MSK L9 Skin and Wound Infections Flashcards Preview

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Flashcards in MSK L9 Skin and Wound Infections Deck (69):
1

Soft tissue infection common organisms:


Staphyococcus aureus:


Streptococcus pyogenes

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Staphyococcus aureus:




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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Streptococcus pyogenes

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

Binding
Invasion
Toxin production

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Staph. Aurues

capsules

11 serotypes (serotype 5,8 most common)

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Staph. Aurues surface

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

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Strep. Pyogenes capsule

Hyaluronic acid (capsule formed from preventing phagocytosis)

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Strep. Pyogenes surface

➢ 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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Stap.aureus tissue degrading organisms

➢ DNAase
➢ Staphylokinase
➢ Hyaluronidase
➢ Lipase
➢ Coagulase (haemolysins

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Strep. Pyogenes tissue degrading organisms

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

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Staph.aureus Both produce toxins that damage host cells

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

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

Enterotoxins (7 types)
Toxis shock syndrome toxin

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Staph.aureus Other toxins

Epidermolytic toxin (exfoliatin)

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Strep. Pyogenes Both produce toxins that damage host cells

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

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

Streptpcoccal pyrogenic (erythrogenic) exotoxins (SPEs)

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Impetigo: Description

Pustular vesicles developing into crusting plaques non scarring

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Impetigo: Caused by

Streptococcus pyogenes or staph. Aureus

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Impetigo: Bullous impetigo caused by

Staph. Aureus epidermolytic toxin

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Impetigo: Bullous impetigo

Causes skin separation at stratum granulosum layer

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Dermatophyte infections: Description

Fungal infections

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Dermatophyte infections: Examples

Athletes foot
Ring worm

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Dermatophyte infections: Cause

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

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Hair Follicle based infections: Predominant cause

Staph aurues

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Hair Follicle based infections: Folliculitis sometimes due to

Garm ive rods

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

Propionibacterium acnes

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Hair Follicle based infections: Carbuncle

Necrotising infection of skin

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Hair Follicle based infections: Furunculosis

Boils

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Leprosy (Hansen’s disease) Epi

10-20 million people affect in tropics

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Leprosy (Hansen’s disease) Caused by

Myocobacterium leprae confined to man (nonculturable)

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Leprosy (Hansen’s disease) Restricted mainly to

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

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Leprosy (Hansen’s disease) Incubation period

6 months. Sometimes decades

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Leprosy (Hansen’s disease) Treatment

Dapsone
Rifampicin
Clofazamine (6-12 months)

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Leprosy (Hansen’s disease) Pathology of Leprosy

M. leprae is an obligate intracellular pathogen

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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

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Leprosy (Hansen’s disease)Tuberculoid leprosy response

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

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Leprosy (Hansen’s disease) Lepromatuos leprosy response

B-cell activation
Eosinophil activation
Acute phase response
Less inflammation

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Leprosy (Hansen’s disease) Tuberculoid presentation

Well defined lesions (small numbers)

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Lepromatous leprosy presentation

Extensive ill (defined lesions (extensive numbers)

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Secondary Infections of Skin: Infected eczema

Usually staphylococcus aureus, occasionally Streptococcus pyogenes

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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

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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.

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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

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Cellulitis: Caused by

Streptococcus pyogenes

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Cellulitis: Less commonly other causes

Beta-haemolytic streptococci or staphylococcus aureus

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Cellulitis: Occasionally caused by

Strep. Pneumonia or Haemophilus influenza (pre HIB)

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Cellulitis: Facial cellulitis

Erysipelas (cheeks) and periorbatalitis

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Necrotising fasciitis (streptococcal gangrene)

Strep. Pyogenes
Sometimes staph aureus

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Gas gangrerr(clostridial cellulitis)

Clostridium spp, often mixed cultures

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Synergistic necrotising fasciits/gangrer

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

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Synergistic necrotising fasciitis/gangre include

Founeir’s gangre
Meleney’s preogressive bacterial synergistic gangre

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Fournier’s gangrene

Affects perineum and male gentalia

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Meleney’s progressive bacterial synergistic gangrene

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

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Lethal toxins of Clostridium perfringens: (produces lethal toxins)

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

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Alpha – lecithinase (phospholipase C)

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

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Beta

Necrotizing

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Epsilon

Permease

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Iota

Dermonnecrotic, ADP ribosylating

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Gamma

Haemolysin

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Delta

Haemolysin, cytolysin

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Kappa

Collagenase, necrotizing

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Tetanus: Caused

Clostridium tetani

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Tetanus: Pathology

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

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Tetanus:Muscles spasms

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

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Tetanus:Prevention by

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

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Bites: Pathology

Local suppuration; cellulitis and lymaphedenaopathy; osteomyelitis and septic arthritis

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Bites: Human bites

Usually yield mixed oral flora, including anaerobes

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Animal bites

Similar plus capnocytophaga spp.,Pasteurella multocida

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Rodents

Can harbour francisella tularensis (tularaemia)

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bite prevention

Cleaning and debridement, antibiotic prophylaxis (co-amoxiclav)

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