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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
Give some examples of hospital-acquired infections
S. aureus E. coli Clostridium difficle
26
Compare enveloped to non-enveloped viruses
``` Enveloped = lipid=envelope from the host cell e.g. measles, ebola Non-enveloped = adenovirus, calcivirus ```
27
What are the features of a DNA virus
Segmented genomes Reassortment of 2 viruses Half of the DNA codes immune resistant proteins
28
What is the basic viral life cycle
``` 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 ```
29
What is the HIV life cycle
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
How are viruses detected
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
How can viruses be analysed
Viruses will form plaques in monolayers - Assay Some viruses (HIV) do not form plaques but fuse = Syncytia Antibody generation
32
How are viral infection diagnosed
``` Amplify genomes using PCR Detect using IDA or ELISA Look for viral particles Cytopathic effect Antibodies (Serology) High density fluorescent markers ```
33
Describe propagation
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
What is attenuation
The virus becomes so different that it is unable to grow as well in humans. Can be used for vaccines
35
What are the viral routes
``` 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
What is tropism
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
What are the modes of transmission for HIV
T cells - CD4, CCR5, CXCR4 (GP120)
38
What are the modes of transmission for Measles
Dendritic cells- CD155, SLAM, Neetin 4
39
What are the modes of transmission for influenza
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
What is pathogenicity
Ability to infect
41
Describe an acute infection and give examples
Infection followed by viral clearance. Smallpox, dengue, polio
42
Describe persistant infection
Latent, slow, transforming infection that is not cleared by adaptive immunity. Chronic or lifelong. HIV, varicella zoster
43
Compare the different types of vaccines
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
Why was smallpox eradicated
No animal reservoir 100% penetrance Obvious symptoms
45
What are the modern aims
eliminate polio and measles | Polio has two versions: live (Sabin) and inactive (Salk)
46
What is genomics
Identifying host cell genes that viruses need
47
Give examples of successful viral therapy
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
What are the features of influenza
Infects water fowl and mutation meant it infected humans. Changes in epitope means it can escape immunity.
49
Define antigenic shift
When mutation adapt a virus for replication and transmission in humans and on its spread it displaces the previous strain
50
What is reassortment
Combination of 2 viruses that infect the same cells
51
How was west nile virus, norovirus and SARS introduced
WNV- Mosquitos and birds from Asia to USA Norovirus - small RNA SARS - bats
52
Why may new viruses emerge
Zoonosis Genetic variation Increased exposure (travelling or by vector) New discoveries
53
Define zoonosis
Crossing of an animal pathogen into humans
54
Define the host range barrier
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
Define quasispecies
A group of viruses related by a similar mutation(s), competing within a highly mutagenic environment.
56
What is fitness cost
resistant pathogens are unable to spread beyond the treated patient
57
What is a live attenuated vaccine and give an example
Whole virus with reduced virulence e.g. MMR
58
What is an inactivated vaccine and give an example
Dead form of a pathogen e.g. Flu
59
What is a toxoid vaccine and give an example
Injection of the toxin that causes the disease e.g. Tetanus
60
What is a conjugate vaccine and give an example
Binding of weak antigen to a strong antigen e.g. pneumococcus
61
Describe the MenC vaccine
All in one paediatric vaccine. Includes whooping cough, tetanus, diphtheria, meningitis, septicaemia, polio 1,2,3,
62
Describe fungi
Saprophytes that digest food extracellular Spread via spores over large distances eukaryotes
63
What makes fungi different to bacteria
Membrane bound nucleus Cell wall DNA vs RNA Harder to treat
64
How may allergies be caused by fungi
Sensation to the spores causes allergic reaction e.g. asthma, rhinitis
65
What is mycotoxicases
Inhalation or ingestion of a mycotoxins typically by eating poisonous mushroom. Certain crops -> aspergillum flavus -> aflatoxin -> hepatic carcinoma
66
What is Mycoses
Fungal infection in animals e.g. candida
67
What are the three types of mycoses
Superficial - rash in all ages OUTERMOST Mucosal - immunosuppressed Systemic - Catheter, gut surgery, chemo DEEP
68
what are the 3 targets for fungi
cell membrane (ergosterol) DNA synthesis Cell wall
69
What is latency
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
What is oncogenesis
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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