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RACP Written Exam > Infectious Disease > Flashcards

Infectious Disease Flashcards

1
Q

Which are the live vaccines

A

“MOBY-VRT”:

  • MMR
  • Oral polio (IPV is ok)
  • BCG
  • Yellow fever
  • Varicella (and varicella zoster)
  • Rotavirus
  • Oral Typhoid (inactivated parenteral vaccine is ok)
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2
Q

When are live vaccines contraindicated?

A
  • > 20mg prednisolone / day
  • HIV positive with CD4<200
  • anti-TNF meds
    (+ some primary immunodeficiencies)
Other immunosuppressants (eg. azathioprine, MTX) - risk unclear.
Suggest being off all these Rx for at least one month (best 3 months) before giving

Note: other inactivated vaccines may be safe but ineffective - may not make protective antibody response

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3
Q

Criteria for DHF:

A
  • fever / recent acute fever
  • haemorrhagic manifestations
  • low platelet count (≤100,000)
  • leaky capillaries:
    • raised haematocrit (20% or more above baseline)
    • low albumin
    • pleural or other effusions
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4
Q

Criteria DSS:

A

4 criteria for DHF plus evidence of circulatory failure (rapid, weak pulse, hypotension)

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5
Q

Standard short course of Tx of Tb:

A

2HRZE / 4HR

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6
Q

5 Mechanisms of Antibiotic Action:

A
  1. Cell wall synthesis inhibition
  2. Protein synthesis inhibition
  3. Nucleic acid synthesis inhibition
  4. Cell membrane disruption
  5. DNA damage
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7
Q

Which classes of antibiotics inhibit cell wall synthesis? How?

A
  1. Beta-lactams (penicillins, cephalosporins, carbapenems) - bind to PBPs and prevent cross-linking of peptidoglycans
  2. Glycopeptides (vancomycin, teicoplanin) - bind molecular building blocks
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8
Q

Which classes of antibiotics inhibit protein synthesis? How?

A
  1. Macrolides (erythromycin) - inhibits translocation - 50s subunit
  2. Aminoglycosides (gentamicin, amikacin) - inhibit mRNA translation - 30s subunit
  3. Tetracyclines (doxycycline) - prevent elongation of peptide chain - 30s subunit
  4. Chloramphenicol
  5. Linezolid
  6. Fusidic acid
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9
Q

How do antibiotics inhibit DNA (nucleic acid) synthesis? Which classes?

A

(a) Inhibit DNA gyrase (and topoisomerase II):
- Quinolones (ciprofloxacin)

(b) Inhibit folic acid synthesis:
- Trimethoprim (dihydrofolate reductase innhibition)
- Sulphamethoxazole

(c) Inhibit RNA polymerase:
- Rifamycins (rifampicin)

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10
Q

Which antibiotics disrupt cell membrane synthesis?

A

Colistin

Daptomycin

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11
Q

Which class of antibiotics acts by causing DNA damage via free radicals?

A

Nitroimidazoles (metronidazole)

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12
Q

Explain the difference between gram positive and gram negative bacteria

A

-

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13
Q

Gram positive (purple) “bunches of grapes” on microscopy - which organism?

A

S. aureus

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14
Q

Gram positive chains. Which bacterial spp?

A

Streptococcus

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15
Q

Gram negative intracellular diplococci. Which organism?

A

Neisseria meningitidis

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16
Q

Rash after some antibiotics may indicate Dx other than allergy. Which antibiotics? Which alternate Dx?

A

Acute EBV infection + amoxycillin / ampicillin –> erythematous rash

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17
Q

4 main mechanisms of antibiotic resistance and an example of each:

A
  1. Altered target sites
    eg. Penicillin-binding proteins (PBPs) altered in MRSA and penicillin-resistant S.pneumoniae
  2. Inactivating enzymes
    Eg. Beta-lactamases, aminoglycoside-modifying enzymes
  3. Decreased permeability
    Gram negative bacteria
    Eg. Loss of porins in enterobacteriaceae –> resistance to beta lactams
    Eg. Enterobacteriaceae and pseudomonas - trimethoprim and some fluorquinolones
  4. Active Efflux
    Tetracyclines (rare mechanism)
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18
Q

Types of beta-lactamases:

A

Beta lactamases hydrolyse and thus inactivate beta-lactams.

  1. Some inhibited by beta-lactamse-inhibitors (clavulanic acid, tazobactam, sulbactam) - eg. S. aureus
  2. ESBL (extended-spectrum beta lactamase): various types; usually enterobacteriaceae (E.coli, K.pneumoniae, Enterobacter spp.). Resistance to penicillins and all cephalosporins. Plasmid mediated.
    Treat with carbapenems.
  3. Carbapenemase / Metallobetalactamase: Eg. New Delhi Metallobetalactamase (NDM-1) in enterobacteriaceae
  4. Chromosomal betalactamases:
    All gram negatives, but many do not produce in significant amounts (H. influenzae, E.coli, P. mirabilis, Shigella, Salmonella); Klebsiella produces a penicillinase so is still susceptible to cephalosporins.
    The ESCAPPM group have inducible chromosomally-mediated betalactamase production. They may appear susceptible in vitro but resistance is activated in vivo when exposed.
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19
Q

Four mechanisms by which bacteria acquire resistance:

A
  1. Plasmid transfer during direct cell-to-cell contact [conjugation]

Plasmids are circular molecules of dsDNA independent of the chromosome.

  1. Bacteriophages transfer bacerial DNA [transduction]

A bacteriophage is a bacterial virus that replicates within the bacterial cell and can incorporate a piece of bacterial SNA into the asembled viral particle, which is then transferred to the next bacterial cell it infects.

  1. Uptake of naked DNA from the environment [transformation]

Transposons are “jumping genes” - mobile segments of DNA that move to different positions in the genome.

  1. Chromosomal mutation
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20
Q

ESCAPPM bacteria - which organisms and what is the significance?

A 
E = Enterobacter
S = Serratia
C = Citrobacter
A = Acetinobacter
P = Pseudomonas
P = Proteus (non-mirabilis)
M = Morganella morganii

These organisms have INDUCIBLE chromosomally-mediated betalactamase production (against penicillins and cephalosporins).

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21
Q

What does ‘retrovirus’ mean?

A

A virus (RNA virus) that uses the process of reverse transcription to integrate its genome into host DNA

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22
Q

What type of virus is HIV?

A 
Retrovirus
Lentiviridae family (lenti = slow)
23
Q

HIV subtypes - what do they mean?

(i) HIV1 vs HIV2 (ii) M/O/N (iii) A/B/C etc

A

(i) HIV1 = most of HIV we see; HIV2 = theoretically less virulent, rare, seen in West Africa.

(ii) TYPES
M = ‘Most’ (Major)
O = ‘Other’ (never see - geographically restricted to West Africa)
N = ‘New’ (never see)

(iii) Type M has multiple SUBTYPES
(HIV mutating all the time)
B = most common in first-world residents (‘rich white people’)
C = more common in SSH Africa, immigrants

24
Q

What is ‘tropism’ wrt HIV’s entry to cells?

A

The ability to enter different cells and establish productive infection.

HIV uses different co-receptors to gain entry to different cells, eg.
CxCR4 - T cell lines
CCR5, CCR3, CCR2a - macrophage entry
CCR6 - macrophage and T cell entry

25
Q

What is the process of cell entry for HIV?

A
  1. Attachment - on contact with cell
  2. CD4 binding (firmer)
  3. Conformational change - triggered by CD4 binding:
    viral protein (GP120) changes shape to bind to co-receptor
  4. Co-receptor binding
  5. Membrane fusion
26
Q

What are the main receptors used for HIV entry?

A
  1. CD4 receptor
  2. Co-receptors - essential for viral entry
    (a) CCR5 - macrophage entry (m-tropic)
    (b) CXCR4 - T cell entry (t-tropic)
27
Q

HIV CCR5 co-receptor - what is the significance?

A

Most HIV is CCR5 tropic (“R5 virus”) ie. uses CCR5 co-receptor to enter macrophages.
CCR5 seen in primary infection and early infection.
R5 is required for initial infection!
Can block CCR5 receptors without harming humans.

28
Q

HIV CXCR4 co-receptor - what is the significance?

A

CXCR4 tropic HIV (“X4 virus”) uses CXCR4 co-receptors to enter T cells.
This develops with disease progression in approximately 40% of patients (ie. emerges late - virus develops ability to use X4).

Some HIV viruses will be dual-tropic (R5X4) - perhaps during transition from R5 to X4.

Unfortunately blocking CXCR4 receptors causes severe toxicity.

29
Q

What is retroviral integrase?

A

Retroviral integrase is an enzyme produced by a retrovirus (such as HIV) that enables its genetic material to be integrated into the DNA of the infected cell.

30
Q

What is retroviral protease?

A

HIV protease cleaves newly synthesized polyproteins at the appropriate places to create the mature protein components of an infectious HIV virion.
Without effective HIV protease, HIV virions remain uninfectious.

31
Q

What is retroviral reverse transcriptase?

A

Enzyme used to generate complementary DNA (cDNA) from an RNA template ( = ‘reverse transcription’)

Used by the retrovirus to convert single-stranded genomic RNA into double-stranded cDNA which can integrate into the host genome.

32
Q

How does HIV go from exposure to widespread dissemination within the host?

A

mucosal exposure to HIV-1

> selective infection by R5 strains

> fusion of dendritic cells and CD4+ lymphocytes

> transport of virus to regional lymph nodes

> spread of infection to activated CD4+ T lymphocytes
[explosive replication of virus]

> entry of virus infected cells into bloodstream

> widespread dissemination

33
Q

Which cells are targets of HIV?

A
  1. CD4+ T lymphocytes
    • Massive and early depletion of resting memory T-cells in the GIT
  2. Monocytes and macrophages
    • CD4+ and CCR5, CXCR4 CCR3 receptors present
    • Tissue macrophages in brain (glial cells), lung, gut, BM monocyte
    precursors, lymphoid tissue macrophages
    • Macrophages are chronically infected and serve as a reservoir
  3. Dendritic cells
    • allow HIV entry, but productive infection is rare
  4. Thymic progenitor cells
  5. CD34+ progenitor cells

Long-lived cells that turnover slowly act as a reservoir and a barrier to infection (when do eventually turn over they release more virus –> reinfection)

34
Q

Which mechanisms help the host resist HIV?

A
  1. CCR5 receptor mutation
    - delta 32 is best known mutation
    - 10% caucasions heterozygous: slower progression
    - 1% caucasians homozygous: highly resistant to infection (would only be infected if had blood transfusion with X4 strain)
  2. SDF-1 (CXCR4-binding chemokine) mutation: enhances survival with untreated HIV

many other examples exist

35
Q

Explain the pattern of disease progression in untreated HIV

A

Peak of viral load - correlates with seroconversion illness (if present)
Also correlates with initial CD4 count nadir

Immune reaction then drives viral load down and CD4 count rebounds somewhat - steady state reached between virus and CD4 cells (clinical latency)

Over time the immune system is exhausted and CD4 counts drop, viral load increases and opportunistic infection develop (progression to AIDS)

36
Q

Factors for favourable course of HIV progression (if untreated):

A

VIRAL:
- attenuated strain (eg. D nef) - nef gene deletion; Sydney blood bank cohort did well, until eventual HIV dementia and AIDS

HOST:

  • Genetic: CCR5 delta 32 mutation (heterozygous - homozygous would resist initial infection)
  • HLA: B57 - allergic to abacavir, but do better overall!
  • Age: extremes of age –> poorer prognosis
37
Q

Risk of developing AIDS within next 3 years is related to which 2 factors primarily (if untreated)?

A

Mellors 1996:

  • Lower CD4 count
  • Higher viral load

Eg. If CD4 count >750 then risk in next 3 years low
Eg. If viral load <500 - almost none develop AIDS in next 3 years

However, all this has changed as treatment of all cases now recommended

38
Q

What is the microbial translocation theory in HIV?

A
  • Massive depletion MALT (mucosa-associated lymphoid tissue) in early HIV infection
  • Rebound of T cell count in blood may not occur in gut
  • Leakage of microbial products (eg. LPS from GN cell wall) across gut wall leads to CHRONIC IMMUNE ACTIVATION
  • This is lowered but not eliminated with HAART
  • Theory: contributes to non-AIDS complications in HIV (eg. CVD)
39
Q

What is the main barrier to HIV cure and the focus of research for cure?

A

With current therapy HIV can be eliminated from pool of rapidly-replicating cells.

However, latency in slower-replicating cells cannot currently be eradicated (can treat to undetectable level, but not eliminate).

Aim of research is to identify and then target cells harbouring latent virus, or drive latent virus out of these cells to enable treatment.

40
Q

CD4 T cells are detroyed by multiple mechanisms in HIV infection. What are these?

A
  1. Direct infection of CD4+ T cell (GIT>blood)
2. Indirect
• Immune activation (microbial translocation)
• Apoptosis
• Innocent bystander
• Syncytium formation
  1. Infection of CD4 progenitor cells (CD34+) and
    thymocyte depletion
41
Q

Why are patients infected with HIV still at risk of opportunistic infection after rebound of CD4 count with HAART?

A

Both memory and naive T cells lost with HIV infection.

Only a small population of memory cells remain.

HAART stimulates CLONAL EXPANSION of this population –> normal number of T cells but with limited repertoire.

Therefore, while don’t usually see opportunistic PJP with CD4 >200, continue with bactrim for at least 6 months once regain this count.

42
Q

Why is it that HIV is a rapidly changing virus? Why can resistance to medications develop quickly?

A

Reverse transcription errors happen frequently (1 or more error per genome, 10 billion replications per day) - reverse transcriptase is a low fidelity enzyme.

Errors can lead to: escape from host immune responses, drug resistance, changes in cell tropism.

Selection pressure exerted by ARVs if ongoing viral replication (lack of adherence, high initial viral load).

43
Q

Does HIV genotype testing tell you whether a patient will respond to a particular ARV?

A

NO.
NOT sensitivity testing.
Only identifies mutations that have been associated with reduced drug susceptibility.

Useful to decide which treatments UNLIKELY to be effective (NOT what they WILL respond to).
Do not currently have ability for HIV phenotyping.

In patients on treatment:
Tests predominant viral quasispecies at the time (ie. the quasispecies selected by the patient’s CURRENT therapy).

44
Q

When is HIV genotype testing indicated, and why?

A
  1. At HIV Dx (Ie. ART naive patients, prior to commencing HAART) - to look for transmitted resistance (uncommon, as treat early).
  2. When HAART is failing (but good adherence - only test while STILL ON Rx) - want to look for resistant strains. If off Rx then wild type will have overgrown.
45
Q

When NOT to do HIV genotype?

A
  1. Stopped taking HAART
  2. Suppressed viral load (not possible)
  3. Will not change management (patient refuses to take or change medication)
46
Q

Which forms (4) of congenital heart disease are associated with the highest risk of IE?

A
  1. Cyanotic congenital heart disease
  2. Right-sided lesions
  3. Tetralogy of Fallot
  4. VSD with Aortic Regurgitation

(Congenital HD makes up 2-18% of all IE; incidence 15-140x gen pop)

47
Q

Modified Duke criteria - what are the 3 major criteria for IE?

A
  1. Positive blood cultures: either (a) OR (b)
(a) 2 cultures with typical organism: 
> S. viridans group
> S. bovis (now gallolyticus) 
> S. aureus
> Enterococcus
> HACEK
(b) persistently positive BCs (3/3 or majority of 4+) consistent with IE
  1. Endocarditis (a) and / or (b)
(a) Echo evidence:
> vegetations
> abscess
> partial dehiscence of prosthetic valve
(b) NEW regurgitant murmur
(NOT a change in an old murmur)
  1. Coxiella burnetti:
    culture or serology (antiphase I IgG antibody titer >1:800)
48
Q

Modified Duke criteria - what are the 5 minor criteria for IE?

A
  1. Fever >38’
  2. Predisposition:
    predisposing heart condition or IDU
  3. Positive blood cultures consistent with IE that do not meet major criteria
    (NOT single culture of CoNS or an organism that does not cause IE)
  4. Vascular phenomena:
    major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, Janeway lesions
  5. Immunologic phenomena:
    RF +ve, nephritis (haematuria), Osler’s nodes, Roth spots, clubbing
49
Q

Definite IE by the Duke criteria:

A

Pathological criteria: histology or gram stain / culture results from surgical or autopsy specimens.

Clinical criteria:
2 M
1 M + 3m
5 m

50
Q

Possible IE by the Duke criteria:

A

1M + 1m
or
3m

51
Q

Rejected IE by the Duke criteria:

A

Firm alternate diagnosis

Resolution with antibiotic therapy ≤4 days

No pathologic evidence of IE at surgery or autopsy after antibiotic therapy for ≤ 4 days

Does not meet criteria for possible infective endocarditis (ie. 1M+1m or 3m)

52
Q

What is the significance of Streptococcus gallolyticus (previously bovis) on blood cultures in possible IE?

A

Often a GIT or GUT source.
Associated with colonic polyps or tumours –> therefore need colonoscopy.

3rd most common cause of IE
Increasing AB resistance

53
Q

What is the significance of Streptococcus milleri (or anginosus) group on blood cultures in possible IE?

A

Often associated with invasion / abscess formation.

Can present as acute or subacute
15% of Strept IE
A subgroup of S. viridans group

54
Q

What are the differences between nmMRSA and mMRSA?

A

mMRSA (multiresistant MRSA or sometimes referred to as healthcare-associated MRSA) are strains that have adapted to spread
and cause infections in the healthcare setting. The major hospital-associated strain in Australia is resistant to all penicillins,
cephalosporins and methicillin (oxacillin), plus three or more of the non-beta-lactam antibiotics (erythromycin, cotrimoxazole,
gentamicin, rifampicin, fusidic acid, ciprofloxacin, tetracycline).
• mMRSA first appeared in the 1960s and has typically been linked to persons with healthcare associated risk factors
such as hospitalisation or nursing home care, chronic dialysis, antibiotic treatment, or exposure to invasive devices
or procedures.
nmMRSA (non-multiresistant MRSA or sometimes referred to as community-associated MRSA) are strains that have arisen in the
community and cause similar types of infection to other strains of S. aureus found in the community. They are usually resistant to
all penicillins, cephalosporins and methicillin (oxacillin), plus up to two of the non-beta-lactam antibiotics (erythromycin,
cotrimoxazole, gentamicin, rifampicin, fusidic acid, ciprofloxacin, tetracycline).
• nmMRSA infections usually occur in a person who does not have any prior history of a healthcare exposure such as
hospitalisation, surgery, permanent intravenous lines or other indwelling devices, or haemodialysis.
• nmMRSA strains of S. aureus are different from mMRSA strains.
• The most frequent infections caused by nmMRSA are skin and soft tissue infections that typically present as boils,
abscesses, or cellulitis.

RACP Written Exam (7 decks)

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