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Principles Of Medicine > Microbes > Flashcards

Microbes Flashcards

Immune evasion, Microbial therapies

1
Q

What is pyogenic s.aureus disease?

A

Pus producing - hydrolytic enzymes and cytotoxins cause tissue destruction

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2
Q

What is systemic s.aureus disease?

A

Mediated by toxins functioning as super antigens

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3
Q

How does s.aureus protect itself from phagocytosis?

A

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

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4
Q

How does catalase protect the s.aureus?

A

Breaks down peroxides produced by neutrophils and macrophages

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5
Q

What do cytotoxins produced by s.aureus do?

A

Lyse erythrocytes, neutrophils, macrophages plus other host cells

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6
Q

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

A

Lipases, nuckeases, hyaluronidase causing tissue destruction

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7
Q

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

A

Grow aerobically & anaerobically

Over a wide range of temps

In the prescence of high salt concentration

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8
Q

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

A

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

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9
Q

List the 7 pyogenic diseases caused by S.Aureus

A 
Impetigo
Folliculitis
Furuncles (boils) and carbuncles
Wound infections
Pneumonia
Endocarditis
Osteomyelitis
Septic arthritis
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10
Q

List 3 S aureus toxin mediated diseases

A

Food poisoning
Scalded skin syndrome
Toxic shock syndrome

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11
Q

Describe impetigo and folliculitis

A

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

Folliculitis is impetigo involving hair follicles

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12
Q

Describe furuncles (boils) and carbuncles

A

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

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13
Q

Describe wound infections

A

Erythema and pus at site. MRSA common

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14
Q

Describe pneumonia

A

Abscess in lungs

Common in very young and old

Usually follows viral infection of R tract

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15
Q

Describe endocarditis

A

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

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16
Q

Describe osteomyelitis

A

Destruction of bones, particularly in highly vascularized areas in children

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17
Q

Describe septic arthritis

A

Infection of join spaces (swollen, reddened joint)

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18
Q

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

A

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

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19
Q

Describe scalded skin syndrome

A

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

20
Q

Describe toxic shock syndrome

A

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

21
Q

What is the treatment for localised infection?

A

Incision and drainage

22
Q

What is the treatment for systemic infection?

A

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

Food poisoning - identify source

23
Q

Prevention methods for s.aureus

A

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

24
Q

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

A
  1. Hide antigens
  2. Disrupt functions
  3. Prevent detection
  4. Degrade antibodies
  5. Modify antigenicity
25
Q

Give 1 ways s.aureus hides from antibodies

A

Capsule hides antigens on surface and less complement is deposited

26
Q

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

A

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

27
Q

Name 2 antigen evasion strategies not specific to S.aureus

A

Proteases cleave antibodies (group B strep [IdeS])

Antigenic variation ( n.gonorrhoaea [Opa and LOS antigens])

28
Q

What happens when neutrophils are recruited?

A
  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

  1. Priming
  2. Chemotaxis - down gradient of complement components and bacterial proteins
  3. Activation
  4. Opsonisation
  5. Phagocytosis, inflammation, degranulation - reactive O2 species, antimicrobial molecules
29
Q

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

A

C3a and C5a

30
Q

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

A

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

31
Q

How do neutrophils detect osonised microorganisms?

A

Fc receptors, complement receptors

32
Q

What is an opsonin?

A

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

33
Q

Describe two chemotaxis receptors of neutrophils

A

C5aR detects C5a

FPR1 detects fMLP (formulated peptides released by bacteria)

34
Q

How does s. Aureus inhibit chemotaxis and activation?

A

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

35
Q

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

A

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

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

36
Q

How does s. Aureus evade neutrophils?

A

Produces toxins to kill them

Expresses molecules that are receptor antagonists, binding an inhibiting the function of activatory receptors

37
Q

What happens during the classical complement pathway?

A
  • 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!
38
Q

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

A

C5b, C6, C7, C8, C9

39
Q

Which are the proinflammatory fragments of the complement cascade?

A

C3a and C5a

40
Q

What are the two types of C3 convertase?

A

C4b-2b - classical and MBL

C3bBb - alternative

41
Q

Which fragments label the target pathogen for elimination by phagocytosis?

A

C3b and C4b

42
Q

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

A

SSL7 binds C5

43
Q

What does the Efb protein do and what produces it?

A

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

44
Q

Which protein does SCIN bind to?

A

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

45
Q

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

A

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)

Principles Of Medicine (6 decks)

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