Skin and Soft Tissue Infections Flashcards
1
Q
Erysipelas
A
- Caused by group A streptococci or streptococcus pyogenes
- 70-80 of cases affect the lower extremeties, 20% affect the face
- Predisposing factors:
- Lympoedema
- Venous stasis
- Obesity
- Diabetes
- EtOH
- Streptococcal bacteraemia occurs in approximately 5% of cases
- Clincal features of site
- Painful
- Bright red
- Oedematour
- Peau d’orange
- Rarely cultured from surface of skin
2
Q
Scarlet Fever
A
- Most commonly dure to S.pyogenes, rarely similar with S.aureus
- Scarlatiniform rash:
- Fine, red, rough textured
- Blanching
- Begins on chest, armpits and behind ears
- ==> Desquamation after 2-5 days
- Symptoms due to exotoxin production
3
Q
Staphylococcal Scalded Skin Syndrome
A
- Commonly seen in infancy/early childhood
- Production of a circulating epidermolytic toxin ==> intradermal cleavage at the granular layer and desquamation
- Onset over a few hours to days , recovery within 5-7 days
- Worse sites tend to be face, neck, axilla and groin
- Scald-like appearance ==> large flaccid bulla
- Perioral crusting typical
- Intraepidermal blistering
- Very painful
- Caused by phage group II, benzylpenicillin-resistant (coagulase positive) staphylococci
- Tx - abx and analgesia
4
Q
Toxic Shock Syndrome
A
- Toxic shock syndrome is an uncommon but severe acute illness with fever, widespread red rash accompanied by involvement of other body organs.
- Caused by the release of exotoxins from toxigenic strains of the bacteria Staphylococcus aureus and Streptococcus pyogenes
- Most commonly S.aureus ==> producing toxic shock syndrome toxin-1 (TSST-1)
- Alternatively staphylococcal enterotoxin B or C
- ==> Massive amounts of cytokines (cell-mediator chemicals):
- Fever
- Rash
- Low blood pressure
- Tissue injury
- Shock
- ==> Massive amounts of cytokines (cell-mediator chemicals):
- Tx - IV abx and supportive
5
Q
Cellulitis
A
- An acute spreading infection of the skin extending deeper than erysipelas and involves the subcutaneous tissues. Blood cultures positive in 2-4%.
- Most often caused by S. aureus and Group A Streptococci but other beta haemolytic Streptococci eg. Groups C and G are implicated.
- Consider predisposing factors – eg occupation for Erysipeloid (contact with meat/fish), immunocompromised, disasters/earthquakes/hurricanes
- May mean organisms may be more diverse eg. Vibrio vulnificus, Enterobacteriaceae, Pasteurella multocida
- Treatment should include antibiotics active against the most common isolates. Eg. Flucloxacillin, Benzyl-penicillin
- Remember MRSA
- May need to be more broad spectrum for eg. diabetic foot.
6
Q
Subcutaneous Tissue Infections
A
- Rapidly progressive cellulitis with extensive necrosis of the subcutaneous tissues and overlying skin
- Necrotising fasciitis Types I and II (Type I = polymicrobial, Type II = Streptococcus pyogenes
- Gas gangrene and anaerobic cellulitis (Clostridial/non-Clostridial). Clostridial cellulitis does not involve the deep fascia vs gangrene
- Progressive bacterial synergistic gangrene
- Fournier’s Gangrene
- Gangrenous cellulitis in immunocompromised patients
- Usually secondary to direct spread from an adjacent site or penetrating injury
- Occasionally secondary to bacteraemic spread eg. Pseudomonas aeruginosa in the immunocompromised
7
Q
Necrotising Fasciitis
A
- An uncommon severe infection involving the subcutaneous soft tissues, particularly the superficial and often deep fascia
- Usually an acute rapidly progressing process
- Risk factors
- For Type I: pre-exisiting conditions such as IDDM, EOH, elderly, male
- For Type II, IVDU
8
Q
Necrotising Fasciitis - Clinical Features
A
- An uncommon severe infection involving the subcutaneous soft tissues, particularly the superficial and often deep fascia
- Usually an acute rapidly progressing process.
- Risk factors
- For Type I: pre-exisiting conditions such as IDDM, EOH, elderly, male
- For Type II, IVDU
- Exquisitely tender in the early stages, erythematous and swollen, rapidly progressing to skin breakdown and bullae formation within 3-5 days
- Frank cutaneous gangrene, area becomes anaesthetic secondary to thrombosis of small blood vessels and destruction of superficial nerves
- Anaesthesia is a worrying clue and may pre-date obvious skin changes.
9
Q
Necrotising Fasciitis - Diagnosis
A
- A swab may not be enough
- Aspiration of pus or fluid
- Biopsy of tissues
- Serology eg ASO (anti-streptolysin O) titres
- Culture and antibiotic sensitivities of organisms grown
10
Q
Necrotising Fasciitis - Treatment
A
- Surgical drainage of pus and debridement of dead tissue
- ==> Extensive and often disfiguring surgery
- Antibiotics
- Against staphylococci and streptococci
- Against anaerobes
- May need high doses
- High dose intravenous immunoglobulin (IVIG) - anecdotal benefit
- Clearance of Staphylococcal carriage
- Nutrition and supportive care
- Hygeine
11
Q
Necrotising Fasciitis - Antibiotic Regimens
A
- High dose benzyl-penicilin + flucloxacillin + metronidazole
- Cephalosporins + metronidazole
-
Meropenem + vancomycin or imepenem + vancomycin
- Addition of high dose clindamycin for Type II (Streptococcus pyogenes)
12
Q
Gas Gangrene
A
- Usually the result of trauma
- Contamination of wound with spores of Clostridia, usually Clostridium perfringens
- May also occur after bowel surgery
- Other organsism are also involved in a synergistic infection
13
Q
Gas Gangrene - Treatment
A
- Antibiotics depends on culture results
- Until known broad spectrum antibiotics eg. benzyl-penicillin + gentamicin + metronidazole or piperacillin/tazobactam or meropenem
- Essential to include anaerobic cover
- Surgery
- Hyperbaric oxygen
14
Q
Anthrax
A
- Caused by Bacillus anthracis
- At risk groups:
- Tanners
- Wool workers
- Vets
- Farmers
- Forms:
- Cutaneous anthrax = malignant pustule
- Pulmonary anthrax = due to inhalation of spores – high mortality
- Treatment = penicillin