62 - Skin and Soft Tissue Infection Flashcards
What bacteria on skin?
Coagulase-negative staphylococci
Staph. aureus
Propionibacterium
Corynebacterium spp.
Molluscum contagiosum causes
a skin infection
Apparently, need to look up
HPV, Orf, Cowpox
Herpes simplex - pathogenesis
- virus gains entry via sensory nerve endings and migrates to dorsal root ganglion
- viral DNA exists as episomes and no virus-coded proteins are present to stimulate an immune resopnse
- reactivated and migrates back out to sensory nerve ending and causes clinical manifestation
Herpes simplex - clinical presentation
Triggered e.g. by infection or stress
Primary (infants) - extensive, painful lesions also inside mouth (but rarely seen as not there long)
Secondary (all ages) peri-oral (genital), weeping, vesicular
Herpes simplex - diagnosis
Vesicle fluid - PCR for herpes virus DNA, immunofluorescence, culture
Herpes simplex - treatment
Cold sores - topical acyclovir
Genital herpes - oral acyclovir
Herpes zoster - history
previous chickenpox
triggered by physical or emotional insult preceded by tingling and/or pain
Herpes zoster - examination
weeping, vesicular rash
dermatomal distribution
Herpes zoster - treatment
oral aciclovir/valaciclovir
IV aciclovir
seek specialist advice if needed
Molluscum contagiosum - causative agent
molluscum contagiosum virus - poxvirus
Molluscum contagiosum - examination
raised, pearly lesions up to 3mm which are umbilicated
Molluscum contagiosum - diagnosis
clinical
Molluscum contagiosum - treatment
none - lesions usually disappear in 6-18 months
various topical preps + physical treatments
Bacterial infections - causative agents
Staph. aureus
Group A B-haemolytic streptococci (S. pyogenes)
S.aureus
Gram +ve cocci in clumps
Normal nasal flora in 30% of people
Large # of virulence factors e.g. DNAse, coagulase, teichoic acid
Exotoxins: epidermolytic toxins, toxic shock syndrome toxin, Panton-valentine leukocidin
S.pyogenes
Gram +ve cocci in chains
Express many virulence factors: adhesins, M proteins, hyaluronic acid capsule, hyaluronidase, C5a peptidase, Streptolysins O and S, pyrogenic exotoxins
Impetigo
Infection of epidermis (superficial)
Impetigo - causative agent
S. aureus, S.pyogenes
Impetigo - history
often occurs at site of skin damage
Impetigo - examination
plaque-like lesions with yellowish exudate.
thick scabs called honey crusted lesions
Impetigo - diagnosis
clinical diagnosis and bacterial culture
Impetigo - complications
Epidermolytic toxin production (ETA & ETB)
Manifests as localised ‘bullous impetigo’
or general: staph. scalded skin syndrome (SSSS) - looks like burned skin
Erysipelas - where does it infect
Infection of dermis - deeper than superficial
Erysipelas - causative agent
S. pyogenes
Erysipelas - history
often occurs at site of skin damage
face or shin
preceded by pain & tenderness
Erysipelas - examination
fever and malaise
well-demarcated inflamed lesion - red, swollen, painful and hot
lymph node enlargement
Erysipelas - diagnosis
clinical diagnosis
culture rarely helpful (will not grow)
Cellulitis - causative agents
S.aureus
S.pyogenes
Pasteurella multocida (animal bites)
Haemophilus influenzae
Cellulitis - history
site of skin penetration
any part of body
Cellulitis - examination
fever and malaise
diffuse inflamed lesion: erythema, swelling, tenderness, heat
Cellulitis - diagnosis
Clinical
Broad differential
Microbiology - lesion swabs (85% +ve)
Lesion aspirates and skin biopsy (20%) - not recommended routinely
Blood cultures (positive in only 2-4% of cases) only if severe sepsis or systemic signs of infection
Anthrax - causative factor
Bacilus anthracis - spore-forming aerobic gram+ve bacillus
Anthrax - where from?
acquired from imported wool, hair and animal hides
Anthrax - epidemiology
woolsorters’ disease
West African drum skin makers and injecting drug use
Anthrax - patterns of disease
Cutaneous anthrax (mortality
Necrotising fasciitis -
infection of skin and subcut tissues
Necrotising fasciitis - causative agents
Type one: polymicrobial - enteric gram -ve bacilli
anaerobes
Type two: strep. pyogenes
Necrotising fasciitis - history
spontaneous or at site of skin penetration for any part of the body
Necrotising fasciitis - examination
fever and malaise
dark, rapidly spreading, necrotic lesion
Necrotising fasciitis - diagnosis
microscopy and culture
Debrided material and blood culture
Necrotising fasciitis - treatment
IV ATX
surgical debridement
Anaerobic infections
Uncommon due to availability of O2
Anaerobic infections - gas gangrene
clinically similar to synergistic gangrene
palpable cutaneous gas
usually post op infection
Anaerobic infections - causative agent
Clostridium perfringens (anaerobic gram+ve bacillus)
Anaerobic infections - treatment
IV antibiotics
Surgical debridement
Empiric therapy for Staph. aureus or pyogenes
Flucloxacillin (with fusidic acid or mupirocin or impetigo)
Penicillin alergy: erythromycin + clarithromycin; vancomycin; linezolid
Empiric therapy for necrotising fasciitis
need to cover anaerobes, enterobacteriaceae, strepcocci and staphylococci
drugs: meropenem + clindamycin
Empiric therapy for anaerobic infections
anti-anaerobic agents e.g. metronidazole
Empiric therapy for high risk for MRSA
vancomycin, linezolid
Dermatophyte infections - skin
Tinea corporis, tinea pedis (athletes foot), tinea cruris
Dermatophyte infections - nails
Onychomycosis
Dermatophyte infections - scalp
tinea capitis (scalp ringworm, kerion)
Dermatophyte infections - causative agents
Tricophyton spp.
Microsporum spp.
Dermatophyte infections - pathogenesis
Dermatophyte use keratin as nutritional substrate
Usually restricted to stratum corneum
Rarely penetrate the living cells of the epidermis
Dermatophyte infections - diagnosis
skin scrapings - microscopy and culture
Dermatophyte infections - treatment
topical or systemic antifungal agents
Topical antifungal agents
Clotrimazole, terbinafine
Systemic antifungal therapy
For scalp and nail infections
Terbinafine, itraconazole, griseofulvin
