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P Intergrated Y2 > CP Microbiology x8 lectures > Flashcards

CP Microbiology x8 lectures Flashcards

1
Q

Define - Antibiotic

A

Chemical products of microbes that inhibit or kill other organisms

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2
Q

Define Antimicrobial agents

A

-Antibiotics
-Synthetic compounds with similar effect
-Semi-synthetic i.e. modified from antibiotics
Different antimicrobial activity/spectrum, pharmacological properties or toxicity

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3
Q

Define Bacteristatic

A

Inhibit bacterial growth

Protein synthesis inhibitors

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4
Q

Define Bactericidal

A

Kill bacteria

Cell wall-active agents

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5
Q

Define minimum inhibitory concentration (MIC)

A

Minimum concentration of antibiotic at which visible growth is inhibited

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6
Q

Define Synergism

A

Activity of two antimicrobials given together is greater than the sum of their activity if given separately

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7
Q

Define Antagonsim

A

One agent diminishes the activity of another

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8
Q

Define indifference

A

Activity unaffected by the addition of another agen

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9
Q

Define clinical relevance

A

Synergism

β-lactam/aminoglycoside combination therapy of streptococcal endocarditis

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10
Q

What are antibacterial mechanisms

A

Inhibition of critical process in bacterial cells

  • Antibacterial targets
  • Enzymes, molecules or structures

Selective toxicity

  • Target not present in human host
  • Target significantly different in human host
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11
Q

What are antibiotic targets

A 
Cell wall
Protein synthesis 
DNA synthesis
RNA synthesis
Plasma membrane
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12
Q

What is the major component of bacterial cell wall

A

Peptidoglycan
polymer of glucose-derivatives, N-acetly muramic acid NAM and N-acetly glucosamine NAG

Not present in animal cells therefore ideal for selective toxicity

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13
Q

What drugs are cell wall synthesis inhibitors

A

β-lactams

Glycopeptides

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14
Q

Explain β-lactams

A
  • Benzylpenicillin
  • All contain β-lactam ring
  • Four-membered ring structure (C-C-C-N)
  • Structural analogue of D-alanyl-D-alanine
  • Interfere with function of “penicillin binding proteins”
  • Transpeptidases enzymes involved in the peptideoglycan cross-linking
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15
Q

What areβ-lactam antibiotics

example drugs

A

Penicillins
Benzylpenicillin (PEN), amoxicillin, flucloxacillin
Relatively narrow spectrum

Cephalosporins
Cefuroxime (CXM), ceftazidime etc.
Broad spectrum

Carbapenems
Meropenem (MER), imipenem
Extremely broad spectrum

Monobactams
Aztreonam (AZT)
Gram-negative activity only

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16
Q

What are glycopeptides

A
  • Vancomycin, teicoplanin
  • Large molecules, bind directly to terminal D-Alanyl-D-Alanine on NAM pentapeptides
  • Inhibit binding of transpeptidases and thus peptideoglycan cross-linking
  • Gram-positive activity
  • Unable to penetrate Gram-negative outer membrane porins
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17
Q

In bacteria where does protein synthesis occur

A

Ribosome
- ribonucleoprotein complexes
- Catalyze peptide bond formation and synthesize polypeptides
Stages: initiation, elongation, termination, and ribosome recycling
50S (large) and 30S (small) subunits combine to form 70S initiation complex
S=Svedberg units; relative sedimentation rate

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18
Q

What do aminoglycosides do

A

Protein synthesis inhibitors
Gentamicin, amikacin
Bind to 30S ribosomal subunit
Mechanism of action not fully understood

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19
Q

What are Macrolides, Lincosamides, stretogamins (MLS)

A 
protein synthesis inhibitors
Erythromycin, clarithromycin (macrolides)
Clindamycin (lincosamide)
Bind to 50S ribosomal subunit1
Blockage of exit tunnel
Inhibit protein elongation
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20
Q

What does tetracycline do?

A 
Protein synthesis inhibitor 
Tetracyclines (tetracycline, doxytetracycline)
Bind to 30S ribosomal subunit
Inhibit RNA translation
Interfere with binding of tRNA to rRNA
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21
Q

actions of oxazolidines

A 
Oxazolidinones
Linezolid
Inhibits initiation of protein synthesis
Binds to 50S ribosomal subunit
Inhibits assembly of initiation complex
May also bind to 70S subunit
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22
Q

What are mupirocin and fusidic acid

A

protein synthesis inhibitors

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23
Q

Examples of DNA synthesis inhibitors

A

Trimethoprim and sulfonamides
Inhibit folate synthesis
Folic acid is a purine synthesis precursor

Trimethoprim
Dihydrofolate reductase

Sulfonamides
Dihydropteroate synthetase

Combined as co-trimoxazole (trimethoprim-sulfamethoxazole)

Quinolones1 and fluoroquinolones2
Inhibit one or more of two related enzymes
DNA gyrase and topoisomerase IV
Involved in remodelling of DNA during DNA replication
Supercoiling/strand separation

Examples
Nalidixic acid1, ciprofloxacin2, levofloxacin2

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24
Q

RNA synthesis inhibitors

A

Rifampicin
RNA polymerase inhibitor
Prevents synthesis of mRNA

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25
Q

Plasma membrane agents

A

Daptomycin
Cyclic lipopeptide
Inserts lipophilic tail into cell membrane resulting in depolarisation and ion loss
Effective in Gram-positives only

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26
Q

Adverse effects of all drugs

A

Nausea, vomiting, headache, skin rashes etc.
Infusion reactions
Allergic reactions
Generation of antibiotic resistance (see separate lecture)
Selection of resistant strains in patient
Preferential colonisation on exposure to resistant strains
Fungal infection
Superficial and invasive candidiasis
Clostridium difficile infection

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27
Q

Antibiotic specific adverse effects

  • aminoglycosides
  • B-Lactams
  • Linezolid
A

Aminoglycosides
Reversible renal impairment on accumulation
Therapeutic drug monitoring indicated

B-lactams
Main problems are allergic reactions
Generalised rash 1-10%
Anaphylaxis approx. 0.01%

Linezolid
Bone marrow depression

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28
Q

B lactams and allergy

A 
Intolerance
Nausea, diarrhoea, headache etc.
Minor allergic reactions
Non-severe skin rash
Severe allergic reactions
Anaphylaxis, urticaria, angio-oedema, bronchospasm, severe skin reaction (Stevens-Johnson syndrome)

Safe to use cephalosporins and carbapenems in patients with non-severe penicillin allergy

Safe to use aztreonam in patients with any penicillin allergy

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29
Q

Antibiotics and C diff

A

Common precipitating antibiotics
Cephalosporins
Ciprofloxacin (esp. ribotype 027)
Clindamycin

Less common precipitating antibiotics
Benzylpenicillin
Aminoglycosides
Glycopeptides
Piperacillin-tazobactam

May be precipitated by any antibiotics

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30
Q

What are the following antibiotics used to treat

  • Flucloxacillin
  • Benzylpenicillin
  • cephalosporins
  • metronidazole
  • vancomycin
  • meropenem
A

Flucloxacillin - Staphylococcus aureus (not MRSA)
Benzylpenicillin – Streptococcus pyogenes
Cephalosporins (avoid in elderly) – Gram-negative bacilli
Metronidazole – anaerobes
Vancomycin – Gram-positives (MRSA)
Meropenem – most clinically-relevant bacteria

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31
Q

what are the pharmacokinetic considerations

A

Important determinant of in vivo efficacy is concentration at site of action

CSF
β-lactams
Good availability in presence of inflammation
Aminoglycosides and vancomycin
Poor availability
Urine
Trimethoprim and β-lactams
Good availability
MLS antibiotics
Poor availability
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32
Q

What are pharmacodynamic considerations

A

Concentration dependent
Main determinant of bacterial killing is the factor by which concentration exceeds MIC
Administered intermittently to achieve high peaks
Aminoglycosides

Time dependent
Main determinant of killing is the amount of time for which antibiotic concentration exceeds MIC
Administered frequently to maintain high level
Β-lactams

In vitro phenomena applied in vivo

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33
Q

What is combination therapy

A

To increase efficacy
Synergistic combination may improve outcome
β-lactam/aminoglycoside in streptococcal endocarditis

To provide adequately broad spectrum
Single agent may not cover all required organisms
Polymicrobial infection
Empiric treatment of sepsis

To reduce resistance
Organism would need to develop resistance to multiple agents simultaneously
Antituberculous chemotherapy

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34
Q

What are the antibiotic resistant organisms

A
  • Meticillin-resistant Staphylococcus aureus (MRSA)
  • Vancomycin/glycopeptide-resistant enterococci (VRE/GRE)
  • Extended-spectrum β-lactamase-producing Enterobacteriaceae (ESBL)
  • NDM-1 producing Gram-negative bacilli
  • Multi-drug resistant tuburculosis (MDR-TB)
  • Extremely-drug resistant tuberculosis (XDR-TB)

Others

  • Enterobacteriaceae resistant to amoxicillin, ciprofloxacin, gentamicin, carbapenems etc.
  • Pseudomonas resistant to ceftazidime, carbapenems etc.
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35
Q

How does resistance affect the treatment of infection

A

Empiric therapy
-Risk of under-treatment
If “traditional” antibiotic is used
-Risk of excessively broad-spectrum treatment
-If risk of resistance is taken into account

Targeted therapy
Requires use of alternatives which may be:
-Expensive
E.g. linezolid, tigecycline, daptomycin vs. flucloxacillin for MRSA
-“Last line”
E.g. meropenem vs. ciprofloxacin for multi-resistant Enterobacteriaceae
Toxic
-E.g. colistin vs. meropenem for NDM-1 producers

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36
Q

Why is sensitivity testing important

A
  • To enable transition from “empiric” to “targeted” antibiotic therapy
  • To explain treatment failures
  • To provide alternative antibiotics in case of
  • Treatment failure
  • Intolerance/adverse effects
  • To provide alternative oral antibiotics when IV therapy no longer required
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37
Q

How does disk susceptability work

A

1) add organism
2) add antibiotics
3) incubate
4) read and interrupt result
- zone of inhibition
5) clinical interpretation

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38
Q

How does liquid medial (microtitre) susceptibility work

A

1) add antibiotic vary concentrations
2) add organism
3) incubate
4) read MIC
5) compare with breakpoint
6) interpret results

Range - more resistant –> more susceptible

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39
Q

Uses and Limitations of susceptibility testing

A

-The infection may not be caused by the organism that has been tested
-The correlation between antimicrobial sensitivity and clinical response is not absolute
-A patient with an infection caused by a specific micro-organism is more likely to respond if treated with an antibiotic to which the organism is “sensitive” than one to which it is “resistant”
-Certain organisms are “clinically resistant” to antimicrobial agents even where in vitro testing indicates susceptibility
Resistance genes may be expressed in vivo in response to antibiotic exposure
E.g. AmpC β-lactamase genes in Enterobacteriaceae
Hence the need for “clinical interpretation”

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40
Q

What are the mechanisms for antibiotic resistance

A
  • No target – no effect
  • Reduced permeability – drug can’t get in
  • Altered target – no effect
  • Over-expression of target – effect diluted
  • Enzymatic degradation – drug destroyed
  • Efflux pump – drug expelled
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41
Q

What are reasons for Absent target

A

Fungi/virus

infection is not bacterial

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42
Q

Reasons for reduced permeability

A

1)Vancomycin:Gram-negative bacilli
Gram-negatives have an outer membrane that is impermeable to vancomycin

2) Gentamicin:anaerobic organisms
Uptake of aminoglycosides requires an O2 dependent active transport mechanism

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43
Q

Reasons for target alteration

A

1)Flucloxacillin: MRSA
Altered penicillin-binding protein (PBP2’, encoded by MecA gene) does not bind β-lactams

2)Vancomycin: VRE
Altered peptide sequence in Gram-positive peptideoglycan (D-ala D-ala  D-ala D-lac)
Reduces binding of vancomycin 1000-fold1

3)Trimethoprim: Gram-negative bacilli
Mutations in dhr (dihydrofolate reductase gene)

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44
Q

What drugs are effected by enzymatic degradation

A

1) Penicillins and cephalosporins: β-lactamases (including ESBLs and NDM-1)
2) Gentamicin: aminoglycoside modifying enzymes
3) Chloramphenicol: chloramphenicol acetyltransferase (CAT)

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45
Q

Drug efflux - causes?

A

Multiple antibiotics, specially in Gram-negative organisms1

Antifungal triazoles and Candida spp.

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46
Q

How does resistance occur

A 
Antibiotic-modifying enzymes
Β-lactamases (including ESBL)
Penicillins, cephalosporins
Aminoglycoside-modiying enzymes
Gentamicin

Altered antibiotic targets
Penicillin-binding protein 2’ (“PBP two prime”) in MRSA
Peptide sequence in VRE peptidoglycan

Resistance genes encoded in plasmids
Circular DNA sequences transmitted within species and (less commonly) between species
Mainly by conjugation

Horizontal transfer of resistance
Enabled by transposons and integrons
DNA sequences designed to be transferred from plasmid to plasmid and/or from plasmid to chromosome
Often contain “cassettes” with multiple resistance genes

Vertical transfer of resistance
Chromosomal or plasmid-borne resistance genes transferred to daughter cells on bacterial cell-division

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47
Q

Consequences of antibiotic exposure

A

1) Sensitive strains exposed to antibiotics at sub-lethal concentrations
2) Chance of survival will be enhanced by development of resistance
3) Resistant strain will out-compete sensitive strains
4) Resistance perpetuated by vertical transfer

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48
Q

How to avoid problems with antibiotics

A

Never use an antibiotic unless absolutely necessary
Always use the most “narrow-spectrum” agent available
Use combination therapy if indicated
Be willing to consult expert information sources

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49
Q

What was the estimated number of people living with HIV in 2012

A

2.3million (1.9-2.7 million)

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50
Q

Pathogenesis of viral infections

  • acute
  • chronic
A

Acute - flu, measles, mumps
Chronic
- latent (with/without recurrence) - Herpes simplex, cytomegalovirus
-Persistent - HIV, Hep B, Hep C

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51
Q

What do viruses consist of

A 
Nucleic acid (DNA, RNA)
Protein - structural coat, enzymes
Lipid evelope
Obligate intracellular parasite
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52
Q

How does viral replication occur

A

1) Virus attachment to cell (via receptor)
2) Cell Entry
3) Virus Uncoating
4) Early proteins produced – viral enzymes
5) Replication
6) Late transcription/translation – viral structural proteins
7) Virus assembly
8) Virus release

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53
Q

What are examples of polymerases

  • DNA to DNA
  • DNA to RNA
  • RNA to RNA
  • RNA to DNA
A

1) DNA to DNA -Eukaryotes, DNA viruses
2) DNA to RNA, Eukaryotes, DNA viruses
3) RNA to RNA- RNA viruses
4) RNA to DNA, Retroviruses (HIV), Hepatitis B virus

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54
Q

What is the structure of a nucleotide

A

Base, Ribose sugar, triphosphate

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55
Q

What is AZT - azidothymidine

A

Inhibits HIV replication

NRTI - nucleoside reverse transcriptase inhibitor

56
Q

What are NRTIs

Examples x2

A

Nucleoside reverse transcriptase inhibitors
Pyrimidine analogues
-Thymidine analogues
-Zidovudine

Cytosine analogues
-Lamivudine

Purine analogues (Adenine and Guanidine)

  • Abacavir
  • Tenofovir
57
Q

HBV - what is it

A

Hep B virus
contains reverse transcriptase enzyme,
Lamividine and tenofovir active against HBV

58
Q

What are NNRTIs

examples x2

A

Non-nucleotide reverse transcription inhibitors

1) Efavirenz
2) Nevirapine

59
Q

What are protease inhibitors

A 
Atazanavir
Darunavir
Fospamprenavir
Lopinavir
Nelfinavir
Ritonavir*
Saquinavir
60
Q

Newer HIV drugs
Fusion Inhibitor
Integrase inhibitor
Chemokine receptor antagonists

A

1) Fusion inhibitor
Enfuviritide (T20, given by IM injection)

2) Integrase Inhibitors
Raltegravir

3) Chemokine receptor
antagonsits (Co-receptor)
Maraviroc (CCR-5)

61
Q

What is HAART

how does HAART work

A 
Highly Active Antiretroviral Therapy
2 NRTIs + NNRTI
2 NRTIs + boosted PI
Started when CD4 falls
Aim to switch off virus replication
Taken life long
Suppression >10yrs achieved
Now problems with toxicity
62
Q

What HIV mutation is immune to Lamivudine

What will this mutation lead to

A

M184V
Strain with mutation will become dominant
Lamivudine will no longer be an effective treatment option

63
Q

How is HIV “cured”

A

HIV suppressed on antivirals
Existing CD4 lymphocytes destroyed by conditioning
Stem cells reconstituted with HLA-matched but delta 32 homozygous allogeneic donor
Antiviral therapy stopped following transplantation
Remained HIV negative (by PCR)
HIV antibody titres have declined

64
Q

How is Hep C virus treated

A

Interferons and ribavirin
(40-90% cure rate)
Increasing number of direct antivirals

65
Q

How do antivirals work

A

block stage of viral replication,

act on virally encoded proteins

66
Q

Types of pathogenic fungi

A

Yeast
Pneumocystis jiroveci
Dimorphic
filamentous fungi

67
Q

what are the anti fungal targets

A

1) DNA synthesis
2) Mitosis
3) Cell membrane (Ergosterol)
4) Protein Synthesis
5) Cell wall - B-1,3-glucan

68
Q

What is Ergosterol

A
  • Found in fungal cell membrane
  • Clusters in phospholipid bilayer
  • regulates membrane permeability
  • required for normal growth and function of fungal cell wall
69
Q

What is the biosynthesis of Ergosterol

A 
Squalene 
(Squalene epoxidase)
Lansterol
(Lansterol 14a demethylase)
Ergosterol
70
Q

What are B-1,3-glucans

A
  • Large polymers of UDP-glucose
  • 50 ‑ 60% of the dry weight of the fungal cell wall
  • Form a fibrous network on the inner surface of the cell wall
  • Synthesized by β-1,3-glucan synthase
71
Q

What are the classes of anti fungal drugs

A 
Polyenes
Allylamines
Azoles
Echinocandins
Others
72
Q

Polyenes

  • modes of action
  • examples
A

Mode of action
Association with ergosterol
Formation of pore-like molecular aggregates
Aqueous vs. non-aqueous pores1
Loss of membrane integrity and leakage of K+
Cell death

Examples
Amphotericin B
Nystatin

73
Q

What is Amphotericin B

A

Spectrum of activity
Most fungi of medical importance
Aspergillus spp., Candida spp., Cryptococcus spp.

Adverse effects
Allergic reactions
Nephrotoxicity
Pores are formed in ergosterol-free membranes

74
Q

Lipid Associated Amphotericin B

A

Several different formulations

  • Liposomal AmB (L-AmB)
  • AmB lipid complex (ABLC)
  • AmB colloidal dispersion (ABCD)

Minimize delivery of AmB to kidney cells
Delivery targeted to fungal cells and/or reticulo-endothelial system
Reduce nephrotoxicity

75
Q

Clinical Uses
Amphotericin B
Nystatin

A

Amphotericin B

  • Not orally absorbed
  • serious sytemic infections

Nystatin

  • Not absorbed orally
  • superficial infections
  • too toxic for systemic use
76
Q

Allylamines

  • how do they work
  • example
A

Inhibit ergosterol syntheisis
- squalene epoxidase

Terbinafine

  • broad spectrum
  • liver toxicity adverse effect
77
Q

Clinical uses of Allylamines

A

Dermatophyte infections

  • topical - athletes foot, tinea corporis, (ring worm)
  • systemic (oral) use - scalp ringworm, onychomycosis
78
Q

Azoles

- what are they

A

Synthetic compound containing 5 membered azole ring

  • Imidazoles - 2 N atoms
  • Triazoles - 3 N atoms
79
Q

What is the mode of action of Azoles, and spectrum of activity

A

inhibit ergosterol synthesis
build up non-ergosterol 14a-sterols in cell membrane

Spectrum
- essentially broad
exception - Fluconazole to treat aspergillus spp.

80
Q

Uses of Imdazole
uses of triazoles

give examples of drugs for BOTH

A 
Imidazole 
- TOXIC
- rarely used systemically
= Clotrimazole
- superficial infections 
- candidiasis, dermatophytes
Triazole
- less toxic
-systemic use common
= Fluconazole
= Itraconazole
= Voriconazole
- systemic infections, aspergillosis, candidiasis
81
Q

Adverse effects and drug interactions of Azoles?

A

Hepatotoxicity
- mild liver enzyme abnormalities (7% fluconazole)

Drug interactions - inhabit cytochrome P-450 enzymes
- increase conc of all drugs metabolised by Cy-P450

82
Q

What is the anti fungal spectrum of

  • fluconazole
  • Itraconazole/ voriconazole
  • Isavuconazole/Posaconazole
A

1) Fluconazole - Yeasts
2) Itraconazole/voriconazole - yeast, aspergillus
3) Posaconazole, isavuconazole
- yeast, aspergillus, mucoraceous moulds

83
Q

Echinocandins

  • action
  • example
  • adverse effects
  • clinical use
A

inhibtion of B-1,3-glucan synthase

Anidulafungin
Caspofungin
Micafungin

minimal - rash, nausea vomiting

clinical - systemic infections
parenteral formulation only

84
Q

5- fluorocytosine

  • what is it?
  • mode of action
  • spectrum of activity
  • adverse effects
  • clinical use
A

synthetic analogue of cytosine

inhibits RNA/protein synthesis, and DNA synthesis but converting 5 flurouracil and 5 flurodeoxyurindine monophosphate

  • yeast only, candida, cryptococcus
  • bone marrow suppression
  • crytococcal meningitis (comb with AmB)
85
Q

Griseofluvin

  • action
  • spectrum
  • adverse effects
  • clinical use
A
  • inhibition of fungal mitosis
  • dermatophytes
  • minimal adverse effects
  • dermatophytes infections in kids
86
Q

What antifungals need Therapeutic drug monitoring

A

Itraconazole
5-fluorocytosine
Voriconazole

87
Q

Define parasite

A

The parasite derives all benefits from the association and the host may either be harmed or may suffer the consequences of this association

88
Q

Define symbiosis

A

living together; close, long term interaction between two different species

89
Q

Define Mutualism

A

an association in which both species benefit from the interaction

90
Q

Define Commensalism

A

an association in which the parasite only is deriving benefit without causing injury to the host

91
Q

What are the classes of host and define them

A

Definitive host
Either harbours the adult stage of the parasite or where the parasite utilizes the sexual method of reproduction
In the majority of human parasitic infections, man is the definitive host

Intermediate host
Harbours the larval or asexual stages of the parasite
Some parasites require two intermediate hosts in which to complete their life cycle

Paratenic host
Host where the parasite remains viable without further development

92
Q

Classification of parasites

A

Protozoa - micro

Helminths - macro

93
Q

Giadria lamblia
Entamoeba sp
P.Falciparum

are all examples of what

A

Protozoa

94
Q

Cestode - Taenia sp
Trematode - schistosoma sp
Intestinal nematode - Ascaris Lumbeicoides
Tissue Nematode - Wuchereria bancrofti

are all examples of what

A

Helminths

95
Q

Ascariasis Lumbricoides

  • what type of parasite
  • how is it acquired
  • infection rate?

Lung Migrations
Intestinal phase

Treatment?
Control?

A
  • Macro parasite , Intestinal Nematode
  • Ingestion of eggs, poor hygiene
  • 1 billion affected,

Lung
Loefflers syndrome - dry cough, dyspnea, wheeze, eosinophilic pneumonitis

Intestinal
Malnutrition, migration to hepatobilary tree, intestinal obstruction

Treatment - Albendazole
- prevents glucose absorption
Control - educated, community deworming

96
Q

Schistosomiasis

  • type
  • caused by
  • causes?
  • Immediate host?
  • clinical features
  • Treatment
  • control
A

Macro parasitite - helminth, fluke
aka - Bilharzia disease

S. haematobium
S. manson S. intercallatum
S. japonicum
S. mekongi

Immediate host - snap
causes - bladder cancer, liver cirrhosis

Swimmers itch, fever, haematuria, bladder fibrosis, portal hypertension, liver cirrhosis

Treatment - Praziquantel
Treat longterm complications
Control - kill snails, chemoprophylaxis, avoid snail infested water, education

97
Q

Hydatid Disease

  • type
  • host
  • caused by?
  • clinical
  • control
A

Macro parasite - tapeworm
Human accidental host, sheep
Echinococcus sp

Cysts - 70% liver 20% lungs
mass effect, bacterial infection

control - worm dogs, hand hygiene

98
Q

Malaria

  • type
  • causes by
  • vector?
  • clinical
  • control
A 
Micro parasite - protozoa, sporozoan  (plasmodium)
P. falciparum
P. vivax
P. ovale
P. malariae

Mosquitoes

Clinical - fever, rigors, cerebral malaria, renal failure, hypoglycaemia, pulmonary oedema, circulatory collapse, anaemia, bleeding, DIC

Control - insecticide, larvicidal spray of breeding pool, bed nets, chemoprophylaxis

99
Q

Cryptosporidiosis

  • cause
  • causes
  • how is it spread
  • clinical
  • treatment
  • control
A 
micro parasite - sporozoan 
Cryptosporidium parvum/  hominis 
- Diarrhoeal disease
- faecal oral spread
- 2-10day incubation
- watery diarrhoea with mucus, bloating, cramp, fever, vomiting
- usually self-limiting

Treatment - symptomatic - rehydration, nitazoxanide
Immunocompromised - Paromomycin, HAART

Control - Hand hygiene, boil water, pasteurise dairy products

100
Q

Common anti protozoal treatments

A 
Metronidazole
Pentamidine
Nitazoxanide
Pyrimethamine
Anti malarials
 - treatment
 - prophylaxis
101
Q

Common anti Helminthic treatments

A

Albendazole
Mebendazole
Ivermectin
Praziquantel

102
Q

When is IgM produced
What does IgG give
What are the materanal antibodies

A
  • acute infection
  • Long term immunity
  • IgG and IgA (breast milk)
103
Q

Measles

  • Virus
  • transmission
  • infectivity
  • incubation
  • clinical features
  • complications
  • Treatment
  • Prevention
A
  • Paramyxovirus (single strand RNA virus)
  • Person to person, Droplet
  • 1st day of symptoms –> 4 days after rash gone
  • 7-18days incubation

Clinical Features

  • Rash - erythematous, maculopapular
  • Fever
  • Koplik’s spots
  • Prodrome - fever, malais, 3 C’s

Complications

  • otitis media
  • pneumonia
  • diarrhoea
  • acute encephalitis 1/2000
  • Subacute sclerosing pan encephalitis 1/25000
  • Death

Treatment - Supportive, antibiotic for superinfection
Prevention - MMR live vaccine
Human normal immunoglobulin

104
Q

What are the 3 c’s

A

Conjunctivitis, coryza, cough

105
Q

Chicken Pox

  • virus
  • transmission
  • incubation
  • infectivity
  • clinical features
  • complications
  • treatment
  • prevention
A
  • Viral Zoster Virus - herpes virus
  • Respiratory spread, 15min face to face
  • 14 days incubation
  • 2 days before rash –> after dried up

Clinical features
Fever, malaise, anorexia
Rash - centripetal, vesicular

Complications

  • Pneumonitis
  • CNS involvement
  • Foetal varicella syndrome
  • Zoster
  • Death

Treatment

  • Acyclovir - oral
  • Chlorpheniramine - for itch
  • supportive

Prevention

  • Vaccine - 2 live doses
  • VZ immunoglobulin
106
Q

Rubella

  • Virus
  • Transmission
  • Incubation
  • Infectivity
  • clinical features
  • complications
A
  • Togavirus (RNA virus)
  • Droplet spread/ airborne
  • 14-21 days incubatoin
  • 1 week pre rash 4 days post

Clinical Features
Prodrome
Lymphadenopathy
Rash - nonspecific

Complications
thrombocytopenia
post infection encephalitis
arthritis

107
Q

Rubella in pregnancy

  • what is congenital rubella syndrome
  • treatment
A
  • Foetal Damage
    cataracts, deafness, cardiac abnormalities, microcephaly, small birth wieght, inflammatory lesions - brain, liver, lungs, bone marrow.

Foetal damage rare post 16/40
deafness reported 20/40

Treatment - non available

  • immunoglobulin to pregnant woman
  • vaccine - MMR
108
Q

Parvovirus B19 (slapped cheek)

  • Virus
  • transmission
  • incubation
  • foetal disease
  • clinical
  • treatment
  • control
A

B19 - DNA virus

  • Respiratory secretions
  • 4-14 days incubation
  • anaemia, hydrops in foetus, risk of miscarriage
clinical 
minor respiratory illness
slapped cheek
arthralgia
aplastic anaemia
anaemia in immunosuppressed

Treatment
none - self limiting
blood transfusion

control
- hard as infectous before rash

109
Q

Enteroviral infections

A

90% asymptomatic
hand foot and mouth
fever/rash syndromes
meningitis - PCR of CSF

Treatment - supportive, good hygiene to prevent infection

110
Q

Respiratory Syncytial Virus (RSV)

  • virus
  • Bronchiolitis
  • Diagnosis
  • Treatment
A

Pneumovirus
Bronchiolitis - under 1yo, life threatening, reinfection common

Dx - PCR nasopharyngeal secretions
Rx - O2, manage fever, fluid intake
Immunoglobulin, monoclonal abs, Palivizumab
manage at home

111
Q

Metapneumovirus

  • what is it
  • causes
  • Diagnosis
  • Treatment
A

Paramyxovirus
Respiratory illness similar to RSV
Dx - PCR
Rx - supportive only

112
Q

Adenovirus

  • Clinical
  • Dx
  • Rx
A 
10% childhood Resp infections
C- mild URTI, conjunctivitis, diarrhoea
Dx- respiratory panel PCR, eye swap PCR
Rx - none
cidofovir if immunocompromised
113
Q

Parainfluenza

  • virus
  • transmission
  • clinical
  • Dx
  • Rx
A 
Paramyxovirus
Person to person inhalational
C - croup, bronchiolitis, URTI
Dx - multiplexed PCR
Rx - none
114
Q

Rhinovirus

  • Virus
  • Clincal
A

Picornaviridae

C - URTI, runny nose,

115
Q

Rotavirus

  • Virus
  • Transmission
  • Incubation
  • Clinical
  • Dx
  • Rx
  • Prevention
A 
Reovirus (RNA)
Faecal oral route
1-2 days incubation
C- Diarrhoea, vommiting, risk mortality
Dx - PCR
Rx - rehydration
Prevetion - oral live vaccine
116
Q

Norovirus

  • transmission
  • course
  • Dx
  • Rx
A

Person to person, food borne
12-60hour course
Dx - PCR
Rx - rehydration

117
Q 
Mumps
- virus
- transmission
- infecitivty
- incubation
- Preventions
- clinical
- complications
Treatment
A 
Paramyxoviridae family
Droplet, direct contact, fomites
pre parotid swelling and post
2-4 weeks incubations
Prevention - MMR
C - prodrome, earache, tenderness over ipsilateral parotid, pyrexia 40 degrees
swelling decreases after 1 weeks
Complications
submandibular/sublingual sialadenitis
oophoritis
meningitis
encephalitis
renal function abnormality
Pancreatitis
epididymo-orchitis

Rx - Supportive/symptomatic

118
Q

why immunise

A

prevent disease
halt carriage and transmission
eliminate > eradicate disease

119
Q

when does a primary immune response occur

A

IgM antibody

weeks following 1st exposure to antigen

120
Q

When does secondary immune response occur

A

IgG - immunological memory
faster and more powerful
2nd exposure to antigen

121
Q

Active immunity vaccination concepts

  • live
  • inactivated organisms
  • components of organisms
  • inactivated toxins
A

Live: MMR, BCG, Yellow fever, Varicella
Act like the natural infection
Inactivated organisms: pertussis, typhoid, IPV
Components of organisms: influenza, pneumococcal
Inactivated toxins: diphtheria, tetanus

122
Q

Passive immunity vaccination concepts

  • vertical transmission
  • injected human immunoglobulin
A

Vertical transmission of auto-antibodies from mother to foetus & breastfeeding

Injection of human immunoglobulin
HNIG – pooled plasma
Specific – tetanus, botulism, hep B, rabies, varicella

123
Q

Live vaccination

  • advantages
  • disadvantages
A

Advantages
Single dose often sufficient to induce long-lasting immunity
Strong immune response evoked
Local and systemic immunity produced

Disadvantages
Potential to revert to virulence
Contraindicated in immunosuppressed patients
Interference by viruses or vaccines and passive antibody
Poor stability
Potential for contamination

124
Q

Inactivated vaccines

  • advantages
  • disadvantages
A

Advantages
Stable
Constituents clearly defined
Unable to cause the infection

Disadvantages 
Need several doses
Local reactions common 
Adjuvant needed 
keeps vaccine at injection site
activates antigen presenting cells
Shorter lasting immunity
125
Q

NHS vaccination programe

2mnths - 70 years

A 
2 mth: DTaP/IPV/Hib + pneumo + rota
3 mth: DTaP/IPV/Hib + Men C + rota
4 mth: DTaP/IPV/Hib + pneumo
12 mth: Hib/Men C + MMR + pneumo
24 - 48 mth: annual flu
40 mth: dTaP/IPV + MMR
12 years: HPV for girls
14 years: Td/IPV + Men C
65 years: pneumo + annual flu
70 years: shingles
126
Q

How are pathogenic organisms eliminated

  • Environmental
  • Equipment decontamination
  • Antisepsis
  • Antibiotic Prophylaxis
A

Environmental cleaning and decontamination

  • H2O2 room decontamination
  • Spillage management
  • Laundry

Equipment decontamination

  • Sterilisation
  • Disinfection

Antisepsis

  • Surgical skin prep
  • MRSA decolonisation

Antibiotic prophylaxis
Perioperative
Post-exposure

127
Q

What is an example of removing source/ reservoir

A

hand hygiene

environmental cleaning and decontamination

128
Q

How is transmission minimised

A
  • Hand Hygiene
  • Personal protective equipment
  • Equipment decontamination
  • source and protective isolation
  • disposable equipement
129
Q

How is eliminated entry/exit acheived

A

Antisepsis
-Surgical skin prep

Asepsis
-Insertion and management of invasive devices

Air handling

  • Air filtration and laminar flow
  • Positive pressure ventilated lobby (PPVL) rooms

Sharps management

Patient management
-Minimise use and duration of invasive devices

130
Q

How can susceptibility to infection be reduced

A

Antibiotic stewardship
- lower C.diff

immunisation

131
Q

What is Sterilization

- methods

A

complete killing or removal of all types of microorganisms

Methods

  • Heath - moist/dry
  • Chemical - gas/liquid
  • Filtration
  • Ionising Radiation
132
Q

How does sterilisation by heat work

  • moist heat
  • dry heat
A

Moist
- Autoclave - steam under high-pressure

Dry
- Oven - controlled temp cycles 160 2hrs or 170 1hr

133
Q

What is disinfection

- what needs to be considered

A

Removal or destruction of sufficient numbers of potentially harmful micro-organisms to make an item safe to use

Chemical disinfectant - effect on micro-organisms, chemical properties, physical effects, harmful effects

134
Q

What is antisepsis

A

applied to damaged skin or living tissues

Requires a disinfectant with minimal toxicity

135
Q

How are surgical instruments reprocessed

A

Sterilization

Moist heat decontamination

136
Q

How is a flexible endoscope reprocessed

A

High level disinfection

chemical disinfection

137
Q

How is syringe needle processed

A

Sterilization
irradiation pre use
disposal after use

P Intergrated Y2 (13 decks)

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