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Immunology and infection > Immune Evasion > Flashcards

Immune Evasion Flashcards

1
Q

How does S.aureus cause disease

A

Localised pyogenic or pus producing disease characterised by tissue destruction mediated by hydrolytic enzymes and cytotoxins

Diseases mediated by toxins function as superantigens producing systemic disease

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2
Q

What are the properties of s. aureus

A
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3
Q

What hydrolytic enzymes and cytotoxins does s.aureus have

A
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4
Q

What toxins does S.aureus have

A

Enterotoxins - heat stable and acid resistant toxins responsible for food poisoning

Exfoliative toxins A and B causing the superficial layers of skin to peel off (scalded skin syndrome)

Toxic shock syndrom toxin - heat and protease resistant toxin that mediates multiorgan pathology

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5
Q

What is the epidemiology of S aureus

A

Common cause of infection in community and hospital because bacteria easily spread person to person and through direct contact or exposure

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6
Q

What are the symptoms of S aureus

A

Impetigo - localised skin infection characterized by pus filled vesicles on a reddened or erythematous base

Folliculitis - involving hair follicles

Furuncles and carbuncles - large, puss filled skin nodules, progress to deeper layers of the skin and spread into blood

Woud infections

Pneumonia

Endocarditis- endothelial lining of heart

Osteomyelitis

Septic arthritis

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7
Q

S aureus toxin mediated sdiseased

A

Toxic shock syndrome

Scalded skin syndrome

Food poisoning

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8
Q

Treatment, prevention and control of S aureus

A

Localised infections managed by incision and drainage

Antibotic therapy

Vancomycin - intravenous

Oral therapy - trimethoprim-sulfamethoxazole, clindamycin, doxycycline

Cleansing of wounds

Thorough hand washing

T

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9
Q

How can we detect bacteria

A

LPS in gram negative bacteria

LTA in gram positive bacteria

Flagella on certain bacteria

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10
Q

Why must neutrophil responses be balanced

A

Balanced to prevent infection but to also prevent damage to the host

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11
Q

How do neutrophils get activated

A
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12
Q

Where is S aureus present

A

In nose 30% of the population

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13
Q

What is antibody opsonisation

A

Antibodies bind bacterial antigens allowing

  • deposition of complement in classical complement pathway
  • Neutrophils and other pagocytes the ability to detect invading microbes
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14
Q

How does s aureus evade antibody opsinisation

A

S.aureus express capsule on its surface - polysaccharide

SpA binds to IgG Fc region not FAB, prevents deposition of complement, prevent bacteria being recognised by Fc receptors. Also portein Sbi

SSL10 - binds to Fc region, prevent complement and detection. Also Sak

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15
Q

What bacteria utilised capsule evasion

A

E coli

Pseudomonas aeruginosa

S pneumonia

S agalactiae

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16
Q

S aureus SSL10 inform

A
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17
Q

What are other bacteria that bind to Fc region

A

Streptococcus dysgalactiae - protein G binds IgG

Peptostreptococcus magnus - protein L binds IgG

Streptococcus agalactiae - beta protein binds IgA

18
Q

Which bacteria cleaves proteases

A

Group B streptococcus (cleaves IgG class)

Porphyromonas gingivalis

Streptococcus pyogenes

Neisseria gonorrhoeae

Haemophilus influenzae

19
Q

What is antigenic variation

A

Surface structure cahnges

N gonorrhoeae (Opa and lOS antigens)

S pneumoniae (Cap)

20
Q

What are the key steps of the complement cascade

A

Initiation

Formation of C3 convertase

Formation of C5 convertase

MAC formation

21
Q

What is the significance of SCIN S.aureus

A

SCIN protein binds C3bBb and inhibits formation of C3 convertase and C5 convertase

Prevents C3B deposition - presents opsonisation , unabel to detect S aureus

Prevent C3a and C5a formation

22
Q

What is the significance of S aureus Efb

A

Binds to C3d in C3, induces conformational change

Factor B cannot bind to C3 - no formation of C3 convertase C3bBb

No conversion of C3 by C3 convertase required for the formation of C5 convertase

C3dg is unable to be recognised by CR2 by phagocytes

Other bacteria release proteins binding C3 - m catarrhalis

23
Q

What proteases cleave complement components

A

S pyogenes (SpeB)

P gingivalis (Kgp)

N meningitidis (MalP)

P aeruginosa (AprA)

24
Q

What bacteria can acquire host derived complement regulators

A

C3b inactivated by fH on bacterial surface - s aureus, s agalactiae, h influenzae, salmonella, a baumannii, n meningitids

C4BP degrades C2a from C3 convertases - b pertussis

25
Q

Examples of immune receptors on neutrophils

A

TLR receptors - conserved microbial structures

CLEC receptors - microbial carbohydrates

FPR receptors - formylated peptides

Fc receptors - (SIGNAL THROUGH ITAM)

Complement receptors

Cytokine receptors

Chemoattractant receptors

LAIR receptors - ITIM - inhibitary to ITAM

SIGLEC receptors

LILR

CEACAM

26
Q

How does S aureus inhibit chemotaxis

A
27
Q

How does S aureus inhibit phagocytosis

A

FLIPr inhibitors Fc y receptors (IgG)

SSL5 innhibits Fc a receptors (IgA)

28
Q

What are additional methods of neutrophil evasion

A

Kill neutrophils with toxins

Bind and inhibit functions of activating receptors

29
Q

What are other bacteria neutrophil evasion

A

Bind inhibitory receptors

Inhibit effects of antimicrobials - upon phagocytosis or granulation

Manipulate intracellular signalling

Modify bacterail surface

30
Q

What are some other ways of immune evasion

A

Antigenic variation

Inactivating antibodies or complement

Resisting phagocytosis

Suppressing the host adaptive immune response - interfering with cytokines or inhibiting MHC expression

Establishing latency

31
Q

Antibody response to viral evasion

A
32
Q

How do you resolve infection

A

Oo

33
Q

How do viruses escape antibody recognition

A

Rhinovirus - Antigenically distinct serotypes

HIV - multiple clades or quasi-species

HBV and Ebola - surface antigens which mop up antibody stopping it reaching infected cell

Dengue virus - exists as 4 serotypes

34
Q

How is interferon induced

A
35
Q

How do interferons work

A
36
Q

Facts about IFN - Beta and IFN - alpha

A

Secreted by all cells

One gene for IFN-beta

37
Q

Facts about IFN - gamma

A

Produced by activated T cells and NK cells

Signals through a different receptor IFN-gamma R

Type 2 IFN

38
Q

Facts about IFN - lambda

A

Signals through recepotrs IL28R and IL10- ebta that are mainly present on epithelila cells surfaces

39
Q

Why is it significant that viruses like hep B and influenza can block production of IFN

A

Inhibition of IFN transcription(HBV) or influenza

40
Q

What do natural killer cells do

A

Activated by IFN-a and interleukin 12 which activates macrophages with IFN - gamma

NK kill virus infected cells

Finds a cell displaying fewer than normal MHC (cytomegalovirus or herpes smiple virus), released toxic substances which kill cell

41
Q

What do macrophages and dendritic cells do

A

Macrophages filter viral particles from blood

Macrophages inactivate opsonized virus particles

Immature and plasmactyodi DC produce IFN-alpha and other cyotkines

DC initiate and determine nature of CD4 and CD8 T cell response

42
Q

What is the role of T cells

A

Essential for controlling enveloped and noncytolytic viral infections

Recognise viral peptides by MHC molecules on cell surfaces

Antigenic viral peptides come from any viral protein

CD8 cytotoxic T cells respond to viral peptide - class 1 MHC protein

CD4 TH2 response may be detrimental if they prematurely limit TH1 inflammatory and cytolytic responses

Viruses encode proteins (herpes and cytomegalovirus) that interfere with MHC anitgen processing pathway

HIV kills CD4 and alters macrophag efunction

Herpes prevent CD8 killing

Immunology and infection (14 decks)

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