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Etiology :
- Industrialized nations : most commonly caused by S. aureus
- developing nations : common cause by Group A streptococcus
Pathogenesis.
- Intact skin is usually resistant to colonization or impetiginization, possibly
due to absence of fibronectin receptors for teichoic acid moieties on
S. aureus & group A streptococcus.
- In a typical sequence, S. aureus spreads from nose to normal skin
(approximately 11 days later) and then develop into skin lesions (after
another 11 days).
Differential Diagnosis :
Seborrheic dermatitis, Atopic dermatitis, Allergic contact dermatitis,
Epidermal dermatophyte infections, Tinea capitis, Herpes simplex,
Varicella, Herpes zoster, Scabies, Pediculosis capitis
Histologically
T0PICAL SYSTEMIC
First line Mupirocin bid Dicloxacillin 250-500 mg PO qid for 5-7 days
Fusidic acid bid Amoxicillin plus clavu 25 mg/kg tid; 250-500 mg qid
lanic acid; cephalexin
The complications :
- spread by autoinoculation or by insect vectors
- post-streptococcal sequela (glomerulonephritis)
SUPERFICIAL FOLLICULITIS
- Irritant folliculitis : exposure to mineral oils, tar products, & cutting oils
- Acne vulgaris
- drug-induced acneform eruptions
- rosacea
- hidradenitis suppurativa
- acne necrotica of the scalp, and
- eosinophilic folliculitis of HIV disease
DEEP FOLLICULITIS
Sycosis barbae : a deep folliculitis with perifollicular inflammation
in the bearded areas of the face and upper lip
- If untreated : lesions may become more deeply seated and chronic
- treatment : with warm saline compresses and local antibiotics
(mupirocin or topical clindamycin) may be sufficient to
control infection.
More extensive cases require systemic antibiotic therapy
20
Furuncles and Carbuncles
A furuncle or boil is a deep-seated inflammatory
nodule that develops around a hair follicle,
usually from a preceding, more superficial
folliculitis and often evolving into an abscess.
Differential Diagnosis :
- Cystic acne
- Kerion
- Hidradenitis suppurativa
- Ruptured epidermal inclusion cyst Furuncular myiasis
- Apical dental abscess
- Osteomyelitis
Figure 24.10 A
furuncle or a
boil begins as a
tender, inflamed
nodule that
usually
becomes
fluctuant,
points, and
ruptures.
CARBUNCLES
Fever and malaise are often present, and the patient may appear
quite ill.
The involved area is red and indurated, and multiple pustules soon
appear on the surface, draining externally around multiple hair
follicles.
Histologic examination
furuncle shows a dense polymorphonuclear inflammatory process in the
dermis and subcutaneous fat
In carbuncles, multiple abscesses, separated by connective-tissue
trabeculae, infiltrate the dermis and pass along the edges of the hair
follicles, reaching the surface through openings in the undermined
epidermis.
Lesions about the lips and nose raise the specter of spread via the
facial and angular emissary veins to the cavernous sinus.
- incision and drainage, when the lesions are large, painful, and
fluctuant
Abscess
Abscesses caused by S. aureus commonly occur in folliculocentric
infections : folliculitis, furuncles, and carbuncles.
31
Erysipelas
37
Cellulitis
Cellulitis is an infection of the deep dermis & subcutaneous tissue
caused most commonly by str.pyogenes & S. aureus.
Predisposition factor : lymphedema, alcoholism, DM, IV drug abuse, &
peripheral vascular disease.
Pathogenesis
- bacteria may gain access to the dermis via an external / a break in
the skin barrier (immunocompetent patient) or a hematogenous
route (immunocompromised patient)
- the lesion usually has ill defined, non palpable borders. In severe
infections may occur : vesicles, bullae, pustules or necrotic tissue.
- the erythema rapidly become intense & spreads. The area become
infiltrated & pits on pressure. Sometimes the central part become
nodular & surmounted by a vesicle that ruptures & discharges pus &
necrotic material. Streaks of Lymphangitis may spread from the area to
the neighboring lymph glands.
- complication (rare) : acute glomerulonephritis, lymphadenitis, &
subacute bacterial endocarditis
recurrent cellulitis (damage to lymphatic vessel)
gangrene, abscesses, & sepsis
Pathology
- in dermis : infiltrate lymphocytes & neutrophils
edema & dilation of lymphatics & small blood vessels
in severe dermal edema may be seen subepidermal bullae
Laboratory examination
- diagnosis cellulitis usually clinical
- the leukocyte count is usually normal / slightly elevated
- culture & sensitivities should be obtained, if sign & symptom do not
improve after 24 – 36 hours of treatment : the primary site of infection,
aspiration of the advancing edge, skin biopsy, or blood culture
- blood culture are almost always negative in immunocompetent host
Treatment
- immobilization & elevation of the area affected
- application of wet dressing to area with bullae or exudate
- treatment should be targeted against Str.pyogenes & S.aureus
- mild cases require a 10 days course of an oral antibiotic
- hospitalization & parenteral antibiotic : fasial cellulitis or seriously ill
(Intravenous penicillinase-resistant penicillins or first generation
cephalosporin are usually effective)
FIGURE A. Cellulitis. The lower FIGURE B. Cellulitis after puncture trauma. The
extremity is swollen, erythematous, and forearm is swollen, erythematous, and tender;
tender; there is blistering and crusting. there is abscess formation, blistering, and
crusting.
Adapted from Wolff K, Johnson RA, Suurmond D. In. Fitzpatrick’s Color Atlas & Synopsis of Clinical Dermatology. New York:Mc Graw Hill, 2005;p598.
Pictures of SSSS . Late stage of staphylococcal
scalded-skin syndrome
(A) erythema, more superficial blisters with
Generalized desquamation
desquamation of large sheets.
with large sheets
B. Superficial erosions around the eye with
underlying denuded skin.
C. Characteristic crusting with superficial
erosions noted on face of this 10- month-old child
with SSSS.
References
1. Craft N, Lee PK, Zipoli MT, Weinberg AN, Swartz MN, Johnson RA.
Superficial Cutaneous Infections and Pyodermas. In. Freedberg IM,
Eisen AZ, Wolff K, et al: eds. Fitzpatrick’s Dermatology in general
medicine. 7th ed. New York : Mc Graw-Hill Book Co, 2008: 1649-709.
2. Wolff K, Johnson RA, Suurmond D. In. Fitzpatrick’s Color Atlas &
Synopsis of Clinical Dermatology. New York:Mc Graw Hill, 2005;p598
3. Halpern AV, Heymann WR. Bacterial diseases. In. Bolognia JL,
Jorizzo JL, Rapini RP, eds. Dermatology. 2nd ed. New York : Mosby
elsevier, 2008 :p. 1075-106
4. Odom RB , James WD, Berger TG. Andrews’ diseases of the skin. 9th
ed. Philadelphia : WB. Saunders Co, 2000
Classification of Infectious Folliculitis
Bacterial folliculitis
· Staphylococcus aureusfolliculitis
· Periporitis staphylogenes
· Superficial (follicular or Bockhart impetigo)
· Deep (sycosis) [may progress to
furuncle (boil) or carbuncle]
· Pseudomonas aeruginosa folliculitis ("hot tub" folliculitis)
· Gram-negative folliculitis (occurs at the site of acne vulgaris, usually the
face, with long-term antibiotic therapy)
· Syphilitic folliculitis (secondary; acneform)
Fungal folliculitis
· Dermatophytic folliculitis
· Tinea capitis
· Tinea barbae
· Majocchi granuloma
· Pityrosporum folliculitis
· Candida folliculitis
Viral folliculitis
· Herpes simplex virus folliculitis
· Follicular molluscum contagiosum
Infestation
· Demodicidosis
Table 2. Organisms, Antimicrobial Agents of Choice, and Alternatives
Penicillin-intermediate resistance