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Skin disseases by  dr. zewudu
 

Skin disseases by dr. zewudu

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    Skin disseases by  dr. zewudu Skin disseases by dr. zewudu Document Transcript

    • Infectious conditions of the skin Bacterial infection of the skin (pyodermas) Normal skin is heavily colonized by bacterial normal flora, which are more numerous and diverse in occluded sites. The most common are nonpathogenic gram-positive bacteria such as Staphylococcus epidermidis (coagulase-nega-tive). Staphylococcus aureus is not one of the normal floras of the skin; it does, however, colonize the nares, perineum, and/or axillae in approximately 20% of individuals. Group A –β hemolytic streptococcus (GAS) (Streptococcus pyogenes) usually colonizes the skin first and then the nasopharynx. An intact stratum corneum is the most important defense against invasion of pathogenic bacteria. Bacterial skin infection is one of the commonly encountered problems in the tropics. When the normal protective functions of the skin are altered by trauma (scratching and excoriation), pre existing and/or coexisting skin diseases like, eczema, scabies or venous or lymphatic insufficiency, pathogenic organisms get access to the skin to establish infection. Impetigo  Impetigo is a contagious superficial (stratum corneum) pyogenic infection of the skin.  Two main clinical forms are recognized: non-bullous impetigo (or impetigo contagiosa) and bullous impetigo.  Impetigo presents as either a primary pyodermal of intact skin or a secondary infection due to preexisting skin disease or traumatized skin.  Impetigo rarely progresses to systemic infection, although post streptococcal glomerulonephritis may occur as a rare systemic complication.  Impetigo occurs in individuals of all ages. However, children younger than 6 years have a higher incidence of impetigo than adults.  Bullous impetigo is most common in neonates and infants Causative agents of impetigo 1 | P a g e
    • The commonest type of impetigo is non-bullous impetigo contagiosa  It is usually caused by group Aβ streptococcus,  In some geographical areas Staphylococcus aureus or by both organisms together.  Bullous impetigo → Staphylococcus aureus Clinical features Non-bullous impetigo/ impetigo contagiosa :  The characteristic lesion is a fragile vesicle or pustule that readily ruptures and becomes a honey-yellow, adherent, crusted papule or plaque and with minimal or no surrounding redness unless cellulites exists.  Usually occurs on hands and face.  Scalp impetigo is commonly associated with pre existing Tinea captis  Lesions develop on either normal or traumatized skin or are superimposed on a preexisting skin condition (e.g., tinea capitis, scabies, varicella, atopic dermatitis).  Lesions are located at exposed parts of the body (e.g., scalp, arms, legs), sparing the palms and soles. Localized lymphadenopathy usually is present, and nodes may be tender. Bullous impetigo:  The characteristic lesion is a vesicle that develops into a superficial flaccid bulla on intact skin, with minimal or no surrounding redness.  Initially, the vesicle contains clear fluid that becomes turbid.  The roof of the bulla ruptures, often leaving a peripheral collarette of scale if removed; it reveals a moist red base. Management Local management for small lesions: -  Wash with betadine solution or normal saline/ salt and water.  Potassium permanganate 1 in 1000 solution soaking twice a day until the pus exudates dry up.  Gentian violet (GV) paint 0.5% apply BID. 2 | P a g e
    •  Topical antibiotics can be used, such as 2% mupirocin, Gentamycine, Fucidic acid can be used but costly. Systemic treatment: -  For extensive impetigo contagiosa, a single dose of benzathin penicillin coupled with local care.  Oral amoxacyllin or Ampicillin can also be used.  For Bullous impetigo: - cloxacillin 500 mg po QID for 7 to 10 days. In cases, with an allergy to penicillin, erythromycin can be given.  The underlining skin conditions such as eczemas, scabies, fungal infection, or pediculosis should be treated.  When impetigo is neglected it becomes ecthyma, a superficial infection which involves the upper dermis which may heal forming a scar.. Folliculitis  It is an infection of the hair follicles.  It occurs on hair bearing areas of the skin. Application of greasy substance such as Vaseline is a predisposition.  The most common etiologic agent is staphylococcus aureus. However, fungi and virus can also cause it.  A furuncle is an acute, deep-seated, red, hot, tender nodule or abscess that evolves around the hair follicle and is caused by staphylococcus aureus.  A carbuncle is a deeper infection comprised of interconnecting abscesses usually arising in several adjacent hair follicles.  Furuncle and carbuncle are common in obese, diabetic patients and immunosuppressive conditions. Management of folliculitis  Avoid greasy applications on the skin.  Mupiricine topically can be used.  Systemic antibiotics: - cloxacillin or erythromycin is choices of treatment.  For deep abscesses (furuncle and carbuncle) incision and drainage is mandatory. Cellulitis and Erysipelas 3 | P a g e
    •  Cellulitis is bacterial infection and inflammation of loose connective tissue (dermis subcutaneous tissue)  Erysipelas is a bacterial infection of the dermis and upper subcutaneous tissue; characterized by a well-defined, raised edge reflecting the more superficial (dermal) involvement Etiology  The most common etiologic agent is group A β hemolytic streptococcus. However, Staphylococcus aureus can also cause cellulites.  In young children, Hemophilus influenza type B should be considered as a possible etiology for cellulites especially of the face (facial cellulitis). Clinical features  The difference between the conditions is oftentimes fluid and more of academical.  Except in mild cases, there is constitutional upset with fever and malaise.  Classical erysipelas starts abruptly and systemic symptoms may be acute and severe, but the response to treatment is more rapid.  Erythema, heat, swelling and pain or tenderness are constant features in both.  In erysipelas, the edge of the lesion is well demarcated and raised, but in cellulitis it is diffuse.  In erysipelas, blisters are common and severe cellulitis may also show bullae or necrosis of epidermis and can rarely progress to fasciitis or myositis. Lymphangitis and lymphadenopathy are frequently associated with cellulitis.  The leg is the commonest site for cellulites. A skin break, usually a wound even if superficial, an ulcer, or an inflammatory lesion including interdigital fungal or bacterial infection, may be identified as a portal of entry.  Erysipelas may occur on the face or extremities and usually accompanied by malaise and fever. Complications 4 | P a g e
    •  Without effective treatment, complications are common - fasciitis, myositis, subcutaneous abscesses, and septicemia.  Pretibial cellulitis can result in osteomyelitis from contiguous spread.  Post streptococcal glomerulonephritis can occur in some cases.  If Lymphangitis is not treated properly, it can lead to lymphoedema. Management  Treat the fever and pain and elevate the affected part.  Crystalline penicillin or procaine penicillin is the first line therapy and oral Ampicillin or Amoxicillin may be used for mild infection and after the acute phase resolves. The antibiotics should be continued for 10- 14 days. Follow up:  Response to the antibiotic  For proper timing of surgical intervention. Erythrasma Def. Erythrasma is a chronic superficial infection of the intertriginous areas of the skin. It is caused by over growth of Corynebacterium minutissimum, which usually is present as a normal flora of the skin.  A warm, humid climate, obesity and Diabetes is a predisposing factor. It is commonly seen among adults.  Among normal populations, mild toe-cleft scaling maceration is common.  Clinically manifest with pink, brawn scaly macules or macerated white areas.  it occurs most commonly in the groins, axillae and the intergluteal and submammary flexures, or between the toes.  In the groins, it affects the area of one or both thighs in contact with the scrotum. Dark faintly scaly patch on both sides of inner thigh with ill defined margins. Differential diagnosis (DDx):  Pityriasis versicolor does not usually affect the wet areas  On the thighs, groins and pubic area, Tinea cruris may be simulated, but the relative lack of inflammation, complete absence of vesiculation and absence of satellite lesions point against Tinea. 5 | P a g e
    •  It is difficult to differentiate erythrasma of the toe clefts from Tinea pedis or Candida infection.  Since most patients have both Candida and erythrasma, it may worsen if only one condition is treated. Treatment  Erythrasma responds well to most topically applied azole antifungal agents, such as 1%clotrimazole and 2% miconazole.  The duration of therapy varies, but 2 weeks is usually sufficient for topical fucidin and erythromycin.  Oral erythromycin and tetracycline for 2 weeks is can also be used but relapse is a problem in some patients.  In these cases, the usual approach adopted is to give long-term antiseptic soaps, such as povidone-iodine and to use drying agents, such as powders, in the affected areas. Pitted Keratolysis  Pitted keratolysis (PK) presents 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, usually associated with pedal hyperhidrosis, caused by Corynebacterium  Age of Onset- Young adults.  Sex - Males than females.  Predisposing Factors- Hyperhidrosis of the feet; occlusive footwear.  Skin Lesions Pits in stratum corneum. Pits can remain discrete or, more often, become confluent, forming large areas of eroded stratum corneum.  Involved areas are white when stratum corneum is fully hydrated.  Symmetric or asymmetric involvement of both feet  Distribution: - Toe webs; all or heel of foot in contact with shoe.  Usually asymptomatic-Foot odor is common  Uncommonly, itching, burning, tender-ness.  Often mistaken for Tinea pedis. 6 | P a g e
    • Management  Wash affected site with lather from benzoyl peroxide bar or wash.  Reduce moisture in shoes with agents such as aluminum chloride or formaldehyde 10%  Wear less occlusive footwear or open shoes.  Daily applications of agents such as benzoyl peroxide gel or topical antibiotics such as erythromycin are usually effective.  azole antifungal agents, such as 1%clotrimazole and 2% miconazole. Intertriginous Infections and Intertrigo  Intertrigo (Latin: inter between, trigo rubbing) is a nonspecific inflammation of opposed skin, occurring in the submammary region, axillae, groins, and gluteal folds.  With increased moisture and maceration, the stratum corneum becomes eroded.  The problem is more common in obese individuals who have more skin with more folds.  Intertriginous infections caused by bacteria (groups A and B streptococcus, Corynebacterium minitissimum, Pseudomonas aeruginosa) and fungi (dermatophytes, Candida, and Malassezia furfur) must be ruled out.  Dermatoses such as psoriasis vulgaris (inverse pattern), seborrheic dermatitis, and atopic dermatitis also occur in body folds, presenting as erythema or erythematous plaques.  Intertrigo is diagnosed in the presence of erythema symptoms or pruritus, tenderness, or increased sensitivity, excluding infectious causes.  For acutely symptomatic intertrigo, moist dressings and/or Castellani’s paint give immediate symptomatic relief.  Powders with antibacterial/antifungal activity are helpful for preventing recurrence.  Tetracycline and antifungals topical or systemic  Potassium permanganete 1:1000 solution soak to dry oozing lesions and as antiseptic action  Johnson powder to avoid the irritation from sweat  In some cases, zinc oxide ointment reduces friction at involved sites.  Mild topical corticosteroid preparations for a short time 7 | P a g e
    •  Wide underwears  Weight reduction is ideal but often not possible. Superficial fungal infection of the skin Superficial fungal infections of the skin are one of the most common dermatologic conditions seen in clinical practice. Therefore, recognition is important for primary care physicians. However, making the correct diagnosis can be difficult, because these infections can have an atypical presentation or be confused with similar-appearing conditions. Superficial fungal infections can be divided into three broad categories: dermatophytic infections, Pityriasis versicolor and cutaneous candidasis Dermatophytes Specifically Trichophyton, Epidermophyton and Microsporum species, are responsible for most superficial fungal infections. The term "Tinea" refers exclusively to dermatophyte infections. Dividing infections into the body region most often affected can help in identification of the problem. Tinea Capitis  Tinea capitis is a dermatophytic infection of the hair of head and scalp.  usually found in children, and young adolescents.  Most infections occur in preschool-aged children.  Around puberty, sebum production by sebaceous glands becomes active, and as a result, it tends to disappear. Presentation  Commonest presentation is scaly patches on the scalp with variable degree of hair loss and generalized scaling that resembles seborrhic dermatitis may occur on the scalp. 8 | P a g e
    •  Cervical lymphadenopathy can occur when there is secondary bacterial infection.  Keroin is a form of Tinea capitis with accentuated inflammatory response. It is boggy, nodular tender mass which may form pus.  An unusual scaling reaction known as favus may give the scalp a waxy or doughy appearance with thick crusted areas. Differential diagnosis (DDx)  Differential diagnosis of Tinea capitis includes seborrheic dermatitis, dandruff, scalp psoriasis, atopic dermatitis, scalp impetigo, and alopecia areata  The finding of large areas of alopecia that have early pustule formation favors a diagnosis of Tinea capitis over alopecia areata Investigation KOH preparation and looking for the fungal elements from skin scraping ,nail or hair. Treatment  Tinea capitis should be treated with systemic therapy. Griseofulvin in a dose of 10-20 mg per kg for six weeks to 8weeks is the first-line treatment of Tinea capitis. Griseofulvin should be taken after fatty meal for better absorption.  Ketoconazole 2-4mg per kg for ten days, itraconazole and terbinafine (Lamisil) are good alternatives.  Topical treatment can be added to decrease the transmission and accelerate resolution.  Whitefield ointment is preferred in the absence of secondary bacterial infection. Other family members should also be examined and treated. Tinea corporis  Tinea corporis is dermatophytosis of the glabrous skin of the trunk and extremities. 9 | P a g e
    •  Lesions are round, scaly patches that have a well defined, enlarging border and a relatively clear central portion.  The active edge often contains follicular papules.  Itching is variable and not diagnostic  Tinea corporis can assume a giant size (Tinea incognito) when steroids are applied for cosmetic reasons or as a result of miss diagnosis. Differential Diagnosis (DDx)  Lichen simplex chronicus, numular eczema, atopic eczema, psoriasis, lichen planus. Investigation  KOH from active edge of lesion.  Fungal culture only in doubtful cases if the KOH is negative. Treatment  Small and single lesion can be treated with topical agents.  Clotrimazole 1%, ketoconazole 2%, meconazole 1%. BID for two weeks   Systemic: o ketoconazole 2-4mg per kg of weight for 10 days. o Itraconazole and fluconazole are choices if available. o Griseofulvin is also effective for the treatment of Tinea corporis. Tinea pedis 10 | P a g e
    •  Tinea pedis is fungal infection of the feet and is usually related to sweating and warmth, and use of occlusive footwear.  Men between 20 and 40 years of age are most frequently affected.  The infection often presents as white, macerated areas in the 3rd or 4th toe webs.  It may also present with a classic pattern on the dorsal surface of the foot or as chronic dry, scaly hyperkeratosis of the soles and heels.  Itching is also common with vesicular or bullous lesion.  It is transmitted by direct contact or sharing of shoes, towels or bath. Treatment  Topical anti fungal creams or ointments applied regularly for 4 - 6 wks.  Systemic treatments provide better skin penetration than most topical preparations,  traconazole, terbinafine and griseofulvin are good choices for oral therapy.  Systemic Itraconazole and terbinafine are more effective than griseofulvin.  Once-weekly dosing with fluconazole is another option, especially in noncompliant patients.  Personal hygiene (foot hygiene) is highly advised. Tinea versicolor (Pityriasis versicolor) Pityriasis versicolor (PV) is a chronic asymptomatic scaling dermatosis associated with the superficial overgrowth of the hyphal form of Pityrosporum ovale, characterized by well-demarcated scaling patches with variable pigmentation, occurring most commonly on the trunk. Synonym: Tinea versicolor 11 | P a g e
    • It is a common, benign, superficial cutaneous (stratum corneum) fungal infection at the level of stratum corneum characterized by hypo pigmented or hyperpigmented macules and patches with faint scale on the chest and the back. Etiology: Malassezia furfur (Pityrosporon ovale,)  It is a lipophilic yeast that normally resides in the keratin of skin and hair follicles of individuals 15 years of age or older  M furfur is a member of normal flora of the skin found in 18% of infants and 90- 100% of adults.  It is an opportunistic organism, causing pityriasis versicolor, Pityrosporum folliculitis, and implicated in the pathogenesis of seborrheic dermatitis.  Pityrosporum infections are not contagious, but an overgrowth of resident cutaneous flora occurs under certain favorable conditions.  Predisposing factors include – o Genetic predisposition, o Warm and humid environments-ingresses skin surface humidity o Excessive sweating o Immunosuppression, malnutrition, o High levels of cortisol appear to increase susceptibility—both in Cushing’s syndrome and with prolonged administration of glucocorticoids (topical as well as systemic). o Application of grease such as cocoa butter predisposes young children to PV.  Incidence In temperate zones: 2%. o In sub-tropical and tropical zones: 40%. 12 | P a g e
    • o Season In temperate zones, appears in summertime; fades during cooler months.  In physically active individuals, may persist year round.  Presentation  Skin lesions Macules, sharply marginated, round or oval in shape, varying in size.  Gently rubbing or straching the skin is best to appreciate fine scaling.  Treated or burned-out lesions lack scale.  Skin, lesions are light brown. In dark-skinned individuals, dark brown macules.  In time, individual lesions may enlarge, merge, forming extensive geographic areas.  Distribution Upper trunk, upper arms, neck, abdomen, axillae, groins, thighs, genitalia.  Facial, neck, and/or scalp lesions occur in patients applying creams/ointments or topical glucocorticoid preparations.   DIFFERENTIAL DIAGNOSIS  Hypopigmented PV Vitiligo, pityriasis alba, postinflammatory hypopigmentation, tuberculoid leprosy.  Scaling Lesions Tinea corporis, seborrheic dermatitis, pityriasis rosea, guttate psoriasis, nummular eczema. Investigation 13 | P a g e
    • The clinical presentation of Pityriasis versicolor is distinctive, and the diagnosis is made without potassium hydroxide (KOH) examination. Treatment  Patients should be informed that causative agent is a normal flora of the skin hence it is not transmitted  Any skin color alterations resolve within 1-2 months after treatment.  Recurrence is common if the patient is not given enough dose of treatment..  Topical agents  Selenium sulfide (2.5%) lotion or shampoo Apply daily to affected areas for 10 to 15 min followed by shower, for 1 week  Sodium thiosulphate solution apply daily for one week  Propylene glycol 50% solution (in water): Apply bid for 2 weeks  Ketoconazole shampoo applied same as selenium sulfide shampoo  Azole creams (ketoconazole, econazole, micronazole, clotrimazole) Apply daily or bid for 2 weeks  Terbinafine 1% solution Apply bid for 7 days  Systemic therapy  Ketoconazole 200 mg/d PO for 7–days or 400 mg once; repeat in 1 week or 400 mg stat, repeat in 1 month  Fluconazole 400–600 mg stat; repeat in 1 week Itraconazole 200 mg bid for one day; 200 mg for 5–7 days  Secondary prophylaxis 14 | P a g e
    •  Ketoconazole shampoo once or twice a week.  Selenium sulfide (2.5%) lotion or shampoo.  Propylene glycol 50% solution once a month Candidiasis  Candidiasis is most frequently caused by the yeast Candida albicans, and less often by other Candida spp. Superficial infections of mucosal surface (oropharynx, genitalia) are common in other-wise healthy individuals; infections of the esophagus and/or tracheobronchial tree occur in the set-ting of significant immunocompromise.  Cutaneous candidiasis commonly occur in moist, flexural sites. These fungi live on all surfaces of our bodies. Under certain conditions, they can become so numerous that they cause infections, particularly in warm and moist areas.  Invasive, disseminated candidiasis occurs in immunocompromised individuals, usually after invasion of the gastrointestinal tract. Synonyms: Candidosis, moniliasis. The factors associated with increased colonization rates.  Broad-spectrum antibiotics by compromising the mucocutaneous protective bacterial flora  Depressed cell-mediated immunity either acquired or congenital  Diabetes mellitus  Systemic corticosteroid treatment  Hematological malignancies and solid tumors  Severe traumas and burns  Premature birth 15 | P a g e
    • Three of every four women have at least one bout of vulvovaginal candidiasis (VVC) during their lifetime. More than 90% of HIV positive patients experience oropharyngeal candidiasis (OPC), and 10% have at least one episode of esophageal candidiasis. Candidal colonization is at the highest levels during the extremes of ages, in neonates and people older than 65 years Cutaneous candidiasis Cutaneous candidiasis is a superficial infection occurring on moist, occluded cutaneous sites; many patients have predisposing factors such as increased moisture at the site of infection, diabetes, or alterations in systemic immunity A. Candida Intertrigo:  Affects any site where the skin surfaces are in close proximity with warm and moist environment.  Erythema. Pruritus, tenderness, pain  Initial pustules on erythematous base become eroded and confluent. Subsequently, fairly sharply demarcated, polycyclic, erythematous, eroded patches with small pustular lesions at the periphery (satellite pustulosis).  Pruritic rash that begins with vesiculopustules, which enlarge and rupture, causing maceration and fissuring.  Satellite lesions frequently are found that may coalesce and extend into larger lesions.  Distribution- Inframammary axillae, groins, perineal, intergluteal cleft. b. Interdigital  Erosio interdigitalis blastomycetica. 16 | P a g e
    •  Initial pustule becomes eroded, with formation of superficial erosion or fissure, surrounded by thickened white skin  May be associated with Candida onychia or paronychia.  Distribution- On hands, usually between third and fourth fingers; on feet, similar presentation as interdigital tinea pedis. b. Diaper Dermatitis  Irritability, discomfort with urination, defecation, changing diapers  Erythema, edema with papular and pustular lesions; erosions, oozing, collarette-like scaling at the margins of lesions involving perigenital and perianal skin, inner aspects of thighs and buttocks Paronychia and onychomycosis  Frequently, paronychia and onychomycosis are associated with immersion of the hands in water.  Patients present with a painful and erythematous area around and underneath the nail and nail bed, warm, glistening, tense, and tender.  There is secondary nail thickening, ridging, discoloration, and occasional nail loss in chronic cases. Mucosal candidiasis Oropharyngeal candidiasis (OPC)  Symptoms include: asymptomatic, sore, and painful mouth, burning mouth or tongue, dysphagia,.  whitish thick patches on the oral mucosa and when removed show erythematous base.  Physical examination reveals a diffuse erythema and white patches that appear on the surfaces of the buccal mucosa, throat, tongue, and gums. 17 | P a g e
    •  The presence of retrosternal pain, epigastric pain, nausea, and vomiting may suggest esophageal candidiasis Vulvovaginal candidiasis:  This is the second most common cause of vaginitis.  The patient's history includes vulvar pruritus, vaginal discharge, dysuria, and dyspareunia.  The vagina and labia are erythematous, with a thick curd like discharge. Candida balanitis:  Candida balanitis is acquired through sexual intercourse with a partner who has vulvovaginal candidiasis.  A patch resembling thrush appears on the glans and may spread to the thighs, gluteal folds, buttocks, and scrotum. Investigation  Wet mount: for hyphae, pseudohyphae, or budding yeast cells.  KOH smear: to demonstrate fungal elements. Treatment Candida intertrigo , Diaper Dermatitis and Interdigital  Topical azoles and polyenes, including clotrimazole, miconazole, and nystatin, are effective.  Castellani’s paint  Potassium permanganate 1:1000 solution soak BID until it dries  Topical or systemic antibiotics -individualised 18 | P a g e
    •  Mild topical steroids for a brief time enhances the healing especially for intertigo and diaper dermatitis  Systemic azoles and polyenes for 5-10 days  Keeping the infected area dry is important. Paronychia –  the most important intervention is drainage followed by oral antifungal therapy with either ketoconazole, fluconazole or itraconazole.  Single daily dose of itraconazole taken for 3-6 months or a pulsed-dose regimen that requires a slightly higher dose daily for 7 days, followed by 3 weeks off therapy. The cycle is repeated every month for 3-6 months. Oropharyngeal candidasis (OPC): -  Topical (nystatin, clotrimazole, amphotericin B oral suspension) or  systemic oral azoles (fluconazole, itraconazole, ketoconazole). Vulvovaginal candidiasis –  Azole suppository or pessaries , in resistant case systemic therapy for 10 days.  Imidazole cream topically for 3 – 7 days plus 1 dose of 150mg Fluconazole P.O.  Ketokonazole 200 mg daily for 5-7 days Viral infections Warts Warts or verrucae are benign growths on the skin or mucous membranes that cause cosmetic problems as well as pain and discomfort.. Etiology and epidemiology  The etiologic agents are various strains of Human papilloma virus (HPV). 19 | P a g e
    •  The incubation period of a wart is 2 to 9 months during which time an excessive proliferation of skin growth slowly develops.  They can be spread by direct or indirect contact or autoinoculation.  They are seen on people of all ages but most commonly appear in children and teenagers  The hosts’ immunity clears the warts within two years in 2/3 of the cases so treatment is often unnecessary Clinical forms  Most types of HPV have an affinity for the skin and produce common warts (verruca vulgaris), flat warts (verruca plana), and plantar or foot warts (verruca plantaris).  Several other types of HPV have an affinity for mucous membranes and some of these cause ano-genital warts (condyloma acuminata) which is mostly sexually transmitted infection.  Certain strains of HPV increase the risk of malignancy especially cervical cancer.  In immunodeficiency states warts can become fulminantly widespread and difficult to treat. Treatment  There is no single effective treatment for warts.  Management is based on the age of the individual as well as the size, number, and location of warts.  Common warts, especially in children, do not necessarily need to be treated, because they exhibit a high rate of spontaneous remission.  Without treatment, however, spread can occur. Cutaneous warts • Salicylic acid 25% ointment twice daily followed by cutting or scraping • Preparation of salicylic acid 5-20% and lactic acid 5-20% in collodion are easier to use • Topical 5% 5-fluoro-uracil cream (efudex) • Podophyllin 10-25% solution • Electrodessication and curettage • Freezing with liquid nitrogen if available. 20 | P a g e
    • For genital warts • Podophyllin 10-25% solution. Protect the skin around the wart with Vaseline apply the podophyllin with a match stick carefully on the top of the war and wash after 6 hours. Repeat every week. It is contraindicated in pregnancy. • Phenol 80% can be used in the same fashion to Podophyllin. • Cauterization • Topical 5% 5-fluoro-uracil cream (efudex) • Cryotherapy with liquid nitrogen Molluscum contagiosum  Molluscum contagiosum is a self-limited epidermal viral infection, characterized clinically by skin-colored papules that are often umbilicated, occurring in children and sexually active adults.  In HIV-infected individuals, however, numerous large mollusca often arise on the face, causing significant cosmetic disfigurement.  Molluscum contagiosum is a viral infection of the skin that causes discrete papules that may be mistaken for warts. Etiologic agent: Poxvirus Clinical presentation  It is common in children and some time in immunocompromised adults.  The rash of molluscum contagiosum is characterized by discrete, 2 to 5 mm papules that are flesh-colored (skin color) and dome-shaped with a central umbilication (depressed centre).  In children, the rash is most often found on the face, trunk and extremities.  In adults it appears in the pubic and genital region it is a sexually transmitted infection. 21 | P a g e
    •  Molluscum contagiosum is a self-limited disease, meaning it will eventually go away on its own. Each lesion generally lasts for about 6 to 9 months, but they can last for several years. Treatment  In children not touching it is probably the best approach because it disappears spontaneously without scars, however, if it is on the eyelid it may damage the cornea by friction - Indications for treatment  Cryosurgery - Using liquid nitrogen to freeze the lesion  Curettage  Salicylic Acid (Compound W) - A solution applied to the lesion with or without tape occlusion Herpes simplex Infection One of the most prevalent infections worldwide The infection is life long It affects: • Skin • Mucous membrane • CNS Etiologic Agents: - Herpesvirus hominis  HSV 1 and HSV 2 50% homology  HSV 1 – orolabial herpes (commoner), 50% give Hx of lesions  HSV 2 – genital herpes (herpes progenitalis) -20% are asymptomatic -20% have recurrent genital ulcer -60% subclinical (unrecognizable) Mode of Transmission:  HSV 1 - Oral secretions or directly from the lesions  HSV 2 – Sexual contact after sexual activity is started  Through birth canal neonatal infection  May imply child abuse if it is found in children 22 | P a g e
    •  HSV 1 and HSV 2 can infect and reactivate the same anatomical area. Pathogenesis: Fig 1. Pathogenesis of herpes simplex virus What causes latency? What causes reactivation? (Precipitating factors)  Local/systemic immuno-suppression  Trauma to the skin site or ganglion  UV rays  Fever 23 | P a g e HSV at mucosal/ Abraded skin surface Entry of the virus Attachment to cells Multiplication/ Replication in the nucleus Cytopathic effect on cells Discharged virions Ascending of the virus transaxonally to the sensory / Autonomic ganglion Multiplication and spread to other nerves Resolution of the primary infection Latency Reactivation Primary infection Latency Transmission can occur in all stages; more at the primary Reactivation stage
    •  Immunity to HSV infection: - Both CMI and Humeral, but CMI is much more important to protect from a lethal disease, the severity of the infection and frequency of recurrence and latency Epidemiology:  Most of the infections are sub clinical which makes serology very important to assess the epidemiology = seroepidemiology  HSV – 2: The worldwide prevalence is increasing. - The major cause of genital ulcer disease worldwide - Very infectious and infection is lifelong. - Asymptomatic infection and transmission possible. - Forms a positive loop hole with HIV infection (co infection with HIV virus) The prevalence of HSV - 2 is higher in developing countries:  Urban than rural  In sub-Saharan Africa and Caribbean 50% in adults  Overall prevalence higher in women than in men (5 – 10% higher)  It starts with sexual activity and with younger age at first age.  Seropositivity increases with years of sexual activity.  Also increases with number of lifetime partners  Lack of circumcision in males  Current or recent sexually transmitted infection (STIs) HSV and HIV Bi-directional Interaction:  HIV and HSV2 manifest a bi-directional interaction.  HSV2 increases HIV replication the efficiency of HIV acquisition and transmission and the disease progression to AIDS whereas  HIV may increase susceptibility to HSV2 and increase HSV2 shedding, HSV2 recurrence rate and severity of clinical manifestations. 24 | P a g e
    • Orolabial Herpes  Lesions on the lips and face = HPV – 1, the initial infection is usually asymptomatic  Gengivostomatitis occurs chiefly in children and young adults, most often just like bacterial tonsilopharyngitis  The most common form of orolabial herpes is cold sore or fever blister caused by recurrent HSV1 (95%). Manifestations: -  Grouped blisters on erythematous base on the lips, cheeks, eyelids, intraoral.  Prodromal symptoms:- tingling, burning, itching in 24 hrs.  In most patients recurrent orolabial herpes is more a nuisance than a disease. Treatment  Lips: In our setting Gentian, violet 0.5% is effective  If available sunblocks reduces recurrence. Eg. Zinc oxide paste , zinc oxide ointment or zinc oxide and  Topical antiseptic or antibiotic e.g betadine ointment 3 times daily for bacterial super infection.  For recurrent infections Acyclovir 200mg PO for 5 days can be given. 25 | P a g e
    • Herpetic Whithlow  Infection of pulp of fingertips, it could appear after touching a primary lesion of ones owns lesion or that of others.  In children – HSV – 1, Adults – HSV – 2, common in females  Health workers may acquire and transmit it. Genital Herpes (herpes progenitalis)  Usually due to HSV - 2 causing 85% ( >15% can be caused by HSV -1) of initial infections and up to 98% of recurrent lesions  In the mid 1980’s because of the change in the sexual behavior, the prevalence of HSV – 1 began to increase.  In developed countries up to 40% of the anogenital herpes in women is caused by HSV – 1  HSV – 1 is associated with less recurrence rate than HSV – 2 Genital herpes → transmitted by skin-to-skin contact  Incubation Period: 5 days  Asymptomatic shading occurs in all sites (vagina, cervix, and mucous membranes) even through normal appearing skin and mucous membranes.  Grouped blisters and erosions in the vagina, vulva, penis … continues to develop in 7 – 14 days.  Lesions are bilateral and symmetrical, inguinal lymph nodes may be enlarged, fever and flu like symptom may be there.  Pain, dysuria, and dysparunia may also be observed.  Previous HSV – 1 lessens the severity resembling recurrent genital herpes.  Most HSV – 2 will have recurrence even if the initial infection was asymptomatic which is estimated to be 6 times more frequent than HSV – 1 Recurrence: Nature: 24 hrs prodromal symptoms → 24 hrs vesicles appear → 24 – 36 hrs ulceration → 2 – 3 days healing: TOTAL: 7 days recurrence  Genitalia and upper buttocks are the common sites for occurrence  Healing without scar  Social stigma – the emotion from recurrent lifelong disease 26 | P a g e
    •  Guilt  Blamefulness of the presumed source (i.e. partner) Frequency: 6 – 12 times a year → deserve prophylaxis Treatment of Genital herpes  Betadine or potassium solutions sitz baths 3 times daily.  Gentian violet 0.5%, Zinc oxide and castor oil to sooths.  Alternatively betadine ointment or oxytetracycline ointment 3 times daily.  Acyclovir cream can also be given 5 times daily.  Severe infections or infection in immunodeficient patients: if available give acyclovir 200 -400 mg 5 times daily for 5-10 days OR  Famciclovir 250mg orally three times a day for 7--10 days, OR  Valacyclovir 1 g orally twice a day for 7--10 days. Neonatal Intrauterine HSV -2 - 70% HSV -1 - 30%  Intrauterine: Rare but devastating neonatal infection, encephalitis  Risks: active lesion in the mother (30 – 50% rate of acquisition)  Recurrence: 2 – 5%  In all cases, CS delivery is mandatory.  Manifestations: Skin vesicles, Encephalitis, Hepatitis, Pneumonia, Coagulopathy  Mortality rate (M/R) >50% in ideal setting.  Without skin infection, it is difficult to diagnose. Varicella /Chickenpox Def Chickenpox or Varicella is the highly contagious primary infection caused by varicella-zoster virus. 27 | P a g e
    •  It is characterized by successive crops of pruritic vesicles that evolve to pustules, crusts, and at times, scars.  Chickenpox can be severe in adulthood, complicated by pneumonia and encephalitis. Etiology  Varicella-zoster virus (VZV) that infects 98% of populations  Primary VZV infection → varicella or chickenpox  Reactivation within the nerve cell and traveling down the neuron to the skin → Herpes zoster (HZ) or shingles Age of Onset 90% of cases occur in children younger than 10 years and 5% in older than 15 years of age. Transmission  Airborne droplets as well as direct contact.  Patients are contagious several days before exanthem appears and until last crop of vesicles.  Crusts are not infectious.  VZV also aerosolized from skin of individuals with herpes zoster and can cause varicella. Pathogenesis Varicella-zoster virus → enter through mucosa of upper resp. tract and oropharynx → local replication primary viremia → reticuloendothelial system → secondary viremia and dissemination to skin and mucous membranes→ virus replication and ballooning degeneration of epithelial cells → VZV passes from the skin lesions to the sensory nerves→ sensory ganglia → latent infection→ immunocompromise → VZV replication in sensory ganglia→ travels down the sensory nerve→ dermatomal pain followed by skin lesions→→ Herpes zoster (HZ) or shingles. Since the neuritis precedes the skin involvement, pain appears before the skin lesions are visible. Clinical manifestation Incubation Period → 14 days (range, 10 to 23 days). Skin Lesions  Exanthem usually quite pruritic → vesicular lesions evident in successive crops. 28 | P a g e
    •  Initial lesions are papules (often not observed) and quickly evolve to vesicles and initially appear as small “drops of water”, with surrounding erythema.  Vesicles become umbilicated and rapidly evolve to pustules and crusts over an 8- to 12-h period.  With subsequent crops, all stages of evolution may be noted simultaneously, i.e.,papules, vesicles, pustules, crusts.  Lesions are much more dense in adults.  First lesions begin on face and scalp, spreading to trunk and extremities density highest on trunk and face  Crusts fall off in 1 to 3 weeks, leaving a pink, somewhat depressed base. Complications  Bacterial superinfection is the commonest complication  Staphylococci or streptococci → impetigo, furuncles, and cellulites  Varicella Pneumonia  Meningoencephalitis Management  Symptomatic therapy  Pruritus → calamine lotion → Oral antihistamines  Fever → possible link between aspirin and Reye’s syndrome in children with chickenpox.  Complications → topical and/or systemic antibiotics  Antiviral agents o For severe and complicated chickenpox and immunocompromised individuals o For healthy → If begun within 24 h after onset of varicella, decreases the severity and reduces secondary cases. Acyclovir 20 mg/kg (800 maximum) qid for 5 days Valacyclovir, Famciclovir Herpes Zoster Def: - Herpes zoster (HZ) is an acute dermatomal infection associated with reactivation of varicella-zoster 29 | P a g e
    •  Virus (VZV) and is characterized by unilateral pain and a vesicular or bullous eruption limited to a dermatome(s) innervated by a corresponding sensory ganglion.  The major morbidity is postherpetic neuralgia (PHN). Epidemiology Age More than 66% are older than 50 years of age 5% of cases in children younger than 15 years of age. .Risk Factors  diminishing immunity to VZV with advancing age, Malignancy, chemotherapy, radiotherapy and HIV infection Clinical manifestation  Prodromal stage: neuritic pain or paresthesia and tenderness precedes for 2 to 3 weeks.  Constitutional Symptoms: flu-like symptoms such as headache, malaise, fever  Acute vesiculation: 3 to 5 days. Skin lesions may be pruritic but in themselves are not painful  Papules (24h) → vesicles-bullae (48 h) → pustules (96 h) → crusts (7 to 10 days). New lesions continue to appear for up to 1 week.  Necrotic and gangrenous lesions sometimes occur.  Some scarring is very common → the dermatomal pattern is pathognomonic of HZ scar.  Distribution Unilateral, dermatomal  Two or more contiguous dermatomes may be involved  Hematogenous dissemination to other skin sites in 10% of healthy individuals  Site of predilection Thoracic (50%) Trigeminal (10 to 20%) lumbosacral and cervical (10 to 20%).  Mucous Membranes Vesicles and erosions occur in mouth, vagina, and bladder depending on dermatome involved. 30 | P a g e
    •  General Examination Regional nodes draining the area are often enlarged and tender.  Sensory or Motor Nerve Changes Detectable by neurological examination.  Eye In ophthalmic zoster, nasociliary involvement of VI (ophthalmic) branch of the trigeminal nerve occurs in about one-third of cases and is heralded by vesicles on the side and tip of the nose.  Complications include uveitis, keratitis, conjuctivitis, retinitis, optic neuritis, glaucoma, proptosis, cicatricial lid retraction, and extraocular muscle palsies. An ophthalmologist should always be consulted.  Sensory defects (temperature, pain, touch) and (mild) motor paralysis, e.g., facial palsy  Zoster Sine Zoster→Nerve involvement can occur without cutaneous zoster  Crust formation: days to 2 to 3 weeks.  PHN: months to years. Chronic Stages PHN  Described as “burning,” “ice-burning,” “shooting,” or “lancinating,” can persist for weeks, months, or years after the cutaneous involvement has resolved.  . Chronic stages: depression is very common in individuals with PHN.  Pain with HZ is associated with neural inflammation, nerve infection during the acute reactivation, and neural inflammation and scarring with PHN.  In most cases of HZ, 50% of individuals are pain-free 50 days after onset of symptoms  95% pain-free at 6 months.  Only 1 to 2% have PHN after 6 months.  Dissemination of zoster—20 or more lesions outside the affected or adjacent dermatomes—occurs in up to 10% of patients, usually in immunosuppressed patients.  Motor paralysis occurs in 5% of patients, especially when the virus involves the cranial nerves. MANAGEMENT 31 | P a g e
    •  Goals of management o Relieve constitutional symptoms o minimize pain o reduce viral shedding and prevent viral dissemination or other o prevent secondary bacterial infection o speed crusting of lesions and healing o ease physical, psychological,emotional discomfort o prevent or minimize PHN. Antiviral therapy  In individuals at high risk for reactivation of VZV infection, oral acyclovir can reduce the incidence of HZ.  In prodromal stage: begin antiviral agent if diagnosis is considered likely antiviral therapy begun 72 h accelerates healing of skin lesions, decreases the duration of acute pain, and decrease the frequency of PHN when given in adequate dosage.  Acyclovir 800 mg PO qid for 7–10 days.  For ophthalmic zoster and HZ in the immuno compromised host, acyclovir should be given intravenously.  Acyclovir hastens healing and lessens acute pain if given within 48 h of the onset of the rash.  Valacyclovir 1000 mg PO tid for 7 days.  Famciclovir 500 mg PO tid for 7 days Supportive therapy for acute HZ  Constitutional symptoms Bed rest, NSAIDs.  Sedation Pain often interferes with sleep. Sleep deprivation and pain commonly result in depression .  Carbamazepine 100 to 200 mg po bid Or  amitrptyline 50- 100 mg po daily  Application of moist dressings (water, saline, Burow’s solution) to the involved dermatome is soothing and alleviates pain. Chronic stages (PHN)  carbamazepine: 200 mg bid  Amitrptyline 50 to 100 mg PO daily 32 | P a g e
    •  5% phenol in calamine lotion topical – phenol has anesthetic effects 33 | P a g e
    • Parasitic infection of the skin Cutaneous Leishmaniasis Def: leishmaniasis is the result of infection with intracellular protozoan parasite belonging to the genus leishmania The parasites are found in two forms ⋅ Amastogots- round, oval , nonflagellated found in thea macrophages of humans and other mammalian hosts ⋅ Promastigotes – flagellated elongated –found in the sandflies Transmission ⋅ Sandfies are the vectors of leishmaniasis ⋅ They transmit the disease from infected animals to humans and from human to human Clinical presentation ⋅ There are four different forms of leishmaniasis with quite different clinical manifestations ⋅ The variation in clinical manifestation depend on the host immune response and the virulence of the leishmania species ⋅ Like leprosy, vigorous immune response results in localized cutaneous disease which can resolve spontaneously and visceral or diffuse cutaneous leishmanisis represent the other extreme where the immune response is week. Visceral leishmainiasis kala azar ⋅ It is the most sever form of the disease if untreated the mortality is almost 100% ⋅ It presents with irregular bouts of fever ⋅ Progressive weight loss ⋅ Anemia and pancytopenia ⋅ Massive e spenomegaly and heptomengaly ⋅ It is a chronic and progressive illness complicated by other intercurrent infections ⋅ It is found in Sudan and south west Ethiopia Mucocutaneous leishmaniasis –Espundia 34 | P a g e
    • ⋅ It produces lesions which can lead to extensive and disfiguring distruction of the mucous membranes of the nose, mouth and throat cavities ⋅ Not seen in our country Cutaneous leishmaniasis ⋅ Clinical forms of cutaneous leishmaniasis Diffused cutaneous leishmaniasis (DCL) ⋅ Analogous to lepromatous leprosy, individuals wioth fail to mount immune responses to the leishmania parasite ⋅ Patients develop multiple, widespread cutaneous papules and nodules allover ⋅ Diffused cutaneous leishmaniasis is found in Ethiopia but rare in other parts of the world ⋅ It is caused by L. aethiopica species Localized cutaneous leishmaniasis ⋅ Cutaneous leishmaniasis is the most common form of leishmaniasis. ⋅ Cuased by L. tropica ⋅ Very common in Ethiopia ⋅ Small erythematous papules appear 2-3 weeks after on the site of the bite of sandfies ⋅ Lesions occur on the exposed part of the body commonly on the face neck and extremities ⋅ ⋅ Progressively the papules expand – develop to nodules which ulcerate at the top, indurated and forms crust. It heals spontaneously over a year or two leaving a depressed scar Recidivance cutneous leishmaniasis and post kala azar dermamal leishmanisis are rare forms of the cutneous type Diagnosis  Cutaneous leishmaniasis can be diagnosed by detecting the parasites in skin scrapings stained with Giemsa or Wright’s stain.  Amastigotes are much easier to find in recent or active lesions than in chronic or healing lesions. 35 | P a g e
    •  A delayed hypersensitivity test, the Montenegro skin test, is useful for the cutaneous and mucocutaneous forms, but is usually negative in the diffuse cutaneous form.  Visceral leishmaniasis is usually diagnosed by direct detection of the parasites found in peripheral blood, spleen, bone marrow, or lymph nodes. Treatment ⋅ localized Cutaneous leishmaniasis eventually heals in one or two years ⋅ Large, multiple of diffused lesions of the face head and neck need to be treated ⋅ Immunocopromised patients should be treated immediately because it can become visceral leishmaniasis in the individuals Topical therapy ⋅ Locale therapy ⋅ Cryotherapy- freezing with liquid nitrogen with a temperature of colder than -80o ⋅ Intra- lesional antimonial compounds – sodium stibogluconiate ⋅ Systemic ⋅ sodium stibogluconiate 20mg/kg for 10-20 days in the hospitals- associated with a lot of side effects ⋅ pentamidine IV/IM 4mg/kg alternate days for 3 doses ⋅ amphotericine B 10-20 mg/kg for 100 20 days ⋅ fluconazole 200 mg daily po for 6 weeks ⋅ ketokonazole 400mg daily for 6 weeks ⋅ allopurinol 300-600mg daily for 6 weeks plus fluconazole or ketokonazole Onchocerciasis – River blindness ⋅ Def. Onchocerciasis is caused by the filarial nematode (round worm) onchocerca volvulus affecting the skin and the eyes leading to chronic prurtic onchodermatitis and blindness Life cycle of the parasite ⋅ Blackflies of the genus Simulium bites an individual with onchocerca volvulus → the microfilaria develop into infective larvae within the blackfies →transmitted in to an other individual during the blood meal of the blackflies ⋅ Blackfies bread in fast moving water bodies(rivers) 36 | P a g e
    • ⋅ They can travel up to 200 km and transmit the disease. Pathogenesis ⋅ Infective larvae enter the human skin by the blackfly→ larvae mature into adult worms that are encapsulated in fibrous tissue and reside in the subcutaneous tissue and fascia. The adult worms produce microfilaria which migrate and enter the blood stream. ⋅ The microfilaria in the skin, eyes and lymph nodes induce inflammation and pathology Epidemiology ⋅ There are many foci in Ethiopia ⋅ Affects young adults usually farmers who stay working in the fields ⋅ Milky-white lesions on the pretibial area in adults is an indicator of oncocerciasis in a community Clinical manifestations ⋅ The incubation period is 1-2 years the micrifilaria can survive in humans for for up to 2-3 years and the adult worms 10-15 years ⋅ A person with onchocerciasis may be asymptomatic ⋅ The skin and the eyes are the two most affected organs Skin manifestations ⋅ The manifestations of the skin are different with the chronicity of the disease and the load of the microflilaria. Different patterns of skin manifestations can exists on an individual A. Acute popular ochodermatitis ⋅ This is the first stage with widespread small pruritic papules that may progress to vesicles and pustule in most severe cases ⋅ There may be erythema and edema this stage affects the face ,extremities and trunk B. Chronic popular onchodermatitis ⋅ The skin lesions at this stage are macular and lichenoid papules ⋅ Pruritus is common and postinflammatory hyperpigmantations are present ⋅ The buttocks, thighs, waist and shoulders are affected mostly C. Lichenified onchodermatitis 37 | P a g e
    • ⋅ Hyperpigmented and hyperkeratotic pruritic papule,plaques more confuante and lichenified wuth increasing severity and time ⋅ Lower extremities and buttocks are affected with lymphadenopathy D. Atrophic ⋅ Longstanding onchodermatitis resultes in atrophic lesions with hyperkeratosis component “lizard skin” ⋅ Depigmentation and follicular hypepigmentation in longstanding onchodermatitis gives the picture of “ leopard skin” ⋅ Pruritus is rare at this stage ⋅ The shin area involved bilaterally and this is used to screen for Onchocerciasis in an endemic area E. Palpable onchocercal nodule ⋅ These nodules are containing the adult worms are asymptomatic , found on the bony prominences of the iliac crest, sacrum ribs scapula and skull F. Hanging groin is an other clinical finding associated with Onchocerciasis ⋅ It consists of inelastic skin in the inguinal area with lymphadenopathy ⋅ Lymphedema of the lower extremities and the external genitalia Ocular involvement ⋅ This is the most devastating aspect of the disease with blindness a potential outcome ⋅ ocular findings include chorioretinitis , iritis optic atrophy and keratitis ⋅ Patients with onchodermatitisis should be evaluated by ophthalmologist ⋅ In Ethiopian endemic foci Patients commonly have microfilaria in the anterior chamber but the prevalence of blindness due to onchocerciasis is said to be not very much common. ⋅ This could be probably due to species difference and the dressing stile of people whereby shoulder and trunk are covered and extremities exposed hence the bite sites blackfies and the locations of the onchocercal nodules are limited to the waist Diagnosis ⋅ Clinical and epidemiological findings ⋅ Identification of the microfilaria in the skin snip- or adult worms from the nodules 38 | P a g e
    • ⋅ In heavily infected individuals microfilaria may be found in the blood and other body fluids ⋅ Slit lamp examination of the anterior chamber of the eyes Differential diagnosis ⋅ Hypersensitivity reactions ⋅ atopic eczemas, ⋅ contact allergic eczemas ⋅ scabies ⋅ Pruritic popular eruption Treatment ⋅ Ivermetin 6 mg po stat and repeat every 6 months in for 12- 15 years endemic areas that is the life span the adult worms in humans ⋅ Currently recommended  Ivermetin 6 mg po stat plus  doxycycline 100 mg daily for 6 weeks this regimen is reapted every 3months for a total of 18 months  doxycycline is to kill the comitial bacteria present in the adult worms that is responsible for sustenance of the viability of the adut worms and reproduction ⋅ Diethylecarbamazine DEC in multiple doses is associated with acute reactions known as the Mazzotti reaction. ⋅ Mazzotti reaction is due to rapid killing of the microfilaria in the tissues – severe allergic reaction- like illness- including generalized itching, urticarial edema of the skin, maculopopular eruptions swelling and tenderness of the lypmnodes, fever and hypotension ⋅ Ocular reactions may cause loss of vision ⋅ DEC is started small dose first with antihistamins and progressively higher doses to avoid this reaction ⋅ Both Ivermetin and DEC kill the microfilaria but not the adults ⋅ Ivermectin is slow acting and it is preferred drug for the treatment and control of may filarial diseases. ⋅ Surgical removal of the onchocercal nodules 39 | P a g e
    • 40 | P a g e
    • Scabies  Definition: - scabies is one of the commonest intensely pruritic, highly contagious infectious conditions of the skin caused by a mite Sarcoptis scabei and transmitted by close personal and sexual contacts Historically  It has been recognized as a disease for over 2500 years.  In 1687 Francesco Redi identified Sarcoptes scabei Scabies is one of the first diseases with a known cause.  In Latin, scabere means to scratch.  Romans used the term to describe any pruritic skin disease; so, it has been known as the great imitator Etiologic agent Sarcoptes scabei var. hominis, the female measures 0.4mm long and 0.3mm broad and the smaller male is 0.2mm long and 0.15 mm broad. Epidemiology  Commoner in children and adolescents  It is a disease of disadvantaged community  Epidemic occurs during wars and social upheavals  Endemic in many developing countries Transmission Pathogenesis  Female and male make mating on the surface of the skin.  The male mite dies and the gravid female mite burrows into the epidermis lays up to 3 eggs per day for the duration of her 30-60 day lifetime.  In a typical infestation host harbors 8-11 adult female mites. The eggs hatch in 3-4 days and the larvae leave the burrow to mature on the skin.  Fewer than 10% of the eggs laid result in mature mites.  Type IV hypersensitivity reaction to the mites, their eggs, or scybala (packets of feces) occurs approximately 30 days after infestation Clinical features 41 | P a g e
    • Classic scabies:  The lesions are erythematous, excoriated, papulovesicular and found bilaterally.  It starts on the wrist, finger webs and on the medial sides of fingers, the flexor aspect of the wrist, the elbows and the anterior axillary folds, the genitalia and inner thighs and the gluteal folds  More disseminated presentation in infants and toddlers. Scabies in infants and young children  Distribution and morphology:- generalized  The face the scalp, palms an soles are affected  Papules, vesicle and pustules  Secondary eczematization and impetiginazation are common Crusted (Norwegian) scabies  In 1848, Danielssen and Boeck described a highly contagious variant of scabies occurring in immunocompromised patients, elderly or mentally incompetent patients.  Thousands to million mites are found instead of the normal 8-11 mites in the normal host. But 2-3% of HIV/ AIDS patients manifest Norwegian scabies.  In Norwegian scabies, pruritus may not be there (in about 50% of the cases do not itch)  It is psoriasiform and generalized with nail changes and scalp involvement  Skin becomes thickened and involves all part of skin including face, palms and sales. DDX Acropustulosis of Infancy, Atopic Dermatitis, Contact Dermatitis …. Diagnosis of scabies  Itching, worse at night  Presence of similar condition in the family or intimate contacts  Characteristic distribution of lesions  Demonstration of the mite, eggs or feces 42 | P a g e
    •  Therapeutic test Management • Treat with a scabicide agent • All family members and close contacts should receive treatment at the same time • Provide antihistamines to alleviate pruritus. • Treatment of secondary infections. • For crusted scabies, crust and scale impair scabicide penetration. • Bed linens, clothing, and towels should be washed in a warm cycle • Sun exposing is the best method of decontamination the mite in our setup • Decontamination of clothing, bed linens, etc, must coincide with medical treatment • Infected individuals should avoid skin-to-skin contact with uninfected individuals • Trim finger nails Scabicide agents • Lindane (gamma benzene hexachloide) 1% lotion or cream – single application • Benzyl benzoate 25% lotion – for 3 consecutive days o For small children add 50% water to make it 12.5% and 75% water for infants • Permethrin (Elimite) -- 5% cream – single application- treatment of choice but costly • Crotamiton (Eurax) -- 10% lotion or cream - 2 times daily for 10 days • Sulfur in petrolatum -- 10% - for 07 days • Ivermectin - 9-18 mg PO in 2 doses, 1 wk apart 200 mcg/kg twice - effective for common as well as crusted scabies in epidemic outbreaks 43 | P a g e
    • Method of application • Apply neck to toe, to Benzyl benzoate lotion advice not to wash between applications • Advice to reapply if hands are washed during the day. Complications of scabies • Bacterial super infection • Eczematization • Nodule formation • Urticaria Treatment of complications: - Use antibiotic and anti histamine. Causes of therapeutic failure • Improper counseling • Poor compliance of patient • Inadequate application • Improper application • Not treating family members who have close contacts Leprosy  Leprosy is a chronic infectious disease caused by Mycobacterium leprae that mainly affects the skin, eyes, testes, peripheral nerves and the mucosa of the upper respiratory tract but capable of affecting any tissue or organ.  Its chronic nature is punctuated by acute episodes called reactions during which nerve damage occurs, which marks leprosy form other infectious diseases  The disease is dreaded because of the damage (nerves) that occurs in weak and anaesthetic hands and feet, as well as in blindness and facial disfigurement  Worldwide 2 million people are estimated to be disabled by the consequences of leprosy. Etiology  Armauer Hansen In 1873 the Norwegian scientist demonstrated the bacterial etiology of leprosy (Hansen’s disease and Hanseniasis)  It has not been possible to culture M. leprea on artificial media 44 | P a g e
    •  But was possible to growing M. leprea bacillus in the mouse foot pad and armadillos, leading to development of new chemotherapeutic agents leprosy bacillus. M. leprae  A member of the family Mycobacteriacae  straight or slightly curved rod-shaped organism  It is Gram-positive, and strongly ‘acid fast’ following staining with basic fuchsin, which stains the bacteria pink.  M. leprae divides every (generation time) 2-3 weeks, this is the rational of giving rifampicine monthly  The optimal growth of M. leprae is observed at 27–30 ºC — reflected clinically affecting the cooler areas of the body such as the skin, nasal mucosa, and superficial peripheral nerves (particularly Schwann cells) are the predominant sites of infection. Epidemiology  The global burden of the disease has decreased tremendously since the introduction of multidrug treatment (MDT) in 1982 by WHO.  From an estimated 12 million in 1985 to 0.6 million in 2002  The success of multidrug therapy provided the basis on which the concept of elimination developed  In 1991 WHO had declared to eliminate leprosy by the year 2000 through active case detection and MDT  Elimination was defined as a prevalence of less than 1 case per 10 000 population  It has brought a remarkable reduction in the prevalence of leprosy by 85%  But the annual number of new-cases detected globally has never been fallen significantly  Higher incidence African countries ==123,412 new cases/yr  Due to active case detection and MDT, in leprosy endemic countries of the world the prevalence has fallen dramatically but the number of new cases detected annually has never been changing 45 | P a g e
    •   Case detection and MDT alone could not eliminate leprosy because of the following Contributing to the pool of M. leprae are: o MDT can only be started after the diagnosis is made. o The existence of ‘healthy’ carriers capable of transmitting the infection o Organism, host and environment related factors in the development of leprosy and its transmission  Poverty and low socioeconomic status are the cofactors in the development of leprosy- our leprosy control programs should remain active and strengthened.  In Europe, leprosy elimination was achieved long before the discovery of multidrug therapy due to improvement in the standard of living. Mode of transmission and pathogenesis  Leprosy is not a highly infectious disease.  The principal means of transmission is by aerosol spread from infected nasal secretions to exposed nasal and oral mucosa.  Leprosy is not generally spread by means of direct contact through intact skin, though close contacts are most vulnerable.  The incubation period is 6 months to 40 years or longer. 46 | P a g e
    •  The mean incubation period is 4 years for tuberculoid leprosy (TT) and 10 years for lepromatous leprosy (LL).  Cases of Lepromatous leprosy are the main reservoirs of the bacillus o The long incubation period and o the high density of the bacillus in these cases makes them to be major transmitters  The areas most commonly affected are the superficial peripheral nerves, skin, mucous membranes of the upper respiratory tract, anterior chamber of the eyes, and testes.  These areas tend to be cool parts of the body.  The strength of the host's immune system influences the clinical form of the disease  A strong cell-mediated immunity (CMI) response of the host to M. leprea results in mild forms of disease, with a few well-defined nerves involved and lower bacterial loads.  Relatively absent cell-mediated immunity results in lepromatous leprosy, with widespread lesions, extensive skin and nerve involvement, and high bacterial loads, long time to show the manifestations and get treatment.  Therefore, a spectrum of disease exists such that cell-mediated immunity dominates in mild forms of leprosy and decreases with increasing clinical severity. Clinical features and classification  Leprosy has a bimodal age distribution, with peaks at 10-14 and 35-44 years of age  Up to 95 % of individuals exposed to infection are naturally protected, are able to mount an efficient immune response, and do not suffer from the disease.  In those who suffer from the disease, are classified as either paucibacillary (PB) or multibacillary leprosy Symptoms 47 | P a g e
    • o 90% of patients have a history of numbness first, sometimes years before the skin lesions appear o Sensory loss -Temperature is the first sensation that is lost. Patients cannot sense extremes of hot or cold. o The next sensation lost is light touch, then pain, and finally deep pressure. These losses are especially apparent in the hands and feet; therefore, the chief complaint may be a burn or ulcer in an anesthetic extremity o The skin lesions appear later during the course of the disease Physical: Assess for physical signs in 3 general areas: 1. For cutaneous lesions- assess the number and distribution of skin lesions. A hypopigmented macule/plaque with a raised border is often the first cutaneous lesion. Plaques are also common. o Lesions may or may not be hypoesthetic. o Borderline disease often appears with lesions on the buttocks. 2. Neuropathies-assess for areas of hypoesthesia (light touch, pinprick, temperature and anhidrosis), especially peripheral nerve trunks and cutaneous nerves. o The most common nerve affected is the posterior tibial nerve. Others commonly damaged are the ulnar, median, lateral popliteal, and facial nerves. o Besides sensory loss, there may be associated tenderness and motor loss. 3. Eye damage is most often seen with facial lesions.  Lagophthalmos (inability to close the eye), a late finding in LL, reduced corneal reflex, leaving dry eyes and reduced blinking are due to Cranial nerve involvement. Slit skin smear:  Tissue smear testing/slit-skin smears: An incision is made in the skin, and the scalpel blade is used to obtain fluid from a lesion.  The fluid is placed on a glass slide and stained by using the Ziehl-Neelsen acid- fast method 48 | P a g e
    •  The bacterial index (BI) is then determined as the number of organisms per 100 bacilli.  This test is useful because it detects the most infectious patients. Diagnostic criteria for leprosy:  The diagnosis of leprosy is primarily a clinical one.  The following criteria have a sensitivity of 97% with a positive predictive value of 98% in diagnosing leprosy.  Based on one or more of 3 signs: o Hypopigmented or reddish patches with definite loss of sensation o Thickened peripheral nerves o Acid-fast bacilli on skin smears or biopsy material Classification of leprosy The Ridley-Jopling classification is used to differentiate types of leprosy and helps in determining the prognosis A general classification of disease is based on the number of skin lesions present and the number of bacilli found on tissue smears. Paucibacillary disease -indeterminate leprosy [IL], TT, smear negative BT with fewer than 5 lesions and no bacilli on smear testing. Multibacillary disease -Five or more lesions with or without bacilli (smear positive BT, borderline leprosies and LL) is considered multibacillary disease. Indeterminate Leprosy ⋅ This is a benign form, relatively unstable ⋅ seldom bacteriologically positive ⋅ Presenting flat, ill-defined, macular lesions on the skin. ⋅ There is no loss of sensation. 49 | P a g e
    • ⋅ The lesions can be hypo-pigmented or erythmatous. ⋅ They may heal without any treatment( in 75% of the cases), or may persist without progressing indefinitely or may evolve into tuberculoid or lepromatous kinds of leprosy. Tuberculoid Leprosy (TT)  Skin lesions are few. One erythematous large plaque is usually present, with well-defined borders that are elevated and that slope down into an atrophic center.  The lesions can become annular with the central healing.  They can be found on the face and limbs  Lesions can be dry and scaly, hypohidrotic, and hairless.  Another presentation involves a large, asymmetric hypopigmented macule.  Both types of lesions are anesthetic and involve alopecia.  Spontaneous resolution can occur in a few years, leaving pigmentary disturbances or scars. Progression can also occur, leading to borderline- type leprosy.  In rare instances in which a patient is untreated for many years, the lepromatous type can develop.  Neural involvement is common in TT; it leads to tender, thickened nerves with subsequent loss of function.  The great auricular nerve, common peroneal, ulnar, radial cutaneous and posterior tibial nerves are often prominent.  Nerve damage can happen early, resulting in wrist drop or foot drop. Borderline Tuberculoid Leprosy (BT) 50 | P a g e
    • ⋅ In borderline tuberculoid leprosy the resistance to M. leprae is somewhat less than in tuberculoid patients and this is reflected by the clinical aspects of the lesions. ⋅ The lesions are less sharply defined and less hypopigmented than in tuberculoid leprosy. ⋅ The healing in centre is absent or slow and incomplete, resulting in broad infiltrated edges. ⋅ Satellite lesions around the main lesion are common. ⋅ Often repeated crops of new lesions occur, thus number of lesions is more. ⋅ The distribution of the lesions remains asymmetrical. ⋅ Skin smears may be weakly to moderately positive for acid-fast bacilli in the active stage of disease or may be negative. ⋅ Skin smear showed a bacteriological index of 1+ Borderline borderline leprosy (BB): Cutaneous lesions consist of numerous, red, irregularly shaped plaques that are less well defined than those in the tuberculoid type. Their distribution may mimic those of the lepromatous type, but they are relatively asymmetric. Anesthesia is only moderate. Regional adenopathy may be present. Disease is unstable, improve, or worsen. Borderline lepromatous leprosy (BL): Lesions are numerous and consist of macules, papules, plaques, and nodules. Annular punched-out–appearing lesions that look like inverted saucers are common. Anesthesia is often absent. 51 | P a g e
    • As with the other forms of borderline leprosy, the disease may remain in this stage, improve, or regress. Skin smear showed a BI of 3+ Lepromatous Leprosy (LL)  Lepromatous leprosy presents with wide spread lesions, sometimes pauples or nodules distributed symmetrically.  The skin may be smooth and shiny, but skin changes do not occur in LL until late.  Therefore, early LL lesions have little or no loss of sensation, nerves are not thickened, and sweating is normal. Nerve loss occurs slowly and progressively.  The skin lesions can be more or less infiltrated.  Skin smears are strongly positive for acid fast bacilli with big globi.  Skin smears from normal looking skin may also be positive.  In the picture a patient with lepromatous leprosy with numerous nodules and papules distributed symmetrically.  Skin smear examination showed a BI of 5-6+  Alopecia affects the lateral aspects of the eyebrows (madarosis), spreading to the eyelashes and then the trunk. Scalp hair remains intact.  Lepromatous infiltrations can be diffuse, nodules (called lepromas), or plaques.  The diffuse type results in a thickened skin appearance of a leonine facies.  Neuritic lesions are symmetric and slow to develop.  Eye involvement occurs, causing pain, photophobia, decreased visual acuity, glaucoma, and blindness. 52 | P a g e
    •  Testicular atrophy results in sterility and gynecomastia.  Lymphadenopathy and hepatomegaly can result from organ infiltration.  Stridor and hoarseness are a result of laryngeal involvement.  Nasal infiltration can cause a saddle-nose deformity.  Brawny edema of the lower extremities is a late finding.  Unlike the other types of leprosy, LL cannot convert back to the less severe borderline or tuberculoid types of disease.  Lepra reactions are complications that occur in 50% of patients after the start of therapy or occasionally before therapy Management  Currently the main features of leprosy control is based on early detection of new cases and followed by treatment with effective chemotherapy namely the multidrug therapy with special emphasis on providing quality patient care o leprosy patients.  The goals of pharmacotherapy are to stop the infection, reduce morbidity, prevent complications, and eradicate the disease.  MDT prevents dapsone resistance, quickly reduces contagiousness, and reduces relapses, reactions, and disabilities.  Patients are considered noninfectious within 1-2 weeks of treatment (usually after the first dose). These drugs are conveniently packaged in monthly calendar blister packs.  Paucibacillary disease can be treated with a combination of 2 drugs, whereas multibacillary disease requires triple-drug therapy.  Single skin lesions (paucibacillary) can be treated with a single dose of 3 drugs.  The length of treatment depends on the type of disease and on the access to drugs.   Paucibacillary disease: Dapsone 100 mg/d plus rifampin 600 mg supervised once a month for 6 months 53 | P a g e
    •  Multibacillary disease: Dapsone 100 mg/d plus rifampin 600 mg supervised once a month plus clofazimine 300 mg supervised once a month and 50 mg/d for 1 year  Single skin lesion: A single dose of rifampin 600 mg, ofloxacin 400 mg, and minocycline 100 mg  In patients taking dapsone, CBCs should be checked frequently early during the therapy and then less frequently later during therapy.  Skin lesions usually resolve within the first year of treatment, though some may persist for up to 5 years in multibacillary disease.  Potential deformities can be prevented by educating patients about how to minimize existing nerve damage and by treating any sequelae of this damage.  Close follow-up is important to ensure patient compliance Leprosy reactions  Reactional states occur in one third of patients and are acute inflammations of the disease.  A leprous reaction should be considered a medical emergency requiring immediate care. These states can result in permanent neurologic sequelae, resulting in disability and deformity.  Patients at the highest risk are those with multibacillary leprosy and/or preexisting nerve impairment. Lepra type I (reversal) reactions  Usually affect patients with borderline disease. Reversal reactions are type IV cell-mediated allergic hypersensitivities.  Reactions occur before , during and after treatment  Puberty, pregnancy, and childbirth can also precipitate type I reactions.  These reactions usually result in skin erythema, with edema and tenderness of peripheral nerves. 54 | P a g e
    •  Pre-exisiting lotions become abruptly erythematous, swollen and new letions appear on clinically normal skin.  Edema of the extremities  Nerves become painful, tender and swollen  Sudden onset of sensory or motor function loss  The peak time for type I reactions is during the first 2 months of therapy and for up to 12 months.  Prednisolone 40 mg po daily tapering slowly for a minimum of 6 months  Corticosteroid treatment is aimed at controlling acute inflammation, relieving pain, and reversing nerve and eye damage.  With treatment, approximately 60-70% of the patient's nerve function is recovered.  If neuritis is absent, nonsteroidal anti-inflammatory drugs (NSAIDs) may be helpful. Lepra type II reactions, or erythema nodsum leprosum -ENL  Occur in multibacillary patients and most often in LL –up to 75% of the cases .  These reactions are type III humoral hypersensitivities, with a systemic inflammatory response to immune complex deposition.  The most common presenting symptoms are crops of painful erythematous nodules of the skin and subcutaneous tissue.  The reaction usually manifests after a few years of therapy and relapse intermittently over several years.  Associated fever, malaise, arthralgias, neuralgia, iridocyclitis, dactylitis, orchitis, and proteinuria may be present. 55 | P a g e
    •  The use of clofazimine in MDT substantially reduced the incidence of ENL to 5%. Clofazimine has also been used to treat ENL.  The real challenge in managing leprosy is the treatment of reactional states.  Systemic steroids are effective in reducing inflammation and edema in reversal reactions; therefore, they are the most helpful medications in preventing nerve damage.  Prednisone 40-80 mg/d should be given for 5-7 days then tapered slowly over 3- 6 months. This long course is necessary to decrease the severity of disabilities and deformities.  Clofazimine can also be used as a steroid-sparing agent for reversal reactions.  Thalidomide is ineffective for the treatment of reversal reactions, but it is highly effective with ENL. Other complications  Injuries can result in ulcerations, cellulitis, scarring, and bony destruction.  Foot ulcers caught early should be treated with rest because they heal if they are not subject to weightbearing.  Contractures can develop and result in fixation. Common sequelae include clawing of hands and feet.  Eye damage can result in loss of the corneal reflex, lagophthalmos, ectropion, entropion, and blindness.  Neuropathy induced by leprosy can result in trauma, pressure necrosis or secondary infection that goes unnoticed, leading to amputation of digits or limbs.  Wrist and foot drop are also common.  Skin drying and fissures can be caused by autonomic disruption. 56 | P a g e
    • Lymphedema /elephantiasis ⋅ It is on of the most disfiguring, disabling and common condition ⋅ Lymphedema is accumulation of lymphatic fluid in the interstitial space as a result of blockade of the lymphatic flow from many causes accumulated lymphatic fluid contains high proteins and fats which organizes in the interstitial space to result in non pitting swelling in long standing cases ⋅ The epidermal changes associated with lymphedema include :  Verrucous and papillomatous growths and hyperkeratisis ,  Fissuring and maceration of the folds and toe webs  Huge and hunging folds of the skin are see in severe and longstanding cases ⋅ Lymphedema is a cause of physiologic immune compromisation in the affected linb→lyphostasis → Maceration and fissuring and the high protein content of the lymphatic fluid serving as a culture for infectious organisms→ recurrent and severe infections cellulitis → that leads to further damage to the lymphatic vessel and nodes → calls for further lymphatic insufficiency and lymphedema Causes of lymphedema 1. Podoconiosis –Mossy Foot –Non- Filarial Elephantiasis ⋅ It is due to silicate crystals in the red, fertile volcanic soil in most highlands of Ethiopia and central and eastern African countries ⋅ As individuals walk bare foot, Aluminium and magnesium silicates get into the skin and lymphatic vessels → lead to sclerosis and fibrotic obstruction of the lymphatics. ⋅ People who walk bare foot are in the highlands of Ethiopia commonly have it ⋅ There are some genetic predispositions to develop podoconiosis as all who walk barefoot in the volcanic soil do not develop it ⋅ Probably it is the commonest cause of lymphedema in Ethiopia 57 | P a g e
    • ⋅ It startes as bilateral swelling of the foot and the legs the toes show veruvous and papillomatous overgrowths with macerations in between. ⋅ Recurrent cellulites is common manifesting as pain in the limb, fever, chills and tenderness in the regional lymph nodes 2. Lymphatic filariasis ⋅ Among the lymphatic filariasis Wichereria bancrofti is the one found south-west Ethiopia and across the equatorial bet in other African countries ⋅ It is transmitted by a mosquito vector ⋅ Infective microfilaria enters the lymphatic vessel and matures into adult worm → adult worm mate in the lymphatic vessels or nods →release microfilaria in to the blood stream ⋅ Mature adult worms provoke chronic inflammation with eosinophilic infiltrate in the lmphatic vessels →dilation / scaring and obliteration of the lymphatic vessels Presentation ⋅ Acute form presents as lymphangitis which is recurrent over 6-10 years associated with lymphadenitis, orechitis and fever ⋅ Massive Lymphedema with hypertrophic snd fibrotic skin folds hydrocele and chyluria ⋅ Lab ⋅ peripheral blood eosinophila ⋅ Hematuria and /protienuria ⋅ Microfilaria in the blood and other body fluids ⋅ Recurrebt bacteria infection ⋅ Cellulites / erysipelas causes fibrotic changes to the lymphatic vessels and nods leading to lymphatic insufficiency and lymphedema , which will further call for bacterial infection 3. cellulitis/ erysipelas · Recurrent cellulitis/ erysipelas causes destruction of the lymphatics 4. Tuberculosis lyphadenitis can cause lymphedema 5. STIs 58 | P a g e
    • · Lymphogranuloma Venoreum and Lymphogranuloma Inguinale can cause destruction and scarring of the lymph nodes and result in lymphedema 6. Malignancies such as Kaposis sarcoma Management of a patient with lymphedema 1. Movement Exercise and movement of the affected limb enhances the lymphatic drainage profoundly While the patient is sitted, dangling the affected limb in dependent position and creating steady state of limb causes more lymphostasis. Therefore movement of the legs even when at sitting position is very much important. 2. Elevation To elevate the affected limb to a certain level enhances the lymphatic drainage significantly Even when the patient is sleeping the affected limb should be elevated using some methods like pillows or raising bed from the other end. 3. Foot Hygiene Soak and wash the limb with in soapy water with much attention to the toe webs Dry the limb and massage with vegetable oil to prevent dryness and cracking The oil also helps to prevent the growth of infectious agents Massaging should be up wards started from the upper thigh progressively the foot and the toes Or Soaking with potassium permanganate 1: 1000 solutions for 20 minutes daily or twice a day then dry it up and apply vegetable oil is superior to using soaps alone 4. Shoes Wearing protective boots is mandatory to prevent trauma and infection Boots can be improvised ones made from local workshops in such a way it helps to apply pressure on the swollen legs and enhance lymphatic drainage 5. Monthly benzanthin penicillin 2.4 mega unit I.M stat 59 | P a g e
    • Benzanthin penicillin can stay in the body and prevent bacterial infection for 3-4 weeks It prevents the occurrence of bacterial cellulitis (group A- β hemolytic streptococcal ) which is the commonest complication manifesting as acute episodes of fever and pain in the limb Bacterial cellulitis causes series morbidity and even mortality It also leads to further lymphatic copromisation and further infection (forms a vicious cycle) yet preventable by monthly Benzanthin penicillin 2.4 mega unit I.M stat 6. When microfilaria origin can not be ruled out Ivermectin If the causes if lymphedema is from lymphatic filariasisi- Wichereria bancrofti or if the possibility could not be ignored, give ivermectin 6mg po stat and to be repeatedly give every year in endemic area 7. Diligent teach and training the patients on these elements of treatment Patients and/or their relatives should be trained with demonstration on this management package This management principle should be given to the patients in a written form in their own language and level of understanding to be reviewed and practiced at home Eczemas Eczemas Def; Eczemas are groups inflammatory skin conditions manifesting either as acute eczematous lesions, which are characterized by active papules; erythema, excoriations and oozing (weeping), sub acute eczemas, also have excoriation, erythema with papules and scales or as a chronic eczematous lesion, characterized by thickening of the skin, and accentuation of the creases (lichenification) and hyperpigmentations Eczemas can be of endogenous in origin eg atopic eczema, seborrhoec eczema, eczemas from varicose veins (stasis eczema), nummular eczema…or of exogenous origin like contact allergic eczema, contact irritant eczema. Atopic dermatitis 60 | P a g e
    • The term atopy is a Greek word meaning "out of place” or strange. Atopic diathesis is the hereditary tendency to develop allergies to food and inhalant substances as manifested by eczema, asthma and hay (allergic conjunctivitis and allergic rhinitis) fever is called atopy. Epidemiology  The prevalence of atopic diseases appears to be rising.  Atopic dermatitis now affects up to 20% of the population.  Onset <5 years of age in 90% cases  Factors in atopic dermatitis  It is the interaction of genetics and environmental factors that results atopic eczema.  More than ¼ of the offsprings of atopic mother develop atopic dermatitis in the first 3 months of life.  If one parent is atopic, more than 50% of the children would develop allergic symptoms by the age of two years and  If both parents are affected, the chance of the of child to have allergic symptoms would be about 79%.  Personal or family history of asthma, or atopic dermatitis in up to 80% of cases Diagnostic Criteria for Atopic Dermatitis The diagnosis of atopic eczema is made by constellation of criteria. Major criteria: one should have three of the following major criteria. 1. pruritus 2. Typical morphology and distribution A. Flexural lichenification in adults B. Facial and extensor involvement in children 3. Chronic or chronically relapsing dermatitis 4. Personal or family history of atopic diseases (asthma , allergic rhinitis, allergic conjunctivitis and atopic eczema ) Minor Criteria One Must Have Three of the Following  Dryness of the skin (xerosis, xeroderma)  Ichthiosis/hyperlinear palms and soles 61 | P a g e
    •  IgE reactivity  Elevated serum IgE  Early stage of onset  Tendency to cutaneous infection  Pityriasis alba  Itching when sweating  Intolerance to wool and lipid solvents perifollicular accentuation For young infants the diagnostic criteria is modified The three major criterias are 1. family history of atopic diseases 2. Typical facial or extensor dermatitis 3. Evidence of pruritus Three minor features are:  Xerosis/ ichthiosis / hyperlinearity of palms and soles  Perifollicular accentuation  Post auricular fissure  Chronic scalp scaling Clinical presentation of atopic eczema  The hallmark of atopic eczema is pruritus and dryness of the skin.  Long standing pruritus results in lichenified dry skin, which would call for further scratching, and in this way the itch -scratch cycle establishes which assumes a vicious form.  The flexures like the popilitial fossa, wrist, and anticubital fossa are affected.  The pattern of distribution in atopic eczemas depends on the age and activity of the disease.  Based pattern of distribution atopic eczemas are classified in to: a. Infantile eczema (from 2 months up to 2 years), b. Childhood atopic eczema (from 2 years to 10 years) and c. atopic eczema of adolescents and adults. 62 | P a g e
    • Infantile Atopic eczema  Atopic dermatitis usually starts in the first year of life.  During this phase, there is facial erythema, vesicles, oozing and crusting located mainly on the face, scalp, forehead and extensor surface of the extremities.  Buttocks and diaper area are frequently spared. Childhood eczema:  The lesions tend to be drier and scaly.  Flexor surfaces and skin creases are predominantly involved.  Facial lesions with eyelid involvement and lesions around the neck also occur.  Lichenification from chronic itching and scratching occur over flexor surfaces.  Psychological effects often are very prominent for exacerbation Adolescent and adult atopic dermatitis:  Flexural predilection of lesions persists.  Localized, eczematous or lichenified plaques often predominates the clinical picture.  Prurigo papules and nodules tend to occur.  Resolved cases show dryness and irritability of the skin with a tendency to itch with sweating and other triggers.  Recurrent and persistent hand dermatitis is a frequent feature. TREATMENT General Measures  Counseling; that it is not curable but controllable by treatments;  Avoidance of factors that promotes dryness, itching or inflammation, such as excessive bathing and exposure to volatile chemicals (gasoline, kerosene)  Avoidance of contact with local irritants like woolen garments; use soft cotton garments.  Clothing and linens should be washed in mild detergents and rinsed well. 63 | P a g e
    •  Soaps should be used when they are necessary  Emollients – liquid paraffin, Vaseline, olive oil used after bath  Antihistamines - Non-sedating antihistamines like cetirizine, loratadine or fexofenadine may be used to alleviate pruritus  In severe cases, hospitalization for a short period may promote rapid reduction of symptoms mainly by providing a changed environment Specific Specific measures are aimed at modifying the following pathogenetic factors: dryness, inflammation, infection, and itching.  High potency steroids are used for a short period to rapidly reduce inflammation, however they should not be used on the face.  Maintenance therapy, if needed is best done with mild steroids like hydrocortisone.  On face and intertriginous areas, mild steroids should be used; mid-potency formulations are used for trunk and limbs.  Topical steroids are applied initially twice or thrice a day after the symptoms are lessened, frequency of application should be reduced.  Intermittent use if topical steroid may be alternated with application of emollients.  Ointments are superior to creams or lotions. Severe :  A short course of systemic steroids (prednisolone, triamcinolone) may occasionally be needed to suppress acute flare-ups  Emollients – liquid paraffin, Vaseline, olive oil used after bath  Antihistamines - Non-sedating antihistamines like cetirizine, loratadine or fexofenadine may be used to alleviate pruritus .  Infections and colonization with Staphylococcus aureus may aggravate or complicate Atopic dermatitis Erythromycin, or cloxacillin is usually prescribed 64 | P a g e
    • Course and prognosis  Most infantile and childhood cases improve over time and the prevalence of atopic dermatitis diminishes significantly in older ages (from 20% during infancy and childhood to 1% in adulthood).  Children usually tend to outgrow the condition -up to ¾.of them  In the remaining 1/4 o Some patients’ disease may persist through adulthood. o Very few continue to have severe form of the disease through adulthood o In others, a tendency for dry and irritable skin that easily develops eczematous changes may persist after AD resolves. o A propensity for recurrent hand dermatitis may remain in adults who had AD in their childhood.  Many children with atopic eczema later on develop allergic rhinitis or bronchial asthma 65 | P a g e
    • Pityriasis alba (PA) · Pityriasis alba (PA) a common disfiguring hypomelanosis, which, as the name indicates, is a white area (alba) with scaling (pityriasis.) · It is observed in a large number of children. Hypopigmented, ill-defined lesions usually on the cheeks of children and young adults with brown or black skin. · Its pathogenesis is unknown, but believed it is a form of atopic eczematous dermatitis, but there is no spongosis (the “hallmark” of allergic eczema). · Age - 90% of the cases range from 6 to 12 years of age. · In young adults, PA quite often occurs on the arms and trunk.  Curiously, PA is not often observed after age 30.  The lesions are light brown or pale white and occur most often on the face (especially the cheeks); extensive PA can be seen on the upper extremities and trunk.  On histologic examination, melanocytes are shown to be reduced in number and there are fewer melanosomes, but transfer of melanosomes does occur.  The lesions disappear spontaneously in the winter in temperate climates. Common mistakes in Pityriasis alba diagnosis and management 66 | P a g e
    •  Medical practitioners usually mistake it for Tinea facie [fungal infection of the face] and treat it with Whitfield’s ointment. Whitfield’s ointment (the Vaseline ) induces photosensitivity and Pityriasis alba assumes a different form of dermatosis, hyperpigmented patch with faint scales with a hypopigmented margins. Now it is called melanodermatitis lichenoidus.  Mangement of Pityriasis Alba  Management is satisfactory with low-potency corticosteroids  Hydrocortisone cream or ointment1%  Betamethasone valerate 0.01-0.025%  Avoid frequent washing and soaps  Vegetable oil or other moisturizers are useful  It is self-limiting condition Seborrheic Dermatitis  Seborrheic dermatitis is a papulosquamous disorder patterned on the sebum- rich areas of the scalp, the face, and the trunk.  In addition to sebum, this dermatitis is linked to Pityrosporum ovale, immunologic abnormalities, and activation of complement.  It is commonly aggravated by changes in humidity, trauma (eg, scratching), seasonal changes, and emotional stress.  The severity varies from mild dandruff to exfoliative erythroderma.  Seborrheic dermatitis may worsen in Parkinson disease and in AIDS. 67 | P a g e
    •  Seborrheic dermatitis is associated with normal levels of P ovale but an abnormal immune response. Epidemiology  The incidence of seborrheic dermatitis is 3-5%, with a worldwide distribution.  In infants, it occurs as cradle cap or commonly as a flexural eruption or rarely as erythroderma  After infancy seborrhea dermatitis is unknown until after adolescence when the sebaceous glands become active again  Etiopathogenesis  Pityrosporum organisms are probably not the cause but a cofactor linked to a T-cell depression, increased sebum levels, and an activation of the alternative complement pathway Clinical presentation  Skin lesions present as greasy scale over red, inflamed skin.  Infectious eczematoid dermatitis, with oozing and crusting, suggests secondary infection.  A seborrheic blepharitis may occur independently → eyelids.  Distribution follows the oily and hair-bearing areas of the head and the neck, such as the scalp, the forehead, the eyebrows, the lash line, the nasolabial folds, the beard, and the postauricular skin. Presternal or interscapular involvement is more common than the nonscaling intertrigo of the umbilicus, axillae, inframammary and inguinal folds, perineum, or anogenital crease that may also be present.  Because seborrheic dermatitis is uncommon in preadolescent children, and Tinea capitis is uncommon after adolescence, dandruff in a child is more likely to represent a fungal infection. Commonly seborrheic dermatitis is secondarly infected by bacteria. 68 | P a g e
    • Treatment  Topical corticosteroids, creams, lotions depending on the site and nature of the lesions  In severe cases systemic prednisolone for a short time may be beneficial  Systemic ketoconazole or shampoos can be given if it is severe.  Dandruff responds to more frequent shampooing with Salicylic acid, tar, selenium, sulfur, and zinc all are effective in shampoos and may be alternated.  Selenium sulfide (2.5%) or ketoconazole shampoos may help by reducing P. ovule scalp reservoirs.  When sever Ketokonazole 200mg tab can be given for 2 to 3 week and Antibiotics if it is infected Contact dermatitis Contact dermatitis is an inflammatory response of the skin to substances coming in contact. The two forms of Contact dermatitis 1. Irritant contact dermatitis 2. Allergic contact dermatitis 1. Irritant contact dermatitis  irritant dermatitis results from exposure of the skin to agents that overwhelm the normal functions of the skin and cause direct injury  An irritant is any agent, which is capable of producing cell damage if applied for sufficient time and in sufficient concentration.  irritant dermatitis is one of the commonest type of skin conditions  Immunological memory is not involved and dermatitis occurs without prior sensitization.  Many chemicals penetrate the skin and alter or damage skin cells.  Dermatitis arises when the defense or repair capacity of the skin is exhausted, or when the penetration of chemicals excites an inflammatory response  Strong irritants will induce a clinical reaction in almost all individuals 69 | P a g e
    •  Many weaker irritants induce damage by gradually exhausting the stratum corneum/ horny layer, denaturing the keratin, removing stratum corneum lipids and altering the water-holding capacity of the skin  This eventually leads to damage to the living cells of the epidermis.  Irritants contact dermatitis affects everyone at a level of exposure, individual susceptibility depend on the site, age and individual predisposition; atopics eczema or those with coexistent or recently healed eczema or any other dermatitis are more vulnerable  Irritant eczema is very common and much common in individuals who have other forms of eczema or dermatosis because inflamed skin is irritated easily  Irritant contact eczema can predispose to contact allergic eczema by enhancing the entry of sensitizing agents onto the skin via the damage it results Common irritants • Water • Detergents, soaps • Body secretions like urine, feacal matter saliva • Industrial cleaning agents, including solvents and abrasives • Alkalis, including cement • Acids • Cutting oils • Organic solvents  Certain, mostly 'wet', occupations, have an increased risk of irritant contact dermatitis; these are listed in  Occupations associated with irritant contact dermatitis 1. Cleaning 2. Food preparation 3. Hairdressing 70 | P a g e
    • 4. Agriculture, horticulture, forestry 5. Metal work 6. Construction 7. Medical, dental, veterinary Clinical features of irritant contact eczema  Irritant contact dermatitis has a spectrum of clinical features, which ranges from a little dryness, redness or chapping through various types of eczematous dermatitis to an acute caustic burn  Acute (toxic) irritant contact dermatitis is often the result of a single overwhelming exposure to an irritant or caustic chemical.  Erythema, edema, inflammation, pain and vesiculation  In more severe cases there may be exudation, bullae formation and tissue necrosis Eg. toxic irritant dermatitis from Nairobi flay (in Amharic –“Almaz bale chirra”)  Chronic irritant dermatitis; 'wear and tear dermatitis';  This type of dermatitis develops as a result of a series of repeated and damaging insults to the skin  Minimal Erythema, scaling , fissuring and dryness Irritant Hand eczema – 'housewife'- eczema  Prolonged contact to water and soap - working in the kitchen, washing cloths, handling vegetables  Nurses and surgeons who frequently scrub and wear gloves busy in the operation theaters  Patchy 'housewife'-type eczema affecting principally the dorsa, sides and webs of the fingers,  or a 'ring' eczema-both are patterns associated with wet work and exposure to detergent  Starts as dryness can develop into patchy or diffuse erythema with scaling, fissuring and even vesiculation. Destraction of the proximal nail fold associated with Candidiasis of finger webs and/ or Candida paronychia  The etiology of hand eczema is often complex.  Constitutional, irritant and allergic factors frequently co-exist 71 | P a g e
    •  Allergy can never be completely excluded, nor is any pattern of hand dermatitis pathognomonic for a single causation  Management o Avoid contact to water and detergents o Topical corticosteriodes o Treat the attending Candida paronychia or finger-web infection or bacteria infection o Dry the oozing wet eczema with potassium permanganate 1: 1000 solution soak BID until it gets dry or if it dry, scaly apply Vaseline: paraffin 50:50 to lubricate Diaper dermatitis · Irritant dermatitis develops in situations of prolonged or too frequent contact with degraded urine or faeces /faecal residues in infants. · Sweat, occlusion, irritant cleansers, secondary infection and secondary medicament allergy are all additional complicating factors · It occurs most frequently in the very young, or in the elderly in situations of urinary or faecal incontinence. · Sufficiently frequent changes of diapers and keep the area dry in infants are important · Mild strength topical steroids antibiotic and antifungal agents for secondary infection Management irritant contact eczemas · Treatment consists of removing all adverse factors, whether these be mechanical, physicochemical or chemical. · Topical steroids enhance healing · Treatment of the complications – infection · If it is oozing – dry it with potassium permanganate 1: 1000 solution soak BID until it gets dry or if it dry, scaly apply Vaseline: paraffin 50:50 to lubricate · Cetrizine or claritin for the Pruritus · Uncomplicated irritant contact dermatitis heals within 2 weeks if all noxious stimuli are removed, while full functional recovery may take 6 weeks or longer. 2. Allergic contact dermatitis 72 | P a g e
    •  Allergic contact dermatitis affects only individuals previously sensitized to the contactant. · The causes of contact allergic dermatitis are countless and varies with the genetic make-up of individuals and form one society to the other  A cell-mediated type IV delayed hypersensitivity reaction results from specific antigens penetrating the epidermal skin layer.  The antigen is transported via the dermis and to the regional lymph nodes where it induces sensitization of the immune system, which results in the development of sensitized T lymphocytes against the substance. Sensitization process takes two weeks but once this occurs within 48-72 hours inflammatory response condenses sensitized T lymphocytes to the sensitizing substance that manifests as eczema – called contact allergic dermatitis · On subsequent presentation of the antigen on the skin surface, sensitized T lymphocytes come to the site within 48-72 hours, illicit inflammation against the sensitizer – allergic dermatitis · This can be usually life long unless the sensitizing agent is not avoided Clinical manifestation · The presentation is eczematous lesions; the first location varies with area of exposure to the sensitizer but later can become widespread · Itching can be severe followed by rash localized to the contactant firs · In acute cases it manifests by erythema, faint papules, edema, vesicles and oozing and crusting and · In chronic stage scaling, excoriation, hyperpigmentation and lichenification can be there. · The distribution varies depending on the exposure to the contactant however hands are the commonest sites. Nickel contact allergic dermatitis · Nickel is common cause of contact dermatitis in adults and more common in women. · Ear piercing and the wearing of cheap metal earrings are important causes of sensitivity 73 | P a g e
    • · Women are usually sensitized by objects worn close to the skin-costume jeweler or metal accessories on clothing · And men are more frequently sensitized by watches, watch buckles or belt rings and spectacle frames. · It may start at the ears, under jeans studs and brassière fasteners. · The eruption may be papular, and either diffuse or consisting only of excoriated papules on almost normal-looking skin. · Some patients seek treatment because of spread of dermatitis to distant regions. Robber contact allergic dermatitis · Rubber is also common cause of contact allergic dermatitis · The presentation differs on the mode of contact · Foot eczema –from contact to rubber in the Shoes and slippers or hand eczema from gloves and rubber handles · Foot eczema could also be from the dyes in the leather industry Allergic contact dermatitis from textiles · This type of eczema presents in the covered parts of the body and more on the pressure and tight areas where the cloths come in contact to the skin more, such as the nap, Shoulders, axillary regions and waist areas, Management · The possible allergens are too many but proper history and physical findings may make the likely offender to be recognized · Patch test is not available · History on site of onset, progression, occupation, habits and hobbies is useful · Treatment Avoid the agent if recognized Topical steroids and if severe systemic for a short time Antipruritics Treat the coplications 74 | P a g e
    • Lichen Simplex Chronicus Def: - Lichen simplex chronicus (LSC) is thickening of the skin with variable scaling that arises secondary to repetitive scratching or rubbing. LSC is not a primary process. Rather, a person senses pruritus in a specific area of skin (with or without underlying pathology) and causes mechanical trauma to the point of lichenification.  LSC is found on the skin in regions accessible to scratching.  Pruritus provokes rubbing that produces clinical lesions, but the underlying pathophysiology is unknown.  A relationship likely exists between central and peripheral neural tissue and inflammatory cell products in the perception of itch and ensuing changes in LSC.  The possible interplay among primary lesions, psychic factors, and the intensity of pruritus additively influence the extent and severity of LSC  Pruritus is usually described as much worse during periods of inactivity, usually at bedtime and during the night.  Touch and emotional stress also may provoke pruritus, which is relieved by moderate-to-severe rubbing and scratching.  LSC occurs mostly in mid-to-late adulthood, with highest prevalence in persons aged 30-50 years.  CM  lichenified, firm, rough plaques with exaggerated skin lines are noted.  Pigmentary changes (especially hyperpigmentation) are seen variably as in any dermatitic lesion. 75 | P a g e
    •   Common sites LSC • Scalp, Nape of neck, • Extensor forearms and elbows • Vulva and scrotum • Upper medial thighs, knees, lower legs, and ankles  Management  Treatment is aimed at reducing pruritus and minimizing existing lesions because rubbing and scratching cause LSC.   Topical steroids are the current treatment of choice because they decrease inflammation and itch while concurrently softening the hyperkeratosis.  Because lesions are by nature chronic, treatment most likely is very long.  Occasionally, occlusion is used to increase potency and enhance delivery of the steroids and also provides a physical barrier to the scratching.  Keratolytes (3% - 5% Salicylic acid) could be used in lichenfied lesion to remove the hyperkeratosis. Acne vulgaris  Acne vulgaris is a common skin disease that affects 85-100% of people at some time during their lives.  It is characterized by noninflammatory follicular papules or comedones and by inflammatory papules, pustules, and nodules in its more severe forms. 76 | P a g e
    •  Acne vulgaris affects the areas of skin with the densest population of sebaceous follicles; these areas include the face, the upper part of the chest, and the back. Four key factors are responsible for the development of an acne lesion: 1. Follicular epidermal hyperproliferation and hyperkeratinization, This is due to the increased level of adrenal derived androgen, dehydroepiandrosterone sulfate induces hyperproliferation. 2. Excess sebum, - Excess sebum is also a key factor in the development of acne vulgaris. - The amount of sebum produced and the degree and the severity of the acne are strongly correlated. - Sebum excretion is under hormonal control. Androgens stimulate sebocyte differentiation and sebum production, whereas estrogens have an inhibitory effect. - Most men and women with acne have normal circulating levels of androgen hormones. An end-organ hyperresponsiveness to androgens has been hypothesized. 3. Propionibacterium acnes, - P acnes is a microaerophilic organism present in many acne lesions. P acnes stimulate inflammation by producing proinflammatory mediators that diffuse through the follicle wall. 4. Inflammation - Inflammation may be a primary phenomenon or a secondary phenomenon and plays a role in the development of acne comedones, papules, pustules, and nodules in a sebaceous distribution characterize acne vulgaris. The face may be the only involved skin surface, but the chest, the back, and the upper arms are often involved 5. Genetic predisposition – but mode of inheritance is unknown 77 | P a g e
    • 6. Mechanical factors – excessive rubbing of the skin and use of oily cosmetics may induce acne lesion.  An external cause is seldom identifiable in acne vulgaris. Some cosmetic agents and hair pomades may worsen acne.  Medications that can promote acne include steroids, lithium, some antiepileptics, and iodides.  Congenital adrenal hyperplasia, polycystic ovary syndrome, and other endocrine disorders with excess androgens may trigger the development of acne vulgaris. Acne vulgaris may also be influenced by genetic factors. Normal Pilosebaceous Unit and pathogenesis of acne 78 | P a g e
    • DIFF ER EN 79 | P a g e
    • Management Treatment should be directed toward the known pathogenic factors involved in acne. These include follicular hyperproliferation, excess sebum, P acnes, and inflammation. The grade and the severity of the acne help in determining, which of the following treatments, alone or in combination, is most appropriate. Topical treatments Each works a little differently.  Benzoyl peroxide (2.5-10%) at night is best at killing P. acnes and may reduce oil production.  Resorcinol, salicylic acid, and sulfur help break down blackheads and whiteheads.  Salicylic acid also helps cut down the shedding of cells lining the follicles of the oil glands.  Topical medications are available in many forms, such as gel, lotion, cream, soap, or pad.  Topical antibiotic: -  Topical antibiotics are mainly used for their role against P acnes.  They may also have anti-inflammatory properties.  The development of resistance is lessened if topical antibiotics are used in combination with benzoyl peroxide.  Erythromycin and clindamycin alone or in combination with benzoyl peroxide.  80 | P a g e
    •  Topical retinoids are comedolytic and anti-inflammatory.  They cause epidermal differentiation and, thus, normalize follicular hyperproliferation and hyperkeratinization.  Adapalene, tazarotene, and tretinoin are in common use.  They are applied once daily to clean, dry skin. Systemic treatment  Tetracycline, (minocycline, docycyline and tetracycline, or erythromycin BID for one month then daily for 2-4 moths).  Trimethoprim, alone or in combination with sulfamethoxazole, are systemic antibiotics and anti-inflammatory.  Isotretinoin is a systemic retinoid that is highly effective in the treatment of severe, recalcitrant acne vulgaris  Patients with moderate to severe inflammatory acne may be treated with prescription of topical or oral medicines, alone or in combination. Advice needs to be given to the patient 1. Chronicity of the problem 2. Not to squeeze acne lesion 3. Washing with warm water but has to avoid irritants 4. Not to use steroids 5. Avoid applying greasy substances such as ointments and creams Pigmetary disorders 81 | P a g e
    • Vitiligo Def: - Vitiligo is an acquired condition of unknown cause whereby the melanocytes (pigment producing cells) have destroyed and disappeared from the affected skin. Lesions appear as totally white, none scaling, sharply demarcated macules.  It may affect the skin, mucous membranes, eyes, inner ear or hairs leaving milky-white patches.  The usual type of vitiligo is called 'Vitiligo Vulgaris' (means: common vitiligo).  Variant types include linear, segmental, trichrome and inflammatory vitiligo. Epidemiology  It occurs 1% of the population all ethnic groups and both sexes are affected equally, but exceptionally more visible on darker skin.  The disease can begin at any age but the peak incidence is in the 10 to 30 year.  It is hereditary in one third of the cases. Pathogenesis  It is believed that vitiligo is an autoimmune disorder whereby certain white blood cells direct the destruction of melanocytes.  People with vitiligo are also somewhat more prone to other autoimmune diseases, such as alopecia areata, autoimmune thyroid disorders, Addison's disease, pernicious anemia, and diabetes mellitus. 82 | P a g e
    • Clinical presentation  Vitiligo can affect any area of the skin and mucous membranes, but the most common areas are the extensor boney surfaces (back of the hand, elbows, and knees) and the periorofafial area (around the mouth, eyes, anus and genitalia).  The involvement of the hairy areas results in the depigmentation of the hair.  The macules of vitiligo are round or oval. They may become confluent as they enlarge, resulting in large patch with irregular borders but very well demarcated.  The diagnosis of vitiligo is usually straightforward, and no special testing is needed.  While vitiligo is a cosmetic problem and does not affect the health directly, however, it is disfiguring and become profoundly psychologically traumatic especially when it occurs in people with dark skin. Treatment  The goal of the therapy is to deal with the cosmetic disfigurement. Treatments for repigmentation are prolonged and the results are suboptimal.  Steroid creams twice a day with sun light exposure are initial treatment and results require three to six months.  If over-dosed or over-used then side effects include local skin damage  Crud coal tar 5-10% to be applies in the morning and steroid creams in the evening for three months and see the response.  dapsone 100mg po daily or 2-4 mg /Kg can be triad 83 | P a g e
    •  For extensive vitiligo, oral medications for repigmentation can be tried. The treatment most commonly used is PUVA (Psoralen and Ultra-Violet A light).  Cosmetics camouflage that can be used to match most skin hues when medical treatment is not helpful. Course and prognosis The Course and prognosis of vitiligo is unpredictable. In some cases spontaneous repigmentation occurs but in most of the cases it is chronic and slowly progressive. Many patients suffer from social stigmatization (the white leprosy). Hyperpigmentation Def: Hyperpigmentation is the increase in the natural color of the skin.  Skin color is influenced by a person’s genetic makeup as environmental factors.  It is determined by the amount of pigment or melanin that is produced melanocytes in the epidermis.  Natural pigment is nature’s way of protecting the skin from ultraviolet light  Uneven pigmentation of the skin may be a natural occurrence or related to ultraviolet light, infection, hormones, drugs, acne or topical chemicals applied to the skin. Common conditions with hyperpigmentation Melasma  Melasma is an acquired skin condition presenting as brown patches on sun-exposed areas. 84 | P a g e
    •  It presents as symmetric hyperpigmented macules or patches, which can be confluent or punctate.  The cheeks, the upper lip, the chin, and the forehead are the most common locations, but it can occasionally occur in other sun-exposed locations.  Chloasma is a synonymous term sometimes used to describe the occurrence of melasma during pregnancy Race: it is much more common in dark-skinned races, particularly Hispanics, Asians, Indians, people from the Middle East, and Northern Africa, tend to have melasma more than others Sex: Melasma mostly occurs in women (90%) and only 10% of those affected are men Age: Melasma is rare before puberty and most commonly occurs in women during their reproductive years. Causes melasma The precise cause of melasma is unknown. 1. A genetic predisposition is a major factor in the development of melasma. More than 30% of patients have a family history of melasma. 2. A direct relationship with female hormonal activity appears to be present because it occurs with pregnancy (called chloasma, or the “mask of pregnancy) and with the use of oral contraceptive pills. 3. The most important factor in the development of melasma is exposure to sunlight. . People with skin of color have more active melanocytes than those with light skin and produce a large amount of pigment under normal conditions, but this production increases even 85 | P a g e
    • further when stimulated by light exposure or an increase in hormone levels. Without the strict avoidance of sunlight, potentially successful treatments for melasma are doomed to fail. The macular hyperpigmentation of melasma is tan-brown in color and occurs in 1 of 3 patterns: centrofacial, malar, and mandibular. Treatment  While there is no cure for melasma, many treatments have been developed.  Melasma may disappear after pregnancy; it may remain for many years, or a lifetime.   Sunscreens are essential in the treatment of melasma.  They should be broad spectrum, protecting against both UVA and UVB rays from the sun. A SPF 30 or higher should be selected.  In addition, physical sunblock lotions and creams such as zinc oxide and titanium oxide may be used to block ultraviolet radiation and visible light.  Sunscreens should be worn daily, whether or not it is sunny outside, or be it in the outdoors or indoors.  Bleaching agents; Creams contain low concentrations of hydroquinone are most commonly-used depigmenting agent. This is often effective for mild forms of melasma when applied at night and a sunscreen in the morning. It takes about three months to see substantially improvement.  Remember, a sunscreen should be applied daily in addition to the bleaching cream. Some bleaching creams are combined with a sunscreen.  Remember Special care must be taken not to prescribe Hydroquinone because all concentrations can lead to skin irritation, phototoxic reactions with secondary postinflammatory hyperpigmentation, and irreversible exogenous ochronosis. 86 | P a g e
    •   Regardless of the treatments used, all will fail if sunlight is not strictly avoided.  Avoid sun exposure using hats and other forms of shade combined with the application of a broad-spectrum sunscreen at least daily. Post inflammatory  Post inflammatory skin darkening is a common occurrence after irritation or injury to the skin.  It is more prominent in dark-skin, however, it is also seen in lighter-skin individuals.  After irritation or injury to the skin, the pigment cells (melanocytes), instead of being incorporated into the keratinocytes in the epidermis, melanin leak to the upper part of the dermis deposit.  Examples include following acne, trauma or infection or inflammation to the skin.  This is a condition that usually clears with time, although it can last for months to years. Immediate treatment is important, as this will help to determine the outcome and ultimate appearance of the area. 87 | P a g e
    • Acanthosis Nigricans (AN)  Acanthosis Nigricans (AN) is characterized by symmetrical, hyperpigmented, velvety plaques that may occur in almost any location but most commonly appear on the intertriginous areas of the axilla, groin, and posterior neck.  The posterior neck is the most commonly affected site in children. The vulva is the most commonly affected site in females who are hyperandrogenic and obese. Epidemiology  Acanthosis Nigricans (AN) is much more common darker skin pigmentation.  The prevalence is the highest at 13.3% in African and less than 1% in the whites.  The incidence of AN is equal for men and women.  AN may be present at any age, although it is found more commonly in the adult population  Many of these patients have an underlying insulin-resistant state and hyperinsulinemia that is the cause of their AN.  The severity of the insulin resistance varies from sub-clinical to overt diabetes mellitus.  Very few patients with AN may have associated with underlying abdominal malignancy is often an aggressive tumor.  AN has been reported with many kinds of cancer but, by far, the most common underlying malignancy is an adenocarcinoma of gastrointestinal origin, usually a gastric adenocarcinoma. Lab  Perform a basic workup for underlying malignancy. Screen for diabetes. 88 | P a g e
    • Treatment  The goal of therapy is to correct the underlying disease process. Treatment of the lesions of AN is for cosmetic reasons only.  Likewise, weight reduction in obesity-associated AN may result in resolution of the dermatosis.  No treatment of choice exists for AN. Dermatosis papulosa nigra (DPN)  Dermatosis papulosa nigra (DPN) is a benign cutaneous condition common among blacks.  It is usually characterized by multiple, small, hyperpigmented, asymptomatic papules on the face of adult blacks.  The condition may be cosmetically undesirable to some patients.  DPN is likely to be genetically determined, with 40-54% of patients having a family history of involvement.  DPN is believed to be caused by a nevoid developmental defect of the pilosebaceous follicle.  The incidence in the black population rises from about 5% in the first decade of life to over 40% by the third. The peak incidence rate of the lesions is in the sixth decade of life  Female preponderance was noted at a proportion of roughly 2: 1. Clinical presentation  Dermatosis papulosa nigra (DPN) is characterized by multiple, firm, smooth, dark brown to black, flattened papules that measure 1-5 mm in diameter.  Lesions occur mainly on the malar area of the face and the forehead, although they also may be found on the neck, upper back, and chest. 89 | P a g e
    • Treatment  No treatment generally is indicated for DPN unless lesions are cosmetically undesirable.  Aggressive therapeutic modalities result in postoperative hyperpigmentation or hypopigmentation , scarring or keloid formation.  Therefore, conservative treatment is advisable. Photoallergic and/or Phototoxic Dermatitis  Medications are a frequent cause of sudden skin pigmentation.  Most of the pigmentation is seen in sun-exposed areas suggesting an interaction between ultraviolet light and the ingested medication.  Some known medications that can cause skin pigmentation include anti- malarial medications, anti-seizure medications, and minocycline.  Ingestion of metal preparations that contain mercury, silver, bismuth, arsenic, lead or gold can also contribute to hyperpigmentation.  Most of the time, a relationship is established between drug ingestion and darkening or irritation of the skin. 90 | P a g e
    • Keloids And Hypertrophic Scars 1. Keloids And Hypertrophic Scars  Keloids represent excessive proliferation of collagen (scar tissue) after trauma to the skin.  A scar is made up of collagen fibers deposited in the skin by the fibroblasts to hold the wound closed.  With keloids, the fibroblasts continue to multiply even after the wound is filled in.  Thus keloids project above the surface of the skin and form large mount of scar tissue where as hypertrophic scars are limited to the area of injury and may fade with time.  Keloids are relatively common. The incidence is highest in the age group 10-30 years. Blacks are porn to have keloids: in African population, the prevalence is approximately 6%.  Clinically Keloids appears as an elevated, firm, protuberant nodule or plaque.  New and actively growing keloids often itch but stable and long standing ones are asymptomatic.  Keloids may form on any part of the body, although the upper chest, shoulders and upper back are especially prone to keloid formation.  Symptoms include pigmentation of the skin, itchiness, redness, unusual sensations and pain. Treatments include:  Steroid (triamcinolon) monthly injections; the keloid usually becomes less noticeable and flattens in three to six month's time.  Cryosurgery (freezing) with or without steroid injection  For severe cases, surgical excised and x-ray treatments to the site immediately afterwards, usually the on the same day to be repeated weekly for four to five times.  Surgical removal alone is contraindicated 91 | P a g e
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    • Exfoliative Dermatitis Erythroderma Syndrome “Skin Failure” The exfoliative erythroderma syndrome (EES) is a serious, at times life- threatening reaction pattern of the skin characterized by generalized and uniform redness and scaling Involving practically the entire skin (>90% surface) and associated with systemic “toxicity,” generalized lymphadenopathy, and fever. In the acute and sub acute phases, there is rapid onset of generalized vivid red erythema and fine branny scales; the patient feels hot and cold, shivers, and has fever. In dark skinned ones eythema is not evident but exfoliation.  In the chronic EES, the skin thickens, and scaling continues and becomes lamellar. There is a loss of scalp and body hair, the nails become thickened and separated from the nail bed (onycholysis), and there may be hyperpigmentation or patchy loss of pigment in patients whose normal skin color is brown or black. About 50% of the patients with EES have a history of a preexisting dermatosis, which is recognizable only in the acute or subacute stages. The most frequent preexisting skin disorders are (in order of frequency) psoriasis, eczematous dermatitis (atopic, allergic contact, seborrheic), adverse cutaneous drug reaction, lymphoma, and pityriasis rubra pilaris. Drugs most commonly implicated in erythroderma are found In 10 to 20% of patients it is not possible to identify the cause by history or histology. Pathogenesis  The metabolic response to exfoliative dermatitis may be profound. 93 | P a g e
    •  Large amounts of warm blood are present in the skin due to the dilatation of capillaries, and there is considerable heat dissipation through insensible fluid loss and by convection. Also, there may be high output cardiac failure.  The loss of scales through exfoliation can be considerable, up to 9 g/m2 of body surface per day, and this may contribute to the reduction in serum albumin and the edema of the lower extremities so often noted in these patients. Systemic changes associated with exfoliative dermatitis and erythroderma i. Hypothermia and hyperthermia ii. Fluid and electrolyte disturbance –prerenal failure iii. Sepsis –septic shock iv. Pyrexia occurs due to pyrogens transcutaneously. v. Hypoprotienemia from exfoliation vi. Anemia –from excessive loss and decreased absorption of hematinics vii. Vitamin deficiency states –excessive denand and decreased absorption from the GI viii. By unknown mechanism they have they have GIT disorders such as malabsorption. Possible Etiology of Exfoliative Dermatitis in Adults  Undetermined or unclassified 23%  Psoriasis 23%  Atopic dermatitis, eczema 16%  Drug allergy 15%  Lymphoma, leukemia 11%  Allergic contact dermatitis 5%  Seborrheic dermatitis 5%  Stasis dermatitis with “id” reaction 3%  Pityriasis rubra pilaris 2% 94 | P a g e
    •  Pemphigus foliaceus 1% Physical examination Appearance of Patient frightened, red, “toxic.” Skin is red, thickened, and scaly. Dermatitis is uniform involving the entire body Surface except for pityriasis rubra pilaris, where EES spares sharply defined areas of normal skin. Thickening leads to exaggerated skin folds; scaling may be fine and branny, and may be barely perceptible or large, up to 5 cm, and lamellar. Palms and Soles Usually involved, with massive hyperkeratosis and deep fissures in pityriasisrubra pilaris, Sézary’s syndrome, and psoriasis. Hair - Thinning of hair, even alopecia, except for EES arising in eczema or psoriasis. Nails - Onycholysis, shedding of nails. General Examination Lymph nodes generalized, rubbery, and usually small; enlarged in Sézary’s syndrome. Edema of lower legs and ankles. Diagnosis Diagnosis is not easy, and the history of the preexisting dermatosis may be the only clue. Also, pathognomonic signs and symptoms of the preexisting dermatosis may help, e.g., dusky-red color in psoriasis and yellowish-red in pityriasis rubra pilaris; typical nail changes of psoriasis; lichenification, erosions, and excoriations in atopic dermatitis and scaly eczematous lesions starting form the scalp and seborrheic area may suggest seborrheic eczema. Course and Prognosis Prognosis depends on underlying etiology. Despite the best attention to all details, patients may succumb to infections or, if they have cardiac problems, to cardiac failure (“high output” failure) or to the effects of the prolonged glucocorticoid therapy that may be required. Management 95 | P a g e
    • This is an important medical problem that should be dealt with in a modern inpatient dermatology facility with experienced personnel. The patient should be hospitalized in a single room, at least for the beginning workup and during the development of a therapeutic program. The hospital room conditions (heat and cold) should be adjusted to the patient’s needs; most often these patients need a warm room with many blankets. Topical Water baths with added bath oils, followed by application of bland emollients. Systemic oral glucocorticoids for remission induction and for maintenance (except in psoriatic EES); systemic and topical therapy as required by underlying condition.Supportive cardiac, fluid, electrolyte, protein replacement therapy as required. Skin Manifestations of HIV/AIDS  Up to 92% of HIV/AIDS patient will have one or more skin disorders during the course their illness  The cutaneous manifestations occurring in HIV infection are mostly due to the alterations in the immune system. Presenting with atypical presentation, more disseminated disease, or being resistant to conventional therapies and patient having related disorders eg candidiasis, H. zoster – etc and the general condition of the patient wasted etc  The cutaneous marker are helpful to asses the stage of HIV/AIDS progression where there are no CD4 count and viral load measurements are not available. 1- Seroconversion illness: - Acute primary HIV infection may lead to a transient, generalized, morbilliform eruption on the trunk and the arms. Some 25% will have exanthema 96 | P a g e
    • 2- Skin conditions at early and intermediate stage of the disease With the onset of immunosuppression, skin changes are nonspecific such as common disorders with atypical clinical features, including recurrent varicella zoster, numerous hyperkeratotic warts, treatment-resistant seborrhoeic dermatitis, and oral hairy leukoplakia A. Seborrhoeic dermatitis 85%  seborrheic dermatitis–like eruptions are observed in 85% of patients with AIDS. It may be the initial cutaneous manifestation of HIV disease.  The eruption, which is characterized by widespread inflammatory and hyperkeratotic lesions in seborrhoeic areas, may progress to erythroderma in some patients.  Seborrheic dermatitis may be increased in patients with AIDS- associated dementia or CNS disease.  The immune alterations caused by HIV infection may lead to psoriasis and Reiter syndrome. In some instances, pre-existing psoriasis may become more severe with disseminated plaques and pustules. B. Pityriasis rosea  It may accompany HIV disease with extensive erythematous plaques skin lesion with history of herald patches. They can have repeated episodes of pityriasis rosea. C. Scabies can be found in all forms of HIV. Classical scabies occurs commonly with HIV.  Norwegian (crusted) Scabies Atypical scabies which is characterized by wide spread hyperkeratotic plaque occurs on palms and soles, scaly maculopapular eruption or crusted can occur in classical sites but can also be generalized involving face and all parts of the body D Xerosis (dryness of the skin) and acquired ichthyosis: 25-30% 97 | P a g e
    •  Generalized dry skin syndrome is frequently observed in patients with HIV infection. Xerosis may be the initial clinical manifestation of AIDS, and it is often a cause of pruritus.  Acquired ichthymosis may begin on the lower extremities and disseminate in advanced HIV disease. Acquired ichthymosis may be a marker of concomitant infection with HIV-1 and human lymphotropic virus II in persons who uses intravenous drugs and who have profound helper T – cell depletion. E Herpes zoster- with lower CD4 counts CD4 counts (300-400cell/mm3) it tends to be mutidermatomal or hemorrhagic, disseminated or even ulcerated or recurrent and it also can occur outside limited dermatome. 98 | P a g e
    • F Human papilloma virus (HPV) infection  In patients infected with HIV, widespread or recalcitrant warts may be observed on the oral mucosa, the face, the perianal region, and the female genital tract.  The perianal and cervical lesions may be difficult to treat. Large plantar warts caused by HPV-66 and an epidermodysplasia verruciformis like eruption (numerous plane warts on sun exposed parts of the body), which is believed to be associated with HPV infection, have also been reported in patients infected with HIV. G Pruritic papular eruption (PPE)  PPE is a common cutaneous manifestation in patients infected with HIV.  It manifests as small, itchy, red or skin-colored papules on the head, the neck, and the upper part of the trunk.  The cause is not known.  About 81.25% of patients with PPE have advanced immunosuppression. 3-Skin conditions with advanced disease - In the later stages of HIV disease, chronic HSV, MC, and CMV appears. Mycobacterial infections and mucocutaneous candidiasis occur. a) Oral pharyngeal candidasis b) Oral hairy leukoplakia  Epstein-Barr virus (EBV) has been implicated in the pathogenesis of oral hairy leukoplakia. Oral hairy leukoplakia, which is characterized by filiform white papules localized on the sides of the tongue, may develop in patients infected with HIV.  Oral hairy leukoplakia has no malignant potential, but it may be the initial sign of progressive immunosuppression. White plaques may be confused with oral candidiasis, lichen planus, and geographic tongue. 99 | P a g e
    • c) Eosinophilic folliculitis manifests as an idiopathic, highly pruritic, papulopustular eruption of sterile pustules around hair follicles involving the face, the neck, the trunk, and the extremities. d) Herpes ulcer – chronic herpes simplex ulcer More than 1 month Chronic perianal and perioral herpetic ulcers caused by HSV and disseminated CMV infection. Recurrent oral and anogenital HSV is common in patients infected with HIV, and it may lead to chronic ulcerations. In pediatric patients, herpes simplex stomatitis is more common than varicella zoster virus (VZV), and it may become chronic and ulcerative. e) Cytomegalovirus infection f) Molluscum contagiosum (MC) in adults. Usually occurs in children, but with HIV it can occur in adults. Molluscum contagiosum can become confluent and giant. MC nodules can occur with HIV. g) Bacillary angiomatosis, which is caused by Bartonella henselae and rarely by Bartonella quintana, is usually manifested by red papules and nodules Skin disorders at any stage of HIV Bacterial infections  Impetigo and folliculitis may be recurrent and persistent in HIV disease, particularly in children.  Disseminated furunculosis, gingivitis, gangrenous stomatitis, and abscess formation can occur in patients with HIV infection. Fungal infections Superficial fungal infections 100 | P a g e
    •  Recurrent and persistent mucocutaneous candidiasis is common in patients with HIV infection.  Recurrent vaginal candidiasis is the most common presentation of HIV infection in women.  In adults, generalized dermatophytosis, or Tinea capitis, which is typically caused by Trichophyton rubrum, may suggest HIV infection.   Pityriasis versicolor may be persistent, generalized and recurrent in patients with HIV infection. Deep fungal infections  Cutaneous Cryptococcus may be observed in patients with HIV infection, but it is rare.  Clinical manifestations include cellulitis; papules; plaques; ulcers; or translucent dome-shaped papules with central umbilication, resembling MC.   Cutaneous histoplasmosis may lead to red papules, cellulites - like eruption, ulcerations, acneiform papules, or molluscum - like lesions in patients infected with HIV.  Systemic coccidioidomycosis may disseminate to the skin, usually as hemorrhagic papules or nodules Cutaneous drug eruptions 10%  Sulfonamides may cause urticaria; erythema multiforme; toxic epidermal necrolysis; and systemic reactions, including fever, leukopenia, thrombocytopenia, hepatitis, and nephritis.  Toxic epidermal necrolysis has been reported with antibiotics, fluconazole, clindamycin, phenobarbital, and chlormezanone in patients with HIV. 101 | P a g e
    •  Drug eruptions have been reported as the most common cause of erythroderma in patients infected with HIV.  Photosensitivity has been reported in patients with advanced HIV disease. Photo-induced lichenoid drug reactions may be seen particularly in dark-skinned patients. Aphthosis:- Severe aphthous stomatitis may be associated with HIV disease. Autoimmunity, atopic disease, and urticaria  Thrombocytopenic purpura, vitiligo, alopecia areata, sicca syndrome, pemphigoid, and other autoimmune blistering diseases have been reported in association with HIV disease.  Atopic disease may be reactivated by HIV disease. Atopic eczema may be severe in children infected with HIV. Increased serum IgE levels have been found in these children. However, increased IgE levels were not correlated with atopic symptoms.  Urticaria may occur primarily or as a drug eruption in HIV disease. Hair and nail disorders  Diffuse alopecia or alopecia areata may be associated with HIV disease and may be inflammatory and permanent.  Generalized alopecia can occur in patients with HIV who are treated with indinavir, an antiretroviral protease inhibitor.  Elongation of the eyelashes and softening and straightening of the scalp hair may be observed in HIV disease.  Beau lines, telogen effluvium, and pallor of the nail beds are the general effects of the chronic illness.  Proximal subungual onychomycosis is usually a sign of HIV disease 102 | P a g e
    • HIV-associated malignancies Kaposi sarcoma: -  KS was the first reported malignancy in association with HIV infection.  The worldwide incidence of KS in patients with AIDS may approach 34%.  KS is believed to be a proliferation of endothelial cells induced by human herpesvirus type 8 (HHV-8).  KS begins as pink macules that become disseminated and palpable. Purplish or brown macules and plaques may become nodular. Mucosal involvement is common.  The clinical progression of KS in patients infected with HIV is more aggressive than the other clinical types of KS. AIDS-related B-cell non-Hodgkin lymphomas may lead to skin nodules. 103 | P a g e
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