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Microbiology Flashcards

1
Q

Define infectivity

A

The ability of a pathogen to establish an infection

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2
Q

Define virulence

A

Ability of a pathogen to cause disease

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3
Q

What does E. coli do

A

Caused by food/ water contamination, Toxins released into the blood stream via the large intestine. Causes kidney failure

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4
Q

What does staphylococcus aureus do

A

Releases toxins and enzymes

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5
Q

What does Neisseria Meningiditis do

A

Releases respiratory endotoxin, damages RBCs, causes shock.

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6
Q

Give an example of a bacteria that enters the faeco-oral route

A

Cholera, E. Coli

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7
Q

Give an example of a bacteria that enters the GI tract

A

E. coli, Sigella spp., Vibrio Cholerae, Salmonella, Listeria

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8
Q

What bacteria causes tonsilitis

A

Streptococcus Pyogenes

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9
Q

Describe severe sepsis/ shock

A

Poor tissue diffusion. sepsis = Sepsis + lactic acidosis. Shock = sepsis +hypotension (increase in permeability and vasodilation)

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10
Q

What is the treatment for sepsis

A

Antibiotic
Blood Products
Fluids and vasopressors to increase blood pressure

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11
Q

What is the minimal inhibitory concentrations

A

Lowest concentration of antibiotic required to inhibit growth

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12
Q

What is the breakpoint

A

Breakpoint is the clinically achievable MIC

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13
Q

Why are hospital acquired diseases transmissible

A

High density of ill people - lots of pathogens
People moving - spread
Open wounds - easy portal of entry
Insertion of devices e.g. catheter, cannulas
Antibiotic therapy - antibiotic resistance

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14
Q

What are antimicrobials

A

Any substance or chemical that kills a microbe or inhibits its growth

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15
Q

What are the classes of antimicrobials and what do they do

A

Beta-lactams - inhibits cell- wall synthesis + murein assembly
Tetracyclines - efflux/membrane pumps, inhibits translation
Chloramphenicols- inhibits translation
Quinolones - target site modification, DNA gyrase + topoisomerase
Sulphanamides - blocking uptake or influx
Aminoglycosides - inhibits protein synthesis, RNA proofreading and damages the cell membrane
Macrolides - inhibits translation via ribosome

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16
Q

How does resistance lead to increased mortality, morbidity and cost

A

Increased time to effective therapy.
Requirement for additional approaches – e.g. surgery.
Use of expensive therapy (newer drugs).
Use of more toxic drugs e.g. vancomycin.
Use of less effective ‘second choice’ antibiotics.

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17
Q

Give some examples of gram -ve AB resistant pathogens and gram +Ve resistant pathogens

A

E. coli
Salmonella spp
Klebsiella spp
Neisseria gonorrhoeae

Staphylococcus aureus
Streptococcus pneumoniae
Clostridium difficle
Mycobacterium tuberculosis

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18
Q

Give reasons as to why AB treatment may fail

A

Inappropriate choice for organism
Poor penetration of AB into target site
Inappropriate dose (half life)
Inappropriate administration (oral vs IV)
Presence of AB resistance within commensal flora e.g. secretion of beta-lactamase

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19
Q

Describe rifampicin, vancomycin, linezolid and daptomycin

A

rifampicin - targets a subunit of RNA polymerase
vancomycin - targets the lipid component of cell wall synthesis
linezolid - inhibits initiation of protein synthesis
daptomycin - targets the cell membrane

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20
Q

What are the pathways of resistance

A

Altered target sites
Antibiotic inactivation
Altered metabolism
Decreases drug accumulation

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21
Q

Describe treatment of multi-drug resistant pathogens

A 
Temporarily withdraw certain antibiotics
Only use them for dangerous infections
Reduce broad-spectrum antibiotics
Identify resistant strains
Combination therapy
Adjust current antibiotics
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22
Q

Describe selective toxicity

A

The large number of differences between mammals and bacteria result in multiple targets for antibiotic therapy

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23
Q

Give the sources of antibiotic resistance genes

A

Plasmids – Multiple copies that often carry mutliple AB res genes – selection for one maintains resistance to all.
Transposons integrate into chromosomal DNA. Allow transfer of genes from plasmid to chromosome and vice versa.
Naked DNA. DNA from dead bacteria released into environment.

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24
Q

Give some non-genetic mechanisms of AB resistance

A 
Biofilm
Intracellular location
Slow growth
Spores
Persisters
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25
Q

Give some examples of hospital-acquired infections

A

S. aureus
E. coli
Clostridium difficle

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26
Q

Compare enveloped to non-enveloped viruses

A 
Enveloped = lipid=envelope from the host cell e.g. measles, ebola
Non-enveloped = adenovirus, calcivirus
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27
Q

What are the features of a DNA virus

A

Segmented genomes
Reassortment of 2 viruses
Half of the DNA codes immune resistant proteins

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28
Q

What is the basic viral life cycle

A 
Virus locates target cell
Binding to receptors
Nucleocapsid enters
Formation go early (regulation) then late (structural) proteins
Replication of the viral genome
Assembly of new virus
Release
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29
Q

What is the HIV life cycle

A

HIV binds to CCR5/ CXCR4
Viral proteins and mRNA released
Host proteases hydrolyse the protein capsid
Reverse transcriptase generates DNA from RNA
Integrase integrates the DNA into host genome
Host cell produces proteins
Proteases cleave into constituent proteins
Host membrane used as the lipid envelope

30
Q

How are viruses detected

A

Using the cytopathic effect = effect of the virus lysing the cell (could be due to shut down of protein synthesis or viral protein accumulation)

31
Q

How can viruses be analysed

A

Viruses will form plaques in monolayers - Assay
Some viruses (HIV) do not form plaques but fuse = Syncytia
Antibody generation

32
Q

How are viral infection diagnosed

A 
Amplify genomes using PCR
Detect using IDA or ELISA
Look for viral particles
Cytopathic effect
Antibodies (Serology)
High density fluorescent markers
33
Q

Describe propagation

A

Continuous lines of viral growth leads to mutation and therefore evolution. If the genome is small, it can be synthesised and mutation can be added for vaccinations.

34
Q

What is attenuation

A

The virus becomes so different that it is unable to grow as well in humans. Can be used for vaccines

35
Q

What are the viral routes

A 
Latrogenic - HCW e.g. contaminated needles
Nosocomial - hospital acquired
Vertical - Parent to offspring
Horizontal - All other forms
Germ- line - part of host cell genome
36
Q

What is tropism

A

The place where the virus replicated. May be determined by expression of the host cell receptor e.g. T cells and HIV, Ability to replicate in one cell type e.g. polio, extracellular factors e.g. influenza and proteases

37
Q

What are the modes of transmission for HIV

A

T cells - CD4, CCR5, CXCR4 (GP120)

38
Q

What are the modes of transmission for Measles

A

Dendritic cells- CD155, SLAM, Neetin 4

39
Q

What are the modes of transmission for influenza

A

Enters through endosomes
The receptors is ubiquitous - found everywhere
Low endosomal pH triggers fusion where HA cleavage is required for exposure of fusion peptide
Clara cells (innate immune system) secrete many proteases, allowing cleavage of HA to activate the virus
Viruses that have not been cleaved are inactive so tropism is determined by availability of host proteases

40
Q

What is pathogenicity

A

Ability to infect

41
Q

Describe an acute infection and give examples

A

Infection followed by viral clearance. Smallpox, dengue, polio

42
Q

Describe persistant infection

A

Latent, slow, transforming infection that is not cleared by adaptive immunity. Chronic or lifelong. HIV, varicella zoster

43
Q

Compare the different types of vaccines

A

Attenuated - rapid, broad, long-lived, but may revert, Adenovirus, influenza, measles
Inactivation - Safe, may be from wild-type, frequent and will need boosts, Hep A, polio
Purified subunit - influenza
Cloned subunit - hep B, HPV

44
Q

Why was smallpox eradicated

A

No animal reservoir
100% penetrance
Obvious symptoms

45
Q

What are the modern aims

A

eliminate polio and measles

Polio has two versions: live (Sabin) and inactive (Salk)

46
Q

What is genomics

A

Identifying host cell genes that viruses need

47
Q

Give examples of successful viral therapy

A

Acyclovir for herpes which is a nucleoside analogue for deoxyguanosine without a3’ OH. It must be thymidine kinase which is only present in viruses.
Zidovudine AZT for HIV. It is a nucleoside and used in HAART

48
Q

What are the features of influenza

A

Infects water fowl and mutation meant it infected humans. Changes in epitope means it can escape immunity.

49
Q

Define antigenic shift

A

When mutation adapt a virus for replication and transmission in humans and on its spread it displaces the previous strain

50
Q

What is reassortment

A

Combination of 2 viruses that infect the same cells

51
Q

How was west nile virus, norovirus and SARS introduced

A

WNV- Mosquitos and birds from Asia to USA
Norovirus - small RNA
SARS - bats

52
Q

Why may new viruses emerge

A

Zoonosis
Genetic variation
Increased exposure (travelling or by vector)
New discoveries

53
Q

Define zoonosis

A

Crossing of an animal pathogen into humans

54
Q

Define the host range barrier

A

Viruses adapted to infect animals hosts are compromised in their ability to replicate and spread in humans due to the genetic difference between host factors and what the virus needs.

55
Q

Define quasispecies

A

A group of viruses related by a similar mutation(s), competing within a highly mutagenic environment.

56
Q

What is fitness cost

A

resistant pathogens are unable to spread beyond the treated patient

57
Q

What is a live attenuated vaccine and give an example

A

Whole virus with reduced virulence e.g. MMR

58
Q

What is an inactivated vaccine and give an example

A

Dead form of a pathogen e.g. Flu

59
Q

What is a toxoid vaccine and give an example

A

Injection of the toxin that causes the disease e.g. Tetanus

60
Q

What is a conjugate vaccine and give an example

A

Binding of weak antigen to a strong antigen e.g. pneumococcus

61
Q

Describe the MenC vaccine

A

All in one paediatric vaccine. Includes whooping cough, tetanus, diphtheria, meningitis, septicaemia, polio 1,2,3,

62
Q

Describe fungi

A

Saprophytes that digest food extracellular
Spread via spores over large distances
eukaryotes

63
Q

What makes fungi different to bacteria

A

Membrane bound nucleus
Cell wall
DNA vs RNA
Harder to treat

64
Q

How may allergies be caused by fungi

A

Sensation to the spores causes allergic reaction e.g. asthma, rhinitis

65
Q

What is mycotoxicases

A

Inhalation or ingestion of a mycotoxins typically by eating poisonous mushroom. Certain crops -> aspergillum flavus -> aflatoxin -> hepatic carcinoma

66
Q

What is Mycoses

A

Fungal infection in animals e.g. candida

67
Q

What are the three types of mycoses

A

Superficial - rash in all ages OUTERMOST
Mucosal - immunosuppressed
Systemic - Catheter, gut surgery, chemo DEEP

68
Q

what are the 3 targets for fungi

A

cell membrane (ergosterol)
DNA synthesis
Cell wall

69
Q

What is latency

A

Latent infection where viral genomes are maintained but no virus is seen until episodes of reactivation when host immunity wanes. Herpes viruses eg Herpes Simplex, Varicella Zoster

70
Q

What is oncogenesis

A

Viruses can encode oncogenes
They interere with the cell cycle to enhance their own replication
Hep B and C can cause hepatocellular carcinoma
Epstein Barr Virus can lead to lymphomas and carcinomas

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