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Infectious Agents > Clinical Micro > Flashcards

Clinical Micro Flashcards

1
Q

Subacute sclerosing panencephalitis is associated with which slow virus ?

A

Measles virus

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2
Q

Which slow virus is associated with progressive rubella panencephalitis ?

A

Rubella virus - v rare complication

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3
Q

Progressive multi focal leukoenceohalopathy (PML) is associated with which slow virus ?

A

JC Polyomavirus

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4
Q

What are the criteria for slow viruses?

A
  • prolonged incubation (months to years)
  • clinical course of infection leading to death
  • pathology limited to single organ - the brain
  • limited to single host species
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5
Q

Which was the first transmissible spongiform encephalopathy to be described ?

A

Scrapie, from sheep and goats

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6
Q

First human transmissible spongiform encephalopathy to be described ?

A

Kuru

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7
Q

Differences in CJD and vCJD?

A

Onset: CJD= 55-70, vCJD= 14-52
Symptoms: CJD= dementia + myoclonus, vCJD= behavioural + ataxia
Clinical course: CJD=rapid, vCJD= insidious onset, prolonged course
Path: CJD= PrPSC in synapses vCJD= prominent florid plaques

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8
Q

Pathogenesis of sporadic CJD

A

Spontaneous Transformation of normal host-encoded prion proteins to aberrantly folded protease resistant forms - it is NOT transmitted

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9
Q

Pathogenesis of vCJD ?

A

Linked with BSE, Transmitted by eating infected meat, in particular parts of CNS

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10
Q

What is gerstman-straussler-Scheinker syndrome (GSS)

A

Rare inherited prion disease, characterised by adult onset of loss of memory and dementia, ataxia and pathological deposition of amyloid b plaques
(TSE)

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11
Q

Prions are resistant to inhibition by ?

A
  • extremely heat resistant
  • irradiation
  • DNAse
  • RNAse
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12
Q

Prions are susceptible to ?

A
  • urea
  • phenol
  • other protein denaturing treatment
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13
Q

Classic epidemiological study

A

John snow, cholera

a removal of broad street pump in soho, London, broke cycle of infection

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14
Q

Outline Koch postulates (4)

A
  • the microorganism must be present in all cases of the disease
  • the pathogen can be isolated from hist and grown in pure culture
  • the pathogen form pure culture must cause disease with typical symptoms (when inoculated in lab animal)
  • the pathogen must be re isolated from artificially inoculated subjects
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15
Q

21st century version of Kochs postulates applied to virulence genes ?

A
  • gene encoding virulence should be present in virulent strains
  • should not be present or should be silent in a virulent strains
  • disruption of gene -> avirulent (or intro =VV)
  • gene must be expressed during infection and Abs should be raised
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16
Q

Outline the 3 basic steps in infection cycle

A
  1. Pathogen must encounter and adhere to host
  2. Multiply within hist
  3. Be dispersed to encounter another host
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17
Q

Examples of healthy carriers of pathogens ?

A
  • neisseria meningitidis (back of nose and throat)

- streptococcus pneumoniae (nasopharyngeal)

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18
Q

Name the two clinical manifestations of leprosy and outline the pathological reason for the difference

A
  1. Paucibacilliary - stronger cellular immune response

- 5 skin lesions

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19
Q

Who discovered leprosy?

A

Dr Hansen, Norwegian physician,1873

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20
Q

What event bought leprosy to Europe ?

A

Soldiers which had joined the crusades returning home to Europe

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21
Q

Which world health programmes has helped Duce the cases of leprosy ?

A

World health assembly initiative

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22
Q

Average incubation of leprosy?

A

7 years

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23
Q

Which form of leprosy has high bacterial load ?

A

Lepromatous aka multibacilliary (MB)

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24
Q

Treatment of paucibacillary leprosy?

A

Rifampicin and dapsone - 6 months

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25
Q

Dapsone mechanism of action

A
  • Inhibits folic acid production (but is not a sulphonamide)

- has anti inflammatory and immunomodulatory effects

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26
Q

Treatment of lepromatous leprosy ?

A

Rifampicin, clofazimine and dapsone (1 year)

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27
Q

What stain is used in the observation of mycobacterium ?

A

Ziehl-Neelson stain

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28
Q

Outline process of Ziehl-Neelson stain of mycobacterium

A
  • slide flooded with string carbol fuschin
  • slide heated until dye steams
  • kept hot for 10 mins
  • Carbol fuschin washed off
  • slide flooded with mineral acid + acid
  • this de colourises everything other than mycobacteria
  • then stained with methylene blue
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29
Q

Describe cell wall of mycobacteria

A
  • Peptidoglycan layer covalently linked to arabinogalactan which is linked to mycolic acids
  • 60% lipids
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30
Q

Who first discovered M. Tuberculosis ?

A

German bacteriologist, Robert Koch, 1882

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31
Q

How many people die of TB each year worldwide ?

A

> 2m

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32
Q

How many new cases of TB occur worldwide per year ?

A

> 8m

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33
Q

What media does M. tuberculosis grow well on ?

A

Egg based e.g. Lowenstein-Jenson medium

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34
Q

Average time for M. tuberculosis to be grown on conventional culture ?

A

4-6 weeks

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35
Q

Which dye can be used as an alternative to Ziehl-Neelson and makes screening large numbers of slides easier ?

A

Auramine-Rhodamine stain - same principle but with fluorescent dyes

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36
Q

Earliest reports of TB

A

2400BC

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37
Q

Drug treatment for pulmonary TB

A

6 months of isoniazid and rifampicin with the first 2 months supplemented with pyrazinamide and ethambutol

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38
Q

Controlling factors of syphilis

A

Posey and promiscuity

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39
Q

What year did syphilis arrive in England ?

A

1498

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40
Q

What year did syphilis return to America ?

A

1800

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41
Q

Who inoculated himself with pus of a patient with gonorrhoea symptoms

A

John hunter, 1767

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42
Q

Who and when was the organism causing gonorrhoea discovered?

A

Albert Neisser, German physician and bacteriologist,1878

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43
Q

When and who by was the causative organism of chancroid identified ?

A

1889, August Ducrey, Italian physician and bacteriologist

Haemophilus ducreyi

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44
Q

When does primary syphilitic lesion appear?

A

Chancre appears at end of incubation period at site of inoculation

45
Q

How long do chancre last ?

A

2 to 3 weeks then heal spontaneously

46
Q

How long father primary syphilis does the secondary stage occur ?

A

6 to 8 weeks after primary chancre heals spontaneously

47
Q

Symptoms of secondary syphilis

A
  • generalised symptoms of infection e.g. Malaise
  • generalised lymphadenopathy
  • characteristic non itchy rash
  • snail track ulcers in mouth, patchy ulcers, iritis
48
Q

How long may seconds syphilis last?

A

Months to years

49
Q

When does the latent stage of syphilis occur and how long does it last ?

A

After last lesions of secondary syphilis have healed, may last 3 to 30 years

50
Q

What amount of untreated syphilis cases progress to tertiary syphilis ?

A

1/3

51
Q

Physical appearance of congenital syphilis ?

A
  • Hutchinson teeth
  • mulberry molars
  • saddle nose
  • sabre shins
52
Q

Symptoms of tertiary syphilis

A
  • gummatous lesions of skin, bone, mucous membranes

- CNS= tabes dorsalis, generalised paresis of the insane

53
Q

3 antibodies appearing in serum in syphilis infection ?

A
  • lipoidophil or reagin antibody
  • antibody to Reiter protein
  • specific antibodies to T. pallidum antigens
54
Q

Which antigen provokes the lipoidal antibody ?

A

Cardiolipin

55
Q

How is Cardiolipin antigen produced ?

A

Prepared from alcoholic extract of beef heart muscle

56
Q

The addition of which compounds make the Cardiolipin antigen test more sensitive ?

A

Lecithin and cholesterol

57
Q

When do antibodies to Cardiolipin appear after infection with syphilis ?

A

1-3 weeks

58
Q

What is added to the RPR test to aid visualisation as an improvement on the VDRL test ?

A

Carbon particles

59
Q

Which specific treponemal test becomes positive first in syphilis infection ?

A

FTA-ABS (fluorescent treponemal Ab absorption)

60
Q

How is FTA-ABS carried out ?

A
  • treponemal antigens fixed to slide
  • slide flooded with serum
  • if anti-trep Abs present they will adhere to trep Ags that are stuck to slide
  • slide washed and flooded with fluorescently labelled anti-human antiserum
  • fluorescent Abs stick to human Abs which are stuck to the Ags
  • final wash to remove unbound Abs
61
Q

Which specific treponemal test remains positive despite therapy as a marker of last infection ?

A

TPHA

- treponema pallidum haemaglutination test

62
Q

Which test has superseded TPHA test ? What modifications ?

A

TPPA

  • treponema pallidum particle agglutination test
  • RBCs replaced by gelatine particles to reduce risk of false positives and increase sensitivity
63
Q

First line treatment for syphilis (primary, secondary and early latent)?

A

Benzathine penicillin (2.4 mega units IM, Single dose)

64
Q

Second line treatment for syphilis (primary, secondary and early latent)?

A

Azithromycin (oral, single dose)

65
Q

Paper on lab diagnosis of syphilis

A

Ratnam, 2005

66
Q

Paper of treatment history and development of syphilis

A

Tampa et al, 2014

67
Q

Paper on the history of syphilis?

A

Nguyen 2013

68
Q

TB genetic predisposition study ?

A

Schurr, 2011

69
Q

Paper on leprosy

A

Pinheiro, 2011

70
Q

Paper on food spoilage

A

Rawat, 2015

71
Q

Paper on wine making and brewing ?

A

McClure, 1976

72
Q

Antibiotic definition and reference ?

A

‘A chemical compound made by microorganisms that inhibit or kill other microorganisms at low concentrations’ (Waksman,1945)

73
Q

Most simple way to determine the antibiotic susceptibility ?

A

Disk diffusion test

74
Q

7 targets of antivirals ?

A
  • entry
  • uncoating
  • reverse transcriptase (retroviruses and DNA-RT)
  • integration in to host genome
  • protease inhibitors
  • virus replication
  • assembly
75
Q

Examples of synthetic antibiotics

A

Sulphonamides and trimethoprim

76
Q

Example of semi synthetic antibiotic

A

Ampicillin

77
Q

How to determine MIC and MBC of antibiotics ?

A

Serial dilution broth then plate out

  • MIC = conc of largest dilution that prevents growth in tube but not when plated out
  • MBC = dilution of last plate to show no growth
78
Q

Example of antibiotics which are antagonistic together and why ?

A

Penicillin and erythromycin (B-lactam and Macrolide)

- erythromycin inhibits protein synthesis and so inhibits the growing cell wall that is actively targeted by penicillin

79
Q

Examples of synergistic pairs

A
  • sulphonamides and trimethoprim

- penicillin and gentamicin (increase penetration)

80
Q

Exact target of B-lactams ?

A
  • Transpeptidases aka PBPs involved in transpeptidation (cross linking) of peptidoglycan by preventing cleavage of the terminal D-alanine residue
  • also stimulate activity of autolysins
81
Q

6 antibiotics (2 classes) targeting the cell wall?

A
  • B-lactams
  • glycopeptides
  • fosfomycin
  • cycloserine
  • isoniazid
  • teixobactin
82
Q

Mechanism of action of glycopeptides ?

A

Inhibit transglycosylation and so prevents elongation of peptidoglycan chain and therefore inhibits subsequent transpeptidation as well

83
Q

Mechanism of resistance in B-lactams ?

A
  • B-lactamases

- modified PBPs with lower affinity (target mod)

84
Q

Which mechanism of resistance in B-lactams is more common in Gram positive bacteria ? Give example

A

Altered PBP

- mutant PBP2a in S. aureus by mutation in MecA gene -> MRSA (lower affinity)

85
Q

Mechanism of resistance in glycopeptides

A

Reprogramming if D-ala D-ala substrate
- e.g. To D-ala D-Lac in vancomycin resistance

*resistance rarer than in other antibiotic classes

86
Q

Mechanism of action and resistance in fosfomycin

A
  • inhibits MurA, 1st enzyme in PG synthesis pathway
  • resistance = sub mutation in active site (cysteine->aspartate), target mod unable to bind

*resistance develops rapidly so not used much clinically

87
Q

Mechanism of action of clycoserine ?

A
  • inhibits 2 steps in PG synthesis
  • competitive inhibitor of L-ala racemase converting L-ala to D-ala
  • inhibits D-ala D-ala synthetase
88
Q

Mechanism of resistance in clycoserine?

A

Over expression of D-ala racemase gene (upregulation of target)

89
Q

Clinical indication for cycloserine ?

A

Drug resistant TB

  • or other resistant infections where all other therapies failed (salvage therapy)
  • neurotoxic
90
Q

Mode of action of isoniazid

A

Inhibits synthesis of mycolic acids

91
Q

Mechanism of action of Teixobactin?

A

Bids to lipid II, precursor if PG, Preventing cell wall synthesis

92
Q

What antibiotic class is the newly developed (2015) antibiotic with Gram negative activity ?

A

Ceftolozane

*administered with B-lactamase inhibitor (tazobactam)

93
Q

How does ceftolozane evade the usual resistance mechanism of P. aeruginosa ? (4)

A
  • particularly high affinity for PBP
  • low affinity for class C B-lactamases (cephalosporinases)
  • enters OM through alternative porin (not OprD)
  • not a substrate of the usually up regulated efflux pump
94
Q

Mechanism of action of polymyxins?

A

Binds to LPS in gram negative outer membrane and subsequently disrupts outer and inner membranes

95
Q

Which antibiotics disrupt membrane integrity ? (3)

A
  • polymyxins
  • Gramicidin
  • possibly metronidazole as secondary target after DNA gyrase
96
Q

What antibiotic class is gentamicin ?

A

Aminoglycosides

97
Q

Which is the only class of antibiotics which inhibit protein synthesis that are bacteriocidal ?

A

Aminoglycosides

98
Q

Most common new traits conferring resistance to antibiotics ? (3)

A
  1. Alteration of drug target
  2. Encoding of new enzymes which hydrolyse drug
  3. Prevention of binding to target e.g. Efflux pump
99
Q

Main mechanism of resistance effecting all aminoglycosides ?

A
  • decreased uptake/accumulation of drug

- bacterial expression of enzymes modifying drug

100
Q

Which 3 classes of antibiotic exhibit cross resistance due to a shared target on the 50S ribosome (23S)

A

Macrolides, lincosamides and streptogrammins (MLS antibiotics)

101
Q

Which organisms are intrinsically resistance to aminoglycosides ?

A

Anaerobic bacteria - lack oxidative metabolism to drive uptake

102
Q

Why is the claim that a drug with 2 targets less likely to develop resistance false ? E.g. teixobactin

A

Most clinically relevant resistance is modification of the drug not the target

  • therefore as one drug, the chances are no less likely than other
  • combo therapy more likely to be effective
103
Q

Usual mechanism of resistance in mycobacteria ?

A
  • Point mutation in chromosomal DNA

- target modification

104
Q

Define conjugation

A

Transfer of genetic material between two bacteria by direct cell-cell contact via bridge-like structure, sex pilus

105
Q

Describe HGT by transformation

A

Transfer of genetic material in which free DNA (I.e. From lysed cell), is taken up and incorporated into the genome of another bacterium

106
Q

Describe HGT by transduction

A

DNA transferred from one bacterium to another by a viral vector e.g. Bacteriophage

107
Q

3 processes errors may occur in to produce mutational resistance ?

A
  • polymerisation
  • exonucleolytic proofreading
  • strand-directed mismatch
108
Q

2 mechanisms by which resistance increases in prevalence ?

A
  • clonal expansion

- horizontal dissemination

109
Q

2 classes of antibiotic acting on the 30S ribosome

A
  • Aminoglycoside

- tetracycline

Infectious Agents (4 decks)

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