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Infection and Immunity > Bacterial Pathogenesis and Immune Evasion > Flashcards

Bacterial Pathogenesis and Immune Evasion Flashcards

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1
Q

What is balanced pathogenicity?

A

Balance between properties of the microbe and properties of the host (pathogenic mechanisms and defensive mechanisms)

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2
Q

What are some pathogenic mechanisms?

A

Adhesins
Toxins
Capsule

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3
Q

What are some defensive mechanisms?

A

Natural barriers
Defensive cells
Complement
Immune response

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4
Q

What do virulence factors do?

A

Promote colonisation and adhesion
Evade host defences
Promote tissue damage

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5
Q

What are some virulence factors?

A

Adherence factors
Invasion factors
Capsules
Endotoxins
Exotoxins
Siderophores

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6
Q

What do adherence factors do?

A

Colonise mucosal sites by using pili to adhere to cells

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7
Q

What are invasion factors?

A

Surface components and secreted effector proteins

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8
Q

What are capsules?

A

Polysaccharides
Protect from opsonisation and phagocytosis

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9
Q

Describe endotoxins

A

Lipopolysaccharide on gram negatives
Lipoteichoic acids on gram positives
Cause fever, changes in BP, inflammation, lethal shock

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10
Q

What are exotoxins?

A

Protein toxins and enzymes produced and/or secreted

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11
Q

What are siderophores?

A

Iron-binding factors to compete with the host for iron haemoglobin, transferrin and lactoferrin

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12
Q

What are the types of pathologic effects of infection?

A

Direct
Via innate immune mechanisms
Via adaptive immune mechanisms (hypersensitivity)

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13
Q

Describe the pathogenesis and defence to Bordetella pertussis (whooping cough)

A

Pathogenesis - numerous toxins, non-invasive
Defence - mucosal and systemic antibody to toxins and adhesins

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14
Q

Describe the pathogenesis and defence to Vibrio cholerae

A

Pathogenesis - non-invasive enteritis
Defence - neutralising and adhesion Abs, antitoxin Abs

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15
Q

Describe pathogenesis and defence to Neisseria meningitidis

A

Pathogenesis - nasopharynx carriage; bacteriaemia, meningitis, endotoxaemia
Defence - killed by lytic, opsonised by Ab then phagocytosed and killed

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16
Q

Describe the pathogenesis and defence to Staphylococcus aureus

A

Pathogenesis - locally invasive and toxins
Defence - Opsonised by Ab and complement, killed by phagocytes

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17
Q

Describe the pathogenesis and defence to Mycobacterium tuberculosis

A

Pathogenesis - invasive, immunopathology granuloma
Defence - macrophage activation by cytokines from T cells

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18
Q

Describe the pathogenesis and defence to Streptococcus pneumoniae

A

Pathogenesis - inflammatory, toxin causes damage, carriage invasion
Defence - muco-ciliary clearance, splenic filtration, complement activation, Ab opsonisation

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19
Q

What are the stages of infection?

A

Acquisition
Colonisation - adherence
Penetration
Multiplication and spread
Immune avoidance
Damage
Transmission
Resolution

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20
Q

What are the mechanisms of microbial interactions with immunity?

A

Extracellular - pneumolysin, superantigens, toxins
Capsule - inhibition C3b and Ig deposition, -ve phagocytosis
Surface structures - protein A, M protein, LPS
Direct secretion of effector proteins into cells - type 3 secretion systems
Intracellular survival mechanisms

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21
Q

What are some receptors for adhesins?

A

Glycolipids
Glycoproteins
Transmembrane proteins
Mucins

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22
Q

Give examples of bacterial adhesins

A

Fimbriae/pili
Capsular polysaccharides
LPS
Lipoteichoic acid
Outer membrane proteins
Flagella
Curli - Salmonella, bind to fibronectin and laminin

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23
Q

Describe adherence in E coli

A

P fimbriae bind P blood group on uroepithelial cells

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24
Q

Describe adherence in Neisseria gonorrhoeae

A

Pili attach to mucosal cells
Non-piliated mutants are less pathogenic

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25
Describe adherence in Vibrio cholerae
Fimbriae bind intestinal epithelial cell receptors
26
Describe adherence in Strep pyogenes
Lipoteichoic acid binds to epithelial cell
27
What is the function of M protein in Streptococcus pyogenes?
Acts as adhesin and structural component of cell wall
28
Describe Neisseria-host interactions
Pili allow anchorage to epithelial cells Tight adherence maintained by Opa proteins Invasion and transcytosis Formation of granulocyte Invasion and intracellular accommodation Formation of monocyte Systemic infection of endothelial cells
29
Describe promoted phagocytosis as a host-pathogen interaction
Some pathogens allow themselves to be phagocytosed instead of evading phagocytosis as the next step in their pathogenicity is after being phagocytosed They manipulate the phagocyte such that they do not get killed when they are engulfed e.g. Streptococcus pyogenes
30
What can E. coli manipulate host cells to do?
Form attachments pedestals for them to adhere to
31
Describe attachment and pedestal formation by EPEC
Bundle forming pili (bfp) mediate the initial attachments to the microvilli of the host cell Type 3 secretion systems are activated Bacterial translocation intimin receptor (Tir) is secreted and injected onto host cell and binds to intimin Loss of microvilli Actin rearrangements lead to formation of pedestal
32
Describe what is meant by attaching and effacing lesion
Microvillus elongation Effacement of apical membrane - destruction of microvilli Pedestal formation
33
Where is E. coli commensal?
The gut
34
What can E. coli cause?
Diarrhoea Dystentery Haemolytic uraemic syndrome (HUS) Urinary tract and kidney infections Septicaemia Pneumonia and meningitis
35
What are virulence factors of E. coli?
Toxins Adhesins Invasins
36
Describe ETEC infection
Traveller's diarrhoea Secretory No inflammation No structural changes Toxins = LT and ST cGMP at membrane
37
Describe EPEC infection
Diarrhoea Attaching and effacing lesions
38
Describe EIEC infection
Dysentery Specific serotypes
39
Describe EHEC infection
O157:H7 Verotoxin (Shiga-like toxin) Intense inflammation HUS Dysentery (not so invasive) Attaching and effacing lesions
40
Describe the role of Tir in type 3 secretion systems
Release of Tir from bacteria when bfp facilitates attachment to host Tir is then phosphorylated and is injected into the host membrane Allows binding of intimin (adhesin protein) Activation of cytoskeletal rearrangements and pedestal formation
41
Describe the molecular structure of a type 3 secretion system
Pore complex - YopBD, LcrV Needle - YscF Basal body - Ysc secretory proteins
42
What are YOPS?
YOPS - Yersinia outer membrane proteins Bacterium Yersinisa pestis secretes YOPS into macrophage and PMNs Each YOP has different effects
43
What effects does YopE have?
Actin rearrangement via GTPases Cell rounding Anti-phagocytic
44
What effects does YopH have?
YopH is a tyrosine phosphatase Negative phagocytosis - YopH blocks ability of cell to undergo phagocytosis
45
What effects does YopJ/P have?
Blocks TNF and MAP kinase release Induces apoptosis
46
What effects does YopA/O have?
A serine protease so will breakdown several proteins
47
What effects does YopT have?
Actin rearrangement
48
What are molecular syringes?
Gram negative bacteria that inject effectors into a host cell
49
Give some examples of molecular syringes
Salmonella gut epithelium invasion Modification macrophage phagosome Yersinia inhibition neutrophil and macrophage function Shigella macrophage invasion and escape from phagosome Cell-to-cell spread EHEC and EPEC adhesion to gut epithelium Legionella inhibition phagolysosomal fusion
50
Why is site of infection of intracellular pathogens commonly the macrophage?
It is the first cell to encounter the pathogen It can subvert bacterial recognition and phagocytic pathways to encourage infection
51
What are some examples of intracellular pathogens?
M. tuberculosis Listeria monocytogenes - gram positive Legionella pneumophila - gram negative Leishmania - protozoa Histoplasma capsulatum - fungi Salmonella typhi - gram negative Francisella tularensis - gram negative Coxiella burnettii - ricketsia
52
How do bacteria interfere with cellular functions?
Adhesion to receptors e.g. adhesins and integrins Manipulation of cytoskeleton by invasive and non-invasive organisms, pedestal formation by E. coli Manipulation of cytoskeleton for movement of intracellular organism e.g. Shigella Endosomal trafficking e.g. M. tuberculosis Manipulation of lysosomal function e.g. S. typhi Escape from phagosome e.g. Legionella -ve protein synthesis e.g. diphtheria Membrane disruption Pore forming toxins Blocking of phagocytosis e.g. Yersinia
53
How does staphylococci prevent phagocytosis?
Produces leucocidins that kill the cell Have protein A on their surface which binds Abs the wrong way round (binds Fc portion of IgG) preventing opsonisation Expression of Fc receptors similar to protein A
54
What is the purpose of capsules on bacteria?
Block phagocytosis e.g. meningococci, Haemophilus influenzae
55
How do intracellular pathogens cause infection?
Promote uptake via CR, Fc receptors Prepares cell for invasion by class 3 secretion e.g. Shigella Prevents phagosome-lysosome fusion e.g. M.tb escape P-L to cytoplasm e.g. Listeria Resist oxidative killing by producing catalase/peroxidases that block MHC, IFN receptors and TNF release
56
Describe listeria cell-cell invasion
Listeria phagocytosed and endosome formation Listeriolysin (intracellular pore forming toxin) released from endosome into cytoplasm Other effector proteins released that take control of actin filament formation inside cell Actin re-arrangement allows transport of bacteria through the cell and from one cell to another
57
What are the roles of complement?
Induces inflammatory response Promotes chemotaxis Increases phagocytosis by opsonisation Increases vascular permeability Mast cell degranulation Lysis of cell membranes Activates macrophages (C3a) Removal of immune complexes
58
How do bacteria avoid complement?
Surface components of bacterial polysaccharide capsules are poor activators of complement Long side chains (O antigens) fix C3b and prevent access to the membrane Capsules rich in sialic acid promote interaction with H and I factors hat promote MAC dissociation e.g. Group B Streps, N. meningitidis, E coli K1 Outer layer of G-ve bacteria can rapidly shed C5b-C9 MAC C3a and C5a proteases Coat themselves with non-complement fixing IgA
59
Describe the importance of opsonisation
Uncoated by Abs, bacteria are phagocytosed poorly When coated with Ab, adherence to phagocytosis is enhanced
60
Give examples of opsonins
IgG1 and 3 IgM C3b CRP
61
What are the phagocyte receptors?
Fc CR3
62
Name some bacteria that have capsules
Neisseria meningitidis Haemophilus influenzae Streptococcus pneumoniae (G+ve) E. coli K1
63
What does presence of a sialic acid or hyaluronic acid capsule result in?
Decreased complement binding/activation Decreased opsonisation Decreased phagocytosis
64
How can the host's immune defences cause damage?
Overactivity of immune defences e.g. with endotoxins produced by G-ve bacteria Types of hypersensitivity e.g. type 4 hypersensitivity granuloma in TB Cross-reaction with host e.g. Strep pyogenes in Rheumatic fever
65
Describe how S. aureus stimulates IL8
Surface protein A binds epithelial TNF-a receptor (TNFR1) Stimulates proinflammatory signalling Induces IL8 secretion Increased neutrophil recruitment Necrotising destructive pneumonia S. aureus stimulation of IL8 is detrimental to the host
66
Describe cross reactivity in Strep pyogenes infection
Abs against strep antigens are produced - group A carbohydrate and M protein These Abs cross-react with antigens of the host Binding of Ab to host Ag activates complement and leads to inflammatory responses and hypersensitivity reactions
67
What are some sites of cross reactivity in Strep pyogenes infection?
Myocardium - rheumatic heart disease Synovium - reactive arthritis Brain - Sydenhams chorea Kidney - post-streptococcal acute glomerulonephritis

Infection and Immunity (33 decks)

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