Painful Skin Lesions

Question 1

Impetigo

Answer 1

• Common inf. of the superficial layer of the epidermis
• Most often Gram + (Strep pyogenes/ Staph aureus)
• Highly contagious
• Bullous/ non-bullous (blisters)
• Outbreaks kindergarten

Question 2

Impetigo Pathophysiology

Answer 2

Need a break in skin barrier:
- Scratching
- Dermatophytosis (highly contagious, fungal, red/silvery ring-like rash on skin/scalp)
- Varicella
- HSV (blister pops = infection)
- Thermal burns
- Surgery
- Trauma

Question 3

S Aureus & GABHS colonization

Answer 3

• Group A beta haemolytic Strep from other individuals
• S Aureus part of commensal Flora (can become pathological or get from other carriers)

Question 4

Bullous impetigo

Answer 4

• Exfoliative toxins of S. aureus = exfoliatins A & B
• These toxins cause loss of adhesion btwn keratinocytes (skin cells) in epidermis
• Specifically target Desmoglein I protein (chain keeping skin cells tog.)= adhesion molecule linking keratinocytes

Question 5

Folliculitis

Answer 5

• Inflammation of hair follicle
• Infectious/ non-infectious

Question 6

Infectious Folliculitis

Answer 6

1. Bacteria (most common)
   - Staph Aureus
   - pseudomonas aeruginosa (hot tub Folliculitis)
2. Virus
   - HSV > H zoster
   - Molluscum contagiosum
3. Fungi & yeasts
   - Malassezia
   - Candida
   - Dermatophytes (Trichophyton tonsurans)
4. Parasites (least common)
   - demodex
   - scabies

Question 7

Non-infectious Folliculitis

Answer 7

• irritation from regrowing hairs (shaving, waxing)
• occlusion eg: moisturizers (thick)
• chemicals
• drugs
  = corticosteroids (prednisone), androgens (male hormones, testosterone), adrenocorticotrophic hormone (ACTH), lithium, isoniazid (INH - TB treatment), phenytoin & B-complex vitamins

Question 8

Boils (Furuncle)

Answer 8

• localized deep suppurative necrotic form of Folliculitis = dermis & subcutaneous tissue (inflammation)
• S. Aureus most common
• access through skin & invade hair follicle
• develops in moist/ sweaty areas = scalp, face, buttocks, axillae & areas with friction & perspirations
• group = carbuncle

Question 9

Abscess

Answer 9

• manifestations of S. Aureus skin & soft tissue infections, formed to contain the nidus of inf.
• PMNs (neutrophils) = primary cellular host defense against S. Aureus inf. & major component of S. Aureus abscesses
• S. Aureus = several molecules that contribute to formation

Question 10

Process of formation of mature abscess

Answer 10

1. 0-2 hrs (infection)
   - need break in skin for S. Aureus = epidermis, dermis into subcutis
2. 2-24 hrs (inflammatory response)
   - polymorphic nucleocytes = neutrophils to fight off inf.
3. 2-6 days (abscess formation)
   - leucocytes = liquefaction & coagulative necrosis
4. 6-14 days (mature abscess)
   - fibrous capsule = keep inf. from infiltrating rest of tissue

Question 11

Cellulitis

Answer 11

• non-necrotizing inflammation of the skin & subcutaneous tissue, acute infection
• breach in the skin, portal of entry may not be obvious
• organisms on skin & appendages = cellulitis & multiply
• Strep pyogenes, lesser S. Aureus
• Group A Strep = most common, produce virulence factors eg: pyrogenic exotoxins (A, B, C & F) & Strep superantigen
• rare cases = occur from hematogenous spread from S. Pneumoniae & marine vibrio species
  Neisseria meningitidis, pseudomonas aeruginosa, brucella species & legionella species

Question 12

Clinical features of cellulitis

Answer 12

• erythema, warmth, edema, tenderness = cytokine & neutrophil response from bacteria breaching epidermis

Question 13

Risk factors for cellulitis

Answer 13

• culprit = breakdown in skin barrier eg: skin injuries, surgical incisions, intravenous site punctures, fissures btwn toes, insect bites, animal bites & other skin infections
• patients with comorbidities eg: DM, venous insufficiency, peripheral arterial disease & lymphedema

Question 14

Herpes virus

Answer 14

More than 100 types
- HSV 1 & 2 (cold sores/ genital herpes)
- VZV (chicken pox/ shingles)
- CMV
- EBV
- human HSV 6, 7 & 8

Question 15

HSV pathophysiology

Answer 15

• dissemination of HSV inf. = people with impaired T-cell immunity (eg: organ transplant receipts & AIDS patients)
• HSV inf. complicate burn wounds/ damaged skin eg: atopic dermatitis
• close personal contact, inoculation of virus in susceptible mucosal surfaces

Question 16

HSV unique properties

Answer 16

• capacity to invade & replicate in nervous system
• establishment & maintenance of latent inf. in nerve cell ganglia proximal to site of inf.
• reactivation & replication of latent HSV, area supplied by ganglia = latency established, induced by various stimuli (eg: fever, trauma, emotional stress, sunlight, menstruation)
  HSV-1 reactivates more frequently in oral rather than genital region
  HSV-2 reactivates 8-10 times more commonly in genital region

Question 17

HSV progression summary

Answer 17

1. Establishes primary infection within host
2. Enters sensory nerve terminals at peripheral sites
   (Retrograde axonal transport)
3. Enters trigeminal nerve ganglion
4. Establishes latency
   (Triggering factors)
5. Reactivation of virus
   (Travels from dorsal root ganglion along sensory nerves)
6. Reaches epidermis & the epidermal-dermal junction
7. = Recurrent infection (small, painful vesicles)

Question 18

Shingles (Herpes Zoster)

Answer 18

• 2 distinct syndromes (chickenpox, shingles)
• chickenpox initial, after infection resolves, viral particles remain dorsal root/ sensory ganglia, lay dormant for years to decades (multiple erythematous vesicles)
• latent period, host immunological mechanisms suppress replication of virus, VZV reactivates
• shingles after = immune system can’t suppress viral replication, VZV reactivates in dermatomal distribution
• VZV activated at spinal root/ cranial nerve neurons
• inflammation in dorsal root ganglion accompanied by hemorrhagic necrosis of nerve cells (painful lesions)
• cutaneous rash due to herpes zoster coincides with profound VZV specific T-cell proliferation
• trigger= virus replicates & travels through sensory nerves, to skin surface

Question 19

Chickenpox & dermatomes

Answer 19

• anatomical location of involved dermatome = determines specific manifestation
• cervical & lumbar roots involved, motor involvement, may be overlooked, evident depending on virulence or extent of migration
• contagious to person with no previous immunity to VZV = chickenpox
• someone has shingles comes into contact with person with no exposure to VZV = chickenpox

Question 20

Acute complications of Varicella

Answer 20

• bacterial sepsis
• pneumonia
• encephalitis
• haemorrhagic

Question 21

Acute complications of Zoster

Answer 21

• vasculopathy
• myelopathy
• postherpetic neuralgia
• retinal necrosis
• cerebellitis
• meningoencephalitis
• myelitis
• cranial nerve palsies
• Gastrointestinal ulcers
• pancreatitis
• hepatitis