13.1 Painful Skin Lesions Flashcards
List the main reasons for painful skin lesions
Skin infections (mostly)
Bacterial:
- Impetigo
- Folliculitis
- Boil
- Abscess
- Cellulitis
Viral:
- Herpes simplex
- Shingles / H Zoster
Impetigo
Overview
Pathophysiology
- Common infection of the epidermis {most superficial layer}
- Most often Gram + (Streptococcus pyogenes or Staphylococcus aureus)
- Highly contagious (outbreaks in kindergardens)
- Classified as bullous or non bullous (causes blisters or don’t)
Pathophysiology
- Needs a break in skin barrier eg
•Scratching
•Dermatophytosis (fungal infec)
•Varicella (blisters)
•Herpes simplex infection
•Thermal burns
•Surgery
•Trauma
How are you exposed to:
GABHS
S aureus
GABHS- From other individuals
GABHS - Group A Beta Haemolytic Strep
S Aureus- Part of commensal flora; can also get from other carriers
Bullous Impetigo
Pathogenesis
Forms blisters:
- Exfoliative toxins of S aureus termed exfoliatins A and B
- These toxins cause loss of adhesion between the keratinocytes in the epidermis
- Specifically target Desmoglein I protein which is an adhesion molecule linking keratinocytes
Pathogenesis and clinical findings
- Slide 7
Infective Folliculitis
Pathogens
Bacteria: most common
- Staph Aureus
- Pseudomonas Aeruginosa (Hot tub folliculitis)
Virus:
- Herpes simplex > H zoster
- Molluscum contagiosum
Fungi and yeasts:
- Malassezia
- Candida
- Dermatophytes (Trichophyton tonsurans)
Parasites
- Demodex
- Scabies
Non-infective folliculitis
Pathogens
- Irritation form regrowing hairs (shaving, waxing)
- Occlusion- eg Thick Moisturisers (Vaseline)
- Chemicals
- Drugs
• Corticosteroids, androgens (male hormones), adrenocorticotrophic hormone (ACTH), lithium, isoniazid (INH), phenytoin and B-complex vitamins
Superficial folliculitis
Aetiology
Slide 11 for overview
Boils (Furuncle)
Def
Organism
Def: Localized deep suppurative necrotic form of folliculitis which involve the dermis and the subcutaneous tissue
Organism
- S. aureus is most common organism
- Gains access through the skin and invades the hair follicle
- Usually develops in moist or sweaty areas such as the scalp, face, buttocks, axillae, and areas that are subject to friction and perspiration.
- group of furuncles coalesce to form a carbuncle
Folliculitis{superficial} ➡️ Furuncle {deep into dermis & subcutaneous tissue} ➡️ Carbuncle {few follicles involved}
Slide14
Abscess
General
Pathogenesis
- Abscesses are a frequent manifestation of S. aureus skin and soft tissue infections and are formed, in part, to contain the nidus of infection
- PMN’s (neutrophils) are the primary cellular host defense against S. aureus infections and a major component of S. aureus abscesses.
- S. aureus produces several molecules that also contribute to the formation of abscesses
Pathogenesis
- break in skin
- enter through dermis, epidermis, subcutaneous tissue, soft tissue
- polymorphic neutrocyts (neutrophils)
- neutrophils causes liquefactive and coagulative necrosis
- formation of fibrous capsule (to round off infec and stop from infiltrating rest of tissue)
Cellulitis
Def
Pathogenesis
Organism
Clinical Features
Risk factors
Def
- Non-necrotizing inflammation of skin and subcutaneous tissues, (from acute infection)
Pathogenesis
- follows a breach in the skin, although a portal of entry may not be obvious
- Organisms on the skin and its appendages gain entrance to the dermis and multiply to cause cellulitis
Organisms
- Most likely organism Strep pyogenes, (lesser extent S aureus)
- Group A Streptococci, the most common bacteria to cause cellulitis, can also produce virulence factors such as pyrogenic exotoxins (A, B, C, and F) and streptococcal superantigen
- Rare: cellulitis can occur from hematogenous spread from organisms like S pneumoniae (pneumococcus) and marine Vibrio species. Neisseria meningitidis, Pseudomonas aeruginosa, Brucella species, and Legionella species
Clinical features
- Erythema, warmth, edema, and tenderness to palpation resulting from cytokine and neutrophil response from bacteria breaching the epidermis.
RF:
- any culprit that could cause a breakdown in the skin barrier such as skin injuries, surgical incisions, intravenous site punctures, fissures between toes, insect bites, animal bites, and other skin infections
- Patients with comorbidities such as diabetes mellitus, venous insufficiency, peripheral arterial disease, and lymphedema are at higher risk of developing cellulitis.
HSV
General
Unique properties
General
- Dissemination of herpes simplex infection can occur in people with impaired T-cell immunity (eg organ transplant recipients and AIDS patients)
- Herpes simplex infection can also complicate burn wounds or damaged skin such as in atopic dermatitis
- HSV is transmitted by close personal contact, and infection occurs via inoculation of virus into susceptible mucosal surfaces
Unique properties
- Capacity to invade and replicate in the nervous system
- Establishment and maintenance of latent infection in nerve cell ganglia proximal to the site of infection
- Reactivation and replication of latent HSV, always in the area supplied by the ganglia in which latency was established, can be induced by various stimuli (eg, fever, trauma, emotional stress, sunlight, menstruation)
- HSV-1 reactivates more frequently in the oral rather than the genital region. On the other hand,
- HSV-2 reactivates 8-10 times more commonly in the genital region
HSV
Pathogenesis
- establishes prim infec within host
⬇️ - enters sensory nerve terminals at peripheral sites
⬇️ retrograde axonal transport - enters trigeminal nerve ganglion
⬇️ - establishes latency
⬇️ triggering factors - reactivation of virus
⬇️ travels from dorsal root ganglion along sensory nerves - reached epidermis & at epidermal-dermal junction
⬇️ - results in recurrent infec
Slide 23
Shingles (Herpes Zoster)
Distinct syndromes
General
Two distinct syndromes
- Chickenpox initial. After this infection resolves, viral particles remain in the dorsal root or other sensory ganglia, where they may lay dormant for years to decades.
- Shingles- Latent period, host immunologic mechanisms suppress replication of the virus, but VZV reactivates
General
- VZV is activated at the spinal root or cranial nerve neurons
Dermatomes
- The anatomic location of the involved dermatome often determines the specific manifestations. When cervical and lumbar roots are involved, motor involvement, which is often overlooked, may be evident, depending on the virulence or extent of migration
- This infection is contagious to persons with no previous immunity to VZV = then they develops chickenpox
Pathogenesis of Varicella zoster
Slide 27 + 28
