Skin infection

1. Skin infection

3. Impetigo Two clinical patterns of impetigo : bullous and nonbullous. Bullous impetigo : S. aureus. Nonbullous impetigo :most commonly caused by group A streptococcus (several decade ago) most commonly caused by S. aureus , group A streptococcus, or by both organism (currently, in industrialized nations) Group A streptococcus (common cause of nonbullous impetigo in developing nations)

4. Nonbullous impetigo This type accounts for >70 percent of cases of impetigo Lesions commonly arise on the skin of the face (especially around the nares) or extremities after trauma

5. Nonbullous impetigo Disrupt the integrity of the epidermis, providing a portal of entry of impetiginization The initial lesion is a transient vesicle or pustule that quickly evolves into a honey-colored crusted plaque

7. Bullous impetigo phage group II S. aureus Bullous impetigo occurs more commonly in the newborn and in older infants Characterized by the rapid progression of vesicles to flaccid bullae

8. Bullous impetigo Bullae usually arise on areas of grossly normal skin. Bullae initially contain clear yellow fluid that subsequently becomes dark yellow and turbid and their margins are sharply demarcated without an erythematous halo. Bullae are superficial, and within a day or two they rupture and collapse, at times forming thin, light brown to golden-yellowcrusts

9. Management Local treatment with mupirocin ointment and removal of crusts andmaintenance of cleanliness is sufficient to cure mild cases. Extensive cases, by the administration of antibiotics : Dicloxacillin, erythromycin, amoxicillin plus clavulanic acid, cephalexin, cefaclor, cefprozil, clindamycin

11. Ecthyma S. aureus and/or group A streptococcus Untreated staphylococcalor streptococcal impetigo can extend more deeply, penetrating the epidermis, producing a shallow crusted ulcer

12. Ecthyma Most commonly on the lower extremities of children or neglected elderly patients or individuals with diabetesellitus. Poor hygiene and neglect are key elements in pathogenesis. The ulcer has a “punched out” appearance When the dirty grayish-yellow crust and purulent material are debrided. The margin of the ulcer isindurated, raised, and violaceous and the granulating base extends deeply into the dermis.

13. Management Same as for staphylococcal impetigo

15. Folliculitis Begins within hair follicle Superficial folliculitis Deep folliculitis

16. Superficial folliculitis Small fragile dome shaped pustule occur at infundibulum of hair follicle Scalps of children and in bread area, axillae, extremities, and buttocks of adults

17. Deep folliculitis Bearded areas of the face and upper lip

19. Furuncles Deep-seated inflammatory nodule that develops about a hair follicle Neck, face, axillae, buttocks

21. Carbuncles More extensive, deeper, communicating, infiltrated lesion that develops when suppuration occurs in thick inelastic skin Extremely painful lesion at the nape of neck, back or thighs

22. Carbuncles Risk : DM, anemia, hypogammagolbulinemia, neutrophil function defect

23. Diagnosis Pus gram stain : gram positive cocci Pus culture Blood culture

27. Paronychia Acute paronychia : S. aureus Chronic or recurent paronychia : Candida albican

32. Staphylococcal scalded skin syndrome Fever Generalized exanthematous disorder with cutaneous tenderness, wide spread blistering and superficial denudation/derquamation Desquamations begins, initially on face, and extends to involve most of the body Most common : neonates, young children

33. Staphylococcal scalded skin syndrome S. aureus Children under 5 years of age, and particularly neonates, are most commonly affected Explained by the importance of mature renal function in the clearance of epidermolytic toxins.

34. Treatment Eradication of staphylococcal from the focus of infection Intravenous penicillinase-resistant antistaphylococcal antibiotics Oral antibiotic therapy can be substituted within several days or sooner Supportive skin care, and appropriate attention to fluid and electrolyte management

35. Significant mortality (2 to 3 percent), and the morbidity from occasional children who developcellulitis, sepsis, and pneumonia should not be ignored. Adult patients with scalded-skin syndrome are more likely to be immunosuppressed andsuffering from other medical problems. They are much more likely than children to have staphylococcal bacteremia and have a poorer prognosis.

38. Erysipelas Painful, bright-red, edematous indurated plaque with an advancing raised border, sharply demarcated from the surrounding normal skin. Face or lower extremities Group A streptococcus S. aureus

41. Cellulitis Many of the features of erysipelas but extends into the subcutaneous tissues Cellulitis is differentiated from erysipelas by two physical findings: cellulitic lesions are not raised and its demarcation from uninvolved skin is indistinct.

42. Cellulitis S. aureus, group A and other streptococci (B, C, and G), E. coli, enterobacteriaceae and anaerobes

43. Laboratory CBC : leukocytosis Aspiration or swab Blood culture

44. Complication Local gangrene, necrotizing fasciitis, localized abscess, severe sepsis, infective endocarditis, septic arthritis, cavernous sinus thrombosis Post streptococcal glomerulonephritis Lymphatic obstruction

46. Necrotizing fasciitis Characterized by rapid progression of infection with extensive necrosis of subcutaneous tissues and overlying skin

47. Necrotizing fasciitis Type I Mixed of facultative and anaerobic microbes : nongroupable streptococci, enterococci, anaerobic streptococci, staphylococci, bacteroides spp., E. coli

48. Necrotizing fasciitis Type II Almost always a group A streptococcus Group C and G : rare Group B : early postpartum

49. Management Mild case : intramuscular procaine penicillin, or with oral penicillin, erythromycin, clindamycin Extensive infection and underlying medical problem : intravenous aqueous penicillin Severe case : higher dose, penicillinase-resistant semisynthetic penicillin and/or vancomycin (staph)

50. Local measures Erysepelas and cellulitis : bed rest with immobilization elevation of the involved area to reduce local edema cool, sterile saline dressings

51. Surgical intervention Necrotizing soft tissue infection : Early and complete surgical debridement of necrotic tissue in combination with appropriate drainage and high-dose antibiotics