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MSK L9 Skin and Wound Infections Flashcards

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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
Hair Follicle based infections: Acne vulgaris may be caused or exacerbated by
Propionibacterium acnes
26
Hair Follicle based infections: Carbuncle
Necrotising infection of skin
27
Hair Follicle based infections: Furunculosis
Boils
28
Leprosy (Hansen’s disease) Epi
10-20 million people affect in tropics
29
Leprosy (Hansen’s disease) Caused by
Myocobacterium leprae confined to man (nonculturable)
30
Leprosy (Hansen’s disease) Restricted mainly to
Skin, peripheral nerves and nasal epithelium by poor growth at 37C (opt. 30C)
31
Leprosy (Hansen’s disease) Incubation period
6 months. Sometimes decades
32
Leprosy (Hansen’s disease) Treatment
Dapsone Rifampicin Clofazamine (6-12 months)
33
Leprosy (Hansen’s disease) Pathology of Leprosy
M. leprae is an obligate intracellular pathogen
34
Leprosy (Hansen’s disease) Spectrum of disease from:
1. Tuberculoid – few well-demarcated lesions, few bacilli seen, granulomatous picture → non infectious? 2. Lepromatous – widely disseminated diffuse lesions containing many bacilli; infections
35
Leprosy (Hansen’s disease)Tuberculoid leprosy response
Cell-mediated immune response (inc. delayed-type hypersensitivity)
36
Leprosy (Hansen’s disease) Lepromatuos leprosy response
B-cell activation Eosinophil activation Acute phase response Less inflammation
37
Leprosy (Hansen’s disease) Tuberculoid presentation
Well defined lesions (small numbers)
38
Lepromatous leprosy presentation
Extensive ill (defined lesions (extensive numbers)
39
Secondary Infections of Skin: Infected eczema
Usually staphylococcus aureus, occasionally Streptococcus pyogenes
40
Secondary Infections of Skin: Leg ulcers, pressure sores, burns
Many species isolated including: 1. Staphylococcus aurues 2. Streptococcus pyogenes 3. Pseudoomonas aeruginosa 4. Anaerobic bacteria
41
Infection of wounds:
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
Wound infection: factors increasing risk of infection:
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
Cellulitis: Caused by
Streptococcus pyogenes
44
Cellulitis: Less commonly other causes
Beta-haemolytic streptococci or staphylococcus aureus
45
Cellulitis: Occasionally caused by
Strep. Pneumonia or Haemophilus influenza (pre HIB)
46
Cellulitis: Facial cellulitis
Erysipelas (cheeks) and periorbatalitis
47
Necrotising fasciitis (streptococcal gangrene)
Strep. Pyogenes | Sometimes staph aureus
48
Gas gangrerr(clostridial cellulitis)
Clostridium spp, often mixed cultures
49
Synergistic necrotising fasciits/gangrer
Mixed cultures, aerobic and micro-aerophillic or anaerobic cocci, bacteroids or fusobacterium. Often affect muscle
50
Synergistic necrotising fasciitis/gangre include
Founeir’s gangre | Meleney’s preogressive bacterial synergistic gangre
51
Fournier’s gangrene
Affects perineum and male gentalia
52
Meleney’s progressive bacterial synergistic gangrene
Usually after abdominal surgery, more slowly progressing than other gangrenes.
53
Lethal toxins of Clostridium perfringens: (produces lethal toxins)
``` Alpha – lecithinase (phospholipase C) Beta Epsilon Iota Gamma Delta Kappa ```
54
Alpha – lecithinase (phospholipase C)
Causes extensive haemolysis Plateleta aggregation in blood vessles Prevents neutrophil infiltration of local tissue
55
Beta
Necrotizing
56
Epsilon
Permease
57
Iota
Dermonnecrotic, ADP ribosylating
58
Gamma
Haemolysin
59
Delta
Haemolysin, cytolysin
60
Kappa
Collagenase, necrotizing
61
Tetanus: Caused
Clostridium tetani
62
Tetanus: Pathology
Bacteria grow in dead, anaerobic tissue sand produce tetanospasmin toxin Toxin binds to nerve endings; inhibit neurotransmitter release, blocking nerve impulses
63
Tetanus:Muscles spasms
Lock jaw, difficulty swallowing, stiff neck, rigid abdominal muscles
64
Tetanus:Prevention by
Toxoid immunization, treatment with immune globulin (binds free toxin)
65
Bites: Pathology
Local suppuration; cellulitis and lymaphedenaopathy; osteomyelitis and septic arthritis
66
Bites: Human bites
Usually yield mixed oral flora, including anaerobes
67
Animal bites
Similar plus capnocytophaga spp.,Pasteurella multocida
68
Rodents
Can harbour francisella tularensis (tularaemia)
69
bite prevention
Cleaning and debridement, antibiotic prophylaxis (co-amoxiclav)

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