Dermato venerology science

Hand, foot & mouth disease Epidemiology In young children (adult can also). Occur in warmer month month of summer& earl autumn. Patophisiology Cause :Enterovirus, Coxacie virus A16. Person to person, oral-oral, fecal-oral, respiratory rules via contact with nose & throat discharges, respiratory droplets, bister fluid &/ sheed. Moderately to highly contagious : most contagious during firstweek. Not transmited to or from pet or animals EC: foot & mouth disease of catle, sheep, swire. Clinical features Brief prodorme to several days, low grade fever, malaise, vomiting, loss of appetite, abdominal pain or respiratory symptoms. Combination of oral & cutaneous finding. Oral lesion are more frequent, ginggiva, bucal mucosa, tongue & hard palate. Early lesion : Small, paintfull,3-7 mmm erymathous, macula, papula progress to form grey, thin- walled vesicles Ulceratifa. Average number of oral lesion 5-10. Lesi2 yang kecil dapat bersatu besar. Cutaneous lesion appear concomitant, with or shortly after mucosal lesion. Hands are more common than feet. Can be > 100 lession, painful, hot proritic. Usually infection in mild lesion residue with out treatment & complication in7-10 days. Diagnosis: Diagnosis is made clinically with: Ferver with ulceration, hand &foot exantem. Viral culture of the throat, secretions, blister fluid, stool &blood. Skin biopsy intraepidermal or subepidermal vesicles with liticular &ballooning degeneration. Diferential diagnosis: Apthous stomaitis not associated with systemic symptoms &cutaneus lesion. Herpangina: ussualy ulcerations of posterior pharynx, soft palate, tonsil or uvula. Herpes viral infection. Varicella: more generalized in face & trunk. 3&4 are more often.

Group A stereptococcal infection : not associated witf hand &foot vesicular eruption. Erythema multiforme: lesions are more targetoid& persisten Treatment Usually resolves spontaneously in weeks with supportive care tropical oralviscous Lidocaine or aptitous ulcer, oral acylovir. Peventive: good hand-mwashing technicque after diaple changes & scaled clothing laundered.

Measels (robeolla)- very often. Epidemiology. Etiology : paramyxovirus : morbilivirus. Differ from morbus (plaque). Spread wit direct contact with infectious droplet or air borne spread. Common in winter & spring. The first disease of six exanthematous disease Patophisiology. Incubation of this ss RNAvirus from exposure to onset of symptoms 8-12 days. There is conflicting information as to whether the rash as the result of Ag-Ab complex deposition or direct invation of local tissue by the virus. Clinical feature. During incubation period: virus may be culture & from the mucosa. Symptomatic prodorme phase (4 days): fever, malaise, cough, conjunctivitis, coryza (3c robeola). Prior to rash :koplik spot: white to bluish spot on an erythemathous base, found on bucal mucosa fading by the time apparent of cutaneous eruption. The rash begins on thhe hand & neck downward. Rash forms over 3 days the sickest time Rash fades in the same order it appear brownish or coopery. The leg lesion ussualy stays individually & discrete. Faad & lesion usually confluent. Complication: Pneumonia, encephalitis, exacerbation of TBC, sub acute scleroting pan encephalopaty late complications. Diagnosis& DD Diagnosis made clinically. Blood, urine, pharynk culture. Treatment: Supportive therapy. Vit A (200.000 IU for 3 dose).

Measles spesific imunoglobuline for infant <1 years old, imunocompromised patients, pregnant woman. Beware of 2nd infection. PROPHYLACTI are not recommended. Prevention :immunization. Rubella Patophisiology. Incubation 14-21 days. The virus. Intrauterin infection: first semester. Clinical features : Prodorma period : mild VR/ Low grade fever, conjunctivitis, headache, lymphadenopati (cervical, aciphital, postauricular). Flushy macular & popular start on face rapidly migrated to trunk, face become clear. Pruritus & mild desquamation. Trombositopeni. Diagnosa: Cell culture. Heamaglutination- inhibition for antirubella antibody test. IgM for detected intra uterine infection, Neonatal rubella: cardiac ,ocular, auditory, ortophedia. Treatment: Supportive treatment. Best treatment is prevention through immunization.

HIV disease Epidemiology: Transmited by sexual contact, Contaminated IV instrument, trans placentaly, needle stick injuries. Patofisiologi Untreated infection of HIV cause a depletion of Cd4 & lymphosites Impaired imunity. Clinical features Exantem of HIV occurs after exposure &inoculation

Symptoms may be relatively abrupt in onset & associated with fever, malaise, mtalgia, sorethroat & lymphadenopaty. Truncal macular of macular-papular erythematous or morbiliform eruption face & uperbody. Roseolar like on the face, neck, shoulder & trunk. Eruption usually resoluted within 2 weeks. Diagnose: Confirmation of seroconvertion to the HIV virus. Elisa test can detect 1-3 month after infection. Examination for P-se antigen, PCR (recently use) or HIVRNA assay. May detect within the first month. Treatment.

Parasite manifestation Infertation & parasiter 1. Scabies (the most common). Epidemiology Pathophysiology Clinical features Diagnosis & Differential Treatment Epidemiology: Sarcoptes scabiei variation hominis, is the ectoparasitic mite that causes the human infection called scabies. Infestations are acquired through direct cutaneus contact with another infested person. Most commonly affected are children. Millitary barrachs, nursing home, day care centers commonly experience out breaks. Patofisiologi: Scabies mite is arounded, 8 legged arthropod. The female mite burrows inside the epidermis creating tunnel, 2-3 eggs/day are produced, the eggs batch within 4 days releasing larvae, which molt a adults in up to 14 days, a life span of approximately 30 days. The male mite follows and dies after a mating. Can live up to 30 hours away from human host. Mites feed on intercellular fluid for nutrition and hydration. Clinical features Intense pruritus, particulary at night, occurs from delayed hypersensitivity response to antigens found in the saliva, feces, and eggs of the mites. Symptom occurs 2-6 weeks after initial infestation, however, symptoms may appear as early as 24-48 hours after infestation. In the imunocomprimized itching may be absent heavier infestation, more contagious due to the high concentration of mites in the epidermis crusted scabies/ NORWEGIAN SCABIES. NB: scabies tidak selalu gatal misalnya pada orang yang belum pernah terkena scabies, baru timbul gatal lama.terutama pada pasien immunocomprimised.

 Mites are typically found in adults in intertriginous areas such as web patch of fingers and toes, groin, axillae, wrists, genitalia & intergluteal cleft. In children scabies affecting the palms, soles, scalp. Skin lession includes burrows, erythematous, papule, pustules. Itching leads to scratching, produce excoriated skin, scaling, crusting & hiperpigmentation. Borrow lesions is a strong clue to the diagnostic, typically presents as ashort, zigzag line with a small black dot at the end.The like is the tunnel and black dot is the mite it self. Pathognomic clinical sign of scabies in men is erythematous papules/nodules on the glans penis. Dignosis Clinical history, visualization of the mite eggs, fecal pellets. An ectoparasite preparat is performed by applying a dab of immersion oil on suspected skin lesion, scrapping the lesion with # 15 scalpel blade/ensuring the epidermis in removed by noting bleeding in the skin after the scape, placing the scrapings in immersion oil on a glass slide and viewy via light microscope. Diagnosis Differential Atopic dermatis bedakan dgn history Contact dermatitis Dermatitis herpetiformis Folliculitis Impetigo Insect bites Xerosis Treatment Permethrin cream 5% ( scabimid ) ; spread over the skin from head to toe and under nails, avoiding the eyes and mouth, before bed and is rinsed off in after an 8-14 hours duration, then repeated in 1 week. Ivermectin 200 mg/kg oral single dose tepeated in 1 week/include Immunocomprimised. Pruritus can be treated with adjunctive therapy, oral antihistamine, topical steroid moisturizing. Inform patients that pruritus may continue for up to 4 weeks after affective treatment. Follow up after 4 weeks. Launderiy all clothing and bedding

2. Lice Lice are glegged, wringles,blood sucking athropods tjhat infest humans. Three spec of lice that cause infestation inhuman: 1) Pedicullus humanus capitis/ head louse. 2) Pedicullus humanus corporis/ body louse 3) Phihinus pubs/pubic or crab louse Head lice Can infest the scalp at any level of social class, most commonly affected chidren. African American have lowest rates of head lice infections, why? Because of their hair types African kribo/kriting. Body lice Found on the clothing of homeless, refuges, unsanitary condition. Pubic lice considerated to be a STD (sexual transmitted Dissosiation) Pathofiosiology Transmition can occurs asa result of direct contact/ expose to contaminated items, such as bedding fowels,sharing of items, such as combs,bushes,hats xport and equipment. Cant transmitted to/from animals. Live for 30 days, up to 3 days without host. After mating, female lice produces up to 120 eggs, that of lued tohair shaft/ head pudi louse or clothing/ body loose.The eggs hatch within 9 days. After infestation has accured, the lice begins takingblood neals from their host, 3 6 hours. Clinical feature Prority due to the lice feces, body part, lice saliva when lice feed. It maytake weeks to months for the proritus to develop. If the patient has had aprecious infestation, the prurity to may begin much faster 1-2 days. Erythematous maculy, papuly, wheals as a cutaneous immune response where the lice have taken blood meals. Secondary bacterials infections may develop as result of slkin as excoriation due to scratching, if chronic, this infections may lead to licheniflaction ( penebalan kulit ) & hyperpigmentation skin. Low grade fever lymphadenopathy & anemia. Chronic infestations can cause a bluish ( paha ) macilan discoloration of the skin on the abdomen and things referred to as macular ceruleae. Diagnosis

 Direct examination & observation of adult lice or nits on skin, clothing/hair. Head lice often be found in the retro auricular & hape of the reac area. Pubic lice can infest the eye lashes & is called phthiriasis palpebrarum. Diagnosis differential Scalp folliculitis Seborrheic dermatitis Atopic dermatitis Psoriasis Insect bites Scabies Treatment Dermethrin 1% ( cream rinse ) 5 % ( cream ) 2 treatments 1 week apart are required. Single, oral dose of luermectin at 200 mEq/kg repeated in 10 days fode effective in the eradication. Clean individuals personal belonging & environtment Commercial environment pesticides should not becaused. Secondary infection antibodies Treatment head lice 1 % permethrin clean rinse to damp scalp for 10 minutes repeated in 1 week in resistant case, increase duration for 30 minutes, use 5% permethrin cream overnight. Repeated in 1 week Investigating to source Metal nit cob Shave the head Treatment body lice Focus desinfectan of clothing & bed Permethrin ( dose like head lice ) Repeated 1 weeks Treatment public lice Dont forget perineal region Topical 5% permethrin cream. For pthriasis palpebrarum, trimetropim bactrim 2 dd, sulfametoxazole/tetracycline 10 days, betroleum jelly tothe eye lasses. Five times a day for 10 days.

Bacterial infection IMPETIGO. Cause by staphy aureus, most common. Also by streptococcus pyogenes/ hemoliticus. Frequently seen in children. Can occur primarily as primary infection or secondarial eevent. Bulous impetigo. Caused by phage 71 type coagulase positive staph-aureus or related group2 phage type, occurs primarily in newborn infants (age 4-10 days). Its highly confergious in nurseries, but occur in adult in warmer climates. Primary infection: Infected children. Pets. Fingernails. Hair cutteries Secondary infection: Scabies. Herpes simplex. Insect bites. Dermatitis.

Patofisiology: Infection arises as the result of superficial breaks in the skin,which allow bacteria to invade. Histologically there is vesicopulmonale containing few cocci, neutrophhyls & epidermal debris. A mild inflammatory reaction is seen in the dermis. IN bullous impetigo, S aureus produces a toxin capable of producing a spleit in the superficial epidermis, resulting in bullae formation. Clinical features. Impetigo generally begins as a superficial vesicle or pustule, which ruptures turning in to Crusted evatin honey comb app The lesions are typically found on the nose, cheek, lips, chin. Impetigo contangiosa Superficial erythematous macule develop into vaesicule or bullae.

These lesions rupture releasing a staw coloured disharge, which dried and give a honey colloured cruta, there may be local lymphadenopaty. Occurd primarily on exposed parts of the body face, hands. Bullous impetigo. Vesiclles & bullae arise with surrounding erythema. These easily rupture forming an eruption. Lession most commonly occur on the face, hands of the children. Diagnose Predominantly a clinical diagnosis. Lessions mar be culture for isolation & sensitivity. Circular patches,especially in children, may resemble tinea, however tinea usually has more scalp, erymatheous in the edge of the placque. Diferential diagnose: Ecthyma. Herpes simplex. Varicella. Pemphigus vulgaris. Contact dermatitis. Bullous pemphigus. Treatment Topical & combined with oral antibiotics, cephalosporin. Soak eith warm compress. Reccurent patient ,may be harboring S.Aureus in their nares. Most cases respond quickly to therapy without scarring. Echtyma: Caused by S. Pyogenes&/ S. Aureus. Usually seen in patients with preceeding trauma, poor hyigiene, malnutririon, drug abuse, HIV. (Lecturer by : Dr.Wong Hendra,Sp.Kulkel)

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Notes from : T-Pen/2002 Writers: Irene M E/2002 Lisa limbardo/2002