Skin and Wound Infections Flashcards
Basic structure and function of the skin
Anatomical defence barrier against microorganisms
Epidermis
- 95% keratinocytes
- stratified squamous epithelium
Dermis
- blood vessels, capillary beds, lymphatics, nerve endings, glands
- connective tissue to cushion body
Subcutis (surrounded by superficial and deep fascia)
Muscle
Structures for defence in the skin
Skin surface
- microbiota
- acid mantle (dry, high salinity, acidic)
- sebum
- continual skin desquamation
- antimicrobial peptides
Epidermis
- CD8 T cells
- specialised dendritic cells
Dermis
- innate immune cells (macrophages, dendritic cells)
- mast cells
- innate lymphoid cells
- CD4 and CD8
Mechanisms of defence
Mechanical: oil film, keratin, dermis Chemical: acidic pH of skin, fatty acids in oil fit Biological: resident microbiome Cellular: phagocytes, lymphocytes Immunological: antibodies, lymphokines
Classification of skin and soft tissue infections
Cellulitis and superficial infections
- primary pyodermas
- cutaneous involvement in systemic bacterial and mycotic infections e.g. disseminated s. aureus (scalded skin syndrome), candidiasis, scarlet fever
Subcutaneous tissue infections
- necrotising fasciitis
Secondary to breached skin defence
- decubitus/ diabetic ulcer
- burns
- surgical wounds/ bite wounds
Wound infections: Predisposing factors (host)
*Malnutrition, anaemia, weight loss
*Dehydration, shock
*Extreme age
Malignancy
Drugs (steroids, cytotoxic)
Alcoholism
*Diabetes, uraemia, cirrhosis
Infection in other areas
Wound infections: 5 Predisposing factors (local)
Type of wound Site of wound Time lapse from injury to treatment Number and virulence of bacteria Presence of dead/ devitalised tissue
Types of wound
Based on degree of contamination
Clean
- only normal skin organisms involved; GI tract, respiratory tract and GU tract not involved
Clean-contaminated
- GIT/ GU and Resp tract entered but without unusual contamination (i.e. mucosal organisms) e.g. endoscopy
Contaminated
- Wound with spillage expected, sterile techniques can’t be maintained e.g. incision of the GIT/GU or Resp
Dirty
- perforated viscus e.g. trauma or open wound
Site of wound
Inadequate blood supply increases susceptibility to infection (as there is decrease in cellular and humoral defence cells due to less flow)
Extremities: DM, PVD
Presence of devitalised tissue
Devitalised tissue –> poor blood supply
Retained foreign bodies –> promote infection
Necrotic devitalised tissue should be debrided to achieve source control
Number and virulence of bacteria
Extent of infection is proportional to number of pathogens and their virulence
Most commonly:
- virulent: s. aureus, grp A/C/G streptococci
Avirulent bacteria cause wound infection if excess in number (minimised by aseptic techniques and sterilisation techniques)
Causative organisms can be exogenous (personnel, environment, surgical equipment) or endogenous (normal flora e.g. GN bacilli, enterococcus)
Wound infection: clinical presentations, diagnosis, treatment, prevention
Redness, swelling, warmth, pain Loss of function Purulent discharge Systemic e.g. fever, chills Non-union, wound dehiscence
Diagnosis
- often clinical
- culture and gram stain: debrided tissue or biopsy at infected margin of wound
- superficial wound swab not useful due to presence of colonisers (except in presence of genuine pus)
Treatment
- incision and drainage of pus
- remove devitalised tissue and foreign bodies
- antibiotics targeting suspected org\
Prevention
- control underlying illness e.g. DM
- operation: bowel decontamination, antibiotic prophylaxis
- aseptic technique
- decrease operation time and tissue trauma/haematoma
Soft tissue infections causative organisms
Bacteria: S. aureus, Strep pyogenes
Virus: HSV (cold sores, genital infection), VZV, Coxsackie A (hand foot mouth)
Fungal: Candida
Parasite: Sarcoptes scabiei
Staphylococci
Impetigo Folliculitis --> Furuncles --> Carbuncles Cellulitis Cutaneous/ Subcutaneous Abscesses Thrombophlebitis
Scalded skin syndrome (exfoliative toxin, very severe)
Toxic shock syndrome (intravaginal tampon contamination)
Streptococci
Mostly strep pyogenes (grp A), sometimes grp G
Impetigo (overlap) Erysipelas Cellulitis (overlap) Necrotising fasciitis Myositis
Superficial skin and soft tissue infections
Impetigo (epidermis)
Erysipelas (dermis)
Cellulitis (subcutis)
Folliculitis/ furuncle/ carbuncle (hair follicle and subcutis)
Impetigo: organism, site of infection, clinical features, variations, treatment
Organism: Strep pyogenes, S. aureus
Infection of EPIDERMIS
Clinical features:
- usually in children
- hot, humid environment
- in exposed areas
- initially papules –> vesicular –> rupture to form golden “honey crust”
Highly contagious – scratching causing spreading
Variations:
- bullous impetigo – specific group of s. aureus lead to formation of bulla (large vesicles)
- ecthyma – penetrate through epidermis and form punch out lesions
Treatment:
- local hygiene care
- cloxacillin (staph) and ampicillin (strep)
Erysipelas: organism, site of infection, distribution, clinical features, treatment
Organism: Strep pyogenes
Infection of DERMIS
Clinical features:
- 80% lower extremities, 20% face
- distinctive type of superficial cellulitis confined to dermis with *prominent lymphatic involvement
- infants, young children and older adults
- painful, bright red, oedematous, indurated (beau d’orange) appearance
- SHARPLY DEMARCATED from adjacent normal skin
- usually with fever
Treatment:
- cloxacillin
Cellulitis: organism, site of infection, distribution, clinical features, treatment
Organism: Strep pyogenes, s. aureus
Infection of SUBCUTIS
Clinical features:
- diffuse area of erythema and oedema with ILL-DEFINED edges
- no fluctuation or pus
- generally no fever
- accompanied by lymphadenitis and lymphangitis
Treatment:
- elevation, immobilisation
- antibiotic (cloxacillin and ampicillin)
- no incision and drainage unless pus present (same applies for other superficial skin infections)
Necrotising fasciitis: organisms, course, site of infection, clinical features, Fournier’s gangrene, diagnosis, treatment
Organism: Strep pyogenes (MC), s. aureus, vibrio vulnificans (seawater), anaerobes
(frequently mixed aerobic and anaerobic infections)
- following cuts, insect bites or surgery
RAPID PROGRESSIVE necrosis of subcutaneous tissue and superficial fascia (along FASCIAL PLANE)
- overlying skin –> cellulitis +/- blister or cyanosis –> necrosis due to destruction of blood supply (within hours)
- VERY HIGH MORTALITY
Clinical features:
- “cellulitis” with fever, pain and swelling –> must have NF as DDx!!!
- pain out of proportion to signs (beyond area of erythema)
- haemorrhagic bullae or blisters
- Fournier’s gangrene = involving sputum and perineum
Diagnosis:
- exudate and tissue for culture of aerobes and anaerobes
Treatment:
- AGGRESSIVE surgical debridement
- antibiotics
Skin ulcers: primary vs secondary, organisms, diabetic and decubitus ulcers (pathogenesis, organisms, treatment, prevention)
Primary (uncommon e.g. cutaneous anthrax)
Secondary (secondary infection of an ulcer e.g. decubitus/ diabetic)
Organisms: staph, strep, GN bacilli, anaerobes, yeast
Diabetic foot ulcer
- DM with vascular disease, neuropathy, sugary blood nutritious for bacterial growth
- mixed aerobes and anaerobes
- complication –> osteomyelitis
- treatment: incision and drainage, antibiotics
- prevention: optimise blood glucose control, foot hygiene
Decubitus ulcer
- prolonged pressure –> tissue ischemia –> necrosis –> ulcer
- mixed aerobes and anaerobes
- treatment: antibiotics, debridement
- prevention: movement and turning
Bites: onset, organism, diagnosis, treatment
Infection common, usually within 24 hrs
Organism: mixed aerobes and anaerobes (normal oral flora of inflicting animal)
- dog: s. aureus, pasteurella canis
- cat: pasteurella multocida, bartonella species
- human: streptococci, s, aureus
Diagnosis:
- culture of wound/ discharge
Treatment:
- surgical debridement and antibiotics (cefuroxime and metronidazole)
- tetanus toxoid +/- tetanus IG
+/- rabies vaccination (animal bites)
Burns: injury, risks for infection, organisms, treatment
Destruction of cutaneous mechanical barrier
- Avascularity of burn wounds
- plasma proteins leak –> decrease plasma Ig and albumin –> increase risk of local and distal infections
- neutrophil dysfunction
Colonisation of non-viable tissues then viable tissues
- s. aureus, candida, p. aeruginosa, enterobacteriaceae, coag neg staph (any org is possible!)
Treatment:
- debridement
- topical/ systemic antibiotics
Soft tissue infections: General diagnosis/ specimens and management
Diagnosis:
- clinical features
- culture and gram stain of:
- – pus or needle aspirate
- – biopsy from advancing edge (cellulitis)
- – deep tissue culture/ ulcer base (superficial not useful)
- – blood culture (systemic infection)
Management:
- removal of infected material by drainage and debridement
- antibiotics
- local wound care
- prevention
Others (furuncle/ carbuncle, paronychia, gas gangrene)
Furuncle (boil) and carbuncle
- s. aureus
- furuncle = intracutaneous abscess in hair follicle –> carbuncle if subcutaneous extension (usually at neck or upper back)
- drainage, cloxacillin for carbuncle
Paronychia
- s. aureus
- infection of subcutaneous tissue around nails (usually due to biting of hangnail)
Gas gangrene
- c. perfringens
- following major trauma/ bowel surgery/ amputation
- tissue degrading enzymes e.g. lecithinase causes tissue necrosis and forms anaerobic environment
- rapidly spreading gangrene of muscle, blackening tissue, foul smelling discharge, crepitus, toxaemia
- treatment: wide excision/ amputation, antibiotics, hyperbaric oxygen
