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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 routes of bacterial transmission

A 
expected = maternal microbiota to the newborn
Unexpected = surgery
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25
How may upper respiratory tract affect other organs
Spread to adjacent tissue (ear, brain) Spread to the blood stream (bacteraemia) Spread to the lower respiratory tract (bronchitis, pneumonia)
26
Give an example of an upper respiratory bacteria
neisseria meningiditis
27
What kind of bacteria infect the urogenital tract. Give an extrinsic and intrinsic route
intrinsic bacteria (E. coli). Ex- catheter, In- Bacteria
28
How may bacteria enter through skin
Wounds Skin diseases Insect bites I.V.
29
What kind of diseases may entry through skin diseases cause
Gangrene Cellulitis Bacteraemia
30
What bacteria causes tonsilitis
Streptococcus Pyogenes
31
Give an example of a bacteria that enters the GI tract
E. coli, Sigella spp., Vibrio Cholerae, Salmonella, Listeria
32
Give an example of a bacteria that enters the faeco-oral route
Cholera, E. Coli
33
What does Neisseria Meningiditis do
Releases respiratory endotoxin, damages RBCs, causes shock.
34
What does E. coli do
Caused by food/ water contamination, Toxins released into the blood stream via the large intestine. Causes kidney failure
35
What does staphylococcus aureus do
Releases toxins and enzymes
36
What is the infective dose and how is it measured
Minimum amount of pathogen required establish disease. Measured in colony-forming units
37
Define infectivity
The ability of a pathogen to establish an infection
38
Define virulence
Ability of a pathogen to cause disease
39
What feature contribute to infectivity
``` Transmission to host Colonisation Tropism (final niche and motility) Replication speed Evasion of the immune system ```
40
What features contribute to virulence
Toxin production Degrading enzymes Interruption of host cell processes Immune evasion
41
What is the process of shock
SIRS - Sepsis - Severe sepsis/shock - MODS
42
Describe SIRS
Severe Inflammatory Response Syndrome. Features include a temp. above 38 or below 36, respiratory rate above 20, heart rate above 90, WBC count above 10,000 or below 4000
43
Describe sepsis
SIRS and an infection . An overreaction and dysregulation. Includes skin warmth, decrease in mental ability, pain and breathing difficulty
44
Describe severe sepsis/ shock
Poor tissue diffusion. sepsis = Sepsis + lactic acidosis. Shock = sepsis +hypotension (increase in permeability and vasodilation)
45
Describe MODS
Multiple Organ dysfunction syndrome.
46
What is the treatment for sepsis
Antibiotic Blood Products Fluids and vasopressors to increase blood pressure
47
What are the sepsis risk factors
``` Genetic Microbiome Nutrition Stress Immunosuppression ```
48
What are the hospital-acquired diseases therapies
Antibiotics, bactericidal, bacteriostatic, anti-septic
49
What is the minimal inhibitory concentrations
Lowest concentration of antibiotic required to inhibit growth
50
What is the breakpoint
Breakpoint is the clinically achievable MIC
51
Why are hospital acquired diseases transmissible
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
What are antimicrobials
Any substance or chemical that kills a microbe or inhibits its growth
53
What are the classes of antimicrobials and what do they do
Beta-lactams - inhibits cell- wall synthesis Tetracyclines - efflux/membrane pumps Chloramphenicols- inhibits protein synthesis Quinolones - target site modification Sulphanamides - blocking uptake or influx Aminoglycosides - inhibits protein synthesis Macrolides - inhibits protein synthesis
54
What are the pathways of resistance
Altered target sites Antibiotic inactivation Altered metabolism Decreases drug accumulation
55
What is the basic resistance mechanism
``` Colony of bacteria present, some are resistant Antibiotic kills bacteria Resistant ones remain No competition for resources Resistant strain replicates ```
56
how does morbidity, mortality, length of stay and cost relate to resistance
More exposure to hospital pathogens, more illness, more drugs, cost of a bed
57
Which pathogens are multi-drug resistant
Gram -ve = E. Coli, Salmonella Neisseria Gonorrhoeae Gram +ve = Staphylococcus Aureus, S. Pneumoniae, clostridium dificcile Mycobacterium = M. Tuberculosis
58
Treatment of multi-drug resistant pathogens
``` Temporarily withdraw certain antibiotics Only use them for dangerous infections Reduce broad-spectrum antibiotics Identify resistant strains Combination therapy Adjust current antibiotics ```
59
What is the size of a virus
20-100nm
60
Compare enveloped to non-enveloped viruses
``` Enveloped = lipid=envelope from the host cell e.g. measles, ebola Non-enveloped = adenovirus, calcivirus ```
61
What are the features of a DNA virus
Segmented genomes Reassortment of 2 viruses Half of the DNA codes immune resistant proteins
62
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 ```
63
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
64
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)
65
How can viruses be analysed
Viruses will form plaques in monolayers - Assay Some viruses (HIV) do not form plaques but fuse = Syncytia Antibody generation
66
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 ```
67
Consideration for viral testing
Who will use it and where Source of the specimen Test purpose Stage of disease
68
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.
69
What is attenuation
The virus becomes so different that it is unable to grow as well in humans. Can be used for vaccines
70
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 ```
71
Describe viral transmission in terms of viraemia
Site of entry - blood (primary viraemia) - organ - Amplification - main organ through blood (secondary viraemia)
72
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
73
What are the modes of transmission for HIV
T cells - CD4, CCR5, CXCR4 (GP120)
74
What are the modes of transmission for Measles
Dendritic cells- CD155, SLAM, Neetin 4
75
What are the modes of transmission for influenza
endosomes, receptors found everywhere (ubiquitous). Low pH means HA fuses, Clara secrete, cleavage protein
76
What does counteraction of the host defence involve
Effects of replication Strength of the host immune system Ability of the virus to spread
77
What is pathogenicity
Ability to infect
78
Describe an acute infection and give examples
Infection followed by viral clearance. Smallpox, dengue, polio
79
Describe persistant infection
Latent, slow, transforming infection that is not cleared by adaptive immunity. Chronic or lifelong. HIV, varicella zoster
80
What gives acute infection epidemic potential
Transmission before the symptoms arise
81
How can polio strains vary in virulence
A single mutation can cause it to be live or to cause flaccid paralysis
82
What is the relationship between siblings and varicella zoster
1st child is milder while second is much worse
83
What is prophylaxis
Preventing the disease before the etiologic agent is acquired by vaccination or giving a drug before infection
84
What is therapy
Treating the disease after host infection
85
Compare vaccines and antivirals
prophylactic vs therapeutic Herd immunity or target group vs defined target group - very sick or over the counter government vs individuals
86
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
87
Smallpox
``` 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 ```
88
Why was smallpox eradicated
No animal reservoir 100% penetrance Obvious symptoms
89
Modern aims
eliminate polio and measles | Polio has two versions: live (Sabin) and inactive (Salk)
90
Describe selective drugs
Drugs are very specific to their viruses | An accurate diagnosis is required to inform correct drug choice
91
Why is combination therapy used
High mutation rate causes resistance development
92
What is genomics
Identifying host cell genes that viruses need
93
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
94
What are the features of influenza
Infects water fowl and mutation meant it infected humans. Changes in epitope means it can escape immunity.
95
What is reassortment
Combination of 2 viruses that infect the same cells
96
Define antigenic shift
When mutation adapt a virus for replication and transmission in humans and on its spread it displaces the previous strain
97
how was HIV introduced to humans
From simian virus - bushmeat trade. Quasispecies
98
How was west nile virus, norovirus and SARS introduced
WNV- Mosquitos and birds from Asia to USA Norovirus - small RNA SARS - bats
99
Why may new viruses emerge
Zoonosis Genetic variation Increased exposure (travelling or by vector) New discoveries
100
Define zoonosis
Crossing of an animal pathogen into humans
101
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.
102
Define quasispecies
A group of viruses related by a similar mutation(s), competing within a highly mutagenic environment.
103
What is fitness cost
resistant pathogens are unable to spread beyond the treated patient
104
Compare active and passive immunisation
``` Active = body makes its own antibodies (memory cells and protection against future infection) Passive = antibodies given directly ```
105
What is a live attenuated vaccine and give an example
Whole virus with reduced virulence e.g. MMR
106
What is an inactivated vaccine and give an example
Dead form of a pathogen e.g. Flu
107
What is a subunit vaccine and give an example
Strong immunity to antigens e.g. Hep B
108
What is a toxoid vaccine and give an example
Injection of the toxin that causes the disease e.g. Tetanus
109
What is a conjugate vaccine and give an example
Binding of weak antigen to a strong antigen e.g. pneumococcus
110
Describe the MenC vaccine
All in one paediatric vaccine. Includes whooping cough, tetanus, diphtheria, meningitis, septicaemia, polio 1,2,3,
111
Describe fungi
Saprophytes that digest food extracellular Spread via spores over large distances eukaryotes
112
What makes fungi different to bacteria
Membrane bound nucleus Cell wall DNA vs RNA Harder to treat
113
How may allergies be caused by fungi
Sensation to the spores causes allergic reaction e.g. asthma, rhinitis
114
What is mycotoxicases
Inhalation or ingestion of a mycotoxins typically by eating poisonous mushroom. Certain crops -> aspergillum flavus -> aflatoxin -> hepatic carcinoma
115
What is Mycoses
Fungal infection in animals e.g. candida
116
What are the three types of mycoses
Superficial - rash in all ages OUTERMOST Mucosal - immunosuppressed Systemic - Catheter, gut surgery, chemo DEEP
117
what are the 3 targets for fungi
cell membrane (ergosterol) DNA synthesis Cell wall

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