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Infection and Immunity > Bacterial Pathogenesis and Immune Evasion > Flashcards

Bacterial Pathogenesis and Immune Evasion Flashcards

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
Q

Describe adherence in Vibrio cholerae

A

Fimbriae bind intestinal epithelial cell receptors

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26
Q

Describe adherence in Strep pyogenes

A

Lipoteichoic acid binds to epithelial cell

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27
Q

What is the function of M protein in Streptococcus pyogenes?

A

Acts as adhesin and structural component of cell wall

28
Q

Describe Neisseria-host interactions

A

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
Q

Describe promoted phagocytosis as a host-pathogen interaction

A

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
Q

What can E. coli manipulate host cells to do?

A

Form attachments pedestals for them to adhere to

31
Q

Describe attachment and pedestal formation by EPEC

A

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
Q

Describe what is meant by attaching and effacing lesion

A

Microvillus elongation
Effacement of apical membrane - destruction of microvilli
Pedestal formation

33
Q

Where is E. coli commensal?

A

The gut

34
Q

What can E. coli cause?

A

Diarrhoea
Dystentery
Haemolytic uraemic syndrome (HUS)
Urinary tract and kidney infections
Septicaemia
Pneumonia and meningitis

35
Q

What are virulence factors of E. coli?

A

Toxins
Adhesins
Invasins

36
Q

Describe ETEC infection

A

Traveller’s diarrhoea
Secretory
No inflammation
No structural changes
Toxins = LT and ST cGMP at membrane

37
Q

Describe EPEC infection

A

Diarrhoea
Attaching and effacing lesions

38
Q

Describe EIEC infection

A

Dysentery
Specific serotypes

39
Q

Describe EHEC infection

A

O157:H7
Verotoxin (Shiga-like toxin)
Intense inflammation
HUS
Dysentery (not so invasive)
Attaching and effacing lesions

40
Q

Describe the role of Tir in type 3 secretion systems

A

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
Q

Describe the molecular structure of a type 3 secretion system

A

Pore complex - YopBD, LcrV
Needle - YscF
Basal body - Ysc secretory proteins

42
Q

What are YOPS?

A

YOPS - Yersinia outer membrane proteins
Bacterium Yersinisa pestis secretes YOPS into macrophage and PMNs
Each YOP has different effects

43
Q

What effects does YopE have?

A

Actin rearrangement via GTPases
Cell rounding
Anti-phagocytic

44
Q

What effects does YopH have?

A

YopH is a tyrosine phosphatase
Negative phagocytosis - YopH blocks ability of cell to undergo phagocytosis

45
Q

What effects does YopJ/P have?

A

Blocks TNF and MAP kinase release
Induces apoptosis

46
Q

What effects does YopA/O have?

A

A serine protease so will breakdown several proteins

47
Q

What effects does YopT have?

A

Actin rearrangement

48
Q

What are molecular syringes?

A

Gram negative bacteria that inject effectors into a host cell

49
Q

Give some examples of molecular syringes

A

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
Q

Why is site of infection of intracellular pathogens commonly the macrophage?

A

It is the first cell to encounter the pathogen
It can subvert bacterial recognition and phagocytic pathways to encourage infection

51
Q

What are some examples of intracellular pathogens?

A

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
Q

How do bacteria interfere with cellular functions?

A

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
Q

How does staphylococci prevent phagocytosis?

A

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
Q

What is the purpose of capsules on bacteria?

A

Block phagocytosis
e.g. meningococci, Haemophilus influenzae

55
Q

How do intracellular pathogens cause infection?

A

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
Q

Describe listeria cell-cell invasion

A

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
Q

What are the roles of complement?

A

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
Q

How do bacteria avoid complement?

A

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
Q

Describe the importance of opsonisation

A

Uncoated by Abs, bacteria are phagocytosed poorly
When coated with Ab, adherence to phagocytosis is enhanced

60
Q

Give examples of opsonins

A

IgG1 and 3
IgM
C3b
CRP

61
Q

What are the phagocyte receptors?

A

Fc
CR3

62
Q

Name some bacteria that have capsules

A

Neisseria meningitidis
Haemophilus influenzae
Streptococcus pneumoniae (G+ve)
E. coli K1

63
Q

What does presence of a sialic acid or hyaluronic acid capsule result in?

A

Decreased complement binding/activation
Decreased opsonisation
Decreased phagocytosis

64
Q

How can the host’s immune defences cause damage?

A

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
Q

Describe how S. aureus stimulates IL8

A

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
Q

Describe cross reactivity in Strep pyogenes infection

A

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
Q

What are some sites of cross reactivity in Strep pyogenes infection?

A

Myocardium - rheumatic heart disease
Synovium - reactive arthritis
Brain - Sydenhams chorea
Kidney - post-streptococcal acute glomerulonephritis

Infection and Immunity (33 decks)

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