Skin and Soft Tissue Pathology Flashcards
4 commensal skin flora
Coagulase -ve staphylococci
Staph A
Proprionibacterium-acne
Corynebacterium
5 common commensal skin viruses
Herpes viruses (HSV, VZV) Moluscum contagiosum HPV Orf Cowpox
Which virus is transmitted from sheep and results in ulcerative skin lesions
Orf
HZV pathogenesis
Vesicle forms which grows to form an ulcer. When it ruptures, it releases vesicle fluid containing infectious particles. Virus gains entry via sensory nerve endings and migrates along the nerve to the DRG where it remains latent and the immune response is not stimulated. When reactivated, the virus migrates outwards to sensory nerve endings and causes the clinical manifestations of infection- preceded by tingling
Triggers of reactivation of HSV
Infection or stress
Primary infections of HSV
Extensive, painful lesion, occurs only once. Rare. Normally HSV1. HSV2 is usually genital herpes.
Secondary infections fo HSV
All ages, recurrent infection. Peri-oral. Weeping, vesicular
Diagnosis of HSV
Clinical
Vesicle fluid contains virus-PCR
Treatment for HSV
Cold sores- topical aciclovir
Genical herpes/immunocompromised- oral aciclovir
Another name for strep pyogenes
Beta haemolytic streptococci
Usual causative organisms for bacterial skin infections
Staph A
Strep P
H. Influenzae
Pasteurella mulficida (grow in cat and dog’s mouths)
Gram +ve cocci in clusters. Catalase +ve. Normal nasal flora in 30% population
Staph A
Name some virulence factors of Staph A
DNAase
Coagulase
Teichoic acid
Exotoxin production e.g. epidemolytic toxins A & B, toxic shock syndrome toxin, PVL-boils
Really nasty bacteria, gram +ve cocci in chains. Catalase -ve.
Strep Pyogenes
Name some virulence factors of strep P
Adhesins M. proteins (antiphagocytic) Streptolysins O and S Hyaluronic capsule (antiphagocytic) Hyaluronidase (facilitates intestinal spread) C5a peptidase (anticomplementary)
Describe the rash in VZV
Weepeing, vesicular rash
Treatment for VZV
Oral aciclovir//valaciclovir
IV aciclovir if older, lower immune system or increased susceptibility to shingles
Causative organism for molluscum contagiosum
Molluscum contagiosum virus-poxvirus
Describe the appearance of molluscum contagiosum
Raised pearly lesions, umbilicated (central depressions) No sequelae.
Treatment of molluscum contagiosum
None. Usually disappear within 6-18 months. Physical treatments some times appropriate if disfiguring.
Causative organism for Impetigo
S. Aureus/S.Pyogenes
Often occurs at site of skin damage, superficial, thick scabs-‘honey crusted lesions’, with yellow exudate. often around the nose.
Impetigo
Local manifestation of impetigo
Bullous impetigo
Generalised manifestation of impetigo
Staph scalded skin syndrome
Pathogenesis of impetigo
Desmosermal glycoprotein desmoglein-1 which is requied for cell to cell adhesion in the superficial epidermis is inactivated by ETA and ETB (epidermolytic toxin)
Causative organism for erysipelas
S. pyogenes
Erysipelas
Infection of dermis
Ocurs at site of skin damag, often face or shin. Preceded by pain and tenderness, well demarcated inflamed lesions-red, swollen, painful or hot. Fever, malaise and local lyphadenopathy.
Cellulitis
Infection of skin and subcutanous tissues, not bilateral.
Causative organisms of cellulitis
S. aureus
S. pyogenes
Pasteurella multicida (animal bites)
H. influenza
What bacteria might give rise to peri-orbital cellulitis?
H. influenza
Causative organism for anthrax
Bacillus anthracis-spore forming aerobic gram +ve bacillus, acquired from imported animal hides or wool.
Describe the skin lesions in anthrax
Malignant pustular-eschar- dry dark scab
may develop into septicaemia
Risk factors for anthrax
Drum skin exposure
Injecting drug users
Describe the different types of anthrax
Cutaneous anthrax-readily treated
Inhalation/septicaemic antrhax-high mortality
Necrotising fasciitis
Infection of the skin and SC tissue. Spontaneous or at site of skin penetration. Any part of the body. Dark, rapidly spreading, necrotic lesion. Fever and malaise.
Describe the 2 types of Necrotising fasciitis
Type 1: polymicrobial - enteric gram -ve bacilli and anaerobes i.e. normal bowel flora.
Type 2: strep pyogenes- acquired.
Another word for perineal necrotising fasciitis
Fournier’s or syndergistic gangrene
Diagnosis of necrotising fasciitis
Blood or debrided material
Treatment for necrotising fasciitis
IV-antibiotics
or surgical debridement
Anaerobic Infections
Uncommon-ready availibility of O2.
Gas gangrene- similar to NF but with a palpable SC gas. Usually post operative at the site of surgery.
Common causative organism of gas gangrene
Clostridium perfringens
Treatment of gas gangrene
IV antibiotics
Surgical debridement
Treatment for impetigo (causative organism staph A)
Fusidic acid or mopirocen
Empiric bacterial skin infection treatment for those with a penicillin allergy
Erythromycin/clarithromycin/vancomycin/linezolid
Treatment for NF
Need to cover anaerobic bacteria so meropenem and clindamycin. Metronidazole is an anti-anaerobic agent.
Dermatophyte
Superficial fungal infection
Skin fungal infection
Tinea corporis, tinea pedis (athlete’s foot)
Nail fungal infections
Onychomycosis
Scalp infections
Tinea capitis (scalp ringworm)
Describe Pityriasis Versicolour
What I have on my back- hypopigmented patches that come out in the summer- fungal infection
Causative organsims for dermatophyte infections
Tricophytum e.g T. rubum- circulates among humans
Microsporum- e.g. M.canis- circulates among animals
What level of the skin do you usually get dermatophyte infections?
Usually restricted to stratum corneum- rarely penetrate the lining cells of the epidermis. Use keratin as a nutritional substrate
Topical antifungal therapy
Clotrimazole
Terbinafine
Scalp and nale infections- systemic antifungal therapy
Terbinafine, itraconazole, friseofluin
