Bacterial Skin Infections Flashcards

1
Q

Most common causes of skin infections in immunocompromised people?

A

Staphylococci and streptococci
Infections begin with break in skin barrier
May see unusual or more severe infections

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2
Q

Medications that work for most bacterial skin infections?

A

first generation cephalosporins, pecillinase-resistant penicillins (MRSA becoming an increasing problem)

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3
Q

What organisms make up the normal skin flora?

A

Function to prevent skin infections:

  • staph epidermidis
  • corynebacterium spp –> intertriginous areas
  • propionibacterium spp: sebaceous glands (acne)
  • gram negative bacteria in axillae and groin
  • yeasts (pityrosporum spp) on skin rich in sebaceous glands like central chest and upper back
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4
Q

Characteristics of Impetigo

A
  • most common cutaneous infection in children
  • causative pathogens: s. aureus, Group A strep (beta hemolytic) or both
  • staph more predominant now
    two clinical variants –> nonbullous (crusted) and bullous
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5
Q

Epidemiology of impetigo

A

usually affects young children
occurs year round
heat, humidity, crowding and poor hygiene predispose
spread by direct contact, autoinoculation
nasal colonization may serve as a source of infection for s. aureus

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6
Q

Common presentation of impetigo

A

often located around nose and mouth

  • moist, honey colored crusts on erythematous base
  • fever, systemic symptoms are rare
  • may itch
  • may be preceded by skin trauma
  • often complicates atopic dermatitis to cause secondary impetiginization
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7
Q

Presentation of Bullous impetigo

A

May arise without obvious trauma

  • large, flaccid bullae may develop
  • blisters rupture leaving shiny, shallow erosions
  • adenopathy, systemic symptoms are rare
  • cleavage result of epidermo;ytic toxin produced by staph (exfoliatin)
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8
Q

Treatment of Bullous impetigo

A
  • antibiotic coverage should cover for both staph and strep.
  • for mild cases: mupurocin cream
  • widespread/complicated cases: penicillinase-resistant penicillins or first generation cephalosporins
  • culture/sensitivities recommended due to rise of resistant organisms
    Recurrent cases: treat nares with mupurocin, body with chlorhexidine (hibiclens) or bleach baths soaking for 15min
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9
Q

Complications of impetigo

A
  • may progress to ecthyma (deeper infection)
  • staph scalded skin syndrome
  • glomerulonephritis (not rheumatic fever) can complicate strep A impetigo.
    Antibiotic tx doesnt prevent nephritis
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10
Q

Appearance of staphylococcus scalded skin syndrome

A

Skin just peals off leaving a smooth base

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11
Q

Characteristics of staphylococcus scalded skin syndrome

A
  • diseases resulting from toxin produced by bacteria
  • most common causes are s. aureus, phage group 1 strains
    They produce exotoxins like exfoliatin (ETA and B) that circulate systemically, split the skin at superficial granular layer
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12
Q

Epidemiology of staph scalded skin syndrome

A

affects children less than 6, rarely immunosuppressed adults, especially with renal failure

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13
Q

typical clinical picture of staph scalded skin syndrome

A
  • site of infection may or may not be apparent
  • prodrome of malaise, fever, irritability
  • skin becomes tender then develops symmetrical sundron-like erythema around facial orficies, neck and flexures
  • skin superficially blisters, then sloughs leaving behind moist skin, scales
  • heals without scarring 10-14days
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14
Q

Diagnosis of staphylococcus scalded skin syndrome

A

diagnosis is primarily clinical

  • cultures from affected skin, blisters negative
  • may culture staph from nare, conjunctiva, small foci of infection (pustules)
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15
Q

What is the prognosis for scalded skin syndrome?

A
  • good in healthy children (3% mortality)
  • bad in adults (over 50% all adults, up to 100% in adults with underlying disease)
  • Must be distinguished from toxic epidermal necrolysis
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16
Q

What is toxic epidermal necrolysis?

A

Usually a drug reaction, full thickness of skin sloughing, leads to widespread denudation, mucosae are involved, high mortality, treated in burn units with or without IVIg.

17
Q

Histological different between SSS and TEN?

A

SSS splits the corneum/granulosum away from the rest of the epidermis leaving a smooth base.
TEN –> you seen eosinophils in the base layers of the epidermis.

18
Q

Folliculitis, furuncles and carbuncles etiology

A
  • bacterial infections of hair follicle
  • S. aureus usual pathogen –> predilection for hair follcle
  • gram negative organisms occasionally cause folliculitis
    E.g. hot tub folliculitis –> pseudomonas
  • some yeasts cause folliculitis –> Candida, Pityrisporum
19
Q

Risk factors for folliculitis, furuncles and carbuncles?

A

trauma, maceration, occlusion, diabetes, immunosuppression

20
Q

Variation in the lesion of folliculitis, furuncles and carbuncles?

A

Depth of infection determines the lesions:
- Superficial –> folliculitis
- entire follicle and surrounding tissue –> furuncle (boil)
- multiple coalescing furuncles, deep tissues –> carbuncle
Caurbuncle can ulcerate

21
Q

Characteristics and Treatment of hot-tub folliculitis?

A
  • can be from both swimming pools and hot tup
  • caused by pseudomonas aeruginosa
  • treat with ciprofloxacin instead of cephalexin
  • seen on body - torso
22
Q

Treatment for folliculitis in general

A

Topical mupurocin for superficial folliculitis

  • abscesses may rupture or require incision and drainage
  • antibiotic therapy may be needed:
    1. widespread lesions or critical areas
    2. immunosuppressed children
    3. valvular heart disease or prosthesis
    4. lesions not responding to local therapy, those with cellulitis
    5. antibiotic coverage: penicillinase-resistant penicillins (dicloxicillin); first generation cephalosporin; fluoroquinolone for hot tup folliculitis
    6. seek and tx for nasal/perineal colonization if recurrent
    7. community acquired MRSA more often cause of very painful, virulent furuncles; do cultures