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MCD > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Give 3 bacterial features

A
  • No membrane bound organelles
  • Haploid
  • May have flagella
  • Very small and unicellular
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2
Q

What are the forms of bacteria

A

Cocci, Bacili, Spinilli

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3
Q

Describe the grams stain process

A

Add violet dye
iodine
rinse with alcohol
Red dye

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4
Q

Why do bacteria have difference results from gram stain

A

Gram negative bacteria have two membranes so the violet dye is lost to one of them and the red counterstain is absorbed instead -> pink colour

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5
Q

Which type of bacteria cannot use a gram stain

A

Mycobacterium

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6
Q

What stain must be used for mycobacterium

A

Acid-fast as they do not decolourise

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7
Q

Give 2 examples of gram -ve bacteria

A

Shigella, Salmonella, E.Coli etc.

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8
Q

Give 2 examples of gram +ve bacteria

A

Streptococcus pneumoniae

Staphylocuccus Aureus

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9
Q

What do bacterial pathogens do

A 
Colonise
Persist
Replicate
Disseminate
Cause disease
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10
Q

Give examples of extracellular bacteria

A

Staphylococcus Aureus
Streptococcus Pneumoniae
Neisseria

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11
Q

Give examples of Intracellular bacteria

A 
Shigella
Salmonella 
E. Coli
Chlamydia
Coxiella
Mycobacteria
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12
Q

How do chlamydia, mycobacteria and Shigella survive

A

Inhibit fusion of the lysosome with the phagosome

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13
Q

How does coxiella survive

A

Survives in the phagosome

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14
Q

How do listeria and shigella survive

A

Escapes the phagosome

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15
Q

What is the purpose of the flagella and give an example of a bacteria that uses it

A

Movement and salmonella

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16
Q

What is the injectisome and give an example of a bacteria that uses it

A

manipulates the host actin cytoskeleton so that the bacteria can enter and move. Salmonella and Listeria

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17
Q

What are the three mechanisms of horizontal gene transfer

A

Transformation
Confugation
Transuction

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18
Q

Describe transformation and give bacterial examples

A

Uptake of naked DNA and integration into the host genome. Neisseria and streptococcus

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19
Q

Describe conjugation and give bacterial examples

A

Transferring a plasmid that gives antibiotic resistance. The plasmid is OriT which transfers via a mating bridge. The new plasmid is produced via semi-conservative replication. Gram -ve and +ve

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20
Q

Describe transduction and give bacterial examples

A

Bacteriophages insert DNA and cleave the bacterial DNA, packaging it into bacteriophages which then travel to other bacterium to inject material.

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21
Q

What contributes to evolution of bacteria

A

Pathogenicity island, horizontal gene transmission, selection pressure, rapid replication, genetic variation

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22
Q

What is a pathogenicity island

A

Pathogenicity Isalnds are a class of non-core genomes that are acquired by HORIZONTAL TRANSMISSION; they can be revealed by aligning pathogenic genomic DNA and a closely-relate non-pathogen.

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23
Q

Compare intrinsic sources to extrinsic sources

A 
Intrinsic = non-sterile sites e.g. mouth, respiratory tract, sinus, lower genital tract, stomach etc.
Extrinsic = other people or living things e.g. animals, food, water
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24
Q

Compare expected vs unexpected routes of bacterial transmission

A 
expected = maternal microbiota to the newborn
Unexpected = surgery
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25
Q

How may upper respiratory tract affect other organs

A

Spread to adjacent tissue (ear, brain)
Spread to the blood stream (bacteraemia)
Spread to the lower respiratory tract (bronchitis, pneumonia)

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26
Q

Give an example of an upper respiratory bacteria

A

neisseria meningiditis

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27
Q

What kind of bacteria infect the urogenital tract. Give an extrinsic and intrinsic route

A

intrinsic bacteria (E. coli). Ex- catheter, In- Bacteria

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28
Q

How may bacteria enter through skin

A

Wounds
Skin diseases
Insect bites
I.V.

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29
Q

What kind of diseases may entry through skin diseases cause

A

Gangrene
Cellulitis
Bacteraemia

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30
Q

What bacteria causes tonsilitis

A

Streptococcus Pyogenes

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31
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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32
Q

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

A

Cholera, E. Coli

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33
Q

What does Neisseria Meningiditis do

A

Releases respiratory endotoxin, damages RBCs, causes shock.

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34
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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35
Q

What does staphylococcus aureus do

A

Releases toxins and enzymes

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36
Q

What is the infective dose and how is it measured

A

Minimum amount of pathogen required establish disease. Measured in colony-forming units

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37
Q

Define infectivity

A

The ability of a pathogen to establish an infection

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38
Q

Define virulence

A

Ability of a pathogen to cause disease

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39
Q

What feature contribute to infectivity

A 
Transmission to host
Colonisation
Tropism (final niche and motility)
Replication speed
Evasion of the immune system
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40
Q

What features contribute to virulence

A

Toxin production
Degrading enzymes
Interruption of host cell processes
Immune evasion

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41
Q

What is the process of shock

A

SIRS - Sepsis - Severe sepsis/shock - MODS

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42
Q

Describe SIRS

A 
Severe Inflammatory Response Syndrome.
temp. above 38 or below 36
respiratory rate above 20 
heart rate above 90
WBC count above 10,000 or below 4000
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43
Q

Describe sepsis

A

SIRS and an infection . An overreaction and dysregulation. Includes skin warmth, decrease in mental ability, pain and breathing difficulty

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44
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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45
Q

Describe MODS

A

Multiple Organ dysfunction syndrome.

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46
Q

What is the treatment for sepsis

A

Antibiotic
Blood Products
Fluids and vasopressors to increase blood pressure

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47
Q

What are the sepsis risk factors

A 
Genetic 
Microbiome
Nutrition
Stress
Immunosuppression
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48
Q

What are the hospital-acquired diseases therapies

A

Antibiotics, bactericidal, bacteriostatic, anti-septic

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49
Q

What is the minimal inhibitory concentrations

A

Lowest concentration of antibiotic required to inhibit growth

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50
Q

What is the breakpoint

A

Breakpoint is the clinically achievable MIC

51
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

52
Q

What are antimicrobials

A

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

53
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

54
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.

55
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

56
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

57
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

58
Q

What are the pathways of resistance

A

Altered target sites
Antibiotic inactivation
Altered metabolism
Decreases drug accumulation

59
Q

What is the basic resistance mechanism

A 
Colony of bacteria present, some are resistant
Antibiotic kills bacteria
Resistant ones remain
No competition for resources
Resistant strain replicates
60
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
61
Q

Describe selective toxicity

A

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

62
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.

63
Q

Give some non-genetic mechanisms of AB resistance

A 
Biofilm
Intracellular location
Slow growth
Spores
Persisters
64
Q

Give some examples of hospital-acquired infections

A

S. aureus
E. coli
Clostridium difficle

65
Q

What are the risk factors for hospital acquired infections

A

High number of ill people! (immunosuppression)
Crowded wards
Presence of pathogens
Broken skin – surgical wound/IV catheter
Indwelling devices - intubation
AB therapy may suppress normal flora
Transmission by staff – contact with multiple patients

66
Q

What is the size of a virus

A

20-100nm

67
Q

Compare enveloped to non-enveloped viruses

A 
Enveloped = lipid=envelope from the host cell e.g. measles, ebola
Non-enveloped = adenovirus, calcivirus
68
Q

What are the features of a DNA virus

A

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

69
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
70
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

71
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)

72
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

73
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
74
Q

Consideration for viral testing

A

Who will use it and where
Source of the specimen
Test purpose
Stage of disease

75
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.

76
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

77
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
78
Q

Describe viral transmission in terms of viraemia

A

Site of entry - blood (primary viraemia) - organ - Amplification - main organ through blood (secondary viraemia)

79
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

80
Q

What are the modes of transmission for HIV

A

T cells - CD4, CCR5, CXCR4 (GP120)

81
Q

What are the modes of transmission for Measles

A

Dendritic cells- CD155, SLAM, Neetin 4

82
Q

What are the modes of transmission for influenza

A

endosomes, receptors found everywhere (ubiquitous). Low pH means HA fuses, Clara secrete, cleavage protein

83
Q

What is pathogenicity

A

Ability to infect

84
Q

Describe an acute infection and give examples

A

Infection followed by viral clearance. Smallpox, dengue, polio

85
Q

Describe persistant infection

A

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

86
Q

What gives acute infection epidemic potential

A

Transmission before the symptoms arise

87
Q

How can polio strains vary in virulence

A

A single mutation can cause it to be live or to cause flaccid paralysis

88
Q

What is the relationship between siblings and varicella zoster

A

1st child is milder while second is much worse

89
Q

What is prophylaxis

A

Preventing the disease before the etiologic agent is acquired by vaccination or giving a drug before infection

90
Q

What is therapy

A

Treating the disease after host infection

91
Q

Compare vaccines and antivirals

A

prophylactic vs therapeutic
Herd immunity or target group vs defined target group - very sick or over the counter
government vs individuals

92
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

93
Q

Describe the progression of smallpox

A 
success of the cowpox vaccination
other strains grown on animals skin 
Sporadic flare of epidemics
WHO invested $2.5 million
1977- last case in Somalia (endgame) - ring vaccination of everyone in the area
94
Q

Why was smallpox eradicated

A

No animal reservoir
100% penetrance
Obvious symptoms

95
Q

What are the modern aims

A

eliminate polio and measles

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

96
Q

Describe selective drugs

A

Drugs are very specific to their viruses

An accurate diagnosis is required to inform correct drug choice

97
Q

Why is combination therapy used

A

High mutation rate causes resistance development

98
Q

What is genomics

A

Identifying host cell genes that viruses need

99
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

100
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.

101
Q

What is reassortment

A

Combination of 2 viruses that infect the same cells

102
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

103
Q

how was HIV introduced to humans

A

From simian virus - bushmeat trade. Quasispecies

104
Q

How was west nile virus, norovirus and SARS introduced

A

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

105
Q

Why may new viruses emerge

A

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

106
Q

Define zoonosis

A

Crossing of an animal pathogen into humans

107
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.

108
Q

Define quasispecies

A

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

109
Q

What is fitness cost

A

resistant pathogens are unable to spread beyond the treated patient

110
Q

Compare active and passive immunisation

A 
Active = body makes its own antibodies (memory cells and protection against future infection)
Passive = antibodies given directly
111
Q

What is a live attenuated vaccine and give an example

A

Whole virus with reduced virulence e.g. MMR

112
Q

What is an inactivated vaccine and give an example

A

Dead form of a pathogen e.g. Flu

113
Q

What is a subunit vaccine and give an example

A

Strong immunity to antigens e.g. Hep B

114
Q

What is a toxoid vaccine and give an example

A

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

115
Q

What is a conjugate vaccine and give an example

A

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

116
Q

Describe the MenC vaccine

A

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

117
Q

Describe fungi

A

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

118
Q

What makes fungi different to bacteria

A

Membrane bound nucleus
Cell wall
DNA vs RNA
Harder to treat

119
Q

How may allergies be caused by fungi

A

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

120
Q

What is mycotoxicases

A

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

121
Q

What is Mycoses

A

Fungal infection in animals e.g. candida

122
Q

What are the three types of mycoses

A

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

123
Q

what are the 3 targets for fungi

A

cell membrane (ergosterol)
DNA synthesis
Cell wall

MCD (13 decks)

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