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Cardio > MSK L9 Skin and Wound Infections > Flashcards

MSK L9 Skin and Wound Infections Flashcards

1
Q

Soft tissue infection common organisms:

A

Staphyococcus aureus:

Streptococcus pyogenes

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2
Q

Staphyococcus aureus:

A
  1. Gram positive found in clusters/tetrads
  2. A very versatile pathogen
  3. Colonises nostrils of many healthy individuals (Groin and axilla also) - commensual
  4. Readily acquires antibiotic resistance (MRSA)
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3
Q

Streptococcus pyogenes

A
  1. Group A
  2. Gram positive (chains)
  3. Agar → haemolytic reaction (beta haemolysis)
  4. Common cause of throat infections, also causes skin infection and rapidly progressing invasive infection
    a. Pharyngitis
    b. Quinsy
  5. Invariably penicillin sensitive
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4
Q

Staph. Aureus and Strep.pyogens have many similar virulence factors:

A

Binding
Invasion
Toxin production

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5
Q

Staph. Aurues

capsules

A

11 serotypes (serotype 5,8 most common)

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6
Q

Staph. Aurues surface

A

➢ Protein A binds IgG (Fc region)
➢ Fibrinogen binding protein (clumping factor)
➢ Fibronectin binding protein
➢ Collagen binding protein

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7
Q

Strep. Pyogenes capsule

A

Hyaluronic acid (capsule formed from preventing phagocytosis)

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8
Q

Strep. Pyogenes surface

A

➢ M protein and M-like proteins bind: IgG and IgA (Fc region), fibrinogen and fibronectin;
➢ Protein F1, F2 & others bind fibronectin;
➢ Epa binds collagen

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9
Q

Stap.aureus tissue degrading organisms

A 
➢	DNAase
➢	Staphylokinase
➢	Hyaluronidase
➢	Lipase
➢	Coagulase (haemolysins
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10
Q

Strep. Pyogenes tissue degrading organisms

A 
➢	DNAases A-D
➢	Streptokinase
➢	Hyaluronidase
➢	Amylase
➢	Esterase
➢	NADase
➢	Proteinase (Haemolysins
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11
Q

Staph.aureus Both produce toxins that damage host cells

A

a-, Beta-, y- Delta- toxins (haemolysins)

Leucocidins

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12
Q

Staph.aureus Both produce ‘superantigens’ (pyrogenic) – induce host immune response

A

Enterotoxins (7 types)

Toxis shock syndrome toxin

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13
Q

Staph.aureus Other toxins

A

Epidermolytic toxin (exfoliatin)

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14
Q

Strep. Pyogenes Both produce toxins that damage host cells

A

Streptolysin O (oxygen unstable) and S (oxygen stable) → Rheumatic fever

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15
Q

Strep. Pyogenes Both produce ‘superantigens’ (pyrogenic) – induce host immune response

A

Streptpcoccal pyrogenic (erythrogenic) exotoxins (SPEs)

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16
Q

Impetigo: Description

A

Pustular vesicles developing into crusting plaques non scarring

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17
Q

Impetigo: Caused by

A

Streptococcus pyogenes or staph. Aureus

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18
Q

Impetigo: Bullous impetigo caused by

A

Staph. Aureus epidermolytic toxin

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19
Q

Impetigo: Bullous impetigo

A

Causes skin separation at stratum granulosum layer

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20
Q

Dermatophyte infections: Description

A

Fungal infections

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21
Q

Dermatophyte infections: Examples

A

Athletes foot

Ring worm

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22
Q

Dermatophyte infections: Cause

A

Caused by colosation of keratinised structures (stratum corneum, hair , nails) by keratinase – producing fungi (Epidermophyton floccosum, Trichophyton spp & Microsporum spp.

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23
Q

Hair Follicle based infections: Predominant cause

A

Staph aurues

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24
Q

Hair Follicle based infections: Folliculitis sometimes due to

A

Garm ive rods

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25
Q

Hair Follicle based infections: Acne vulgaris may be caused or exacerbated by

A

Propionibacterium acnes

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26
Q

Hair Follicle based infections: Carbuncle

A

Necrotising infection of skin

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27
Q

Hair Follicle based infections: Furunculosis

A

Boils

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28
Q

Leprosy (Hansen’s disease) Epi

A

10-20 million people affect in tropics

29
Q

Leprosy (Hansen’s disease) Caused by

A

Myocobacterium leprae confined to man (nonculturable)

30
Q

Leprosy (Hansen’s disease) Restricted mainly to

A

Skin, peripheral nerves and nasal epithelium by poor growth at 37C (opt. 30C)

31
Q

Leprosy (Hansen’s disease) Incubation period

A

6 months. Sometimes decades

32
Q

Leprosy (Hansen’s disease) Treatment

A

Dapsone
Rifampicin
Clofazamine (6-12 months)

33
Q

Leprosy (Hansen’s disease) Pathology of Leprosy

A

M. leprae is an obligate intracellular pathogen

34
Q

Leprosy (Hansen’s disease) Spectrum of disease from:

A
  1. Tuberculoid – few well-demarcated lesions, few bacilli seen, granulomatous picture → non infectious?
  2. Lepromatous – widely disseminated diffuse lesions containing many bacilli; infections
35
Q

Leprosy (Hansen’s disease)Tuberculoid leprosy response

A

Cell-mediated immune response (inc. delayed-type hypersensitivity)

36
Q

Leprosy (Hansen’s disease) Lepromatuos leprosy response

A

B-cell activation
Eosinophil activation
Acute phase response
Less inflammation

37
Q

Leprosy (Hansen’s disease) Tuberculoid presentation

A

Well defined lesions (small numbers)

38
Q

Lepromatous leprosy presentation

A

Extensive ill (defined lesions (extensive numbers)

39
Q

Secondary Infections of Skin: Infected eczema

A

Usually staphylococcus aureus, occasionally Streptococcus pyogenes

40
Q

Secondary Infections of Skin: Leg ulcers, pressure sores, burns

A

Many species isolated including:

  1. Staphylococcus aurues
  2. Streptococcus pyogenes
  3. Pseudoomonas aeruginosa
  4. Anaerobic bacteria
41
Q

Infection of wounds:

A
  1. Clean surgical wound – few bacteria
  2. Chronic wound contaminated with viable organisms
    a. Wound infection local symptoms delayed healing
    i. Sepsis (systemic effects due to spread of organisms/toxins or
    ii. Removal of bacteria by host defences etc.
42
Q

Wound infection: factors increasing risk of infection:

A
  1. Presence of foreign material
  2. Presence of dead tissue/clots
  3. Poor perfusion of wound site
  4. Delayed healing
  5. Heavy microbial contamination
  6. General health of patient
43
Q

Cellulitis: Caused by

A

Streptococcus pyogenes

44
Q

Cellulitis: Less commonly other causes

A

Beta-haemolytic streptococci or staphylococcus aureus

45
Q

Cellulitis: Occasionally caused by

A

Strep. Pneumonia or Haemophilus influenza (pre HIB)

46
Q

Cellulitis: Facial cellulitis

A

Erysipelas (cheeks) and periorbatalitis

47
Q

Necrotising fasciitis (streptococcal gangrene)

A

Strep. Pyogenes

Sometimes staph aureus

48
Q

Gas gangrerr(clostridial cellulitis)

A

Clostridium spp, often mixed cultures

49
Q

Synergistic necrotising fasciits/gangrer

A

Mixed cultures, aerobic and micro-aerophillic or anaerobic cocci, bacteroids or fusobacterium. Often affect muscle

50
Q

Synergistic necrotising fasciitis/gangre include

A

Founeir’s gangre

Meleney’s preogressive bacterial synergistic gangre

51
Q

Fournier’s gangrene

A

Affects perineum and male gentalia

52
Q

Meleney’s progressive bacterial synergistic gangrene

A

Usually after abdominal surgery, more slowly progressing than other gangrenes.

53
Q

Lethal toxins of Clostridium perfringens: (produces lethal toxins)

A 
Alpha – lecithinase (phospholipase C)
Beta
Epsilon
Iota
Gamma
Delta
Kappa
54
Q

Alpha – lecithinase (phospholipase C)

A

Causes extensive haemolysis
Plateleta aggregation in blood vessles
Prevents neutrophil infiltration of local tissue

55
Q

Beta

A

Necrotizing

56
Q

Epsilon

A

Permease

57
Q

Iota

A

Dermonnecrotic, ADP ribosylating

58
Q

Gamma

A

Haemolysin

59
Q

Delta

A

Haemolysin, cytolysin

60
Q

Kappa

A

Collagenase, necrotizing

61
Q

Tetanus: Caused

A

Clostridium tetani

62
Q

Tetanus: Pathology

A

Bacteria grow in dead, anaerobic tissue sand produce tetanospasmin toxin
Toxin binds to nerve endings; inhibit neurotransmitter release, blocking nerve impulses

63
Q

Tetanus:Muscles spasms

A

Lock jaw, difficulty swallowing, stiff neck, rigid abdominal muscles

64
Q

Tetanus:Prevention by

A

Toxoid immunization, treatment with immune globulin (binds free toxin)

65
Q

Bites: Pathology

A

Local suppuration; cellulitis and lymaphedenaopathy; osteomyelitis and septic arthritis

66
Q

Bites: Human bites

A

Usually yield mixed oral flora, including anaerobes

67
Q

Animal bites

A

Similar plus capnocytophaga spp.,Pasteurella multocida

68
Q

Rodents

A

Can harbour francisella tularensis (tularaemia)

69
Q

bite prevention

A

Cleaning and debridement, antibiotic prophylaxis (co-amoxiclav)

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