells
mollaret’s recurrent meningitis usually associated with HSV-2

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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

Dex helps with s.pneumonia, h.influenza (hearing loss)

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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? particularly CD4 <100

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 produced

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42
Q

What is the other name with streptococcus gallotyicus?

A

AKA strep bovis
associated with colon pathology such as cancer

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43
Q

What are HACEK organisms?

A

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

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44
Q

What are examples of culture-negative endocarditis?

A

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

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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

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46
Q

How to treat streptococcal IE specific therapy?

A

Depends on penicillin MIC

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47
Q

How to treat enterococcal IE?

A
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48
Q

What are some oral options for Infective endocarditis?

A

Many thing, but can trial linezolid + rifampicin

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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)

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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)

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51
Q

What is the IE prophylaxis?

A
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52
Q

What is the CURB-65 score?

A
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53
Q

When can you use steroids with pneumonia?

A
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54
Q

What is Multi-drug resistant tuberculosis?

A

TB resistant to isoniazid and rifampicin.

note isolated rifampicin every rare, usually indicated MDR

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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

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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

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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

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58
Q

Is Q.gold affected by BCG vaccine?

A

NO

unlike mantoux test

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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

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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

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61
Q

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

A

subacute presentation

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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.

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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
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64
Q

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

A

Cefepime

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65
Q

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

A

anti-biofilm activity

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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 integrase 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 (survival benefit)

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

necrotizing inflammation with transmural infection of the damaged bowel wall.

Mx- medical

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? And what is it?

A

Candida albicans

hepatosplenic candidiasis syndrome is an inflammatory response to fungi invaded by portal vasculature. presents after engraftment.

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

Drugs and common opportunistic infection

A
  • TNF-alpha inhibitors (infliximab >adalimumab > etanercept): Hep B, HSV, tuberculosis, nocardia, PJP, candida
  • Anti-B lymphocyte (rituximab)- Hepatitis B
  • IL-17 (secukinumab)- mucocutaneous and URT infections
  • JAKi – increase risk of VZC (herpes)
  • Bruton tyrosine kinase inhibitors- aspergillus, PJP, cryptococcus
  • Integrin (natalizumab)- PML
  • Eculizumab- Neisseria
101
Q

Describe the management of common fungi

A

aspergillus: voriconazole, isavuconazole or amphotericin B

zygermycosis/mucormycosis: amphotericin then posaconazole or isoconazole

Candida: echinocandins, azoles

cryptococcal meningitis: 5-FU

102
Q

What are examples of bugs that cause mucurmycosis and Scedosporium

A

mucurmycosis: mucoracea, absidia, rhizomucor, Rhizopus

Scedosporium: S.apiospermum, S.prolificans

103
Q

how long before a solid organ transplant should you avoid live transplants?

A

28 days

104
Q

What common food sources cause diarrhoea?

A
  • Beef: STEC, c.perfinges
  • Poultry: campylobacter, salmonella
  • Pork: yersinia
  • Shellfish: vibrio parahaemolyticus, norovirus
  • Eggs: non-typhoidal salmonella
  • Unpasteurised milk or dairy produce- non-typhoidal salmonella, campylobacter, yersinia, S.aureus endotoxin
  • Rice: bacillus cereus
105
Q

What common microorganisms are associated with certain infections?

A
  • Reactive arthritis: campylobacter, salmonella, shigella, yersinia
  • Gullain barre syndrome: campylobacter
  • Haemolytic uraemic syndrome: shiga-toxin producing E.coli (STEC)
  • Extraintestinal sites of infection: mycotic aneurysm, aortitis with salmonella
  • Appendicitis-like presentation: yersinia
  • Liver abscess: entamoeba histolytica
106
Q

What is the incubation period for norovirus? Transmission and symptoms?

A

Incubation period: 10-50 hours

transmission: faecal-oral route, droplet spread; contact with fomites; food, water or environmental contamination

Symptoms: sudden onset vomiting +/- watery diarrhoea, fever, can be asymptomatic. Lasts 2-3 days.

107
Q

Describe the management of C.Diff

A

*Asymptomatic: no treatment
*Mild: stop abx
*Moderate: PO vancomycin 125mg q6hrly or fidaxomicin 200mg BD for 10 days
*Severe: PO/NGT vancomycin +/- metronidazole or; or fidaxomicin
*Fulminant- (hypotension or shock; ileus or megacolon)
* PO vancomycin 500mg q6hrly plus IV metronidazole
* Early surgical view

First recurrence: PO vancomycin, tapering course; or fidaxomicin

Multiple recurrences (>2)- consider faecal microbiota transplant (FMT)
* Bezlotoxumab (monoclonal antibody against c.diff) +standard treatment

108
Q

What is immunity to influenza A and B mediated by?

A

IgG and IgA antibodies against haemagglutinin

109
Q

Describe the incubation period for COVID-19, MPOX, rabies, typhoid, rocky mountain spotted fever, dengue

A

Acute (<10 days): dengue, influenza, zika , chikunguya, Rocky Mountain
Intermediate (10-21 days), malaria, viral hemorrhagic fever, typhoid, MPOX
Chronic (>21 days): malaria, hepatitis, TB

  • COVID-19: 2-14 days
  • Rabies 4 days to years
109
Q

What is the investigation and treatment of typhoid?

A

classically has ‘rose spots’

Diagnosis: Culture stool and blood. Bone marrow culture most sensitive, but not usually warranted
Widal test

Treatment:
o Empiric: azithromycin or ceftriaxone
o Infection in Pakistan: carbapenem
o Dexamethasone adjunctive treatment in severe infection
o Assessment for chronic carriage and eradication (e.g. ciprofloxacin 500mg BD for.4 weeks)

110
Q

Describe phases of dengue fever and treatment

A

Febrile phase: fever, headache, sore throat, transaminitis

Critical phase: capillary permeability (extravasation of fluid- pleural effusion, ascites, haemoconcentration, intravascular volume depletion), thrombocytopenia and disordered coagulation (internal haemorrhage), severe dengue (organ involvement- can see myocarditis, hepatitis, CNS involvement).

Recovery phase

Treatment and prevention
o Supportive therapy: use of fluids +/- whole blood
o Vaccine: dengvaxia (live, 3 doses over 12 months)

111
Q

Describe the clinical presentation of chikunguya infection and treatment

A

acute
fever, sore bones and muscles, rash
severe: Encephalitis, myocarditis, hepatitis, pneumonitis, pancreatitis, multiorgan failure

Diagnosis: PCR

Treatment: supportive

112
Q

Describe the clinical presentation of Zika virus, diagnosis and treatment

A

Acute
a lot are asymptomatic
Symptoms: fever, rash, joint pain, body aches, headaches, red watery eyes (non-purulent conjunctivitis), swelling of hands and feet

113
Q

Viruses and relation to eyes

A

ZIKA-red watery eyes (non-purulent conjunctivitis)
DENGUE- retro-orbital headache
measles- conjunctival injection and crusty eyes

114
Q

Fever in returned traveller

A
115
Q

What is Wolbachia?

A

Used as vector control to get rid of mosquitos

116
Q

What are the main causes of cellulitis?

A

B-haemolytic streptococci (s.dysgalactiae) + group A (s.pyogenes), staph aureus (purulent)

If marine exposure –> vibrio, aeromonas speciies

Dog/cat bite: pasteurella multicoda, capnocytophagia canimorsus

117
Q

Management of necrotising soft tissue infection

A

IV clindamycin or linezolid

118
Q

List CURB65

A

confusion
urea >7
RR >30
BP systolic <90
Age >65

if 0-1 it is low severity, if 2= mod severity, 3-5 is high severity

119
Q

What is the management of genital herpes?

A

first episode- valaciclovir for 7-10 days, acyclovir 400mg TDS for 7-10 days

recurrent episodes: valaciclovir 500mg BD for 3 days, acyclovir 800mg TDS for 2 days, famciclovir 1gm PO for 1 day

120
Q

Describe what tremponema palladium looks like

A

Corkscrew-shaped, motile microaerophillic bacterium

121
Q

Describe the natural history of syphillis

A

o Early syphilis (<2 years) 1/3 spontaneous resolution, 1/3 infected without clinical disease (Latent phase), 1/3 tertiary syphilis

122
Q

Is a chancre in syphillis painless or painful?

A

Painless

note secondary syphillis occurs 2-8 weeks after the chancre

123
Q

What are some ocular findings in latent syphillis?

A

Argyll Robertson pupils
optic atrophy

124
Q

Describe the tests for syphillis

A

Direct test: dark ground microscopy, direct fluorescent antigen (DFA), tremponemal NAAT (PCR)

Serology test
- screening test: chemiluminescence immunoassay (CMIA) or enzyme immunoassay (EIA)
- treponema test (TPPA), TPHA
- non-treponemal test (Rapid plasma reagin test RPR, VDRL, measure of disease activity)’

Once infected, syphilis serology stays positive for life
- RPR/VDRL used to determine cure and re-infection
o 2 titre (4 fold) reduction in RPR= cure
o 2 titre (4 fold) increase in RPR post cure = re-infection

125
Q

Describe the treatment of syphillis

A

Early: 2.4 million units IM benzathine penicillin G as a single dose OR procaine benzylpenicillin 1.5g IM, daily for 10 days

Late: 2.4 million units IM benzathine penicillin G once weekly for 3 weeks OR procaine benzylpenicillin 1.5g IM, daily for 15 days

o If neurological involvement: 2.4g procaine penicillin plus probenecid OR benzylpenicillin OR doxycycline

o Tertiary: benzylpenicillin 1.8g IV QID for 15 days

126
Q

Describe the treatment of chlamydia and gonorrhoea

A

Chlamydia
- asymptomatic: doxycycline 100 mg orally, 12-hourly for 7 days OR for pregnant women or patients likely to be nonadherent to doxycycline: azithromycin 1 g orally, as a single dose.

IF causing PID: Cef + doxy/azithro

127
Q

What are the HACEK organisms?

A
  • Haemophilus species
  • Aggregatibacter actinomycetemcomitans
  • Cardiobacterium hominis
  • Eikenella corrodens
  • Kingella kingae
128
Q

Describe the vaccine schedule in a post-splenectomy patient

A

pneumococcal: PCV13 (conjugate) then 8 weeks later PPV23 (polysaccharide)

Meningococcal

HiB

Influenza annually

129
Q

Describe the treatment of CMV

A

Ganciclovir or valganciclovir
Foscarnet
Cidofovir
Marabivir

Prophylaxis: Valganciclovir, letermovir

130
Q

What CD cell is implicated in infectious mononucleosis/EBV?

A

CD8+ T cells

131
Q

How to treat pregnant woman who have been exposed to varicella

A

Post-exposure prophylaxis with varicella immunoglobulin if <4 days and non-immune.

Consider oral acyclovir if exposure >4 days

Do NOT give varicella vaccine to pregnant woman due to risk of congenital disease

Highest risk of fetal varicella syndrome during 12-28 weeks gestation

132
Q

What are koplik spots?

A

seen in measles

133
Q

What deficiency in measles prolongs recovery and worsens measles recovery?

A

Vitamin A deficiency

134
Q

What is the Japanese encephalitis virus?

A

RNA virus of genus flavivirus

135
Q

What to do if expose to rabies/monkey bite?

A

Rabies immunoglobulin and rabies vaccination now

136
Q

Genital ulcers, what are painful and what not?

A

Painful: herpes, H.ducreyi (usually only one present)

Painless: C.trachomantis, T.pallidum

137
Q

What is ceftaroline?

A

5th generation cephalosporin

acts against gram +ve bacteria and resistant strep pneumo

138
Q

What is Dalvavancin and oritavancin?

A

2nd generation lipo-glycopeptide family
inhibits bacterial cell wall biosynthesis

long half life

139
Q

What is first line therapy for new delhi mutation?

A

Ceftazidime- avibactam + aztreonam

Avibactam is used to protect aztreonam against b-lactamase enzymes, allowing aztreonam to work

superior to previous colistin-based combination therapy

140
Q

What type of virus is dengue?

A

mosquito-transmitted flavivirus

vectors: aedes aegypti, a.albopictus, a.polynesiensis

141
Q

Yellow fever vaccination as a single dose is protective, true or false?

A

true

141
Q

What is the gram stain for scrub typhus?

A

gram -ve coccobacillus
trasmitted by chigger mites

142
Q

What are the symptoms of scrub typhus? treatment?

A

usually begin within 10 days of being bitten: fever, headaches, diffuse myalgias, mental status changes, lymphadenopathy, rash, pneumonia

treatment: doxycycline

143
Q

What is Lyme disease?

A

a tick-borne illness caused by spirochete borreliella species in america, Europe and asia

erythema migraines
fatigue, HA, neck stiffness, myalgia, arthralgia, lymphadenopathy, fever

Neuroborreliosis: lymphocytic meningitis, cranial nerve palsies, encephalomyelitis

carditis: AV block +/- my-pericarditis

treatment: CNS disease give ceftriaxone, cefotaxime or penicillin
isolated facial nerve palsy –> doxycycline

144
Q

African trypanosomiasis

A
145
Q
A

Leprosy (Leonine facies)

146
Q

Vomiting, diarrhoea, peri-oral paresthesias, metallic taste, blurred vision, temperature-related dysesthesias (cold stimuli perceived as hot) after eating coral fish in Fiji:

A

Ciguatera fish poisoning

147
Q

Meningoencephalitis after swimming in a fresh and warm water source:

A

Primary amoebic meningoencephalitis (Naegleria fowleri)

148
Q

Regarding HIV testing, how soon can it be detected?

A

Within 3 days
according to the timing:
HIV NAAT > p24 4th generation assay antibody and p24 detection > 3rd generation assay antibody

149
Q

Describe first, second, third and 4th generation testing for HIV

A
150
Q

Tenofovir alafenamide (TAF) vs tenofovir disoproxil fumarate (TDF)

A

TAF is a prodrug of TDF converted to TDF intracellularly, therefore it has less systemic effects

therefore TAF has less BMD loss and less renal toxicity

151
Q

Is hepatitis B DNA or RNA?

A

Hepatitis B is a DNA virus which replicates by reverse transcription

152
Q

How are emtricitabine and lamidudine related?

A

emtricitabine (FTC) is a fluroinated lamivudine (3TC)

153
Q

Describe treatment of HIV + HBV coinfection

A

emtricitabine AND tenofovir

do not use emtricitabine or lamuvidine alone as resistance to HBV occurs quickly.

if tenofovir cannot be used- then you can use entecavir- but it only has weak HIV activity

154
Q

Describe the timing of IRIS in cryptococcosis

A

weeks or months after ARVs and anti fungal RX for meningitis

can get fevers, headache, seizures, CN palsies, new MRI lesions

all culture negative

Mx: NSAIDS or pred

155
Q

Which conditions are associated with immune reconstitution inflammatory syndrome (IRIS)?

A

sarcoidosis, Grave’s, increased folliculitis

MTB, MAI, cryptococcus, CMV

156
Q

Describe side effects of amphotericin B

A

renal failure
renal tubular acidosis 1

157
Q

how to distinguish between mucormycosis and aspergillus in the lab?

A

mucor is non-septate
aspergillus is septate

158
Q

Prophylaxis for CMV?

A

Prophylaxis: letermovir, valganciclovir

treatment: ganciclovir, valganciclovir, cidofovir, maribavir

Also can do pre-emptive strategy: check weekly, and if >1000 IU/mL of CMV DNA or 5-fold rise- then treat with ganciclovir, valganciclovir

159
Q

Which type of organ transplant carry a higher risk of acquiring CMV disease?

A

lung and bowel transplant recipients rather than kidney and liver transplant

160
Q
A

Aisha (47 decks)

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