Microbes

Question 1

What is pyogenic s.aureus disease?

Answer 1

Pus producing - hydrolytic enzymes and cytotoxins cause tissue destruction

Question 2

What is systemic s.aureus disease?

Answer 2

Mediated by toxins functioning as super antigens

Question 3

How does s.aureus protect itself from phagocytosis?

Answer 3

Polysaccharide capsule and coagulase which causes fibrinogen to convert to insoluble fibrin causing blood clots

Question 4

How does catalase protect the s.aureus?

Answer 4

Breaks down peroxides produced by neutrophils and macrophages

Question 5

What do cytotoxins produced by s.aureus do?

Answer 5

Lyse erythrocytes, neutrophils, macrophages plus other host cells

Question 6

What do hydrolytic enzymes does s.aureus produce and what are their function?

Answer 6

Lipases, nuckeases, hyaluronidase causing tissue destruction

Question 7

What is a key property of s.aureus linked with food poisoning?

Answer 7

Grow aerobically & anaerobically

Over a wide range of temps

In the prescence of high salt concentration

Question 8

What toxins does s.aureus produce and what are their properties?

Answer 8

Enterotoxins - heat stable + acid resistant -> food poisoning

Exfoliative toxins A&B - superficial layers of skin peel off

Toxic shock syndrome - heat & protease resistant mediates multiorgan pathology

Question 9

List the 7 pyogenic diseases caused by S.Aureus

Answer 9

Impetigo
Folliculitis
Furuncles (boils) and carbuncles
Wound infections
Pneumonia
Endocarditis
Osteomyelitis
Septic arthritis

Question 10

List 3 S aureus toxin mediated diseases

Answer 10

Food poisoning
Scalded skin syndrome
Toxic shock syndrome

Question 11

Describe impetigo and folliculitis

Answer 11

Localized skin infection characterized by pus-filled vesicles on reddened/erythematous base

Folliculitis is impetigo involving hair follicles

Question 12

Describe furuncles (boils) and carbuncles

Answer 12

Large, pus filled skin nodules, can progress deeper and spread

Question 13

Describe wound infections

Answer 13

Erythema and pus at site. MRSA common

Question 14

Describe pneumonia

Answer 14

Abscess in lungs

Common in very young and old

Usually follows viral infection of R tract

Question 15

Describe endocarditis

Answer 15

Infection of endothelial lining of heart, progresses rapidly and high mortality

Question 16

Describe osteomyelitis

Answer 16

Destruction of bones, particularly in highly vascularized areas in children

Question 17

Describe septic arthritis

Answer 17

Infection of join spaces (swollen, reddened joint)

Question 18

How is food poisoning caused and what are the symptoms and progression?

Answer 18

Heat stable enterotoxin, 2-4 hours cramps, vomiting, diarrhoea. Resolved in 24 hours

Question 19

Describe scalded skin syndrome

Answer 19

Localized infection causing outermost layer of skin to peel off caused by exfoliative toxins A&B

Question 20

Describe toxic shock syndrome

Answer 20

Localized infection but toxins affect multiple organs (fever, hypotension, erythematous rash, high mortality rate unless ABs promptly administered and local infection managed)

Question 21

What is the treatment for localised infection?

Answer 21

Incision and drainage

Question 22

What is the treatment for systemic infection?

Answer 22

IV - Vancomycin
Oral therapy- trimethoprim- sulfamethoxazole, clindamycin, doxycycline

Food poisoning - identify source

Question 23

Prevention methods for s.aureus

Answer 23

Proper cleansing of wounds
Use of disinfectant
Hand washing and covering exposed skin
No vaccine currently available

Question 24

What are the main mechanisms bacteria use to evade opsonisation by antibodies?

Answer 24

1. Hide antigens
2. Disrupt functions
3. Prevent detection
4. Degrade antibodies
5. Modify antigenicity

Question 25

Give 1 ways s.aureus hides from antibodies

Answer 25

Capsule hides antigens on surface and less complement is deposited

Question 26

Name and describe 2 proteins s.aureus uses to prevent antibody detection

Answer 26

S.aureus surface protein A (SpA) binds IgG Fc region so Fc receptors on immune cells can't detect Secreted SSL10 binds IgG to inhibit detection

Question 27

Name 2 antigen evasion strategies not specific to S.aureus

Answer 27

Proteases cleave antibodies (group B strep [IdeS]) Antigenic variation ( n.gonorrhoaea [Opa and LOS antigens])

Question 28

What happens when neutrophils are recruited?

Answer 28

1. C5a binds to C5aR and C3a binds to C3aR Endothelial cells express ICAM Adhesion occurs and neutrophils roll along endothelial surface of blood vessels 2. Priming 3. Chemotaxis - down gradient of complement components and bacterial proteins 4. Activation 5. Opsonisation 6. Phagocytosis, inflammation, degranulation - reactive O2 species, antimicrobial molecules

Question 29

What happens during inflammation and which complement components are proinflammatory agents?

Answer 29

C3a and C5a

Question 30

Which pathogen specific receptors (PRRs) do neutrophils express and what do they do?

Answer 30

They prime and activate neutrophils TLR receptors detect conserved microbial structures eg. Lipopolysaccharides (LPS, gram -ve cell wall) and lipoteichoic acid (LTA, gram +ve cell wall), flagella CLEC detect microbial carbohydrates FPR detect formulated peptides released by bacteria

Question 31

How do neutrophils detect osonised microorganisms?

Answer 31

Fc receptors, complement receptors

Question 32

What is an opsonin?

Answer 32

An opsonin is any molecule that enhances phagocytosis by marking an antigen for an immune response or marking dead cells for recycling.

Question 33

Describe two chemotaxis receptors of neutrophils

Answer 33

C5aR detects C5a FPR1 detects fMLP (formulated peptides released by bacteria)

Question 34

How does s. Aureus inhibit chemotaxis and activation?

Answer 34

Secretes CHIPs which binds C5aR and FPR1 with a higher affinity than C5a and fMLPs

Question 35

How does a.aureus interact with receptors, thus preventing phagocytosis?

Answer 35

FLIPr binds Fcg receptors (IgG) preventing detection of IgG opsonised bacteria SSL5 binds Fca receptors (IgA) preventing detection of IgA opsonised bacteria

Question 36

How does s. Aureus evade neutrophils?

Answer 36

Produces toxins to kill them | Expresses molecules that are receptor antagonists, binding an inhibiting the function of activatory receptors

Question 37

What happens during the classical complement pathway?

Answer 37

- Immunoglobulins bind to pathogen surface - C1q binds to Fc region and activates C1r which activates C1s - C1s activates a serine protease which cleaves C4 into C4a and b, c4b binds to pathogen surface - C1s cleaves C2 to C2a and b - C2b binds C4b forming C4b-2b complex (C3 convertase) - C3 convertase cleaves C3 to C3a and C3b which binds to C3 convertase forming C4b-2b-3b complex (C5 convertase) OR C3b binds to surface of pathogen - C5 binds to C3b part of C5 convertase and is cleaved into C5a and C5b - Opsonisation is complete!

Question 38

Which components is the membrane attack complex (MAC) composed of?

Answer 38

C5b, C6, C7, C8, C9

Question 39

Which are the proinflammatory fragments of the complement cascade?

Answer 39

C3a and C5a

Question 40

What are the two types of C3 convertase?

Answer 40

C4b-2b - classical and MBL C3bBb - alternative

Question 41

Which fragments label the target pathogen for elimination by phagocytosis?

Answer 41

C3b and C4b

Question 42

Which protein does s.aureus produce that inhibits MAC formation?

Answer 42

SSL7 binds C5

Question 43

What does the Efb protein do and what produces it?

Answer 43

S.aureus Binds C3d part of C3, inducing a conformation change which prevents binding of factor B to C3, and C3dg binding CR2. It essentially prevents C3 being cleaved to C3b

Question 44

Which protein does SCIN bind to?

Answer 44

C3bBb - inhibits formation of C3 convertade and C5 convertase, preventing C3b deposition, C3a formation, C5a formation.

Question 45

Describe 2 complement evasion strategies not covered by SCIN, SSL7 or Efb

Answer 45

Proteases cleave complement components Aquired host derived complement regulators eg. fH on bacterial surface inactivates C3b and C4BP is associated with FI and degrades C2a from C4b2a (C3 convertases)