SKINSCABIESEtilogy:Scabies is caused by burrowing and release of toxic or antigenic substances by the female mite Sarcoptes scabiei var. hominis. Spread:1. Physical contact with an affected individual. 2. The children and sexual partner of an affected individual 3. Only rarely by fomites (clothes) because mite dies within 23 days.Clinical Manifestations:1. In an immunocompetent host, scabies is frequently heralded by intense pruritus, particularly at night. 2. Threadlike burrows are the classic lesion of scabies but may not be seen in infants. 3. In infants, bullae and pustules are relatively common. 4. The eruption may also include superimposed eczematous dermatitis. 5. The palms, soles, face, and scalp are often affected. 6. In older children and adolescents, preferred sites are the interdigital spaces, wrist flexors, anterior axillary folds, ankles, buttocks, umbilicus and belt line, groin, genitals in men, and areolas in women. 7. The head, neck, palms, and soles are generally spared. 8. Complications:1. Untreated, scabies may lead to eczematous dermatitis, impetigo, ecthyma, folliculitis, furunculosis, cellulitis, lymphangitis, and id reaction. 2. Children have developed glomerulonephritis from streptococcal impetiginization of scabies lesions. 3. In some tropical areas, scabies is the predominant underlying cause of pyoderma. Diagnosis:1. This can often be made clinically but is confirmed by microscopic identification of mites, ova, and scybala in epithelial debris. 2. Scrapings are most often positive when obtained from burrows or fresh papules. 3. A reliable method is application of a drop of mineral oil on the selected lesion, scraping of it with a No. 15 blade, and transferring the oil and scrapings to a glass slide or a KOH preparation.Norwegian Scabies:1. This variant of human scabies is highly contagious and occurs mainly in individuals who are:1. Mentally and physically debilitated, 2. Who are institutionalized 3. Down syndrome; 4. patients with poor cutaneous sensation (leprosy, spina bifida), 5. patients who have severe systemic illness (leukemia, diabetes), 6. Immunosuppressed patients (HIV infection). DD:1. Drug eruptions, dermatitis herpetiformis, and folliculitis. 2. Eczematous lesions may mimic atopic dermatitis and seborrheic dermatitis, Treatment:1. Application of permethrin 5% cream (Elimite) to the entire body from the neck down, with particular attention to intensely involved areas, is standard therapy. Scabies is frequently found above the neck in infants, necessitating treatment of the scalp. The medication is left on the skin for 812 hr. If necessary, it may be reapplied in 1 wk for another 812 hr period. 2. Ivermectin has been used successfully as single-dose therapy in refractory cases, particularly in HIV-infected patients. 200 g per kg3. The entire family should be treated, as should caretakers of the infested child. 4. Clothing, bed linens, and towels should be thoroughly laundered.

Impetigo1. Impetigo is an acute, highly contagious gram-positive bacterial infection of the superficial layers of the epidermis. Impetigo occurs most commonly in children, especially those who live in hot, humid climates. 2. Impetigo occurs in 2 forms: bullous and nonbullous.3. Nonbullous impetigo:a. It is the more common form, constituting approximately 70% of impetigo cases. b. Nonbullous impetigo, also known as impetigo contagiosa c. It is caused by Staphylococcus aureus, group A beta hemolytic streptococci (GABHS, also known as Streptococcus pyogenes), or a combination of both. d. Methicillin-resistant S aureus (MRSA), which can be hospital or community acquired, is an increasingly common cause of impetigo; 4. Bullous impetigo:a. It is caused almost exclusively by S aureus. b. It is a toxin-mediated erythroderma in which the epidermal layer of the skin sloughs, resulting in large areas of skin loss. 5. Impetigo can also present as folliculitis, which is considered to be impetigo of the hair follicles caused by S aureus. 6. Treatment of impetigo typically involves local wound care along with antibiotic therapy. Antibiotic therapy for impetigo may be with a topical agent alone or a combination of systemic and topical agents7. For antibiotic therapy, the chosen agent must provide coverage against both Staphylococcus aureus and Streptococcus pyogenes. Community-acquired methicillin-resistant S aureus (MRSA) infection most commonly manifests as folliculitis or abscess, rather than impetigo; thus, beta-lactam drugs remain an appropriate initial empiric choice. 8. Topical mupirocin is adequate treatment for single lesions of nonbullous impetigo or small areas of involvement. It is applied to the affected area 2 to 3 times daily. A 7-day course is usually standard.9. Complications:a. Poststreptococcal glomerulonephritisb. Sepsis, osteomyelitis, arthritis, endocarditis, pneumonia, cellulitis, lymphangitis or lymphadenitis, guttate psoriasis, toxic shock syndrome, and staphylococcal scalded skin syndrome.HYPOPIGMENTED MACULE1. Tinea versicolor: Infection of the skin by Trichophyton Manifests as patchy hypopigmentation and sometimes hyperpigmentation Commonly found on the trunk 2. Vitiligo Progressive patchy depigmentation Common on hands, arms, face, neck Associated with thyroid disease 3. Pityriasis alba Related to eczema Hypopigmented patches on the face 4. Postinflammatory hypopigmentation May occur after any type of cutaneous inflammation More obvious in dark-skinned individuals Duration is weeks to months 5. Post-topical steroid hypopigmentation Topical steroids, particularly fluorinated, may cause thinning, atrophy, and hypopigmentation with prolonged use More common on the face and perineum 6. Tuberous sclerosis (TS) A neurocutaneous disorder affecting the brain, eyes, kidney, skin, and heart Systemic symptoms are preceded by ash-leaf macules, which are usually present in affected infants Other skin findings are shagreen patches, adenoma sebaceum, periungual fibromas Mental retardation, seizures are common 7. Congenital oculocutaneous albinism May involve the hair, skin, or eyes Inherited in autosomal recessive, autosomal dominant, and X-linked forms Variable degree of hypopigmentation Photophobia is a frequent finding Patients are prone to skin cancer 8. Partial albinism (piebaldism) Eg> Waardenburg syndromeWhite forelock, nonpigmentad patches on the face, trunk, elbows, and knees Facial dysmorphism, a white forelock, and hypopigmentation May be accompanied by hearing deficit