Viral Diseases Herpes Simplex Virus (HSV) Painful, recurrent vesicular eruption of mucocutaneous surfaces HSV-1: Oral-labial lesions

HSV-2: Genital lesions Virus spreads through epidermal cells fuse into giant cells  Local host inflammatory response erythema + swelling Initial infxn passed by direct contact in local nerve ganglia virus remains dormant Clinical Tzanck smear of vesicle base: multinucleated giant cells *VSV has same appearance on Tzanck, so cx or direct IF Ab staining needed for definitive dx Oral or IV Acyclovir  Frequency + severity of recurrences Daily acyclovir, famciclovir suppressive therapy  Pts w/ >6 outbreaks per year  Pts w/ EM In AIDs pts HSV can persist, ulcers remaining resistant to antiviral therapy

Primary episodes: longer, more severe than recurrences Onset: preceded by prodromal tingling, burning, pain  Can also present w/ lymphadenopathy, fever, discomfort, malaise, edema Recurrences: limited to mucocutaneous areas innervated by involved nerve  Recurrent oral (HSV-1): common cold sore - cluster of crusted vesicles on erythematous base. Trigger: sun, fever  Recurrent genital (HSV-2): Unilateral, cluster of blisters on erythematous base, less pain + systemic involvement than primary Pruritic papules + vesicles on elbows, knees, buttocks, neck, and scalp Prodrome: malaise, fever, headache, myalgia 24 hrs before rash onset Pruritic lesions over 2-3 days (dewdrop on rose petal)  Lesions in all stages of development over entire body  Palms and sole SPARED! In adults: More severe  Systemic complications (pneumonia, encephalitis)

Dermatitis Herpetiformis Varicella (Chickenpox)

Associated w/ celiac disease (15-25% have it) Transmission: respiratory droplet or direct Incubation: 10-20 days Contagious: 24 hrs before eruption until lesions crust In first trimester  Microcephaly  Chorioretinitis  IUGR  Cataracts

Bx: Granular IgA on dermal papillae clinical

Dapsone Gluten-free diet Self-limited in healthy children- Benadryl Infants, children, adults: Vaccine Adults: Acyclovir Neonates:  VZIG if mom contracted w/in 5 days of delivery

Herpes Zoster

Recurrence of VZV in specific nerve

Lesions preceded by intense local pain then arise as grouped blisters on erythematous base  Dermatomal In immunocompromised: can lead to  severe local dz  Disseminated cuteanous dz  Systemic dz Older pts: Postherpetic neuralgia

clinical

Acyclovir **Pain control most important

Molluscum contagiosum

Poxvirus infxn MC in young children + AIDS pts Spread = physical contact

Tiny waxy papules, central umbilication Asymptomatic unless inflamed/irritated Children: trunk, extremities, face Adults: genitalia, perineal region AIDS: Face, large **If see giant molluscum contagiosum HIV

Clinical Confirmed by expressing/staining contents of papules y Giemsa or Wright s stain Large inclusion or molluscum bodies

Any local destructive method:  Curetting, freezing, or trichloroacetic acid Resolve spontaneously over months-years @ untreated in children

Verruca/condyl oma (Warts)

Pathogen: many different types of HPV Location: skin, mucous membranes, other pithelia Usually benign, some subtypes of HPV (16 + 18) squamous malignancies Spread: direct contact HPV hyperproliferation of infected cells *Long latency period. Children sometimes acquire HPV at birth w/ no manifestation until years later

Common warts: Most prevalent HPV  Hands  Palmer + Plantar: grown downward into skin flatter appearance Genital: Cauliflower-like papule or nodule appearing  Glans penis, vulva, perianal region Mucous membranes: velvety + white  Oral, genital, laryngeal mucosa (transmitted to infants by mothers w/ genital HPV)

Clinical Acetowhitening (mucosal lesions)

Destruction of tissue:  Curette, cryotherapy, or acid keratolytics Genital warts:  Local podophyllin, trichloroacetic acid, imiquimod, or 5-FU Cervix:  Must be monitored cytologically + histologically for evidence of malignancy

BACTERIAL INFECTIONS
Impetigo Superficial, weeping local infxn Primarily in children Pathogen: Group A strep (B-hemolytic) and Staph Spread = direct contact ERYSIPELAS Group A Strep Common type: Pustules, honey-colored crusts on erythematous base; Face Bullous type: Acral; Large stable blisters  Almost always caused by S. aureus  Can evolve into SSSS Pts have hx of trauma or pharyngitis Small red patch on cheek Turns into painful, raised, shiny red plaque Scarlet fever S. pyogenes sunburn w/ goosebumps appearance Strawberry tongue Salmonella typhi Small pink papules on trunk ( rose spots ) in groups of 10-20 PLUS gallbladder disease! Pathogen: Crynebacterium More common in diabetics Gram stain: + filamentous rods Cellulitis Deep, local infxn involving CT, subq tissue, or muscle in addition to skin Common pathogen: Staph or group A strep. Originating from damaged skin or systemic source of infxn Community acquired MRSA is common risk Risk factors:  Diabetes  IV drug use  Venous stasis  Immune compromise Necrotizing fasciitis Deep infxn along fascial plan severe pain followed by anesthesia Pathogen: S. pyogenes or Clostridium perfringens **Fournier gangrene = localized to scrotum + perineal area Erythema quickly spreads over hrs-days  Margins move into normal skin  Skin becomes dusky/purplish necrosis  If skin is open, gloved fingers can easily pass btw two layers to reveal yellow-green necrotic fascia Most important signs: tissue necrosis, putrid discharge, bullae, severe pain, gas production, rapid burrowing through fascial planes, lack of classical tissue inflammatory signs, intravascular volume loss Folliculitis Inflammation of hair follicle Pathogen: Staph, Strep, and Gram Bacteria, occasionally yeast (Candida, Pityrosporum ovale) *Pseudemonas aeruginosa Mechanical (ingrown hairs) risk: Diabetes, Immunosuppression Can be critical problem in AIDs pts (intensely pruritic + resistant to therapy) Acne Chronic inflammatory condition of pilosebaceous unit Pathogenesis: y Hormonal activation of sebaceous glands y Comedo (plugged sebaceous follicle) y Propionibacterium acnes in follicle inflammation y Meds (lithium, corticosteroids) Begins at puberty Face, back, upper chest (greatest density of sebaceous follicles) Comedo:  Open comedones (blackheads)  Close comedones (whiteheads) Inflammatory:  Comedo ruptures Scar: picking at papules Clinical Mild comedonal acne topical retinoid: y Tretinoin (retin-A) + benzoyl peroxide Mild popular or pustular acne  Topical Erythromycin/ clindamycin  Systemic: tetracycline (photosensitivity), erythromycin **Severe acne or moderate acne, primarily nodulocystic, failing previous tx or have scarring Isoretinoin (Accutane) y Teratogen!! y Associated w/ depression y *Monthly blood tests (B-hcg, LFTs, cholesterol, TGs) Clinical r/o perirectal and anal abscess Incision + Drainage hot tub folliculitis Tiny pustule- usually has hair penetrating it Furuncle: deeper hair follicle abscess  Larger and more painful  May disseminate to adjacent follicles carbuncle Clinical Mild: Topical antibiotics Severe: Systemic antibiotics Large lesions: incised, drained, cultured to r/o MRSA Hx of trauma or recent surgery to affected area Sudden onset of pain + swelling at site anesthesia Biopsy (from edge of lesion) Strep: Penicillin G Aerobic: metronidazole or 3 -gen cephalosporin
rd

Clinical

Antibiotics w/ anti-staph activity

Penicillin

Penicillin

Cholecystectomy for chronic carrier state

Erythrasma

Brownish-red patches w/ fine scales  Along major skin folds

Woods light exam: coral-red fluorescence

Erythromycin (erythrasma = erythromycin)

Red, hot, swollen, tender skin Fever + chills common Regional lymphadenopathy

Clinical Wound culture (may help aid + sensitivities) Blood cx (when bacteremia suspected) R/o abscess, urticaria, contact dermatitis, osteomyelitis, and necrotizine fasciitis

Oral antibiotics 7-10 days Systemic toxicity, comorbid conditions, DM, extremes of age, hand or orbital involvement:  IV antibiotics

Local radiographs or CT : air in tissue

SURGICAL EMERGENCY! Early + aggressive surgical debridement

pustule (large/nodular)

Pilonidal cysts

Abscesses in sacrococcygeal region Repetitive trauma plays role Starts as folliculitis abscess complicated by perineal microbes (Bacteroides) MC btw 20-40, Men > women Risk: deep/hairy natal clefts, Obesity, Sedentary lifestyle

Abscess at natal cleft tender, fluctuant, warm and indurated *May develop into perianal fistulas

FUNGAL INFECTION Tinea versicolor Infection w/ Malassezia furfur (normal skin yeast) Risk: Humid and sweaty conditions, oily skin, Cushings syndrome, Immunosuppression Chest and back Small, scaly patches of varying color Pale, velvety pink or whitish, hypopigmented macules or hyperpigmented (thickened scale)  Do not tan and are NOT scaly  Scale on scraping Oral: painless white plaques, cannot easily be scraped off Risk: antibiotics, steroids, diabetes Skin: pink, circular, erythematous macules that converge, with smaller satellete lesions nearby in skinfolds Infants: diaper area along inguinal folds Diaper: Topical nystatin Dermatophyte infections Dermatophytes live only in tissues with keratin (skin, nails, and hair) Organisms: Microsporum, Trichophyton, Epidermophyton Risk: Pets, diabetes, peripheral circulation, immune compromise, chronic maceration of skin (athetic activities) Tinea corporis: scaly, pruritic eruption w/ sharp, irregular border central clearing  Immunocompromised or children following contact w/ infected pet Tinea pedis/manuum: Chronic interdigital scaling w/ erosions btw toes ( athletes foot ) or thickened, scaly skin on soles  Assymmetric involvement of hands typical Tinea crurus ( jock itch ): chronic infxn of groin (spares scrotum) Tinea capitis ( ringworm ): diffuse, scaly scalp eruption similar to sebhorreic dermatitis Clinical KOH prep: hyphae Topical or systemic antifungals *Tinea capitis must be treated w/ systemic drugs Clinical KOH prep: spaghetti and metaballs pattern of hyphae and spores Topical selenium sulfide daily x 1 week Ketoconazole shampoo *Inform pt. change in pigmentation takes months to return to normal

Candidasis

Clinical KOH prep: hyphae + pseudospores

Oral: Oral fluconazole; Nystatin swish and swallow Skin: Topical antifungals; keep skin clean and dry

PARASITIC Lice Live off blood Head louse: scalp, layes eggs as nits attached to hair Body louse: clothing; bites only body Pubic lice ( crabs ): anticoagulant in saliva blue bites Pubic louse: pubic hair Spread: body contact or sharing bedclothes/garments Secrete local toxins pruritis Scabies Pathogen: Sarcoptes scabiei (mates on skin surface female digs passage into stratum corneum lays eggs). Burrowing pruritis intensity when allergy develops Spread: close contact Hx of pruritis in several family members Pruritis may persist 2 weeks after tx, so provide symptomatic tx Intense pruritis, especially at night + after hot showers MC sites: hands, axillae, genitals Exam: track seen, erythematous, excoriated papules Mite may be identifiable by scraping intact tunnels and looking under microscope Severe pruritis, secondary bacterial infection of excoriations Classroom epidemics common Body lice: inadequate hygiene, crowded living conditions Seen on hair follicles or clothing Head lice:  OTC pyrethrin (RID) + mechanical removal of nits Body lice:  Wash body, clothes, and bedding thoroughly  Topical permethrin or pyrethrin Pubic: RID

Overnight: 1-2 applications of 5% permethrin cream from neck down *Contacts treated as well! Oral ivermectin

ISCHEMIC DISORDERS Decubitus ulcers Continuous pressure on skin restricts microcirculation Ischemic necrosis Incontinence of urine or stool ulceration MC in bedridden pts High grade: surgical debridement Risk: underlying bony predominance, fat, lack mobility, lack cutaneous sensation Venous stasis ulcers Near lateral or medial malleolus Associated w/ lower extremity edema Compression (unna boots or compression sockings) + Elevation macerates skin Grade III: destruction of structures beneath skin (muscle or fat) Low grade: wound care (hydrocolloid dressings) Grade I: Perisstent redness Grade II: Ulceration Clinical *Prevention is key!  Routinely move bedridden pts (special beds)

Arterial insufficiency Neuropathic ulcers Gangrene Necrosis of body tissue Dry: insudfficient blood flow to tissue; atherosclerosis Wet: baterial infxn w/ skin flora Gas: clostridium perfringens infxn

Heel + tips of toes Very PAINFUL Underside of foot + toes At pressure points. PAINLESS Dry:  Early: dull ache, cold, and pallor of flesh  w/ necrosis (usually toe) becomes bluish-black, dry, and shriveled  Risk: Diabetes, vasculopathy, smoking Wet:  tissue appears bruised, swollen, or blistered w/ pus Gas:  At site of recent injury/surgery  Swelling around injury, skin turns pale then dark red  Bacteria rapidly destructive of tissue gas separates Clinical Surgical debridement, amputation if necessary *Antibiotics alone do NOT suffice (d/t inadequate blood flow) but given as adjuvant to surgery Gas gangrene:  Hyperbaric O2 (toxic to anaerobic C. perfringens)  Susceptible pts should maintain careful foot care and avoid trauma

healthy tissue predisposes to infxn  MEDICAL EMERGENCY!

MISCELLANEOUS SKIN DISORDERS Acanthosis nigrans Sin in intertriginous zones (genital and axillary regions, nape of neck) is hyperkeratotic + hyperpigmented w/ velvety appearance Associated w/  DM  Obesity  HAIR-AN Syndrome  Cushing disease  Gi adenocarcinoma (paraneoplastic syndrome) Lichen planus Chronic inflammatory dermatosis involving skin + mucous membranes Middle-aged women between 30 and 60 Intense pruritis, can be induced by drugs, associated w/ Hep. C P disease:  Planar, Polygonal, Purple  Pruritis, Persistent  Penile, Perioral, Koebner s phenomenon Rosacea Chronic inflammatory condition w/ facial flushing, localized erythema, telangiectasia, papules, and pustules Women, middle-aged 30-50, abnormal flushing response to various substances Do NOT have comedones (vs. acne) Environmental triggers (infectious agents, sunlight, certain foods/drinks) Pityriasis rosea Acute dermatitis pink + scaly Rxn to viral infxn w/ HHV 6 or 7  Tends to occur in mini-epidemics among young adults Initial lesion: Herald patch (several cm + erythematous w/ a peripheral scale) Days-weeks: multiple tiny, symmetric papules w/ fine cigarette paper scale.  Christmas tree pattern : papules arranged alone skin lines on pts back Pts generally asymptomatic Clinical KOH (r/o fungus) Differential:  Secondary syphilis (RPR) (Systemic sx)  Guttate psoriasis (smaller, thicker scale)  Drug eruptions Clinical Histo: total absence of melanocytes r/o: postinflammatory hypopigmentation, scleroderma, piebaldism, toxin exposure (phenolated cleaners = toxic to melanocytes) Early: Central facial erythema w/ telangiectasias Later: Papules and pustules Associated findings:  Ocular keratitis (gritty sensation in eyes)  Rhinophyma (sebaceous gland hyperplasia of nose) Clinical Urinary 5-HIAA (r/o carcinoid syndrome) Serology (r/o SLE) Voilaceous, flat-topped, polygonal papules Wickmans striae (white stripes), esp. on mucous membranes Koebner s Phenomenon: lesions appear at site of trauma Histology: lichnoid pattern band of T lymphocytes at epidermal-dermal jxn w/ damage to basal layer Mild: topical steroids Severe: Systemic steroids Oral mucosa: Tretinoin gel *Most cases resolve spontaneously 6-18 mo. Oral have more chronic course. Fasting glucose to r/o insulin resistance Topical retinoids but typically not treated Encourage to lose weight!!

Avoid triggers that aggravate vasodilation (coffee, tea, hot drinks, spicy foods, chocolate, alcohol) Mild: low-potency topical steroids or topical metronidazole Severe cases: Both oral + topical therapy Heal w/out tx in 2-3 weeks Skin lubrication, topical antipruritics, systemic antihistamines Severe: short course of systemic steroids

Vitiligo

Disease of depigmentation Chronic + Progressive Serologic markers of autoimmune dz  Anithyroid Abs, DM, pernicious anemia Pts w/ malignant melanoma may develop antimelanocyte immune response vitiligo

Small, sharply demarcated, depigmented macules/patches on otherwise normal skin  Hands, face, genitalia Peri-orificial lesions or lesions on finger tips Total depigmentation (vs. lightened in tinea versicolor)

Topical/systemic psoralens Exposure to sunlight or PUVA Must wear sunscreen (depigmented skin lacks protection)

DYSPLASIAS Seborrheic keratosis Benign thickening s of epidermis Very common, almost in all pts >40 When may erupt suddenly, may be part of paraneoplastic syndrome (d/t tumor production of epidermal growth factors) NO malignant potential! Actinic keratosis Pre-malignant lesion  Predisposes pt to SCC in situ Outdoor occupation (excessive sunlight) Middle aged/Older men Dry, scaly papules w/ erythematous base  Sandpaper-like texture Face, lower lip, hand dorsum, forearms, bald scalp, ears
nd

MC = back and chest >50 years Exophytic, waxy brown, stuck on appearing papules/plaques May become irritated spontaneously or by external trauma (esp. in groin, breast, or axillae)

Clinical diagnosis Histo: hyperplasia of benign, basaloid epidermal cells w/ horn pseudocysts (prominent follicular openings) r/o actinic keratosis, lentigo (focal in melanocytes), SCC, and BCC Clinical Bx (r/o SCC): intraepidermal atypia over sun-damaged dermis DDx: Bowens disease (form of SCC in situ) Clinical Confirmation: Biopsy  Necessary for dx + therapy  Intraepidermal atypical keratinocytes w/ penetration of BM by malignant epidermal cells growing into dermis Graded histologically

No treatment necessary d/t benign nature Removed for cosmetic reasons

Cryosurgery, topical 5-FU, or topical imiquimod If carcinoma suspected:  Excision/curettage Advise pts to use sun protection Surgical excision or radiation

Squamous cell carcinoma

2 MC skin tumor locally destructive effects + potential for metastasis + death MCC = UV light Other:  Chemical carcinogens  prior radiation therapy  chronically draining infectious sinuses (osteomyelitis) Older adults w/ sun-damaged skin, arising from actinic keratosis

Arise from actinic keratosis rarely metastasize Lips down or ulcers that won t heal more likely to metastasize

Keratoacanthoma

Benign epithelial tumor

Looks like SCC but develops more rapidly and may regress spontaneously Varying degrees of pigmentation, ulceration, and depth of growth Upper lip up Pearly nodule w/ rolled border Clinical Confirmation: biopsy  Islands of proliferating epithelium resebling basal layer of epidermis Differential:  Benign tumors  Hypopigmented melanocytic nevi  Melanoma  Dermatitis  Psoriasis  Pagets disease First growth phase: horizontal-intraepidermal flat but in diameter (typical of lentigo maligna or melanoma in situ) Later: vertical growth phase (dermal invasion)  Pruritis = early sign of malignant change Characteristics:  Irregular pigment  Irregular contour + border  Nodule and ulcer formation  Changes in size/shape/color/contour/surface Classic variant:  Multicentric vascular macules + coalescent papules/plaques on lower extremities  Elderly Ashkenazi Jewish or Mediterranean descent More disseminated cases:  African KS (endemic KS)  Immunocompromised Epidemic HIV-associated KS  Aggressive form of dz  Most common HIV-associated malignancy Total excision biopsy Malignancy determined histologically Staged by Breslow s thickeness and tumor-node-metastasis (TMN) Clark s level = another classification system linking melanoma depth to prognosis

Similar to SCCs

Basal cell carcinoma

MC Malignant skin tumor Slow growing, locally destructive, virtually NO metastatic potential MC Risk: Chronic UV light Multiple lesions on non-sun-exposed areas more suggestive of arsenic exposure or inherited basal cell nevus syndrome Location: Face, other sun-exposed areas

Excision, curettage and electrodesiccation/cautery, deep cryotherapy, superficial radiation therapy, and Mohs surgery Cure rates >95%

Melanoma

MC life-threatening dermatologic dz Risk:  Short, intense bursts of sun exposure (esp. in childhood + w/ intermittent exposure)  Congenital melanocytic nevi,  # of nevi,  Dysplastic nevi,  Immunosuppression Genetics: Familial atypical mole, Melanoma (FAM-M) syndrome

Confined to skin:  Excision w/ margins  LN dissection for staging Malignant:  Potential to relapse after several years  Pts w/ early melanoma at low risk for relapse but high risk for subsequent melanomas  Pt. surveillance essential Palliative

Kaposi s Sarcoma (KS)

Vascular proliferative dz attributed to herpesvirus, HHV-8, also called Kaposi s sarcomaassociated herpesvirus (KSHV)

Hx and clinical impression Biopsy: spindle cells (elongated tumor cells) w/ +HHV-8 staining  Presence of viral protein LANA in tumor cells

Mycosis fungoides (CTCL)

Slow, progressive neoplastic proliferation of T cells. Not a fungus. Pathogenesis: Chronic immunostimulation helper T cells to gather in epidermis Risk: Industrial exposure to irritation chemicals Chronic, More common in men

Early lesion: nonspiecific, psoriatic-appearing plaque palpable, pruritic Stage 1: limited plaques, papules, + patches <10% BSA w/ NO nodes Stage II: limited or generalized skin involvement + palpable LNs or u1 skin tumors w/ multicentric, confluent reddish-brown nodules Stage III: generalized erythroderma Stage: IV: biopsy positive LNs or internal organ spread Pts may have dermatopathic lymphadenopathy w/out actual tumor involvement of node. However, internal organs can be involved (LNs, liver, spleen)

Clinical + Histology Sezary or Lutzner cells (cerebriform lymphocytes) Early lesion: clinically indistinguishable from dermatitis @ Histological diagnosis indicated for any dermatitis that is chronic + resistant to treatment

Stage I: Topical steroids, retinoids, chemo, or PUVA Stage II: Systemic retinoids, interferon, monoclonal antibodies, or chemo Photopheresis = mainstay of tx More extensive/advanced: Radiation therapy

Sezary s syndrome: leukemic phase of CTCL circulating Sezary cells in peripheral blood, erythroderma, + lymphadenopathy

Lupus erytehmatosus (discoid, subacute, SLE)

Multisystem autoimmune dz related to Abmediated cellular attack + deposition of AgAb complexes Risk: African Americans Usually affects women of childbearing age

Nonspecific sx: fever, anorexia, weight loss, symmetric joint pain *Have 4 criteria D Discoid rash O - Oral ulcers P Photosensitivity A Arthritis M Malar rash I Immunologic criteria N Neuro sx (Lupus cerebritis, seizures) E Elevated ESR R Renal dz (proteinuria, casts) A ANA + (highly sensitive, not specific) S Serositis (pleural or pericardial effusion) H Hematologic abnormalities (Anemia, Leukopenia, thrombocytopenia)

Mild joint sx: NSAIDS Acute exacerbations:  Corticosteroids Progressive refractory cases:  Corticosteroids  Hydroxychloroquine  Cyclophosphamide  azathioprine

Scleroderma

Inflammation excessive deposition of type I and III collagen progressive tissue fibrosis CREST Syndrome (limited form) Diffuse form: skin, GI, GU, renal, pulmonary, and cardiovascular systemis Risk:  Female  Age 35-50

Raynauds, dysphagia, mask-like face, tight skin Symmetric thickening of skin face and/or distal extremities Associated w/ CREST Syndrome (limited form):  Calcinosis  Raynauds phenomenon  Esophageal dysmotility  Sclerodactyly  Telangiectasias Diffuse form:  Pulmonary fibrosis  Cor pulmonale  Acute renal failure  Malignant HTN Macroglossia, waxy papules on face Primary systemic (AL) and Seconary systemic (AA): Kidneys, heart, liver Alzheimers dz: Brain

RF and ANA may be + Anticentromere Abs (specific for CREST) Anti-Scl-70 (antitopoisomerase 1) Abs associated w/ diffuse dz and poor prognosis

Acute flairs:  Corticosteroids  D-penicillamine (for skin changes inhibits collagen cross-linking)  Ca2+ channel blockers amlodipine, nifedipine (for raynauds)  ACEIs for renal dz + prevention of scleroderma renal crisis

*Mortality is d/t pulmonary HTN and complications of pulmonary HTN Dx: Clinical Bx (confirms): Congo red stain apple green birefringence under polarized light Seizure control Stop EtOH Then phlebotomy

Amyloidosis

Extracellular deposition of protein fibrils Dz of elderly

Tuberous sclerosis Porphyra cutanea tarda Associated w/ Hep. C

Retinal phacomas, seizures, MR, sebaceous adeomas, ash-leaf hypopigmented macules NO abd pain + red urine Vesicles on back of hand after drinking alcohol, drugs, estrogens

Lyme disease

Tick-borne Pathogen: Borrelia burgdorferi Carrier: Ixodes ticks on whitetailed deer and white-footed mice Summer months Endemic to northeast

Onset of rash w/ fever, malaise, fatigue, headache, myalgias, and/or arthralgias Primary (early-localized):  Erythema migrans (small erythematous macule/papule at tick-biting site expands slowly weeks-days)  Border macular or raised, central clearing ( bulls eye ) Secondary (early disseminated):  Migratory polyarthropathy  Neurologic phenomena (bells palsy)  Meningitis  Myocarditis rd  Conduction abnormalities (3 deg. Block) Tertiary (late disease):  Arthritis  Subacute encephalitis (memory loss + mood change)

Clinical dx of erythema migrans:  ELISA (+ = exposure)  Western Blot (confirms)  Tissure cx + PCR (not routinely done)

Early: Doxycycline CNS + arthritic:  Ceftriaxone