FOM Flashcards
1
Q
What is a pathogen?
A
- organism that causes or is capable of causing disease
2
Q
What is a commensal?
A
- organism which colonises the host but causes no disease in normal circumstances
3
Q
What is an opportunist pathogen?
A
- only causes disease if host defences are compromised
4
Q
What is virulence/pathogenicity?
A
- degree to which a given organism is pathogenic
5
Q
What is the asymptomatic carriage?
A
- pathogen carried harmlessly at tissue site where it causes no disease
6
Q
How does a coccus appear under microscope?
A
- small and round
7
Q
Describe gram stain results
A
- blue: positive
- pink: negative
8
Q
Gram postive vs gram negative
A
- positive: tend to be rich in peptidoglycan
- negative: have very little peptidoglycan, rich in lipopolysaccharide
9
Q
Describe innate immunity
A
- first line of body immune defence
- active immediately after antigen enters body
- not antigen specific, not highly effective, no immunological memory
10
Q
What is the first line of defence?
A
- barrier: skin, mucosal membrane
- acts as a mechanical barrier and has acidic environment
11
Q
What happens in the early phase of innate immunity?
A
- activation of tissue resident immune cells and inflammation
- 0-4 hours. Dendritic cells and macrophages hone into area
12
Q
Soluble mediators released by macrophages
A
- secretion of cytokines, histamine prostaglandins and leukotrienes
13
Q
Role of complement in innate immunity
A
- contain nine proteins: C1-9. Present in plasma, synthesise in liver
- activated by extracellular pathogens
- promote inflammation. Act in enzymatic cascade. Produce effector molecules
14
Q
Soluble mediator released by mast cell
A
- activation by complement and secretion of histamine prostaglandins and leukotrienes
- make it easier for non-local cells to access
- increase permeability of blood vessels
15
Q
Describe second phase of innate immunity
A
- neutrophils
- 4-96 hours
- monocytes: able to differentiate into other immune cells
- complement entry into inflamed tissue
16
Q
Describe adaptive immunity
A
- highly antigen specific, effective elimination mechanisms, memory cells allow quick and effective response
17
Q
Disadvantages of adaptive immunity
A
- takes a few days
- ineffective for pathogens not previously been in contact with
18
Q
Disadvantages of innate immunity
A
- not antigen specific, not highly effective, no immunologic memory
19
Q
What does the activation of T cells involve?
A
- dendritic cells present peptide antigen to T cells
- T cells are activated and proliferate: T cell receptors
20
Q
Role of dendritic cells in adaptive immunity
A
- break down bacteria into smaller chunks and present them on surface
- bound to MHC (major histocompatibility complex) molecules
21
Q
Where do T cells typically reside?
A
- paracortex of lymph node
22
Q
MHC class I present only what cell?
A
- CD8 T cells (Cytotoxic)
23
Q
MHC class II only present what cells?
A
- CD4 T cells
24
Q
What does the activation of B cells involve?
A
- detect bacterial/viral antigen using B cell receptor
- CD4 activates B cell and B cells further activates CD4 cell
- causes activation, proliferation and differentiation: plasma cells turn into antibodies
25
What occurs after B cells differentiate into plasma cells?
- migrate from cortex to medulla
- secretion of antigen-specific antibodies
- all antibodies would have same specificity but soluble versions of initial B cell receptors
26
How do phagocytes recognise pathogens?
- Pathogen Associated Molecular Patterns (PAMPs): unique features found on non-self
- using Pathogen Recognition Receptors (PRRs)
27
What does PRR binding to PAMP lead to?
- activation of macrophages and uptake of pathogen
28
How does the recognition and activation of T cells occur?
- dendritic cells present antigen to T cells (MHC molecules)
- antigen detected by T cell receptor
29
How does the recognition and activation of B cells occur?
- detect whole antigen using B cell receptor. Causes activation, proliferation and differentiation
30
What are the five types of immunoglobulin?
- IgM, IgG, IgA, IdE, IgD
31
What are the ways antibodies fight extracellular infection?
- neutralise toxins by direct binding
- agglutination and opsonises them
- form complexes which activate classical complement pathway
- directly activate effector cells
32
How do antibodies have the ability to recognise a huge number of different antigens?
- single antigen receptor on surface
- fine tuning during course of response
- surface complementary to antigen
- specificity achieved in antigen-binding sites
33
Describe features of the viral particle
- all contain proteinaceous capsid/nucleocapsid 'cage' surrounding viral nucleic acid
- contain viral-encoded membrane proteins that bind to cells and deliver virion across plasma membrane
34
Role of the viral particle
- protects viral genome from environment
- delivers viral genome into uninfected cells
- binds uninfected cells
35
What are non-enveloped viruses?
- rely purely on capsid to protect genome, bind to cells and deliver genome across plasma membrane
36
What are enveloped viruses?
- surround capsid protein with a lipid membrane acquired from infected cell.
- contain viral-encoded membrane proteins that bind to cells and deliver the virion across the plasma membrane
37
What are the three broad types of viruses?
- DNA viruses
- RNA viruses
- reverse-transcribing viruses
38
How do DNA viruses replicate?
- need DNA polymerase to replicate genome
- DNA genome as template for mRNA transcription
39
How do RNA viruses replicate?
- need novel RNA-dependent RNA polymerase to their genome
- either use genome as mRNA for protein or transcribe mRNAs from their genome
- positive-sense
- negative-sense
40
How do reverse-transcribing viruses replicate?
- carry novel reverse transcriptase polymerase in with their viral particles
- mRNAs encoding viral proteins arise from nuclear transcription from DNA copies
- single strand introduce DNA copy of genome into host DNA
41
What is R (reproductive number)?
- average number of successful transmissions per infectious individual in a population
42
What are examples of non-specific markers of infection?
- C-reactive protein
- Procalcitonin
43
What are the ways disease can be caused in infection?
- damage directly by pathogen
- damage mediated via overactive/inappropriate natural (innate) immune mechanisms
- damage mediated via inappropriate adaptive immune mechanisms
44
What is a vaccination?
- deliberate induction of adaptive immune response to pathogen by injecting a vaccine
45
What is immunisation?
- deliberate provocation of adaptive immune response by introducing antigen into body
46
How is active immunisation achieved?
- administration of all/part of / modified product of micro organism to evoke immune response
- mimicking natural infection
47
What forms of vaccines are involved in active immunisation?
- live attenuated
- inactivated
- Detoxified endotoxins
48
How is passive immunisation achieved?
- administration of preformed antibody to a recipient for prevention and amelioration of infectious disease
49
What does DALY mean?
- disability-adjusted life years
50
What does YLL mean?
- number of life years lost
51
What does YLD mean?
- number of years lost due to disability
52
What is Basic Reproductive Number RO?
- indicator of how contagious an infective organism is in a susceptible population
53
What is RO dependent on?
- density
- incubation periods
- latent periods
- mode of transmission
54
How is RO used in vaccination?
- used to determine what % of population would need to be vaccinated for herd immunity
55
What is colonisation?
- presence of bacteria with growth and multiplication but without invasion
- can be colonisation without infection
56
What are factors which promote colonisation?
- pili
- fimbriae
- adhesins
- biofilms
57
What is invasiveness?
- ability of pathogen to invade
- includes: colonisation factors, secreted factors that enable invasion into host cells
- evasion of immune system
58
What are the different antibiotic mechanisms?
- binding to cell wall, inhibition of synthesis. Cause lysis
- interference with nucleic acid/function
- inhibition of DNA gyrase
- inhibition of ribosomal activity and protein synthesis
- inhibition of folate synthesis and carbon unit metabolism
59
What do beta lactams do?
- interrupt bacterial cell wall formation
60
Examples of beta lactams?
- penicillins, glycopeptides, cephalosporin
61
What type of bacteria does penicillin work on?
- gram positive bacteria
62
What does adding an amino group do to penicillin?
- turn into ampicillin
- has some effectiveness against gram positive and negative bacteria
63
Describe how some bacterias may have penicillin resistance?
- some bacteria can alter penicillin binding protein so antibiotics cannot bind
- secrete enzymes
64
Examples of antibiotics interrupting nucleic acid/function
- metronidazole
- rifampicin
65
What type of antibiotics inhibit DNA gyrase?
- fluoroquinolone
66
What is a disadvantage of antibiotics inhibiting protein synthesis?
- although protein is prevented from being made, bacteria is not killed instantly
- generally not suitable for serious hospital infections
67
Examples of antibiotics inhibiting protein synthesis
- aminogycosides, tetracyclines, macrolides, chloramphenicol
68
Why cannot trimethoprim be used in pregnant women?
- inhibit folate synthesis essential for DNA synthesis
- cause baby to develop spina bifida
69
What are the mechanisms of antibiotic resistance?
- have inactivating enzymes
- modified impermeable cell envelope
- expel drug from efflux systems
- modify drug targets to prevent binding
- drug bypassed by changing metabolic pathway
70
What is an efflux system?
- pump out unwanted toxic substances through specific efflux pumps
71
