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Lihat Materi | |
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Pioderma
PYODERMAS Agnes Sri Siswati Dermatolo-vereology department Faculty of Pyodermas are bacterial infections of the skin caused by pyogenic bacteria. Normal skin is heavily colonized by bacterial flora, which are more numerous and diverse in occluded sites. The most common are various nonpathogenic gram-positive bacteria such as staphylococcus epidermidis. Staphylococcus aureus and Streptococcus pyogenes can cause superficial infections of epidermis or extending into the dermis. The infections may arise as primary infections in minor superficial breaks in the skin or as secondary infections of preexisting dermatoses. I. IMPETIGO AND ECHTYMA Definition: Impetigo represents a superficial skin infection caused by gram positive bacteria. The early lesions are pustules, which quickly break to form crust. Epidemiology: Impetigo occurs most commonly in children. Etiology : - Staphylococcus aureus can cause non bullous impetigo. - Streptococcus pyogenes (Group A â-hemolytic Streptococcus) cause bullous impetigo. Predisposing factors: - Warm temperature - High humidity - Presence of skin disease (especially atopic dermatitis) - Age - Prior antibiotic therapy - Crowded living condition - Neglected minor trauma Symptoms: - Impetigo variable pruritus - Echtyma pain and tenderness Physical examination: Non bullous impetigo. The most commonly encountered clinical finding as that of a crust, which usually honey-colored, that call golden- yellow crusts. Intact pustules are usually not found. When the crust is removed, a superficial glistening base is revealed. Impetigo does not extend deeply, so ulcerations are not present Lesions can be found anywhere, but most frequently are located on the face. Bullous impetigo. Vesicle and bullae containing clear yellow or slightly turbid fluid without surrounding erythema, arising on normal-appearing skin. If vesicle or bullae rupture, a hallow moist erosion forms. Echtyma. Ulceration with a thick adherent crust, tender and indurated Laboratory examinations: Gram stain. Gram-positive cocci, in chains or clusters, with in neutrophils. Culture. S, aureus; Group A â-hemolytic Streptococcus Management: Prevention. Benzoyl peroxide wash (soap bar) Therapy. Both topical and systemic antibiotics have been advocated for treating impetigo. Topical preparations such bacitracin or neomycin, especially for small lesions. For extensive lesions systemic antibiotics are indicated II. FOLLICULITIS Folliculitis is an inflammatory reaction in the hair follicles caused by bacteria, usually Staphylococcus aureus. Folliculitis is characterized by a follicular papule, pustule, erosion or crust at the follicular infundibulum. Predisposing factors: - Shaving hairy region such as beard area, axillae and leg - Occlusion of hair bearing area - Topical climate with high temperature and humidity - Topical glucocorticoid - Systemic antibiotics promotes growth of gram negative bacteria - Diabetes Mellitus - Immunosuppressant Distributions: Face, beard area, Scalp, neck, leg, trunk, buttocks Sympto: Usually non tender, slightly tender or pruritus Skin lesion: Papule or pustules confined to the ostium of the hair follicle, surrounded by erythematous hallo. Rupture of pustules leads to superficial erosions or crusts. Superficial infection heals without scarring. Laboratory examinations: Gram stain. Gram-positive cocci, in chains or clusters, with in neutrophils. Culture. Staphylococcus aureus Management: Prophylaxis. Correct underlying predisposing condition. Washing with antibacterial soap or benzoyl peroxide preparation. Therapy. Topical antibiotics. Response to therapy is usually good, but recurrences are common. Extension of infection can progress to abscess or furuncle. III. ABSCESS, FURUNCLE AND CARBUNCLE An abscess is a circumscribed collection of pus appearing as an acute or chronic localized inflammation, associated with tissue destruction. Furuncle is an acute, deep-seat, red, hot, tender nodule or abscess. A carbuncle is a deeper infection comprised of interconnecting abscess usually arising in several contagious hair follicles. Epidemiology: Children, adolescent and young adult, but more common in boys. Etiology: Staphylococcus aureus, much less commonly other organisms. Predisposing factors: - Chronic S. aureus carrier state - Diabetes Mellitus - Obesity - Poor hygiene - Bactericidal defects - Chemo tactic defects Symptom: Throbbing pain and invariably exquisite tenderness Carbuncles may be accompanied by low-grade fever and malaise. Skin lesions: Lesions are red, hot, and painful/tender. Abscess. May arise in any organ or structure. Abscess that present on the skin arise in the dermis, subcutaneous, fat, muscle or variety of deeper structures. A well-formed abscess is characterized by fluctuance of central portion of the lesion. Occur at any cutaneus site. Furuncle. Initially, a firm tender nodule, with a central necrotic plug. Nodule becomes fluctuant with abscess formation below necrotic plug often topped by central pustule. After rupture or drainage of pustule and discharge of necrotic plug, a nodule with cavitations remains. Carbuncle. Evolution is similar to that of furuncle. Comprised of several to multiple, adjacent, coalescing furuncles. Characterized by multiple loculated dermal and subdermalabscess, superficial pustules, necrotic plug and sieve-like openings draining pus. Laboratory examinations: Gram positive cocci within leukocyte and extra cellular space. Management: Most cases resolve within incision, drainage and systemic antibiotic treatment. Prevention. Antibacterial soap bathing Surgery. Incision and drainage. Systemic and topical antibiotics IV. ERYSIPELAS AND CELLULITIS Cellulitis is an acute, spreading infection of dermal and subcutaneous tissues, characterized by a red, hot, tender area of the skin, often on the site bacterial entry. Erysipelas more localized and superficial than cellulitis. Etiology: Adult. Staphyloccocus aureus, Group A â hemolytic Streptoccocus Children. Hemophylus influenzae Pathogenesis: Cellulitis and erysipelas can arise via portal of entry through any mucocutaneous site or less commonly, spread hematogenously to soft tissue. Following entry, infection spreads to tissue spaces and cleavage plane as hyaluronidases break down polysaccharideground substances, fibrinolisins digest fibrin barriers, lechitinases destroy cell membranes. Symptom Incubation period Few days. Prodrome. Occurs less often than commonly thought. Malaise, anorexia, fever, chills can develop rapidly before cellulitis is apparent clinically. Skin lesions: Portals of entry. Breaks in skin, ulcers, or chronic dermatosis. Plaque red, hot, edematous and shiny, very tender area of skin of varying size. Border usually sharply defined, irregular and slightly elevated. Vesicle or bullae aroud the border. Adult. Distribution on lower leg, interdigital, trunk. Children on cheek, periorbital area, head and neck Lymph nodes can be enlarged and tender regionally. Laboratory examinations: Hematology. WBC and ESR may be elevated Gram’s stain may show bacteria, chain or cluster of gram-positive cocci Management: Supportive. Rest, immobilization, elevation, moist heat, analgesia Therapy. Systemic Antibiotic V. HIDRADENITIS Hidradenitis suppurativa is a chronic, suppuratie, cicatricial disease of apocrine gland-bearing skin in the axillae, or the anogenital region( males more often Hve anogenital and females axillary involvement Etiology: A variety of pathogens may secondary co;onize or infect lesions. Predisposing factors: - Obesity - Apocrine duct obstruction, secondary bacterial infection Symptom: Intermittent pain and marked point tenderness related to abscess formationin axillae and/or anogenital area Skin lesions: Initial lesion: inflammatory nodule/abscess that may resolve or point to surfaceand drain purulent/seropurulent material, relationship to hair follicle usually not apparent. Lesions moderatly to exquisitely tender. Management: Hidradenitis suppurativa is not simply an infection and that combination medical management and surgical management programme are needed. Medical management. Intralesion triamcinolone, systemic antibiotic, prednisone and oral isotretinoin. Surgical management. Incise and drain acute abscesses, exsisechrinic reccurent Secondary Infections 1. Intertrigo 2. Toe web Infections 3. Acut Infectious Eczematoid Dermatitis 4. Pyoderma Secondary to Eczema OTHERS 1. Pitted keratolysis 2. Staphylococcal Scalded Skin Syndrome (S4) Staphylococcal Scalded Skin Syndrome (S4)/ Ritter’s disease Staphylococcal Scalded Skin Syndrome (S4) is an toxin mediated epidermolytic disease characterized by erythema, widespread detachment of the superficiallayer of epidermis, resembling scalding, and occuring mainly in newborn and infants younger than 2 years. Epidemiology: Most common in infants and young children Etiology: Staphylococcus aureus of pjage group II, mostly type 71 Pathogenesis: Staphylococcus aureus colonizes nose, conjunctivae with or without causing clinically apparent infection, producing an exotoxin that transported hematogrnously to the skin.Teh exfoliative toxin causes acantholysis nad intradermal cleavege within the stratum granulosum. Skin symptom Early eryhematous areas are very tender Skin lesion: Localized form. Intact flaccis bullae, cluster. Ruptur of the bullae result in moist red and/or crust erosive lesions Generalized form. Exotoxin-induce changes: micromacular scarlatiniform rash or diffuse, illdefine erythemaand a fine, stippled, sandpaper appearance occur initially. Condition become generalized, resembling scalding. With epidermolysis, epidermis appear wrinkle and can be removed by gentle pressure. Laboratory examinations: Gram’s stain and bacterial culture Management: General care. Hospitalization is recomanded for neonates and young children, especially if skin sloughing is extensive and parental compliance questionable. Topical therapy. Systemic antimocobial therapy. Adjuvant therapy. Replace significant water and electrolyte loss ontervenously in severe cases. Pitted keratolysis Pitted keratolysis present as defects in the thickly keratinized skin of the plantar foot with sculpted pits of variable depth, depending on the thickness of the stratum corneum. Etiology: Micrococcus sedentarius. Age of onset: young adult Predisposing factors: - Hyperhidrosis of the feet - Occlusing footwear Skin symptom: Usually asymptomatic. Foot odor. Skin lesion: Pits in strarum corneum. 1 to 8 mm in diameter. Pits can remain discreteore, more often become confluent, forming large areas of eroded stratum corneum. Involve areas are whiw when stratum corneum is fully hydrated. Course and prognosis: Persist and recurs until the underlying prediaposing factors are corrected. Management: Prevention. Topical therapy. Daily applications of agents such as benzoyl peroxide gel or topical antibotic such erythromycin are usually effective.
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